Ordinary Differential Equations/First Order

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==First Order Differential Equations==

The simplest types of differential equations to solve are the '''first order equations'''. These are equations where the highest derivative in the equation is the first. So, a first order equation is a function &lt;math&gt;F(x,y,y^{\prime})&lt;/math&gt;; there are no occurrences of &lt;math&gt;y^{\prime \prime}&lt;/math&gt; or higher derivatives. 

There are two easily solved types of first order equations. These are equations with '''separable variables''' and '''linear equations'''. This chapter covers how to solve and graph any equation in one of these forms, or reducible to these forms. Other types of differential equations, such as '''non-linear equations''', are not covered yet.


=== Separable First Order Differential Equations===

*[[../Separable 1|Explanation]]
*[[../Separable 2|Examples]]
*[[../Separable 3|Problems]]
*[[../Separable 4|Answers]]

=== First Order Linear Differential Equations===

*[[../First Order Linear 1|Explanation]]
*[[../First Order Linear 2|Examples]]
*[[../First Order Linear 3|Problems]]
*[[../First Order Linear 4|Answers]]

=== Exact Differential Equations===

*[[../Exact 1|Explanation]]
*[[../Exact 2|Examples]]
*[[../Exact 3|Problems]]
*[[../Exact 4|Answers]]

=== Substitution Methods===

*[[../Substitution 1|Explanation]]
*[[../Substitution 2|Examples]]
*[[../Substitution 3|Problems]]
*[[../Substitution 4|Answers]]

=== Graphing Differential Equations===
[[File:Slope_Field_2b.png|thumb|Slope field and some solutions of y'=x]]
*[[../Graphing 1|Slope Fields]]
*[[../Isoclines 1|Isoclines]]

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=== Related Books 相關書籍 ===
{{Print version}}
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* [[voy:Chinese phrasebook|Chinese Phrasebook]] (on WikiVoyage)
* [[Min Nan|Taiwanese (Southern Min / Min Nan)&lt;br /&gt;臺語（閩南語）]]
* [[Cookbook:Cuisine of China]]

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__NOTOC__
= Table of contents =
== Text / 课文 ==
=== Introduction / 介绍 ===
: [[Chinese/About Chinese|About Chinese&lt;br&gt; 中文是什么？]] {{stage short|100%|Jan 24, 2005}}
: [[Chinese/How To Use This Textbook|How to use this textbook&lt;br&gt; 如何使用这本教科书]] {{stage short|100%|Jan 24, 2005}}
: [[Chinese/How To Study Chinese|How to study Chinese&lt;br&gt; 如何学习中文]] {{stage short|100%|Jan 24, 2005}}

== Pronunciation ==
: [[Chinese/Pinyin Pronunciation|Pinyin Pronunciation Basics]] {{stage short|100%|Jan 24, 2005}}
: [[Chinese/Pronunciation of Initials|Pronunciation of Initials]] 
: [[Chinese/Pronunciation of Finals|Pronunciation of Finals]] 
: [[Chinese/Possible Initial-Final Combinations|Possible Initial-Final Combinations]] 
: [[Chinese/Using Tones|Using Tones]]

= Text / 课文 =
# [[:Chinese (Mandarin)/Lesson 1|Hello! - 第一课：你好！]] {{stage short|100%|Jan 24, 2005}}
# [[:Chinese (Mandarin)/Lesson 2|Are you busy today? - 第二课：今天你忙不忙?]] {{stage short|75%|Jan 24, 2005}}
# [[:Chinese/Lesson 3|An introduction to particles - 第三课：助词]] {{stage short|75%|Jan 24, 2005}}
# [[:Chinese (Mandarin)/Lesson 4|Word order and Verbs - 第四课：词序和动词]] {{stage short|00%|Jan 24, 2005}}
# [[:Chinese (Mandarin)/Lesson 5|Measure words/Counters - 第五课：量词]] {{stage short|75%|August 16, 2009}}
# [[:Chinese (Mandarin)/Lesson 6|More on interrogatives - 第六课：疑问助词]] {{stage short|00%|Jan 24, 2005}}
# [[:Chinese (Mandarin)/Lesson 7|What's this? - 第七课：这是什么?]] {{stage short|100%|Jan 24, 2005}}
# [[:Chinese (Mandarin)/Lesson 8|Who is she? - 第八课：她是谁?]] {{stage short|25%|Jan 24, 2005}}
# [[:Chinese (Mandarin)/Lesson 9|Where is the railway station? - 第九课：火车站在哪里？]] {{stage short|00%|Oct 5, 2008}}
# [[:Chinese (Mandarin)/Lesson 10|A telephone conversation - 第十课：电话]] {{stage short|00%|Dec 30,2009}}
# [[:Chinese (Mandarin)/Lesson 11|Taiwan&lt;br&gt;第十一课：台湾]] {{stage short|00%|Dec 30,2009}}
# [[:Chinese (Mandarin)/Lesson 12|Mandarin is so interesting!&lt;br&gt;第十二课：汉语真有趣]] {{stage short|00%|Dec 30,2009}}
# [[:Chinese (Mandarin)/Lesson 13|I'm sick&lt;br&gt;第十三课：我生病了]] {{stage short|00%|Dec 30,2009}}
# [[:Chinese (Mandarin)/Lesson 14|Drinking tea&lt;br&gt;第十四课：喝茶]] {{stage short|00%|Dec 30,2009}}
# [[:Chinese (Mandarin)/Lesson 15|China&lt;br&gt;第十五课：中国]] {{stage short|00%|Sep 12，2010}}
# [[:Chinese (Mandarin)/Lesson 16|Basic Chinese History&lt;br&gt;第十六课：基本中国历史]] {{stage short|00%|Jan 12，2012}}
# [[:Chinese (Mandarin)/Lesson 17|Basic Heteronym in Chinese&lt;br&gt;第十七课：基础多音字]] {{stage short|50%|Jul 4，2026}}

== Introduction / 介绍 ==
{{:Chinese/About Chinese}}
{{:Chinese/How To Use This Textbook}}
{{:Chinese/How To Study Chinese}}

= Pronunciation =
{{:Chinese/Pinyin Pronunciation}}
{{:Chinese/Pronunciation of Initials}}
{{:Chinese/Pronunciation of Finals}}
{{:Chinese/Using Tones}}

= Lessons / 课程 =
{{:Chinese (Mandarin)/Lesson 1}}
{{:Chinese (Mandarin)/Lesson 2}}
{{:Chinese (Mandarin)/Lesson 3}}
{{:Chinese (Mandarin)/Lesson 4}}
{{:Chinese (Mandarin)/Lesson 5}}
{{:Chinese (Mandarin)/Lesson 6}}
{{:Chinese (Mandarin)/Lesson 7}}
{{:Chinese (Mandarin)/Lesson 8}}
{{:Chinese (Mandarin)/Lesson 9}}
{{:Chinese (Mandarin)/Lesson 10}}
{{:Chinese (Mandarin)/Lesson 11}}
{{:Chinese (Mandarin)/Lesson 12}}
{{:Chinese (Mandarin)/Lesson 13}}
{{:Chinese (Mandarin)/Lesson 14}}
{{:Chinese (Mandarin)/Lesson 15}}
{{:Chinese (Mandarin)/Lesson 16}}
{{:Chinese (Mandarin)/Lesson 17}}
== Appendices / 附录 ==
{{:Chinese/Common Phrases}}
{{:Chinese/Everyday_Phrases}}
{{:Chinese (Mandarin)/Chinese-English Dictionary}}
{{:Chinese (Mandarin)/English-Chinese Dictionary}}
{{:Chinese (Mandarin)/Key to the Exercises}}
{{:Chinese (Mandarin)/Greetings}}
{{:Chinese (Mandarin)/Table of Initial-Final Combinations}}
{{:Chinese (Mandarin)/Numbers}}
{{:Chinese (Mandarin)/Nations of the World}}
{{:Chinese (Mandarin)/Radicals}}
{{:Chinese (Mandarin)/Slang}}
{{:Chinese (Mandarin)/Development History}}
{{:Chinese (Mandarin)/Contributors}}
{{:Chinese (Mandarin)/Contributor's Guide}}
{{:Chinese (Mandarin)/Planning}}

= License =
== GNU Free Documentation License ==
{{:GNU Free Documentation License}}</text>
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| Category = Salad dressing recipes
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| Time = 8 h, 10 minutes
| Rating = 1
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{{Nutrition Summary|
|ServingSize=1/12 of recipe
|Servings=12
|Cals=148
|FatCals=124
|TotalFat=1.2 g
|SatFat=0.3 g
|Cholesterol=1.3 mg
|Sodium=45.5 mg
|Carbs=0.2 g
|Fiber=0.1 g
|Sugars=0.1 g
|Protein=0.4 g
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From the original recipe contributor:&lt;blockquote&gt;''&quot;This is a recipe I created when I realized that our bottled salad dressing was frozen and couldn't thaw quickly enough. It is very easy to make from ingredients usually already on hand. You can vary the amounts, or even substitute low-fat ingredients according to your personal taste. Tastes even better when chilled over night!&quot;''&lt;/blockquote&gt;

==Ingredients==
* 1 ½ [[Cookbook:Lemon|lemons]], juiced 
* 1 [[Cookbook:Cup|cup]] freshly [[Cookbook:Grating|grated]] [[Cookbook:Parmesan Cheese|Parmesan cheese]]
* 2 [[Cookbook:Teaspoon|teaspoons]] [[Cookbook:Garlic Salt|garlic salt]]
* ¾ cup [[Cookbook:Mayonnaise|mayonnaise]]
* 1 cup [[Cookbook:Milk|milk]]

==Procedure==
# Mix together lemon juice, Parmesan cheese, garlic salt, and mayonnaise until smooth.
# Stir in milk, adjusting the amount or adding a little water, to make the dressing as thin or thick as you like.
# Cover and refrigerate 8 hours, or overnight.

==Notes, tips, and variations==
* Instead of garlic salt, crush a clove of [[Cookbook:Garlic|garlic]] and mix into the dressing with a little [[Cookbook:Salt|salt]] (to taste).

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Welcome to the '''Technical Assistance reading room'''. Get assistance on questions related to [[w:MediaWiki|MediaWiki]] markup, CSS, JavaScript, and such as they relate to Wikibooks. '''This is not a general-purpose technical support room'''.

To submit a ''bug notice or feature request'' for the MediaWiki software, visit [[phabricator:|Phabricator]].

To get more information about the ''MediaWiki software'', or to download your own copy, visit [[mw:|MediaWiki]]

There are also two IRC channels for technical help: {{Channel|mediawiki}} for issues about the software, and {{channel|mediawiki-core}} for [[m:WMF|WMF]] server or configuration issues.
{{clear}}
[[Category:Reading room]]

== Survey (proposed direction for Wishlist) ==

&lt;bdi lang=&quot;en&quot; dir=&quot;ltr&quot; class=&quot;mw-content-ltr&quot;&gt;You are invited to voice your opinion on a new [[m:Talk:Community Wishlist#Proposed direction for Wishlist|community-proposed direction]] for the [[m:Community Wishlist|Community Wishlist]]. {{Int:Feedback-thanks-title}} [[User:MediaWiki message delivery|MediaWiki message delivery]] ([[User talk:MediaWiki message delivery|discuss]] • [[Special:Contributions/MediaWiki message delivery|contribs]]) 03:07, 29 May 2026 (UTC)&lt;/bdi&gt;
&lt;!-- Message sent by User:기나ㅏㄴ@metawiki using the list at https://meta.wikimedia.org/w/index.php?title=User:%EA%B8%B0%EB%82%98%E3%85%8F%E3%84%B4/MassMessage&amp;oldid=30604233 --&gt;

== A location in a page. ==

Hi,&lt;br&gt;
A location in a page can be specified with empty span such as &lt;nowiki&gt;&lt;span id=&quot;location&quot;&gt;&lt;/span&gt;&lt;/nowiki&gt;, although not tidy. Can someone suggest another possibility or two, please?&lt;br&gt;
Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 13:22, 14 June 2026 (UTC)

:: ... &lt;a id=&quot;location&quot;&gt;&lt;/a&gt; is a little more compact than span. Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 01:56, 20 June 2026 (UTC)
::: &lt;a doesn't work but &lt;nowiki&gt;&lt;div id=&quot;location&quot;&gt;&lt;/nowiki&gt; works as in [[Oberon/System_Variants|Oberon/System_Variants]].
::: Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 15:18, 21 June 2026 (UTC)

== Template usage. ==

Hi,&lt;br&gt;
(1) A template declared in my account namespace works. Declared in the book namespace it doesn't work. Both cases are demonstrated in my [[User:PeterEasthope/sandbox]]. Declaration in the book is more direct; better not to depend upon an individual account. Ideas? Thx.

(2) If the desktop browser window is narrowed or the sandbox is viewed on a smartphone, the display is as illustrated [https://easthope.ca/WikimediaTemplate.jpg here]. How can the black perimeter frame be shrunk automatically to fit the background color boxes?

Thx,        ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 15:35, 21 June 2026 (UTC)

== Viewing unreviewed changes, and recent changes, for a particular book ==
I've recently started editing [[Chess Opening Theory]] after a long hiatus. Two things
* How can I view recent edits, for this book alone. I'm aware of [[Using_Wikibooks/How_To_Edit_A_Wikibook#Watching All Pages in a Book|Watching All Pages in a Book]], which was well hidden on the page on editing, rather than on tracking changes (since rectified), but the advice there is unhelpful. Option 1 is entirely impractical, as one cannot add hundreds of pages one does not know about, and Option 2 simply doesn't work. For example, at this moment, there are 12 relevant edits listed in the main [[Special:RecentChanges]] page (which goes back to 9 July), but the suggested [https://en.wikibooks.org/wiki/Special:RecentChangesLinked/Chess_Opening_Theory Related Changes] only lists pages directly linked from the top level.
* Similarly, how can one see the unreviewed changes for this book (or even all the books, where I can at least manually filter). I noticed a whole lot going back more than a month and approved most of them, but this was only through some tedious digging around through user contributions and page histories.
**Partially answering this question myself, there's [https://en.wikibooks.org/w/index.php?title=Special%3APendingChanges&amp;namespace=&amp;tagFilter=&amp;limit=50&amp;category=&amp;size= this page]. Which brings up a followup question. My contributions page doesn't list the changes I've approved (only the one I declined). Is there a way to see these? [[User:Greenman|Greenman]] ([[User talk:Greenman|discuss]] • [[Special:Contributions/Greenman|contribs]]) 21:38, 13 July 2026 (UTC)
Thanks! [[User:Greenman|Greenman]] ([[User talk:Greenman|discuss]] • [[Special:Contributions/Greenman|contribs]]) 21:29, 13 July 2026 (UTC)

:At the risk of sounding pedantic, a hack for the first problem whereby [[Special:RecentChangesLinked/Chess_Opening_Theory]] only shows changes that are linked to the top page of the book directly and not all sub-pages or sub-sub-sub-pages, etc. is to just make them all linked from the top page. This can be done with a template that may make it a little more pretty or discreet than a huge list of links. ―[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''&lt;span style=&quot;color:black&quot;&gt;v&lt;/span&gt;f&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:53, 14 July 2026 (UTC)
::Thanks, but this doesn't really help. Besides having to add thousands of links to the front page, which certainly shouldn't be displayed there, when someone adds a new variation (which is what a large portion of the edits are), the new entry won't appear on Recent Changes until specifically linked from the front page. [[User:Greenman|Greenman]] ([[User talk:Greenman|discuss]] • [[Special:Contributions/Greenman|contribs]]) 17:23, 15 July 2026 (UTC)
:@[[User:Greenman|Greenman]] I think using the book categories at [[Special:UnreviewedPages]] might be helpful here—is [https://en.wikibooks.org/w/index.php?title=Special%3AUnreviewedPages&amp;namespace=0&amp;category=Book%3AChess+Opening+Theory this] approximately what you're looking for? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:24, 16 July 2026 (UTC)</text>
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      <text bytes="6964" sha1="39pa6pzkw7k5s35matp4uozw2vdyu8s" xml:space="preserve">__NEWSECTIONLINK__ {{Discussion Rooms}} {{Shortcut|WB:TECH}} {{TOC left}}
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Welcome to the '''Technical Assistance reading room'''. Get assistance on questions related to [[w:MediaWiki|MediaWiki]] markup, CSS, JavaScript, and such as they relate to Wikibooks. '''This is not a general-purpose technical support room'''.

To submit a ''bug notice or feature request'' for the MediaWiki software, visit [[phabricator:|Phabricator]].

To get more information about the ''MediaWiki software'', or to download your own copy, visit [[mw:|MediaWiki]]

There are also two IRC channels for technical help: {{Channel|mediawiki}} for issues about the software, and {{channel|mediawiki-core}} for [[m:WMF|WMF]] server or configuration issues.
{{clear}}
[[Category:Reading room]]

== Survey (proposed direction for Wishlist) ==

&lt;bdi lang=&quot;en&quot; dir=&quot;ltr&quot; class=&quot;mw-content-ltr&quot;&gt;You are invited to voice your opinion on a new [[m:Talk:Community Wishlist#Proposed direction for Wishlist|community-proposed direction]] for the [[m:Community Wishlist|Community Wishlist]]. {{Int:Feedback-thanks-title}} [[User:MediaWiki message delivery|MediaWiki message delivery]] ([[User talk:MediaWiki message delivery|discuss]] • [[Special:Contributions/MediaWiki message delivery|contribs]]) 03:07, 29 May 2026 (UTC)&lt;/bdi&gt;
&lt;!-- Message sent by User:기나ㅏㄴ@metawiki using the list at https://meta.wikimedia.org/w/index.php?title=User:%EA%B8%B0%EB%82%98%E3%85%8F%E3%84%B4/MassMessage&amp;oldid=30604233 --&gt;

== A location in a page. ==

Hi,&lt;br&gt;
A location in a page can be specified with empty span such as &lt;nowiki&gt;&lt;span id=&quot;location&quot;&gt;&lt;/span&gt;&lt;/nowiki&gt;, although not tidy. Can someone suggest another possibility or two, please?&lt;br&gt;
Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 13:22, 14 June 2026 (UTC)

:: ... &lt;a id=&quot;location&quot;&gt;&lt;/a&gt; is a little more compact than span. Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 01:56, 20 June 2026 (UTC)
::: &lt;a doesn't work but &lt;nowiki&gt;&lt;div id=&quot;location&quot;&gt;&lt;/nowiki&gt; works as in [[Oberon/System_Variants|Oberon/System_Variants]].
::: Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 15:18, 21 June 2026 (UTC)

== Template usage. ==

Hi,&lt;br&gt;
(1) A template declared in my account namespace works. Declared in the book namespace it doesn't work. Both cases are demonstrated in my [[User:PeterEasthope/sandbox]]. Declaration in the book is more direct; better not to depend upon an individual account. Ideas? Thx.

(2) If the desktop browser window is narrowed or the sandbox is viewed on a smartphone, the display is as illustrated [https://easthope.ca/WikimediaTemplate.jpg here]. How can the black perimeter frame be shrunk automatically to fit the background color boxes?

Thx,        ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 15:35, 21 June 2026 (UTC)

== Viewing unreviewed changes, and recent changes, for a particular book ==
I've recently started editing [[Chess Opening Theory]] after a long hiatus. Two things
* How can I view recent edits, for this book alone. I'm aware of [[Using_Wikibooks/How_To_Edit_A_Wikibook#Watching All Pages in a Book|Watching All Pages in a Book]], which was well hidden on the page on editing, rather than on tracking changes (since rectified), but the advice there is unhelpful. Option 1 is entirely impractical, as one cannot add hundreds of pages one does not know about, and Option 2 simply doesn't work. For example, at this moment, there are 12 relevant edits listed in the main [[Special:RecentChanges]] page (which goes back to 9 July), but the suggested [https://en.wikibooks.org/wiki/Special:RecentChangesLinked/Chess_Opening_Theory Related Changes] only lists pages directly linked from the top level.
* Similarly, how can one see the unreviewed changes for this book (or even all the books, where I can at least manually filter). I noticed a whole lot going back more than a month and approved most of them, but this was only through some tedious digging around through user contributions and page histories.
**Partially answering this question myself, there's [https://en.wikibooks.org/w/index.php?title=Special%3APendingChanges&amp;namespace=&amp;tagFilter=&amp;limit=50&amp;category=&amp;size= this page]. Which brings up a followup question. My contributions page doesn't list the changes I've approved (only the one I declined). Is there a way to see these? [[User:Greenman|Greenman]] ([[User talk:Greenman|discuss]] • [[Special:Contributions/Greenman|contribs]]) 21:38, 13 July 2026 (UTC)
Thanks! [[User:Greenman|Greenman]] ([[User talk:Greenman|discuss]] • [[Special:Contributions/Greenman|contribs]]) 21:29, 13 July 2026 (UTC)

:At the risk of sounding pedantic, a hack for the first problem whereby [[Special:RecentChangesLinked/Chess_Opening_Theory]] only shows changes that are linked to the top page of the book directly and not all sub-pages or sub-sub-sub-pages, etc. is to just make them all linked from the top page. This can be done with a template that may make it a little more pretty or discreet than a huge list of links. ―[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''&lt;span style=&quot;color:black&quot;&gt;v&lt;/span&gt;f&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:53, 14 July 2026 (UTC)
::Thanks, but this doesn't really help. Besides having to add thousands of links to the front page, which certainly shouldn't be displayed there, when someone adds a new variation (which is what a large portion of the edits are), the new entry won't appear on Recent Changes until specifically linked from the front page. [[User:Greenman|Greenman]] ([[User talk:Greenman|discuss]] • [[Special:Contributions/Greenman|contribs]]) 17:23, 15 July 2026 (UTC)
:@[[User:Greenman|Greenman]] I think using the book categories at [[Special:UnreviewedPages]] might be helpful here—is [https://en.wikibooks.org/w/index.php?title=Special%3AUnreviewedPages&amp;namespace=0&amp;category=Book%3AChess+Opening+Theory this] approximately what you're looking for? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:24, 16 July 2026 (UTC)
::@[[User:Greenman|Greenman]] I think you're also looking for [[Special:Log/review]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:32, 16 July 2026 (UTC)</text>
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{{ombox|type=content|text='''To request a rename or usurpation''', go to the global request page at Meta [[meta:SRUC|here]].&lt;br /&gt;''Please do not post those requests here!''}}
{{Clear}}
Welcome to the '''Administrative Assistance reading room'''.  You can request assistance from [[WB:ADMIN|administrators]] for handling a variety of problems here and alert them about problems which may require special actions not normally used during regular content editing. Please be patient as administrators are often quite busy with either their own projects or trying to perform general maintenance and cleanup.

You can deal with most vandalism yourself: [[Wikibooks:Dealing with vandalism|fix it]], then [[Wikibooks:Templates/User_notices|warn the user]]. If there is repeated vandalism by one user, lots of vandalism on a single page, or vandalism from many users, tell an admin here, or in [irc://irc.freenode.net/wikibooks #wikibooks] (say &lt;code&gt;!admin&lt;/code&gt; to get attention).

For more general questions and assistance that doesn't require an administrator, please use the [[WB:HELP|Assistance Reading Room]].
{{clear}}

[[Category:Reading room]]

== Emirati yahzota reported by MathXplore ==

* {{userlinks|Emirati yahzota}}

Long-term abuse, [[:w:Wikipedia:Sockpuppet investigations/Muhammad Ali Rajab]] &lt;!-- USERREPORTED:/Emirati yahzota/ --&gt; [[User:MathXplore|MathXplore]] ([[User talk:MathXplore|discuss]] • [[Special:Contributions/MathXplore|contribs]]) 12:18, 2 July 2026 (UTC)

:I deleted their page addition. @[[User:MarcGarver|MarcGarver]] could we get a CU here? Thanks! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:28, 3 July 2026 (UTC)
::Nothing to see on CU. [[User:MarcGarver|MarcGarver]] ([[User talk:MarcGarver|discuss]] • [[Special:Contributions/MarcGarver|contribs]]) 11:07, 13 July 2026 (UTC)

== Protecting Pages ==

Hello, Admins,

My name is Kayden Swanson, and I have proudly created ''[[The Geoguide]].'' But I would like to remove the ability for fellow users to edit it to prevent vandalism and preserve my prized creation I have made for school. Could you permanently lock it so others cant edit it while I still can? [[User:Kayden Swanson|Kayden Swanson]] ([[User talk:Kayden Swanson|discuss]] • [[Special:Contributions/Kayden Swanson|contribs]]) 02:41, 6 July 2026 (UTC)

:Hi @[[User:Kayden Swanson|Kayden Swanson]]! Unfortunately, that is not an appropriate justification for protecting a page here at Wikibooks per the [[Wikibooks:Protection policy|protection policy]]. Notably, {{tq|&quot;Preemptive full protection of pages is contrary to the open nature of Wikibooks&quot;}}. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:15, 6 July 2026 (UTC)
::NOOOOOOOOOOOOOOOOOOOOOOOOOOOOO okay that's fine  [[User:Kayden Swanson|Kayden Swanson]] ([[User talk:Kayden Swanson|discuss]] • [[Special:Contributions/Kayden Swanson|contribs]]) 00:26, 8 July 2026 (UTC)
::: I'm sorry, but that's not within the scope of the protection policy. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 12:39, 8 July 2026 (UTC)
:::If you really want a stable version, you can make a PDF of the existing content and link it. See [[Help:Print versions]] and {{tl|Print version}}/{{tl|PDF version}}. ―[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''&lt;span style=&quot;color:black&quot;&gt;v&lt;/span&gt;f&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 19:15, 10 July 2026 (UTC)

== Prudhvifmsdh reported by MathXplore ==

* {{userlinks|Prudhvifmsdh}}

Spam &lt;!-- USERREPORTED:/Prudhvifmsdh/ --&gt; [[User:MathXplore|MathXplore]] ([[User talk:MathXplore|discuss]] • [[Special:Contributions/MathXplore|contribs]]) 12:39, 8 July 2026 (UTC)
: {{done}}. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 13:07, 8 July 2026 (UTC)

== I'm unable to create a page ==

Hello, I wanted to created the page [[English in Use/Agreement]]. I thought I would use a modified version of a Wikipedia article (https://en.wikipedia.org/wiki/Agreement_in_the_English_language). It's already written like a textbook, so I did some improvements and clicked &quot;published&quot;, but I got the error:

&lt;blockquote&gt;Welcome to Wikibooks!Your edit has triggered an automated filter and has been disallowed. It looks like your edit has added a large amount of content to this page.If you copied the content from another website, please do not add it without rewriting it in your own words. Unless the content is in the public domain (published before 1923), it is almost certainly copyrighted and cannot be added to Wikibooks.If all of the content is your own work and you cannot find anything to link, feel free to ask for the edit to be performed at the reading room. If you have received this message in error, you may report it here.&lt;/blockquote&gt;

What should I do? Can you help me? [[User:Justtocreateapage|Justtocreateapage]] ([[User talk:Justtocreateapage|discuss]] • [[Special:Contributions/Justtocreateapage|contribs]]) 20:43, 10 July 2026 (UTC)

:@[[User:Justtocreateapage|Justtocreateapage]] An editfilter is preventing your edit. In my opinion, you did not do anything wrong and the filter is wrong, but an admin (=not me) would need to fix it. [[User:Der-Wir-Ing|Der-Wir-Ing]] ([[User talk:Der-Wir-Ing|discuss]] • [[Special:Contributions/Der-Wir-Ing|contribs]]) 20:52, 10 July 2026 (UTC)
:: {{re|Justtocreateapage}} As a new user you face harsher requirements. You should make useful edits to Wikibooks first. If you want to use a modified version of a WP article, [[Wikibooks: Requests for import|requesting an import]] is the proper venue. This [[Help: Importing|preserves the edit history]]. ‑‑[[User:Kai Burghardt|Kai Burghardt]] ([[User talk:Kai Burghardt|discuss]] • [[Special:Contributions/Kai Burghardt|contribs]]) 21:15, 10 July 2026 (UTC)
:::Okay, thanks you all. I'll request for an import then [[User:Justtocreateapage|Justtocreateapage]] ([[User talk:Justtocreateapage|discuss]] • [[Special:Contributions/Justtocreateapage|contribs]]) 21:39, 10 July 2026 (UTC)
::::{{done}} ―[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''&lt;span style=&quot;color:black&quot;&gt;v&lt;/span&gt;f&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 21:50, 10 July 2026 (UTC)

== Unprotection/edit request ==

Hi, would an admin please temporarily unprotect the non-MediaWiki pages at [[User:TenshiBot/Errors]]? As for the MediaWiki pages, would an admin go through them and replace the &lt;nowiki&gt;&lt;center&gt;&lt;/nowiki&gt; tags and replace it with &lt;nowiki&gt;&lt;div style=&quot;text-align: center&quot;&gt;&lt;/nowiki&gt;? [[User:Tenshi Hinanawi|Tenshi Hinanawi]] ([[User talk:Tenshi Hinanawi|discuss]] • [[Special:Contributions/Tenshi Hinanawi|contribs]]) 23:10, 11 July 2026 (UTC)
: Unprotecting, fixing, and protecting back would take too long—I know just the thing, which is using JWB. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 02:35, 12 July 2026 (UTC)
: [[User:Tenshi Hinanawi|Tenshi Hinanawi]], I've done what JWB could process; should there be way more in your bot's error log, let me know. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:02, 12 July 2026 (UTC)
::There's still a lot of the &lt;nowiki&gt;&lt;font&gt;&lt;/nowiki&gt; tags which need replacing in the talk page archives. [[User:Tenshi Hinanawi|Tenshi Hinanawi]] ([[User talk:Tenshi Hinanawi|discuss]] • [[Special:Contributions/Tenshi Hinanawi|contribs]]) 10:11, 12 July 2026 (UTC)
::: I can replace those, but should it be &lt;code&gt;div&lt;/code&gt; or &lt;code&gt;span&lt;/code&gt;? [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 14:35, 12 July 2026 (UTC)
::::Span, though the font tag's parameters need to be converted as well, see [https://github.com/TenshiSWR/TenshiBot/blob/958b59d1a5e14a31ab8b46f66db54ebdba63e101/tasks/linterrors/obsolete_HTML_tags.py#L15-L52 the code] and the [https://html.spec.whatwg.org/multipage/rendering.html#:~:text=When%20a%20font%20element%20has%20a%20color,%27color%27%20property%20to%20the%20resulting%20color. HTML spec] for this. [[User:Tenshi Hinanawi|Tenshi Hinanawi]] ([[User talk:Tenshi Hinanawi|discuss]] • [[Special:Contributions/Tenshi Hinanawi|contribs]]) 14:56, 12 July 2026 (UTC)
== NSSGGuarding reported by MathXplore ==

* {{userlinks|NSSGGuarding}}

Spam &lt;!-- USERREPORTED:/NSSGGuarding/ --&gt; [[User:MathXplore|MathXplore]] ([[User talk:MathXplore|discuss]] • [[Special:Contributions/MathXplore|contribs]]) 12:17, 13 July 2026 (UTC)

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      <sha1>gjf7scdlrhpizk3akelplx448tshep1</sha1>
    </revision>
  </page>
  <page>
    <title>Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nc3</title>
    <ns>0</ns>
    <id>182938</id>
    <revision>
      <id>4654687</id>
      <parentid>3279617</parentid>
      <timestamp>2026-07-16T15:04:50Z</timestamp>
      <contributor>
        <username>Greenman</username>
        <id>7490</id>
      </contributor>
      <comment>/* Caro-Kann Defence - Advance Variation */ title</comment>
      <origin>4654687</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="2063" sha1="qh31npere0bri7l4hsvt3pjlrlpdvzd" xml:space="preserve">{{Chess Opening Theory/Position|=
|Caro-Kann Defence - Advance Variation|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |pd|pd|pd|pd|=
   |  |  |pd|  |  |  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
||
}}
=Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=

A sounder response than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Bd3]], and more ambitious than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Nf3]], 4. Nc3 has helped revitalize the Advance Variation of the Caro-Kann.

It is almost always met with 4...e6, with black aiming ultimately to play c5.

==Theory table==
{{Chess Opening Theory/Table}}.

'''1.e4 c6 2.d4 d5 3.e5 Bf5 4.Nc3'''
&lt;table border=&quot;0&quot; cellspacing=&quot;0&quot; cellpadding=&quot;4&quot;&gt;
	&lt;tr&gt;
		&lt;th&gt;&lt;/th&gt;
                &lt;th align=&quot;left&quot;&gt;4&lt;/th&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...e6|e6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Qb6|Qb6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...a6|a6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...h5|h5]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Qd7|Qd7]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...h6|h6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Qc8|Qc8]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...a5|a5]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...c5|c5]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Nd7|Nd7]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...b5|b5]]&lt;/td&gt;
	&lt;/tr&gt;

&lt;/table&gt;

{{ChessMid}}

==References==
{{reflist}}
{{Wikipedia|Caro-Kann}}
* Nunn's Chess Openings. 1999. [[w:John Nunn|John Nunn]] (Editor), Graham Burgess, John Emms, Joe Gallagher. {{ISBN|1-8574-4221-0}}.
* Modern Chess Openings: MCO-14. 1999. [[w:Nick de Firmian|Nick de Firmian]], [[w:Walter Korn|Walter Korn]]. {{ISBN|0-8129-3084-3}}.
{{BCO2}}
{{Chess Opening Theory/Footer}}


{{ChessStub}}</text>
      <sha1>qh31npere0bri7l4hsvt3pjlrlpdvzd</sha1>
    </revision>
    <revision>
      <id>4654688</id>
      <parentid>4654687</parentid>
      <timestamp>2026-07-16T15:06:45Z</timestamp>
      <contributor>
        <username>Greenman</username>
        <id>7490</id>
      </contributor>
      <comment>expand</comment>
      <origin>4654688</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="2178" sha1="a0d0txkxn0z8maafc32n43xf18jvift" xml:space="preserve">{{Chess Opening Theory/Position|=
|Caro-Kann Defence - Advance Variation|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |pd|pd|pd|pd|=
   |  |  |pd|  |  |  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
||
}}
=Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=

A sounder response than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Bd3]], and more ambitious than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Nf3]], 4. Nc3 has helped revitalize the Advance Variation of the Caro-Kann.

White usually plans to harass Black's bishop with g4 and h4-h5, and Nc3 takes away the e4 square from the bishop.

It is almost always met with 4...e6, with black aiming ultimately to play c5.

==Theory table==
{{Chess Opening Theory/Table}}.

'''1.e4 c6 2.d4 d5 3.e5 Bf5 4.Nc3'''
&lt;table border=&quot;0&quot; cellspacing=&quot;0&quot; cellpadding=&quot;4&quot;&gt;
	&lt;tr&gt;
		&lt;th&gt;&lt;/th&gt;
                &lt;th align=&quot;left&quot;&gt;4&lt;/th&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...e6|e6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Qb6|Qb6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...a6|a6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...h5|h5]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Qd7|Qd7]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...h6|h6]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Qc8|Qc8]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...a5|a5]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...c5|c5]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...Nd7|Nd7]]&lt;/td&gt;
	&lt;/tr&gt;
	&lt;tr&gt;
		&lt;th align=&quot;right&quot;&gt;&lt;/th&gt;
		&lt;td&gt;[[/4...b5|b5]]&lt;/td&gt;
	&lt;/tr&gt;

&lt;/table&gt;

{{ChessMid}}

==References==
{{reflist}}
{{Wikipedia|Caro-Kann}}
* Nunn's Chess Openings. 1999. [[w:John Nunn|John Nunn]] (Editor), Graham Burgess, John Emms, Joe Gallagher. {{ISBN|1-8574-4221-0}}.
* Modern Chess Openings: MCO-14. 1999. [[w:Nick de Firmian|Nick de Firmian]], [[w:Walter Korn|Walter Korn]]. {{ISBN|0-8129-3084-3}}.
{{BCO2}}
{{Chess Opening Theory/Footer}}


{{ChessStub}}</text>
      <sha1>a0d0txkxn0z8maafc32n43xf18jvift</sha1>
    </revision>
    <revision>
      <id>4654689</id>
      <parentid>4654688</parentid>
      <timestamp>2026-07-16T15:11:49Z</timestamp>
      <contributor>
        <username>Greenman</username>
        <id>7490</id>
      </contributor>
      <comment>/* Theory table */ Update templates</comment>
      <origin>4654689</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="1496" sha1="laz47kcm25b8i19afgspul4zo63esuo" xml:space="preserve">{{Chess Opening Theory/Position|=
|Caro-Kann Defence - Advance Variation|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |pd|pd|pd|pd|=
   |  |  |pd|  |  |  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
||
}}
=Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=

A sounder response than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Bd3]], and more ambitious than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Nf3]], 4. Nc3 has helped revitalize the Advance Variation of the Caro-Kann.

White usually plans to harass Black's bishop with g4 and h4-h5, and Nc3 takes away the e4 square from the bishop.

It is almost always met with 4...e6, with black aiming ultimately to play c5.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=4... e6
|eval1=

|name2=
|line2=4... Qb6
|eval2=

|name3=
|line3=4... a6
|eval3=

|name4=
|line4=4... h5
|eval4=

|name5=
|line5=4... Qd7
|eval5=
}}

{{ChessMid}}
{{Wikipedia|Panov-Botvinnik Attack}}

==References==
{{reflist}}
{{Wikipedia|Caro-Kann}}
* Nunn's Chess Openings. 1999. [[w:John Nunn|John Nunn]] (Editor), Graham Burgess, John Emms, Joe Gallagher. {{ISBN|1-8574-4221-0}}.
* Modern Chess Openings: MCO-14. 1999. [[w:Nick de Firmian|Nick de Firmian]], [[w:Walter Korn|Walter Korn]]. {{ISBN|0-8129-3084-3}}.
{{BCO2}}
{{Chess Opening Theory/Footer}}


{{ChessStub}}</text>
      <sha1>laz47kcm25b8i19afgspul4zo63esuo</sha1>
    </revision>
    <revision>
      <id>4654692</id>
      <parentid>4654689</parentid>
      <timestamp>2026-07-16T15:16:24Z</timestamp>
      <contributor>
        <username>Greenman</username>
        <id>7490</id>
      </contributor>
      <comment>templates</comment>
      <origin>4654692</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="1443" sha1="4k7ab1x7q71myqko4cfwfmo29856a3f" xml:space="preserve">{{Chess Opening Theory/Position|=
|Caro-Kann Defence - Advance Variation|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |pd|pd|pd|pd|=
   |  |  |pd|  |  |  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
||
}}
=Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=

A sounder response than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Bd3]], and more ambitious than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Nf3]], 4. Nc3 has helped revitalize the Advance Variation of the Caro-Kann.

White usually plans to harass Black's bishop with g4 and h4-h5, and Nc3 takes away the e4 square from the bishop.

It is almost always met with 4...e6, with black aiming ultimately to play c5.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=4... e6
|eval1=

|name2=
|line2=4... Qb6
|eval2=

|name3=
|line3=4... a6
|eval3=

|name4=
|line4=4... h5
|eval4=

|name5=
|line5=4... Qd7
|eval5=
}}

{{ChessMid}}

==References==
{{reflist}}
{{Wikipedia|Caro-Kann}}
* Nunn's Chess Openings. 1999. [[w:John Nunn|John Nunn]] (Editor), Graham Burgess, John Emms, Joe Gallagher. {{ISBN|1-8574-4221-0}}.
* Modern Chess Openings: MCO-14. 1999. [[w:Nick de Firmian|Nick de Firmian]], [[w:Walter Korn|Walter Korn]]. {{ISBN|0-8129-3084-3}}.
{{BCO2}}
{{Chess Opening Theory/Footer}}</text>
      <sha1>4k7ab1x7q71myqko4cfwfmo29856a3f</sha1>
    </revision>
    <revision>
      <id>4654695</id>
      <parentid>4654692</parentid>
      <timestamp>2026-07-16T15:26:23Z</timestamp>
      <contributor>
        <username>Greenman</username>
        <id>7490</id>
      </contributor>
      <comment>/* Caro-Kann Defence - Advance Variation, Van Der Wiel Attack */ MOS</comment>
      <origin>4654695</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="1453" sha1="8drdrrbb6vq4hqtz0he3h7xqevg48v8" xml:space="preserve">{{Chess Opening Theory/Position|=
|Caro-Kann Defence - Advance Variation|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |pd|pd|pd|pd|=
   |  |  |pd|  |  |  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
||
}}
=5. Nc3 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=

A sounder response than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Bd3]], and more ambitious than [[Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nf3|4. Nf3]], 4. Nc3 has helped revitalize the Advance Variation of the Caro-Kann.

White usually plans to harass Black's bishop with g4 and h4-h5, and Nc3 takes away the e4 square from the bishop.

It is almost always met with 4...e6, with black aiming ultimately to play c5.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=4... e6
|eval1=

|name2=
|line2=4... Qb6
|eval2=

|name3=
|line3=4... a6
|eval3=

|name4=
|line4=4... h5
|eval4=

|name5=
|line5=4... Qd7
|eval5=
}}

{{ChessMid}}

==References==
{{reflist}}
{{Wikipedia|Caro-Kann}}
* Nunn's Chess Openings. 1999. [[w:John Nunn|John Nunn]] (Editor), Graham Burgess, John Emms, Joe Gallagher. {{ISBN|1-8574-4221-0}}.
* Modern Chess Openings: MCO-14. 1999. [[w:Nick de Firmian|Nick de Firmian]], [[w:Walter Korn|Walter Korn]]. {{ISBN|0-8129-3084-3}}.
{{BCO2}}
{{Chess Opening Theory/Footer}}</text>
      <sha1>8drdrrbb6vq4hqtz0he3h7xqevg48v8</sha1>
    </revision>
  </page>
  <page>
    <title>OpenClinica User Manual</title>
    <ns>0</ns>
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      <id>4654723</id>
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      <contributor>
        <username>GerbenRienk</username>
        <id>339385</id>
      </contributor>
      <minor />
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      <text bytes="1173" sha1="sc4juj8aoy9adwz23ed5d0oni9c3gd5" xml:space="preserve">{{OpenClinica_User_Manual/Templates:Content}}

== About this book==
This book is an unofficial voluntary work done by [[/Authors|OpenClinica users]].

=== Introduction ===
OpenClinica is open source clinical trial software used for Electronic Data Capture (EDC) in clinical research. This book contains a series of guides to help users learn how to use OpenClinica for clinical data management. It was used since 2003 by many organisations, especially in the academic and non-profit sector. In 2015 the company OpenClinica LLC announced that it would no longer update the software. 

A group of dedicated users decided to make a fork of the code and launched [https://libreclinica.org/ LibreClinica] Almost all information found here can be applied to LibreClinica as well.

A list of available versions of openclinica can be found [https://distros.openclinica.com/ here].
==== Installing OpenClinica Community edition ====
The software download includes installation instructions, but for those in difficulty, this manual includes an [[OpenClinica_User_Manual/InstallationCheckList|Installation checklist]].

{{Alphabetical|O}}
{{Shelves|Business software}}
{{status|25%}}</text>
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  </page>
  <page>
    <title>Aros/User/Applications</title>
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        <id>301139</id>
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      <minor />
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==Introduction==


[[#Graphical Image Editing Art]]
[[#Office Application]]
[[#Audio]]

[[#Misc Application]]
[[#Games &amp; Emulation]]

[[#Application Guides]]

[[#top|...to the top]]


[[#top|...to the top]]

Most apps can be opened on the Workbench (aka publicscreen pubscreen) which is the default display option but can offer a custom one set to your configurations (aka custom screen mode promotion). These custom ones tend to stack so the possible use of A-M/A-N method of switching between full screens and the ability to pull down screens as well 

If you are interested in creating or porting new software, see [http://en.wikibooks.org/wiki/Aros/Developer/Docs here]

{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Internet Applications 
!width:10%;|AROS(x86)
!width:10%;|Commodore-Amiga OS 3.1 (68k)
!width:10%;|Hyperion OS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;Web Online Browser [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=network/browser Odyssey 2.0], [https://www.arosworld.org/infusions/forum/viewthread.php?thread_id=1175&amp;highlight=odyssey&amp;rowstart=100 Odyssey 3.0], 
|&lt;!--Amiga OS--&gt;[https://aminet.net/comm/www Amelinium], [https://blog.alb42.de/programs/amifox/ amifox] with [https://github.com/alb42/wrp wrp server], IBrowse*, Voyager*, [https://github.com/amigazen/aweb3/ AWeb 3.6 src], [https://github.com/matjam/aweb AWeb Src], [http://aminet.net/package/comm/www/NetSurf-m68k-sources Netsurf], [], 
|&lt;!--AmigaOS4--&gt;[ Odyssey OWB], [ Timberwolf (Firefox port 2011)], [http://amigaworld.net/modules/newbb/viewtopic.php?forum=32&amp;topic_id=32847 OWB-mui], [http://strohmayer.org/owb/ OWB-Reaction], IBrowse*, [http://os4depot.net/index.php?function=showfile&amp;file=network/browser/aweb.lha AWeb], Voyager, [http://www.os4depot.net/index.php?function=browse&amp;cat=network/browser Netsurf], 
|&lt;!--MorphOS--&gt;Wayfarer, [http://fabportnawak.free.fr/owb/ Odyssey OWB], [ Netsurf], IBrowse*, AWeb, [], 
|-
|&lt;!--Sub Menu--&gt;YouTube, Dailymotion website downloading videos audio [https://github.com/yt-dlp/yt-dlp yt-dlp], [],  
|&lt;!--AROS--&gt;[], [https://blog.alb42.de/amitube/ Amitube], 
|&lt;!--Amiga OS--&gt;[https://blog.alb42.de/amitube/ Amitube], [ smtube], 
|&lt;!--AmigaOS4--&gt;[https://blog.alb42.de/amitube/ Amitube], getVideo, Tubexx, [https://github.com/walkero-gr/aiostreams aiostreams], 
|&lt;!--MorphOS--&gt;[ ytsearch], [https://blog.alb42.de/amitube/ Amitube], [http://morphos.lukysoft.cz/en/vypis.php?kat=5 getVideo], Tubexx 
|-
|&lt;!--Sub Menu--&gt;E-mailing SMTP POP3 IMAP based 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=network/email SimpleMail], [http://sourceforge.net/projects/simplemail/files/ src], [https://github.com/jens-maus/yam YAM] 
|&lt;!--Amiga OS--&gt;[http://sourceforge.net/projects/simplemail/files/ SimpleMail], [https://github.com/jens-maus/yam YAM]
|&lt;!--AmigaOS4--&gt;SimpleMail, YAM, 
|&lt;!--MorphOS--&gt; SimpleMail, YAM
|-
|&lt;!--Sub Menu--&gt;IRC 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=network/chat WookieChat], [https://sourceforge.net/projects/wookiechat/ Wookiechat src], [http://archives.arosworld.org/index.php?function=browse&amp;cat=network/chat AiRcOS], Jabberwocky, 
|&lt;!--Amiga OS--&gt;Wookiechat, AmIRC 
|&lt;!--AmigaOS4--&gt;Wookiechat 
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=5 Wookiechat], [http://morphos.lukysoft.cz/en/vypis.php?kat=5 AmIRC], 
|-
|&lt;!--Sub Menu--&gt;Instant Messaging IM like [https://github.com/BlitterStudio/amidon Hollywood lang based Mastodon client], BlueSky AT protocol, Facebook(TM), Twitter X (TM), Bitlbee IRC Gateway and others 
|&lt;!--AROS--&gt;[https://github.com/kaffeine1/telegram-amiga telegram-amiga], [http://archives.arosworld.org/index.php?function=browse&amp;cat=network/chat jabberwocky], 
|&lt;!--Amiga OS--&gt;[http://amitwitter.sourceforge.net/ AmiTwitter], CLIMM, SabreMSN, jabberwocky, 
|&lt;!--AmigaOS4--&gt;[http://amitwitter.sourceforge.net/ AmiTwitter], SabreMSN,
|&lt;!--MorphOS--&gt;[http://amitwitter.sourceforge.net/ AmiTwitter], [http://morphos.lukysoft.cz/en/vypis.php?kat=5 PolyglotNG], SabreMSN,
|-
|&lt;!--Sub Menu--&gt;Torrents 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=network/p2p ArTorr], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;CTorrent, Transmission 
|&lt;!--MorphOS--&gt;MLDonkey, Beehive, [http://morphos.lukysoft.cz/en/vypis.php?kat=5 Transmission], CTorrent, 
|-
|&lt;!--Sub Menu--&gt;FTP 
|&lt;!--AROS--&gt;Plugin included with Dopus Magellan, MarranoFTP, 
|&lt;!--Amiga OS--&gt;[http://aminet.net/package/comm/tcp/AmiFTP AmiFTP], AmiTradeCenter, ncFTP, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=5 Pftp], [http://aminet.net/package/comm/tcp/AmiFTP-1.935-OS4 AmiFTP], 
|-
|&lt;!--Sub Menu--&gt;WYSIWYG Web Site Editor
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Internet Radio Streaming Audio [http://www.gnu.org/software/gnump3d/ gnump3d], [http://www.icecast.org/ Icecast2] Server (Broadcast) and Client (Listen), [ mpd], [http://darkice.sourceforge.net/ DarkIce], [http://www.dyne.org/software/muse/ Muse], 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=audio/misc ], Mplayer (Icecast Client only), 
|&lt;!--Amiga OS--&gt;[https://github.com/sandlbn/TuneFinder TuneFinder C Src], [https://github.com/sandlbn/TuneFinderMUI TuneFinderMUI], [http://amigazeux.net/anr/ AmiNetRadio], [], [], 
|&lt;!--AmigaOS4--&gt;[http://www.tunenet.co.uk/ Tunenet], 
|&lt;!--MorphOS--&gt;Mplayer, AmiNetRadio, 
|-
|&lt;!--Sub Menu--&gt;VoIP (Voice over IP) with SIP Client (Session Initiation Protocol) or Asterisk IAX2 Clients Softphone (skype like) 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;AmiPhone with Speak Freely, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Weather Forecast 
|&lt;!--AROS--&gt;[http://sourceforge.net/projects/zunetools/files/ WeatherBar], [http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/workbench AWeather], []
|&lt;!--Amiga OS--&gt;[http://amigazeux.net/wetter/ Wetter], [https://github.com/emartisoft/AmiWeatherForecasts AmiWeatherForecasts src], 
|&lt;!--AmigaOS4--&gt;[http://os4depot.net/?function=showfile&amp;file=utility/workbench/flipclock.lha FlipClock], 
|&lt;!--MorphOS--&gt;[http://amigazeux.net/wetter/ Wetter], 
|-
|&lt;!--Sub Menu--&gt;Street Road Maps Route Planning GPS Tracking  
|&lt;!--AROS--&gt;[https://blog.alb42.de/programs/muimapparium/ MuiMapparium] [https://build.alb42.de/ Build of MuiMapp versions], 
|&lt;!--Amiga OS--&gt;AmiAtlas*, UKRoutePlus*, [http://blog.alb42.de/ AmOSM], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;[http://blog.alb42.de/programs/mapparium/ Mapparium], 
|-
|&lt;!--Sub Menu--&gt;Clock and Date setting from the internet (either ntp or websites) [https://www.timeanddate.com/worldclock/ World Clock], [http://www.time.gov/ NIST], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=network/misc ntpsync],  
|&lt;!--Amiga OS--&gt;ntpsync 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Newsgroups
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;[http://newscoaster.sourceforge.net/ Newscoaster], [https://github.com/jens-maus/newsrog NewsRog], [ WorldNews], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|}

&lt;nowiki&gt;*&lt;/nowiki&gt; Commercial product.


==Graphical Image Editing Art==
{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Image Editing
!width:10%;|AROS(x86)
!width:10%;|Commodore-Amiga OS 3.1(68k)
!width:10%;|Hyperion OS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;Pixel Raster Artwork [https://github.com/LibreSprite/LibreSprite LibreSprite based on GPL aseprite], [https://github.com/abetusk/hsvhero hsvhero], [], 
|&lt;!--AROS--&gt;[https://sourceforge.net/projects/zunetools/files/ZunePaint/ ZunePaint], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/edit LunaPaint], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/edit GrafX2], [ LodePaint needs OpenGL], 
|&lt;!--Amiga OS--&gt;[http://www.amigaforever.com/classic/download.html PPaint], GrafX2, [https://github.com/grovdata/Amiga_Sources/blob/master/software.md DeluxePaint], [http://www.amiforce.de/perfectpaint/perfectpaint.php PerfectPaint], Zoetrope, Brilliance2*, 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=graphics/edit LodePaint], GrafX2, 
|&lt;!--MorphOS--&gt;Sketch, Pixel*, GrafX2, [http://morphos.lukysoft.cz/en/vypis.php?kat=3 LunaPaint]
|-
|&lt;!--Sub Menu--&gt;Image viewing 
|&lt;!--AROS--&gt;[http://sourceforge.net/projects/zunetools/files/ ZuneView], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/viewer LookHere], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/viewer LoView], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/viewer PicShow] , [http://amigaworld.net/modules/newbb/viewtopic.php?mode=viewtopic&amp;topic_id=31400&amp;forum=32&amp;start=80&amp;viewmode=flat&amp;order=0#583458 Picture Album], 
|&lt;!--Amiga OS--&gt;PicShow, PicView, Photoalbum,
|&lt;!--AmigaOS4--&gt;WarpView, PicShow, flPhoto, Thumbs, [http://amigaworld.net/modules/newbb/viewtopic.php?mode=viewtopic&amp;topic_id=31400&amp;forum=32&amp;start=80&amp;viewmode=flat&amp;order=0#583458 Picture Album], 
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=3 ShowGirls], [http://amigaworld.net/modules/newbb/viewtopic.php?mode=viewtopic&amp;topic_id=31400&amp;forum=32&amp;start=80&amp;viewmode=flat&amp;order=0#583458 Picture Album]
|-
|&lt;!--Sub Menu--&gt;Photography retouching / Image Manipulation like Photoshop(tm)  
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/edit RNOEffects], [https://sourceforge.net/projects/zunetools/files/ ZunePaint], [http://sourceforge.net/projects/zunetools/files/ ZuneView], 
|&lt;!--Amiga OS--&gt;[ Tecsoft Video Paint aka TVPaint], Photogenics*, ArtEffect*, ImageFX*, XiPaint, fxPaint, ImageMasterRT, Opalpaint, 
|&lt;!--AmigaOS4--&gt;WarpView, flPhoto, [http://www.os4depot.net/index.php?function=browse&amp;cat=graphics/edit Photocrop]
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=3 ShowGirls], ImageFX*, 
|-
|&lt;!--Sub Menu--&gt;Manage RAW picture folder galleries like Darktable, RAWtherapy, etc 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Graphic Format Converter - ICC profile support sRGB, Adobe RGB, XYZ and linear RGB 
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;GraphicsConverter, ImageStudio, [http://www.coplabs.org/artpro.html ArtPro]
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Thumbnail Generator [], 
|&lt;!--AROS--&gt;[http://sourceforge.net/projects/zunetools/files/ ZuneView], [http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/shell Thumbnail Generator]
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Icon Editor
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/iconedit Archives], [http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/workbench Icon Toolbox], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=graphics/iconedit IconEditor]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;2D Pixel Art Animation 
|&lt;!--AROS--&gt;Lunapaint
|&lt;!--Amiga OS--&gt;PPaint, AnimatED, Scala*, GoldDisk MovieSetter*, Walt Disney's Animation Studio*, ProDAD*, [https://github.com/historicalsource/DeluxePaint DeluxePaint src], Brilliance
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=3 Titler] 
|-
|&lt;!--Sub Menu--&gt;2D SVG based MovieSetter type 
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;MovieSetter*, Fantavision*
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Morphing 
|&lt;!--AROS--&gt;[ GLMorph]
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;2D Cad (qcad-&gt;LibreCAD, etc.) 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;Xcad, MaxonCAD
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;3D Cad like FreeCad, BRL-CAD, OpenSCAD, AvoCADo, etc. using dxf, obj (vertices), blend, 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;XCad3d*, DynaCADD*, Cycas, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;3D Model Rendering of glft (json) gbl (png jpg), usdz (USD files with materials, textures, and animations), FBX Filmbox is a proprietary Autodesk format, 
|&lt;!--AROS--&gt;POV-Ray
|&lt;!--Amiga OS--&gt;[http://www.discreetfx.com./amigaproducts.html CINEMA 4D]*, POV-Ray, Lightwave3D*, Real3D*, Caligari24*, Reflections/Monzoom*, [https://github.com/privatosan/RayStorm Raystorm src], Tornado 3D
|&lt;!--AmigaOS4--&gt;Blender, POV-Ray, Yafray
|&lt;!--MorphOS--&gt;Blender, POV-Ray, Yafray
|-
|&lt;!--Sub Menu--&gt;3D Format Converter [], [], 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/?function=showfile&amp;file=graphics/convert/ 3doc.i386-aros], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=showfile&amp;file=graphics/convert/ivcon.lha IVCon]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt; 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Screen grabbing display 
|&lt;!--AROS--&gt;[ Screengrabber], [http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/misc snapit], [http://archives.arosworld.org/index.php?function=browse&amp;cat=video/record screen recorder], []
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Grab graphics music from apps [https://github.com/Malvineous/ripper6 ripper6], [],
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt; 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|}

&lt;nowiki&gt;*&lt;/nowiki&gt; Commercial product.

[[#top|...to the top]]

==Office Application==
{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Office
!width:10%;|AROS (x86)
!width:10%;|[http://en.wikipedia.org/wiki/Amiga_software Commodore-Amiga OS 3.1] (68k)
!width:10%;|[http://en.wikipedia.org/wiki/AmigaOS_4 Hyperion OS4] (PPC)
!width:10%;|[http://en.wikipedia.org/wiki/MorphOS MorphOS] (PPC)
|-
|&lt;!--Sub Menu--&gt;Word-processing 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=office/wordprocessing Cinnamon Writer], [https://finalwriter.godaddysites.com/ Final Writer 7*], [https://github.com/sodero/MUI-Vim/releases MUI-Vim], [https://www.arosworld.org/infusions/forum/viewthread.php?thread_id=1995&amp;rowstart=20&amp;pid=12668#post_12668 Slovo], [], 
|&lt;!--AmigaOS--&gt;[ Softwood FinalCopy II*], Haage AmigaWriter*, Digita WordWorth*, Softwood FinalWriter*, Micro-Systems Excellence 3*, Arnor Protext, Rashumon, [ InterWord], [ KindWords], [WordPerfect], [ New Horizons Flow], [ CygnusEd Pro], [ Micro-systems Scribble], 
|&lt;!--AmigaOS4--&gt;AbiWord, [ CinnamonWriter]
|&lt;!--MorphOS--&gt;[ Cinnamon Writer], [http://www.meta-morphos.org/viewtopic.php?topic=1246&amp;forum=53 scriba], [http://morphos.lukysoft.cz/en/index.php Papyrus Office], 
|-
|&lt;!--Sub Menu--&gt;Spreadsheets 
|&lt;!--AROS--&gt;[https://blog.alb42.de/programs/leu/ Leu], [https://archives.arosworld.org/index.php?function=browse&amp;cat=office/spreadsheet], 
|&lt;!--AmigaOS--&gt;[https://aminet.net/package/biz/spread/ignition-src Ignition Src 1.3], [MaxiPlan 500 Plus], [OXXI Plan/IT v2.0 Speadsheet], [ Superplan], [ Creative Developments TurboCalc], [ ProCalc], [ InterSpread], [Digita DGCalc], [ Gold Disk Advantage], [ Micro-systems Analyze!]
|&lt;!--AmigaOS4--&gt;Gnumeric, [https://ignition-amiga.sourceforge.net/ Ignition], 
|&lt;!--MorphOS--&gt;[ ignition], [http://morphos.lukysoft.cz/en/vypis.php Papyrus Office], 
|-
|&lt;!--Sub Menu--&gt;Presentations
|&lt;!--AROS--&gt;[http://www.hollywoood-mal.com/ Hollywood]*, 
|&lt;!--Amiga OS--&gt;[http://www.hollywoood-mal.com/ Hollywood]*, MediaPoint, PointRider, Scala*, 
|&lt;!--Amiga OS4--&gt;[http://www.hollywoood-mal.com/ Hollywood]*, PointRider 
|&lt;!--MorphOS--&gt;[http://www.hollywoood-mal.com/ Hollywood]*, PointRider
|-
|&lt;!--Sub Menu--&gt;Databases 
|&lt;!--AROS--&gt;[http://sdb.freeforums.org/ SDB], [http://archives.arosworld.org/index.php?function=browse&amp;cat=office/database BeeBase], 
|&lt;!--Amiga OS--&gt;Precision Superbase 4 Pro*, Arnor Prodata*, BeeBase, Datastore, FinalData*, AmigaBase, Fiasco, Twist2*, [Digita DGBase], [], 
|&lt;!--AmigaOS4--&gt;BeeBase, SQLite, 
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=6 BeeBase], 
|-
|&lt;!--Sub Menu--&gt;PDF Viewing and editing digital signatures 
|&lt;!--AROS--&gt;[http://sourceforge.net/projects/arospdf/ ArosPDF via splash], [https://github.com/wattoc/AROS-vpdf vpdf wip], 
|&lt;!--Amiga OS--&gt;APDF 
|&lt;!--AmigaOS4--&gt;AmiPDF 
|&lt;!--MorphOS--&gt;APDF, vPDF, 
|-
|&lt;!--Sub Menu--&gt;Printing 
|&lt;!--AROS--&gt;Postscript 3 laser printers and Ghostscript internal, [ GutenPrint], 
|&lt;!--Amiga OS--&gt;[http://www.irseesoft.de/tp_what.htm TurboPrint]* 
|&lt;!--AmigaOS4--&gt;(some native drivers), 
|&lt;!--MorphOS--&gt;early TurboPrint included, 
|-
|&lt;!--Sub Menu--&gt;Note Taking markdown support like Obsidian like, joplin, OneNote, EverNotes, xournalpp, etc 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Study and analyse, collect, organize, annotate, cite, and share
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;PIM Personal Information Manager - Day Diary Planner Calendar App 
|&lt;!--AROS--&gt;[ ], [ ], [ ], 
|&lt;!--Amiga OS--&gt;Digita Organiser*, On The Ball, Everyday Organiser, [ Contact Manager], 
|&lt;!--AmigaOS4--&gt;AOrganiser, 
|&lt;!--MorphOS--&gt;[http://polymere.free.fr/orga_en.html PolyOrga], 
|-
|&lt;!--Sub Menu--&gt;Accounting
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=office/misc ETB], LoanCalc, [ ], [ ], [ ], 
|[ Digita Home Accounts2], Accountant, Small Business Accounts, Account Master, [ Amigabok], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Project Management Research 
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;SuperGantt, SuperPlan, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;System Wide Search 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=utility/filetool Finder], [], [], 
|&lt;!--Amiga OS--&gt; 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;System Wide Dictionary - multilingual [http://sourceforge.net/projects/babiloo/ Babiloo], [http://code.google.com/p/stardict-3/ StarDict], 
|&lt;!--AROS--&gt;[ ],  
|&lt;!--AmigaOS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;System wide Thesaurus - multi lingual
|&lt;!--AROS--&gt;[ ], 
|Kuma K-Roget*, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Sticky Desktop Notes (post it type) 
|&lt;!--AROS--&gt;[http://aminet.net/package/util/wb/amimemos.i386-aros AmiMemos], [https://aminet.net/package/util/wb/amimemos.src-aros AmiMemos Src], [], 
|&lt;!--Amiga OS--&gt;[http://aminet.net/package/util/wb/StickIt-2.00 StickIt v2], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;DTP Desktop Publishing 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/edit RNOPublisher], 
|&lt;!--Amiga OS--&gt;[http://pagestream.org/ Pagestream]*, Professional Pro Page*, Saxon Publisher, Pagesetter, PenPal, 
|&lt;!--AmigaOS4--&gt;[http://pagestream.org/ Pagestream]* 
|&lt;!--MorphOS--&gt;[http://pagestream.org/ Pagestream]* 
|-
|&lt;!--Sub Menu--&gt;Scanning 
|&lt;!--AROS--&gt;[ SCANdal], [], 
|&lt;!--Amiga OS--&gt;FxScan*, ScanQuix* 
|&lt;!--AmigaOS4--&gt;SCANdal (Sane)
|&lt;!--MorphOS--&gt;SCANdal
|-
|&lt;!--Sub Menu--&gt;OCR
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/convert gOCR] 
|&lt;!--AmigaOS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;[http://morphos-files.net/categories/office/text Tesseract] 
|-
|&lt;!--Sub Menu--&gt;Text Editing
|&lt;!--AROS--&gt;Jano Editor (already installed as Editor), [http://archives.arosworld.org/index.php?function=browse&amp;cat=development/edit EdiSyn], [http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/text/edit Annotate], [https://archives.arosworld.org/index.php?function=browse&amp;cat=development/edit Vim], [http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/text/edit FrexxEd] [https://github.com/vidarh/FrexxEd src], [ NoWinEd], 
|&lt;!--Amiga OS--&gt;[https://aminet.net/package/text/edit/TurboText20 TurboText20 ttx], Annotate, MicroGoldED/CubicIDE*, CygnusED*, Protext*, NoWinED, 
|&lt;!--AmigaOS4--&gt;Notepad, Annotate, CygnusED*, NoWinED, 
|&lt;!--MorphOS--&gt;MorphOS ED, NoWinED, GoldED/CubicIDE*, CygnusED*, Annotate, 
|-
|&lt;!--Sub Menu--&gt;Office Fonts [http://sourceforge.net/projects/fontforge/files/fontforge-source/ Font Designer] 
|&lt;!--AROS--&gt;[ ], [ ], 
|&lt;!--Amiga OS--&gt;TypeSmith*, SaxonScript (GetFont Adobe Type 1), 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Drawing Vector
|&lt;!--AROS--&gt;[http://sourceforge.net/projects/amifig/ ZuneFIG previously AmiFIG]
|&lt;!--Amiga OS--&gt;Drawstudio*, ProVector*, ArtExpression*, Professional Draw*, AmiFIG, MetaView, [https://gitlab.com/amigasourcecodepreservation/designworks Design Works Src], [], 
|&lt;!--AmigaOS4--&gt;MindSpace, [http://www.os4depot.net/index.php?function=browse&amp;cat=graphics/edit amifig], 
|&lt;!--MorphOS--&gt;SteamDraw, [http://aminet.net/package/gfx/edit/amifig amiFIG], 
|-
|&lt;!--Sub Menu--&gt;video conferencing (jitsi) 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;source code hosting
|&lt;!--AROS--&gt;Gitlab, 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Remote Desktop (server)
|&lt;!--AROS--&gt;[http://sourceforge.net/projects/zunetools/files/VNC_Server ArosVNCServer], 
|&lt;!--Amiga OS--&gt;[http://s.guillard.free.fr/AmiVNC/AmiVNC.htm AmiVNC], [http://dspach.free.fr/amiga/avnc/index.html AVNC]
|&lt;!--AmigaOS4--&gt;[http://s.guillard.free.fr/AmiVNC/AmiVNC.htm AmiVNC] 
|MorphVNC, vncserver
|-
|&lt;!--Sub Menu--&gt;Remote Desktop (client) login and connect to another machine 
|&lt;!--AROS--&gt;[https://sourceforge.net/projects/zunetools/files/VNC_Client/ ArosVNC], [http://archives.arosworld.org/index.php?function=browse&amp;cat=network/misc rdesktop], 
|&lt;!--Amiga OS--&gt;[http://twinvnc.free.fr/index.php?menu=01&amp;lang=eng TwinVNC], [http://dspach.free.fr/amiga/vva/index.html VVA], [http://www.hd-zone.com/ RDesktop]
|&lt;!--AmigaOS4--&gt;[http://twinvnc.free.fr/index.php?menu=01&amp;lang=eng TwinVNC], [http://www.hd-zone.com/ RDesktop]
|[http://twinvnc.free.fr/index.php?menu=01&amp;lang=eng TwinVNC], [http://www.hd-zone.com/ RDesktop]
|-
|&lt;!--Sub Menu--&gt;notifications 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;Ranchero 
|&lt;!--AmigaOS4--&gt;Ringhio 
|&lt;!--MorphOS--&gt;MagicBeacon 
|-
|&lt;!--Sub Menu--&gt;Biometric facial logins and fingerprint security features 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt; 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt; 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|}

&lt;nowiki&gt;*&lt;/nowiki&gt; Commercial product.

[[#top|...to the top]]

==Audio==
{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Audio
!width:10%;|AROS(x86)
!width:10%;|Commodore-Amiga OS 3.1(68k)
!width:10%;|Hyperion OS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;Playing playback Audio like MP3, [https://github.com/chrg127/gmplayer NSF], [https://github.com/kode54/lazyusf miniusf .usflib], [], etc 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=video/play Mplayer], [ HarmonyPlayer hp], [http://www.a500.org/downloads/audio/index.xhtml playcdda] CDs, [ WildMidi Player], [https://bszili.morphos.me/ UADE mod player], [], [RNOTunes ], [ mp3Player], [], 
|&lt;!--Amiga OS--&gt;AmiNetRadio, AmigaAmp, playOGG, 
|&lt;!--AmigaOS4--&gt;TuneNet, SimplePlay, AmigaAmp, TKPlayer
|AmiNetRadio, Mplayer, Kaya, AmigaAmp
|-
|&lt;!--Sub Menu--&gt;Editing Audio 
|&lt;!--AROS--&gt;[ Audio Evolution 4] 
|&lt;!--Amiga OS--&gt;[ Samplitude Opus Key], [https://sourceforge.net/projects/hd-rec/ HD-Rec Src], [http://www.sonicpulse.de/eng/news.html SoundFX], 
|&lt;!--AmigaOS4--&gt;[https://sourceforge.net/projects/hd-rec/ HD-Rec], AmiSoundED, [http://os4depot.net/?function=showfile&amp;file=audio/record/audioevolution4.lha Audio Evolution 4] 
|[http://www.hd-rec.de/HD-Rec/index.php?site=home HD-Rec], 
|-
|&lt;!--Sub Menu--&gt;Editing Tracker Music
|&lt;!--AROS--&gt;[https://github.com/hitchhikr/protrekkr Protrekkr], [ Schism Tracker], [http://archives.arosworld.org/index.php?function=browse&amp;cat=audio/tracker MilkyTracker], [http://www.hivelytracker.com/ HivelyTracker], [ Radium in AROS already],  [http://www.a500.org/downloads/development/index.xhtml libMikMod], 
|&lt;!--Amiga OS--&gt;MilkyTracker, HivelyTracker, DigiBooster, Octamed SoundStudio, 
|&lt;!--AmigaOS4--&gt;MilkyTracker, HivelyTracker, GoatTracker
|MilkyTracker, GoatTracker, DigiBooster, 
|-
|&lt;!--Sub Menu--&gt;Editing Music [], [https://github.com/kmatheussen/camd CAMD] and/or staves and notes manuscript 
|&lt;!--AROS--&gt;[http://bnp.hansfaust.de/ Bars and Pipes for AROS], [ Audio Evolution], [], 
|&lt;!--Amiga OS--&gt;[http://bnp.hansfaust.de/ Bars'n'Pipes], MusicX* David &quot;Talin&quot; Joiner &amp; Craig Weeks (for Notator-X), Deluxe Music Construction 2*, [https://github.com/timoinutilis/midi-sequencer-amigaos Horny c Src], HD-Rec, [https://aminet.net/package/mus/midi/dominatorV1_51 Dominator], 
|&lt;!--AmigaOS4--&gt;[https://sourceforge.net/p/hd-rec/code/HEAD/tree/ HD-Rec Src], Rockbeat, [http://bnp.hansfaust.de/download.html Bars'n'Pipes], [http://os4depot.net/index.php?function=browse&amp;cat=audio/edit Horny], Audio Evolution 4, 
|&lt;!--MorphOS--&gt;Bars'n'Pipes, 
|-
|&lt;!--Sub Menu--&gt;Sound Sampling 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=audio/record Audio Evolution 4], [http://www.imica.net/SitePortalPage.aspx?siteid=1&amp;did=162 Quick Record], [https://archives.arosworld.org/index.php?function=browse&amp;cat=audio/misc SOX to get AIFF 16bit files], [https://github.com/aros-development-team/AROS/tree/master/workbench/tools/AHIRecord AHIRecord], 
|&lt;!--Amiga OS--&gt;[https://aminet.net/package/mus/edit/AudioEvolution3_src Audio Evolution 3 c src], [ Samplitude-MS Opus Key], Audiomaster IV*, 
|&lt;!--AmigaOS4--&gt;[https://github.com/timoinutilis/phonolith-amigaos phonolith c src], HD-Rec, Audio Evolution 4,
|&lt;!--MorphOS--&gt;[https://sourceforge.net/p/hd-rec/code/HEAD/tree/ HD-Rec Src], Audio Evolution 4,
|-
|&lt;!--Sub Menu--&gt;Live Looping or Audio Misc - Groovebox like
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;CD/DVD burn
|[https://code.google.com/p/amiga-fryingpan/ FryingPan], 
|&lt;!--Amiga OS--&gt;FryingPan, [http://www.estamos.de/makecd/#CurrentVersion MakeCD], 
|&lt;!--AmigaOS4--&gt;FryingPan, AmiDVD, 
|[http://www.amiga.org/forums/printthread.php?t=58736 FryingPan], Jalopeano, 
|-
|&lt;!--Sub Menu--&gt;CD/DVD audio rip
|Lame, [http://www.imica.net/SitePortalPage.aspx?siteid=1&amp;cfid=0&amp;did=167 Quick CDrip],
|&lt;!--Amiga OS--&gt;Lame,  
|&lt;!--AmigaOS4--&gt;Lame, 
|Lame,  
|-
|&lt;!--Sub Menu--&gt;MP3 v1 and v2 Tagger
|&lt;!--AROS--&gt;id3ren (v1), [http://archives.arosworld.org/index.php?function=browse&amp;cat=audio/edit mp3info], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|
|-
|&lt;!--Sub Menu--&gt;Audio Convert
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=audio/misc Sox], [], 
|&lt;!--Amiga OS--&gt;[http://aminet.net/package/mus/misc/SoundBox SoundBox], [http://aminet.net/package/mus/misc/SoundBoxKey SoundBox Key], [http://aminet.net/package/mus/edit/SampleE SampleE], sox 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;DJ mixing jamming 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Radio Automation Software [http://www.rivendellaudio.org/ Rivendell], [http://code.campware.org/projects/livesupport/report/3 Campware LiveSupport], [http://www.sourcefabric.org/en/airtime/ SourceFabric AirTime], [http://www.ohloh.net/p/mediabox404 MediaBox404], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Speakers Audio Sonos Mains AC networked wired controlled 
*2005 ZP100 with ZP80 
*2008 Zoneplayer ZP120 (multi-room wireless amp)  ZP90 receiver only with CR100 controller, 
*2009 ZonePlayer S5, 
*2010 BR100 wireless Bridge (no support),   
*2011 Play:3
*2013 Bridge (no support), Play:1,  
*2016 Arc,   Play:1,   
*Beam (Gen 2),   Playbar,  Ray,   Era 100,   Era 300,   Roam,   Move 2,   
*Sub (Gen 3),   Sub Mini,  Five,  Amp  S2 
|&lt;!--AROS--&gt;SonosController 
|&lt;!--Amiga OS--&gt;SonosController
|&lt;!--AmigaOS4--&gt;SonosController
|&lt;!--MorphOS--&gt;SonosController
|-
|&lt;!--Sub Menu--&gt;Smart Speakers 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt; 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|}

&lt;nowiki&gt;*&lt;/nowiki&gt; Commercial product.

[[#top|...to the top]]

==Video Creativity and Production==
{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Video
!width:10%;|AROS(x86)
!width:10%;|Commodore-Amiga OS 3.1(68k)
!width:10%;|Hyperion OS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;Playing Video 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=video/play Mplayer VAMP], [http://www.a500.org/downloads/video/index.xhtml CDXL player], [http://www.a500.org/downloads/video/index.xhtml IffAnimPlay], [], 
|&lt;!--Amiga OS--&gt;Frogger*, AMP2, MPlayer, RiVA*, MooViD*, 
|&lt;!--AmigaOS4--&gt;DvPlayer, MPlayer 
|&lt;!--MorphOS--&gt;MPlayer, Frogger, AMP2, VLC 
|-
|&lt;!--Sub Menu--&gt;Streaming Video and game streaming like OBS studio, Parsec, [https://github.com/lizardbyte/sunshine sunshine], [https://github.com/moonlight-stream/moonlight-qt moonlight], etc 
|&lt;!--AROS--&gt;Mplayer, 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;Mplayer, Gnash, Tubexx 
|&lt;!--MorphOS--&gt;Mplayer, OWB, Tubexx
|-
|&lt;!--Sub Menu--&gt;Playing DVD 
|&lt;!--AROS--&gt;[http://a-mc.biz/ AMC]*, Mplayer 
|&lt;!--Amiga OS--&gt;AMP2, Frogger 
|&lt;!--AmigaOS4--&gt;[http://a-mc.biz/ AMC]*, DvPlayer*, AMP2,  
|&lt;!--MorphOS--&gt;Mplayer 
|-
|&lt;!--Sub Menu--&gt;Screen Recording
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=video/record Screenrecorder], [ ], [ ], [ ], [ ], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;Screenrecorder, 
|-
|&lt;!--Sub Menu--&gt;Create and Edit Individual Video NLE 
|&lt;!--AROS--&gt;[ Mencoder], [ Quick Videos], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/edit AVIbuild], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/misc FrameBuild], FFMPEG, 
|&lt;!--Amiga OS--&gt;[ MainConcept Mainactor Broadcast*], [http://en.wikipedia.org/wiki/Video_Toaster Video Toaster*], MacroSystem MovieShop 4.3*, proDAD Adorage*, [ IOSpirit VHI studio]*, [Gold Disk ShowMaker], [], 
|&lt;!--AmigaOS4--&gt;FFMpeg/GUI 
|&lt;!--MorphOS--&gt;Blender, Mencoder, FFmpeg
|-
|&lt;!--Sub Menu--&gt;Subtitle editor 
|&lt;!--AROS--&gt;[https://aminet.net/package/text/edit/Slarti_Arosx86ABIv0 Slarti_Arosx86ABIv0], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;IP-based video production workflows with High Dynamic Range (HDR), 10-bit color collaborative NDI, 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Blogging like Lemmy or kbin
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;VR face recognition for Vtubers 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;VR chatting Live 2D models with Cubism type editor 
&lt;pre&gt;
Model data (cmo3)
Basic motions (can3)
Background image (png)
Set of files for embedding (runtime folder)
• Model data (moc3)
• Motion data (motion3.json)
• Model settings file (model3.json)
• Physics settings file (physics3.json)
• Display auxiliary file (cdi3.json)
&lt;/pre&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;VR chatting chatters .VRML models - standardized 3D file format for VR avatars 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;V-tubers V-tubing like Vseeface with Openseeface tracker or Vpuppr (virtual puppet project) for 2d / 3d art models rigging rigged LIV 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt; 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|}

&lt;nowiki&gt;*&lt;/nowiki&gt; Commercial product.

[[#top|...to the top]]


==Misc Application==
{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Misc Application
!width:10%;|AROS(x86)
!width:10%;|Commodore-Amiga OS 3.1 (68k)
!width:10%;|Hyperion OS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;File Management 
|&lt;!--AROS--&gt;DOpus4, [https://github.com/BlitterStudio/dopus5 DOpus Magellan aka DOpus 5], [ Scalos], [ ], 
|&lt;!--Amiga OS--&gt;DOpus2, DOpus 4, [http://sourceforge.net/projects/dopus5allamigas/files/?source=navbar DOpus Magellan DOpus5], ClassAction, FileMaster, [http://www.amiga.org/forums/showthread.php?t=4897 DirWork 2]*, [https://github.com/RudolphRiedel/DiskMaster2 DiskMaster2 src], 
|&lt;!--AmigaOS4--&gt;DOpus4, DOpus5, Filer, AmiDisk 
|&lt;!--MorphOS--&gt;DOpus4, DOpus5 
|-
|&lt;!--Sub Menu--&gt;File Verification / Repair 
|&lt;!--AROS--&gt;md5 (works in linux compiling shell), [http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/filetool workpar2] (PAR2),  [http://zakalwe.fi/~shd/foss/cksfv/files/ compile cksfv from website], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;Par2, 
|-
|Application Installer 
|&lt;!--AROS--&gt;[], [ InstallerNG], 
|&lt;!--Amiga OS--&gt;InstallerNG, Grunch, 
|&lt;!--AmigaOS4--&gt;Jack
|&lt;!--MorphOS--&gt;Jack 
|-
|&lt;!--Sub Menu--&gt;Compression archiver [https://github.com/FS-make-simple/paq9a paq9a], [], 
|&lt;!--AROS--&gt;XAD system is a toolkit designed for handling various file and disk archiver
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[https://aminet.net/package/util/pack/decrunchmania_os4 Crunchmania CrM2 depacker], 
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Binary Hexadecimal Editor 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=development/edit Zaphod], [],
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Repository
|&lt;!--AROS--&gt;[ Git]
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;Git
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Filesystem Partition Editor formatter Disk Management
|&lt;!--AROS--&gt;[https://www.arosworld.org/infusions/forum/viewthread.php?thread_id=1440&amp;highlight=partition&amp;pid=8821#post_8821 QuickPart], [ HDToolBox]
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Filesystem Repair and backups 
|&lt;!--AROS--&gt;ArSFSDoctor, 
|&lt;!--Amiga OS--&gt;[https://aminet.net/package/disk/bakup/quarterback_src Quarterback Tools C and asm src], [ ], [ ], [ ], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;System Disk check, integrity and history [https://github.com/smartmontools/smartmontools smart tools], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;[], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Multiple File renaming
|&lt;!--AROS--&gt;DOpus 4 or 5, 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Anti Virus
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;VChecker, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Random Wallpaper Desktop changer [ DOpus5], [ Scalos],  
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Alarm Clock, Timer, Stopwatch, Countdown 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/workbench DClock], [http://aminet.net/util/time/AlarmClockAROS.lha AlarmClock], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Fortune Cookie Quotes Sayings 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/misc AFortune], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;C/C++ IDE 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/text/edit FrexxEd], [https://github.com/vidarh/FrexxEd FrexxEd src], Annotate, Murks, 
|&lt;!--Amiga OS--&gt;[http://devplex.awardspace.biz/cubic/index.html Cubic IDE]*, Annotate, 
|&lt;!--AmigaOS4--&gt;CodeBench , [https://gitlab.com/boemann/codecraft CodeCraft], 
|&lt;!--MorphOS--&gt;[http://devplex.awardspace.biz/cubic/index.html Cubic IDE]*, Anontate, 
|-
|&lt;!--Sub Menu--&gt;Computer Languages Translation [https://tetracorp.github.io/guide/reverse-engineering-amiga.html ], [https://amigasourcecodepreservation.gitlab.io/amiga-assembler-insider-guide/ ], [https://github.com/kermitfrog/Amiga-Re-Engineering Rust, Ghidra and FS-UAE], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;[https://bitbucket.org/rhinoid/convert68000toc/src/main/ convert m68k seka asm-one to c], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Gui Creators
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=development/guitool MuiBuilder], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;[ MuiBuilder],  
|-
|&lt;!--Sub Menu--&gt;Catalog .cd .ct Editors 
|&lt;!--AROS--&gt;FlexCat
|&lt;!--Amiga OS--&gt;[http://www.geit.de/deu_simplecat.html SimpleCat], FlexCat
|&lt;!--AmigaOS4--&gt;[http://aminet.net/package/dev/misc/simplecat SimpleCat], FlexCat
|[http://www.geit.de/deu_simplecat.html SimpleCat], FlexCat
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|}

&lt;nowiki&gt;*&lt;/nowiki&gt; Commercial product.


==Misc Application 2==
{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Misc Application
!width:10%;|AROS(x86)
!width:10%;|Commodore-Amiga OS 3.1(68k)
!width:10%;|Hyperion OS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;System 
|&lt;!--AROS--&gt;[ SysExplorer], [ SysMon], [ Scout], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;OSK On Screen Keyboard
|&lt;!--AROS--&gt;[], 
|&lt;!--Amiga OS--&gt;[https://aminet.net/util/wb/OSK.lha OSK]
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Screen Magnifier Magnifying Glass Magnification 
|&lt;!--AROS--&gt;[http://www.onyxsoft.se/files/zoomit.lha ZoomIT], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Comic Book CBR CBZ format reader viewer 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/viewer comics], [http://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/viewer comicon], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Ebook Reader 
|&lt;!--AROS--&gt;[https://blog.alb42.de/programs/#legadon Legadon EPUB],[]
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Ebook Converter 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Text to Speech tts [https://github.com/JonathanFly/bark-installer Bark], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=audio/misc flite], 
|&lt;!--Amiga OS--&gt;[http://www.text2speech.com translator], 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=search&amp;tool=simple FLite]
|&lt;!--MorphOS--&gt;[http://se.aminet.net/pub/aminet/mus/misc/ FLite]
|-
|&lt;!--Sub Menu--&gt;Speech Voice Recognition Dictation - [http://sourceforge.net/projects/cmusphinx/files/ CMU Sphinx], [http://julius.sourceforge.jp/en_index.php?q=en/index.html Julius], [http://www.isip.piconepress.com/projects/speech/index.html ISIP], 
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Speech Voice Changer [], [], [], [], 
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Screen Display Blanker screensaver 
|&lt;!--AROS--&gt;Blanker Commodity (built in), [https://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/screenblanker GarshneBlanker], [http://sourceforge.net/projects/gblanker/ GBlanker Src], [], 
|&lt;!--Amiga OS--&gt;MultiCX, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;ModernArt Blanker, 
|-
|}


==Misc Application 3==
{|  class=&quot;wikitable sortable&quot; 
|- 
!width:30%;|Misc Application
!width:10%;|AROS(x86)
!width:10%;|Commodore-Amiga OS 3.1(68k)
!width:10%;|Hyperion OS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;Fractals mandelbrot, etc 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/misc ], 
|&lt;!--Amiga OS--&gt;ZoneXplorer, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Landscape Rendering 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=graphics/raytrace WCS World Construction Set], 
|&lt;!--Amiga OS--&gt;[ Vista Pro], [http://en.wikipedia.org/wiki/World_Construction_Set World Construction Set]
|&lt;!--AmigaOS4--&gt;[ WCS World Construction Set],
|&lt;!--MorphOS--&gt;[ WCS World Construction Set],
|-
|&lt;!--Sub Menu--&gt;Astronomy [https://sourceforge.net/projects/skychart/ skychart freepascal], [], [], 
|&lt;!--AROS--&gt;[ Digital Almanac (ABIv0 only)], 
|&lt;!--Amiga OS--&gt;[http://aminet.net/search?query=planetarium Aminet search], [http://aminet.net/misc/sci/DA3V56ISO.zip Digital Almanac], [https://aminet.net/package/misc/sci/da3sourceV58 Src c V58], [ Galileo renamed to Distant Suns]*, [], 
|&lt;!--AmigaOS4--&gt;[http://sourceforge.net/projects/digital-almanac/ Digital Almanac], Distant Suns*, [http://www.digitaluniverse.org.uk/ Digital Universe]*,
|&lt;!--MorphOS--&gt;[http://www.aminet.net/misc/sci/da3.lha Digital Almanac], [http://www.aminet.net/package/misc/sci/da3-mos-src Src c V56], 
|-
|&lt;!--Sub Menu--&gt;Astrology [https://sourceforge.net/projects/skylendar/ skylendar], [https://github.com/CruiserOne/Astrolog Astrolog], [https://www.astrolog.org/astrolog/astfile.htm Astrology alt site], [https://saravali.github.io/download.html Maitreya], [https://github.com/alamahant/Asteria Asteria], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;PCB design
|&lt;!--AROS--&gt; 
|&lt;!--Amiga OS--&gt;[ ], [ ], [ ], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Digital Signage
|&lt;!--AROS--&gt;Hollywood, Hollywood Designer 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Genealogy History Family Tree Ancestry Records (FreeBMD, FreeREG, and FreeCEN file formats or GEDCOM GenTree)
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt; [ Origins], [ Your Family Tree], [ ], [ ], [ ], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Languages 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;Fun School, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Mathematics ([http://www-fourier.ujf-grenoble.fr/~parisse/install_en.html Xcas], etc.), 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/scientific mathX] 
|&lt;!--Amiga OS--&gt;Maple V, mathX, Fun School, GCSE Maths, [ ], [ ], [ ], 
|&lt;!--AmigaOS4--&gt;Yacas 
|&lt;!--MorphOS--&gt;Yacas 
|-
|&lt;!--Sub Menu--&gt;Maths Graph Function Plotting
|&lt;!--AROS--&gt;[https://blog.alb42.de/programs/#MUIPlot MUIPlot], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;App Utility Launcher Dock toolbar  
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=utility/docky BoingBar], [], 
|&lt;!--Amiga OS--&gt;[https://github.com/adkennan/DockBot Dockbot],
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;3D Printer [https://github.com/OrcaSlicer/OrcaSlicer OrcaSlicer]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;BASIC Computer Language 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=development/language Basic4SDL], [ Ace Basic], [ X-AMOS], [SDLBasic], [ Alvyn], 
|&lt;!--Amiga OS--&gt;[http://www.amiforce.de/main.php Amiblitz 3], [http://amos.condor.serverpro3.com/AmosProManual/contents/c1.html Amos Pro], [http://aminet.net/package/dev/basic/ace24dist ACE Basic], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;sdlBasic
|-
|&lt;!--Sub Menu--&gt;HAM radio, amateur radio, packet radio  [], [], [], [https://cemaxecuter.com/ Dragon OS], [https://github.com/km4ack/73Linux with 73 link update], [https://www.youtube.com/watch?v=YAL5KNePRSg video for], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;[https://www.amigarealm.com/amiga/amicomms/comm4.htm Comm4], [https://www.amigarealm.com/archives/comms/aarug/ TNC Terminal Node Controller with packets over serial connections on Yaesu or Woxum handheld], [https://aminet.net/comm/misc AmiCom], [ with 7Plus file encoder/decoder], [ mksstv], [ RTTYam], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|}

&lt;nowiki&gt;*&lt;/nowiki&gt; Commercial product.


==Games &amp; Emulation==

Some emulators/games require OpenGL to function and to adjust ahi prefs channels, frequency and unit0 and unit1 and 
[http://aros.sourceforge.net/documentation/users/shell/changetaskpri.php changetaskpri -1]

Rom patching  https://www.marcrobledo.com/RomPatcher.js/ https://www.romhacking.net/patch/ (ips, ups, bps, etc) and this other site supports the latter formats https://hack64.net/tools/patcher.php 

Free public domain roms for use with emulators can be found [http://www.pdroms.de/ here] as most of the rest are covered by copyright rules. If you like to read about old games see [http://retrogamingtimes.com/ here] and [http://www.armchairarcade.com/neo/ here] and a [http://www.vintagecomputing.com/ blog] about old computers. Possibly some of the [http://www.answers.com/topic/list-of-best-selling-computer-and-video-games best selling] of all time. [http://en.wikipedia.org/wiki/List_of_computer_system_emulators Wiki] with emulated systems list.

[https://archive.gamehistory.org/ Archive of VGHF], [https://library.gamehistory.org/ Video Game History Foundation Library search]


{|  class=&quot;wikitable sortable&quot; 
|- 
!width:10%;|Games [http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer Emulation]
!width:10%;|AROS(x86)
!width:10%;|AmigaOS3(68k)
!width:10%;|AmigaOS4(PPC)
!width:10%;|MorphOS(PPC)
|-
|&lt;!--Sub Menu--&gt;Games Emulation Amstrad CPC 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer], [ Caprice32 (OpenGL &amp; pure SDL)], [ Arnold], [https://retroshowcase.gr/cpcbox-master/], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://os4depot.net/index.php?function=browse&amp;cat=emulation/computer]
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=2], 
|-
|&lt;!--Sub Menu--&gt;Games Emulation Apple2 and 2GS
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Arcade 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem Mame], [ SI Emu (ABIv0 only)], 
|&lt;!--Amiga OS--&gt;Mame, 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem xmame], amiarcadia, 
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=2 Mame], 
|-
|&lt;!--Sub Menu--&gt;Games Emulation Atari 2600 [], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem Stella], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Atari 5200 [https://github.com/wavemotion-dave/A5200DS A5200DS], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Atari 7800
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Atari 400 800 130XL [https://github.com/wavemotion-dave/A8DS A8DS], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer Atari800], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Atari Lynx
|&lt;!--AROS--&gt;[http://myfreefilehosting.com/f/6366e11bdf_1.93MB Handy (ABIv0 only)], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Atari Jaguar
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Bandai Wonderswan 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation BBC Micro and Acorn Electron [http://beehttps://bem-unix.bbcmicro.com/download.html BeebEm], [http://b-em.bbcmicro.com/ B-Em], [http://elkulator.acornelectron.co.uk/ Elkulator], [http://electrem.emuunlim.com/ ElectrEm], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Dragon 32 and Tandy CoCo [http://www.6809.org.uk/xroar/ xroar], [], 
|&lt;!--AROS--&gt;[], [], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Commodore C16 Plus4
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Commodore C64
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer Vice (ABIv0 only)], [], 
|&lt;!--Amiga OS--&gt;Frodo, 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem viceplus], 
|&lt;!--MorphOS--&gt;Vice, 
|-
|&lt;!--Sub Menu--&gt;Games Emulation Commodore Amiga
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer Janus UAE], Emumiga, 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://os4depot.net/index.php?function=browse&amp;cat=emulation/computer UAE], 
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=2 UAE], 
|-
|&lt;!--Sub Menu--&gt;Games Emulation Japanese MSX MSX2 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Mattel Intelivision
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Mattel Colecovision and Adam
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Milton Bradley (MB) Vectrex [ Vectrex OpenGL], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation PICO8 Pico-8 fantasy video game console [https://github.com/egordorichev/pemsa-sdl/ pemsa-sdl], [https://github.com/jtothebell/fake-08 fake-08], [https://github.com/Epicpkmn11/fake-08/tree/wip fake-08 fork], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Nintendo Gameboy
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem vba no sound], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem vba]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Nintendo NES
|&lt;!--AROS--&gt;[ EmiNES], [http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem Fceu], [https://github.com/takahirox/nes-js?tab=readme-ov-file nes-js], [https://github.com/bfirsh/jsnes jsnes], [https://github.com/angelo-wf/NesJs NesJs], 
|&lt;!--Amiga OS--&gt;AmiNES, [http://www.dridus.com/~nyef/darcnes/ darcNES], 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem amines]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Nintendo SNES
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem Zsnes], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem warpsnes]
|&lt;!--MorphOS--&gt;[http://fabportnawak.free.fr/snes/ Snes9x], 
|-
|&lt;!--Sub Menu--&gt;Games Emulation Nintendo N64 
*HLE and plugins [ mupen64], [https://github.com/ares-emulator/ares ares], [https://github.com/N64Recomp/N64Recomp N64Recomp], [https://github.com/rt64/rt64 rt64], [https://github.com/simple64/simple64 Simple64], 
*LLE [], 
|&lt;!--AROS--&gt;[http://code.google.com/p/mupen64plus/ Mupen64+],
|&lt;!--Amiga OS--&gt;[http://code.google.com/p/mupen64plus/ Mupen64+], [http://aminet.net/package/misc/emu/tr-981125_src TR64], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;[ Nintendo Gamecube Wii]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;[ Nintendo Wii U]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;[https://github.com/yuzu-emu Nintendo Switch]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation NEC PC Engine 
|&lt;!--AROS--&gt;[], [], [https://github.com/yhzmr442/jspce js-pce], 
|[http://www.hugo.fr.fm/ Hugo], [http://mednafen.sourceforge.net/ Mednafen], 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem tgemu]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sega Master System (SMS)
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem Dega], [http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem sms], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem osmose]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sega Genesis/Megadrive
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem gp no sound], [http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem DGen], 
|&lt;!--Amiga OS--&gt;[http://code.google.com/p/genplus-gx/ Genplus], 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem genesisplus]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sega Saturn 
*HLE [https://mednafen.github.io/ mednafen], [http://yabause.org/ yabause], [], 
*LLE [], [], 
|&lt;!--AROS--&gt;?
|&lt;!--Amiga OS--&gt;[http://yabause.org/ Yabause], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sega Dreamcast 
*HLE [https://github.com/flyinghead/flycast  flycast], [https://code.google.com/archive/p/nulldc/downloads NullDC], 
*LLE [], [], 
|&lt;!--AROS--&gt;?
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sinclair ZX80 and ZX81 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer], [], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sinclair Spectrum 
|[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer Fuse (crackly sound)], [http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer SimCoupe], [ FBZX slow], [https://jsspeccy.zxdemo.org/ jsspeccy], [http://torinak.com/qaop/games qaop], 
|&lt;!--Amiga OS--&gt;[http://www.lasernet.plus.com/ Asp], [http://www.zophar.net/sinclair.html Speculator], [http://www.worldofspectrum.org/x128/index.html X128], 
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/computer]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sinclair QL
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer], [], 
|&lt;!--Amiga OS--&gt;[http://aminet.net/package/misc/emu/QDOS4amiga1 QDOS4amiga]
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation SNK NeoGeo Pocket
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem gngeo], NeoPop, 
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation Sony PlayStation
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/gamesystem FPSE], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem FPSE]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;[ Sony PS2]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;[ Sony PS3]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;[https://vita3k.org/ Sony Vita]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;[https://github.com/shadps4-emu/shadPS4 PS4]
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation [http://en.wikipedia.org/wiki/Tangerine_Computer_Systems Tangerine] Oric and Atmos 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer Oricutron]
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.os4depot.net/index.php?function=browse&amp;cat=emulation/gamesystem Oricutron]
|&lt;!--MorphOS--&gt;[http://aminet.net/package/misc/emu/oricutron Oricutron]
|-
|&lt;!--Sub Menu--&gt;Games Emulation TI 99/4 99/4A [https://github.com/wavemotion-dave/DS994a DS994a], [], [https://js99er.net/#/ js99er], [], [http://aminet.net/package/misc/emu/TI4Amiga TI4Amiga], [http://aminet.net/package/misc/emu/TI4Amiga_src TI4Amiga src in c], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=emulation/computer], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation HP 38G 40GS 48 49G/50G Graphing Calculators
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Emulation TI 58 83 84 85 86 - 89 92 Graphing Calculators
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|}

{|  class=&quot;wikitable sortable&quot; 
|- 
!width:10%;|Games [https://www.rockpapershotgun.com/ General]
!width:10%;|AROS(x86)
!width:10%;|AmigaOS3(68k)
!width:10%;|AmigaOS4(PPC)
!width:10%;|MorphOS(PPC)
|- style=&quot;background:lightgrey; text-align:center; font-weight:bold;&quot;
| Games [https://www.trackawesomelist.com/michelpereira/awesome-open-source-games/ Open Source and others] || AROS || Amiga OS || Amiga OS4 || Morphos 
|-
|&lt;!--Sub Menu--&gt;Games Action like [https://github.com/opentomb/OpenTomb opentomb], [https://github.com/LostArtefacts/TRX TRX formerly Tomb1Main], [https://github.com/TombEngine TombEngine], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/action Thrust], [https://github.com/fragglet/sdl-sopwith sdl sopwith], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/action], [https://archives.arosworld.org/index.php?function=browse&amp;cat=game/action BOH], [], 
|&lt;!--Amiga OS--&gt;[https://github.com/BSzili/OpenLara/tree/amiga/src source of openlara SDL2], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Adventure like [http://dotg.sourceforge.net/ DMJ], [https://github.com/kromenak/gengine Gabriel Knight 3], [http://www.sarien.net/ Sierra Sarien], [https://github.com/klembot/twinejs twine js], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/adventure dmagnetic], [https://archives.arosworld.org/?function=browse&amp;cat=emulation/misc ScummVM], [https://archives.arosworld.org/index.php?function=browse&amp;cat=game/roleplaying frotz infocom], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Board like [https://github.com/aperture-software/colditz-escape escape from colditz], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/board], [http://amigan.1emu.net/releases Africa]
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Cards 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=game/card ], [], 
|&lt;!--AmigaOS--&gt;[http://home.arcor.de/amigasolitaire/e/welcome.html Reko], [https://github.com/samskivert/beschei-en beschei Src], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Misc [https://github.com/michelpereira/awesome-open-source-games Awesome open], [https://github.com/bobeff/open-source-games General Open Source], [https://github.com/SAT-R/sa2 Sonic Advance 2], [https://github.com/velorek1/cwordle Wordle type], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/misc], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games FPS like [https://aminet.net/package/game/shoot/D1X_Rebirth_AGA Descent D1X src], [https://github.com/DescentDevelopers/Descent3 Descent 3], [https://github.com/Fewnity/Counter-Strike-Nintendo-DS Counter-Strike-Nintendo-DS], [https://github.com/Aleph-One-Marathon/alephone Bungie Marathon 1994], [https://zdoom.org/downloads UzDoom opengl 3.3], [https://github.com/ZDoom/gzdoom gzdoom opengl 3+], [https://zdoom.org/downloads LZDoom opengl 2.1], 
|&lt;!--AROS--&gt;Doom, Quake, [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Quake 3 Arena (OpenGL)], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Cube (OpenGL)], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Assault Cube (OpenGL)], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Cube 2 Sauerbraten (OpenGL)], [http://fodquake.net/test/ FodQuake QuakeWorld], [https://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Duke Nukem 3D], [https://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Darkplaces Nexuiz Xonotic], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Doom 3 SDL (OpenGL)], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Hexenworld and Hexen 2], [https://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Aliens vs Predator Gold 2000 avp (openGL)], [https://archives.arosworld.org/index.php?function=browse&amp;cat=game/fps Odamex (openGL doom)], [https://archives.arosworld.org/?function=showfile&amp;file=game/fps/ zgloom], [], [https://archives.arosworld.org/?function=showfile&amp;file=game/fps/ ab3dhd], [], 
|&lt;!--Amiga OS--&gt;Doom, Quake, AB3D, Fears, Breathless, Gloom, 
|&lt;!--AmigaOS4--&gt;Doom, Quake, 
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=12 Doom], Quake, Quake 3 Arena, [https://github.com/OpenXRay/xray-16 S.T.A.L.K.E.R Xray]
|-
|&lt;!--Sub Menu--&gt;Games MMORG like 
|&lt;!--AROS--&gt;[ Eternal Lands (OpenGL)],
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Platform like 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/platform], [ Maze of Galious], [ Gish]*(openGL), [ Mega Mario], [https://archives.arosworld.org/?function=showfile&amp;file=game/platform/ thextech SMBX], [http://www.gianas-return.de/ Giana's Return], [http://www.sqrxz.de/ Sqrxz], [www.sqrxz2.de/ Sqrxz 2], [http://www.sqrxz.de/sqrxz-3/ Sqrxz 3], [http://www.sqrxz.de/sqrxz-4/ Sqrxz 4], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/platform Cave Story], [https://bszili.morphos.me/ Frogatto], [https://bszili.morphos.me/ OpenJazz], [https://archives.arosworld.org/?function=showfile&amp;file=game/platform/ pekkakana2], [ Aquaria], [https://archives.arosworld.org/?function=showfile&amp;file=game/platform/ sonic CD], [], 
|&lt;!--Amiga OS--&gt;[ Giana Sisters], [], 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Puzzle [https://github.com/mariopartyrd/marioparty4/tree/port Party], [https://github.com/mdodis/OpenSolomonsKey OpenSolomonsKey], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/puzzle], [ Cubosphere (OpenGL)], [http://archives.arosworld.org/index.php?function=browse&amp;cat=game/puzzle Candy Crisis], [http://bszili.morphos.me/ TailTale], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Racing [ Trigger Rally], [ VDrift], [http://www.ultimatestunts.nl/index.php?page=2&amp;lang=en Ultimate Stunts], [http://maniadrive.raydium.org/ Mania Drive], [https://github.com/plowteam/donut Simpsons Hit and Run], [], 
|&lt;!--AROS--&gt;[ Super Tux Kart (OpenGL)], [http://www.dusabledanslherbe.eu/AROSPage/F1Spirit.30.html F1 Spirit (OpenGL)], [http://bszili.morphos.me/index.html MultiRacer], [https://bszili.morphos.me/ Speed Dreams], [], 
|&lt;!--AmigaOS--&gt;
|&lt;!--AmigaOS4--&gt;[http://bszili.morphos.me/index.html Speed Dreams], 
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=12], [http://bszili.morphos.me/index.html TORCS], 
|-
|&lt;!--Sub Menu--&gt;Games 1st first person DRPG [https://wiki.rpg.net/index.php/Open_Game_Systems Misc], [https://github.com/OpenEnroth/OpenEnroth OpenEnroth MM], []
|&lt;!--AROS--&gt;[https://github.com/BSzili/aros-stuff Arx Libertatis], [http://www.playfuljs.com/a-first-person-engine-in-265-lines/ js raycaster], [https://github.com/Dorthu/es6-crpg webgl], [https://github.com/sonountaleban/AmiShockolate System Shock], [], [], 
|&lt;!--AmigaOS--&gt;Phantasie, Faery Tale, Dungeon Master, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games 3rd third person action CRPG  [https://sourceforge.net/projects/sumwars/ Summoning Wars], [https://www.solarus-games.org/ Solarus], [https://wiki.rpg.net/index.php/Open_Game_Systems Misc], [https://github.com/alexbatalov/fallout1-ce fallout ce], [https://github.com/rwengine/openrw gta3], [https://github.com/gta-reversed/gta-reversed gta3 sa], [https://github.com/mrxenginner/reVC gta3 vc revc], 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/?function=showfile&amp;file=game/strategy/ fheroes2 homm2], [https://archives.arosworld.org/?function=showfile&amp;file=game/roleplaying/ breakhack], [https://archives.arosworld.org/?function=showfile&amp;file=game/roleplaying/ devilutionx diablo 1 hellfire], [https://archives.arosworld.org/?function=showfile&amp;file=game/roleplaying/ fallout 1], [https://archives.arosworld.org/?function=showfile&amp;file=game/strategy/ stratagus], [https://archives.arosworld.org/?function=showfile&amp;file=game/strategy/ hostile-takeover], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games isometric RPG [https://sourceforge.net/projects/sumwars/ Summoning Wars], [https://www.solarus-games.org/ Solarus], [https://wiki.rpg.net/index.php/Open_Game_Systems Misc], [https://github.com/topics/dungeon?l=javascript Dungeon], [], [https://github.com/clintbellanger/heroine-dusk JS Dusk], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/roleplaying nethack], [https://archives.arosworld.org/index.php?function=browse&amp;cat=game/roleplaying GemRB], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games card based RPG [https://github.com/open-duelyst/duelyst Duelyst], [], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games turn based tactics RPG [], [], [], [], [], [], 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=game/strategy UFO AI], [http://play.freeciv.org/ FreeCiv], [], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Strategy [http://rtsgus.org/ RTSgus], [http://stargus.sourceforge.net/ Stargus], [https://github.com/KD-lab-Open-Source/Perimeter Perimeter], [https://matty77.itch.io/conflict-3049 conflict-3049], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=game/strategy MegaGlest (OpenGL)], [https://archives.arosworld.org/?function=showfile&amp;file=game/strategy/ signus], [https://www.arosworld.org/infusions/forum/viewthread.php?thread_id=1443&amp;rowstart=140&amp;pid=12446#post_12446 Wargus warcraft 2 setup], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=12]
|-
|&lt;!--Sub Menu--&gt;Games Rhythm, Beat, Step [], [], [https://clonehero.net/ clonehero], [https://github.com/MatteoGodzilla/Dj-Engine Dj-Engine], 
|&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=game/misc Frets on Fire], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Shoot Em Ups [http://www.mhgames.org/oldies/formido/ Formido], [http://code.google.com/p/violetland/ Violetland], 
||&lt;!--AROS--&gt;[https://archives.arosworld.org/index.php?function=browse&amp;cat=game/action Open Tyrian], [http://www.parallelrealities.co.uk/projects/starfighter.php Starfighter], [ Alien Blaster], [https://github.com/OpenFodder/openfodder OpenFodder], [https://archives.arosworld.org/?function=showfile&amp;file=game/action/ tbftss The Battle for the Solar System: the Pandora War]
|&lt;!--AmigaOS--&gt;
|&lt;!--AmigaOS4--&gt;[http://www.parallelrealities.co.uk/projects/starfighter.php Starfighter], [ The Battle for the Solar System: the Pandora War]
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Simulations [http://scp.indiegames.us/ Freespace 2], [http://www.heptargon.de/gl-117/gl-117.html GL117], [http://code.google.com/p/corsix-th/ Theme Hospital], [http://code.google.com/p/freerct/ Rollercoaster Tycoon], [http://hedgewars.org/ Hedgewars], [https://github.com/raceintospace/raceintospace raceintospace], [https://github.com/Return-To-The-Roots RTTR Settlers 2], [https://github.com/OoliteProject/oolite oolite elite], [https://github.com/fesh0r/newkind newkind elite], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;SimCity, SimAnt, Sim Hospital, Theme Park, 
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;[http://morphos.lukysoft.cz/en/vypis.php?kat=12]
|-
|&lt;!--Sub Menu--&gt;Games Life Sim [https://github.com/ACreTeam/forest Animal Crossing], [ ], [], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Horror [https://github.com/Mikompilation/MikuPan Fatal Frame], [ ], [], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Sandbox Voxel Open World Exploration [https://github.com/ClassiCube/ Classicube],[http://www.michaelfogleman.com/craft/ Craft], [https://github.com/tothpaul/DelphiCraft DelphiCraft],[https://www.minetest.net/ Luanti formerly Minetest], [ infiniminer], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Battle Royale [https://bruh.io/ Play.Bruh.io], [https://www.coolmathgames.com/0-copter Copter Royale], [https://surviv.io/ Surviv.io], [https://nuggetroyale.io/#Ketchup Nugget Royale], [https://miniroyale2.io/ Miniroyale2.io], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Tower Defense [https://chriscourses.github.io/tower-defense/ HTML5], [https://github.com/SBardak/Tower-Defense-Game TD C++], [https://github.com/bdoms/love_defense LUA and LOVE], [https://github.com/HyOsori/Osori-WebGame HTML5], [https://github.com/PascalCorpsman/ConfigTD ConfigTD Pascal], [https://github.com/GloriousEggroll/wine-ge-custom Wine], []
|&lt;!--AROS--&gt;[https://www.arosworld.org/infusions/forum/viewthread.php?thread_id=1443&amp;rowstart=180&amp;pid=12871#post_12871 Plants vs Zombies PvZ], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Visual Novel Engines [https://github.com/diane1f0cd/VisualNovelTemplate Visual Novel Template], [https://github.com/Kirilllive/tuesday-js Tuesday JS], [https://github.com/tejasnayak25/vnsutra vnsutra], [https://github.com/weetabix-su/renpsp-dev RenPSP], [https://github.com/Galladite27/ONScripter-EN ONScripter-EN], [https://github.com/NathanGuilhot/VNES-Raylib https://github.com/NathanGuilhot/VNES VNES in Raylib], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Virtual Reality VR [https://gitlab.com/madsbuvi/openmw openmw vr], [https://github.com/Team-Beef-Studios/BeefRaiderXR BeefRaiderXR], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Virtual Table Top VTT [ Roll20], [https://www.owlbear.rodeo/ owlbear rodeo], [], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Computer assisted TableTop TTRPG OSR [https://www.rpgsolo.com/play.php RPGSolo], [https://github.com/fpsvogel/solo-ttrpgs Solo TTRPG], [], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games 2D 3D Engines [https://github.com/fegennari/3DWorld 3DWorld], [https://github.com/GarageGames/Torque3D Torque3D], [https://github.com/gameplay3d/GamePlay GamePlay 3D],  [https://www.babylonjs.com/ BabylonJS ], [ Godot], [ Ogre], [ Crystal Space], [https://github.com/JacobHess03/ Dragon-Quest like], [https://github.com/bjornbytes/lovr Lua LOVE for 2D LOVR for 3D], [], 
|&lt;!--AROS--&gt;[https://www.arkhamdev.net/wiki.htm?id=agx Arkham Development antiryadgx 8.9 lts with register], [], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games C based game frameworks [https://github.com/orangeduck/Corange Corange], [https://github.com/scottcgi/Mojoc Mojoc], [https://orx-project.org/ Orx], [https://github.com/ioquake/ioq3 Quake 3], [https://www.mapeditor.org/ Tiled], [https://www.raylib.com/ 2d Raylib], [https://github.com/Rabios/awesome-raylib other raylib], [https://github.com/MrFrenik/gunslinger Gunslinger], [https://o3de.org/ o3d], [http://archives.aros-exec.org/index.php?function=browse&amp;cat=development/library GLFW], [], 
|&lt;!--AROS--&gt;[http://archives.arosworld.org/index.php?function=browse&amp;cat=development/library Raylib 5], 
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games RPGMaker MV/MZ-compatible projects [https://github.com/Psychronic-Games/RPGReactor RPGReactor js],
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games Virtual Pinball [https://github.com/vpinball/vpinball vpinball], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|-
|&lt;!--Sub Menu--&gt;Games unpack unarc [], [], 
|&lt;!--AROS--&gt;
|&lt;!--Amiga OS--&gt;
|&lt;!--AmigaOS4--&gt;
|&lt;!--MorphOS--&gt;
|}


==Application Guides==

[[#top|...to the top]]

===Web Browser===

OWB is now at version 2.0 (which got an engine refresh, from July 2015 to February 2019) and 3.0.

This latest version has a good support for many/most web sites, even YouTube web page now works. 

This improved compatibility comes at the expense of higher RAM usage (now 1GB RAM is the absolute minimum). 

Also, keep in mind that the lack of a JIT (Just-In-Time) JS compiler on the 32 bit version, makes the web surfing a bit slow. 

Only the 64 bit version of OWB 2.0 will have JIT enabled, thus benefitting of more speed. There are tooltypes that can be added to the icon to provide further features JIT, MSE etc 


Certificates from [https://curl.se/docs/caextract.html ca certs], 


DNS tracking blocking with [https://easylist.to/easylist/easylist.txt easylist.txt] in PROGDIR:Conf before starting browser with enabled AdBlock [https://github.com/easylist/easylist/tree/master easylist], [https://gitlab.com/eyeo anti abp], [https://firebog.net/ big blocklist], [https://github.com/StevenBlack/hosts Steves], [], [], 

This can be enabled with OWB Odyssey with Windows -&gt; Content Blocking and Windows -&gt; Messages and enter 

 https://www.youtube.com/api/stats/ads*
 https://www.youtube.com/pagead/adview*
 https://www.youtube.com#@##player-ads*

into your custom filters 


Element blocker browser extension might be needed for [https://github.com/easylist/easylist/wiki/Youtube-Issues youtube], [ mid roll], [ pre roll], [ ],  


OWB speed is much better when running from RAM Disk, the best way is to add the below into your S:User-Startup which copies OWB drawer from Extras:Internet/OWB to RAM Disk: 

So add this :
&lt;pre&gt;
copy Extras:Internet/OWB Ram:OWB/ ALL CLONE &gt;NIL:
copy Extras:Internet/OWB.info Ram: &gt;NIL:
&lt;/pre&gt;
Open RAM Disk and open OWB drawer and double click on OWB icon so that the above icon tooltypes are activated 

Problems are that the copy time is long (around 20 seconds added in the background), but we can make it faster if we delete useless files from the OWB drawer (docs, …)
If you don’t copy the drawer back onto the HD, you won’t save your cache, cookies, passwords… So you need a script for it.


Error messages 

SSL error &quot;cant verify with ca-certificates&quot;, check bios clock time date is correct 

Error 6, try checking networking prefs settings and Save / Use preferences again or a '''few times''' otherwise the network chipset may not be compatible with Aros 


[https://www.google.com/search?q=%s&amp;udm=14 Google search without AI overview] 


===E-mail===

 YAM does not support SSL and most mail providers now switched to encrypted SMTP/POP3 connections


====SimpleMail====

SimpleMail supports IMAP and appears to work with GMail, but it's never been reliable enough, it can crash with large mailboxes.

Please read more on this [http://www.freelists.org/list/simplemail-usr User list]


 GMail

Be sure to activate the pop3 usage in your gmail account setup / configuration first.

pop3: 
pop.gmail.com
Use SSL: Yes
Port: 995

smtp:
smtp.gmail.com (with authentication)
Use Authentication: Yes
Use SSL: Yes
Port: 465 or 587


 Hotmail/MSN/outlook/Microsoft Mail mid-2017, all outlook.com accounts will be migrated to Office 365 / Exchange

Most users are currently on POP which does not allow showing folders and many other features (technical limitations of POP3). With Microsoft IMAP you will get folders, sync read/unread, and show flags. You still won't get push though, as Microsoft has not turned on the IMAP Idle command as at Sept 2013.

If you want to try it, you need to first remove (you can't edit) your pop account (long-press the account on the accounts screen, delete account). Then set it up this way:

1. Email/Password
2. Manual
3. IMAP
4.

* Incoming: imap-mail.outlook.com, port 993, SSL/TLS should be checked
* Outgoing: smtp-mail.outlook.com, port 587, SSL/TLS should be checked
* POP server name pop-mail.outlook.com, port 995, POP encryption method SSL

 Yahoo  Mail

On April 24, 2002 Yahoo ceased to offer POP access to its free mail service. Introducing instead a yearly payment feature, allowing users POP3 and IMAP server support, along with such benefits as larger file attachment sizes and no adverts.

Sorry to see Yahoo leaving its users to cough up for the privilege of accessing their mail. Understandable, when competing against rivals such as Gmail and Hotmail who hold a large majority of users and were hacked in 2014 as well.


Incoming Mail (IMAP) Server

* Server - imap.mail.yahoo.com
* Port - 993
* Requires SSL - Yes

Outgoing Mail (SMTP) Server

* Server - smtp.mail.yahoo.com
* Port - 465 or 587
* Requires SSL - Yes
* Requires authentication - Yes

Your login info

* Email address - Your full email address (name@domain.com)
* Password - Your account's password
* Requires authentication - Yes


Note that you need to enable “Web &amp; POP Access” in your Yahoo Mail account to send and receive Yahoo Mail messages through any other email program.

You will have to enable “Allow your Yahoo Mail to be POPed” under “POP and Forwarding”, to send and receive Yahoo mails through any other email client.

Cannot be done since 2002 unless the customer pays Yahoo a subscription subs fee to have access to SMTP and POP3

* Set the POP server for incoming mails as pop.mail.yahoo.com. You will have to enable “SSL” and use 995 for Port.
* “Account Name or Login Name” – Your Yahoo Mail ID i.e. your email address without the domain “@yahoo.com”.
* “Email Address” – Your Yahoo Mail address i.e. your email address including the domain “@yahoo.com”. E.g. myname@yahoo.com
* “Password” – Your Yahoo Mail password.

Yahoo! Mail Plus users may have to set POP server as plus.pop.mail.yahoo.com and SMTP server as plus.smtp.mail.yahoo.com.

* Set the SMTP server for outgoing mails as smtp.mail.yahoo.com. You will also have to make sure that “SSL” is enabled and use 465 for port. you must also enable “authentication” for this to work.


====YAM Yet Another Mailer====

 YAM does not support SSL and most mail providers have now switched to encrypted SMTP/POP3 connections

This email client is POP3 only if the SSL library is available [http://www.freelists.org/list/yam YAM Freelists]

One of the downsides of using a POP3 mailer unfortunately - you have to set an option not to delete the mail if you want it left on the server. IMAP keeps all the emails on the server.

Possible issues

Sending mail issues is probably a matter of using your ISP's SMTP server, though it could also be an SSL issue.


getting a &quot;Couldn't initialise TLSv1 / SSL error

Use of on-line e-mail accounts with this email client is not possible as it lacks the OpenSSL AmiSSl v3 compatible library

 GMail 
Incoming Mail (POP3) Server - requires SSL: pop.gmail.com
Use SSL: Yes
Port: 995

Outgoing Mail (SMTP) Server - requires TLS: smtp.gmail.com (use authentication)
Use Authentication: Yes
Use STARTTLS: Yes (some clients call this SSL)
Port: 465 or 587

Account Name: your Gmail username (including '@gmail.com')
Email Address: your full Gmail email address (username@gmail.com)
Password: your Gmail password

Anyway, the SMTP is pop.gmail.com port 465 and it uses SSLLv3 Authentication. The POP3 settings are for the same server (pop.gmail.com), only on port 995 instead.


 Outlook.com access

&lt;pre &gt;
Outlook.com SMTP server address: smtp.live.com
Outlook.com SMTP user name: Your full Outlook.com email address (not an alias)
Outlook.com SMTP password: Your Outlook.com password
Outlook.com SMTP port: 587
Outlook.com SMTP TLS/SSL encryption required: yes 
&lt;/pre &gt;


 Yahoo  Mail

&lt;pre &gt;
“POP3 Server” – Set the POP server for incoming mails as pop.mail.yahoo.com. You will have to enable “SSL” and use 995 for Port.
“SMTP Server” – Set the SMTP server for outgoing mails as smtp.mail.yahoo.com. You will also have to make sure that “SSL” is enabled and use 465 for port. you must also enable “authentication” for this to work.
“Account Name or Login Name” – Your Yahoo Mail ID i.e. your email address without the domain “@yahoo.com”.
“Email Address” – Your Yahoo Mail address i.e. your email address including the domain “@yahoo.com”. E.g. myname@yahoo.com
“Password” – Your Yahoo Mail password.
&lt;/pre &gt;

Yahoo! Mail Plus users may have to set POP server as plus.pop.mail.yahoo.com and SMTP server as plus.smtp.mail.yahoo.com.

Note that you need to enable “Web &amp; POP Access” in your Yahoo Mail account to send and receive Yahoo Mail messages through any other email program.

You will have to enable “Allow your Yahoo Mail to be POPed” under “POP and Forwarding”, to send and receive Yahoo mails through any other email client.

Cannot be done since 2002 unless the customer pays Yahoo a monthly fee to have access to SMTP and POP3


 Microsoft Outlook Express Mail 

1. Get the files to your PC.
By whatever method get the files off your Amiga onto your PC. In the YAM folder you have a number of different folders, one for each of your folders in YAM. Inside that is a file usually some numbers such as 332423.283. YAM created a new file for every single email you received.

2. Open up a brand new Outlook Express. Just configure the account to use 127.0.0.1 as mail servers. It doesn't really matter. You will need to manually create any subfolders you used in YAM.

3. You will need to do a mass rename on all your email files from YAM. Just add a .eml to the end of it. Amazing how PCs still rely mostly on the file name so it knows what sort of file it is rather than just looking at it! There are a number of multiple renamers online to download and free too.

4. Go into each of your folders, inbox, sent items etc. And do a select all then drag the files into Outlook Express (to the relevant folder obviously) Amazingly the file format that YAM used is very compatible with .eml standard and viola your emails appear. With correct dates and working attachments.

5. If you want your email into Microsoft Outlook. Open that up and create a new profile and a new blank PST file. Then go into File Import and choose to import from Outlook Express. And the mail will go into there. And viola.. you have your old email from your Amiga in a more modern day format.


===FTP===

Magellan has a great FTP module. It allows transferring files from/to a FTP server over the Internet or the local network and, even if FTP is perceived as a &quot;thing of the past&quot;, its usability is all inside the client. The FTP thing has a nice side effect too, since every Icaros machine can be a FTP server as well, and our files can be easily transferred from an Icaros machine to another with a little configuration effort.

First of all, we need to know the 'server' IP address. Server is the Icaros machine with the file we are about to download on another Icaros machine, that we're going to call 'client'. To do that, move on the server machine and 1) run Prefs/Services to be sure &quot;FTP file transfer&quot; is enabled (if not, enable it and restart Icaros); 2) run a shell and enter this command:

ifconfig -a

Make a note of the IP address for the network interface used by the local area network. For cabled devices, it usually is net0:. Now go on the client machine and run Magellan:

Perform these actions: 1) click on FTP; 2) click on ADDRESS BOOK; 3) click on &quot;New&quot;. 
You can now add a new entry for your Icaros server machine:

1) Choose a name for your server, in order to spot it immediately in the address book. Enter the IP address you got before.

2) click on Custom Options:


1) go to Miscellaneous in the left menu;

2) Ensure &quot;Passive Transfers&quot; is NOT selected;

3) click on Use. We need to deactivate Passive Transfers because YAFS, the FTP server included in Icaros, only allows active transfers at the current stage. Now, we can finally connect to our new file source:


1) Look into the address book for the newly introduced server, be sure that name and IP address are right, and

2) click on Connect. A new lister with server's &quot;MyWorkspace&quot; contents will appear. You can now transfer files over the network choosing a destination among your local (client's) volumes.

Can be adapted to any FTP client on any platform of your choice, just be sure your client allows Active Transfers as well.


===IRC Internet Relay Chat===

Jabberwocky is ideal for one-to-one social media communication, use IRC if you require one to many. 

Just type a message in ''lowercase''' letters and it will be posted to all in the [ AROS irc channel]. Please do not use UPPER CASE as it is a sign of SHOUTING which is annoying.

Other things to type in - replace &lt;message&gt; with a line of text and &lt;nick&gt; with a person's name

&lt;pre&gt;
/help

/list

/who
/whois &lt;nick&gt;

/msg &lt;nick&gt; &lt;message&gt;

/query &lt;nick&gt; 
&lt;message&gt;s
/query

/away &lt;message&gt;
/away

/quit &lt;going away message&gt; 
&lt;/pre&gt;


[http://irchelp.org/irchelp/new2irc.html#smiley Intro guide here]. IRC Primer can be found here in [http://www.irchelp.org/irchelp/ircprimer.html html], [http://www.irchelp.org/irchelp/text/ircprimer.txt TXT], [http://www.kei.com/irc/IRCprimer1.1.ps PostScript].


Issue the command /me &lt;text&gt; where &lt;text&gt; is the text that should follow your nickname.
Example: /me slaps ajk around a bit with a large trout

/nick &lt;newNick&gt;

/nickserv register &lt;password&gt; &lt;email address&gt;

/ns instead of /nickserv, while others might need /msg nickserv

/nickserv identify &lt;password&gt;

Alternatives:
/ns identify &lt;password&gt;
/msg nickserv identify &lt;password&gt;


==== IRC WookieChat ====

WookieChat is the most complete internet client for communication across the IRC Network. WookieChat allows you to swap ideas and communicate in real-time, you can also exchange Files, Documents, Images and everything else using the application's DCC capabilities.


add smilies drawer/directory

 run wookiechat from the shell and set stack to 1000000 e.g. wookiechat stack 1000000

select a server / server window

* nickname 
* user name 
* real name - optional

Once you configure the client with your preferred screen name, you'll want to find a channel to talk in.


servers

* New Server - click on this to add / add extra - change details in section below this click box 
* New Group
* Delete Entry
* Connect to server
* connect in new tab
* perform on connect

Change details

* Servername - change text in this box to one of the below Server: 
* Port number - no need to change
* Server password
* Channel - add #channel from below 
* auto join - can click this 
* nick registration password,

Click Connect to server button above


&lt;pre&gt;
Server: irc.freenode.net
Channel: #aros
&lt;/pre&gt;

irc://irc.freenode.net/aros

&lt;pre&gt;
Server: chat.amigaworld.net 
Channel: #amigaworld or #amigans 
&lt;/pre&gt;

&lt;pre&gt;
On Sunday evenings USA time usually starting around 3PM EDT (1900 UTC)
Server:irc.superhosts.net
Channel #team*amiga  
&lt;/pre&gt;

&lt;pre&gt;
BitlBee and Minbif are IRCd-like gateways to multiple IM networks
Server: im.bitlbee.org 
Port 6667 
Seems to be most useful on WookieChat as you can be connected to several servers at once. One for Bitlbee and any messages that might come through that. One for your normal IRC chat server. 
&lt;/pre&gt;

[http://www.bitlbee.org/main.php/servers.html Other servers],

&lt;pre&gt;
#Amiga.org - irc.synirc.net eu.synirc.net dissonance.nl.eu.synirc.net (IPv6: 2002:5511:1356:0:216:17ff:fe84:68a) 
twilight.de.eu.synirc.net zero.dk.eu.synirc.net us.synirc.net avarice.az.us.synirc.net envy.il.us.synirc.net harpy.mi.us.synirc.net 
liberty.nj.us.synirc.net snowball.mo.us.synirc.net - Ports 6660-6669 7001 (SSL)
&lt;/pre&gt;

&lt;pre&gt;
Multiple server support
&quot;Perform on connect&quot; scripts and channel auto-joins
Automatic Nickserv login
Tabs for channels and private conversations
CTCP PING, TIME, VERSION, SOUND
Incoming and Outgoing DCC SEND file transfers
Colours for different events
Logging and automatic reloading of logs
mIRC colour code filters
Configurable timestamps
GUI for changing channel modes easily
Configurable highlight keywords
URL Grabber window
Optional outgoing swear word filter
Event sounds for tabs opening, highlighted words, and private messages
DCC CHAT support
Doubleclickable URL's
Support for multiple languages using LOCALE
Clone detection
Auto reconnection to Servers upon disconnection
Command aliases
Chat display can be toggled between AmIRC and mIRC style
Counter for Unread messages
Graphical nicklist and graphical smileys with a popup chooser
&lt;/pre&gt;


====IRC Aircos ====

Double click on Aircos icon in Extras:Networking/Apps/Aircos. It has been set up with a guest account for trial purposes. Though ideally, choose a nickname and password for frequent use of irc. 


====IRC and XMPP Jabberwocky====
 Servers are setup and close down at random 
You sign up to a server that someone else has setup and access chat services through them. 

The two ways to access chat from jabberwocky
&lt;pre &gt;
Jabberwocky -&gt; Server -&gt; XMPP -&gt; open and ad-free 
Jabberwocky -&gt; Server -&gt; Transports (Gateways) -&gt; Proprietary closed systems 
&lt;/pre &gt;

The Jabber.org service connects with all IM services that use XMPP, the open standard for instant messaging and presence over the Internet. The services we connect with include Google Talk (closed), Live Journal Talk, Nimbuzz, Ovi, and thousands more. However, you can not connect from Jabber.org to proprietary services like AIM, ICQ, MSN, Skype, or Yahoo because they don’t yet use XMPP components (XEP-0114) '''but''' you can use Jabber.com's servers and IM gateways (MSN, ICQ, Yahoo etc.) instead.

The best way to use jabberwocky is in conjunction with a public jabber server with '''transports''' to your favorite services, like gtalk, Facebook, yahoo, ICQ, AIM, etc.


You have to register with one of the servers, [https://list.jabber.at/ this list] or [http://www.jabberes.org/servers/ another list], [http://xmpp.net/ this security XMPP list],

Unfortunately jabberwocky can only connect to one server at a time so it is best to check what services each server offers. If you set it up with separate Facebook and google talk accounts, for example, sometimes you'll only get one or the other.

Jabberwocky open a window where the Jabber server part is typed in as well as your Nickname and Password.

Jabber ID (JID) identifies you to the server and other users.

Once registered the next step is to goto Jabberwocky's &quot;Windows&quot; menu and select the &quot;Agents&quot; option. The &quot;Agents List&quot; window will open.

Roster (contacts list)

[http://search.wensley.org.uk/ Chatrooms] (MUC) are available

File Transfer - can send and receive files through the Jabber service but not with other services like IRC, ICQ, AIM or Yahoo. All you need is an installed webbrowser and OpenURL.

Clickable URLs - The message window uses Mailtext.mcc and you can set a URL action in the MUI mailtext prefs like SYS:Utils/OpenURL %s NEWWIN.

There is no consistent Skype like (H.323 VoIP) video conferencing available over Jabber. The move from xmpp to Jingle should help but no support on any amiga-like systems at the moment. [http://aminet.net/package/dev/src/AmiPhoneSrc192 AmiPhone] and [http://www.lysator.liu.se/%28frame,faq,nobg,useframes%29/ahi/v4-site/ Speak Freely] was an early attempt voice only contact. SIP and Asterisk are other PBX options.


 Facebook

If you're using the XMPP transport provided by Facebook themselves, chat.facebook.com, it looks like they're now requiring SSL transport. This means jabberwocky method below will no longer work. The best thing to do is to create an ID on a public jabber server which has a Facebook gateway.

&lt;pre &gt;
1. launch jabberwocky
2. if the login window doesn't appear on launch, select 'account' from the jabberwocky menu
3. your jabber ID will be user@chat.facebook.com where user is your user ID
4. your password is your normal facebook password
5. to save this for next time, click the popup gadget next to the ID field

6. click the 'add' button
7. click the 'close' button
8. click the 'connect' button
&lt;/pre &gt;

you're done. you can also click the 'save as default account' button if you want. jabberwocky configured to auto-connect when launching the program, but you can configure as you like. there is amigaguide documentation included with jabberwocky.

[http://amigaworld.net/modules/newbb/viewtopic.php?topic_id=37085&amp;forum=32 Read more here]

for Facebook users, you can log-in directly to Facebook with jabberwocky. just sign in as @chat.facebook.com with your Facebook password as the password


 Twitter

For a few years, there has been added a twitter transport. Servers include [http://jabber.hot-chilli.net/ jabber.hot-chili.net],  and .

An [http://jabber.hot-chilli.net/tag/how-tos/ How-to]

:Read [http://jabber.hot-chilli.net/2010/05/09/twitter-transport-working/ more]

 Instagram 

no support at the moment best to use a web browser based client

 ICQ

The new version (beta) of StriCQ uses a newer ICQ protocol. Most of the ICQ Jabber Transports still use an older ICQ protocol. You can only talk one-way to StriCQ using the older Transports. Only the newer ICQv7 Transport lets you talk both ways to StriCQ. Look at the server lists in the first section to check.

Register on a Jabber server, e.g. this one works: http://www.jabber.de/
Then login into Jabberwocky with the following login data e.g. xxx@jabber.de / Password: xxx Now add your ICQ account under the window-&gt;Agents-&gt;&quot;Register&quot;. Now Jabberwocky connects via the Jabber.de server with your ICQ account.

 Yahoo Messenger

although yahoo! does not use xmpp protocol, you should be able to use the transport methods to gain access and post your replies

 MSN

early months of 2013 Microsoft will ditch MSN Messenger client and force everyone to use Skype...but MSN protocol and servers will keep working as usual for quite a long time....

Occasionally the Messenger servers have been experiencing problems signing in.  You may need to sign in at www.outlook.com and then try again.  It may also take multiple tries to sign in.  (This also affects you if you’re using Skype.)

You have to check each servers' Agents List to see what transports (MSN protocol, ICQ protocol, etc.) are supported or use the list address' provided in the section above. Then register with each transport (IRC, MSN, ICQ, etc.) to which you need access. After registering you can Connect to start chatting.

msn.jabber.com/registered should appear in the window.

From this [http://tech.dir.groups.yahoo.com/group/amiga-jabberwocky/message/1378 JW group] guide which  helps with this process in a clear, step by step procedure.

1. Sign up on MSN's site for a passport account. This typically involves getting a Hotmail address.

2. Log on to the Jabber server of your choice and do the following:

* Select the &quot;Windows/Agents&quot; menu option in Jabberwocky.
* Select the MSN Agent from the list presented by the server.
* Click the Register button to open a new window asking for:
**Username = passort account email address, typically your hotmail address.
**Nick = Screen name to be shown to anyone you add to your buddy list.
**Password = Password for your passport account/hotmail address.
* Click the Register button at the bottom of the new window.

3. If all goes well, you will see the MSN Gateway added to your buddy list. If not, repeat part 2 on another server. Some servers may show MSN in their list of available agents, but have not updated their software for the latest protocols used by MSN.

4. Once you are registered, you can now add people to your buddy list. Note that you need to include the '''msn.''' ahead of the servername so that it knows what gateway agent to use. Some servers may use a slight variation and require '''msg.gate.''' before the server name, so try both to see what works.

If my friend's msn was amiga@hotmail.co.uk and my jabber server was @jabber.meta.net.nz..
then amiga'''%'''hotmail.com@'''msn.'''jabber.meta.net.nz

or another the trick to import MSN contacts is that you don't type the hotmail URL but the passport URL... e.g. Instead of: goodvibe%hotmail.com@msn.jabber.com  You type: goodvibe%passport.com@msn.jabber.com 
And the thing about importing contacts I'm afraid you'll have to do it by hand, one at the time...

 Google Talk

any XMPP server will work, but you have to add your contacts manually. a google talk user is typically either @gmail.com or @talk.google.com. a true gtalk transport is nice because it brings your contacts to you and (can) also support file transfers to/from google talk users.

implement Jingle a set of extensions to the IETF's Extensible Messaging and Presence Protocol (XMPP)

support ended early 2014 as Google moved to Google+ Hangouts which uses it own proprietary format


===Video Player MPlayer===

Many of the menu features (such as doubling) do not work with the current version of mplayer but using

4:3
 mplayer -vf scale=800:600 file.avi

16:9
 mplayer -vf scale=854:480 file.avi

if you want gui use;
 mplayer -gui 1 &lt;other params&gt; file.avi

&lt;pre &gt;
stack 1000000

; using AspireOS 1.xx 
; copy FROM SYS:Extras/Multimedia/MPlayer/ TO RAM:MPlayer ALL CLONE &gt; Nil:

; using Icaros Desktop 1.x 
; copy FROM SYS:Tools/MPlayer/ TO RAM:MPlayer ALL CLONE &gt; Nil:

; using Icaros Desktop 2.x 
; copy FROM SYS:Utilities/MPlayer/ TO RAM:MPlayer ALL CLONE &gt; Nil:

cd RAM:MPlayer
run MPlayer -gui &gt; Nil:
;run MPlayer -gui -ao ahi_dev -playlist http://www.radio-paralax.de/listen.pls &gt; Nil: 
&lt;/pre &gt;

$ mplayer rtsp://127.0.0.1:554/sample_300kbit.mp4


MPlayer supports multicast streaming, and rtp/rtsp protocols (it might require [http://www.live555.com/openRTSP/ live555 library] to work with some streams). But you might have to build it where it's disabled. Also, multicast won't work with some AmiTCP-likes. MIAMI supported it, though.

AROS supports IPv4 (old but works) and this includes the needed address space for RTP.

If you mean multicast via RTP - mplayer handles it. You can even force UDP over TCP

-rtsp-stream-over-tcp

If the rtsp Real Time Streaming Protocol  server needs authentification:

-user -passwd


MPlayer - Menu - Open Playlist and load already downloaded .pls or .m3u file - auto starts around 4 percent cache

MPlayer - Menu - Open Stream and copy one of the .pls lines below into space allowed, press OK and press play button on main gui interface


Old 8bit 16bit remixes chip tune game music 
 
http://www.radio-paralax.de/listen.pls 

http://scenesat.com/

http://www.shoutcast.com/radio/Amiga

http://www.theoldcomputer.com/retro_radio/RetroRadio_Main.htm

http://www.kohina.com/

http://www.remix64.com/

http://retrogamer.net/forum/

http://retroasylum.podomatic.com/rss2.xml

http://retrogamesquad.com/

http://www.retronauts.com/

http://monsterfeet.com/noquarter/

http://www.retrogamingradio.com/

http://www.radiofeeds.co.uk/mp3.asp


[[#top|...to the top]]

====ZunePaint==== 

simplified typical workflow

* importing and organizing and photo management
* making global and regional local correction(s) - recalculation is necessary after each adjustment as it is not in real-time 
* exporting your images in the best format available with the preservation of metadata


Whilst achieving 80% of a great photo with just a filter, the remaining 20% comes from a manual fine-tuning of specific image attributes.


For photojournalism, documentary, and event coverage, minimal touching is recommended. Stick to Camera Raw for such shots, and limit changes to level adjustment, sharpness, noise reduction, and white balance correction.

For fashion or portrait shoots, a large amount of adjustment is allowed and usually ends up far from the original. Skin smoothing, blemish removal, eye touch-ups, etc. are common.  Might alter the background a bit to emphasize the subject.

Product photography usually requires a lot of sharpening, spot removal, and focus stacking.

For landscape shots, best results are achieved by doing the maximum amount of preparation before/while taking the shot. No amount of processing can match timing, proper lighting, correct gear, optimal settings, etc. Excessive post-processing might give you a dramatic shot but best avoided in the long term.


* White Balance - Left Amiga or F12 and K and under &quot;Misc color effects&quot; tab with a pull down for White Balance - color temperature also known as AKA tint (movies) or tones (painting) - warm temp raise red reduce green blue - cool raise blue lower red green 
* Exposure - exposure compensation, highlight/shadow recovery
* Noise Reduction - during RAW development or using external software
* Lens Corrections - distortion, vignetting, chromatic aberrations
* Detail - capture sharpening and local contrast enhancement
* Contrast - black point, levels (sliders) and curves tools (F12 and K) 
* Framing - straighten () and crop (F12 and F) 
* Refinements - color adjustments and selective enhancements - Left Amiga or F12 and K for RGB and YUV histogram tabs - 
* Resizing - enlarge for a print or downsize for the web or email (F12 and D) 
* Output Sharpening - customized for your subject matter and print/screen size


White Balance - F12 and K

scan your image for a shade which was meant to be white (neutral with each RGB value being equal) like paper or plastic which is in the same light as the subject of the picture. Use the dropper tool to select this color, similar colours will shift and you will have selected the perfect white balance for your part of the image - for the whole picture make sure RAZ or CLR button at the bottom is pressed before applying to the image above.


Exposure correction

F12 and K - YUV Y luminosity - RGB extra red tint - move red curve slightly down and move blue green curves slightly up

Workflows in practice

* Undo - Right AROS key or F12 and Z 
* Redo - Right AROS key or F12 and R

First flatten your image (if necessary) and then do a rotation until the picture looks level. 
* Crop the picture. Click the selection button and drag a box over the area of the picture you want to keep. Press the crop button and the rest of the photo will be gone. 
* Adjust your saturation, exposure, hue levels, etc., (right AROS Key and K for color correction) until you are happy with the photo. Make sure you zoom in all of the way to 100% and look the photo over, zoom back out and move around. Look for obvious problems with the picture. 
* After coloring and exposure do a sharpen (Right AROS key and E for Convolution and select drop down option needed), e.g. set the matrix to 5x5 (roughly equivalent Amount to 60%) and set the Radius to 1.0. Click OK.


And save your picture


Implemented or would like to see for simplification and ease of use

basic filters (presets) like black and white, monochrome, edge detection (sobel), motion/gaussian blur, 
* negative, sepiatone, retro vintage, night vision, colour tint, color gradient, color temperature, glows, fire, lightning, lens flare, emboss, filmic, pixelate mezzotint, antialias, etc.

adjust / cosmetic tools such as crop, 
* reshaping tools, straighten, smear, smooth, perspective, liquify, bloat, pucker, push pixels in any direction, dispersion, transform like warp, blending with soft light, page-curl, whirl, ripple, fisheye, neon,  etc. 
* red eye fixing, blemish remover, skin smoothing, teeth whitener, make eyes look brighter, desaturate,

effects like oil paint, cartoon, pencil sketch, charcoal, noise/matrix like sharpen/unsharpen, (right AROS key with A for Artistic effects) 
* blend two image, gradient blend, masking blend, explode, implode, custom collage, surreal painting, comic book style, needlepoint, stained glass, watercolor, mosaic, stencil/outline, crayon, chalk, etc.

borders such as 
* dropshadow, rounded, blurred, color tint, picture frame, film strip polaroid, bevelled edge, etc.

brushes e.g.
* frost, smoke, etc.

and manual control of

fix lens issues including vignetting (darkening), color fringing and barrel distortion, and chromatic and geometric aberration -  lens and body profiles

perspective correction

levels - directly modify the levels of the tone-values of an image, by using sliders for highlights, midtones and shadows

curves -  Color Adjustment and Brightness/Contrast

color balance

one single color transparent (alpha channel (color information/selections) for masking and/or blending ) for backgrounds, etc.

Threshold indicates how much other colors will be considered mixture of the removed color and non-removed colors

decompose layer into a set of layers with each holding a different type of pattern that is visible within the image

any selection using any selecting tools like lasso tool, marquee tool etc. the selection will temporarily be save to alpha 
If you create your image without transparency then the Alpha channel is not present, but you can add later.

File formats like .psd (Photoshop file has layers, masks etc.  contains edited sensor data. The original sensor data is no longer available) .xcf .raw .hdr

Image Picture Formats
* low dynamic range (JPEG, PNG, TIFF 8-bit), 16-bit (PPM, TIFF), typically as a 16-bit TIFF in either ProPhoto or AdobeRGB colorspace -  TIFF files are also fairly universal – although, if they contain proprietary data, such as Photoshop Adjustment Layers or Smart Filters, then they can only be opened by Photoshop making them proprietary.
* linear high dynamic range (HDR) images (PFM, [http://www.openexr.com/ ILM .EXR], jpg, [http://aminet.net/util/dtype cr2] (canon tiff based), hdr, NEF, CRW, ARW, MRW, ORF, RAF (Fuji), PEF, DCR, SRF, ERF, DNG files are RAW converted to an Adobe proprietary format - a container that can embed the raw file as well as the information needed to open it) 
An old version of [http://archives.aros-exec.org/index.php?function=browse&amp;cat=graphics/convert dcraw]

There is no single RAW file format. Each camera manufacturer has one or more unique RAW formats. RAW files contain the brightness levels data captured by the camera sensor. This data cannot be modified. A second smaller file, separate XML file, or within a database with instructions for the RAW processor to change exposure, saturation etc. The extra data can be changed but the original sensor data is still there. RAW is technically least compatible.

A raw file is high-bit (usually 12 or 14 bits of information) but a camera-generated TIFF file will be usually converted by the camera (compressed, downsampled) to 8 bits. The raw file has no embedded color balance or color space, but the TIFF has both. These three things (smaller bit depth, embedded color balance, and embedded color space) make it so that the TIFF will lose quality more quickly with image adjustments than the raw file. The camera-generated TIFF image is much more like a camera processed JPEG than a raw file. A strong advantage goes to the raw file. The power of RAW files, such as the ability to set any color temperature non-destructively and will contain more tonal values.

The principle of preserving the maximum amount of information to as late as possible in the process. The final conversion - which will always effectively represent a &quot;downsampling&quot; - should prevent as much loss as possible.

Once you save it as TIFF, you throw away some of that data irretrievably. When saving in the lossy JPEG format, you get tremendous file size savings, but you've irreversibly thrown away a lot of image data. As long as you have the RAW file, original or otherwise, you have access to all of the image data as captured.

Keyboard equivalence with Photoshop(tm) would help 

File
PHOTOSHOP	SHORTCUT	GIMP
New	Ctrl+n	New
Open	Ctrl+o	Open
Close	Ctrl+w	Close
Save	Ctrl+s	Save
Save as	Shift+Ctrl+s	Save as
Revert	F12	Revert
Print	Ctrl+p	Print
Exit	Ctrl+q	Quit
 
Edit
PHOTOSHOP	SHORTCUT	GIMP
Undo/Redo (1 level)	Ctrl+z	Undo (Redo is Shift+Ctrl+z)
Cut	Ctrl+x	Cut
Copy	Ctrl+c	Copy
Paste	Ctrl+v	Paste
Paste Into	Shift+Ctrl+v	Paste Into
Fill with FG color	Alt+Backspace	Fill with FG color
Fill with BG color	Control+Backspace	Fill with BG color
 
Image/Colors
PHOTOSHOP	SHORTCUT	GIMP
Levels	Ctrl+l	Levels
Auto Contrast	Shift+Ctrl+Alt+l	Stretch Contrast (same?)
Curves	Ctrl+m	Curves
Color Balance	Ctrl+b	Color Balance
Hue/Saturation	Ctrl+u	Hue-Saturation
Desaturate	Shift+Ctrl+u	Desaturate
Invert	Ctrl+i	Invert
Default Colors	d	Default Colors
Switch Colors	x	Switch Colors
 
Layer
PHOTOSHOP	SHORTCUT	GIMP
New Layer	Shift+Ctrl+n	New Layer
Layer via Copy	Ctrl+j	Duplicate Layer
Bring (layer) to Front	Shift+Ctrl+]	Layer to Top
Send (layer) to Back	Shift+Ctrl+[	Layer to Bottom
Bring (layer) Forward	Ctrl+]	Raise Layer
Send (layer) Backward	Ctrl+[	Lower Layer
Select Top Layer	Shift+Alt+]	Select Top Layer
Select Bottom Layer	Shift+Alt+[	Select Bottom Layer
Select One Layer Forward	Alt+]	Select Previous Layer
Select One Layer Backward	Alt+[	Select Next Layer
Merge Down	Ctrl+e	Merge Down
Merge Visible	Shift+Ctrl+e	Merge Visible
Preserve Transparency	/	Keep Transparency
Cycle Modes Forwards	Shift+=	Next Layer Mode
Cycle Modes Backwards	Shift+-	Previous Layer Mode
 
Select
PHOTOSHOP	SHORTCUT	GIMP
Select All	Ctrl+a	Select All
Deselect	Ctrl+d	Select None
Inverse	Shift+Ctrl+i	Invert
Feather	Ctrl+Alt+d	Feather
 
View
PHOTOSHOP	SHORTCUT	GIMP
Zoom In	Ctrl+=	Zoom In
Zoom Out	Ctrl+-	Zoom Out
Fit on Screen	Ctrl+0	Zoom to Fit Window
Actual Pixels	Ctrl+Alt+0	Zoom 1:1
Show/Hide Extras	Ctrl+h	Toggle Show Selection (close enough?)
Show/Hide Guides	Ctrl+'	Toggle Show Guides
Show/Hide Grid	Ctrl+Alt+'	Toggle Show Grid
Show/Hide Rulers	Ctrl+r	Toggle Show Rulers
Snap	Ctrl+;	Snap to Guides
Scroll View Up	Page Up	Scroll Page Up
Scroll View Down	Page Down	Scroll Page Down
Scroll View Left	Ctrl+Page Up	Scroll Page Left
Scroll View Right	Ctrl+Page Down	Scroll Page Right
 
Window/Dialogs
PHOTOSHOP	SHORTCUT	GIMP
?	F5	Tools Dialog
Color Tab	F6	Colors Dialog
Layers Tab	F7	Layers Dialog
Info Tab	F8	Image Information
 
Tools
PHOTOSHOP	SHORTCUT	GIMP
Rectangular Marquee Tool	m	Rect Select Tool
Elliptical Marquee Tool	Shift+m	Ellipse Select Tool
 	*This is a toggle between 'Elliptical Marquee Tool' and 'Rectangular Marquee Tool' in Photoshop	 
Move Tool	v	Move Tool
Lasso Tool	l	Free Select Tool
Magic Wand Tool	w	Fuzzy Select Tool
Crop Tool	c	Crop &amp; Resize Tool
Airbrush Tool	j	Airbrush Tool
Paintbrush Tool	b	Paintbrush Tool
Clone Stamp Tool	s	Clone Stamp Tool
Eraser Tool	e	Eraser Tool
Gradient Tool	g	Blend Tool
Paint Bucket Tool	Shift+g	Bucket Fill Tool
 	*This is a toggle between 'Paint Bucket Tool' and 'Gradient Tool' in Photoshop	 
Blur Tool	r	Convolve Tool
Dodge Tool	o	DodgeBurn Tool
Type Tool	t	Text Tool
Pen Tool	p	Bezier Select Tool
Eye Dropper Tool	i	Color Picker Tool
Zoom Tool	z	Magnify Tool
Previous Brush	,	Previous Brush
Next Brush	.	Next Brush
First Brush	Shift+&lt;	First Brush
Last Brush	Shift+&gt;	Last Brush
Decrease Brush Size	[	Decrease Brush Size
Increase Brush Size	]	Increase Brush Size
Decrease Brush Hardness	{	Decrease Brush Hardness
Increase Brush Hardness	}	Increase Brush Hardness
 
Help
PHOTOSHOP	SHORTCUT	GIMP
Help	F1	Help
Context Help	Shift+F1	Context Help
 
Misc.
PHOTOSHOP	SHORTCUT	GIMP
Last Filter	Ctrl+f	Repeat Last Filter
?	Shift+Ctrl+f	Reshow Last Filter
Preferences	Ctrl+k	Preferences
Liquify	Shift+Ctrl+x	IWarp (close enough?)
Toggle Quick Mask	q	Toggle Quick Mask


Spotlights - triangle of white opaque shape

Cutting out and/or replacing unwanted background or features - select large areas with the selection option like the Magic Wand tool (aka Color Range) or the Lasso (quick and fast) with feather 2 to soften edge or the pen tool which adds points/lines/Bézier curves (better control but slower), hold down the shift button as you click to add extra points/areas of the subject matter to remove. Increase the tolerance to cover more areas. To subtract from your selection hold down alt as you're clicking. 
* Layer masks are a better way of working than Erase they clip (black hides/hidden white visible/reveal). Clone Stamp can be simulated by   and brushes for other areas. 
* Leave the fine details like hair, fur, etc. to later with lasso and the shift key to draw a line all the way around your subject. Gradient Mapping - Inverse - Mask. i.e. Refine your selected image with edge detection and using the radius and edge options / adjuster (increase/decrease contrast) so that you will capture more fine detail from the background allowing easier removal. 
Remove fringe/halo

saving image as png rather than jpg/jpeg to keep transparency background intact.


Implemented [http://colorizer.org/ colour model representations] [http://paulbourke.net/texture_colour/colourspace/ Mathematical approach] - Photo stills are spatially 2d (h and w), but are colorimetrically 3d (r g and b, or H L S, or Y U V etc.) as well. 
* RGB - split cubed mapped color model for photos and computer graphics hardware using the light spectrum (adding and subtracting) 
* YUV - Y-Lightness U-blue/yellow V-red/cyan (similar to YPbPr and YCbCr) used in the PAL, NTSC, and SECAM composite digital TV color [http://crewofone.com/2012/chroma-subsampling-and-transcoding/#comment-7299 video]


Histograms

White balanced (neutral) if the spike happens in the same place in each channel of the RGB graphs. If not, you're not balanced. 
If you have sky you'll see the blue channel further off to the right.

RGB is best one to change colours. These elements RGB is a 3-channel format containing data for Red, Green, and Blue in your photo scale between 0 and 255. The area in a picture that appears to be brighter/whiter contains more red color as compared to the area which is relatively darker. Similarly in the green channel the area that appears to be darker contains less amount of green color as compared to the area that appears to be brighter.  Similarly in the blue channel the area appears to be darker contains less amount of blue color as compared to the area that appears to be brighter. Brightness luminance histogram also matches the green histogram more than any other color - human eye interprets green better e.g. RGB rough ratio 15/55/30%

RGBA (RGB+A, A means alpha channel) .  The alpha channel is used for &quot;alpha compositing&quot;, which can mostly be associated as &quot;opacity&quot;.  AROS deals in RGB with two digits for every color (red, green, blue), in ARGB you have two additional hex digits for the alpha channel.

The shadows are represented by the left third of the graph.  The highlights are represented by the right third.  And the midtones are, of course, in the middle.  The higher the black peaks in the graph, the more pixels are concentrated in that tonal range (total black area). 
By moving the black endpoint, which identifies the shadows (darkness) and a white light endpoint (brightness) up and down either sides of the graph, colors are adjusted based on these points. 
By dragging the central one, can increased the midtones and control the contrast, raise shadows levels, clip or softly eliminate unsafe levels, alter gamma, etc... in a way that is much more precise and creative .


RGB Curves

* Move left endpoint (black point) up or right endpoint (white point) up brightens 
* Move left endpoint down or right endpoint down darkens

Color Curves

* Dragging up on the Red Curve increases the intensity of the reds in the image but 
* Dragging down on the Red Curve decreases the intensity of the reds and thus increases the apparent intensity of its complimentary color, cyan. Green’s complimentary color is magenta, and blue’s is yellow.
&lt;pre&gt;
 Red &lt;-&gt; Cyan
 Green &lt;-&gt;Magenta
 Blue &lt;-&gt;Yellow 
&lt;/pre&gt;

YUV Best option to analyse and pull out statistical elements of any picture (i.e.  separate luminance data from color data). The line in Y luma tone box represents the brightness of the image with the point in the bottom left been black, and the point in the top right as white.  A low-contrast image has a concentrated clump of values nearer to the center of the graph. By comparison, a high-contrast image has a wider distribution of values across the entire width of the Histogram.   A histogram that is skewed to the right would indicate a picture that is a bit overexposed because most of the color data is on the lighter side (increase exposure with higher value F), while a histogram with the curve on the left shows a picture that is underexposed. This is good information to have when using post-processing software because it shows you not only where the color data exists for a given picture, but also where any data has been clipped (extremes on edges of either side): that is, it does not exist and, therefore, cannot be edited.  By dragging the endpoints of the line and as well as the central one, can increased the dark/shadows, midtones and light/bright parts and control the contrast, raise shadows levels, clip or softly eliminate unsafe levels, alter gamma, etc... in a way that is much more precise and creative .

The U and V chroma parts show color difference components of the image. It’s useful for checking whether or not the overall chroma is too high, and also whether it’s being limited too much
Can be used to create a negative image but also 
With U (Cb), the higher value you are, the more you're on the blue primary color. If you go to the low values then you're on blue complementary color, i.e. yellow.
With V (Cr), this is the same principle but with Red and Cyan.
e.g. If you push U full blue and V full red, you get magenta. If you push U full yellow and V full Cyan then you get green.

YUV simultaneously adds to one side of the color equation while subtracting from the other.  
using YUV to do color correction can be very problematic because each curve alters the result of each other: the mutual influence between U and V often makes things tricky. You may also be careful in what you do to avoid the raise of noise (which happens very easily). Best results are obtained with little adjustments

sunset that looks uninspiring and needs some color pop especially for the rays over the hill, a subtle contrast raise while setting luma values back to the legal range without hard clipping.


Free royalty pictures, [www.freeimages.com ], [http://imageshack.us/ ], [http://photobucket.com/ ], [http://rawpixels.net/], [], [], [], 


====Lunapaint====

Pixel based drawing app with onion-skin animation function

 Blocking, Shading, Coloring, adding detail 

&lt;pre&gt;
b BRUSH
e ERASER

alt eyedropper 
v layer tool 

z ZOOM / MAGNIFY &lt; &gt; n 
spc panning 
m  marque 
q lasso 
w same color selection / region 
&lt;/pre&gt;

&lt;pre&gt;
, LM RM
v 
V
f  filter 
F 
.  size 

p 
,  pick color 
[] last / next color 
&lt;/pre&gt;


There is not much missing in Lunapaint to be as good as FlipBook and then you have to take into account that Flipbook is considered to be amongst the best and easiest to use animation software out there. Ok to be honest Flipbook has some nice features that require more heavy work but those aren't so much needed right away, things like camera effects, sound, smart fill, export to different movie file formats etc.

Tried Flipbook with my tablet and compared it to Luna. The feeling is the same when sketching. LunaPaint is very responsive/fluent to draw with. Just as Flipbook is, and that responsiveness is something its users have mentioned as one of the positive sides of said software.

 author was learning MUI. Some parts just have to be rewritten with proper MUI classes before new features can be added.

* add [Frame Add] / [Frame Del]
* whole animation feature is impossible to use. If you draw 2 color maybe but if you start coloring your cells then you get in trouble
* pickup the entire image as a brush, not just a selection ? And consequently remove the brush from memory when one doesn't need it anymore. can pick up a brush and put it onto a new image but cropping isn't possible, nor to load/save brushes.
* Undo is something I longed for ages in Lunapaint.
* to import into the current layer, other types of images (e.g. JPEG) besides RAW64.
* implement graphic tablet features support


**GENERAL DRAWING**

Miss it very much:
UNDO
ERASER
COLORPICKER - has to show on palette too which color got picked.
BACKGROUND COLOR -Possibility to select from &quot;New project screen&quot;

Miss it somewhat:
ICON for UNDO
ICON for ERASER
ICON for CLEAR SCREEN ( What can I say? I start over from scratch very often )
BRUSH - possibility to cut out as brush not just copy off image to brush

**ANIMATING**

Miss it very much:
NUMBER OF CELLS - Possibity to change total no. of cells during project
ANIM BRUSH - Possibility to pick up a selected part of cells into an animbrush

Miss it somewhat:
ADD/REMOVE FRAMES: Add/remove single frame

In general LunaPaint is really well done and it feels like a new DeluxePaint version. It works with my tablet. Sure there's much missing of course but things can always be added over time. So there is great potential in LunaPaint that's for sure. Animations could be made in it and maybe put together in QuickVideo, saving in .gif or .mng etc some day.


LAYERS
-Layers names don't get saved globally in animation frames
-Layers order don't change globally in an animation (perhaps as default?).

EXPORTING IMAGES
-Exporting frames to JPG/PNG gives problems with colors. (wrong colors. See my animatiopn --&gt; My robot was blue now it's &quot;gold&quot; ) I think this only happens if you have layers.
-Trying to flatten the layers before export doesn't work if you have animation frames only the one you have visible will flatten properly all other frames are destroyed. (Only one of the layers are visible on them)
-Exporting images filenames should be for example e.g. file0001, file0002...file0010 instead as of now file1, file2...file10

LOAD/SAVE (Preferences)
-Make a setting for the default &quot;Work&quot; folder.

* Destroyed colors if exported image/frame has layers 
* mystic color cycling of the selected color while stepping frames back/forth (annoying)

&lt;pre&gt;
Deluxe Paint II enhanced key shortcuts 
    NOTE: @ denotes the ALT key

    [Technique]

    F1  - Paint
    F2  - Single Colour
    F3  - Replace
    F4  - Smear
    F5  - Shade
    F6  - Cycle
    F7  - Smooth
     M  - Colour Cycle

    [Brush]

     B  - Restore
     O  - Outline
     h  - Halve brush size
     H  - Double brush size
     x  - Flip brush on X axis
     X  - Double brush size on X axis only
     y  - Flip on Y 
     Y  - Double on Y
     z  - Rotate brush 90 degrees
     Z  - Stretch

    [Stencil]

     `  - Stencil On

    [Miscellaneous]

    F9  - Info Bar
    F10 - Selection Bar
    @o  - Co-Ordinates
    @a  - Anti-alias
    @r  - Colourise
    @t  - Translucent
    TAB - Colour Cycle

    [Picture]

     L  - Load
     S  - Save
     j  - Page to Spare(Flip)
     J  - Page to Spare(Copy)
     V  - View Page
     Q  - Quit

    [General Keys]

     m  - Magnify
     &lt;  - Zoom In
     &gt;  - Zoom Out
     [  - Palette Colour Up
     ]  - Palette Colour Down
     (  - Palette Colour Left
     )  - Palette Colour Right
     ,  - Eye Dropper
     .  - Pixel / Brush Toggle
     /  - Symmetry
     |  - Co-Ordinates
    INS - Perspective Control
    +/- - Brush Size (Fine Control)
     w  - Unfilled Polygon
     W  - Filled Polygon
     e  - Unfilled Ellipse
     E  - Filled Ellipse
     r  - Unfilled Rectangle
     R  - Filled Rectangle
     t  - Type/text tool
     a  - Select Font
    u/U - Undo
     d  - Brush
     D  - Filled Non-Uniform Polygon
    f/F - Fill Options
    g/G - Grid
    h/H - Brush Size (Coarse Control)
     K  - Clear
     c  - Unfilled Circle
     C  - Filled Circle
     v  - Line
     b  - Scissor Select and Toggle
     B  - Brush
    {,} - Toggle between two background colours
&lt;/pre&gt;

====Lodepaint====

Pixel based painting artwork app

====Grafx2====

Pixel based painting artwork app aesprite like 

[https://www.youtube.com/watch?v=59Y6OTzNrhk aesprite workflow keys and tablet use], [], 


====Vector Graphics ZuneFIG====

Vector Image Editing of files .svg .ps .eps


*Objects - raise lower rotate flip aligning snapping 
*Path - unify subtract intersect exclude divide 
*Colour - fill stroke 
*Stroke - size 
*Brushes - 
*Layers - 
*Effects - gaussian bevels glows shadows 
*Text    - 
*Transform - 


 AmiFIG ([http://epb.lbl.gov/xfig/frm_introduction.html xfig manual]) 

[[File:MyScreen.png|thumb|left|alt=Showing all Windows open in AmiFIG.|All windows available to AmiFIG.]]

for drawing simple to intermediate vector graphic images for scientific and technical uses and for illustration purposes for those with talent

;Menu options
* Load - fig format but import(s) SVG
* Save - fig format but export(s) eps, ps, pdf, svg and png
* PAN = Ctrl + Arrow keys 
* Deselect all points

There is no selected object until you apply the tool, and the selected object is not highlighted.

;Metrics - to set up page and styles - first window to open on new drawings

;Tools - Drawing Primitives - set Attributes window first before clicking any Tools button(s) 
* Shapes - circles, ellipses, arcs, splines, boxes,  polygon 
* Lines - polylines
* Text &quot;T&quot; button 
* Photos - bitmaps
* Compound - Glue, Break, Scale 
* POINTs - Move, Add, Remove 
* Objects - Move, Copy, Delete, Mirror, Rotate, Paste 
use right mouse button to stop extra lines, shapes being formed and the left mouse to select/deselect tools button(s)
* Rotate - moves in 90 degree turns centered on clicked POINT of a polygon or square

;Attributes which provide change(s) to the above primitives 
* Color
* Line Width
* Line Style
* arrowheads

;Modes 
Choose from freehand, charts, figures, magnet, etc.

;Library - allows .fig clip-art to be stored 
* compound tools to add .fig(s) together

;FIG 3.2 [http://epb.lbl.gov/xfig/fig-format.html Format] as produced by xfig version 3.2.5 
&lt;pre&gt;
Landscape
Center
Inches
Letter 
100.00
Single
-2
1200 2
4 0 0 50 -1 0 12 0.0000 4 135 1050 1050 2475 This is a test.01
&lt;/pre&gt;

# change the text alignment within the textbox. I can choose left, center, or right aligned by either changing the integer in the second column from 0 (left) to 1 or 2 (center, or right). 
# The third integer in the row specifies fontcolor. For instance, 0 is black, but blue is 1 and Green3 is 13.
# The sixth integer in the bottom row specifies fontface. 0 is Times-Roman, but 16 is Helvetica (a MATLAB default).
# The seventh number is fontsize. 12 represents a 12pt fontsize. Changing the fontsize of an item really is as easy as changing that number to 20.
# The next number is the counter-clockwise angle of the text. Notice that I have changed the angle to .7854 (pi/4 rounded to four digits=45 degrees).
# twelfth number is the position according to the standard “x-axis” in Xfig units from the left. Note that 1200 Xfig units is equivalent to once inch.
# thirteenth number is the “y-position” from the top using the same unit convention as before.

* The nested text string is what you entered into the textbox.
* The “01″ present at the end of that line in the .fig file is the closing tag. For instance, a change to \100 appends a @ symbol at the end of the period of that sentence.

; Just to note there are no layers, no 3d functions, no shading, no transparency, no animation


[[#top|...to the top]]

===Audio===


# AHI uses linear panning/balance, which means that in the center, you will get -6dB. If an app uses panning, this is what you will get. Note that apps like Audio Evolution need panning, so they will have this problem.

# When using AHI Hifi modes, mixing is done in 32-bit and sent as 32-bit data to the driver. The Envy24HT driver uses that to output at 24-bit (always).

# For the Envy24/Envy24HT, I've made 16-bit and 24-bit inputs (called Line-in 16-bit, Line-in 24-bit etc.). There is unfortunately no app that can handle 24-bit recording.


====Music Mods====

Digital module (mods) trackers are music creation software using samples and sometimes soundfonts, audio plugins (VST, AU or RTAS), MIDI.

Generally, MODs are similar to MIDI in that they contain note on/off and other sequence messages that control the mod player. Unlike (most) midi files, however, they also contain sound samples that the sequence information actually plays. MOD files can have many channels (classic amiga mods have 4, corresponding to the inbuilt sound channels), but unlike MIDI, each channel can typically play only one note at once. However, since that note might be a sample of a chord, a drumloop or other complex sound, this is not as limiting as it sounds.

Like MIDI, notes will play indefinitely if they're not instructed to end. Most trackers record this information automatically if you play your music in live. If you're using manual note entry, you can enter a note-off command with a keyboard shortcut - usually Caps Lock.

In fact when considering file size MOD is not always the best option. Even a dummy song wastes few kilobytes for nothing when a simple SID tune could be few hundreds bytes and not bigger than 64kB. AHX is another small format, AHX tunes are never larger than 64kB excluding comments.

[https://www.youtube.com/watch?v=rXXsZfwgil Protrekkr] (previously aka [w:Juan_Antonio_Arguelles_Rius|NoiseTrekkr])

If Protrekkr does not start, please check if the Unit 0 has been setup in the AHI prefs and still not, go to the directory utilities/protrekkr and double click on the Protrekkr icon

*Sample
*Note - Effect 
*Track (column) - Pattern - Order

It all starts with the Sample which is used to create Note(s) in a Track (column of a tracker) 
The Note can be changed with an Effect.  A Track of Note(s) can be collected into a Pattern (section of a song) and these can be given Order to create the whole song.

Patience (notes have to be entered one at a time) or playing the bassline on a midi controller (faster - see midi section above).  Best approach is to wait until a melody popped into your head.

*Up-tempo means the track should be reasonably fast, but not super-fast. 
*Groovy and funky imply the track should have some sort of &quot;swing&quot; feel, with plenty of syncopation or off beat emphasis and a recognizable, melodic bass line. 
*Sweet and happy mean upbeat melodies, a major key and avoiding harsh sounds.
*Moody - minor key

First, create a quick bass sound, which is basically a sine wave, but can be hand drawn for a little more variance. It could also work for the melody part, too.

This is usually a bass guitar or some kind of synthesizer bass. The bass line is often forgotten by inexperienced composers, but it plays an important role in a musical piece. Together with the rhythm section the bass line forms the groove of a song. It's the glue between the rhythm section and the melodic layer of a song.

The drums are just pink noise samples, played at different frequencies to get a slightly different sound for the kick, snare, and hihats.

Instruments that fall into the rhythm category are bass drums, snares, hi-hats, toms, cymbals, congas, tambourines, shakers, etc. Any percussive instrument can be used to form part of the rhythm section.

The lead is the instrument that plays the main melody, on top of the chords. There are many instruments that can play a lead section, like a guitar, a piano, a saxophone or a flute. The list is almost endless. There is a lot of overlap with instruments that play chords. Often in one piece an instrument serves both roles. The lead melody is often played at a higher pitch than the chords.

Listened back to what was produced so far, and a counter-melody can be imagined, which can be added with a triangle wave.

To give the ends of phrases some life, you can add a solo part with a crunchy synth. By hitting random notes in the key of G, then edited a few of them.

For the climax of the song, filled out the texture with a gentle high-pitch pad… …and a grungy bass synth.


The arrow at A points at the pattern order list. As you see, the patterns don't have to be in numerical order. This song starts with pattern &quot;00&quot;, then pattern &quot;02&quot;, then &quot;03&quot;, then &quot;01&quot;, etcetera. Patterns may be repeated throughout a song.

The B arrow points at the song title. Below it are the global BPM and speed parameters. These determine the tempo of the song, unless the tempo is altered through effect commands during the song.

The C arrow points at the list of instruments. An instrument may consist of multiple samples. Which sample will be played depends on the note. This can be set in the Instrument Editing screen. Most instruments will consist of just one sample, though. The sample list for the selected instrument can be found under arrow D.

Here's a part of the main editing screen. This is where you put in actual notes. Up to 32 channels can be used, meaning 32 sounds can play simultaneously. The first six channels of pattern &quot;03&quot; at order &quot;02&quot; are shown here. The arrow at A points at the row number. The B arrow points at the note to play, in this case a C4. The column pointed at by the C arrow tells us which instrument is associated with that note, in this case instrument #1 &quot;Kick&quot;.

The column at D is used (mainly) for volume commands. In this case it is left empty which means the instrument should play at its default volume. You can see the volume column being used in channel #6.

The E column tells us which effect to use and any parameters for that effect. In this case it holds the &quot;F&quot; effect, which is a tempo command. The &quot;04&quot; means it should play at tempo 4 (a smaller number means faster).

Base pattern

When I create a new track I start with what I call the base pattern. It is worthwhile to spend some time polishing it as a lot of the ideas in the base pattern will be copied and used in other patterns. At least, that's how I work. Every musician will have his own way of working. In &quot;Wild Bunnies&quot; the base pattern is pattern &quot;03&quot; at order &quot;02&quot;.

In the section about selecting samples I talked about the four different categories of instruments: drums, bass, chords and leads. That's also how I usually go about making the base pattern. I start by making a drum pattern, then add a bass line, place some chords and top it off with a lead. This forms the base pattern from which the rest of the song will grow.


Drums

Here's a screenshot of the first four rows of the base pattern. I usually reserve the first four channels or so for the drum instruments. Right away there are a couple of tricks shown here. In the first channel the kick, or bass drum, plays some notes. Note the alternating F04 and F02 commands. The &quot;F&quot; command alters the tempo of the song and by quickly alternating the tempo; the song will get some kind of &quot;swing&quot; feel.

In the second channel the closed hi-hat plays a fairly simple pattern. Further down in the channel, not shown here, some open hi-hat notes are added for a bit of variation.

In the third and fourth channel the snare sample plays. The &quot;8&quot; command is for panning. One note is panned hard to the left and the other hard to the right. One sample is played a semitone lower than the other. This results in a cool flanging effect. It makes the snare stand out a little more in the mix.


Bass line

There are two different instruments used for the bass line. Instrument #6 is a pretty standard synthesized bass sound. Instrument #A sounds a bit like a slap bass when used with a quick fade out. By using two different instruments the bass line sounds a bit more ”human”. The volume command is used to cut off the notes. However, it is never set to zero. Setting the volume to a very small value will result in a reverb-like effect. This makes the song sound more &quot;live&quot;.

The bass line hints at the chords that will be played and the key the song will be in. In this case the key of the song is D-major, a positive and happy key.


Chords

The D major chords that are being played here are chords stabs; short sounds with a quick decay (fade out). Two different instruments (#8 and #9) are used to form the chords. These instruments are quite similar, but have a slightly different sound, panning and volume decay. Again, the reason for this is to make the sound more human. The volume command is used on some chords to simulate a delay, to achieve more of a live feel. The chords are placed off-beat making for a funky rhythm.


Lead

Finally the lead melody is added. The other instruments are invaluable in holding the track together, but the lead melody is usually what catches people's attention.

A lot of notes and commands are used here, but it looks more complex than it is. A stepwise ascending melody plays in channel 13. Channel 14 and 15 copy this melody, but play it a few rows later at a lower volume. This creates an echo effect. A bit of panning is used on the notes to create some stereo depth. Like with the bass line, instead of cutting off notes the volume is set to low values for a reverb effect. The &quot;461&quot; effect adds a little vibrato to the note, which sounds nice on sustained notes.

Those paying close attention may notice the instrument used here for the lead melody is the same as the one used for the bass line (#6 &quot;Square&quot;), except played two or three octaves higher. This instrument is a looped square wave sample. Each type of wave has its own quirks, but the square wave (shown below) is a really versatile wave form.

Song structure

Good, catchy songs are often carefully structured into sections, some of which are repeated throughout the song with small variations.

A typical pop-song structure is: Intro - Verse - Chorus - Verse - Chorus - Bridge - Chorus.

Other single sectional song structures are

&lt;pre&gt;
Strophic or AAA Song Form - oldest story telling with refrain (often title of the song) repeated in every verse section melody 
AABA Song Form - early popular, jazz and gospel fading during the 1960s 
AB or Verse/Chorus Song Form - songwriting format of choice for modern popular music since the 1960s 
Verse/Chorus/Bridge Song Form
ABAB Song Form
ABAC Song Form
ABCD Song Form
AAB 12-Bar Song Form - three four-bar lines or sub-sections 
8-Bar Song Form
16-Bar Song Form
Hybrid / Compound Song Forms
&lt;/pre&gt;

The most common building blocks are:

#INTRODUCTION(INTRO)
#VERSE
#REFRAIN
#PRE-CHORUS / RISE / CLIMB
#CHORUS
#BRIDGE
#MIDDLE EIGHT
#SOLO / INSTRUMENTAL BREAK
#COLLISION
#CODA / OUTRO
#AD LIB (OFTEN IN CODA / OUTRO)

The chorus usually has more energy than the verse and often has a memorable melody line. As the chorus is repeated the most often during the song, it will be the part that people will remember.

The bridge often marks a change of direction in the song. It is not uncommon to change keys in the bridge, or at least to use a different chord sequence. The bridge is used to build up tension towards the big finale, the last repetition of chorus.


 Playing

RCTRL:                           Play song from row 0.

LSHIFT + RCTRL:                  Play song from current row.

RALT:                            Play pattern from row 0.

LSHIFT + RALT:                   Play pattern from current row.

Left mouse on '&gt;':               Play song from row 0.

Right mouse on '&gt;':              Play song from current row.

Left mouse on '|&gt;':              Play pattern from row 0.

Right mouse on '|&gt;':             Play pattern from current row.

Left mouse on 'Edit/Record':     Edit mode on/off.

Right mouse on 'Edit/Record':    Record mode on/off.


 Editing 


LSHIFT + ESCAPE:                 Switch large patterns view on/off

TAB:                    Go to next track

LSHIFT + TAB:                    Go to prev. track

LCTRL + TAB:                    Go to next note in track

LCTRL + LSHIFT + TAB:           Go to prev. note in track

SPACE:                           Toggle Edit mode On &amp; Off

(Also stop if the song is being played)

SHIFT SPACE:                     Toggle Record mode On &amp; Off

(Wait for a key note to be pressed

or a midi in message to be received)

DOWN ARROW:                      1 Line down

UP ARROW:                        1 Line up

LEFT ARROW:                      1 Row left

RIGHT ARROW:                     1 Row right

PREV. PAGE:                      16 Arrows Up

NEXT PAGE:                       16 Arrows Down

HOME / END:                      Top left / Bottom right of pattern

LCTRL + HOME / END:              First / last track

F5, F6, F7, F8, F9:              Jump to 0, 1/4, 2/4, 3/4, 4/4 lines of the patterns

+ - (Numeric keypad):           Next / Previous pattern

LCTRL + LEFT / RIGHT:           Next / Previous pattern

LCTRL + LALT + LEFT / RIGHT:    Next / Previous position

LALT + LEFT / RIGHT:           Next / Previous instrument

LSHIFT + M:                      Toggle mute state of the current channel

LCTRL + LSHIFT + M:             Solo the current track / Unmute all

LSHIFT + F1 to F11:              Select a tab/panel

LCTRL + 1 to 4:                 Select a copy buffer


 Tracking 

1st and 2nd keys rows:           Upper octave row

3rd and 4th keys rows:           Lower octave row

RSHIFT:                          Insert a note off

/ and * (Numeric keypad)

or F1 F2:                        -1 or +1 octave

INSERT / BACKSPACE:              Insert or Delete a line in current track

or current selected block.

LSHIFT + INSERT / BACKSPACE:     Insert or Delete a line in current pattern

DELETE (NOT BACKSPACE):          Empty a column or a selected block.


 Blocks

(Blocks can also be selected with the mouse by holding the right button and scrolling the pattern with the mouse wheel).


LCTRL + A:          Select entire current track

LCTRL + LSHIFT + A: Select entire current pattern

LALT + A:          Select entire column note in a track

LALT + LSHIFT + A: Select all notes of a track

LCTRL + X:          Cut the selected block and copy it into the block-buffer

LCTRL + C:          Copy the selected block into the block-buffer

LCTRL + V:          Paste the data from the block buffer into the pattern

LCTRL + I:          Interpolate selected data from the first to the last row of a selection

LSHIFT + ARROWS

PREV. PAGE

NEXT PAGE: Select a block

LCTRL + R:          Randomize the select columns of a selection, works similar to CTRL + I (interpolating them)

LCTRL + U:          Transpose the note of a selection to 1 seminote higher

LCTRL + D:          Transpose the note of a selection to 1 seminote lower

LCTRL + LSHIFT + U: Transpose the note of a selection to 1 seminote higher (only for the current instrument)

LCTRL + LSHIFT + D: Transpose the note of a selection to 1 seminote lower  (only for the current instrument)

LCTRL + H:          Transpose the note of a selection to 1 octave higher

LCTRL + L:          Transpose the note of a selection to 1 octave lower

LCTRL + LSHIFT + H: Transpose the note of a selection to 1 octave higher (only for the current instrument)

LCTRL + LSHIFT + L: Transpose the note of a selection to 1 octave lower (only for the current instrument)

LCTRL + W:          Save the current selection into a file


 Misc 


LALT + ENTER:     Switch between full screen / windowed mode

LALT + F4:        Exit program (Windows only)

LCTRL + S:         Save current module

LSHIFT + S:         Switch top right panel to synths list

LSHIFT + I:         Switch top right panel to instruments list


&lt;pre&gt;
C-x   xh xx xx hhhh             Volume 
B-x   xh xx xx hhhh             Jump to 
A#x  xh xx xx hhhh hhhh   Slide 
F-x    xh xx xx hhhh            Tempo 
D-x   xh xx xx hhhh             Pattern Break 
G#x  xh xx xx hhhh
&lt;/pre&gt;

h Hex 01 02 03 04 05 06 07 08 09 0A 0B 0C 0D 0E 0F 10 11 12 13

d Dec 01 02 03 04 05 06 07 08 09 10  11 12 13 14 15 16 17 18 19

The Set Volume command: C. Input a note, then move the cursor to the effects command column and type a C. Play the pattern, and you shouldn't be able to hear the note you placed the C by. This is because the effect parameters are 00. Change the two zeros to a 40(Hex)/64(Dec), depending on what your tracker uses. Play back the pattern again, and the note should come in at full volume.

The Position Jump command next. This is just a B followed by the position in the playing list that you want to jump to. One thing to remember is that the playing list always starts at 0, not 1. This command is usually in Hex.

Onto the volume slide command: A. This is slightly more complex (much more if you're using a newer tracker, if you want to achieve the results here, then set slides to Amiga, not linear), due to the fact it depends on the secondary tempo. For now set a secondary tempo of 06 (you can play around later), load a long or looped sample and input a note or two. A few rows after a note type in the effect command A. For the parameters use 0F. Play back the pattern, and you should notice that when the effect kicks in, the sample drops to a very low volume very quickly. Change the effect parameters to F0, and use a low volume command on the note. Play back the pattern, and when the slide kicks in the volume of the note should increase very quickly.
This because each part of the effect parameters for command A does a different thing. The first number slides the volume up, and the second slides it down. It's not recommended that you use both a volume up and volume down at the same time, due to the fact the tracker only looks for the first number that isn't set to 0. If you specify parameters of 8F, the tracker will see the 8, ignore the F, and slide the volume up. Using a slide up and down at same time just makes you look stupid. Don't do it...

The Set Tempo command: F, is pretty easy to understand. You simply specify the BPM (in Hex) that you want to change to. One important thing to note is that values of lower than 20 (Hex) sets the secondary tempo rather than the primary.

Another useful command is the Pattern Break: D. This will stop the playing of the current pattern and skip to the next one in the playing list. By using parameters of more than 00 you can also specify which line to begin playing from.

Command 3 is Portamento to Note. This slides the currently playing note to another note, at a specified speed. The slide then stops when it reaches the desired note. 
&lt;pre&gt;
   C-2 1 000 - Starts the note playing
   ---      000
   C-3    330 - Starts the slide to C-3 at a speed of 30.
   ---     300 - Continues the slide
   ---     300 - Continues the slide
&lt;/pre&gt;
Once the parameters have been set, the command can be input again without any parameters, and it'll still perform the same function unless you change the parameters. This memory function allows certain commands to function correctly, such as command 5, which is the Portamento to Note and Volume Slide command. Once command 3 has been set up command 5 will simply take the parameters from that and perform a Portamento to Note. Any parameters set up for command 5 itself simply perform a Volume Slide identical to command A at the same time as the Portamento to Note.

This memory function will only operate in the same channel where the original parameters were set up.
There are various other commands which perform two functions at once. They will be described as we come across them.

C-3  04  ..  ..  09  00 ---&gt; C-3  04  ..  ..  09  00

C-3  04  ..  ..  09  00 ---&gt; C-3  04  ..  ..  09  02

C-3  04  ..  ..  09  00 ---&gt; C-3  04  ..  ..  09  05

C-3  04  ..  ..  09  00 ---&gt; C-3  04  ..  ..  09  08

C-3  04  ..  ..  09  00 ---&gt; C-3  04  ..  ..  09  0A

C-3  04  ..  ..  09  00 ---&gt; C-3  04  ..  ..  09  0D

C-3  04  ..  ..  09  10 ---&gt; C-3  04  ..  ..  09  10

(You can also switch on the Slider Rec to On, and perform parameter-live-recording, such as cutoff transitions, resonance or panning tweaking, etc..)  Note: this command only works for volume/panning and fx datas columns.


The next command we'll look at is the Portamento up/down: 1 and 2. Command 1 slides the pitch up at a specified speed, and 2 slides it down. This command works in a similar way to the volume slide, in that it is dependent on the secondary tempo. Both these commands have a memory dependent on each other, if you set the slide to a speed of 3 with the 1 command, a 2 command with no parameters will use the speed of 3 from the 1 command, and vice versa.

Command 4 is Vibrato. Vibrato is basically rapid changes in pitch, just try it, and you'll see what I mean. Parameters are in the format of xy, where x is the speed of the slide, and y is the depth of the slide. One important point to remember is to keep your vibratos subtle and natural so a depth of 3 or less and a reasonably fast speed, around 8, is usually used. Setting the depth too high can make the part sound out of tune from the rest.
Following on from command 4 is command 6. This is the Vibrato and Volume Slide command, and it has a memory like command 5, which you already know how to use.

Command 7 is Tremolo. This is similar to vibrato. Rather than changing the pitch it slides the volume. The effect parameters are in exactly the same format.   vibrato effect (0x1dxy) x = speed y = depth (can't be used if arpeggio (0x1b) is turned on) 

&lt;pre&gt;
 C-7 00 .. .. 1B37 &lt;-  Turn Arpeggio effect on
  --- .. .. .. 0000
  --- .. .. .. 0000
  --- .. .. .. 0000
  --- .. .. .. 1B38 &lt;- Change datas
  --- .. .. .. 0000
  --- .. .. .. 0000
  --- .. .. .. 0000
  --- .. .. .. 1B00 &lt;- Turn it off
&lt;/pre&gt;

Command 9 is Sample Offset. This starts the playback of the sample from a different place than the start. The effect parameters specify the sample offset, but only very roughly. Say you have a sample which is 8765(Hex) bytes long, and you wanted it to play from position 4321(Hex). The effect parameter could only be as accurate as the 43 part, and it would ignore the 21.

Command B is the Playing List/Order Jump command. The parameters specify the position in the Playing List/Order to jump to. When used in conjunction with command D you can specify the position and the line to play from.

Command E is pretty complex, as it is used for a lot of different things, depending on what the first parameter is. Let's take a trip through each effect in order.
Command E0 controls the hardware filter on an Amiga, which, as a low pass filter, cuts off the highest frequencies being played back. There are very few players and trackers on other system that simulate this function, not that you should need to use it. The second parameter, if set to 1, turns on the filter. If set to 0, the filter gets turned off.

Commands E1/E2 are Fine Portamento Up/Down. Exactly the same functions as commands 1/2, except that they only slide the pitch by a very small amount. These commands have a memory the same as 1/2 as well.

Command E3 sets the Glissando control. If parameters are set to 1 then when using command 3, any sliding will only use the notes in between the original note and the note being slid to. This produces a somewhat jumpier slide than usual. The best way to understand is to try it out for yourself. Produce a slow slide with command 3, listen to it, and then try using E31.

Command E4 is the Set Vibrato Waveform control. This command controls how the vibrato command slides the pitch. Parameters are 0 - Sine, 1 - Ramp Down (Saw), 2 - Square. By adding 4 to the parameters, the waveform will not be restarted when a new note is played e.g. 5 - Sine without restart.

Command E5 sets the Fine Tune of the instrument being played, but only for the particular note being played. It will override the default Fine Tune for the instrument. The parameters range from 0 to F, with 0 being -8 and F being +8 Fine Tune. A parameter of 8 gives no Fine Tune. If you're using a newer tracker that supports more than -8 to +8 e.g. -128 to +128, these parameters will give a rough Fine Tune, accurate to the nearest 16.

Command E6 is the Jump Loop command. You mark the beginning of the part of a pattern that you want to loop with E60, and then specify with E6x the end of the loop, where x is the number of times you want it to loop.

Command E7 is the Set Tremolo Waveform control. This has exactly the same parameters as command E4, except that it works for Tremolo rather than Vibrato.

Command E9 is for Retriggering the note quickly. The parameter specifies the interval between the retrigs. Use a value of less than the current secondary tempo, or else the note will not get retrigged.

Command EA/B are for Fine Volume Slide Up/Down. Much the same as the normal Volume Slides, except that these are easier to control since they don't depend on the secondary tempo. The parameters specify the amount to slide by e.g. if you have a sample playing at a volume of 08 (Hex) then the effect EA1 will slide this volume to 09 (Hex). A subsequent effect of EB4 would slide this volume down to 05 (Hex).

Command EC is the Note Cut. This sets the volume of the currently playing note to 0 at a specified tick. The parameters should be lower than the secondary tempo or else the effect won't work.

Command ED is the Note Delay. This should be used at the same time as a note is to be played, and the parameters will specify the number of ticks to delay playing the note. Again, keep the parameters lower than the secondary tempo, or the note won't get played!

Command EE is the Pattern Delay. This delays the pattern for the amount of time it would take to play a certain number of rows. The parameters specify how many rows to delay for.

Command EF is the Funk Repeat command. Set the sample loop to 0-1000. When EFx is used, the loop will be moved to 1000- 2000, then to 2000-3000 etc. After 9000-10000 the loop is set back to 0- 1000. The speed of the loop &quot;movement&quot; is defined by x. E is two times as slow as F, D is three times as slow as F etc. EF0 will turn the Funk Repeat off and reset the loop (to 0-1000).

effects 0x41 and 0x42 to control the volumes of the 2 303 units

There is a dedicated panel for synth parameter editing with coherent sections (osc, filter modulation, routing, so on) the interface is much nicer, much better to navigate with customizable colors, the reverb is now customizable (10 delay lines), It accepts newer types of Waves (higher bit rates, at least 24). Has a replay routine.

It's pretty much your basic VA synth. The problem isn't with the sampler being to high it's the synth is tuned two octaves too low, but if you want your samples tuned down just set the base note down 2 octaves (in the instrument panel).

so the synth is basically divided into 3 sections from left to right: oscillators/envelopes, then filter and LFO's, and in the right column you have mod routings and global settings.

for the oscillator section you have two normal oscillators (sine, saw, square, noise), the second of which is tunable, the first one tunes with the key pressed. Attached to OSC 1 is a sub-oscillator, which is a sawtooth wave tuned one octave down. The phase modulation controls the point in the duty cycle at which the oscillator starts. The ADSR envelope sliders (grouped with oscs) are for modulation envelope 1 and 2 respectively. you can use the synth as a sampler by choosing the instrument at the top.

In the filter column, the filter settings are: 1 = lowpass, 2 = highpass, 3 = off. cutoff and resonance. For the LFOs they are LFO 1 and LFO 2, the ADSR sliders in those are for the LFO itself.

For the modulation routings you have ENV 1, LFO 1 for the first slider and ENV 2, LFO 2 for the second, you can cycle through the individual routings there, and you can route each modulation source to multiple destinations of course, which is another big plus for this synth. Finally the glide time is for portamento and master volume, well, the master volume... it can go quite loud.

The sequencer is changed too, It's more like the one in AXS if you've used that, where you can mute tracks to re-use patterns with variation.


&lt;pre&gt;
Support for the following modules formats:
669 (Composer 669, Unis 669), 
AMF (DSMI Advanced Module Format), 
AMF (ASYLUM Music Format V1.0), 
APUN (APlayer), DSM (DSIK internal format), 
FAR (Farandole Composer), 
GDM (General DigiMusic), 
IT (Impulse Tracker), 
IMF (Imago Orpheus), 
MOD (15 and 31 instruments), 
MED (OctaMED), 
MTM (MultiTracker Module editor), 
OKT (Amiga Oktalyzer), 
S3M (Scream Tracker 3), 
STM (Scream Tracker), 
STX (Scream Tracker Music Interface Kit), 
ULT (UltraTracker), 
UNI (MikMod), 
XM (FastTracker 2),
Mid (midi format via timidity)
&lt;/pre&gt;


Possible plugin options include [http://lv2plug.in/ LV2],


====Midi - Musical Instrument Digital Interface====

A midi file typically contains music that plays on up to 16 channels (as per the midi standard), but many notes can simultaneously play on each channel (depending on the limit of the midi hardware playing it).

'''Timidity'''

Although usually already installed, you can uncompress the [http://www.libsdl.org/projects/SDL_mixer/ timidity.tar.gz (14MB)] into a suitable drawer like below's SYS:Extras/Audio/ 
 assign timidity: SYS:Extras/Audio/timidity
added to SYSːs/User-Startup

'''WildMidi playback'''


'''Audio Evolution 4 (2003) 4.0.23 (from 2012)'''


*Sync Menu    - CAMD Receive, Send checked 
*Options Menu - MIDI Machine Control - Midi Bar Display - Select CAMD MIDI in / out - Midi Remote Setup 


MCB Master Control Bus 
*Sending a MIDI start-command and a Song Position Pointer, you can synchronize audio with an external MIDI sequencer (like B&amp;P). 
*B&amp;P Receive, start AE, add AudioEvolution.ptool in Bars&amp;Pipes track, press play / record in AE then press play in Pipes 
*CAMD Receive, receive MIDI start or continue commands via camd.library sync to AE 


*MIDI Machine Control
*Midi Bar Display 
*Select CAMD MIDI in / out
*Midi Remote Setup - open requester for external MIDI controllers to control app mixer and transport controls cc remotely 
 Channel   - mixer(vol, pan, mute, solo), eq, aux, fx, 
 Subgroup  - Volume, Mute, Solo 
 Transport - Start, End, Play, Stop, Record, Rewind, Forward 
 Misc      - Master vol., Bank Down, Bank up 


&lt;pre&gt;
q        - quit 

First 3 already opened when AE started 
F1       - timeline window
F2       - mixer 
F3       - control 
F4       - subgroups 
F5       - aux returns 
F6       - sample list 

i        - Load sample to use 

space    - start/stop play 
b        - reset time 0:00


s        - split mode 
r        - open recording window 
a        - automation edit mode with p panning, m mute and v volume 


[ / ]    - zoom in / out 
:        - previous track
*        - next track 

x c v f  - cut copy paste cross-fade 
g        - snap grid 


&lt;/pre&gt;


 '''[http://bnp.hansfaust.de/ Bars n Pipes sequencer]'''

 BarsnPipes debug ... in shell 

Menu (right mouse)  
*Song        - Songs load and save in .song format but option here to load/save Midi_Files .mid in FORMAT0 or FORMAT1 
*Track       - 
*Edit        -
*Tool        - 
*Timing      - SMTPE Synchronizing 
*Windows     - 
*Preferences - Multiple MIDI-in option 

Windows (some of these are usually already opened when Bars n Pipes starts up for the first time) 
*Workflow -&gt; Tracks, .... Song Construction, Time-line Scoring, Media Madness, Mix Maestro, 
*Control  -&gt; Transport (or mini one), Windows (which collects all the Windows icons together-shortcut), .... Toolbox, Accessories, Metronome, 

Once you have your windows placed on the screen that suits your workflow, Song -&gt; Save as Default will save the positions, colors, icons, etc as you'd like them 

If you need a particular setup of Tracks, Tools, Tempos etc, you save them all as a new song you can load each time 

Right mouse menu -&gt; Preferences -&gt; Environment... -&gt; ScreenMode  - Linkages for Synch (to Slave) usbmidi.out.0 and Send (Master) usbmidi.in.0 - Clock MTC 


'''Tracks'''

#Double-click on B&amp;P's icon. B&amp;P will then open with an empty Song. You can also double-click on a song icon to open a song in B&amp;P.
#Choose a track. The B&amp;P screen will contain a Tracks Window with a number of tracks shown as pipelines (Track 1, Track 2, etc...). To choose a track, simply click on the gray box to show an arrow-icon to highlight it. This icon show whether a track is chosen or not. To the right of the arrow-icon, you can see the icon for the midi-input. If you double-click on this icon you can change the MIDI-in setup.
#Choose Record for the track. To the right of the MIDI-input channel icon you can see a pipe. This leads to another clickable icon with that shows either P, R or M. This stands for Play, Record or Merge. To change the icon, simply click on it. If you choose P, this track can only play the track (you can't record anything). If you choose R, you can record what you play and it overwrites old stuff in the track. If you choose M, you merge new records with old stuff in the track. Choose R now to be able to make a record.
#Chose MIDI-channel. On the most right part of the track you can see an icon with a number in it. This is the MIDI-channel selector. Here you must choose a MIDI-channel that is available on your synthesizer/keyboard. If you choose General MIDI channel 10, most synthesizer will play drum sounds. To the left of this icon is the MIDI-output icon. Double-click on this icon to change the MIDI-output configuration.
#Start recording. The next step is to start recording. You must then find the control buttons (they look like buttons on a CD-player). To be able to make a record. you must click on the R icon. You can simply now press the play button (after you have pressed the R button) and play something on you keyboard. To playback your composition, press the Play button on the control panel.
#Edit track. To edit a track, you simply double click in the middle part of a track. You will then get a new window containing the track, where you can change what you have recorded using tools provided. Take also a look in the drop-down menus for more features.


Videos to help understand [https://www.youtube.com/watch?v=A6gVTX-9900 small intro], [https://www.youtube.com/watch?v=abq_rUTiSA4&amp;t=3s Overview], [https://www.youtube.com/watch?v=ixOVutKsYQo Workplace Setup CC PC Sysex], [https://www.youtube.com/watch?v=dDnJLYPaZTs Import Song], [https://www.youtube.com/watch?v=BC3kkzPLkv4 Tempo Mapping], [https://www.youtube.com/watch?v=sd23kqMYPDs ptool Arpeggi-8], [https://www.youtube.com/watch?v=LDJq-YxgwQg  PlayMidi Song], [https://www.youtube.com/watch?v=DY9Pu5P9TaU Amiga Midi], [https://www.youtube.com/watch?v=abq_rUTiSA4 Learning Amiga bars and Pipes], 

Groups like [https://groups.io/g/barsnpipes/topics this] could help 


'''Tracks window'''

* blue &quot;1 2 3 4 5 6 7 8 Group&quot; and transport tape deck VCR-type controls
* Flags 
* [http://theproblem.alco-rhythm.com/org/bp.html Track 1, Track2, to Track 16, on each Track there are many options that can be activated] 

Each Track has a 

*Left LHS  - Click in grey box to select what Track to work on, Midi-In ptool icon should be here (5pin plug icon), and many more from the Toolbox on the Input Pipeline 
*Middle    - (P, R, M) Play, Record, Merge/Multi before the sequencer line and a blue/red/yellow (Thru Mute Play) Tap 
*Right RHS - Output pipeline, can have icons placed uopn it with the final ptool icon(s) being the 5pin icon symbol for Midi-OUT 

Clogged pipelines may need Esc pressed several times 


'''Toolbox (tools affect the chosen pipeline)'''

After opening the Toolbox window you can add extra Tools (.ptool) for the pipelines like keyboard(virtual), midimonitor, quick patch, transpose, triad, (un)quantize, feedback in/out, velocity etc
 right mouse -&gt; Toolbox menu option -&gt; Install Tool... and navigate to Tool drawer (folder) and select requried .ptool 

Accompany B tool to get some sort of rythmic accompaniment, Rythm Section and Groove Quantize are examples of other tools that make use of rythms
[https://aminet.net/search?query=bars Bars &amp; Pipes pattern format .ptrn] for drawer (folder). Load from the Menu as Track or Group 


'''Accessories (affect the whole app)''' 

Accessories -&gt; Install... and goto the Accessories drawer for .paccess like adding ARexx scripting support 


'''Song Construction'''
&lt;pre&gt;
F1  Pencil
F2  Magic Wand
F3  Hand 
F4  Duplicator 
F5  Eraser 
F6  Toolpad 
F7  Bounding box 
F8  Lock to A-B-A 

A-B-A strip, section, edit flags, white boxes, 

&lt;/pre&gt;


Bars&amp;Pipes Professional offers three track formats; basic song tracks, linear tracks — which don't loop — and finally real‑time tracks. The difference between them is that both song and linear tracks respond to tempo changes, while real‑time tracks use absolute timing, always trigger at the same instant regardless of tempo alterations 

'''Tempo Map'''

F1  Pencil
F2  Magic Wand
F3  Hand 
F4  Eraser 
F5  Curve 
F6  Toolpad 


Compositions

Lyrics, Key, Rhythm, Time Signature 

'''Master Parameters'''

Key, Scale/Mode

'''Track Parameters'''

Dynamics 


'''Time-line Scoring'''


'''Media Madness'''


'''Mix Maestro'''


*ACCESSORIES         Allows the importation of other packages and additional modules 
*CLIPBOARD           Full cut, copy and paste operations, enabling user‑definable clips to be shared between tracks.
*INFORMATION         A complete rundown on the state of the current production and your machine.
*MASTER PARAMETERS   Enables global definition of time signatures, lyrics, scales, chords, dynamics and rhythm changes.
*MEDIA MADNESS       A complete multimedia sequencer which allows samples, stills, animation, etc 
*METRONOME           Tempo feedback via MIDI, internal Amiga audio and colour cycling — all three can be mixed and matched as required.
*MIX MAESTRO         Completely automated mixdown with control for both volume and pan. All fader alterations are memorised by the software 
*RECORD ACTIVATION   Complete specification of the data to be recorded/merged. Allows overdubbing of pitch‑bend, program changes, modulation etc
*SET FLAGS           Numeric positioning of location and edit flags in either SMPTE or musical time 
*SONG CONSTRUCTION   Large‑scale cut and paste of individual measures, verses or chorus, by means of bounding box and drag‑n‑drop mouse selections
*TEMPO MAP           Tempo change using a variety of linear and non‑linear transition curves 
*TEMPO PALETTE       Instant tempo changes courtesy of four user‑definable settings.
*TIMELINE SCORING    Sequencing of a selection of songs over a defined period — ideal for planning an entire set for a live performance.
*TOOLBOX             Selection screen for the hundreds of signal‑processing tools available 
*TRACKS              Opens the main track window to enable recording, editing and the use of tools.
*TRANSPORT           Main playback control window, which also provides access to user‑ defined flags, loop and punch‑in record modes.


Bars and Pipes Pro 2.5 is using internal 4-Byte IDs, to check which kind of data are currently processed.
Especially in all its files the IDs play an important role. The IDs are stored into the file in the same order they are laid out in the memory.

In a Bars 'N' Pipes file (no matter which kind) the ID &quot;NAME&quot; (saved as its ANSI-values) is stored on a big endian system (68k-computer) as &quot;NAME&quot;. On a little endian system (x86 PC computer) as &quot;EMAN&quot;.  The target is to make the AROS-BnP compatible to songs, which were stored on a 68k computer (AMIGA).

If possible, setting MIDI channels for Local Control for your keyboard 

http://www.fromwithin.com/liquidmidi/archive.shtml


MIDI files are essentially a stream of event data. An event can be many things, but typically &quot;note on&quot;, &quot;note off&quot;, &quot;program change&quot;, &quot;controller change&quot;, or messages that instruct a MIDI compatible synth how to play a given bit of music.

* Channel     - 1 to 16 -
* Messages    - PC presets, CC effects like delays, reverbs,  etc 
* Sequencing  - MIDI instruments, Drums, Sound design, 
* Recording   - 
* GUI         - Piano roll or Tracker, Staves and Notes 

MIDI events/messages like step entry e.g. Note On, Note Off 

MIDI events/messages like PB, PC, CC, Mono and Poly After-Touch, Sysex, etc 

MIDI sync - Midi Clocks (SPS Measures), Midi Time Code (h, m, s and frames) SMPTE 

Individual track editing with audition edits so easier to test any changes. Possible to stop track playback, mix clips from the right edit flag and scroll the display using arrow keys. 

Step entry, to extend a selected note hit the space bar and the note grows accordingly. Ability to cancel mouse‑driven edits by simply clicking the right mouse button — at which point everything snaps back into its original form. Lyrics can now be put in with syllable dividers, even across an entire measure or section. Autoranging when you open a edit window, the notes are automatically displayed — working from the lowest upwards. 

Flag editing, shift‑click on a flag immediately open the bounds window, ready for numeric input. Ability to cancel edits using the right‑hand mouse button, plus much improved Bounding Box operations.

Icons other than the BarsnPipes icon -&gt; PUBSCREEN=BarsnPipes (cannot choose modes higher than 8bit 256 colors)

Preferences -&gt; Menu in Tracks window - Send MIDI defaults OFF 

Prefs -&gt; Environment -&gt; screenmode (saved to BarsnPipes.prefs binary file) 

Customization -&gt; pics in gui drawer (folder) - 


Can save as .song files and .mid General Midi 

SMF is a “Standard Midi File”  ([http://www.music.mcgill.ca/~ich/classes/mumt306/StandardMIDIfileformat.html SMF0, SMF1 and SMF2]), [https://github.com/stump/libsmf libsmf], [https://github.com/markc/midicomp MIDIcomp], [https://github.com/MajicDesigns/MD_MIDIFile C++ src], [], [https://github.com/newdigate/midi-smf-reader Midi player], 

* SMF0        All MIDI data is stored in one track only, separated exclusively by the MIDI channel.
* SMF1        The MIDI data is stored in separate tracks/channels.
* SMF2 (rarely used) The MIDI data is stored in separate tracks, which are additionally wrapped in containers, so it's possible to have e.g. several tracks using the same MIDI channels.


Would it be possible to enrich Bars N’Pipes with software synth and sample support along with audio recording and mastering tools like in the named MAC or PC music sequencers?
On the classic AMIGA-OS this is not possible because of missing CPU-power. The hardware of the classic AMIGA is not further developed. So we must say (unfortunately) that those dreams can’t become reality

BarsnPipes is best used with external MIDI-equipment. This can be a keyboard or synthesizer with MIDI-connectors. 

&lt;pre&gt;
MIDI can control 16 channels 
There are USB-MIDI-Interfaces on the market with 16 independent MIDI-lines (multi-port), which can handle 16 MIDI devices independently – 16×16 = 256 independent MIDI-channels or instruments 
handle up to 16 different USB-MIDI-Interfaces (multi-device). That is: 16X16X16 = 4096 independent MIDI-channels – theoretically 
&lt;/pre&gt;

&lt;pre&gt;
Librarian MIDI SYStem EXplorer (sysex) - PatchEditor and used to be supplied as a separate program like PatchMeister but currently not at present 
It should support MIDI.library (PD), BlueRibbon.library (B&amp;P), TriplePlayPlus, and CAMD.library (DeluxeMusic) and 
MIDI information from a device's user manual and configure a custom interface to access parameters for all MIDI products connected to the system 
Supports ALL MIDI events and the Patch/Librarian data is stored in MIDI standard format 
Annette M.Crowling, Missing Link Software, Inc.
&lt;/pre&gt;


Composers
&lt;pre&gt;
[https://x.com/hirasawa/status/1403686519899054086 Susumu Hirasawa] 

&lt;/pre&gt;


&lt;pre&gt;
1988 Todor Fay and his wife Melissa Jordan Gray, who founded the Blue Ribbon Inc
1992 Bars&amp;Pipes Pro published 
November 2000, Todor Fay announcement to release the sourcecode of Bars&amp;Pipes Pro 2.5c beta
end of May 2001, the source of the main program and the sources of some tools and accessories were in a complete and compileable state 
end of October 2009 stop further development of BarsnPipes New for now on all supported systems and made freeware 
2013 Alfred Faust diagnosed with incureable illness, called „Myastenia gravis“ (weak muscles) 
&lt;/pre&gt;


 Protrekkr

How to use Midi In/Out in Protrekkr ?

First of all, midi in &amp; out capabilities of this program are rather limited.

# Go to Misc. Setup section and select a midi in or out device to use (ptk only supports one device at a time).
# Go to instrument section, and select a MIDI PRG (the default is N/A, which means no midi program selected).
# Go to track section and here you can assign a midi channel to each track of ptk.
# Play notes :]. Note off works. F'x' note cut command also works too, and note-volume command (speed) is supported.

Also, you can change midicontrollers in the tracker, using '90' in the panning row:

&lt;pre&gt;
    C-3 02 .. .. 0000....


    --- .. .. 90 xxyy.... &lt;&lt; This will set the value 
    --- .. .. .. 0000....    of the controller n.'xx' to 'yy' (both in hex)
    --- .. .. .. 0000....
&lt;/pre&gt;

So &quot;--- .. .. 90 2040....&quot; will set the controller number $20(32) to $40(64).

You will need the midi implementation table of your gear to know what you can change with midi controller messages.

 N.B. Not all MIDI devices are created equal!

Although the MIDI specification defines a large range of MIDI messages of various kinds, not every MIDI device is required to work in exactly the same way and respond to all the available messages and ways of working. For example, we don't expect a wind synthesiser to work in the same way as a home keyboard.

Some devices, the older ones perhaps, are only able to respond to a single channel. With some of those devices that channel can be altered from the default of 1 (probably) to another channel of the 16 possible.

Other devices, for instance monophonic synthesisers, are capable of producing just one note at a time, on one MIDI channel. Others can produce many notes spread across many channels.

Further devices can respond to, and transmit, &quot;breath controller&quot; data (MIDI controller number 2 (CC#2)) others may respond to the reception of CC#2 but not be able to create and to send it.

A controller keyboard may be capable of sending &quot;expression pedal&quot; data, but another device may not be capable of responding to that message.

Some devices just have the basic GM sound set. The &quot;voice&quot; or &quot;instrument&quot; is selected using a &quot;Program Change&quot; message on its own.

Other devices have a greater selection of voices, usually arranged in &quot;banks&quot;, and the choice of instrument is made by responding to &quot;Bank Select MSB&quot; (MIDI controller 0 (CC#0)), others use &quot;Bank Select LSB&quot; (MIDI controller number 32 (CC#32)), yet others use both MSB and LSB sent one after the other, all followed by the Program Change message. The detailed information about all the different voices will usually be available in a published MIDI Data List.


 MIDI Implementation Chart

But in the User Manual there is sometimes a summary of how the device works, in terms of MIDI, in the chart at the back of the manual, the MIDI Implementation Chart.

If you require two devices to work together you can compare the two implementation charts to see if they are &quot;compatible&quot;. In order to do this we will need to interpret that chart.

The chart is divided into four columns headed &quot;Function&quot;, &quot;Transmitted&quot; (or &quot;Tx&quot;), &quot;Received&quot; (or &quot;Rx&quot;), or more correctly &quot;Recognised&quot;, and finally, &quot;Remarks&quot;.

&lt;pre&gt;
The left hand column defines which MIDI functions are being described.
The 2nd column defines what the device in question is capable of transmitting to another device.
The 3rd column defines what the device is capable of responding to.
The 4th column is for explanations of the values contained within these previous two columns.
&lt;/pre&gt;

There should then be twelve sections, with possibly a thirteenth containing extra &quot;Notes&quot;. Finally there should be an explanation of the four MIDI &quot;modes&quot; and what the &quot;X&quot; and the &quot;O&quot; mean.
&lt;pre&gt;
Mode 1: Omni On, Poly; 
Mode 2: Omni On, Mono; 
Mode 3: Omni Off, Poly; 
Mode 4: Omni Off, Mono.
&lt;/pre&gt;
O means &quot;yes&quot; (implemented), X means &quot;no&quot; (not implemented).

Sometimes you will find a row of asterisks &quot;**************&quot;, these seem to indicate that the data is not applicable in this case. Seen in the transmitted field only (unless you've seen otherwise).

Lastly you may find against some entries an asterisk followed by a number e.g. *1, these will refer you to further information, often on a following page, giving more detail.

Basic Channel
But the very first set of boxes will tell us the &quot;Basic Channel(s)&quot; that the device sends or receives on. 
&quot;Default&quot; is what happens when the device is first turned on, &quot;changed&quot; is what a switch of some kind may allow the device to be set to. 
For many devices e.g. a GM sound module or a home keyboard, this would be 1-16 for both. That is it can handle sending and receiving on all MIDI channels.

On other devices, for example a synthesiser, it may by default only work on channel 1. But the keyboard could be &quot;split&quot; with the lower notes e.g. on channel 2. If the synth has an arppegiator, this may be able to be set to transmit and or receive on yet another channel.
So we might see the default as &quot;1&quot; but the changed as &quot;1-16&quot;.

Modes.
We need to understand Omni On and Off, and Mono and Poly, then we can decipher the four modes.

But first we need to understand that any of these four Mode messages can be sent to any MIDI channel. They don't necessarily apply to the whole device.

If we send an &quot;Omni On&quot; message (CC#125) to a MIDI channel of a device, we are, in effect, asking it to respond to e.g. a Note On / Off message pair, received on any of the sixteen channels. Sound strange? Read it again. Still strange? It certainly is. We normally want a MIDI channel to respond only to Note On / Off messages sent on that channel, not any other. In other words, &quot;Omni Off&quot;.

So &quot;Omni Off&quot; (CC#124) tells a channel of our MIDI device to respond only to messages sent on that MIDI channel.

&quot;Poly&quot; (CC#127) is for e.g. a channel of a polyphonic sound module, or a home keyboard, to be able to respond to many simultaneous Note On / Off message pairs at once and produce musical chords.

&quot;Mono&quot; (CC#126) allows us to set a channel to respond as if it were e.g. a flute or a trumpet, playing just one note at a time. If the device is capable of it, then the overlapping of notes will produce legato playing, that is the attack portion of the second note of two overlapping notes will be removed resulting in a &quot;smoother&quot; transition.

So a channel with a piano voice assigned to it will have Omni Off, Poly On (Mode 3), a channel with a saxophone voice assigned could be Omni Off, Mono On (Mode 4).

We call these combinations the four modes, 1 to 4, as defined above. 
Most modern devices will have their channels set to Mode 3 (Omni Off, Poly) but be switchable, on a per channel basis, to Mode 4 (Omni Off, Mono).

This second section of data will include first its default value i.e. upon device switch on. Then what Mode messages are acceptable, or X if none.

Finally, in the &quot;Altered&quot; field, how a Mode message that can't be implemented will be interpreted. Usually there will just be a row of asterisks effectively meaning nothing will be done if you try to switch to an unimplemented mode.

Note Number
&lt;pre&gt;
The next row will tell us which MIDI notes the device can send or receive, normally 0-127.
The second line, &quot;True Voice&quot; has the following in the MIDI specification: 
&quot;Range of received note numbers falling within the range of true notes produced by the instrument.&quot;
My interpretation is that, for instance, a MIDI piano may be capable of sending all MIDI notes (0 to 127) by transposition, but only responding to the 88 notes (21 to 108) of a real piano. 
&lt;/pre&gt;

Velocity
This will tell us whether the device we're looking at will handle note velocity, and what range from 1-127, or maybe just 64, it transmits or will recognise. So usually &quot;O&quot; plus a range or &quot;X&quot; for not implemented.

After touch
This may have one or two lines two it.
If a one liner the either &quot;O&quot; or &quot;X&quot;, yes or no.
If a two liner then it may include &quot;Keys&quot; or &quot;Poly&quot; and &quot;Channel&quot;.
This will show whether the device will respond to Polyphonic after touch or channel after touch or neither.

Pitch Bend
Again &quot;O&quot; for implemented, &quot;X&quot; for not implemented.
(Many stage pianos will have no pitch bend capability.)
It may also, in the notes section, state whether it will respond to the full 14 bits, or not, as usually encoded by the pitch bend wheel.

Control Change
This is likely to be the largest section of the chart.
It will list all those controllers, starting from CC#0, Bank Select MSB, which the device is capable of sending, and those that it will respond to using &quot;O&quot; or &quot;X&quot; respectively.
You will, almost certainly, get some further explanation of functionality in the remarks column, or in more detail elsewhere in the documentation.

Of course you will need to know what all the various controller numbers do. Lots of the official technical specifications can be found at the [www.midi.org/techspecs/ MMA], with the table of messages and control change [www.midi.org/techspecs/midimessages.php message numbers]

Program Change
Again &quot;O&quot; or &quot;X&quot; in the Transmitted or Recognised column to indicate whether or not the feature is implemented. In addition a range of numbers is shown, typically 0-127, to show what is available.
True # (number): &quot;The range of the program change numbers which correspond to the actual number of patches selected.&quot;

System Exclusive
Used to indicate whether or not the device can send or recognise System Exclusive messages. A short description is often given in the Remarks field followed by a detailed explanation elsewhere in the documentation.

System Common - These include the following:
&lt;pre&gt;
MIDI Time Code Quarter Frame messages (device synchronisation).
Song Position Pointer
Song Select
Tune Request
&lt;/pre&gt;
The section will indicate whether or not the device can send or respond to any of these messages.

System Real Time
These include the following:
&lt;pre&gt;
Timing Clock - often just written as &quot;Clock&quot;
Start
Stop
Continue
&lt;/pre&gt;
These three are usually just referred to as &quot;Commands&quot; and listed.
Again the section will indicate which, if any, of these messages the device can send or respond to.
&lt;pre&gt;
Aux. Messages
Again &quot;O&quot; or &quot;X&quot; for implemented or not.
Aux. = Auxiliary.
Active Sense = Active Sensing.
&lt;/pre&gt;
Often with an explanation of the action of the device.

Notes
The &quot;Notes&quot; section can contain any additional comments to clarify the particular implementation.

Some of the explanations have been drawn directly from the MMA MIDI 1.0 Detailed Specification.
And the detailed explanation of some of the functions will be found there, or in the General MIDI System Level 1 or General MIDI System Level 2 documents also published by the MMA.


 OFFICIAL MIDI SPECIFICATIONS

SUMMARY OF MIDI MESSAGES
Table 1 - Summary of MIDI Messages

The following table lists the major MIDI messages in numerical (binary) order (adapted from &quot;MIDI by the Numbers&quot; by D. Valenti, Electronic Musician 2/88, and updated by the MIDI Manufacturers Association.). This table is intended as an overview of MIDI, and is by no means complete.

WARNING! Details about implementing these messages can dramatically impact compatibility with other products. We strongly recommend consulting the official MIDI Specifications for additional information.

MIDI 1.0 Specification

Message Summary Channel Voice Messages [nnnn = 0-15 (MIDI Channel Number 1-16)]

{| class=&quot;wikitable sortable&quot; width=&quot;90%&quot;
! width=&quot;10%&quot;  |Status D7----D0 
! width=&quot;10%&quot;  |Data Byte(s) D7----D0 
! width=&quot;20%&quot;  |Description
|-
|&lt;!--Status--&gt;1000nnnn || &lt;!--Data--&gt;0kkkkkkk 0vvvvvvv || &lt;!--Description--&gt;Note Off event. 
This message is sent when a note is released (ended). (kkkkkkk) is the key (note) number. (vvvvvvv) is the velocity.
|-
|&lt;!--Status--&gt;1001nnnn || &lt;!--Data--&gt;0kkkkkkk 0vvvvvvv || &lt;!--Description--&gt;Note On event. 
This message is sent when a note is depressed (start). (kkkkkkk) is the key (note) number. (vvvvvvv) is the velocity.
|-
|&lt;!--Status--&gt;1010nnnn || &lt;!--Data--&gt;0kkkkkkk 0vvvvvvv || &lt;!--Description--&gt;Polyphonic Key Pressure (Aftertouch). 
This message is most often sent by pressing down on the key after it &quot;bottoms out&quot;. (kkkkkkk) is the key (note) number. (vvvvvvv) is the pressure value.
|-
|&lt;!--Status--&gt;1011nnnn || &lt;!--Data--&gt;0ccccccc 0vvvvvvv || &lt;!--Description--&gt;Control Change. 
This message is sent when a controller value changes. Controllers include devices such as pedals and levers. Controller numbers 120-127 are reserved as &quot;Channel Mode Messages&quot; (below). (ccccccc) is the controller number (0-119). (vvvvvvv) is the controller value (0-127).
|-
|&lt;!--Status--&gt;1100nnnn || &lt;!--Data--&gt;0ppppppp || &lt;!--Description--&gt;Program Change. This message sent when the patch number changes. (ppppppp) is the new program number.
|-
|&lt;!--Status--&gt;1101nnnn || &lt;!--Data--&gt;0vvvvvvv || &lt;!--Description--&gt;Channel Pressure (After-touch). This message is most often sent by pressing down on the key after it &quot;bottoms out&quot;. This message is different from polyphonic after-touch. Use this message to send the single greatest pressure value (of all the current depressed keys). (vvvvvvv) is the pressure value.
|-
|&lt;!--Status--&gt;1110nnnn || &lt;!--Data--&gt;0lllllll 0mmmmmmm || &lt;!--Description--&gt;Pitch Bend Change. This message is sent to indicate a change in the pitch bender (wheel or lever, typically). The pitch bender is measured by a fourteen bit value. Center (no pitch change) is 2000H. Sensitivity is a function of the receiver, but may be set using RPN 0. (lllllll) are the least significant 7 bits. (mmmmmmm) are the most significant 7 bits.
|}

Channel Mode Messages (See also Control Change, above)

{| class=&quot;wikitable sortable&quot; width=&quot;90%&quot;
! width=&quot;10%&quot;  |Status D7----D0 
! width=&quot;10%&quot;  |Data Byte(s) D7----D0 
! width=&quot;20%&quot;  |Description
|-
|&lt;!--Status--&gt;1011nnnn || &lt;!--Data--&gt;0ccccccc 0vvvvvvv || &lt;!--Description--&gt;Channel Mode Messages. 
This the same code as the Control Change (above), but implements Mode control and special message by using reserved controller numbers 120-127. The commands are:
*All Sound Off. When All Sound Off is received all oscillators will turn off, and their volume envelopes are set to zero as soon as possible c = 120, v = 0: All Sound Off
*Reset All Controllers. When Reset All Controllers is received, all controller values are reset to their default values. (See specific Recommended Practices for defaults) c = 121, v = x: Value must only be zero unless otherwise allowed in a specific Recommended Practice.
*Local Control. When Local Control is Off, all devices on a given channel will respond only to data received over MIDI. Played data, etc. will be ignored. Local Control On restores the functions of the normal controllers. 
c = 122, v = 0: Local Control Off
c = 122, v = 127: Local Control On
* All Notes Off. When an All Notes Off is received, all oscillators will turn off. 
c = 123, v = 0: All Notes Off (See text for description of actual mode commands.)
c = 124, v = 0: Omni Mode Off 
c = 125, v = 0: Omni Mode On 
c = 126, v = M: Mono Mode On (Poly Off) where M is the number of channels (Omni Off) or 0 (Omni On) 
c = 127, v = 0: Poly Mode On (Mono Off) (Note: These four messages also cause All Notes Off)
|}

System Common Messages

System Messages (0xF0)

The final status nybble is a “catch all” for data that doesn’t fit the other statuses. They all use the most significant nybble (4bits) of 0xF, with the least significant nybble indicating the specific category.

The messages are denoted when the MSB of the second nybble is 1. When that bit is a 0, the messages fall into two other subcategories.

System Common

If the MSB of the second second nybble (4 bits) is not set, this indicates a System Common message. Most of these are messages that include some additional data bytes.

System Common Messages
Type Status Byte   Number of Data Bytes      Usage 
&lt;pre&gt;
Time Code Quarter Frame	0xF1	1	Indicates timing using absolute time code, primarily for synthronization with video playback systems. A single location requires eight messages to send the location in an encoded hours:minutes:seconds:frames format*.
Song Position	0xF2	2	Instructs a sequencer to jump to a new position in the song. The data bytes form a 14-bit value that expresses the location as the number of sixteenth notes from the start of the song.
Song Select	0xF3	1	Instructs a sequencer to select a new song. The data byte indicates the song.
Undefined	0xF4	0	
Undefined	0xF5	0	
Tune Request	0xF6	0	Requests that the receiver retunes itself**.
&lt;/pre&gt;
*MIDI Time Code (MTC) is significantly complex. Please see the MIDI Specification
**While modern digital instruments are good at staying in tune, older analog synthesizers were prone to tuning drift. Some analog synthesizers had an automatic tuning operation that could be initiated with this command.


System Exclusive

If you’ve been keeping track, you’ll notice there are two status bytes not yet defined: 0xf0 and 0xf7. These are used by the System Exclusive message, often abbreviated at SysEx. SysEx provides a path to send arbitrary data over a MIDI connection. There is a group of predefined messages for complex data, like fine grained control of MIDI Time code machinery. SysEx is also used to send manufacturer defined data, such as patches, or even firmware updates.

System Exclusive messages are longer than other MIDI messages, and can be any length. The messages are of the following format:

0xF0, 0xID, 0xdd, ...... 0xF7
The message is bookended with distinct bytes.

It opens with the Start Of Exclusive (SOX) data byte, 0xF0.
The next one to three bytes after the start are an identifier.
Values from 0x01 to 0x7C are one-byte vendor IDs, assigned to manufacturers who were involved with MIDI at the beginning.
If the ID is 0x00, it’s a three-byte vendor ID - the next two bytes of the message are the value.
&lt;pre&gt;
ID 0x7D is a placeholder for non-commercial entities.
ID 0x7E indicates a predefined Non-realtime SysEx message.
ID 0x7F indicates a predefined Realtime SysEx message.
&lt;/pre&gt;
After the ID is the data payload, sent as a stream of bytes.
The transfer concludes with the End of Exclusive (EOX) byte, 0xF7.
The payload data must follow the guidelines for MIDI data bytes – the MSB must not be set, so only 7 bits per byte are actually usable. If the MSB is set, it falls into three possible scenarios.

An End of Exclusive byte marks the ordinary termination of the SysEx transfer.
System Real Time messages may occur within the transfer without interrupting it. The recipient should handle them independently of the SysEx transfer.
Other status bytes implicitly terminate the SysEx transfer and signal the start of new messages.
 Some inexpensive USB-to-MIDI interfaces aren’t capable of handling messages longer than four bytes.

{| class=&quot;wikitable sortable&quot; width=&quot;90%&quot;
! width=&quot;10%&quot;  |Status D7----D0 
! width=&quot;10%&quot;  |Data Byte(s) D7----D0 
! width=&quot;20%&quot;  |Description
|-
|&lt;!--Status--&gt;11110000 || &lt;!--Data--&gt;0iiiiiii [0iiiiiii 0iiiiiii]  0ddddddd  --- --- 0ddddddd 11110111 || &lt;!--Description--&gt;System Exclusive. 
This message type allows manufacturers to create their own messages (such as bulk dumps, patch parameters, and other non-spec data) and provides a mechanism for creating additional MIDI Specification messages. The Manufacturer's ID code (assigned by MMA or AMEI) is either 1 byte (0iiiiiii) or 3 bytes (0iiiiiii 0iiiiiii 0iiiiiii). Two of the 1 Byte IDs are reserved for extensions called Universal Exclusive Messages, which are not manufacturer-specific. If a device recognizes the ID code as its own (or as a supported Universal message) it will listen to the rest of the message (0ddddddd). Otherwise, the message will be ignored. (Note: Only Real-Time messages may be interleaved with a System Exclusive.)
|-
|&lt;!--Status--&gt;11110001 || &lt;!--Data--&gt;0nnndddd || &lt;!--Description--&gt;MIDI Time Code Quarter Frame.
nnn = Message Type
dddd = Values
|-
|&lt;!--Status--&gt;11110010 || &lt;!--Data--&gt;0lllllll 0mmmmmmm || &lt;!--Description--&gt;Song Position Pointer. 
This is an internal 14 bit register that holds the number of MIDI beats (1 beat= six MIDI clocks) since the start of the song. l is the LSB, m the MSB.
|-
|&lt;!--Status--&gt;11110011 || &lt;!--Data--&gt;0sssssss || &lt;!--Description--&gt;Song Select. 
The Song Select specifies which sequence or song is to be played.
|-
|&lt;!--Status--&gt;11110100 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Undefined. (Reserved)
|-
|&lt;!--Status--&gt;11110101 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Undefined. (Reserved)
|-
|&lt;!--Status--&gt;11110110 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Tune Request. Upon receiving a Tune Request, all analog synthesizers should tune their oscillators.
|-
|&lt;!--Status--&gt;11110111 || &lt;!--Data--&gt; || &lt;!--Description--&gt;End of Exclusive. Used to terminate a System Exclusive dump. 
|}


System Real-Time Messages

{| class=&quot;wikitable sortable&quot; width=&quot;90%&quot;
! width=&quot;10%&quot;  |Status D7----D0 
! width=&quot;10%&quot;  |Data Byte(s) D7----D0 
! width=&quot;20%&quot;  |Description
|-
|&lt;!--Status--&gt;11111000 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Timing Clock. Sent 24 times per quarter note when synchronization is required.
|-
|&lt;!--Status--&gt;11111001 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Undefined. (Reserved)
|-
|&lt;!--Status--&gt;11111010 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Start. Start the current sequence playing. (This message will be followed with Timing Clocks).
|-
|&lt;!--Status--&gt;11111011 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Continue. Continue at the point the sequence was Stopped.
|-
|&lt;!--Status--&gt;11111100 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Stop. Stop the current sequence.
|-
|&lt;!--Status--&gt;11111101 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Undefined. (Reserved)
|-
|&lt;!--Status--&gt;11111110 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Active Sensing. This message is intended to be sent repeatedly to tell the receiver that a connection is alive. Use of this message is optional. When initially received, the receiver will expect to receive another Active Sensing message each 300ms (max), and if it does not then it will assume that the connection has been terminated. At termination, the receiver will turn off all voices and return to normal (non- active sensing) operation. 
|-
|&lt;!--Status--&gt;11111111 || &lt;!--Data--&gt; || &lt;!--Description--&gt;Reset. Reset all receivers in the system to power-up status. This should be used sparingly, preferably under manual control. In particular, it should not be sent on power-up.
|}


Advanced Messages

Polyphonic Pressure (0xA0) and Channel Pressure (0xD0)

Some MIDI controllers include a feature known as Aftertouch. While a key is being held down, the player can press harder on the key. The controller measures this, and converts it into MIDI messages.

Aftertouch comes in two flavors, with two different status messages.

The first flavor is polyphonic aftertouch, where every key on the controller is capable of sending its own independent pressure information. The messages are of the following format:
&lt;pre&gt;
0xnc, 0xkk, 0xpp
n is the status (0xA)
c is the channel nybble
kk is the key number (0 to 127)
pp is the pressure value (0 to 127)
&lt;/pre&gt;
Polyphonic aftertouch is an uncommon feature, usually found on premium quality instruments, because every key requires a separate pressure sensor, plus the circuitry to read them all.

Much more commonly found is channel aftertouch. Instead of needing a discrete sensor per key, it uses a single, larger sensor to measure pressure on all of the keys as a group. The messages omit the key number, leaving a two-byte format
&lt;pre&gt;
0xnc, 0xpp
n is the status (0xD)
c is the channel number
pp is the pressure value (0 to 127)
&lt;/pre&gt;

Pitch Bend (0xE0)

Many keyboards have a wheel or lever towards the left of the keys for pitch bend control. This control is usually spring-loaded, so it snaps back to the center of its range when released. This allows for both upward and downward bends.

Pitch Bend Wheel

The wheel sends pitch bend messages, of the format
&lt;pre&gt;
0xnc, 0xLL, 0xMM
n is the status (0xE)
c is the channel number
LL is the 7 least-significant bits of the value
MM is the 7 most-significant bits of the value
&lt;/pre&gt;
You’ll notice that the bender data is actually 14 bits long, transmitted as two 7-bit data bytes. This means that the recipient needs to reassemble those bytes using binary manipulation. 14 bits results in an overall range of 214, or 0 to 16,383. Because it defaults to the center of the range, the default value for the bender is halfway through that range, at 8192 (0x2000).

Control Change (0xB0)

In addition to pitch bend, MIDI has provisions for a wider range of expressive controls, sometimes known as continuous controllers, often abbreviated CC. These are transmitted by the remaining knobs and sliders on the keyboard controller shown below.


Continuous Controllers

These controls send the following message format:
&lt;pre&gt;
0xnc, 0xcc, 0xvv
n is the status (0xB)
c is the MIDI channel
cc is the controller number (0-127)
vv is the controller value (0-127)
&lt;/pre&gt;

Typically, the wheel next to the bender sends controller number one, assigned to modulation (or vibrato) depth. It is implemented by most instruments.

The remaining controller number assignments are another point of confusion. The MIDI specification was revised in version 2.0 to assign uses for many of the controllers. However, this implementation is not universal, and there are ranges of unassigned controllers.

On many modern MIDI devices, the controllers are assignable. On the controller keyboard shown in the photos, the various controls can be configured to transmit different controller numbers. Controller numbers can be mapped to particular parameters. Virtual synthesizers frequently allow the user to assign CCs to the on-screen controls. This is very flexible, but it might require configuration on both ends of the link and completely bypasses the assignments in the standard.


Program Change (0xC0)

Most synthesizers have patch storage memory, and can be told to change patches using the following command:
&lt;pre&gt;
0xnc, 0xpp
n is the status (0xc)
c is the channel
pp is the patch number (0-127)
&lt;/pre&gt;
This allows for 128 sounds to be selected, but modern instruments contain many more than 128 patches. Controller #0 is used as an additional layer of addressing, interpreted as a “bank select” command. Selecting a sound on such an instrument might involve two messages: a bank select controller message, then a program change.

Audio &amp; Midi are not synchronized, what I can do ?
Buy a commercial software package but there is a nasty trick to synchronize both. It's a bit hardcore but works for me:

 Simply put one line down to all midi notes on your pattern (use Insert key)
 and go to 'Misc. Setup', adjust the latency and just search a value
 that will make sound sync both audio/midi.

The stock Sin/Saw/Pulse and Rnd waveforms are too simple/common, is there a way to use something more complex/rich ?
You have to ability to redirect the waveforms of the instruments through the synth pipe by selecting the &quot;wav&quot; option for the oscillator you're using for this synth instrument, samples can be used as wavetables to replace the stock signals.


Sound banks like soundfont (sf2) or Kontakt2 are not supported at the moment


====DAW Audio Evolution 4====

Audio Evolution 4 gives you unsurpassed power for digital audio recording and editing on the Amiga. The latest release focusses on time-saving non-linear and non-destructive editing, as seen on other platforms. Besides editing, Audio Evolution 4 offers a wide range of realtime effects, including compression, noise gate, delays, reverb, chorus and 3-band EQ.

Whether you put them as inserts on a channel or use them as auxillaries, the effect parameters are realtime adjustable and can be fully automated. Together with all other mixing parameters, they can even be controlled remotely, using more ergonomic MIDI hardware.

Non-linear editing on the time line, including cut, copy, paste, move, split, trim and crossfade actions

The number of tracks per project(s) is unlimited .... AHI limits you to recording only two at a time. i.e. not on 8 track sound cards like the Juli@ or Phase 88.

sample file import is limited to 16bit AIFF (not AIFC, important distinction as some files from other sources can be AIFC with aiff file extention). and 16bit WAV (pcm only)


Most apps use the Music Unit only but a few apps also use Unit (0-3) instead or as well. 
* Set up AHI prefs so that microphone is available. (Input option near the bottom)


stereo++ allows the audio piece to be placed anywhere and the left-right adjusted to sound positionally right

hifi best for music playback if driver supports this option


Load 16bit .aif .aiff only sample(s) to use not AIFC which can have the same ending. AIFF stands for Audio Interchange File Format 

 sox recital.wav recital.aiff

 sox recital.wav −b 16 recital.aiff channels 1 rate 16k fade 3 norm
 sox input.wav        output.aiff bass −b 16 rate 48k

performs the same format translation, but also applies four effects (down-mix to one channel, sample rate change, fade-in, nomalize), and stores the result at a bit-depth of 16.

 rec −c 2 radio.aiff trim 0 30:00

records half an hour of stereo audio 

 play existing-file.wav


24bit PCM WAV or AIFF do not work 

*No stream format handling. So no way to pass on an AC3 encoded stream unmodified to the digital outputs through AHI.
*No master volume handling. Each application has to set its own volume. So each driver implements its own custom driver-mixer interface for handling master volumes, mute and preamps.
*Only one output stream. So all input gets mixed into one output.
*No automatic handling of output direction based on connected cables.
*No monitor input selection. Only monitor volume control. 


select the correct input (Don't mistake enabled sound for the correct input.)
The monitor will feedback audio to the lineout and hp out no matter if you have selected the correct input to the ADC. The monitor will provide sound for any valid input. This will result in free mixing when recording from the monitor input instead of mic/line because the monitor itself will provide the hardware mixing for you. Be aware that MIC inputs will give two channel mono. Only Linein will give real stereo.

Now for the not working part. Attempt to record from linein in the AE4 record window, the right channel is noise and the left channel is distorted. Even with the recommended HIFI 16bit Stereo++ mode at 48kHz.


Channels

Monitor

Gain

Inout

Output

Advanced settings - Debugging via serial port


* Options -&gt; Soundcard In/Out
* Options -&gt; SampleRate
* Options -&gt; Preferences

F6 for Sample File List

Setting a grid is easy as is measuring the BPM by marking a section of the sample. Is your kick drum track &quot;not in time&quot; ? If so, you're stumped in AE4 as it has no fancy variable time signatures and definitely no 'track this dodgy rhythm' function like software of the nature of Logic has. So if your drum beat is freeform you will need to work in freeform mode. (Real music is free form anyway).

If the drum *is* accurate and you are just having trouble measuring the time, I usually measure over a range of bars and set the number of beats in range to say 16 as this is more accurate, Then you will need to shift the drum track to match your grid *before* applying the grid. (probably an iterative process as when the grid is active samples snap to it, and when inactive you cannot see it).

AE4 does have ARexx but the functions are more for adding samples at set offsets and starting playback / recording.


These are the usual features found in DAWs...

* Recording digital audio, midi sequencer and mixer 
* virtual VST instruments and plug-ins 
* automation, group channels, MIDI channels, FX sends and returns, audio and MIDI editors and music notation editor


* different track views 
* mixer and track layout (but not the same as below) 
* traditional two windows (track and mixer)


Mixing - mixdown

Could not figure out how to select what part I wanted to send to the aux, set it to echo and return. Pretty much the whole echo effect. Or any effect.

Take look at page17 of the manual.

When you open the EQ / Aux send popup window you will see 4 sends. Now from the menu choose the windows menu.

Menus-&gt;Windows-&gt; Aux Returns Window

or press F5

You will see a small window with 4 volume controls and an effects button for each. Click a button and add an effects to that aux channel, then set it up as desired (note the reverb effect has a special AUX setting that improves its use with the aux channel, not compulsory but highly useful). You set the amount of 'return' on the main mix in the Aux Return window, and the amount sent from each main mixer channel in the popup for that channel. Again the aux sends are &quot;prefade&quot; so the volume faders on each channel do not affect them.


Tracking


Effects - fade in

To add some echoes to some vocals, tried to add an effect on a track but did not come out. This is made more complicated as I wanted to mute a vocal but then make it echo at the muting point. Want to have one word of a vocal heard and then echoed off. But when the track is mute the echo is cancelled out.

To correctly understand what is happening here you need to study the figure at the bottom of page 15 on the manual. You will see from that that the effects are applied 'prefade' So the automation you applied will naturally mute the entire signal.

There would be a number of ways to achieve the goal,

You have three real time effects slots, one for smoothing like so

Sample -&gt; Amplify -&gt; Delay

Then automate the gain of the amplify block so that it effectively mutes the sample just before the delay at the appropriate moment, the echo effect should then be heard.

Getting the effects in the right order will require experimentation as they can only be added top down and it's not obvious which order they are applied to the signal, but there only two possibilities, so it wont take long to find out.

Using MUTE can cause clicks to the Amplify can be used to mute more smoothly so that's a secondary advantage.

Signal Processing -


Overdub

[[#top|...to the top]]

===Office===

====Spreadsheet Leu====

Support for some xlsx, and ods functions 


====Spreadsheet Ignition====

; Needs ABIv1 to be completed before more can be done

File formats supported 
* ascii #?.txt and #?.csv (single sheets with data only). 
* igs and TurboCalc(WIP) #?.tc for all sheets with data, formats and formulas.

There is '''no''' support for xls, xlsx, ods or uos ([http://en.wikipedia.org/wiki/Uniform_Office_Format Uniform Unified Office Format]) at the moment.

* Always use Esc key after editing Spreadsheet cells.
* copy/paste seems to copy the first instance only so go to Edit -&gt; Clipboard to manage the list of remembered actions. 
* Right mouse click on row (1 or 2 or 3) or column header (a or b or c)  to access optimal height or width of the row or column respectively 
* Edit -&gt; Insert -&gt; Row  seems to clear the spreadsheet or clears the rows after the inserted row until undo restores as it should be...

Change Sheet name by  Object -&gt; Sheet -&gt; Properties

Click in the cell which will contain the result, and click '''down arrow button''' to the right of the formula box at the bottom of the spreadsheet and choose the function required from the list provided. Then click on the start cell and click on the bottom right corner, a '''very''' small blob, which allows stretching a bounding box (thick grey outlines) across many cells This grey bounding box can be used to '''copy a formula''' to other cells.

Object -&gt; Cell -&gt; Properties to change cell format - Currency only covers DM and not $, Euro, Renminbi, Yen or Pound etc. 
Shift key and arrow keys selects a range of cells, so that '''formatting can be done to all highlighted cells'''. 
View -&gt; Overview then select ALL with one click (in empty cell in the top left hand corner of the sheet).

Default mode is relative cell referencing e.g. a1+a2 but absolute e.g. $a$1+$a$2 can be entered.

* #sheet-name to '''absolute''' reference another sheet-name cell unless reference() function used.

;Graphs

use shift key and arrow keys to select a bunch of cells to be graph'ed making sure that x axes represents and y axes represents

* value() - 0 value, 1 percent, 2 date, 3 time, 4 unit ...


;Dates 
* Excel starts a running count from the 1st Jan 1900 and Ignition starts from 1st Jan 1AD '''(maybe this needs to change)'''
Set formatting Object -&gt; Cell -&gt; Properties and put date in days


;Time 
Set formatting Object -&gt; Cell -&gt; Properties and put time in seconds taken


;Database (to be done by someone else)

type - standard, reference (bezug), search criterion (suchkriterium), 
* select a bunch of cells and Object -&gt; Database -&gt; Define to set Datenbank (database) and Felder (fields not sure how?) 
* Neu (new) or loschen (delete) to add/remove database headings e.g. Personal, Start Date, Finish Date (one per row?)
* Object -&gt; Database -&gt; Index to add fields (felder) like Surname, First Name, Employee ID, etc. to ?

Filtering done with dbfilter(), dbproduct() and dbposition().

Activities with dbsum(), dbaverage(), dbmin() and dbmax().

Table sorting -


;Scripts (Arexx)

;Excel(TM) to Ignition - commas ''',''' replaced by semi-colons ''';''' to separate values within functions 
*SUM(), 
*AVERAGE(), MAX(), MIN(), INT(), PRODUCT(), MEDIAN(), VAR() becomes Variance(), Percentile(),
*IF(), AND, OR, NOT 
*LEFT(), RIGHT(), MID() becomes MIDDLE(), LEN() becomes LENGTH(), 
*LOWER() becomes LOWERCASE(), UPPER() becomes UPPERCASE(),
* DATE(yyyy,mm,dd) becomes COMPUTEDATE(dd;mm;yyyy), 
*TODAY(), DAY(),WEEK(), MONTH(),=YEAR(TODAY()), 
*EOMONTH() becomes MONTHLENGTH(), 
*NOW() should be date and time becomes time only, SECOND(), MINUTE(), HOUR(),
*DBSUM() becomes DSUM(),


;Missing and possibly useful features/functions needed for ignition to have better support of Excel files 
There is no Merge and Join Text over many cells, no protect and/or freeze row or columns or books but can LOCK sheets, no define bunch of cells as a name, Macros (Arexx?), conditional formatting, no Solver, no Goal Seek, no Format Painter, no AutoFill, no AutoSum function button, no pivot tables, (30 argument limit applies to Excel)

*HLOOKUP(), VLOOKUP(), [http://production-scheduling.com/excel-index-function-most-useful/ INDEX(), MATCH()], CHOOSE(), TEXT(), 
*TRIM(), FIND(), SUBSTITUTE(), CONCATENATE() or &amp;, PROPER(), REPT(), 
*[https://acingexcel.com/excel-sumproduct-function/ SUMPRODUCT()], ROUND(), ROUNDUP(), *ROUNDDOWN(), COUNT(), COUNTA(), SUMIF(), COUNTIF(), COUNTBLANK(), TRUNC(), 
*PMT(), PV(), FV(), POWER(), SQRT(), MODE(), TRUE, FALSE, 
*MODE(), LARGE(), SMALL(), RANK(), STDEV(), 
*DCOUNT(), DCOUNTA(), WEEKDAY(),


;Excel Keyboard [http://dmcritchie.mvps.org/excel/shortx2k.htm shortcuts needed to aid usability in Ignition] 
&lt;pre&gt;
Ctrl Z - Undo

Ctrl D - Fill Down
Ctrl R - Fill right

Ctrl F - Find
Ctrl H - Replace

Ctrl 1 - Formatting of Cells
CTRL SHIFT ~ Apply General Formatting ie a number 
Ctrl ; - Todays Date 

F2 - Edit cell
F4 - toggle cell absolute / relative cell references

&lt;/pre&gt;


====Document Scanning - Scandal====

Scanner usually needs to be connected via a USB port and not via a hub or extension lead.

Check in Trident Prefs -&gt; Devices that the USB Scanner is not bound to anything (e.g. Bindings None)
If not found then reboot the computer and recheck.

Start Scandal, choose Settings from Menu strip at top of screen and in Scanner Driver choose the ?#.device of the scanner (e.g. epson2.device).

The next two boxes - leave empty as they are for morphos SCSI use only
 or put ata.device (use the selection option in bigger box below) and Unit as 0 this is needed for gt68xx

* gt68xx - no editing needed in s/gt68xx.conf but needs a firmware file that corresponds to the scanner [http://www.meier-geinitz.de/sane/gt68xx-backend/ gt68xx firmwares] in sys:s/gt68xx.
* epson2 - Need to edit the file epson2.conf in sys/s that corresponds to the scanner being used

'''Save''' the settings but do not press the Use button (aros freezes)

Back to the Picture Scan window and the right-hand sections.

Click on the '''Information''' tab and press Connect button and the scanner should now be detected.

Go next to the '''Scanner''' tab next to Information Tab should have Color, Black and White, etc. and dpi settings now. Selecting an option Color, B/W etc. can cause dpi settings corruption (especially if the settings are in one line) so set '''dpi first'''. Make sure if Preview is set or not.

In the '''Scan''' Tab, press Scan and the scanner will do its duty. 
Be aware that nothing is saved to disk yet.

In the Save tab, change format JPEG, PNG or IFF DEEP. Tick incremental and base filename if necessary and then click the Save button. The image will now be saved to permanent storage.


The driver ignores a device if it is already bond to another USB class, rejects it from being usable. However, open Trident prefs, select your device and use the right mouse button to open. Select &quot;NONE&quot; to prevent poseidon from touching the device. Now save settings. It should always work now.

[[#top|...to the top]]

===Emulators===

==== Amiberry ====


==== Amiga Emu - Janus UAE ====

With Amibridge, AROS attempts to make the UAE emulator seem embedded within but it still is acting as an app 

There is no dynarec m68k for each hardware that Aros supports or direct patching of motorola calls to AROS hardware accelerated ones unless the emulator has that included 

Try starting Janus with a priority of -1 like this little script:
&lt;pre&gt;
cd sys:system/AmiBridge/emulator
changetaskpri -1
run janus-uae -f my_uaerc.config &gt;nil:
cd sys:prefs
endcli
&lt;/pre&gt;
This stops Janus hogging all the CPU time.


===Miscellaneous===

====Screensaver Blanker====

Most blankers on the amiga (i.e. aros) run as commodities (they are in the tools/commodities drawer). Double click on blanker.

Control is with an app called Exchange, which you need to run first (double click on app) or  run QUIET sys:tools/commodities/Exchange &gt;NIL: but subsequently can use (Cntrl Alt h).

Icon tool types (may be broken) or command line options 
&lt;pre&gt;
seconds=number 
&lt;/pre&gt;

Once the timing is right then add the following to s:icaros-sequence or s:user-startup

e.g. for 5 minutes

 run QUIET sys:tools/commodities/Blanker seconds=300 &gt;NIL:


*[http://archives.aros-exec.org/index.php?function=showfile&amp;file=graphics/screenblanker/gblanker.i386-aros.zip Garshneblanker] can make Aros unstable or slow. Certain blankers crashes in Icaros 2.0.x like Dragon, Executor.


*[ Acuario AROS version], the aquarium screen saver.

Startup: extras:acuariofv-aros/acuario

Kill: c:break name=extras:acuariofv-aros/acuario

Managed to start Acuario by the Executor blanker.

&lt;pre&gt;
cx_priority=
cx_popkey=    ie CX_POPKEY=&quot;Shift F1&quot; 
cx_popup=Yes or No

&lt;/pre&gt;


&lt;pre&gt;
 Qualifier String    Input Event Class
   ----------------    -----------------
    &quot;lshift&quot;           IEQUALIFIER_LSHIFT
    &quot;rshift&quot;           IEQUALIFIER_RSHIFT
    &quot;capslock&quot;         IEQUALIFIER_CAPSLOCK
    &quot;control&quot;          IEQUALIFIER_CONTROL
    &quot;lalt&quot;             IEQUALIFIER_LALT
    &quot;ralt&quot;             IEQUALIFIER_RALT
    &quot;lcommand&quot;         IEQUALIFIER_LCOMMAND
    &quot;rcommand&quot;         IEQUALIFIER_RCOMMAND
    &quot;numericpad&quot;       IEQUALIFIER_NUMERICPAD
    &quot;repeat&quot;           IEQUALIFIER_REPEAT
    &quot;midbutton&quot;        IEQUALIFIER_MIDBUTTON
    &quot;rbutton&quot;          IEQUALIFIER_RBUTTON
    &quot;leftbutton&quot;       IEQUALIFIER_LEFTBUTTON
    &quot;relativemouse&quot;    IEQUALIFIER_RELATIVEMOUSE
&lt;/pre&gt;


&lt;pre&gt;
    Synonym     Synonym
    String     Identifier
    -------    ----------
    &quot;shift&quot;    IXSYM_SHIFT    /* look for either shift key */
    &quot;caps&quot;     IXSYM_CAPS     /* look for either shift key or capslock */
    &quot;alt&quot;      IXSYM_ALT      /* look for either alt key */

Highmap is one of the following strings:
    &quot;space&quot;, &quot;backspace&quot;, &quot;tab&quot;, &quot;enter&quot;, &quot;return&quot;, &quot;esc&quot;, &quot;del&quot;,
    &quot;up&quot;, &quot;down&quot;, &quot;right&quot;, &quot;left&quot;, &quot;f1&quot;, &quot;f2&quot;, &quot;f3&quot;, &quot;f4&quot;, &quot;f5&quot;,
    &quot;f6&quot;, &quot;f7&quot;, &quot;f8&quot;, &quot;f9&quot;, &quot;f10&quot;, &quot;help&quot;.


&lt;/pre&gt;


[[#top|...to the top]]

==== World Construction Set WCS (Version 2.031) ====

WCS is a fractal landscape software such as Scenery Animator, Vista Pro and Panorama. Open sourced February 2022, World Construction Set [https://3dnature.com/downloads/legacy-software/ legally and for free] and [https://github.com/AlphaPixel/3DNature c source]. 

Announced August 1994 this version dates from April 1996 developed by Gary R. Huber and Chris &quot;Xenon&quot; Hanson&quot; from Questar 

&lt;pre&gt;
Assign &quot;WCSProjects:&quot; &quot;Volume:Dir/Dir/WCSProjects&quot; 
Assign &quot;WCSFrames:&quot;   &quot;Volume:Dir/Dir/WCSFrames&quot; 
&lt;/pre&gt;

&lt;pre&gt;
Load projects .proj by accessing pull down menu Project -&gt; Open then click on CanyonSunset.proj
OK to changing .par file and enlarge Status Log window to show what is happening 
Render by pull down menu Modules -&gt; Render with End equal 1 not 300 then click bottom middle button Render 
&lt;/pre&gt;

[https://www.youtube.com/watch?v=CxQDmf1ZWG0 Youtube walkthrough of above], [], [], 

Also try working with the already built file ColoDemo - Then open with the drop-down menu: Project/Open, then WCSProject:ColoDemo.proj
Which allows you to use altimetric DEM files already included and Loading scene parameters from ColoDemo.par
Once this is done, save everything with a new name to start working exclusively on your project. 
Then drop-down menu and select Save As (&quot;NewName&quot;.proj name), then drop-down menu to open parameter and select Save All ( .par name)


After launching the software, there is a the Module Control Panel composed of five icons. 
It is a dock type shortcut of the first few functions of the drop-down menu 

*Database   - Load (#?.proj), Append, Create, Edit, Save, Dir List (of WCSProject drawer), 
*Data Ops   - Extract / Convert Interp DEM, Import DLG, DXF, WDB and export LW map 3d formats  
*Map View   - Database file Loader leading to Map View Control with option to the Database Editor 
*Parameters - Editor for Motion, Color, Ecosystem, Clouds, Waves, management of altimeter files DEM, sclock settings etc 
*Render     - rendering terrain 

These are more in the pull down menu but not in the dock 
*Motion Editor
*Color Editor
*Ecosys Editor 


Simple minimal workflow 
*Load database (1st icon - 1st)
*Set parameters and save .par file (4th icon)
*Render scene (5th icon) 

[https://www.youtube.com/watch?v=ZbTwwR2qcc4 Youtube], [], 

&lt;pre&gt;
.proj new project name which creates a drawer of additional files 

.binary array, ascii array .xyz , z buffer, DTED .dt0, vista 1990s dem, iff  conversion 
.Obj with .elev, .frd with .hdr maps, - digital elevation model (DEM) is a 3D representation of elevation data in various formats 
USGS 7.5MinDEM, 

.par 


&lt;/pre&gt;


Since for the time being no project is loaded, a query window indicates a procedural error when clicking on the rendering icon (right end of the bar). The menu is quite traditional; it varies according to the activity of the windows. To display any altimetric file in the &quot;Mapview&quot; (third icon of the panel), There are three possibilities:

* Loading of a demonstration project.
* The import of a DEM file, followed by texturing and packaging from the &quot;Database-Editor&quot; and the &quot;Color-Editor&quot;.
* The creation of an altimetric file in WCS format, then texturing.


The altimeter file editing (display in the menu) is only made possible if the &quot;Mapview&quot; window is active.

The software is made up of many windows and won't be able to describe them all. Know that &quot;Color-Editor&quot; and the &quot;Data-Editor&quot; comprise sufficient functions for obtaining an almost real rendering quality. You have the possibility of inserting vector objects in the &quot;Data-Editor&quot; (creation of roads, railways, etc.) 


The Map View (MapView) window

*Database - Objects and Topos
*View     - Align, Center, Zoom, Pan, Move 
*Draw     - Maps and distance 
*Object   - Find, highlight, add points, conform topo, duplicate 
*Motion   - Camera, Focus, path, elevation 
*Windows  - DEM designer, Cloud (.cld) and wave (.wve) editor, 


You will notice that by selecting this window and simply moving the pointer to various points on the map you will see latitude and longitude values ​​change, along with the height.
Drop-down menu and Modules, then select MapView and change the width of the window with the map to arrange it in the best way on the screen. With the Auto button the center. Window that then displays the contents of my DEM file, in this case the Grand Canyon. MapView allows you to observe the shape of the landscape from above
 

ZOOM button

Press the Zoom button and then with the pointer position on a point on the map, press the left mouse button and then move to the opposite corner to circumscribe the chosen area and press the left mouse button again, then we will see the enlarged area selected on the map.
Would add that there is a box next to the Zoom button that allows the direct insertion of a value which, the larger it is, the smaller the magnification and the smaller the value, the stronger the magnification. At each numerical change you will need to press the DRAW button to update the view.

PAN button

Under Zoom you will find the PAN button which allows you to move the map at will in all directions by the amount you want. This is done by drawing a line in one direction, then press PAN and point to an area on the map with the pointer and press the left mouse button. At this point, leave it and move the pointer in one direction by drawing a line and press the left mouse button again to trigger the movement of the map on the screen (origin and end points). Do some experiments and then use the Auto button immediately below to recenter everything.
There are parameters such as TOPO, VEC to be left checked and immediately below one that allows different views of the map with the Style command (Single, Multi, Surface, Emboss, Slope, Contour), each with its own particularities to highlight different details.

Now you have the first basics to manage your project visually on the map. Close the MapView window and go further...


Let's start working on ECOSYSTEMS
If we select Emboss from the MapView Style command we will have a clear idea of ​​how the landscape appears, realizing that it is a predominantly desert region of our planet. Therefore we will begin to act on any vegetation present and the appearance of the landscape.
With WCS we will begin to break down the elements of the landscape by assigning defined characteristics. It will be necessary to determine the classes of the ecosystem (Class) with parameters of Elevation Line (maximum altitude), Relative Elevation (arrangement on basins or convexities with respectively positive or negative parameters), Min Slope and Max Slope (slope). WCS offers the possibility of making ecosystems coexist on the same terrain with the UnderEco function, by setting a Density value.


Ecosys Ecosystem Editor

Let's open it from Modules, then Ecosys Editor. In the left pane you will find the list of ecosystems referring to the files present in our project. It will be necessary to clean up that box to leave only the Water and Snow landscapes and a few other predefined ones. We can do this by selecting the items and pressing the Remove button (be careful not for all elements the button is activated, therefore they cannot all be eliminated).
Once this is done we can start adding new ecosystems. Scroll through the various Unused and as soon as the Name item at the top is activated allowing you to write, type the name of your ecosystem, adding the necessary parameters.
&lt;pre&gt;
Ecosystem1: Name: RockBase Class: Rock Density: 80 MinSlope: 15 UnderEco: Terrain
Ecosystem2: Name: RockIncl Clss: Rock Density: 80 MinSlope: 30 UnderEco: Terrain
Ecosystem3: Name: Grass Class Low Veg Density: 50 Height: 1 Elev Line : 1500 Rel El Eff: 5
Max Slope: 10 – Min Slope: 0 UnderEco: Terrain
Ecosistema4: Name: Shrubs Class: Low Veg Density: 40 Height: 8 Elev Line: 3000
Rel El Eff: -2 Max Slope: 20 Min Slope : 5 UnderEco: Terrain
Ecosistema5: Name: Terrain Class: Ground Density: 100 UnderEco: Terrain
&lt;/pre&gt;

Now we need to identify an intermediate ecosystem that guarantees a smooth transition between all, therefore we select as Understory Ecosystem the one called Terrain in all ecosystems, except Snow and Water .
Now we need to 'emerge' the Colorado River in the Canyon and we can do this by raising the sea level to 900 (Sea Level) in the Ecosystem called Water.
Please note that the order of the ecosystem list gives priority to those that come after. So our list must have the following order: Water, Snow, Shrubs, RockIncl, RockBase, Terrain. It is possible to carry out all movements with the Swap button at the bottom. To put order you can also press Short List. Press Keep to confirm all the work done so far with Ecosystem Editor.
Remember every now and then to save both the Project 'Modules/Save' and 'Parameter/Save All'

EcoModels are made up of .etp .fgp .iff8 for each model 


Color Editor

Now it's time to define the colors of our scene and we can do this by going to Modules and then Color Editor. In the list we focus on our ecosystems, created first.
Let's go to the bottom of the list and select the first white space, assigning the name 'empty1', with a color we like and then we will find this element again in other environments... It could serve as an example for other situations!
So we move to 'grass' which already exists and assign the following colors: R 60 G 70 B50
&lt;pre&gt;
'shrubs': R 60 G 80 B 30
'RockIncl' R 110 G 65 B 60
'RockBase' R 110 G 80 B 80
' Terrain' R 150 G 30 B 30
&lt;pre&gt;
Now we can work on pre-existing colors
&lt;pre&gt;
'SunLight' R 150 G 130 B 130
'Haze and Fog' R 190 G 170 B 170
'Horizon' R 209 G 185 B 190
'Zenith' R 140 G 150 B 200
'Water' R 90 G 125 B 170
&lt;/pre&gt;

Ambient R 0 G 0 B 0

So don't forget to close Color Editor by pressing Keep.
Go once again to Ecosystem Editor and assign the corresponding color to each environment by selecting it using the Ecosystem Color button. Press it several times until the correct one appears. Then save the project and parameters again, as done previously.


Motion Editor

Now it's time to take care of the framing, so let's go to Modules and then to Motion Editor. An extremely feature-rich window will open. Following is the list of parameters regarding the Camera, position and other characteristics:
&lt;pre&gt;
-Camera Altitude: 7.0
-Camera Latitude: 36.075
-Camera Longitude: 112.133
-Focus Attitude: -2.0
-Focus Latitude: 36.275
-Focus Longitude: 112.386
-Camera : 512 → rendering window
-Camera Y: 384 → rendering window
-View Arc: 80 → View width in degrees
-Sun Longitude: 172
-Sun Latitude: -0.9
-Haze Start: 3.8
-Haze Range: 78, 5
&lt;/pre&gt;
As soon as the values ​​shown in the relevant sliders have been modified, we will be ready to open the CamView window to observe the wireframe preview. Let's not consider all the controls that will appear.
Well from the Motion Editor if you have selected Camera Altitude and open the CamView panel, you can change the height of the camera by holding down the right mouse button and moving the mouse up and down. To update the view, press the Terrain button in the adjacent window. As soon as you are convinced of the position, confirm again with Keep. You can carry out the same work with the other functions of the camera, such as Focus Altitude...
Let's now see the next positioning step on the Camera map, but let's leave the CamView preview window open while we go to Modules to open the window at the same time MapView. We will thus be able to take advantage of the view from the other together with a subjective one.


From the MapView window, select with the left mouse button and while it is pressed, move the Camera as desired. To update the subjective preview, always click on Terrain.
While with the same procedure you can intervene on the direction of the camera lens, by selecting the cross and with the left button pressed you can choose the desired view. So with the pressure of Terrain I update the Preview. Possibly can enlarge or reduce the Map View using the Zoom button, for greater precision.
Also write that the circle around the cameras indicates the beginning of the haze, there are two types (haze and fog) linked to the altitude. Would also add that the camera height is editable through the Motion Editor panel.


The sun

Let's see that changing the position of the sun from the Motion Editor. Press the SUN button at the bottom right and set the time and the date. Longitude and latitude are automatically obtained by the program. Always open the View Arc command from the Motion Editor panel, an item present in the Parameter List box.

Once again confirm everything with Keep and then save again.


Animation

The animation part is not left-back and also occupies a window. The settings possibilities are enormous. A time line with dragging functions (&quot;slide&quot;, &quot;drag&quot;...) comparable to that of LightWave completes this window. 


A small window is available for positioning the stars as a function of a date, in order to vary the seasons and their various events (and yes...).

At the bottom of the &quot;Motion-Editor&quot;, a &quot;cam-view&quot; function will give you access to a control panel. Different preview modes are possible. The rendering is also accessible through a window. No less than nine pages compose it. At this level, you will be able to determine the backup name of your images (&quot;path&quot;), the type of texture to be calculated, the resolution of the images, activate or deactivate functions such as the depth buffer (&quot;zbuffer&quot;), the blur, the background image, etc.


Once all these parameters have been set, all you have to do is click on the &quot;Render&quot; button.

For rendering go to Modules and then Render. Select the resolution, then under IMA select the name of the image. Move to FRA and indicate the level of fractal detail which of 4 is quite good. Then Keep to confirm and then reopen the window, pressing Render you will see the result. The image will be opened with any viewing program.


Strengths:

* Multi-window.
* Quality of rendering.
* Accuracy.
* Opening, preview and rendering on CyberGraphX screen.
* Extract / Convert Interp DEM, Import DLG, DXF, WDB and export LW map 3d formats 
* The &quot;zbuffer&quot; function.

Weaknesses:

* No OpenGL management 
* Calculation time.
* No network computing tool.


====Writing CD / DVD - Frying Pan====

Can be backup DVDs (4GB ISO size limit due to use of FileInfoBlock), create audio cds from mp3's, and put .iso files on discs

If using for the first time - click Drive button and Device set to ata.device and unit to 0 (zero)

Click Tracks Button - Drive 1 - Create New Disc or Import Existing Disc Image (iso bin/cue etc.) - Session File open cue file

If you're making a data cd, with files and drawers from your hard drive, you should be using the ISO Builder.. which is the MUI page on the left. (&quot;Data/Audio Tracks&quot; is on the right).

You should use the &quot;Data/Audio tracks&quot; page if you want to create music cds with AIFF/WAV/MP3 files, or if you download an .iso file, and you want to put it on a cd.

Click WRITE Button - set write speed - click on long Write button

Examples

Easiest way would be to burn a DATA CD, simply go to &quot;Tracks&quot; page &quot;ISO Builder&quot; and &quot;ADD&quot; everything you need to burn.

On the &quot;Write&quot; page i have &quot;Masterize Disc (DAO)&quot;, &quot;Close Disc&quot; and &quot;Eject after Write&quot; set.

One must not &quot;Blank disc before write&quot; if one uses a CDR


AUDIO CD from MP3's are as easy but tricky to deal with. FP only understands one MP3 format, Layer II, everything else will just create empty tracks

Burning bootable CD's works only with .iso files. Go to &quot;Tracks&quot; page and &quot;Data/Audio Tracks&quot; and add the .iso


====odf====

Every ODF file is a collection of several subdocuments within a package (ZIP file), each of which stores part of the complete document.

* content.xml – Document content and automatic styles used in the content.
* styles.xml – Styles used in the document content and automatic styles used in the styles themselves.
* meta.xml – Document meta information, such as the author or the time of the last save action.
* settings.xml – Application-specific settings, such as the window size or printer information.


To read document follow these steps:

* Extracting .ods file.
* Getting content.xml file (which contains sheets data).
* Creating XmlDocument object from content.xml file.
* Creating DataSet (that represent Spreadsheet file).
* With XmlDocument select “table:table” elements, and then create adequate DataTables.
* Parse child’s of “table:table” element and fill DataTables with those data.
* At the end, return DataSet and show it in application’s interface.


To write document follow these steps:

* Extracting template.ods file (.ods file that we use as template).
* Getting content.xml file.
* Creating XmlDocument object from content.xml file.
* Erasing all “table:table” elements from the content.xml file.
* Reading data from our DataSet and composing adequate “table:table” elements.
* Adding “table:table” elements to content.xml file.
* Zipping that file as new .ods file.

XLS file format

The XLS file format contains streams, substreams, and records.

These sheet substreams include worksheets, macro sheets, chart sheets, dialog sheets, and VBA module sheets. 
All the records in an XLS document start with a 2-byte unsigned integer to specify Record Type (rt), and another for Count of Bytes (cb). A record cannot exceed 8224 bytes. If larger than the rest is stored in one or more continue records.

* Workbook stream 
**Globals substream
***BoundSheet8 record - info for Worksheet substream i.e. name, location, type, and visibility. (4bytes the lbPlyPos FilePointer, specifies the position in the Workbook stream where the sheet substream starts) 
**Worksheet substream (sheet) - Cell Table - Row record - Cells (2byte=row 2byte=column 2byte=XF format)
***Blank cell record
***RK cell record 32-bit number. 
***BoolErr cell record (2-byte Bes structure that may be either a Boolean value or an error code)
***Number cell record (64-bit floating-point number)
***LabelSst cell record (4-byte integer that specifies a string in the Shared Strings Table (SST). Specifically, the integer corresponds to the array index in the RGB field of the SST)
***Formula cell record (FormulaValue structure in the 8 bytes that follow the cell structure. The next 6 bytes can be ignored, and the rest of the record is a CellParsedFormula structure that contains the formula itself)
***MulBlank record (first 2 bytes give the row, and the next 2 bytes give the column that the series of blanks starts at. Next, a variable length array of cell structures follows to store formatting information, and the last 2 bytes show what column the series of blanks ends on)
***MulRK record 
***Shared String Table (SST) contains all of the string values in the workbook.

ACCRINT(), ACCRINTM(), AMORDEGRC(), AMORLINC(), 
COUPDAYBS(), COUPDAYS(), COUPDAYSNC(), COUPNCD(), COUPNUM(), COUPPCD(), 
CUMIPMT(), CUMPRINC(), 
DB(), DDB(), DISC(), 
DOLLARDE(), DOLLARFR(), 
DURATION(), EFFECT(), FV(), FVSCHEDULE(), 
INTRATE(), IPMT(), IRR(), ISPMT(), MDURATION(), MIRR(), NOMINAL(), NPER(), NPV(), 
ODDFPRICE(), ODDFYIELD(), ODDLPRICE(), ODDLYIELD(), 
PMT(), PPMT(), PRICE(), PRICEDISC(), PRICEMAT(), PV(), RATE(), 
RECEIVED(), SLN(), SYD(), TBILLEQ(), TBILLPRICE(), TBILLYIELD(), 
VDB(), XIRR(), XNPV(), YIELD(), YIELDDISC(), YIELDMAT(),


&lt;pre&gt;
&lt;/pre&gt;


&lt;pre&gt;
&lt;/pre&gt;

&lt;pre&gt;
&lt;/pre&gt;

{{BookCat}}</text>
      <sha1>h76jk6e5illq5v2z2cegis253zh5fbp</sha1>
    </revision>
  </page>
  <page>
    <title>OpenClinica User Manual/InstallationCheckList</title>
    <ns>0</ns>
    <id>238148</id>
    <revision>
      <id>4654726</id>
      <parentid>2739657</parentid>
      <timestamp>2026-07-16T18:39:29Z</timestamp>
      <contributor>
        <username>GerbenRienk</username>
        <id>339385</id>
      </contributor>
      <minor />
      <comment>/* Writing a mail to the OpenClinica community */  removed refernece to the forum, because that is no longer active. Updated the url for the distros.</comment>
      <origin>4654726</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="5548" sha1="9qvzk2csg7j8xn9s2doi1ytly5hm48t" xml:space="preserve">== Checklist for installation problems ==
=== introduction ===

If you followed the installation-instructions and the results are not as expected, this could have a number of reasons. A large number. Before you post a mail to the OpenClinica-mailinglist, saying &quot;my installation did not work: why not?&quot; it is good to check the list of points below. It helps a lot if you can narrow down the problem, for example to &quot;the creation of the Postgres-db was not succesfull&quot;.

=== check that you have the correct version of OpenClinica ===
The [https://distros.openclinica.com/ Download OpenClinica page] offers several different versions of OpenClinica.  If you are just starting off, you will most likely want the latest stable version that looks like OpenClinica-n.n.n (the regular OpenClinica release), rather than OpenClinica-ws-n.n.n (the web services release) or OpenClinica-ws-caBIG-n.n.n (web services with caBIG).

=== check the versions of the software you are running ===
Compare the versions of the software you are running to the requirements listed in the requirements section of the [https://community.openclinica.com/project/openclinica Download OpenClinica page].  Sometimes the latest versions of software (Tomcat or Postgres) are not compatible with the latest version of OpenClinica (e.g. OpenClinica 3.1.4.x isn't compatible with Tomcat 7+ or Postgres 9.0+).

==== non-obvious effects of using non-supported versions ====
Even though your installation appears to be running OK, there can be some bugs that are related to using a non-supported version that aren't apparent until after you've built your first study.

For example with OpenClinica 3.1.4 and 3.1.3.1 (and presumably earlier versions), using Tomcat 6.0.36 instead of the recommended 6.0.32 results the display of an inactive 'Begin New Thread' link in the discrepancy notes pop-up window, both on Linux and Windows systems ([https://mailman.openclinica.com/pipermail/users/2013-August/008634.html see this mail list thread]). This bug prevents more than one discrepancy note being (easily) added to each item in the study, and therefore prevents more than one edit being saved for an item on a CRF that was marked complete, where 'Forced Reason for Change During Administrative Data Entry' is active for the study.

=== check Tomcat is running OK ===

To check this, open a web browser, such as Firefox or Internet Explorer. Type the address of the server you installed  Tomcat on, followed by the portnumber you specified. If you took all defaults this is port 8080. You can use ip-address or the name, so http://www.myserver.org:8080 or http://[ip-address]:8080.

If you installed Tomcat on your local machine, use http://localhost:8080

You should now see a page of the Apache Software Foundation saying &quot;If you're seeing this page via a web browser, it means you've setup Tomcat successfully. Congratulations!&quot;

If you don't see such a page, check your Tomcat log files, you may see an error about Tomcat not being able to allocate memory.  You can either reduce the amount Tomcat is trying to allocate (e.g. reduce the Maximum memory pool value on Windows), or increase the amount available.

=== check Tomcat recognizes OpenClinica ===

To check if Tomcat recognizes OpenClinica correctly, you can use the Tomcat manager-page. But before you can access this page, you must add a user with the tomcat-manager-role to the file tomcat-users.xml This file is located under the Tomcat-directory structure in conf/tomcat-users.xml 
Add two lines to it: &lt;br /&gt;
&lt;role rolename=&quot;manager&quot;/&gt; &lt;br /&gt;
&lt;user username=&quot;tomcat&quot; password=&quot;s3cret&quot; roles=&quot;manager&quot;/&gt;

Shutdown and startup Tomcat. Go to the default page, described above, http://www.myserver.org:8080 or localhost:8080
If you are on the first page of Tomcat, click on the link in the lefthand corner labeled &quot;Tomcat Manager&quot;. In the page that opens, you see a list of all applications. In this list you should see an entry for &quot;OpenClinica 3.0&quot;

=== check OpenClinica is running ===

In the Tomcat Web Application Manager, described above, go to the line with &quot;OpenClinica&quot; and check the third column &quot;Running&quot;: this should be &quot;true&quot;. If it is &quot;false&quot;, click &quot;Start&quot; in the fourth column. If this is the first time for OpenClinica to run, give it time! Tomcat has to go through the archive file, the war, and deploy it. On a slow machine this can take 10 minutes or more.
If the status of OpenClinica is True/Running, then click on the link if the left column to get the OpenClinica login-screen.

=== check Postgres is running ===

For Linux type &quot;ps -u postgres&quot; and if there is output, you're OK.
For Windows, goto Configuration-System-Services and look for PostgreSQL and then check the status.

=== check user clinica and database openclinica exist in Postgres ===

Open psql. Type &quot;\du&quot;. You get a listing of all users and (super)user &quot;clinica&quot; should be on it.
Next type &quot;\l&quot; This will give a list of all databases and one of them should be &quot;openclinica&quot;, owner &quot;clinica&quot;, encoding &quot;UTF8&quot;

=== check your datainfo.properties ===
This is the obvious one: check every line you changed and/or commented out! Especially the username and password of the postgres-user.
Starting from OpenClinica 3.4 there's a strange, but expected behaviour: at first the file datainfo.properties is created in /usr/local/tomcat/webapps/OpenClinica/WEB-INF/classes. But then after restarting the application, the file is moved to /usr/local/tomcat/openclinica.config
Make sure that you edit the right datainfo.properties

{{BookCat}}</text>
      <sha1>9qvzk2csg7j8xn9s2doi1ytly5hm48t</sha1>
    </revision>
  </page>
  <page>
    <title>Wikijunior:The Elements/Arsenic</title>
    <ns>110</ns>
    <id>307047</id>
    <revision>
      <id>4654727</id>
      <parentid>4440164</parentid>
      <timestamp>2026-07-16T19:03:04Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* What does it look, feel, taste, or smell like? */ Added information.</comment>
      <origin>4654727</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="2573" sha1="j168otdw7h4ul5s7c03u3zb5drxce9m" xml:space="preserve">__NOTOC__

[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.

==Where did its name come from?==
The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food.

==Is it dangerous?==
Arsenic is poisonous. It is used in pesticides and other poisons.

== References ==

{{BookCat}}</text>
      <sha1>j168otdw7h4ul5s7c03u3zb5drxce9m</sha1>
    </revision>
    <revision>
      <id>4654728</id>
      <parentid>4654727</parentid>
      <timestamp>2026-07-16T19:08:56Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* How was it discovered? */ Added information</comment>
      <origin>4654728</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="2900" sha1="3zgxqxkt5h6nb1qlsdlt3ol63qd3x7q" xml:space="preserve">__NOTOC__

[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.    Magnus heated arsenic sulfide with soap to produce metallic arsenic. Arsenic compounds were known in ancient times. Ancient people used the mineral orpiment to make bright yellow pigments. The mineral realgar was used for red pigments and poisons. Arabic alchemists first described isolation of arsenic about 800 years ago.

==Where did its name come from?==
The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food.

==Is it dangerous?==
Arsenic is poisonous. It is used in pesticides and other poisons.

== References ==

{{BookCat}}</text>
      <sha1>3zgxqxkt5h6nb1qlsdlt3ol63qd3x7q</sha1>
    </revision>
    <revision>
      <id>4654729</id>
      <parentid>4654728</parentid>
      <timestamp>2026-07-16T19:11:07Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* Where did its name come from? */ Added information</comment>
      <origin>4654729</origin>
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      <text bytes="2978" sha1="8ew3usd82ttwij7azi3gnzil9ww1p9b" xml:space="preserve">__NOTOC__

[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.    Magnus heated arsenic sulfide with soap to produce metallic arsenic. Arsenic compounds were known in ancient times. Ancient people used the mineral orpiment to make bright yellow pigments. The mineral realgar was used for red pigments and poisons. Arabic alchemists first described isolation of arsenic about 800 years ago.

==Where did its name come from?==
The name arsenic likely comes from a Greek word meaning “yellow pigment.” The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food.

==Is it dangerous?==
Arsenic is poisonous. It is used in pesticides and other poisons.

== References ==

{{BookCat}}</text>
      <sha1>8ew3usd82ttwij7azi3gnzil9ww1p9b</sha1>
    </revision>
    <revision>
      <id>4654730</id>
      <parentid>4654729</parentid>
      <timestamp>2026-07-16T19:12:34Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* Where is it found? */ added information</comment>
      <origin>4654730</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="3294" sha1="hk3fapru8qavqdwupwz6xkf5r82hei0" xml:space="preserve">__NOTOC__

[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.    Magnus heated arsenic sulfide with soap to produce metallic arsenic. Arsenic compounds were known in ancient times. Ancient people used the mineral orpiment to make bright yellow pigments. The mineral realgar was used for red pigments and poisons. Arabic alchemists first described isolation of arsenic about 800 years ago.

==Where did its name come from?==
The name arsenic likely comes from a Greek word meaning “yellow pigment.” The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco. Arsenic is found within the Earth’s crust, but rarely in pure form. Most arsenic is bound in minerals such as realgar, orpiment, and arsenopyrite. These minerals exist in regions with hydrothermal veins and volcanos. Arsenic is typically a byproduct of mining and refining metals such as gold, silver, and copper.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food.

==Is it dangerous?==
Arsenic is poisonous. It is used in pesticides and other poisons.

== References ==

{{BookCat}}</text>
      <sha1>hk3fapru8qavqdwupwz6xkf5r82hei0</sha1>
    </revision>
    <revision>
      <id>4654731</id>
      <parentid>4654730</parentid>
      <timestamp>2026-07-16T19:16:18Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* What are its uses? */ added information</comment>
      <origin>4654731</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="3442" sha1="7d8zjpjwvpnciserl0050odjjdg7qcz" xml:space="preserve">__NOTOC__

[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.    Magnus heated arsenic sulfide with soap to produce metallic arsenic. Arsenic compounds were known in ancient times. Ancient people used the mineral orpiment to make bright yellow pigments. The mineral realgar was used for red pigments and poisons. Arabic alchemists first described isolation of arsenic about 800 years ago.

==Where did its name come from?==
The name arsenic likely comes from a Greek word meaning “yellow pigment.” The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco. Arsenic is found within the Earth’s crust, but rarely in pure form. Most arsenic is bound in minerals such as realgar, orpiment, and arsenopyrite. These minerals exist in regions with hydrothermal veins and volcanos. Arsenic is typically a byproduct of mining and refining metals such as gold, silver, and copper.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food. Arsenic is used for electronics and to make certain metal alloys. In glassmaking, small amounts of arsenic help remove bubbles and improve clarity.

==Is it dangerous?==
Arsenic is poisonous. It is used in pesticides and other poisons.

== References ==

{{BookCat}}</text>
      <sha1>7d8zjpjwvpnciserl0050odjjdg7qcz</sha1>
    </revision>
    <revision>
      <id>4654732</id>
      <parentid>4654731</parentid>
      <timestamp>2026-07-16T19:17:49Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* Is it dangerous? */ Added information</comment>
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[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.    Magnus heated arsenic sulfide with soap to produce metallic arsenic. Arsenic compounds were known in ancient times. Ancient people used the mineral orpiment to make bright yellow pigments. The mineral realgar was used for red pigments and poisons. Arabic alchemists first described isolation of arsenic about 800 years ago.

==Where did its name come from?==
The name arsenic likely comes from a Greek word meaning “yellow pigment.” The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco. Arsenic is found within the Earth’s crust, but rarely in pure form. Most arsenic is bound in minerals such as realgar, orpiment, and arsenopyrite. These minerals exist in regions with hydrothermal veins and volcanos. Arsenic is typically a byproduct of mining and refining metals such as gold, silver, and copper.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food. Arsenic is used for electronics and to make certain metal alloys. In glassmaking, small amounts of arsenic help remove bubbles and improve clarity.

==Is it dangerous?==
Arsenic is poisonous. Elemental arsenic and many of its compounds are poisonous. Repeated exposure can cause serious long-term health problems. Handling, storage, and disposal are strictly regulated in industrial settings. Even at low levels arsenic is very hazardous.

When arsenopyrite, realgar, or orpiment are heated in the smelting process, they release arsenic vapor. This vapor rapidly oxidizes to form arsenic trioxide (As₂O₃), a very toxic white smoke. 

== References ==

{{BookCat}}</text>
      <sha1>nqmwz5ur0hn15juqpfrket6bqxji0hf</sha1>
    </revision>
    <revision>
      <id>4654733</id>
      <parentid>4654732</parentid>
      <timestamp>2026-07-16T19:20:28Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* Is it dangerous? */ Added information</comment>
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      <text bytes="4255" sha1="5654n778pnr4wa0q64w05evusq8vx87" xml:space="preserve">__NOTOC__

[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.    Magnus heated arsenic sulfide with soap to produce metallic arsenic. Arsenic compounds were known in ancient times. Ancient people used the mineral orpiment to make bright yellow pigments. The mineral realgar was used for red pigments and poisons. Arabic alchemists first described isolation of arsenic about 800 years ago.

==Where did its name come from?==
The name arsenic likely comes from a Greek word meaning “yellow pigment.” The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco. Arsenic is found within the Earth’s crust, but rarely in pure form. Most arsenic is bound in minerals such as realgar, orpiment, and arsenopyrite. These minerals exist in regions with hydrothermal veins and volcanos. Arsenic is typically a byproduct of mining and refining metals such as gold, silver, and copper.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food. Arsenic is used for electronics and to make certain metal alloys. In glassmaking, small amounts of arsenic help remove bubbles and improve clarity.

==Is it dangerous?==
Arsenic is an interesting but very dangerous element. It appears in colorful minerals. When scientists learned how to separate arsenic from minerals, they discovered its toxicity. Arsenic is poisonous. Elemental arsenic and many of its compounds are poisonous. Repeated exposure can cause serious long-term health problems. Handling, storage, and disposal are strictly regulated in industrial settings. Even at low levels arsenic is very hazardous.

When arsenopyrite, realgar, or orpiment are heated in the smelting process, they release arsenic vapor. This vapor rapidly oxidizes to form arsenic trioxide (As₂O₃), a very toxic white smoke.  

Today, arsenic is used in some industries and in scientific research. Strict rules help protect people from arsenic poisoning. It is important to know where arsenic comes from, how it acts, and why it must be handled with care.  

== References ==

{{BookCat}}</text>
      <sha1>5654n778pnr4wa0q64w05evusq8vx87</sha1>
    </revision>
    <revision>
      <id>4654737</id>
      <parentid>4654733</parentid>
      <timestamp>2026-07-16T19:23:12Z</timestamp>
      <contributor>
        <username>Ladybug62</username>
        <id>740059</id>
      </contributor>
      <comment>/* References */ Added References</comment>
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      <text bytes="4835" sha1="fve9s9wv76cxaudr4rd1nxtfw4f8lob" xml:space="preserve">__NOTOC__

[[File:As-TableImage.svg|thumb|left|500px|Shows the position of Arsenic on the periodic chart.]]
[[File:Arsenic.svg|thumb|55px|Arsenic's symbol on the Periodic Table]]
{{clear}}
Arsenic is a poisonous metalloid.
==What does it look, feel, taste, or smell like?==
[[File:Arsen 1a.jpg|thumb|250px|Elemental arsenic]]
The most stable &amp;mdash; and therefore the most common &amp;mdash; form of pure arsenic is gray.  Gray arsenic has a bright, reflective metallic luster There are also yellow and black forms.  Yellow arsenic is the most unstable and the most toxic. Elemental arsenic is a metallic solid. Its surface is shiny steel-gray.. Arsenic looks like a metal but is classified as a metalloid. It has a brittle, crystalline property that makes it snap or crumble instead of bending.

Other forms of elemental arsenic (allotropes) look different. One allotrope, yellow arsenic is pale yellow. It is unstable and turns into the grey form when exposed to light. Another allotrope, black arsenic is glassy and brittle. It does not have a metallic appearance. 

==How was it discovered?==
Compounds of arsenic have been known since ancient times &amp;mdash; arsenic sulfates, and arsenic oxides.  Pure arsenic is rare in nature.  As far as we know, the first person to isolate pure arsenic was Albertus Magnus, a German friar and bishop, around the year 1250&amp;nbsp;CE.    Magnus heated arsenic sulfide with soap to produce metallic arsenic. Arsenic compounds were known in ancient times. Ancient people used the mineral orpiment to make bright yellow pigments. The mineral realgar was used for red pigments and poisons. Arabic alchemists first described isolation of arsenic about 800 years ago.

==Where did its name come from?==
The name arsenic likely comes from a Greek word meaning “yellow pigment.” The Greek word ''arsenikos'', meaning &quot;male&quot;, &quot;virile&quot; was adopted in Latin as ''arsenicum'', which in French became ''arsenic'', from which the English word arsenic is taken.
&lt;div style=&quot;float:right; border:2px solid #000000; width:250px; margin-left:0.2em; padding:0.4em; background-color:#f0f0ff&quot;&gt;
'''Did You Know?'''
* Arsenic has metallic and nonmetallic properties. It is a metalloid.
* Arsenic comprises about 1.5 ppm (0.00015%) of the Earth's crust.
* Arsenite of lime and arsenate of lead were used widely as insecticides until the discovery of DDT in 1942.
&lt;/div&gt;

==Where is it found?==
Arsenic is a fairly common element on Earth.  A lot of it is mined in China. Other countries that mine a fair amount of arsenic are Chile, Peru, and Morocco. Arsenic is found within the Earth’s crust, but rarely in pure form. Most arsenic is bound in minerals such as realgar, orpiment, and arsenopyrite. These minerals exist in regions with hydrothermal veins and volcanos. Arsenic is typically a byproduct of mining and refining metals such as gold, silver, and copper.

==What are its uses?==
Arsenic is used in some alloys to make them harder. It was sometimes used in ancient times to make bronze harder. It is also used in some pesticides, although these are not used as much as they used to be because of concerns it could hurt people if it gets on their food. Arsenic is used for electronics and to make certain metal alloys. In glassmaking, small amounts of arsenic help remove bubbles and improve clarity.

==Is it dangerous?==
Arsenic is an interesting but very dangerous element. It appears in colorful minerals. When scientists learned how to separate arsenic from minerals, they discovered its toxicity. Arsenic is poisonous. Elemental arsenic and many of its compounds are poisonous. Repeated exposure can cause serious long-term health problems. Handling, storage, and disposal are strictly regulated in industrial settings. Even at low levels arsenic is very hazardous.

When arsenopyrite, realgar, or orpiment are heated in the smelting process, they release arsenic vapor. This vapor rapidly oxidizes to form arsenic trioxide (As₂O₃), a very toxic white smoke.  

Today, arsenic is used in some industries and in scientific research. Strict rules help protect people from arsenic poisoning. It is important to know where arsenic comes from, how it acts, and why it must be handled with care.  

== References ==

{{BookCat}}Ducksters. (2026)'''.''' ''Chemistry for kids: Elements – Arsenic.'' &lt;nowiki&gt;https://www.ducksters.com/science/chemistry/arsenic.php&lt;/nowiki&gt;

Kiddle Encyclopedia. (n.d.). ''Arsenic facts for kids.'' &lt;nowiki&gt;https://kids.kiddle.co/Arsenic&lt;/nowiki&gt;

WeDraw Studio. (n.d.). ''Arsenic element – Periodic table: Properties, uses, and more'' [Video]. Yahoo Video Search. &lt;nowiki&gt;https://video.search.yahoo.com/search/video&lt;/nowiki&gt;

What is Arsenic? History, poison, and modern uses. (n.d.). [Video]. Yahoo Video Search. &lt;nowiki&gt;https://video.search.yahoo.com/search/video&lt;/nowiki&gt;</text>
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  <page>
    <title>Annotated Republic of China Regulations/Regulations for Road Traffic Signs, Markings, and Signals</title>
    <ns>0</ns>
    <id>360163</id>
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      <id>4654768</id>
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      <timestamp>2026-07-17T03:48:28Z</timestamp>
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        <username>TunnelESON</username>
        <id>10882</id>
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      <text bytes="16181" sha1="csnu66ed6pegscd0yuxdy8n3q3ggwz1" xml:space="preserve">{{header
 | title    = Regulations for Road Traffic Signs, Markings, and Signals
 | author   = |override_author= Republic of China (Taiwan) Regulation
 | section  = 
 | previous =
 | next     =
 | notes    = In 2021, the serial comma was dropped to make the &quot;Regulations for Road Traffic Signs, Markings and Signals&quot;.
}}

==History==
Taiwanese traffic control devices use metric measuring units, such as kilometers, meters, and tonnes. Full history is as follows:

{|border=&quot;1&quot;
!Version&lt;ref&gt;https://law.moj.gov.tw/LawClass/LawHistory.aspx?pcode=K0040014 https://www.laws.taipei.gov.tw/Law/LawSearch/LawInformation/FL012456 , accessed 2026-07-17&lt;/ref&gt;!!Date&lt;ref&gt;[http://law.moj.gov.tw/Eng/LawClass/LawSearchNo.aspx?PC=A0030133&amp;DF=&amp;SNo=13 Article 13] of the ''[[b:Annotated Republic of China Laws/Central Regulation Standard Act|Central Regulation Standard Act]]'': &quot;While a regulation stipulated that the regulation shall be enforced from the date of enactment or '''publication''', the regulation shall become effective since the third date of the enactment or publication date.&quot;&lt;/ref&gt; !!Amended articles (± amended; + added; &lt;i&gt;- deleted&lt;/i&gt;)!!Summary and comparison, and/or draft amendment&lt;ref&gt;https://gazette.nat.gov.tw/egFront/browseHistory.do?metaid=91629 , accessed 2026-07-17&lt;/ref&gt;
|-
|'''[[s:zh:道路交通標誌標線號誌設置規則 (民國57年)|1]]'''||'''[[/1968/]]-10-01'''||'''Published 207 new articles:''' [[:File:ROC1968-10-01道路交通標誌標線號誌設置規則1.pdf|1 -&gt; 64]]; [[:File:ROC1968-10-01道路交通標誌標線號誌設置規則2.pdf|65 -&gt; 89]]; [[:File:ROC1968-10-01道路交通標誌標線號誌設置規則3.pdf|90 -&gt; 113]]; [[:File:ROC1968-10-01道路交通標誌標線號誌設置規則4.pdf|114 -&gt; 147]]; [[:File:ROC1968-10-01道路交通標誌標線號誌設置規則5.pdf|148 -&gt; 207]]; [[:File:ROC1968-10-01道路交通標誌標線號誌設置規則6.pdf|Appendix]]; [[:File:ROC1968-10-01道路交通標誌標線號誌設置規則勘誤表.pdf|Errata]]||
|-
|2||[[:File:ROC1977-09-14道路交通標誌標線號誌設置規則修正條文.pdf|1977-09-14]]||±50 crossbucks at rail level crossings||
|-
|3||[[:File:ROC1978-11-30道路交通標誌標線號誌設置規則修正條文.pdf|1978-11-30]]||±101 stationary barricade ±102 movable barricade ±103 traffic cone ±104 work zone control; + 103-1 work zone signs + 103-2 moving work zone signs + 103-3 work zone warning lights||
|-
|'''4'''||'''[[/1981/]]-01-22'''||'''Fully amended all 229 articles.'''||
|-
|5||1981-10-19||±2||
|-
|'''[[s:zh:道路交通標誌標線號誌設置規則 (民國78年)|6]]'''||'''[[/1989/]]-12-15'''||'''Fully amended all 235 articles: [[:File:ROC1989-12-15道路交通標誌標線號誌設置規則1.pdf|1 -&gt; 73]]; [[:File:ROC1989-12-15道路交通標誌標線號誌設置規則2.pdf|73 -&gt; 132]]; [[:File:ROC1989-12-15道路交通標誌標線號誌設置規則3.pdf|132 -&gt; 158]]; [[:File:ROC1989-12-15道路交通標誌標線號誌設置規則4.pdf|158 -&gt; 203]]; [[:File:ROC1989-12-15道路交通標誌標線號誌設置規則5.pdf|203 -&gt; Appendix 3]]; [[:File:ROC1989-12-15道路交通標誌標線號誌設置規則6.pdf|Appendix 3]]; [[:File:ROC1989-12-15道路交通標誌標線號誌設置規則勘誤表.pdf|Errata]]'''||
|-
|7||[[:File:ROC1994-04-09道路交通標誌標線號誌設置規則修正條文.pdf|1994-04-09]]||±13 ±15 ±16 ±18 ±19 ±24&lt;ref name=&quot;images unchanged&quot;&gt;The texts have been amended with the images unchanged.&lt;/ref&gt; ±30&lt;ref name=&quot;images unchanged&quot; /&gt; ±58&lt;ref name=&quot;new images&quot;&gt;New images were added.&lt;/ref&gt; ±59&lt;ref name=&quot;new images&quot; /&gt; ±62 ±63&lt;ref name=&quot;texts unchanged&quot;&gt;The images have been amended with the texts unchanged.&lt;/ref&gt; ±65&lt;ref name=&quot;images unchanged&quot; /&gt; ±74 ±75 ±76 ±77 ±78 ±79 ±80 ±85 ±99 ±118 ±119 ±120 ±121 ±122 ±123 ±124 ±125 ±126 ±127 ±128 ±129 ±130 ±131 ±132 ±133 ±134 ±135 ±140 ±141 ±151 ±152 ±158 ±162 ±166 ±168 ±170 ±171 ±174 ±181 ±182 ±183 ±188 ±190 ±191 ±194 ±231 ±233; + 73-1 + 118-1 + 118-2 + 118-3 + 118-4 + 133-1 + 183-1||
|-
|8||[[:File:ROC1994-06-23道路交通標誌標線號誌設置規則修正條文.pdf|1994-06-23]]||±11 ±12 ±87 ±89 ±98&lt;ref name=&quot;texts unchanged&quot; /&gt; ±108 ±116||
|-
|9||[[:File:ROC1998-11-16道路交通標誌標線號誌設置規則修正條文.pdf|1998-11-16]]||±149 ±167 No Lane Change Markings add Lane Change Prohibited in Either Side (solid line) ±168 No Parking Markings prohibit parking from 7 am to 8 pm (no longer until 11 pm) every day, unless also having signs and supplementary plates.||
|-
|10||[[:File:ROC2000-07-13道路交通標誌標線號誌設置規則修正條文.pdf|2000-07-13]]||±99 ±122 ±164 ±173 ±174 ±183 ±183-1 ±204; + 174-1 + 174-2||
|-
|[[s:zh:道路交通標誌標線號誌設置規則 (民國91年)|11]]||[[:File:ROC2002-10-25道路交通標誌標線號誌設置規則修正條文.pdf|2002-10-25]]||±1 ±15 ±89 ±118-1 ±140 ±179 ±188 ±190 ±194 ±195||[[:File:ROC2002-05-31道路交通標誌標線號誌設置規則修正草案.pdf|2002-05-31 draft]]
|-
|[[:File:ROC2003-09-24道路交通標誌標線號誌設置規則.pdf|12]]||[[:File:ROC2003-09-24道路交通標誌標線號誌設置規則修正條文.pdf|2003-09-24]]||±9&lt;ref name=&quot;images unchanged&quot; /&gt; ±85 ±87 ±95 ±96 ±97 ±98 ±104 ±105 ±109 ±118-4 ±120 ±141 ±173 ±174 ±174-2 ±177 ±179 ±183 ±183-1 ±190 ±221; + 87-1 + 87-2 + 118-5||[[:File:ROC2002-10-11道路交通標誌標線號誌設置規則修正草案.pdf|2002-10-11 ]] and [[:File:ROC2003-05-05道路交通標誌標線號誌設置規則修正草案.pdf|2003-05-05 draft]]s
|-
|13||[[:File:ROC2006-02-22道路交通標誌標線號誌設置規則修正條文.pdf|2006-02-22]]||±9&lt;ref name=&quot;images unchanged&quot; /&gt; The Chinese National Standards are renamed the National Standards of the Republic of China, still abbreviated CNS.||
|-
|14||[[:File:ROC2006-06-28道路交通標誌標線號誌設置規則修正條文.pdf|2006-06-28]] (effective 2006-07-01)||±69 ±174 ±[[:File:ROC2006-06-28道路交通標誌標線號誌設置規則勘誤表.pdf|235 (errata)]]; + 67-1||[[:File:ROC2006-05-05道路交通標誌標線號誌設置規則修正草案.pdf|2006-05-05 draft]]
|-
|[[:File:ROC2006-12-13道路交通標誌標線號誌設置規則.pdf|15]]||[[:File:ROC2006-12-13道路交通標誌標線號誌設置規則修正條文.pdf|2006-12-13]]||±96 ±99 ±105 ±108 ±109||[[:File:ROC2005-06-21道路交通標誌標線號誌設置規則修正草案.pdf|2005-06-21 draft]]
|-
|[[:File:ROC2008-01-01道路交通標誌標線號誌設置規則.pdf|16]]||[[:File:ROC2007-09-17道路交通標誌標線號誌設置規則修正條文.pdf|2007-09-17]] (effective 2007-11-01)||±18 ±43&lt;ref name=&quot;images unchanged&quot; /&gt; ±65&lt;ref name=&quot;new images&quot; /&gt;&lt;ref name=&quot;images unchanged&quot; /&gt; ±68&lt;ref name=&quot;new images&quot; /&gt; ±69&lt;ref name=&quot;new images&quot; /&gt; ±73 ±74 ±87 '''±87-1''' ±89 ±90&lt;ref name=&quot;new images&quot; /&gt; ±95 ±97 ±103 '''±104''' ±118 ±118-4 ±118-5 ±128 ±139 ±140 ±141 ±142 ±145 ±174-1 ±174-2 ±175 '''±178''' ±183 ±183-1 ±185 ±187 ±190 ±191 ±194 '''±198''' ±202 ±203 ±204 ±208 ±212 ±214 ±228 ±230 ±231 ±235; + 70-1 + 84-1 + 90-1 + 105-1 + 185-1 + 189-1; &lt;i&gt;-91 -92 -118-2 -143&lt;/i&gt; (2007-11-02 [[:File:ROC2007-09-17道路交通標誌標線號誌設置規則勘誤表.pdf|Errata]] ±87-1 ±104 ±178 ±198) Motorcycles with engine displacements of at least 550&amp;nbsp;cm&lt;sup&gt;3&lt;/sup&gt; would normally be driven like cars.||[[:File:ROC2005-06-21道路交通標誌標線號誌設置規則修正草案.pdf|2005-06-21]] and [[:File:ROC2007-06-07道路交通標誌標線號誌設置規則修正草案.pdf|2007-06-07 draft]]s
|-
|17||[[:File:ROC2008-04-14道路交通標誌標線號誌設置規則修正條文.pdf|2008-04-14]] (effective 2008-04-15)||±46&lt;ref name=&quot;images unchanged&quot; /&gt; ±67-1 ±68 ±69 ±73 ±154 ±164 ±174 ±175 ±180 ±185 ±235; + 186-1 The Chinese name of a bicycle would be literally changed from &quot;feet-pedaled cycle&quot; (腳踏車) to &quot;self-moving cycle&quot; (自行車) to accommodate electric-assisted bicycles.||[[:File:ROC2008-01-28道路交通標誌標線號誌設置規則修正草案.pdf|2008-01-28 draft]]
|-
|[[:File:ROC2008-06-18道路交通標誌標線號誌設置規則.pdf|18]]||[[:File:ROC2008-06-18道路交通標誌標線號誌設置規則修正條文.pdf|2008-06-18]]||±203 ±212 ±214 ±220 ±226||[[:File:ROC2008-04-02道路交通標誌標線號誌設置規則修正草案.pdf|2008-04-08 draft]]
|-
|[[:File:ROC2009-12-08道路交通標誌標線號誌設置規則.pdf|19]]||[[:File:ROC2009-12-08道路交通標誌標線號誌設置規則修正條文.pdf|2009-12-08]]||±46 ±108 ±118-5||[[:File:ROC2009-06-24道路交通標誌標線號誌設置規則修正草案.pdf|2009-06-24 draft]]
|-
|[[s:zh:道路交通標誌標線號誌設置規則 (民國100年)|20]]||[[:File:ROC2011-05-11道路交通標誌標線號誌設置規則修正條文.pdf|2011-05-11]]||+ 122-1 liquefied petroleum gas station||[[:File:ROC2011-03-09道路交通標誌標線號誌設置規則修正草案.pdf|2011-03-09 draft]]
|-
|21||[[:File:ROC2012-06-20道路交通標誌標線號誌設置規則修正條文.pdf|2012-06-20]]||±69&lt;ref name=&quot;new images&quot; /&gt; ±95&lt;ref name=&quot;texts unchanged&quot; /&gt; ±96 ±97 ±99 ±103 ±105 ±105-2 ±174 ±175||[[:File:ROC2011-12-22道路交通標誌標線號誌設置規則修正草案.pdf|2011-12-22 draft]]
|-
|22||[[:File:ROC2012-06-29道路交通標誌標線號誌設置規則修正條文.pdf|2012-06-29]]||±65&lt;ref name=&quot;images unchanged&quot; /&gt; ±68&lt;ref name=&quot;new images&quot; /&gt; ±69&lt;ref name=&quot;new images&quot; /&gt; ±73 ±74 ±174-1 ±174-2 ±175 ±178 ±190 ±191 Motorcycles &gt; 250&amp;nbsp;cm&lt;sup&gt;3&lt;/sup&gt; or 40 hp would normally be driven like cars.||[[:File:ROC2012-04-18道路交通標誌標線號誌設置規則修正草案.pdf|2012-04-18 draft]]
|-
|[[:File:ROC2012-10-13道路交通標誌標線號誌設置規則.pdf|23]]||[[:File:ROC2012-10-13道路交通標誌標線號誌設置規則修正條文.pdf|2012-10-13]]&lt;ref name=&quot;images unchanged&quot; /&gt;||±1 ±65 ±68 ±69 ±73 ±74 ±174-1 ±174-2 ±175 ±178 ±190 ±191 ±226 The Chinese name of a motorcycle would be literally changed from &quot;motor feet-pedaled cycle&quot; (機器腳踏車) to &quot;motor cycle&quot; (機車).||[[:File:ROC2012-09-06道路交通標誌標線號誌設置規則修正草案.pdf|2012-09-06 draft]]
|-
|24||[[:File:ROC2013-02-07道路交通標誌標線號誌設置規則修正條文.pdf|2013-02-07]]||±28&lt;ref name=&quot;images unchanged&quot; /&gt; ±138&lt;ref name=&quot;images unchanged&quot; /&gt;; + 122-2 + 188-1||[[:File:ROC2012-10-09道路交通標誌標線號誌設置規則修正草案.pdf|2012-10-09 draft]]
|-
|25||[[:File:ROC2013-08-01道路交通標誌標線號誌設置規則修正條文.pdf|2013-08-01]]||±9&lt;ref name=&quot;new images&quot; /&gt; ±[[:File:ROC2013-08-01道路交通標誌標線號誌設置規則勘誤表.pdf|174 (errata)]]&lt;ref name=&quot;images unchanged&quot; /&gt;; + 174-3||[[:File:ROC2013-02-07道路交通標誌標線號誌設置規則修正草案.pdf|2013-02-07 draft]]
|-
|26||[[:File:ROC2014-09-04道路交通標誌標線號誌設置規則修正條文.pdf|2014-09-04]]||±42&lt;ref name=&quot;images unchanged&quot; /&gt; ±69&lt;ref name=&quot;new images&quot; /&gt; ±194 ±200 ±201 ±220; + 55-1||[[:File:ROC2014-06-12道路交通標誌標線號誌設置規則修正草案.pdf|2014-06-12 draft]]
|-
|27||[[:File:ROC2015-05-14道路交通標誌標線號誌設置規則修正條文.pdf|2015-05-14]]||±4 ±149 ±180 ±226 ±229 ±231; + 189-2&lt;ref name=&quot;new images&quot; /&gt;||[[:File:ROC2015-05-14道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2014-11-25道路交通標誌標線號誌設置規則修正草案.pdf|2014-11-25 draft]]
|-
|28||[[:File:ROC2017-06-14道路交通標誌標線號誌設置規則修正條文.pdf|2017-06-14]] (Article 55-2 effective 2018-01-01)||±9&lt;ref name=&quot;images unchanged&quot; /&gt; ±11 ±12 ±15 ±24&lt;ref name=&quot;images unchanged&quot; /&gt; ±93&lt;ref name=&quot;images unchanged&quot; /&gt; ±162 ±164 ±170&lt;ref name=&quot;images unchanged&quot; /&gt; ±174-2 ±180 ±183-1 ±192 ±235; + 55-2&lt;ref name=&quot;new images&quot; /&gt; + 87-3&lt;ref name=&quot;new images&quot; /&gt; + 90-2&lt;ref name=&quot;new images&quot; /&gt; + 132-1&lt;ref name=&quot;new images&quot; /&gt; + 188-2&lt;ref name=&quot;new images&quot; /&gt;||[[:File:ROC2017-06-14道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2016-02-25道路交通標誌標線號誌設置規則修正草案.pdf|2016-02-25]] and [[:File:ROC2016-09-13道路交通標誌標線號誌設置規則修正草案.pdf|2016-09-13 draft]]s
|-
|29||[[:File:ROC2021-01-29道路交通標誌標線號誌設置規則修正條文.pdf|2021-01-29]]||'''±58'''&lt;ref name=&quot;images unchanged&quot; /&gt; ±59&lt;ref name=&quot;images unchanged&quot; /&gt; '''±172'''&lt;ref name=&quot;images unchanged&quot; /&gt; ±174-2 ±180 ±185 ±188 '''±188-2'''&lt;ref name=&quot;new images&quot; /&gt; ±189&lt;ref name=&quot;new images&quot; /&gt; ±211 ±217 '''±224 ±226 ±229 ±231''' (2021-02-23 [[:File:ROC2021-01-29道路交通標誌標線號誌設置規則勘誤表.pdf|Errata]] ±87-1 ±104 ±178 ±198)||[[:File:ROC2021-01-29道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2020-06-17道路交通標誌標線號誌設置規則修正草案.pdf|2020-06-17 dradt]]
|-
|30||[[:File:ROC2022-08-19道路交通標誌標線號誌設置規則修正條文.pdf|2022-08-19]] (Article 55-2 effective 2022-04-30)||±55-2&lt;ref name=&quot;images unchanged&quot; /&gt; ±96&lt;ref name=&quot;new images&quot; /&gt; ±235||[[:File:ROC2022-08-19道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2022-04-12道路交通標誌標線號誌設置規則修正草案.pdf|2022-04-12 draft]]
|-
|[[:File:ROC2023-02-23道路交通標誌標線號誌設置規則.pdf|31]]||[[:File:ROC2023-02-23道路交通標誌標線號誌設置規則修正條文.pdf|2023-02-23]] (Articles 122-1 and 122-2 effective 2023-07-01; Article 183-1 effective 2023-12-31)||±65&lt;ref name=&quot;images unchanged&quot; /&gt; ±122-1&lt;ref name=&quot;texts unchanged&quot; /&gt; ±122-2&lt;ref name=&quot;new images&quot; /&gt; ±183-1&lt;ref name=&quot;images unchanged&quot; /&gt; ±226 ±235; + 122-3||[[:File:ROC2023-02-23道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2022-04-12道路交通標誌標線號誌設置規則修正草案.pdf|2022-04-12 draft]]
|-
|32||[[:File:ROC2024-07-22道路交通標誌標線號誌設置規則修正條文.pdf|2024-07-22]]||±9 ±11 ±73 ±75&lt;ref name=&quot;images unchanged&quot; /&gt; ±78&lt;ref name=&quot;images unchanged&quot; /&gt; ±90 ±110 ±111&lt;ref name=&quot;images unchanged&quot; /&gt; ±154 ±159 ±160&lt;ref name=&quot;images unchanged&quot; /&gt; ±164 ±168&lt;ref name=&quot;new images&quot; /&gt; ±170 ±174-3&lt;ref name=&quot;new images&quot; /&gt; ±180 ±185&lt;ref name=&quot;images unchanged&quot; /&gt; ±186 ±191&lt;ref name=&quot;new images&quot; /&gt; ±194 ±231; + 137-1&lt;ref name=&quot;new images&quot; /&gt; + 159-1&lt;ref name=&quot;new images&quot; /&gt; + 163-1&lt;ref name=&quot;new images&quot; /&gt; + 174-4&lt;ref name=&quot;new images&quot; /&gt;||[[:File:ROC2024-07-22道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2023-12-13道路交通標誌標線號誌設置規則修正草案.pdf|2023-12-13 draft]]
|-
|33||[[:File:ROC2024-10-22道路交通標誌標線號誌設置規則修正條文.pdf|2024-10-22]] (Articles 12 and 67-2 effective 2024-10-01)||±12 ±173 ±235; +67-2&lt;ref name=&quot;new images&quot; /&gt;||[[:File:ROC2024-10-22道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2024-09-16道路交通標誌標線號誌設置規則修正草案.pdf|2024-09-16 draft]]
|-
|34||[[:File:ROC2025-06-30道路交通標誌標線號誌設置規則修正條文.pdf|2025-06-30]]||±170&lt;ref name=&quot;new images&quot; /&gt;||[[:File:ROC2025-06-30道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2025-03-25道路交通標誌標線號誌設置規則修正草案.pdf|2025-03-25 draft]]
|-
|35||[[:File:ROC2026-03-11道路交通標誌標線號誌設置規則修正條文.pdf|2026-03-11]]||±207||[[:File:ROC2026-03-11道路交通標誌標線號誌設置規則總說明與對照表.pdf|Summary and comparison]]; [[:File:ROC2026-01-28道路交通標誌標線號誌設置規則修正草案.pdf|2026-01-28 draft]]
|}

{{BookCat}}</text>
      <sha1>csnu66ed6pegscd0yuxdy8n3q3ggwz1</sha1>
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  </page>
  <page>
    <title>Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nc3/4...e6</title>
    <ns>0</ns>
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        <username>Greenman</username>
        <id>7490</id>
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      <text bytes="649" sha1="jctvbvzfpa8j4ax3ozbqc5i9sonfdyo" xml:space="preserve">{{Chess Opening Theory/Position|=
|Van der Wiel Attack|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |  |pd|pd|pd|=
   |  |  |pd|  |pd|  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
}}
1. e4 c6 2. d4 d5 3. e5 Bf5 4. Nc3 e6
Is one of the most followed continuations of the Caro–Kann Defence: Advanced Variation.
The best followup is 5. g4, questioning Black's bishop on the f5-square.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=5. g4
|eval1=
}}

{{Wikipedia|Caro–Kann Defence}}
{{ChessMid}}
{{ChessFooter}}</text>
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    </revision>
    <revision>
      <id>4654696</id>
      <parentid>4654691</parentid>
      <timestamp>2026-07-16T15:28:34Z</timestamp>
      <contributor>
        <username>Greenman</username>
        <id>7490</id>
      </contributor>
      <comment>MOS</comment>
      <origin>4654696</origin>
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      <format>text/x-wiki</format>
      <text bytes="690" sha1="q4x3m3anm0iwla5w4sp5bec38jghr5s" xml:space="preserve">{{Chess Opening Theory/Position|=
|Van der Wiel Attack|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |  |pd|pd|pd|=
   |  |  |pd|  |pd|  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
}}

=5. Nc3 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=
5. Nc3 is one of the most followed continuations of the Caro–Kann Defence: Advanced Variation.
The best followup is 5. g4, questioning Black's bishop on the f5-square.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=5. g4
|eval1=
}}

{{Wikipedia|Caro–Kann Defence}}
{{ChessMid}}
{{ChessFooter}}</text>
      <sha1>q4x3m3anm0iwla5w4sp5bec38jghr5s</sha1>
    </revision>
    <revision>
      <id>4654697</id>
      <parentid>4654696</parentid>
      <timestamp>2026-07-16T15:29:18Z</timestamp>
      <contributor>
        <username>Greenman</username>
        <id>7490</id>
      </contributor>
      <comment>/* 5. Nc3 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack */ fix header</comment>
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      <text bytes="689" sha1="c8pghqkyhpzc57ocjuvou0lfxphk7xo" xml:space="preserve">{{Chess Opening Theory/Position|=
|Van der Wiel Attack|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |  |pd|pd|pd|=
   |  |  |pd|  |pd|  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
}}

=4... e6 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=
This is one of the most followed continuations of the Caro–Kann Defence: Advanced Variation.
The best followup is 5. g4, questioning Black's bishop on the f5-square.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=5. g4
|eval1=
}}

{{Wikipedia|Caro–Kann Defence}}
{{ChessMid}}
{{ChessFooter}}</text>
      <sha1>c8pghqkyhpzc57ocjuvou0lfxphk7xo</sha1>
    </revision>
  </page>
  <page>
    <title>Hokkien/Pronunciation</title>
    <ns>0</ns>
    <id>376218</id>
    <revision>
      <id>4654763</id>
      <parentid>4645129</parentid>
      <timestamp>2026-07-17T03:36:47Z</timestamp>
      <contributor>
        <username>一隻北極熊</username>
        <id>3609960</id>
      </contributor>
      <comment>/* Tones */</comment>
      <origin>4654763</origin>
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      <format>text/x-wiki</format>
      <text bytes="7624" sha1="5lvt05m4xy4wqakubwlvv8bxmsn7xyw" xml:space="preserve">== Hokkien sounds ==
=== Syllables ===
There are far fewer syllables in the Hokkien language than English.  The syllables are also easily described with the concepts of ''initials'' and ''finals''.  A syllable begins with a single consonant.  This is called the ''initial''.  The rest of the syllable is called the ''final.'' A final can have a single vowel or a diphthong (two vowels that glide from one to the other) and an optional final consonant (''p'', ''t'', ''k'', ''h'', ''m'', ''n'', or ''ng''). Additionally, finals in Hokkien can 
be nasalized.

The pronunciation guide below is based on American English except where otherwise noted.  Not all sounds can be described with English words and some are just approximations at best.  Be sure to listen to actual speakers to ensure that your pronunciation is correct. 


=== Initials ===
{|border=&quot;0&quot; cellspacing=&quot;3&quot; cellpadding=&quot;2&quot; style=&quot;text-align: center&quot;
|-
|'''Tai5-lo5'''
|'''Pronunciation'''
|'''IPA'''
|-
|b
|'''b''' in &quot;'''b'''all&quot;
|b
|-
|p
|'''p''' as in &quot;s'''p'''at&quot;
|p
|-
|ph
|'''p''' as in &quot;'''p'''at&quot;
|pʰ
|-
|m
|'''m''' as in &quot;'''m'''om&quot;
|m
|-
|t
|'''t''' in &quot;s'''t'''op&quot;
|t
|-
|th
|'''t''' as in &quot;'''t'''op&quot;
|tʰ
|-
|n
|'''n''' as in &quot;'''n'''ot&quot;
|n
|-
|l
|'''l''' as in &quot;'''l'''ap&quot;
|l
|-
|g
|'''g''' in &quot;'''g'''ood&quot;
|g
|-
|k
|'''k''' as in &quot;s'''k'''it&quot;
|k
|-
|kh
|'''k''' as in &quot;'''k'''ite&quot;
|kʰ
|-
|ng
|'''ng''' as in &quot;si'''ng'''er&quot;
|ŋ
|-
|h
|'''h''' as in &quot;'''h'''ot&quot;
|h
|-
|j
|Blend of the '''ds''' in &quot;be'''ds'''&quot; and the '''j''' in &quot;'''j'''am&quot;
|dz
|-
|ts
|'''ts''' in &quot;ca'''ts'''&quot; 
|ts
|-
|tsh
|Blend of the '''ts''' in &quot;ca'''ts'''&quot; and the '''ch''' in &quot;'''ch'''urch&quot;
|tsʰ
|-
|s
|'''s''' as in &quot;'''s'''un&quot;
|s
|-
|}


==== Tips on initials ====

* The consonant ''j'' has merged with ''l'' in many speakers, especially in Chuan-chiu, since the early 20th century. It is still frequently written out in the romanization scheme though.

* The triplets ''g'', ''k'', ''kh'' and ''b'', ''p'', ''ph'', as well as ''j'', ''ch'', ''chh'' (voiced unaspirated, unvoiced unaspirated, unvoiced aspirated) are rare among languages and need some practice to correctly distiguish.

* When followed by ''i'', i.e. ''ji'', ''chi'', ''chhi, si'', the consonants ''j'', ''ch'', ''chh'', ''s'', take on the IPA values: [dʑ], [tɕ], [tɕʰ], [ɕ]. No true equivalents in English exist, but [tɕ], [tɕʰ] correspond to Mandarin ''j'', ''q''.

* ''b'' and ''g'' are slightly nasalized, reflecting their development from Old/Middle Chinese ''m'' and ''ng''

=== Finals ===
{|border=&quot;0&quot; cellspacing=&quot;3&quot; cellpadding=&quot;2&quot; style=&quot;text-align: center&quot;
|-
|'''Tai-lo''' 
|'''Pronunciation'''
|'''IPA'''
|-
|a
|'''a''' as in &quot;sp'''a'''&quot;
|a
|-
|ap
|'''op''' as in &quot;t'''op'''&quot;
|ap
|-
|at
|'''ot''' as in &quot;p'''ot'''&quot;
|at̚
|-
|ak
|'''ock''' as in &quot;s'''ock'''&quot;
|ak̚
|-
|ah
|First '''a''' as in &quot;'''aha'''&quot;
|aʔ
|-
|ann
|'''a''' as in &quot;sp'''a'''&quot;
|ã
|-
|am
|'''am''' as in &quot;Vietn'''am'''&quot;
|am
|-
|an
|'''on''' as in &quot;c'''on'''&quot;
|an
|-
|ang
|'''ong''' as in &quot;t'''ong'''s&quot;
|aŋ
|-
|ai
|'''igh''' as in &quot;s'''igh'''&quot;
|ai
|-
|e
|'''e''' as in &quot;b'''e'''t&quot;
|-
|ei
|'''ay''' as in &quot;s'''ay'''&quot;
|-
|em
|'''em''' as in &quot;t'''em'''ple&quot;
|-
|eng
|'''ang''' as in &quot;'''ang'''ry&quot;
|-
|ek
|'''eck''' as in &quot;p'''eck'''&quot;
|-
|i
|'''ee''' as in &quot;t'''ee'''&quot;
|-
|iu
|'''ew''' as in &quot;f'''ew'''&quot;
|-
|im
|'''eem''' as in &quot;s'''eem'''&quot;
|-
|in
|'''een''' as in &quot;s'''een'''&quot;
|-
|ing
|'''ing''' as in &quot;s'''ing'''&quot;
|-
|ip
|'''eep''' as in &quot;sl'''eep'''&quot;
|-
|it
|'''eet''' as in &quot;m'''eet'''&quot;
|-
|ik
|'''ick''' as in &quot;s'''ick'''&quot;
|-
|o
|'''or''' as in &quot;'''or'''&quot; (British English)
|-
|oi
|'''oy''' as in &quot;b'''oy'''&quot;
|-
|ou
|'''o''' as in &quot;n'''o'''&quot;
|-
|on
|'''on''' as in &quot;c'''on'''&quot; (British English)
|-
|ong
|'''ong''' as in &quot;s'''ong'''&quot;
|-
|ot
|'''ot''' as in &quot;h'''ot'''&quot; (British English)
|-
|ok
|'''ock''' as in &quot;s'''ock'''
|-
|u
|'''oo''' as in &quot;t'''oo'''&quot;
|-
|ui
|'''ooey''' as in &quot;g'''ooey'''&quot;
|-
|un
|'''oon''' as in &quot;s'''oon'''&quot;
|-
|ung
|combination of '''ou''' and '''ng'''
|-
|ut
|'''oot''' as in &quot;b'''oot'''&quot;
|-
|uk
|'''ook''' as in &quot;t'''ook'''&quot;
|-
|eu
|'''er''' as in &quot;h'''er'''&quot; (British English, with rounded lips)
|-
|eung
|combination of '''eu''' and '''ng'''
|-
|euk
|'''ork''' as in &quot;w'''ork'''&quot; (British English)
|-
|eui
|'''eui''' as in &quot;d'''eui'''l&quot; (French)
|-
|eun
|'''ine''' as in &quot;eng'''ine'''&quot;
|-
|eut
|'''ut''' as in &quot;p'''ut'''&quot;
|-
|yu
|'''u''' as in &quot;t'''u'''&quot; (French)
|-
|yun
|'''un''' as in &quot;'''union'''&quot;
|-
|yut
|'''Ut''' as in &quot;'''Ut'''ah&quot;
|-
|m
|'''mm''' as in &quot;h'''mm'''&quot;
|-
|ng
|'''ng''' as in &quot;si'''ng'''&quot;
|}

==== Tips on finals ====
* The final consonants ''p'', ''t'', and ''k'' are '''unreleased'''.  This means that they are virtually silent and you hear no &quot;puff of air&quot; at the end of the syllable.  To give a concrete example, say the word &quot;cup&quot; and do not open your lips at the end of the word.  Note how there is no &quot;puff of air&quot; at the end. The ''k'' sound will also shift from being what is termed a '''velar stop''' to a '''glottal stop''' when it is used to add liveliness to final modal particles. The final consonant ''k'' will sometimes disappear in rapid speech as in the expression ''m4 sai2 haa[k]3 hei3''.
* The ''aa'' sounds are a low back vowel which is slightly longer in length and different in quality from the ''a'' sounds.  Be sure to note the difference in these sounds since confusing the two will change the meaning of words.
* The vowel quality in ''ing'', ''it'', and ''ik'' is not the same as in ''in'',''im'', or ''i''.  It's the same difference between the English words &quot;sin&quot; and &quot;seen&quot; (or in grammar school terms a &quot;short&quot; vowel versus a &quot;long&quot; vowel).   While this difference is not as important as the one above since it does not contrast word meanings, you will have a much more obvious &quot;foreign accent&quot; if you do not master these two sounds.
* The ''yu'' sound does not exist in English but it is not hard to produce.  Start by saying a long ''i'' as in &quot;see&quot; and--without changing anything else!--round your lips.  It's a common sound in French so &quot;think French&quot; if you have to.
* The ''eu'' sound does not exist in English either but like the ''yu'' it's just a case of rounding the lips.  Start by saying the ''e'' sound in &quot;bet&quot; and--without changing anything else!--round your lips.
* The ''eui'' sound is simply a fusion of ''eu'' and ''i'' (&quot;eu-ee&quot;) into a single syllable.
* The ''o'' sound does not exist in '''American''' English, but it is in British English.  It is the back rounded vowel that you hear when British people say &quot;more&quot; or &quot;scorn&quot;.  If you listen carefully to a British speaker, you'll notice they do not pronounce the &quot;r&quot; in these words.  It is the quality of the &quot;o&quot; vowel that makes them unique to American speakers' ears.
* The final ''eung'' has a faint, British ''r'' sound riding on the vowel, so the number two would be pronounced somewhat like &quot;leurng&quot;.  Be careful -- pronouncing this sound with an American ''r'' is a common mistake that sounds extremely foreign.
* Only the finals ''m'' and ''ng'' can be used as standalone [[w:nasal consonant|nasal]] syllables.
* Vowels preceding nasal final consonants are not nasalized, yet vowels following nasal consonants are.  You can hold your nose while pronouncing some syllables such as ''sin1'' or ''ngo5'' to test your pronunciation.  It's not critical to get this right, but doing so will reduce any apparent foreign accent.
==Tones==
There are once 8 tones in the Hokkien language, however the 6th tone has now assimilated to the 2nd tone, making it only 7.
[[file:Taiwanese tones.png|thumb|Taiwanese tones]]
===Tone sandhi===
{{stub}}
{{BookCat}}</text>
      <sha1>5lvt05m4xy4wqakubwlvv8bxmsn7xyw</sha1>
    </revision>
    <revision>
      <id>4654769</id>
      <parentid>4654763</parentid>
      <timestamp>2026-07-17T04:13:01Z</timestamp>
      <contributor>
        <username>一隻北極熊</username>
        <id>3609960</id>
      </contributor>
      <comment>added a picture of Hokkien Tone Sandhi</comment>
      <origin>4654769</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="7674" sha1="598vqnpkf6jq9qoavtjw0mrd0ln5rqq" xml:space="preserve">== Hokkien sounds ==
=== Syllables ===
There are far fewer syllables in the Hokkien language than English.  The syllables are also easily described with the concepts of ''initials'' and ''finals''.  A syllable begins with a single consonant.  This is called the ''initial''.  The rest of the syllable is called the ''final.'' A final can have a single vowel or a diphthong (two vowels that glide from one to the other) and an optional final consonant (''p'', ''t'', ''k'', ''h'', ''m'', ''n'', or ''ng''). Additionally, finals in Hokkien can 
be nasalized.

The pronunciation guide below is based on American English except where otherwise noted.  Not all sounds can be described with English words and some are just approximations at best.  Be sure to listen to actual speakers to ensure that your pronunciation is correct. 


=== Initials ===
{|border=&quot;0&quot; cellspacing=&quot;3&quot; cellpadding=&quot;2&quot; style=&quot;text-align: center&quot;
|-
|'''Tai5-lo5'''
|'''Pronunciation'''
|'''IPA'''
|-
|b
|'''b''' in &quot;'''b'''all&quot;
|b
|-
|p
|'''p''' as in &quot;s'''p'''at&quot;
|p
|-
|ph
|'''p''' as in &quot;'''p'''at&quot;
|pʰ
|-
|m
|'''m''' as in &quot;'''m'''om&quot;
|m
|-
|t
|'''t''' in &quot;s'''t'''op&quot;
|t
|-
|th
|'''t''' as in &quot;'''t'''op&quot;
|tʰ
|-
|n
|'''n''' as in &quot;'''n'''ot&quot;
|n
|-
|l
|'''l''' as in &quot;'''l'''ap&quot;
|l
|-
|g
|'''g''' in &quot;'''g'''ood&quot;
|g
|-
|k
|'''k''' as in &quot;s'''k'''it&quot;
|k
|-
|kh
|'''k''' as in &quot;'''k'''ite&quot;
|kʰ
|-
|ng
|'''ng''' as in &quot;si'''ng'''er&quot;
|ŋ
|-
|h
|'''h''' as in &quot;'''h'''ot&quot;
|h
|-
|j
|Blend of the '''ds''' in &quot;be'''ds'''&quot; and the '''j''' in &quot;'''j'''am&quot;
|dz
|-
|ts
|'''ts''' in &quot;ca'''ts'''&quot; 
|ts
|-
|tsh
|Blend of the '''ts''' in &quot;ca'''ts'''&quot; and the '''ch''' in &quot;'''ch'''urch&quot;
|tsʰ
|-
|s
|'''s''' as in &quot;'''s'''un&quot;
|s
|-
|}


==== Tips on initials ====

* The consonant ''j'' has merged with ''l'' in many speakers, especially in Chuan-chiu, since the early 20th century. It is still frequently written out in the romanization scheme though.

* The triplets ''g'', ''k'', ''kh'' and ''b'', ''p'', ''ph'', as well as ''j'', ''ch'', ''chh'' (voiced unaspirated, unvoiced unaspirated, unvoiced aspirated) are rare among languages and need some practice to correctly distiguish.

* When followed by ''i'', i.e. ''ji'', ''chi'', ''chhi, si'', the consonants ''j'', ''ch'', ''chh'', ''s'', take on the IPA values: [dʑ], [tɕ], [tɕʰ], [ɕ]. No true equivalents in English exist, but [tɕ], [tɕʰ] correspond to Mandarin ''j'', ''q''.

* ''b'' and ''g'' are slightly nasalized, reflecting their development from Old/Middle Chinese ''m'' and ''ng''

=== Finals ===
{|border=&quot;0&quot; cellspacing=&quot;3&quot; cellpadding=&quot;2&quot; style=&quot;text-align: center&quot;
|-
|'''Tai-lo''' 
|'''Pronunciation'''
|'''IPA'''
|-
|a
|'''a''' as in &quot;sp'''a'''&quot;
|a
|-
|ap
|'''op''' as in &quot;t'''op'''&quot;
|ap
|-
|at
|'''ot''' as in &quot;p'''ot'''&quot;
|at̚
|-
|ak
|'''ock''' as in &quot;s'''ock'''&quot;
|ak̚
|-
|ah
|First '''a''' as in &quot;'''aha'''&quot;
|aʔ
|-
|ann
|'''a''' as in &quot;sp'''a'''&quot;
|ã
|-
|am
|'''am''' as in &quot;Vietn'''am'''&quot;
|am
|-
|an
|'''on''' as in &quot;c'''on'''&quot;
|an
|-
|ang
|'''ong''' as in &quot;t'''ong'''s&quot;
|aŋ
|-
|ai
|'''igh''' as in &quot;s'''igh'''&quot;
|ai
|-
|e
|'''e''' as in &quot;b'''e'''t&quot;
|-
|ei
|'''ay''' as in &quot;s'''ay'''&quot;
|-
|em
|'''em''' as in &quot;t'''em'''ple&quot;
|-
|eng
|'''ang''' as in &quot;'''ang'''ry&quot;
|-
|ek
|'''eck''' as in &quot;p'''eck'''&quot;
|-
|i
|'''ee''' as in &quot;t'''ee'''&quot;
|-
|iu
|'''ew''' as in &quot;f'''ew'''&quot;
|-
|im
|'''eem''' as in &quot;s'''eem'''&quot;
|-
|in
|'''een''' as in &quot;s'''een'''&quot;
|-
|ing
|'''ing''' as in &quot;s'''ing'''&quot;
|-
|ip
|'''eep''' as in &quot;sl'''eep'''&quot;
|-
|it
|'''eet''' as in &quot;m'''eet'''&quot;
|-
|ik
|'''ick''' as in &quot;s'''ick'''&quot;
|-
|o
|'''or''' as in &quot;'''or'''&quot; (British English)
|-
|oi
|'''oy''' as in &quot;b'''oy'''&quot;
|-
|ou
|'''o''' as in &quot;n'''o'''&quot;
|-
|on
|'''on''' as in &quot;c'''on'''&quot; (British English)
|-
|ong
|'''ong''' as in &quot;s'''ong'''&quot;
|-
|ot
|'''ot''' as in &quot;h'''ot'''&quot; (British English)
|-
|ok
|'''ock''' as in &quot;s'''ock'''
|-
|u
|'''oo''' as in &quot;t'''oo'''&quot;
|-
|ui
|'''ooey''' as in &quot;g'''ooey'''&quot;
|-
|un
|'''oon''' as in &quot;s'''oon'''&quot;
|-
|ung
|combination of '''ou''' and '''ng'''
|-
|ut
|'''oot''' as in &quot;b'''oot'''&quot;
|-
|uk
|'''ook''' as in &quot;t'''ook'''&quot;
|-
|eu
|'''er''' as in &quot;h'''er'''&quot; (British English, with rounded lips)
|-
|eung
|combination of '''eu''' and '''ng'''
|-
|euk
|'''ork''' as in &quot;w'''ork'''&quot; (British English)
|-
|eui
|'''eui''' as in &quot;d'''eui'''l&quot; (French)
|-
|eun
|'''ine''' as in &quot;eng'''ine'''&quot;
|-
|eut
|'''ut''' as in &quot;p'''ut'''&quot;
|-
|yu
|'''u''' as in &quot;t'''u'''&quot; (French)
|-
|yun
|'''un''' as in &quot;'''union'''&quot;
|-
|yut
|'''Ut''' as in &quot;'''Ut'''ah&quot;
|-
|m
|'''mm''' as in &quot;h'''mm'''&quot;
|-
|ng
|'''ng''' as in &quot;si'''ng'''&quot;
|}

==== Tips on finals ====
* The final consonants ''p'', ''t'', and ''k'' are '''unreleased'''.  This means that they are virtually silent and you hear no &quot;puff of air&quot; at the end of the syllable.  To give a concrete example, say the word &quot;cup&quot; and do not open your lips at the end of the word.  Note how there is no &quot;puff of air&quot; at the end. The ''k'' sound will also shift from being what is termed a '''velar stop''' to a '''glottal stop''' when it is used to add liveliness to final modal particles. The final consonant ''k'' will sometimes disappear in rapid speech as in the expression ''m4 sai2 haa[k]3 hei3''.
* The ''aa'' sounds are a low back vowel which is slightly longer in length and different in quality from the ''a'' sounds.  Be sure to note the difference in these sounds since confusing the two will change the meaning of words.
* The vowel quality in ''ing'', ''it'', and ''ik'' is not the same as in ''in'',''im'', or ''i''.  It's the same difference between the English words &quot;sin&quot; and &quot;seen&quot; (or in grammar school terms a &quot;short&quot; vowel versus a &quot;long&quot; vowel).   While this difference is not as important as the one above since it does not contrast word meanings, you will have a much more obvious &quot;foreign accent&quot; if you do not master these two sounds.
* The ''yu'' sound does not exist in English but it is not hard to produce.  Start by saying a long ''i'' as in &quot;see&quot; and--without changing anything else!--round your lips.  It's a common sound in French so &quot;think French&quot; if you have to.
* The ''eu'' sound does not exist in English either but like the ''yu'' it's just a case of rounding the lips.  Start by saying the ''e'' sound in &quot;bet&quot; and--without changing anything else!--round your lips.
* The ''eui'' sound is simply a fusion of ''eu'' and ''i'' (&quot;eu-ee&quot;) into a single syllable.
* The ''o'' sound does not exist in '''American''' English, but it is in British English.  It is the back rounded vowel that you hear when British people say &quot;more&quot; or &quot;scorn&quot;.  If you listen carefully to a British speaker, you'll notice they do not pronounce the &quot;r&quot; in these words.  It is the quality of the &quot;o&quot; vowel that makes them unique to American speakers' ears.
* The final ''eung'' has a faint, British ''r'' sound riding on the vowel, so the number two would be pronounced somewhat like &quot;leurng&quot;.  Be careful -- pronouncing this sound with an American ''r'' is a common mistake that sounds extremely foreign.
* Only the finals ''m'' and ''ng'' can be used as standalone [[w:nasal consonant|nasal]] syllables.
* Vowels preceding nasal final consonants are not nasalized, yet vowels following nasal consonants are.  You can hold your nose while pronouncing some syllables such as ''sin1'' or ''ngo5'' to test your pronunciation.  It's not critical to get this right, but doing so will reduce any apparent foreign accent.
==Tones==
There are once 8 tones in the Hokkien language, however the 6th tone has now assimilated to the 2nd tone, making it only 7.
[[file:Taiwanese tones.png|thumb|Taiwanese tones]]
===Tone sandhi===
[[File:Amoy tones.JPG|thumb|Hokkien Tone Sandhi]]
{{stub}}
{{BookCat}}</text>
      <sha1>598vqnpkf6jq9qoavtjw0mrd0ln5rqq</sha1>
    </revision>
  </page>
  <page>
    <title>Wikibooks:Edit filter/False positives</title>
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    <id>396216</id>
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      <id>4654710</id>
      <parentid>4654615</parentid>
      <timestamp>2026-07-16T16:23:44Z</timestamp>
      <contributor>
        <username>LoveElectronicLiterature</username>
        <id>3414389</id>
      </contributor>
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      <origin>4654710</origin>
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      <text bytes="10134" sha1="5k31ya7j7so8jj4340kxzsdumlcryg2" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
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== SHE-LOVES-BRIAN ==

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: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

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== ~2026-35089-83 ==

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: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

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}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SeaDragon1}} filter log]&lt;/span&gt;)
;Page you were editing
: [[User:SeaDragon1/UTM highlighting test]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test&amp;wpSearchUser=SeaDragon1}} user filter log])&lt;/span&gt;
;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== Earthinators page rewrite ==

I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me. [[User:Earthinators|Earthinators]] ([[User talk:Earthinators|discuss]] • [[Special:Contributions/Earthinators|contribs]]) 06:56, 11 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:26, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:27, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>5k31ya7j7so8jj4340kxzsdumlcryg2</sha1>
    </revision>
    <revision>
      <id>4654711</id>
      <parentid>4654710</parentid>
      <timestamp>2026-07-16T16:27:28Z</timestamp>
      <contributor>
        <username>LoveElectronicLiterature</username>
        <id>3414389</id>
      </contributor>
      <comment>/* {{subst:currentuser}}{{subst:^|DO NOT EDIT THIS LINE}} */ new section</comment>
      <origin>4654711</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="11785" sha1="3gkv1kg2as5ij3lr37zel35ovt7pq45" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
|archive = Wikibooks:Edit filter/False positives/Archive %(counter)d
|algo = old(75d)
|counter = 4
|maxarchivesize = 150K
|minthreadstoarchive = 1
|minthreadsleft = 3
}}

== SHE-LOVES-BRIAN ==

;Username
: [[:b:User:SHE-LOVES-BRIAN|SHE-LOVES-BRIAN]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SHE-LOVES-BRIAN|discuss]]
|[[:b:Special:Emailuser/SHE-LOVES-BRIAN|email]]
|[[:b:Special:Contributions/SHE-LOVES-BRIAN|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SHE-LOVES-BRIAN}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SHE-LOVES-BRIAN}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SHE-LOVES-BRIAN}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 14:35, 5 May 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

;Username
: [[:b:User:~2026-32360-90|~2026-32360-90]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-32360-90|discuss]]
|[[:b:Special:Emailuser/~2026-32360-90|email]]
|[[:b:Special:Contributions/~2026-32360-90|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-32360-90}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-32360-90}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-32360-90}} filter log]&lt;/span&gt;)
;Page you were editing
: [[Chess Opening Theory/1. e4/1...e5/2. Bc4/2...Bc5/3. Qh5/3...Qe7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7&amp;wpSearchUser=%7E2026-32360-90}} user filter log])&lt;/span&gt;
;Description
: Trying to add a language ([[:fi:Shakki/rnb1k1nr;ppppqppp;8;2b1p2Q;2B1P3;8;PPPP1PPP;RNB1K1NR w KQkq]]) was being flagged as unconstructive by the edit filter.
;Date and time
: 15:57, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

:{{EFFP|rf}} [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:57, 15 June 2026 (UTC)

== ~2026-35089-83 ==

;Username
: [[:b:User:~2026-35089-83|~2026-35089-83]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-35089-83|discuss]]
|[[:b:Special:Emailuser/~2026-35089-83|email]]
|[[:b:Special:Contributions/~2026-35089-83|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-35089-83}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-35089-83}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-35089-83}} filter log]&lt;/span&gt;)
;Page you were editing
: [[[[Japanese/Kana]]]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D&amp;wpSearchUser=%7E2026-35089-83}} user filter log])&lt;/span&gt;
;Description
: Tried replacing a dead link with a working version I found when I plugged the link into webarchive, since that's what I presumed I was meant to do when I found a dead link.
;Date and time
: 01:27, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

;Username
: [[:b:User:SeaDragon1|SeaDragon1]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SeaDragon1|discuss]]
|[[:b:Special:Emailuser/SeaDragon1|email]]
|[[:b:Special:Contributions/SeaDragon1|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SeaDragon1}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SeaDragon1}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SeaDragon1}} filter log]&lt;/span&gt;)
;Page you were editing
: [[User:SeaDragon1/UTM highlighting test]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test&amp;wpSearchUser=SeaDragon1}} user filter log])&lt;/span&gt;
;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== Earthinators page rewrite ==

I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me. [[User:Earthinators|Earthinators]] ([[User talk:Earthinators|discuss]] • [[Special:Contributions/Earthinators|contribs]]) 06:56, 11 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:26, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:27, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/wiki/Hereditary_Multiple_Exostoses]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I have been moving my google doc, that I have curated for over 20 years and which is a creative commons non-attribute doc, into the Wikibooks. I copied a great deal of text (public abstracts and citations) and then I edited. I still get the error flag that I have copied text even AFTER I edited. Thank you
;Date and time
: 16:27, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>3gkv1kg2as5ij3lr37zel35ovt7pq45</sha1>
    </revision>
    <revision>
      <id>4654713</id>
      <parentid>4654711</parentid>
      <timestamp>2026-07-16T16:28:54Z</timestamp>
      <contributor>
        <username>LoveElectronicLiterature</username>
        <id>3414389</id>
      </contributor>
      <comment>/* LoveElectronicLiterature */ duplicated my post because I misread the warning that my page was not found. So I redid the post with the full Wikibook URL.</comment>
      <origin>4654713</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="11843" sha1="b1rh9s53b4vp2kaim4942rsxp05e81r" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
|archive = Wikibooks:Edit filter/False positives/Archive %(counter)d
|algo = old(75d)
|counter = 4
|maxarchivesize = 150K
|minthreadstoarchive = 1
|minthreadsleft = 3
}}

== SHE-LOVES-BRIAN ==

;Username
: [[:b:User:SHE-LOVES-BRIAN|SHE-LOVES-BRIAN]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SHE-LOVES-BRIAN|discuss]]
|[[:b:Special:Emailuser/SHE-LOVES-BRIAN|email]]
|[[:b:Special:Contributions/SHE-LOVES-BRIAN|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SHE-LOVES-BRIAN}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SHE-LOVES-BRIAN}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SHE-LOVES-BRIAN}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 14:35, 5 May 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

;Username
: [[:b:User:~2026-32360-90|~2026-32360-90]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-32360-90|discuss]]
|[[:b:Special:Emailuser/~2026-32360-90|email]]
|[[:b:Special:Contributions/~2026-32360-90|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-32360-90}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-32360-90}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-32360-90}} filter log]&lt;/span&gt;)
;Page you were editing
: [[Chess Opening Theory/1. e4/1...e5/2. Bc4/2...Bc5/3. Qh5/3...Qe7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7&amp;wpSearchUser=%7E2026-32360-90}} user filter log])&lt;/span&gt;
;Description
: Trying to add a language ([[:fi:Shakki/rnb1k1nr;ppppqppp;8;2b1p2Q;2B1P3;8;PPPP1PPP;RNB1K1NR w KQkq]]) was being flagged as unconstructive by the edit filter.
;Date and time
: 15:57, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

:{{EFFP|rf}} [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:57, 15 June 2026 (UTC)

== ~2026-35089-83 ==

;Username
: [[:b:User:~2026-35089-83|~2026-35089-83]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-35089-83|discuss]]
|[[:b:Special:Emailuser/~2026-35089-83|email]]
|[[:b:Special:Contributions/~2026-35089-83|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-35089-83}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-35089-83}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-35089-83}} filter log]&lt;/span&gt;)
;Page you were editing
: [[[[Japanese/Kana]]]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D&amp;wpSearchUser=%7E2026-35089-83}} user filter log])&lt;/span&gt;
;Description
: Tried replacing a dead link with a working version I found when I plugged the link into webarchive, since that's what I presumed I was meant to do when I found a dead link.
;Date and time
: 01:27, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

;Username
: [[:b:User:SeaDragon1|SeaDragon1]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SeaDragon1|discuss]]
|[[:b:Special:Emailuser/SeaDragon1|email]]
|[[:b:Special:Contributions/SeaDragon1|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SeaDragon1}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SeaDragon1}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SeaDragon1}} filter log]&lt;/span&gt;)
;Page you were editing
: [[User:SeaDragon1/UTM highlighting test]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test&amp;wpSearchUser=SeaDragon1}} user filter log])&lt;/span&gt;
;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== Earthinators page rewrite ==

I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me. [[User:Earthinators|Earthinators]] ([[User talk:Earthinators|discuss]] • [[Special:Contributions/Earthinators|contribs]]) 06:56, 11 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:26, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:27, 15 July 2026 (UTC)
;Comments
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== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== LoveElectronicLiterature ==

Sorry for duplicate postings! Delete this one. Thank you, 
;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/wiki/Hereditary_Multiple_Exostoses]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I have been moving my google doc, that I have curated for over 20 years and which is a creative commons non-attribute doc, into the Wikibooks. I copied a great deal of text (public abstracts and citations) and then I edited. I still get the error flag that I have copied text even AFTER I edited. Thank you
;Date and time
: 16:27, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>b1rh9s53b4vp2kaim4942rsxp05e81r</sha1>
    </revision>
    <revision>
      <id>4654717</id>
      <parentid>4654713</parentid>
      <timestamp>2026-07-16T16:39:19Z</timestamp>
      <contributor>
        <username>Ternera</username>
        <id>2679710</id>
      </contributor>
      <comment>/* ~2026-40102-72 */ nft</comment>
      <origin>4654717</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="11987" sha1="qvczug3aokbwglnq9usqqcx3wuge4al" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
|archive = Wikibooks:Edit filter/False positives/Archive %(counter)d
|algo = old(75d)
|counter = 4
|maxarchivesize = 150K
|minthreadstoarchive = 1
|minthreadsleft = 3
}}

== SHE-LOVES-BRIAN ==

;Username
: [[:b:User:SHE-LOVES-BRIAN|SHE-LOVES-BRIAN]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SHE-LOVES-BRIAN|discuss]]
|[[:b:Special:Emailuser/SHE-LOVES-BRIAN|email]]
|[[:b:Special:Contributions/SHE-LOVES-BRIAN|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SHE-LOVES-BRIAN}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SHE-LOVES-BRIAN}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SHE-LOVES-BRIAN}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 14:35, 5 May 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

;Username
: [[:b:User:~2026-32360-90|~2026-32360-90]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-32360-90|discuss]]
|[[:b:Special:Emailuser/~2026-32360-90|email]]
|[[:b:Special:Contributions/~2026-32360-90|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-32360-90}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-32360-90}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-32360-90}} filter log]&lt;/span&gt;)
;Page you were editing
: [[Chess Opening Theory/1. e4/1...e5/2. Bc4/2...Bc5/3. Qh5/3...Qe7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7&amp;wpSearchUser=%7E2026-32360-90}} user filter log])&lt;/span&gt;
;Description
: Trying to add a language ([[:fi:Shakki/rnb1k1nr;ppppqppp;8;2b1p2Q;2B1P3;8;PPPP1PPP;RNB1K1NR w KQkq]]) was being flagged as unconstructive by the edit filter.
;Date and time
: 15:57, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

:{{EFFP|rf}} [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:57, 15 June 2026 (UTC)

== ~2026-35089-83 ==

;Username
: [[:b:User:~2026-35089-83|~2026-35089-83]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-35089-83|discuss]]
|[[:b:Special:Emailuser/~2026-35089-83|email]]
|[[:b:Special:Contributions/~2026-35089-83|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-35089-83}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-35089-83}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-35089-83}} filter log]&lt;/span&gt;)
;Page you were editing
: [[[[Japanese/Kana]]]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D&amp;wpSearchUser=%7E2026-35089-83}} user filter log])&lt;/span&gt;
;Description
: Tried replacing a dead link with a working version I found when I plugged the link into webarchive, since that's what I presumed I was meant to do when I found a dead link.
;Date and time
: 01:27, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

;Username
: [[:b:User:SeaDragon1|SeaDragon1]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SeaDragon1|discuss]]
|[[:b:Special:Emailuser/SeaDragon1|email]]
|[[:b:Special:Contributions/SeaDragon1|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SeaDragon1}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SeaDragon1}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SeaDragon1}} filter log]&lt;/span&gt;)
;Page you were editing
: [[User:SeaDragon1/UTM highlighting test]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test&amp;wpSearchUser=SeaDragon1}} user filter log])&lt;/span&gt;
;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== Earthinators page rewrite ==

I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me. [[User:Earthinators|Earthinators]] ([[User talk:Earthinators|discuss]] • [[Special:Contributions/Earthinators|contribs]]) 06:56, 11 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:26, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:27, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== LoveElectronicLiterature ==

Sorry for duplicate postings! Delete this one. Thank you, 
;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/wiki/Hereditary_Multiple_Exostoses]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I have been moving my google doc, that I have curated for over 20 years and which is a creative commons non-attribute doc, into the Wikibooks. I copied a great deal of text (public abstracts and citations) and then I edited. I still get the error flag that I have copied text even AFTER I edited. Thank you
;Date and time
: 16:27, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>qvczug3aokbwglnq9usqqcx3wuge4al</sha1>
    </revision>
    <revision>
      <id>4654718</id>
      <parentid>4654717</parentid>
      <timestamp>2026-07-16T16:39:26Z</timestamp>
      <contributor>
        <username>Ternera</username>
        <id>2679710</id>
      </contributor>
      <comment>/* ~2026-40102-72 */ nft</comment>
      <origin>4654718</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="12131" sha1="mf8tjal62wi273vl6e84to136fmvrum" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
|archive = Wikibooks:Edit filter/False positives/Archive %(counter)d
|algo = old(75d)
|counter = 4
|maxarchivesize = 150K
|minthreadstoarchive = 1
|minthreadsleft = 3
}}

== SHE-LOVES-BRIAN ==

;Username
: [[:b:User:SHE-LOVES-BRIAN|SHE-LOVES-BRIAN]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SHE-LOVES-BRIAN|discuss]]
|[[:b:Special:Emailuser/SHE-LOVES-BRIAN|email]]
|[[:b:Special:Contributions/SHE-LOVES-BRIAN|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SHE-LOVES-BRIAN}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SHE-LOVES-BRIAN}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SHE-LOVES-BRIAN}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 14:35, 5 May 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

;Username
: [[:b:User:~2026-32360-90|~2026-32360-90]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-32360-90|discuss]]
|[[:b:Special:Emailuser/~2026-32360-90|email]]
|[[:b:Special:Contributions/~2026-32360-90|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-32360-90}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-32360-90}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-32360-90}} filter log]&lt;/span&gt;)
;Page you were editing
: [[Chess Opening Theory/1. e4/1...e5/2. Bc4/2...Bc5/3. Qh5/3...Qe7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7&amp;wpSearchUser=%7E2026-32360-90}} user filter log])&lt;/span&gt;
;Description
: Trying to add a language ([[:fi:Shakki/rnb1k1nr;ppppqppp;8;2b1p2Q;2B1P3;8;PPPP1PPP;RNB1K1NR w KQkq]]) was being flagged as unconstructive by the edit filter.
;Date and time
: 15:57, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

:{{EFFP|rf}} [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:57, 15 June 2026 (UTC)

== ~2026-35089-83 ==

;Username
: [[:b:User:~2026-35089-83|~2026-35089-83]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-35089-83|discuss]]
|[[:b:Special:Emailuser/~2026-35089-83|email]]
|[[:b:Special:Contributions/~2026-35089-83|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-35089-83}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-35089-83}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-35089-83}} filter log]&lt;/span&gt;)
;Page you were editing
: [[[[Japanese/Kana]]]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D&amp;wpSearchUser=%7E2026-35089-83}} user filter log])&lt;/span&gt;
;Description
: Tried replacing a dead link with a working version I found when I plugged the link into webarchive, since that's what I presumed I was meant to do when I found a dead link.
;Date and time
: 01:27, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

;Username
: [[:b:User:SeaDragon1|SeaDragon1]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SeaDragon1|discuss]]
|[[:b:Special:Emailuser/SeaDragon1|email]]
|[[:b:Special:Contributions/SeaDragon1|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SeaDragon1}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SeaDragon1}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SeaDragon1}} filter log]&lt;/span&gt;)
;Page you were editing
: [[User:SeaDragon1/UTM highlighting test]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test&amp;wpSearchUser=SeaDragon1}} user filter log])&lt;/span&gt;
;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== Earthinators page rewrite ==

I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me. [[User:Earthinators|Earthinators]] ([[User talk:Earthinators|discuss]] • [[Special:Contributions/Earthinators|contribs]]) 06:56, 11 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:26, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:27, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== LoveElectronicLiterature ==

Sorry for duplicate postings! Delete this one. Thank you, 
;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/wiki/Hereditary_Multiple_Exostoses]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I have been moving my google doc, that I have curated for over 20 years and which is a creative commons non-attribute doc, into the Wikibooks. I copied a great deal of text (public abstracts and citations) and then I edited. I still get the error flag that I have copied text even AFTER I edited. Thank you
;Date and time
: 16:27, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>mf8tjal62wi273vl6e84to136fmvrum</sha1>
    </revision>
    <revision>
      <id>4654719</id>
      <parentid>4654718</parentid>
      <timestamp>2026-07-16T16:40:31Z</timestamp>
      <contributor>
        <username>Ternera</username>
        <id>2679710</id>
      </contributor>
      <comment>/* SeaDragon1 */ ad</comment>
      <origin>4654719</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="12285" sha1="iw9tmgauqcdz8u6kukfrh7ptnzqyxqx" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
|archive = Wikibooks:Edit filter/False positives/Archive %(counter)d
|algo = old(75d)
|counter = 4
|maxarchivesize = 150K
|minthreadstoarchive = 1
|minthreadsleft = 3
}}

== SHE-LOVES-BRIAN ==

;Username
: [[:b:User:SHE-LOVES-BRIAN|SHE-LOVES-BRIAN]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SHE-LOVES-BRIAN|discuss]]
|[[:b:Special:Emailuser/SHE-LOVES-BRIAN|email]]
|[[:b:Special:Contributions/SHE-LOVES-BRIAN|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SHE-LOVES-BRIAN}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SHE-LOVES-BRIAN}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SHE-LOVES-BRIAN}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 14:35, 5 May 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

;Username
: [[:b:User:~2026-32360-90|~2026-32360-90]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-32360-90|discuss]]
|[[:b:Special:Emailuser/~2026-32360-90|email]]
|[[:b:Special:Contributions/~2026-32360-90|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-32360-90}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-32360-90}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-32360-90}} filter log]&lt;/span&gt;)
;Page you were editing
: [[Chess Opening Theory/1. e4/1...e5/2. Bc4/2...Bc5/3. Qh5/3...Qe7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7&amp;wpSearchUser=%7E2026-32360-90}} user filter log])&lt;/span&gt;
;Description
: Trying to add a language ([[:fi:Shakki/rnb1k1nr;ppppqppp;8;2b1p2Q;2B1P3;8;PPPP1PPP;RNB1K1NR w KQkq]]) was being flagged as unconstructive by the edit filter.
;Date and time
: 15:57, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

:{{EFFP|rf}} [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:57, 15 June 2026 (UTC)

== ~2026-35089-83 ==

;Username
: [[:b:User:~2026-35089-83|~2026-35089-83]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-35089-83|discuss]]
|[[:b:Special:Emailuser/~2026-35089-83|email]]
|[[:b:Special:Contributions/~2026-35089-83|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-35089-83}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-35089-83}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-35089-83}} filter log]&lt;/span&gt;)
;Page you were editing
: [[[[Japanese/Kana]]]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D&amp;wpSearchUser=%7E2026-35089-83}} user filter log])&lt;/span&gt;
;Description
: Tried replacing a dead link with a working version I found when I plugged the link into webarchive, since that's what I presumed I was meant to do when I found a dead link.
;Date and time
: 01:27, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

;Username
: [[:b:User:SeaDragon1|SeaDragon1]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SeaDragon1|discuss]]
|[[:b:Special:Emailuser/SeaDragon1|email]]
|[[:b:Special:Contributions/SeaDragon1|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SeaDragon1}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SeaDragon1}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SeaDragon1}} filter log]&lt;/span&gt;)
;Page you were editing
: [[User:SeaDragon1/UTM highlighting test]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test&amp;wpSearchUser=SeaDragon1}} user filter log])&lt;/span&gt;
;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
:{{EFFP|ad|SeaDragon1}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:40, 16 July 2026 (UTC)

== Earthinators page rewrite ==

I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me. [[User:Earthinators|Earthinators]] ([[User talk:Earthinators|discuss]] • [[Special:Contributions/Earthinators|contribs]]) 06:56, 11 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:26, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 20:27, 15 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

== LoveElectronicLiterature ==

Sorry for duplicate postings! Delete this one. Thank you, 
;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
|[[:b:Special:Emailuser/LoveElectronicLiterature|email]]
|[[:b:Special:Contributions/LoveElectronicLiterature|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/wiki/Hereditary_Multiple_Exostoses]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I have been moving my google doc, that I have curated for over 20 years and which is a creative commons non-attribute doc, into the Wikibooks. I copied a great deal of text (public abstracts and citations) and then I edited. I still get the error flag that I have copied text even AFTER I edited. Thank you
;Date and time
: 16:27, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>iw9tmgauqcdz8u6kukfrh7ptnzqyxqx</sha1>
    </revision>
    <revision>
      <id>4654742</id>
      <parentid>4654719</parentid>
      <timestamp>2026-07-16T19:48:46Z</timestamp>
      <contributor>
        <username>Codename Noreste</username>
        <id>3441010</id>
      </contributor>
      <comment>/* Earthinators page rewrite */ Fixed the report.</comment>
      <origin>4654742</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="13340" sha1="hko6qhps6nw0luervhhgvemrpmgtiis" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
|archive = Wikibooks:Edit filter/False positives/Archive %(counter)d
|algo = old(75d)
|counter = 4
|maxarchivesize = 150K
|minthreadstoarchive = 1
|minthreadsleft = 3
}}

== SHE-LOVES-BRIAN ==

;Username
: [[:b:User:SHE-LOVES-BRIAN|SHE-LOVES-BRIAN]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SHE-LOVES-BRIAN|discuss]]
|[[:b:Special:Emailuser/SHE-LOVES-BRIAN|email]]
|[[:b:Special:Contributions/SHE-LOVES-BRIAN|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SHE-LOVES-BRIAN}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SHE-LOVES-BRIAN}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SHE-LOVES-BRIAN}} filter log]&lt;/span&gt;)
;Page you were editing
: Page not specified
;Description
: 
;Date and time
: 14:35, 5 May 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

;Username
: [[:b:User:~2026-32360-90|~2026-32360-90]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-32360-90|discuss]]
|[[:b:Special:Emailuser/~2026-32360-90|email]]
|[[:b:Special:Contributions/~2026-32360-90|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-32360-90}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-32360-90}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-32360-90}} filter log]&lt;/span&gt;)
;Page you were editing
: [[Chess Opening Theory/1. e4/1...e5/2. Bc4/2...Bc5/3. Qh5/3...Qe7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Chess+Opening+Theory%2F1.+e4%2F1...e5%2F2.+Bc4%2F2...Bc5%2F3.+Qh5%2F3...Qe7&amp;wpSearchUser=%7E2026-32360-90}} user filter log])&lt;/span&gt;
;Description
: Trying to add a language ([[:fi:Shakki/rnb1k1nr;ppppqppp;8;2b1p2Q;2B1P3;8;PPPP1PPP;RNB1K1NR w KQkq]]) was being flagged as unconstructive by the edit filter.
;Date and time
: 15:57, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

:{{EFFP|rf}} [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:57, 15 June 2026 (UTC)

== ~2026-35089-83 ==

;Username
: [[:b:User:~2026-35089-83|~2026-35089-83]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-35089-83|discuss]]
|[[:b:Special:Emailuser/~2026-35089-83|email]]
|[[:b:Special:Contributions/~2026-35089-83|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-35089-83}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-35089-83}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-35089-83}} filter log]&lt;/span&gt;)
;Page you were editing
: [[[[Japanese/Kana]]]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D&amp;wpSearchUser=%7E2026-35089-83}} user filter log])&lt;/span&gt;
;Description
: Tried replacing a dead link with a working version I found when I plugged the link into webarchive, since that's what I presumed I was meant to do when I found a dead link.
;Date and time
: 01:27, 15 June 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

;Username
: [[:b:User:SeaDragon1|SeaDragon1]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:SeaDragon1|discuss]]
|[[:b:Special:Emailuser/SeaDragon1|email]]
|[[:b:Special:Contributions/SeaDragon1|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:SeaDragon1}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:SeaDragon1}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=SeaDragon1}} filter log]&lt;/span&gt;)
;Page you were editing
: [[User:SeaDragon1/UTM highlighting test]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=User%3ASeaDragon1%2FUTM+highlighting+test&amp;wpSearchUser=SeaDragon1}} user filter log])&lt;/span&gt;
;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
:{{EFFP|ad|SeaDragon1}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:40, 16 July 2026 (UTC)

==Earthinators==
;Username
: [[:b:User:Earthinators|Earthinators]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:Earthinators|discuss]]
|[[:b:Special:Emailuser/Earthinators|email]]
|[[:b:Special:Contributions/Earthinators|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:Earthinators}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:Earthinators}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=Earthinators}} filter log]&lt;/span&gt;)
;Page you were editing
: [[Earthinators]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Earthinators}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Earthinators&amp;wpSearchUser=Earthinators}} user filter log])&lt;/span&gt;
;Description
: I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me.
;Date and time
: 06:56, 11 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;

:{{EFFP|rf}} [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 19:48, 16 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
|[[:b:Special:Emailuser/~2026-40102-72|email]]
|[[:b:Special:Contributions/~2026-40102-72|contribs]]
|[{{fullurl:b:Special:Log|user={{urlencode:~2026-40102-72}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
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:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== ~2026-40102-72 ==


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:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== LoveElectronicLiterature ==


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: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
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: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
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== LoveElectronicLiterature ==

Sorry for duplicate postings! Delete this one. Thank you, 
;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
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|[{{fullurl:b:Special:Log|user={{urlencode:LoveElectronicLiterature}}}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;logs&lt;/span&gt;]
|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
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;Page you were editing
: [[https://en.wikibooks.org/wiki/Hereditary_Multiple_Exostoses]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fwiki%2FHereditary_Multiple_Exostoses&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I have been moving my google doc, that I have curated for over 20 years and which is a creative commons non-attribute doc, into the Wikibooks. I copied a great deal of text (public abstracts and citations) and then I edited. I still get the error flag that I have copied text even AFTER I edited. Thank you
;Date and time
: 16:27, 16 July 2026 (UTC)
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&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>hko6qhps6nw0luervhhgvemrpmgtiis</sha1>
    </revision>
    <revision>
      <id>4654743</id>
      <parentid>4654742</parentid>
      <timestamp>2026-07-16T19:49:14Z</timestamp>
      <contributor>
        <username>Codename Noreste</username>
        <id>3441010</id>
      </contributor>
      <comment>/* LoveElectronicLiterature */ Duplicate.</comment>
      <origin>4654743</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="11631" sha1="qerve5jm8cv77c9yl0gtujynpgdx1gq" xml:space="preserve">__NONEWSECTIONLINK__ __NOINDEX__ {{Wikibooks:Edit filter/False positives/Header}} {{shortcut|WB:EFFP}} {{User:MiszaBot/config
|archive = Wikibooks:Edit filter/False positives/Archive %(counter)d
|algo = old(75d)
|counter = 4
|maxarchivesize = 150K
|minthreadstoarchive = 1
|minthreadsleft = 3
}}

== SHE-LOVES-BRIAN ==

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;Date and time
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&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;
: {{EFFP|note}} You are autoconfirmed, which means the filter shouldn't trigger on you anymore, but not all of them to be exact. – [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:58, 15 June 2026 (UTC)

== ~2026-32360-90 ==

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;Description
: Trying to add a language ([[:fi:Shakki/rnb1k1nr;ppppqppp;8;2b1p2Q;2B1P3;8;PPPP1PPP;RNB1K1NR w KQkq]]) was being flagged as unconstructive by the edit filter.
;Date and time
: 15:57, 15 June 2026 (UTC)
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:{{EFFP|rf}} [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:57, 15 June 2026 (UTC)

== ~2026-35089-83 ==

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: [[[[Japanese/Kana]]]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=%5B%5BJapanese%2FKana%5D%5D&amp;wpSearchUser=%7E2026-35089-83}} user filter log])&lt;/span&gt;
;Description
: Tried replacing a dead link with a working version I found when I plugged the link into webarchive, since that's what I presumed I was meant to do when I found a dead link.
;Date and time
: 01:27, 15 June 2026 (UTC)
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: {{EFFP|done}}  – [[User:Codename Noreste|&lt;span style=&quot;color: blue&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 21:54, 15 July 2026 (UTC)

== SeaDragon1 ==

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;Description
: Attempted creation of page to test [[User:SeaDragon1/common.js]] (both attempted page creation content and &lt;span style=&quot;font-family: monospace&quot;&gt;common.js&lt;/span&gt; were copied from [[w:Main Page|the English Wikipedia]]).
;Date and time
: 23:26, 3 July 2026 (UTC)
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:{{EFFP|ad|SeaDragon1}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:40, 16 July 2026 (UTC)

==Earthinators==
;Username
: [[:b:User:Earthinators|Earthinators]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:Earthinators|discuss]]
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: [[Earthinators]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=Earthinators}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=Earthinators&amp;wpSearchUser=Earthinators}} user filter log])&lt;/span&gt;
;Description
: I was trying to replace the main page of [[Earthinators]] with a neutral, instructional textbook version ([[Talk:Earthinators|the new text is on the talk page]]). The edit filter blocked me, saying the edit was &quot;potentially unconstructive&quot;. The new version follows Wikibooks guidelines – it’s a textbook, not a promotional page. Please allow the edit or make the change for me.
;Date and time
: 06:56, 11 July 2026 (UTC)
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:{{EFFP|rf}} [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 19:48, 16 July 2026 (UTC)

== ~2026-40102-72 ==


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: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
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|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
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:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== ~2026-40102-72 ==


;Username
: [[:b:User:~2026-40102-72|~2026-40102-72]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:~2026-40102-72|discuss]]
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|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:~2026-40102-72}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=%7E2026-40102-72}} filter log]&lt;/span&gt;)
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: 
;Date and time
: 20:27, 15 July 2026 (UTC)
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:{{EFFP|nft}} [[User:Ternera|Ternera]] ([[User talk:Ternera|discuss]] • [[Special:Contributions/Ternera|contribs]]) 16:39, 16 July 2026 (UTC)

== LoveElectronicLiterature ==


;Username
: [[:b:User:LoveElectronicLiterature|LoveElectronicLiterature]]&lt;span class=&quot;noprint&quot;&gt; {{toolbar|separator=dot
|[[:b:User talk:LoveElectronicLiterature|discuss]]
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|[//tools.wmflabs.org/xtools/pcount/index.php?lang{{=}}en&amp;wiki{{=}}wikibooks&amp;name{{=}}{{urlencode:LoveElectronicLiterature}} &lt;span style{{=}}&quot;color:#002bb8&quot;&gt;count&lt;/span&gt;]
}}&lt;/span&gt; (&lt;span class=&quot;plainlinks&quot;&gt;[{{fullurl:Special:AbuseLog|wpSearchUser=LoveElectronicLiterature}} filter log]&lt;/span&gt;)
;Page you were editing
: [[https://en.wikibooks.org/w/index.php?title=Hereditary_Multiple_Exostoses&amp;veaction=edit&amp;section=7]] &lt;span class=&quot;plainlinks&quot;&gt;([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7}} filter log]) ([{{fullurl:Special:AbuseLog|wpSearchTitle=https%3A%2F%2Fen.wikibooks.org%2Fw%2Findex.php%3Ftitle%3DHereditary_Multiple_Exostoses%26veaction%3Dedit%26section%3D7&amp;wpSearchUser=LoveElectronicLiterature}} user filter log])&lt;/span&gt;
;Description
: I was trying to copy the references and abstracts that I have been maintaining for over 20 years at http COLON SLASH SLASH tinyurl DOT com SLASH MHETalk.  I copied a bunch of references, and then I shortened the description and put the citations in. But I got flagged for copying.  Is there any way to fix this?  thanks!
;Date and time
: 16:23, 16 July 2026 (UTC)
;Comments
&lt;!-- Please leave this area blank for now, but be prepared to answer questions left by reviewing editors. Thanks! --&gt;</text>
      <sha1>qerve5jm8cv77c9yl0gtujynpgdx1gq</sha1>
    </revision>
  </page>
  <page>
    <title>Proto-Turkic/Suffixes used to create new words with new meanings</title>
    <ns>0</ns>
    <id>435365</id>
    <revision>
      <id>4654755</id>
      <parentid>4313571</parentid>
      <timestamp>2026-07-16T22:24:52Z</timestamp>
      <contributor>
        <username>~2026-40190-29</username>
        <id>3614903</id>
      </contributor>
      <comment>/* Dead Verbs */ tiakïgu is altaistic variant, so I removed 'i'</comment>
      <origin>4654755</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="15198" sha1="0x6i43wuh80c2kuwlcrn9p1vggkyuk7" xml:space="preserve">Welcome to seventh lesson of Proto-Turkic.

Languages belonging to the Altaic group are agglutinative languages. New words are always born from roots.

== Suffixes that make nouns (or adjectives, adverbs) from a verb ==
In order to define the suffixes that make nouns from the verb, we first need a root verb. Nouns (or adjectives, adverbs) formed by this method are in close meaning with the root verb.

=== *-Xk&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-k&lt;/ref&gt;&lt;/small&gt; ===
Here are some examples:

'''''*uŕa-''''' (“to be taller, to be longer”) → '''''*uŕak''''' (“far; long (time), late”)

'''''*kīči-''''' (“to tickle”) → '''''*kīčik''''' (“itching, tickling”)

'''''*tīre-''''' (“to support”) → '''''*tīrek''''' (“support”)

'''''*sogï-''''' (“to get cold”) → '''''*sogïk''''' (“cold”)

=== *-Xn&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-in&lt;/ref&gt;&lt;/small&gt; ===
Here are some examples:

'''''*kẹl-''''' (“to come”) → '''''*kẹlin''''' (“bride”)

'''''*yarï-''''' (“to shine”) → '''''*yarïn''''' (“morning, tomorrow”)

'''''*oy-''''' (“to jump”) → '''''*oyun''''' (“game”)

'''''*tüt-''''' (“to smoke, reek”) → '''''*tütün''''' (“tobacco, smoke”)

=== *-gU&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-g%C3%BC&lt;/ref&gt;&lt;/small&gt; ===
'''''*bur-''''' (“to bend”) → '''''*burgu''''' (“trumpet, horn; pipe (of a plant)”)

See dead verbs for more.

=== *-Xĺ&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-i%C4%BA&lt;/ref&gt;&lt;/small&gt; ===
'''''*yum-''''' → '''''*yumuĺ''''' (“work”) (from a dead verb, perhaps from '''''*yum-''''' (“to round”))

The same suffix also has a different function. But that is the subject of ''Suffixes that make verbs from a verb''.

=== *-Ug ===
'''''*kam-''''' (“to gather”) → '''''*kamug''''' (“all, together”)

'''''*agrï-''''' (“to ache, hurt”) → '''''*agrïg''''' (“ache, pain”)

'''''*köpür-''''' (“dead verb”) → '''''*köpürüg''''' (“bridge”)

=== *-gAk ===
'''''*bat-''''' (“to sink; to fit into, get into”) → '''''*batgak''''' (“swamp, marsh”)

See dead verbs for more.

== Suffixes that make nouns (or adjectives, adverbs) from a noun ==
Some suffixes of this type do not change the meaning, and most suffixes have meanings very close to the root.

=== *-Ig&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-ig&lt;/ref&gt;&lt;/small&gt; ===
Here are some examples:

'''''*el''''' (“hand”) → '''''*elig''''' (“hand”)

'''''*siar(ï)''''' (“yellow, white”) → '''''*siarïg''''' (“yellow, white”)

=== *-lXg&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-lig&lt;/ref&gt;&lt;/small&gt; ===
It corresponds to the -ful suffix in English.

Here are some examples:

'''''*kǖč''''' (“power”) → '''''*kǖčlüg''''' (“powerful”)

'''''*köpür''''' (“bridge”) → '''''*köpürlüg''''' (“bridge-ful, with bridges”)

'''''*us''''' (“mind”) → '''''*uslug''''' (“well-behaved, mind-ful”)

'''''*el''''' (“hand”) → '''''*ellig''''' (“fifty; with hand”)

You can give the same meaning by adding this suffix to any word you want. But of course you can't get a new number by adding it to numbers. :) This is only for the number fifty.

=== *-sXŕ&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-si%C5%95&lt;/ref&gt;&lt;/small&gt; ===
It corresponds to the -less suffix in English.

'''''*kǖč''''' (“power”) → '''''*kǖčsüŕ''''' (“powerless”)

'''''*köpürüg''''' (“bridge”) → '''''*köpürügsüŕ''''' (“bridgeless, without bridges”)

'''''*us''''' (“mind”) → '''''*ussuŕ''''' (“mindless, without mind”)

You can give the same meaning by adding this suffix to any word you want.

=== *-lXk&lt;small&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-lik&lt;/ref&gt;&lt;/small&gt; ===
It corresponds to the -ness suffix in English.

'''''*kǖčlüg''''' (“powerful”) → '''''*kǖčlüglük''''' (“powerfulness”)

'''''*bẹ''''' (“I, me”) → '''''*benlik''''' (“me-ness, my pair of shoes”)

'''''*kara''''' (“black, dark”) → '''''*kara(n)lïk''''' (“darkness”)

'''''*it''''' (“dog”) → '''''*itlik''''' (“dogness, dog's pair of shoes”)

'''''*yubka''''' (“thin, slender, unsubstantial”) → '''''*yubkalïk''''' (“thin-ness, slender-ness”)

You can give the same meaning by adding this suffix to any word you want.

=== *-čI ===
This suffix is identical to the English suffix ''-er''.

* '''''*sǖt''''' (“milk”) → '''''*sǖtči''''' (“milkman”)

* '''''*īĺč''''' (“work”) → '''''*īĺčči''''' (“worker”)
* '''''*oyun''''' (“game”) → '''''*oyunčï''''' (“gamer”)

* '''''*sub''''' (“water”) → '''''*subčï''''' (“water seller”)

=== *-XnčI&lt;small&gt;&lt;ref&gt;https://en.m.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-in%C4%8Di&lt;/ref&gt;&lt;/small&gt; ===
Creates ordinal numbers from cardinal numbers.  

The structure of this suffix may have been provided by the fact that the word takes the previous '''*-čI''' suffix after taking the instrumental. 

'''''*bīr''''' (“one”) → '''''*bīrinči''''' (“first”)

'''''*üč''''' (“three”) → '''''*üčünči''''' (“third”)

'''''*altï''''' (“six”) → '''''*altïnčï''''' (“sixth”)

It just makes the noun an adjective. For example, it &lt;u&gt;cannot be used&lt;/u&gt; as &quot;'''**bīrinči kẹltim''' (I came first)&quot;. It should be used as follows: &quot;'''*bīrinči bōlsa kẹltim''' (I came as being first)&quot;. Or there is the word '''*il(i)k''', which you can use in the same sense, although it does not mean exactly the same on its own. (e.g: *'''il(i)k keltim''', ''I came before'').

== Suffixes that make verbs from a verb ==
Such suffixes can answer questions such as who is performing the action, whether it is one person or more than one person, without a second additional sentence. They don't change the meaning of the verb, they just add.

=== Reciprocal (*-X'''ĺ'''č-)&lt;sup&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-i%C4%BA%C4%8D&lt;/ref&gt; &lt;/sup&gt; ===
This appendix indicates that the action was performed by more than one person. The same sentence can be made without this suffix, but this suffix saves extra words. You can get this meaning by adding this suffix to any verb you want.

It is also sometimes used to mean doing something by oneself in some Turkic languages such as Turkish.

'''''*kör-''''' (“to see”) → '''''*körüĺč-''''' (“to see each other; to meet”)

'''''*bạk-''''' (“to look”) → '''''*bạkïĺč-''''' (“to look each other”)

'''''*ur-''''' (“to beat, hit”) → '''''*uruĺč-''''' (“to beat each other; to fight”)

'''''*seb-''''' (“to love”) → '''''*sebiĺč-''''' (“to love each other”)
{| class=&quot;wikitable&quot;
|+Examples
!
!Turkish - Anadolu Türkçesi
!Kazakh - Қазақша
!Chuvash - Чӑвашла
|-
|Original
|Beni onla kar'''ış'''tırma.
|Содан бері біз көр'''іс'''педік.
|Эпир ку тӑван ҫӗршыва ҫап'''ӑҫ'''са ҫӗнтертӗмӗр.
|-
|Transcription
|(the text is already written in latin script)
|Sodan beri biz kör'''is'''pedik.
|Epir ku tăvan şĕršıva şap'''ăş'''sa şĕntertĕmĕr.
|-
|Translation
|Don't '''confuse''' me with him.
|We haven't '''met''' since then.
|We won this war '''fight'''ing.
|}

=== Passiveness and Activeness (*-Xn-, *-n-, *-Xl-, -l-) ===

# Indicates that a job is done by itself
# Creates the passive state

First of all, this can be a bit difficult for non-native speakers to understand. Because the use of these suffixes varies according to the consonant in the last letter.

If the consonant in the last letter is ''t'' or ''n'', it always takes the suffix '''*-Xl'''. If the consonant in the last letter is ''l'', it always takes the suffix '''*-Xn'''. However, other consonants may vary from Turkic languages to Turkic languages and are irregular in some Turkic languages. It has been observed that in Turkish, vowel endings always have ''-n'' suffix and no ''-l'' suffix. On the contrary, the Kazakh word ''bastaw'' takes the suffix ''-l'' and the new verb becomes ''bastalw''. Since there is no ''-l'' suffix in Turkish, ''başlamak'' became ''başlanmak''.

In general, '''*-In''' is used more like in the first item, and '''*-Il''' more like in the second item. In some verbs, a suffix can provide both clauses. For example, since the word '''*kat-''' ends with the letter '''''t''''', it cannot take the suffix '''*-In''' and necessarily provides both with '''*-Il'''.

'''''*seb-''''' (“to love, like”) → '''''*sebil-''''' (“to be loved, liked (by)”), '''''*seb-''''' (“to love, like”) → '''''*sebin-''''' (“rejoice in oneself”)

'''*ker-''' (“to stretch”) → '''''*keril-''''' (“to be stretched (by)”), '''''*ker-''''' (“to stretch”) → '''''*kerin-''''' (“give oneself a stretch”)

'''''*ēn-''''' (“to go down”) → '''''*ēnil-''''' (“to be gone down (by); to go down on one's own”)

'''''*ạt-''''' (“to throw”) → '''''*ạtïl-''''' (“to be thrown (by); to throw on one's own”)

'''''*ạl-''''' (“to take”) → '''''*ạlïn-''''' (“to be taken (by); to take on one's own”)

=== Causative and Transitivised (*-tUr-, *-t-)&lt;sup&gt;&lt;ref&gt;https://en.wiktionary.org/wiki/Reconstruction:Proto-Turkic/-tur&lt;/ref&gt;&lt;/sup&gt; ===
This suffix provides the meaning of making someone do it or causing.

'''''*ol-''''' (“to become”) → '''''*oltur-''''' (“to make someone be, to sit”)

'''''*kẹl-''''' (“to come”) → '''''*kẹltür-''''' (“to cause something come, to bring; to make someone come”)

'''''*öl-''''' (“to die”) → '''''*öltür-''''' (“to make someone die, to kill”)

'''''*seb-''''' (“to love”) → '''''*sebtür-''''' (“to make someone love”)

If it is multiple syllables, it takes the suffix '''*-t'''.

'''''*semir-''''' (“to fatten”) → '''''*semirt-''''' (“to cause something fatten”)

'''''*okï-''''' (“to read”) → '''''*okït-''''' (“to make someone read&quot;) (''Shaz'')

If the last letter is ''t'' or ''n'', it does not take the letter ''t'' even if it is multiple syllables, it takes the form *-tUr.

'''''*ẹlit-''''' (“to hear”) → '''''*ẹlittür-''''' (“to make something heard by someone; to cause someone hear”)

'''''*sebin-''''' (“to love oneself”) → '''''*sebintür-''''' (“to make someone love oneself”)

The word can take from these suffixes twice.

'''''*kẹltür-''''' (“to cause something come, to bring”) → '''''*kẹltürt-''''' (“to make someone cause something come, to make someone bring”)

'''''*öltür-''''' (“to make someone die, to kill”) → '''''*öltürt-''''' (“to cause someone make someone die, to cause someone kill”)

Let's explain with a few examples since it seems confusing.

S/he '''died'''. - Ol '''öl'''tü.

S/he '''kill'''ed him. - Ol anï '''öltür'''tü.

S/he had her '''kill'''ed '''by''' him. - Ol anï anka '''öltürt'''dü.

=== Negation (*-mA-) ===
By adding this suffix to the verbs, the meaning of negation is provided.

* '''''*seb-''''' (“to love, like”) → '''''*sebme-''''' (“to not love, not like”)
* '''''*bar-''''' (“to go”) → '''''*barma-''''' (“to not go”)
See next lesson [[Proto-Turkic/Verbals|8: Verbals]] for more information about negation suffix.

== Suffixes that make verbs from a noun ==

=== *-lA- ===
Here are some examples:

'''''*tïŋ''''' (dead noun) → '''''*tïŋla-''''' (“to listen; to hear; to consider, meditate”)

'''''*āŋ''''' (“intelligence”) → '''''*āŋla-''''' (“to understand; to hear; to discern”)

'''''*yï̄g''''' (“weeping, crying”) → '''''*yï̄gla-''''' (“to weep, cry”) ''(Proto-Shaz)''

'''''*āb''''' (“hunt”) → '''''*ābla-''''' (“to hunt”) ''(Proto-Shaz)''

=== *-lAn- ===
It is provided by the previously mentioned '''*-lA-''' and '''*-n-'''. This suffix gives the meaning of ''to have (something)''. Here are some examples:

'''''*eb''''' (house) → '''''*eblen-''''' (“to have a house; to marry”)

'''''*āb''''' (“hunt”) → '''''*āblan-''''' (“to have a hunt”) ''(Proto-Shaz)''

=== *-Ar-, *-r- ===
This suffix gives the meaning of ''to turn (something)''. It seems to be used only in colors. Here are some examples;

'''''*kȫk''''' (blue) → '''''*kȫker-''''' (“to turn blue”)

'''''*kara''''' (black) → '''''*karar-''''' (“to turn black”)

'''''*siarïg''''' (yellow, white) → '''''*siarïgar-''''' (“to turn yellow, white”)

=== *-gA- ===
Here are some examples:

'''''*kẹr''''' (dead noun) → '''''*kẹrge-''''' (“to need”)

'''''*em''''' (“dead noun”) → '''''*emge-''''' (“to suffer, be tortured”)

Sometimes this verb takes a noun suffix and becomes a noun again, but the suffix '''*-gAk''' added to verbs and '''*-gA-''' added to nouns should not be confused with each other. For example, '''''*bat-''''' is a verb and becomes a noun by taking the suffix '''*-gAk'''. But '''''*kẹr''''' is a noun, and it becomes a verb by taking the suffix '''*-gA-''', and then it becomes a noun again by taking the suffix '''''*-k'''''. In Lir, same noun takes the '''*-lIg''' verb deriavtional suffix from noun.

== Dead Verbs ==

=== Dead Verbs ===
We come across dead verbs from time to time in Proto languages. A noun has taken the noun suffix from the verb lives, but the root verb dies when it is not needed enough. Any root used in ancient inscriptions may no longer survive.

Even after splitting into branchs, new roots can be developed. For example, ''çekmek (to pull)'' used only by the Oghuz and Arghu today may be a late formation. While ''havlamak (to bark)'' in Turkish can be associated with the sound of dogs, the word ''ürümek (to bark)'' should have been used more often than ''havlamak''. Because ''ürümek'' comes from Old Turkic ''ür- (to blow)'' and compare to Mongolic ''uri- (to blow)''. This shows that there is a new root born in Anatolia. That's how verbs don't just die, sometimes new roots can be born no matter what century you're in.

Here are some dead verbs from Proto-Turkic language:

'''''*döle-''''' → '''''*dölek''''' (“tranquil, sedate, quiet”)

'''''*topra-''''' (“to turn into dust, dry out”) → '''''*toprak''''' (“earth, soil”)

'''''*süŋ-''''' (“to battle, war”) → '''''*süŋgü''''' (“lance, spear”)

'''''*buŕa-''''' (“to bear a calf”) → '''''*buŕagu''''' (“calf”)

'''*küde-''' → '''''*küdegü''''' (“bridegroom, son-in-law”)

'''''*takï-''''' → '''''*takïgu''''' (“hen”)

'''''*yum-''''' → '''''*yumuĺ''''' (“work”)

'''''*in-''''' → '''''*ingek''''' (“cow”)

'''''*eĺ-(/eĺč-)''''' → '''''*eĺgek''''' (“donkey”)

'''''*čï̄p-''''' → '''''*čï̄pgan''''' (“furuncle; rash, pimple”) (see next lesson verbals for the suffix)
 Next Lesson: [[Proto-Turkic/Verbals|Verbals]]

== References ==
&lt;references/&gt;
{{BookCat}}</text>
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      <contributor>
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        <id>3371989</id>
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      <text bytes="95686" sha1="by1qs4r6xoh61avps8vqt1tog12ozvz" xml:space="preserve">{| class=&quot;wikitable&quot;
|+
! colspan=&quot;3&quot; |Talk Page Archives
|-
|[[User talk:Kittycataclysm/Archive 2022|2022]]
|[[User talk:Kittycataclysm/Archive 2023|2023]]
|[[User talk:Kittycataclysm/Archive 2024|2024]]

|}

== That IP range calculator ==

Following [[phab:T381138|T381138]], I have now become the maintainer of the IP range calculator you like. You can find it [[toolforge:ftools/general/ip-range-calc.html|here]]. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 23:10, 9 January 2025 (UTC)

:Thank you for the heads-up! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:56, 10 January 2025 (UTC)

== A merge and unmerge from two years ago ==

I was browsing through the history merge log when I saw that you merged [[Cookbook:Chicken Bog]] into [[Cookbook:Chicken Bog I]], and then promptly reverted it. What happened here exactly? Could I correct it? [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 15:55, 10 January 2025 (UTC)

:Good question! I can't remember what I was trying to do, but it looks like I didn't succeed at what I wanted based on the log comment. You're just trying to history merge to get [[Cookbook:Chicken Bog I]] to have continuity of history? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:35, 10 January 2025 (UTC)
::I think I figured out your mistake: it outright moved the revisions from the first page to the second, rather than copying them. This would have caused the other two [[Cookbook:Chicken Bog]] pages to have incomplete histories. I think the only solution would be to XML import the pre-April 2023 revisions from the first page to the other three, and I'm not sure if that's the best idea, and I am technically unable to do so. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 16:49, 10 January 2025 (UTC)

== Undeletion request ==

I wouldn't be surprised if you expected this, but I'd like to ask you to undelete the subpages of [[Rotorcraft Fundamentals]] you just deleted with the summary &quot;Use of copyrighted work without permission. Please read Terms of Use: page needs to be imported for attribution&quot;, so that I can do that. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 19:54, 14 January 2025 (UTC)

:Done! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:57, 14 January 2025 (UTC)
::Upon further investigation, this might actually be a rare case where an [[WB:UT|unmerged transwiki]] is ''preferred'' (this is part of why I stopped calling them &quot;bad transwikis&quot;), since only a small portion of the Wikipedia article (with over 2,000 revisions) was copied over. Importation is generally only needed if the ''majority'' of the page is copied across wikis. I'll just leave a null edit providing attribution and add {{tlx|Copied}}. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 21:19, 14 January 2025 (UTC)

== Reusing [[Cookbook:8 Desserts in 1 Pan]] on wikiHow ==

Hi, I am a user on wikiHow, see [[wikihow:User:Xeverything11]]. I would like to create a new recipe on wikiHow. I wanted to let us know if I can give permission to reuse your contributions to this recipe from Wikibooks to wikiHow. I (as a copyright holder) created this recipe on Wikibooks, but you contributed to this recipe.

If not, I'll use the revision before you contributed since I was the only author. 

Wikibooks uses CC-BY-SA 4.0 while wikiHow uses CC-BY-NC-SA 3.0, which both licenses are incompatible due to ShareAlike conditions.

Thanks [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 08:27, 15 January 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] I'm personally fine with this as long as proper attribution is given back to the original recipe page here. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:52, 20 January 2025 (UTC)
::I adapted this [[wikihow:Make-8-Desserts-in-1-Pan|recipe]] on wikiHow with attribution, and got a Rising Star (an achievement used for best new articles on wikiHow). Thank you! [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 19:49, 24 January 2025 (UTC)

== Wikibooks community ==

Hi, @[[User:Kittycataclysm|Kittycataclysm]]!

I am trying to contribute more to English Wikibooks. My main contributions will focus on the Cookbook, especially on Indonesian recipes. Do you have a community group where we can discuss and share ideas together?

I am looking forward to join. Thank you!

[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 08:47, 16 January 2025 (UTC)

:@[[User:Raflinoer32|Raflinoer32]] Sorry I missed this, and welcome! Are you asking about a Cookbook-specific area for discussion? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:39, 20 January 2025 (UTC)
::Yes. Do you know place for this?
::Thank you 
::[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 09:41, 21 January 2025 (UTC)
:::Honestly, there's not a centralized Cookbook-specific discussion space, especially since there aren't currently a ton of active contributors. Some people ask questions at [[Cookbook talk:Table of Contents]]. I'm currently the most consistently active and involved Cookbook editor, so feel free to ask me questions! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:46, 22 January 2025 (UTC)

== Congratulations! ==

[[File:Admin T-shirt.svg|thumb|You get this now.]]
You are now a permanent administrator. Welcome to the team (I am entitled to say this because I technically got the extension a few hours before you did)!{{FBDB}} [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 10:33, 29 January 2025 (UTC)

:Thanks :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:29, 29 January 2025 (UTC)

== Is there a way to contact a Steward on WikiBooks? ==

Hi {{PAGENAME}},
Is there a way to contact a Steward on WB? I tried to find who the active Stewards are here  at [[Special:ActiveUsers?username=&amp;groups%5B%5D=steward&amp;wpFormIdentifier=specialactiveusers]] but nothing shows up.

The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the [[Wikimania-wiki]], but I just visited the [[wikimania 2014 wiki]] and could not  find this backward link. I tried to ask about this  on the [[Wikimania 2014 main-page talk]] but disovered that the Stewards have protected it. 

Is there a way  wikibookians can communicate with Stewards at WB? Thanks in advance for answering this non-urgent question, and apologies for all the red-links which I can bluify if needed. Cheers [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 16:37, 7 February 2025 (UTC)

:@[[User:Ottawahitech|Ottawahitech]] You can ask this on somewhere like [[metawiki:Steward requests/Miscellaneous]]. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 17:01, 7 February 2025 (UTC)
&lt;s&gt;:@[[User:Ottawahitech|Ottawahitech]] seconding what Leaderboard said—we no longer have any active stewards at enWB.&lt;/s&gt; Had a brain fade there and mixed up stewards with bureaucrats. Yes, meta is the place for this. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:15, 7 February 2025 (UTC)
::@Kittycataclysm,@[[User:Leaderboard|Leaderboard]], or anyone else:
::Some wikibookians prefer for various reasons to post only at wb. I myself am indef-blocked at  META so could not participate at [[metawiki:Steward requests/Miscellaneous]] even if I waned to.
::Since [[Wikimania]] is a topic of interest to all members of the [[wikimedia movement]] why can't wikibookians talk to thier elected representatives here? [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:56, 7 February 2025 (UTC)
:::@[[User:Ottawahitech|Ottawahitech]] I can check with the blocking admin to see if they'd be willing to unblock you, if you'd like. The reason things like these are done at Meta is that Meta is a cross-project coordination platform - stewards ''cannot'' be expected to watch every project after all. Now you could message any steward here on Wikibooks if you really wanted to, but that is not normally a good idea. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 02:26, 8 February 2025 (UTC)
::::Wikimania is the annual conference celebrating all the free knowledge projects hosted by the Wikimedia Foundation (WMF).  It is a wikimedia initiative which is meant to help all of our projects (including wikibooks), gain more readership, educate more wiki-editors, foster better communications, and much more.  The wmf has been hosting  a Wikimania-wiki dedicated to each Wikimania annual event since 2004. These wikis contain a wealth of information, but can  benefit from wiki-improvements, starting from spelling and grammar errors that detract from their to appeal to the general membership. It would be nice if Stewards paid more attention to it.
::::@[[User:Leaderboard|Leaderboard]], I truly appreciate your offer, but  I posted this here not in order to get someone to advocate for one unblocking at META. As I said earlier:
::::* &quot;Some wikibookians prefer for various reasons to post only at wb&quot;
::::* &quot;The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the Wikimania-wiki, but I just visited the wikimania 2014 wiki and could not find this backward link. I tried to ask about this on the Wikimania 2014 main-page talk but disovered that the Stewards have protected it&quot; 
::::I would much rather see more wikimedia members question blocking in general at META. One cannot run such large movement of people from different backgrounds and nationalities simply by silencing minorities  IMIO. [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:12, 8 February 2025 (UTC)

== [[Crystal ball]] ==

That page appears to be a mixture of isolated paragraphs from [[w:Crystal ball|Crystal ball]], hence my tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 03:04, 9 February 2025 (UTC)

:Yep, that seems correct! I also queried it simply because it does not seem suitable for inclusion at all. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:09, 9 February 2025 (UTC)

== Question about an edit suggestion ==

Hi Kittycataclysm,

Thanks for the great work you do as an admin! I wanted to clarify a suggestion you made on a recently published page I’m working on. You recommended splitting it into smaller sections—would you suggest creating separate pages for these sections, or would a higher-level header for some topics be sufficient?

Any specific recommendations you have would be greatly appreciated!

Here’s the link to the page I’m referring to: [[Funding and Finance of Transportation Projects in the United States of America]]

Thank you! [[User:Svrmustafa|Svrmustafa]] ([[User talk:Svrmustafa|discuss]] • [[Special:Contributions/Svrmustafa|contribs]]) 18:19, 18 February 2025 (UTC)

:Hi @[[User:Svrmustafa|Svrmustafa]], and thanks for asking! Splitting refers to creating new pages, each with a smaller amount of content. The main page should then contain a table of contents, and each page can contain a navigation template for easier navigation. I'll create the table of contents based on the current work and move some content to one of those pages as an example for you; then, you can do the rest. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:26, 19 February 2025 (UTC)
::Following up on this—I noticed that you use the term &quot;paper&quot;. However, technically Wikibooks hosts books not papers, so you should probably change this wording. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:38, 19 February 2025 (UTC)
== Talkback ==
{{Talkback|Cookbook talk:Chilli Crab|Recipe Questions}} [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 09:54, 19 February 2025 (UTC)

:@[[User:Kittycataclysm|Kittycataclysm]] I also made [[Cookbook:Prata|this]] [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:15, 19 February 2025 (UTC)

== Hello ==

Can you look at my latest recipe? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 00:10, 28 February 2025 (UTC)

:I saw it! It needs a few corrections, which I'll note. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:23, 28 February 2025 (UTC)
::@[[User:Kittycataclysm|Kittycataclysm]] How do you write recipe summary, correct headers [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 06:04, 28 February 2025 (UTC)
:::Please see [[Cookbook:Policy/Recipe template]]. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:08, 28 February 2025 (UTC)
::::ok [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 02:33, 1 March 2025 (UTC)

== Cookbook ==

Hi there, Kittycataclysm. I wandered over here from Wikipedia, and I'm quite enamoured with this cookbook. I noticed you seem to be the one maintaining it, and I thought I'd reach out. Can I really just start cranking out recipes from public domain cookbooks and my family recipes? It's that simple? I was also wondering about the featured recipes section. There's not very many in there, and I imagine there's not very many folks around to do reviews compared to GAR on Wikipedia. How do you handle content review? Thanks. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:51, 1 March 2025 (UTC)

:Hi @[[User:MediaKyle|MediaKyle]] and welcome! For some context, the Cookbook has been around since the very beginning of Wikibooks, but it had gotten into a bit of disarray over the course of about two decades by the time I found it. I started the long process of overhauling, standardizing, and expanding it just over four years ago—I finished standardizing the recipe formatting and quality a while back and am currently working my way through the ingredient pages before moving on to equipment, techniques, and cuisines. You can absolutely add any public domain recipes as well as your own recipes—they just need to conform to the [[Cookbook:Policy/Recipe template|recipe template]] and [[Cookbook:Policy|Cookbook policy overall]]. It's even better if you've made the recipe and can contribute a nice picture and specific guidance/instructions/notes! Please feel free to ask me any questions. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:27, 1 March 2025 (UTC)
::Oh, and regarding the featured recipes section, I actually haven't gotten around to looking into that yet—there's been a lot to do! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:28, 1 March 2025 (UTC)
::That's great, thanks a lot for your response. This is just delightful. Maybe content review is something that we could collaborate on. There's a lot of recipes in here and it would be nice to know which ones are the best. Question for you, [[:Category:Brown sauces]] is really bothering me. How can I move that to Brown sauce recipes? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:29, 1 March 2025 (UTC)
:::Good catch on that category! It seems like it was created two decades ago and never got corrected—feel free to recategorize those recipes. Thank you also for introducing the hideprefix parameter to the category trees—I didn't realize that was an option, and it reduces the visual clutter! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:38, 1 March 2025 (UTC)
::::My pleasure! As I continue to look at the categories, this is actually worse than I thought. We have both [[:Category:Sauce recipes]] and [[:Category:Recipes for condiments]] and I suspect that's just the beginning. I want to go through and categorize everything properly, but the bones aren't even there... How long do I have to be here before it'll let me create and move around categories? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:40, 1 March 2025 (UTC)
:::::Regarding the categories, the category overhauling is in progress, since I address the category when I overhaul the associated page. The variation in titling is actually somewhat deliberate—I started changing it from &quot;____ recipes&quot; in certain cases to solve a particular categorization problem. Sometimes, there is an item that is used in recipes as an ingredient but for which there are also recipes. For example, [[:Category:Recipes for bread]] versus [[:Category:Recipes using bread]]. The different naming scheme is necessary to properly delineate the categories, and I'm working on implementing it a bit more consistently as I go. While you're still getting started, it would be great if you could check with me when something looks odd or out of place—that way I can take a look and weigh in on whether that's normal or not and maybe provide some context. Just off the top of my head, I think you will have to wait for autoreview status to make move changes. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:56, 1 March 2025 (UTC)
::::::I see what you're saying, I've been trying to wrap my head around that. Maybe it would be beneficial to try to put together some sort of a Cookbook MOS regarding category structure? It's kind of all over the place right now. Using your bread example, would it perhaps make more sense to have [[:Category:Bread recipes]] and [[:Category:Recipes using bread]]? There would be no ambiguity with just those two categories, but when you add the extra [[:Category:Recipes for bread]], that's when things start getting a little whacky. What do you think? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:05, 1 March 2025 (UTC)
:::::::Either that or get rid of [[:Category:Bread recipes]] and keep the other two. But one of these categories gotta go, I reckon. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:07, 1 March 2025 (UTC)
::::::::I see you already had the same thought as me. I think all categories should include &quot;for&quot; or &quot;using&quot;. Take for example, [[:Category:Recipes for pancakes]] as opposed to [[:Category:Pancake recipes]]. Well obviously there's no recipes using pancakes. But for something like [[:Category:Recipes for gravy]], there may also be a need for [[:Category:Recipes using gravy]]. The lack of consistency in this regard means the only way to achieve consistency across the categories is by changing them over to that format. Sorry for clogging up your talk page! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:18, 1 March 2025 (UTC)
:::::::::Same heads-up as below—migrating this over to [[Cookbook talk:Table of Contents]] —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:10, 4 March 2025 (UTC)
:Also, on [[Cookbook:Table of Contents]], could you please add a wikilink for [[Cookbook:Breakfast]], and maybe add cooknav to the top for seamless navigation between all the top level articles? Can't edit that article yet. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:47, 1 March 2025 (UTC)

== More Table of Content Edits ==

Hello again. I've been going through everything and this is my list of suggestions for edits to the table of contents. Unfortunately there's not much else I can do for now, because without autoconfirmed my ability to change anything is very limited. I was going to ask for someone to check off the confirmed box for me at RfP but I can't post there either, so I guess I'll be back in four days.

* Fix Bread wikilink
* Remove &quot;Creaming&quot; from techniques, redirected to Mixing
* [[Cookbook:History of Food and Cooking]] points to redirect, needs capitalized
* [[Cookbook:Low-Carb]] points to redirect, needs capitalized
* [[Cookbook:Cuisine of the Mediterranean]] to [[Cookbook:Mediterranean Cuisine]] for parity
* Remove the S from the cuisine wikilinks on ToC, currently redirecting
* Create [[:Category:Lunch recipes]], wikilink to ToC
* Wikilink [[Cookbook:Dessert]] under Meals
* Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category
* Create [[Cookbook:East Asian Cuisine]] so I can add the recipes from [[:Category:East Asian recipes]] to it; currently is a redlink on the ToC
* Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;
* Appendix and Equipment sections switch places

Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:46, 1 March 2025 (UTC)

:I took the liberty of doing it myself in my userspace. You can just copy it over from [[User:MediaKyle/sandbox]]. Figured I'd save you the trouble of trying to figure out what I'm talking about. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 14:15, 1 March 2025 (UTC)
:Circling back to this! It seems like your suggestions are getting at a couple different things. I'll try to go through them point-by-point below:
:* {{xt|Fix Bread wikilink}} {{done}}
:* {{xt|Remove &quot;Creaming&quot; from techniques, redirected to Mixing}} see below comments on TOC.
:* {{xt|Cookbook:History of Food and Cooking points to redirect, needs capitalized}} {{not done}} for now because I don't fully understand the urgency and I want to triage/prioritize things for you, but please feel free to make this change yourself once you can!
:* {{xt|Cookbook:Low-Carb points to redirect, needs capitalized}} {{not done}} for same reason as above.
:* {{xt|Cookbook:Cuisine of the Mediterranean to Cookbook:Mediterranean Cuisine for parity}} {{not done}} for now just because we do have a lot of cuisine pages that follow the form &quot;Cuisine of ____&quot;. It could be good to standardize, and I had been planning to do that once I got around to the cuisines.
:* {{xt|Remove the S from the cuisine wikilinks on ToC, currently redirecting}} {{not done}} for same reason as other redirects
:* {{xt|Create Category:Lunch recipes, wikilink to ToC}} Not quite sure what you mean here, and I didn't see what it corresponded to in your linked sandbox page
:* {{xt|Wikilink Cookbook:Dessert under Meals}} {{done}}
:* {{xt|Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category}} I'm not sure about this—brunch is in many places considered a separate entity, and I don't necessarily think it would cause confusion. But, overall it's hard to determine whether it should have its own page and TOC link because I haven't actually gotten around to evaluating the meal pages and what role they should play. See also the TOC notes below.
:* {{xt|Create Cookbook:East Asian Cuisine so I can add the recipes from Category:East Asian recipes to it; currently is a redlink on the ToC}} {{done}} for now; however, I'm not sure yet whether it will ultimately make sense to keep that as a content page. I think content pages should be reasonably focused, and it may not be the best to have a cuisine page that is so broad. This is something I planned to consider once I made my way around the overhauling the cuisines.
:* {{xt|Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;}} The reason I made it &quot;Introductory Matter&quot; instead of &quot;Introduction&quot; is because there's already a chapter itself titled &quot;Introduction&quot;—it felt odd to have the entire section titled that as well. Happy to discuss other header options (e.g. &quot;Front Matter&quot;, which is a generally accepted book term)
:* {{xt|Appendix and Equipment sections switch places}} see below comments on TOC.
:* '''Comments on the TOC:''' So, I think a fundamental issue with the current TOC is that it somewhat arbitrarily picks and chooses individual pages to link. It also sometimes direct-links to categories and sometimes to content pages, which I don't think we should do. Because the cookbook is so expansive, it's been established that manual indices intending to capture detail in large areas don't really make sense and quickly get bulky and out-of-date. This is why categorytree is such a useful tool! After thinking on it for a while and making some small tweaks, I think I'd ultimately like to overhaul the TOC and come to a solution that keeps a few broad headers/links to the small handful of the primary content pages while perhaps stashing away more detailed and self-updating lists in a collapsible way to reduce clutter but allow for customizable user navigation. Much to think about, and I'll probably workshop some things on the side to see how they feel.
:Let me know if I've misunderstood anything! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:24, 3 March 2025 (UTC)
::Thanks for the notes! Here's my thoughts:
::* On the Cuisine titling, it actually seems like [[Cookbook:Cuisine of the Mediterranean]] and [[Cookbook:East Asian cuisines]] are the only ones that don't follow the naming scheme, i.e. &quot;[[Cookbook:African Cuisine]]&quot;, and I think that shorter titles are preferable where it makes sense.
::* On your note about East Asian Cuisine, I actually had the same thought after going through the cuisine pages. Having three separate pages for different kinds of Asian cuisine does seem a little silly, doesn't it? Do you think it might be better to combine all of them under one &quot;Asian Cuisine&quot;, but put the different locales under separate headers?
::* On Brunch - I honestly think there's way too much ambiguity around what exactly constitutes as &quot;brunch&quot; to keep that in. I feel as though the term brunch more applies to the time you're eating, rather than the kind of food. I think it would be easier to keep meals that include commonly accepted breakfast foods in the Breakfast category, and things that don't fit neatly into that, into the Lunch category. This would prevent any dilemmas in the future where we can't decide whether something is breakfast or brunch.
::* You're right that it looks a little awkward to have the header as Introduction when there's a page called introduction. I still think that to say &quot;Introductory Matter&quot;, or &quot;Front Matter&quot; as you mentioned, is a little long-winded and reflects a more academic tone than needed for a cookbook. Upon further reflection, I think maybe rather than worrying about the header at this point, we should perhaps think about trying to compile all of those short introductory type pages into one comprehensive introductory page. Then we likely won't even need a header for it on the ToC.
::* The ToC is definitely a bit cluttered, and it bothers me too that there's a real lack of consistency across whether the wikilinks lead to a page or a category. I'm not sure how I would feel about cutting away too much of the navigation from it, though, because just about every page on there does have a reason to be there, it's just that they're not presented very nicely. Some of it can certainly get nested or combined though. I'll play around with it over the next few days in my sandbox as well and let you know if I come up with anything.
::* As an aside, the first thing on my to-do list once my autoconfirmed comes through is to start subcategorizing all of the recipes so that they're all nicely sorted in the category trees. When you have a chance, I'd love to hear your thoughts on what we should use as the standard naming for categories. Once we determine this, I think we can also take the liberty of updating the cookbook MoS to reflect it.
::Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:33, 3 March 2025 (UTC)
:::Note: After writing this, I realized what you were getting at about slashing away some of the subpages. Maybe we can come up with a system where all of those subpages are under their main subpage rather than on the ToC. For example, all the Cuisines are under [[Cookbook:Cuisines]], all techniques under [[Cookbook:Cooking Techniques]], to keep the subpages off the main ToC. Also, I wonder if maybe we should try to make a centralized discussion for this somewhere, in case anyone else wants to join in at some point? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:45, 3 March 2025 (UTC)
::::Heads-up: to make it easier to keep track of these and since I think they deserve their own discussions, I'm going to gradually migrate them over individually to [[Cookbook talk:Table of Contents]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:52, 4 March 2025 (UTC)
:::::Good idea. Can you remove the semi-protection from that talk page? I see no reason why it should be protected. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:23, 4 March 2025 (UTC)

== Cookbook ToC ==

Hi [[User:Kittycataclysm|Kittycataclysm]]. I was just wondering why you didn't respond to my above message, and started a separate sandbox for the ToC instead? It seems as though you don't really want to collaborate. It would be nice if we could work on this together. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 22:43, 2 March 2025 (UTC)

:@[[User:MediaKyle|MediaKyle]] thanks for the ping! I'm sorry you feel like I don't want to collaborate—the opposite is true, and please understand that this is good-faith editing. The reason I haven't responded to the above points is mostly since you've been modifying a bunch of content and adding suggestions lately, and I've been working my way through these while continuing with my routine contributions and real life as well—things happen a little more slowly here than on other projects, and I'm the one person dedicated to the cookbook right now. The reason I created that sandbox was because I saw [[Wikibooks:Reading room/General#Modernize the shelves|your comment]] at the reading room and wanted to play around and think about your suggestion without touching the actual TOC. You're right that it's not the best, and it's been something I've been thinking about for a bit now. Please understand also that it can be overwhelming when a new editor unfamiliar with the Cookbook begins making a high volume of edits and suggestions without having much experience with it or its history—this isn't to say that you don't have good ideas or things worth contributing. In fact, you have already made a few helpful changes, as I've mentioned. I just want to do this properly and take the time to evaluate your suggestions together with the current efforts that are underway, and that can take a bit. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:03, 2 March 2025 (UTC)
::Thanks for getting back to me. While I may be new to Wikibooks, I'm certainly not new to MediaWiki, and I've been working with small wiki projects for a number of years. Perhaps it's been a misunderstanding to some degree, but I've found my reception here to be unusually unwelcoming. The way to do this properly, as you said, would be to have discussions and form consensus. Yesterday, when you reached out to me about adding hideroot to the pages, I gave you my rationale and was more than happy to have a discussion about it, but you did not reply. I noticed a similar situation happened with [https://en.wikibooks.org/wiki/User_talk:Ottawahitech#Category_sorting Ottawahitech], regarding category sorting. I'm aware that you're the main person looking after the cookbook right now, which is why I reached out to you right from the get go.
::I understand why you would want to create your own sandbox to play around with options for the ToC, but I'm sure you can understand why it would draw my attention that you would do this without implementing any of the wikilink fixes I mentioned, or making an attempt to discuss it further. This came across to me as not wanting my help.
::I invite you to check out my page on Wikipedia. I've made contributions across quite a wide area of topics there, as well as the other Wikimedia projects, and this is the first time I've encountered any sort of resistance to my contributions. I think Wikibooks has enormous potential, and I'm very excited to contribute to helping it grow. On most projects, this would be something to be encouraged. I don't feel like &quot;I'm sorry that you feel that way&quot; was really an appropriate response. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:59, 2 March 2025 (UTC)
:::I think you're right that this has been a mix of misunderstanding and miscommunication, and I think I can understand how things came across as unwelcoming! For whatever it's worth, I absolutely plan on circling back to the various discussions at hand (I have all the relevant pages open to return to), but it seems like the order I did things made it seem like I was ignoring you (if I'm understanding correctly). I am pretty busy, so sometimes items on my to-do list do get lost/shunted or it takes me a bit to get around to something—please don't hesitate to give me a ping if it seems like I'm taking a while to get back to something. Looking forward to more collaboration! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:49, 3 March 2025 (UTC)
::::I'm glad you can understand where I'm coming from. To clarify, my intent is not to try to rush you, or to try to push you to make changes that you don't agree with. It's really easy to misinterpret things over the Internet, and I think a short message can go a long way. I apologize if I've caused you any undue stress by coming into the cookbook and unleashing a flurry of alterations, but do rest assured that I'm not married to any of my changes, I'm always open for discussion, and I want to see the cookbook improve just like you do. The great thing about wikis is that no change is permanent. I think we'll have it in tip-top shape in no time! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:19, 3 March 2025 (UTC)

== [[Cookbook:Polish Doughnuts (Paczki)]] ==

Do you see any reason not to just add this to Featured Recipes? At least we know this one works, and it seems like this is now one of the few recipes to have a picture that actually aligns with the recipe used. I was thinking later on we'll come up with a content review system where a couple editors will actually try the recipes nominated for FR, but in the absence of that I'd just add it to the list. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 12:25, 4 March 2025 (UTC)

:I'm fine with adding it to the featured recipes. You're right that we'll want to come up with a good system for this going forward, though it's lower down on my personal priority list at moment. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 March 2025 (UTC)

== [[Cookbook:Cream Cheese American Buttercream]] ==

Hi! I am a wikiHow user and I am planning to adapt this recipe to wikiHow. Since you contributed to this recipe, I wanted to know if I can get permission to reuse your contributions to this recipe. Thanks. [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 21:41, 4 March 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] that's fine with me as long as proper attribution and linking back to the original recipe page here are included at the top. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:28, 4 March 2025 (UTC)

== [[A Companion to Our Literary Journey]] ==

Hi! I feel that we have started to outline the scope in a clearer and more precise way and that’s the work we are going to do with the students this and for the next years, adding more sections and content. Do you think that would be enough? [[User:Ferdi2005|Ferdi2005]] ([[User talk:Ferdi2005|discuss]] • [[Special:Contributions/Ferdi2005|contribs]]) 22:43, 6 March 2025 (UTC)

:Hi @[[User:Ferdi2005|Ferdi2005]]! Yes, this seems to be reasonably outlined. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:51, 7 March 2025 (UTC)

== Exercising care with copyright ==

When deleting a page as a copyright violation, it is important that you '''do not quote any content from the deleted page'''. If you do, then your log entry is itself a copyright violation. I have redacted a recent deletion that you performed because of this. If you want to make sure that none of your past deletions have been problematic for this reason, you can [[quarry:query/90444|run this SQL query]] to get a list of every deletion that could be eligible for redaction. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 18:32, 21 March 2025 (UTC)

:Hi @[[User:JJPMaster|JJPMaster]] and thank you for the message. In the most recent instance that I think you're referencing, I do not see any material in the edit summary that posed a significant risk—I don't believe the few listed words would be a copyright concern. However, I do understand your concern! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:31, 21 March 2025 (UTC)

== Splitting Pages ==

Hi I have recently made the book on the [[History of the Nawabs of Bengal]] and you gave a notice on how you believe it should be split into smaller bits. As I am still new to wikibooks I don't know how to do this. Can you please assist me on renaming the page so I can split the page into multiple pages? @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 19:47, 29 March 2025 (UTC)

:@[[User:Greatswrd|Greatswrd]]: You did it. I've removed the tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 22:44, 29 March 2025 (UTC)
:Like @[[User:JJPMaster|JJPMaster]] said, you're all set! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:53, 29 March 2025 (UTC)
::Thanks! @[[User:JJPMaster|JJPMaster]] @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 10:24, 30 March 2025 (UTC)

== Minecraft book ==

Is it good creating pages like this, [[Minecraft#Husk]]? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 12:43, 9 May 2025 (UTC)

:@[[User:Cactusisme|Cactusisme]] what do you mean? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:18, 10 May 2025 (UTC)
::are we allowed to create pages like that? like for every mob [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:02, 11 May 2025 (UTC)
:::To be honest, I don't think the structure and formatting of the book is very good. Several of the mob pages, for example, have very little information and aren't particularly helpful on their own. If I were working on it, I would restructure the book. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 14:09, 11 May 2025 (UTC)
::::I am planning to do that. [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 04:19, 12 May 2025 (UTC)

== Request to Review Adjusted User Page (XoriantTeam) ==

Hello [[User:Kittycataclysm|Kittycataclysm]],

I hope you're well. I noticed that my user page ([[User:XoriantTeam]]) was recently deleted for appearing promotional or inappropriate for Wikibooks. Thank you for keeping the community standards in check.

I’ve since revised the content with closer attention to neutrality and compliance with Wikibooks guidelines. My intent is to participate constructively, especially in areas related to digital engineering and educational content creation.

If possible, I’d appreciate your help reviewing the revised version. I'm happy to share it or upload it as a file if there’s a preferred method.

Please let me know how best to proceed. I welcome any suggestions and will gladly make further adjustments.

Best regards,  

XoriantTeam [[User:XoriantTeam|XoriantTeam]] ([[User talk:XoriantTeam|discuss]] • [[Special:Contributions/XoriantTeam|contribs]]) 11:02, 15 May 2025 (UTC)

:Hi there—you can publish an updated user page, but I'd caution you against talking about your company. Keep it limited to your involvement with Wikibooks. You may contribute productively here, but further promotional materials are grounds for an indefinite block. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 12:30, 15 May 2025 (UTC)

== Planning to use AWB to update categories on the cookbook ==

Hello. I noticed in recent changes that you were moving some categories using HotCat (e.g. moving Category:Chile recipes to Category:Recipes using chile), which can be time-consuming. Therefore, I plan to help you with moving the cookbook categories by adding myself to enabledusers and enabledbots in [[Wikibooks:AutoWikiBrowser/CheckPageJSON]]. Would this be fine if I assist you and to add myself to the check page? I am familiar with using AWB after testing on a non-Wikimedia project. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:42, 8 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—thank you for the tip! I just installed JWB, so this should make my mass cat changes much faster. Thanks again! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:11, 8 June 2025 (UTC)
:: Thank you for the information. Also, is it okay if I change (for example) [[:Category:Vinegar recipes]] to [[:Category:Recipes using vinegar]] (I can redirect the former category to the latter), given that we should move {{tq|Category:[ingredient] recipes}} to {{tq|Category:Recipes using [ingredient]}} for consistency? [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:57, 8 June 2025 (UTC)
:::Sure thing—go ahead! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:53, 8 June 2025 (UTC)

== Tool for even faster category changes ==

See [[:c:Help:Gadget-Cat-a-lot#As_your_user_gadget]]. I just [https://en.wikibooks.org/w/index.php?title=User:Koavf/common.js&amp;action=history installed it] and used it dozens of times in a click. Let me know if you need any help. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:36, 19 June 2025 (UTC)

:@[[User:Koavf|Koavf]] Thanks! I'm having a little trouble activating it, but I'll keep trying. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:54, 19 June 2025 (UTC)
::A lot of times, a purge will do the trick. See [[:mw:Purge]]. Usually just &lt;kbd&gt;Ctrl+Shift+R&lt;/kbd&gt; once or twice. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:55, 19 June 2025 (UTC)
:::Took several purges, but we're set now! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:16, 19 June 2025 (UTC)

== Advice on when I should run for adminship ==

Hi, I hope you are doing well. I am asking for some advice on when I should run for enwikibooks adminship, given the following below:

Currently, I am doing some optimizations for dark mode on this project, and some of the message box/MediaWiki interface/template pages might be outdated, fully protected, or can use a little help using mw-parser-output. These unfortunately might hinder the process of updating these pages/templates for Vector 2022's dark mode.&lt;br&gt;
Additionally, I have a solid expertise with edit filters, as I have requested some administrators to update deprecated filter variables, switching filters from warn and disallow to disallow only, and I can also monitor the filter log for potential false positives (from local or global filters).

A fellow English Wikibooks administrator also said to me that they are willing to support me in a few months when I run for adminship, as I am generally trusted.

I hold two advanced global permissions, and I hold an edit filter helper permission on the English Wikipedia, to be sure. Thank you for your consideration. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 01:02, 23 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—good question! I agree that you are a trusted user, and I think it would be reasonable for you to run for adminship, especially given our need to fix up technical aspects of the project. If you don't plan to commit to Wikibooks long-term (i.e. you have some projects you'd like to take a few months to complete and then be done), you can always request temporary adminship. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:30, 23 June 2025 (UTC)
:: Thank you for your feedback, but I also plan to monitor for vandalism/spam, and to commit to reduce the administrative assistance reading room backlog, should I be elected for adminship (and I forgot to mention those). Anyway, regarding your feedback, I might run by August or even July, given that I've lately started contributing more often to Wikibooks. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:29, 23 June 2025 (UTC)
::: [[User:Kittycataclysm|Kittycataclysm]], I am pinging you one more time to see if you have read my response above yours. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:34, 26 June 2025 (UTC)
::::Hi @[[User:Codename Noreste|Codename Noreste]]! I'm not sure what you mean—was there an additional question you had? Everything you've outlined seems quite reasonable. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:26, 26 June 2025 (UTC)
::::: Apologies for the confusion, I don't have any questions to ask. I was clarifying that I can help with implementing edit requests and to block obvious vandals and spammers, aside from the skills I mentioned earlier. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:32, 26 June 2025 (UTC)

== how is it you feel able to interfere in my sandbox? ==

you deleted a page in my sandbox that was my way of providing my response to a request from an OpenSCAD dev team leader for a couple of text blurbs for use on a web page of the OpenSCAD site.

now that you have deleted my page i have to recreate the texts from a screenshot to be able to offer the suggestions, which i will 

This kind of high handed treatment is what keeps me from being a wiki-anything contributor .. If it is Wiki policy to interfere in the documentation of an open source project because it is hosted on Wikibooks then i will take up the task of moving our online docs to a site where you cannot interfere.
--
[[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 21:56, 29 June 2025 (UTC)

:Hi @[[User:VulcanWikiEdit|VulcanWikiEdit]]—thanks for bringing this to my attention. I now understand that this was intended to be in your user namespace—I've undeleted it and moved it to the correct namespace for you. Let me know if anything else comes up! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:05, 30 June 2025 (UTC)
::ah .. err .. umm .. well that is a gentle answer to my ire. Thanks for being so gracious [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:29, 30 June 2025 (UTC)
::and .. isn't my sandbox in my namespace by default? [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:30, 30 June 2025 (UTC)
:::No worries—it looks like you didn't add the prefix &quot;User:&quot; before writing out the full page titles, so the pages you created were technically in the project's Main space with the official published materials. Going forward, you can just double-check that the page title starts with &quot;'''User:'''VulcanWikiEdit/sandbox&quot;, and that should keep everything in the right place! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:36, 30 June 2025 (UTC)
::::BTW .. i love the play on cat lover name [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 15:35, 1 July 2025 (UTC)
:::::Thank you! That's very kind. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:46, 1 July 2025 (UTC)

== Regarding the user Codename Tameirao ==

Could this be Matthew again (the Unicode LTA)? I believe it might be him based on his usage of edit summaries, and his usual edits to [[Unicode/Versions]]. I just blocked his recent account, and then I protected and stabilized that Unicode book. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 23:51, 12 August 2025 (UTC)

:I suspect you're right! That seems like a reasonable course of action. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:56, 13 August 2025 (UTC)
:: I recently encountered another possible LTA, see [[Special:Contributions/~2025-55706-6]] (as well as [[Unicode/Roadmap Blocks]]). I can email you more details if you want. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 16:30, 9 September 2025 (UTC)
:::I think this is the same LTA, yes! I've protected [[Unicode/Roadmap Blocks]], but I think it would be a good idea if we could automate this monitoring somewhat using the edit filter. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:07, 9 September 2025 (UTC)
:::: I don't think that was Matthew, as he typically uses edit summaries. The deleted page was not protected, as it was protected before you deleted it; I salted it from creation for one year. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 20:22, 9 September 2025 (UTC)
::::: You might want to look at [[Special:Contributions/Freddy Fazbearing Others]]. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:18, 26 October 2025 (UTC)
::::::Thank you! I went ahead and blocked them. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:54, 28 October 2025 (UTC)

== IP block exempt  ==

Hi Kitty,
I currently have IP block exemption on enwiki, Commons and Wikidata as I use VPNs connected to my internet security software. Can you please grant me the right on wikibooks. I have a strong password and use two factor authentication. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 10:51, 22 August 2025 (UTC)

:Hi @[[User:TarnishedPath|TarnishedPath]]! This doesn't sound unreasonable to me, but I think it would be good if you requested at [[Wikibooks:Requests for permissions]] so we can have a discussion—I have not granted this right before. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:50, 23 August 2025 (UTC)
::Kitty, thanks for pointing me in the right direction. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:25, 23 August 2025 (UTC)
::See [[Wikibooks:Requests_for_permissions#TarnishedPath_(discuss_·_contribs_·_count_·_logs_·_block_log_·_rfp_·_rights)_(IP_Block_Exemption)]] ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:35, 23 August 2025 (UTC)
== You've got mail! ==
{{You've got mail|sig=&lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 00:20, 6 September 2025 (UTC)}}

:Thank you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:06, 6 September 2025 (UTC)

== Are you able to import? ==

I made a few requests over at https://en.wikibooks.org/wiki/Wikibooks:Requests_for_import . [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 22:32, 4 October 2025 (UTC)
: [[User:2005-Fan|2005-Fan]], I'll go ahead and start the imports. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:29, 5 October 2025 (UTC)
::Thank you for your help [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 16:51, 5 October 2025 (UTC)
::: My apologies for not doing this sooner, because some database error appears when I am trying to mass import. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 23:39, 5 October 2025 (UTC)
::::I also tried to make this import earlier and ran into issues with the software. I was hoping it was a temporary bug, but it seems to be persisting. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:01, 6 October 2025 (UTC)
:::::This seems like I should get involved. {{working}}... [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 13:11, 6 October 2025 (UTC)
:::::: I believe there are five pages that have massive page histories they fail to import here. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:13, 6 October 2025 (UTC)
:::::::I backed up the XMLs of them locally but im unsure how much that'd do. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 15:18, 6 October 2025 (UTC)
::::::::Just became an importer. The reason is prob understandable but I cannot upload the XML file to here locally. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 17:23, 10 October 2025 (UTC)

== About the category parameter in the recipe summary template ==

When it uses a &quot;recipe by type&quot; category, should it use a &quot;[type/food] recipes&quot; name or &quot;Recipes for [type/food]&quot;?

I recently operated JWB to change from [[:Category:Dessert recipes]] to [[:Category:Recipes for dessert]] in multiple Cookbook recipes, and from what I've said before, I've changed to ''Recipes for dessert'' in the category parameter of Cookbook recipes. Hope you don't mind that this was over more than 250 changes (not counting the recent category changes after moving some recipe categories). Thanks. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 02:07, 27 October 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—those JWB changes you made seem fine to me! I'm not quite sure what you're asking in your first sentence, though. Assuming I understand correctly: in general, I think the default format should be whatever the actual category name is. BUT if there is a redirect, it ultimately shouldn't matter too much. And, because I'm not convinced of the utility of that infobox parameter in the first place (thinking of removing it), I'm not hugely concerned about it for the time being. Does this help? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:21, 27 October 2025 (UTC)
:: Probably, but I will say the following below (for my first sentence) to clarify:
:: On the &lt;code&gt;|category =&lt;/code&gt; parameter, when placing a recipe category name, should it either be {{tq|Sandwich recipes}} or {{tq|Recipes for sandwiches}}? I hope this clears the confusion. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:39, 27 October 2025 (UTC)

== Please no more Unicode LTA ==

Please don't block me again. I promise I will edit Unicode stuff and add correct information. [[Special:Contributions/&amp;#126;2025-30839-28|&amp;#126;2025-30839-28]] ([[User talk:&amp;#126;2025-30839-28|talk]]) 20:54, 1 November 2025 (UTC)
:&lt;small&gt;I am a bit out of the loop, so correct me if I'm wrong - I'm assuming here&lt;/small&gt; I think the point is that they want you to ''not'' edit the Unicode stuff? Also hi kitty, it's been a ... very long time.. &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:13, 5 November 2025 (UTC)
::Ok so apparently not as long as I thought, but it feels like I've been away for at least a year lol &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:23, 5 November 2025 (UTC)
:::Nice to see you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:41, 5 November 2025 (UTC)

== Administrator and reviewer user right combinations are not needed anymore ==

Given that administrators can review edits in addition to reviewers, I would suggest for you (and other administrators) to kindly remove the reviewer permission from (own) accounts. What I'm saying is that if one holds administrator and reviewer permissions together, they can remove the reviewer permission from their own account and retain their administrator permission. Thanks. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:06, 11 November 2025 (UTC)

:Gotcha—is there a reason it's bad for one user to have both these rights? If so, I can remove my reviewer right. Otherwise, it seems fairly harmless? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:26, 11 November 2025 (UTC)
:: The thing is, administrators have the &lt;code&gt;review&lt;/code&gt; user right, as well as some permissions in the reviewer user group in the administrator toolset. That means that having the reviewer user group together with the admin user group is redundant. Hope this explains it. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 19:59, 11 November 2025 (UTC)
::: @[[User:Kittycataclysm|Kittycataclysm]] &lt;s&gt;I'll do this tomorrow morning, as well as to remove autoreviewed user permissions from users who are reviewers.&lt;/s&gt; ({{doing}}) [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:24, 12 November 2025 (UTC)
: I have removed the autoreviewed user permission from users who are reviewers. As for administrators, I will do so later today. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:40, 13 November 2025 (UTC)

== Nesting in Open Book of Ecovillages and Eco Communities  ==

Hi Kittycataclysm,

I am editor of wikipedia since 2004. We have the habit if we have a concern using the talk page to clarify the case. I am not sure to delete meaningful content without previous notification and doing major redirection without agreeing the main contributor(s) is an adequate admin act and sign of good manner of host (see [[W:Wikipedia:Etiquette|Wikipedia:Etiquette]].)

Yes, It will be not an average book but above the regular. This is the exact case: ''&quot;this may be appropriate, such as with large textbooks that contain subsections with a lot of content.&quot;'' ''for to establish good structural and stylistic practices''

I have a data management certification. If you asking it will have 4 nest level on strict purpose. If you saw the introduction of the [[Open Book of Ecovillages and Eco Communities]] is/will be a global collection making effective collaboration over borders and continents. One structured + categorized(!) page for each community willing to show up. The Postal addresses has also same or larger deepness, this is unavoidable (Country/Postal Code/Location/Street/House/floor/door). Here will looks like: '''Eco-comm/Continent/Regio code/Community name'''

The goal of this system to open bridge + experience highway  for the communities using the same permaculture technics what collected parallelly in [[Open Book of Permaculture]]. That is also part of this knowledge base please dont do simplification steps on that without discussion.

I am kindly asking to revert your edits in this book.

After that I will put a notification template  about 
 &quot;This book is under construction with major changes. Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History. Common clarifications/ guides are on the primary talk page.&quot;


Thanks: [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 02:22, 12 November 2025 (UTC)

:Hi @[[User:Rodrigo|Rodrigo]], and thank you both for your contributions and for reaching out! Yes, I did make the following changes to [[Open Book of Ecovillages and Eco Communities]]:
:* I moved the pages from the [[Eco-comm]] namespace to the [[Open Book of Ecovillages and Eco Communities]] namespace, since the table of contents and pages for a given book should be under that book's namespace.
:* I removed the links to Wikipedia that were on [[Open Book of Ecovillages and Eco Communities]], since outlinking has been discouraged at en.Wikibooks as a matter of practice. Compilations of links may not fall into WB scope as an instructional text, and [[Wikibooks:Requests for deletion/Piano Solo Music: An Encyclopedia|there is precedent for deleting them]]. But, I do see that the tool I used didn't just remove links to enWP, so I will restore the prior revision and ping the tool developer.
:* I flagged it as needing denesting—you're right that nested entries can sometimes be appropriate. In this case, I was primarily flagging for a denest because the table of contents needs to be moved onto the main page, and it shouldn't have hidden navigation within the nested portions.
:Could you clarify which of these edits you do not agree with so I can make sure they are individually addressed? As an aside, it could be helpful to create a [[Help:Local manuals of style|local manual of style]] for the book in order to clearly outline the expectations. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:59, 12 November 2025 (UTC)
::My main concern not about moving and flagging but '''deleting''' [[Eco-comm]] against [[Wikibooks:Deletion policy]] and not mentioning in the clarification even after my notification. Should I note all administrators [[Wikibooks:Please do not bite the newcomers]] - or will they do speedy deleting one by one until I make them individually addressed?
:::The &lt;u&gt; local manual of style&lt;/u&gt; development is ongoing together with the sample pages.
::'''MAIN PAGE'''
::The '''Main page''' and '''Namespace''' is the [[Eco-comm]]. The '''Full Title''' or '''Cover''' is [[Open Book of Ecovillages and Eco Communities]]. Because of the high level of nesting the below extra-long-full-text-title to be avoided the Cover page is a redirection with preface/intro etc.
::'''NESTING '''
:::Featured book with 3 level nesting: [[Social and Cultural Foundations of American Education/Educational Change/Theory]]
:::5 level nesting example: [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]]
::'''Categories''' The [[:Category:Eco-comm]] will let the users make practical sub-categories e.g. [[:Category:Eco-comm/Project/numundo]] [[:Category:Eco-comm/]]
:::
::[[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 03:44, 18 November 2025 (UTC)
:::Thank you for elaborating! I'm unfortunately not sure what you mean about deleting [[Eco-comm]]—are you referring to the fact that I moved it without leaving a redirect? Regarding the nesting, I do honestly think those other books you linked should have their navigation denested since I find their format difficult to parse, and they have some navigation issues. Looping in some other active admins (@[[User:Leaderboard|Leaderboard]] @[[User:MarcGarver|MarcGarver]] @[[User:JJPMaster|JJPMaster]] @[[User:Codename Noreste|Codename Noreste]] (@[[User:SHB2000|SHB2000]]) so they can get eyes on this and voice anything they think is important. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 04:12, 18 November 2025 (UTC)
::::It makes no sense to have some crazy abbreviation as a &quot;main page&quot; or &quot;namespace&quot; (whatever that means in this context) for a book in order to allow it to be deep nested. Nobody needs to type the whole name of the nesting because that's what navigation templates do, and it is a simple matter to override the page title. I also take issue with the statement, above, &quot;Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History.&quot; Anybody can edit, and nobody gets to own and control any work. Taken together, this complaint looks like a case of attempting to assert ownership and to operate against the normal practices of Wikibooks. As such, I am completely aligned with the changes made. [[User:MarcGarver|MarcGarver]] ([[User talk:MarcGarver|discuss]] • [[Special:Contributions/MarcGarver|contribs]]) 12:49, 18 November 2025 (UTC)
:::::That. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 14:59, 18 November 2025 (UTC)
::::Thanks @[[User:MarcGarver|MarcGarver]]@[[User:Leaderboard|Leaderboard]] for the contribution, btw the [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]] also looks crazy long, is'nt it? Lets continue in the [[Wikibooks:Reading_room/General]] keeping this page for personal messages. [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 23:07, 20 November 2025 (UTC)

== Deletions of Wikibook subpages ==

Hello @[[User:Kittycataclysm|Kittycataclysm]],

regarding the [[Thesis Writing Guide]] subpage deletions, should I just recreate them when I keep working on them or was there an automatic deletion that we could undo? This document will grow, but really slowly.

Best,
Tim [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 11:37, 16 December 2025 (UTC)

:Hi @[[User:TimBorgNetzWerk|TimBorgNetzWerk]]! Since there was so little content on the deleted pages, my recommendation would just be for you to gradually recreate the chapters as you go. Does that make sense? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:54, 17 December 2025 (UTC)
::Makes sense, not my ideal solution, but also not far from it :) The end result will be the same, the in-between will just feel a little bit weird from time to time.
::Thank you for taking time to curate and quality-control Wikibooks - wishing wonderful holidays and a happy new year! [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 20:43, 17 December 2025 (UTC)
:::Thank you, and happy holidays to you as well :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:13, 17 December 2025 (UTC)

== help with &quot;Media Literacy and You&quot; == 

{{re|Kittycataclysm}} What do I need to do to get a quality review of ''[[Media Literacy and You]]'', or whatever is needed to remove &lt;nowiki&gt;{{Qr-em|not clear how this is to be structured as a book}}&lt;/nowiki&gt;? 

I ask, because you added that flag just over 2 hours after I created it. I later found that I had accidentally created it as an anonymous user. I've since started using my standard Wikiname, and I tried to respond to the requests both by creating a discussion on the &quot;Discussion&quot; page associated with that book and by upgrading the content. 

The upgrades included adding the &quot;Introduction&quot; chapter by revising an article on Wikiversity that convinced me to start this Wikibook. I have other articles that I plan to rewrite to create 9 of the remaining 11 chapters in the current table of contents, as indicated in this table of contents. 

??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:23, 8 February 2026 (UTC)

:Hi @[[User:DavidMCEddy|DavidMCEddy]]! I removed the query flag, since this is clearly not a test page. I do have concerns about the suitability of this book for Wikibooks, since it seems to be more in line with essays and original research/analysis (which are [[Wikibooks:WIW|out of scope here]]). Wikiversity seems like a very suitable place for them—is there a specific reason you want to move them here? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:24, 8 February 2026 (UTC)

::{{re|Kittycataclysm}} 
::This book is intended to accelerate the diffusion of [[w:Media literacy|media literacy]] by making it easier for humans to (a) access training materials and (b) connect with research on the most important issues that concern them and (c) discuss those issues with others who may believe differently in a nonthreatening context that encourages dialogue and a shared search for what can honestly be said about any particular issue. This is an extension of &quot;The wisdom of polarized crowds&quot; discussed in [[Wikipedia:Reliability of Wikipedia]]. 

::I don't know about you, but I'm frightened by the collapse of nuclear arms control agreements since the year 2000, by global warming, by the threats of the Trump administration to invade Canada and Greenland, etc. If this book project is successful, it will make a material contribution to reversing these trends -- unless this kind of dialogue is [[v:Responding to a nuclear attack|interrupted by a nuclear war]]. 

=== Who is DavidMCEddy ===

::I'm a [[w:Vietnam veteran|Vietnam-era veteran]] with a PhD in statistics and a publication record for which [https://www.researchgate.net/profile/Spencer-Graves-3 ReserchGate has found over 1,200 academic publications that have cited my work.] Since  [https://xtools.wmcloud.org/ec/en.wikipedia.org/DavidMCEddy 2010 I have logged]
*  6,000+ edits in each of Wikipedia and Wikiversity, 
*  1,000+ in Wikimedia Commons, 
* 30,000+ in Wikidata, and 
* almost 1,000 in other Wikimedia Foundation projects like Wikiquote and edits to the Spanish, French and German Wikipedias. 

This includes dozens of research reports posted to Wikiversity under [[v:Category:Freedom and abundance]] and 44 posts under [[v:Category:Media reform to improve democracy]] that provide a platform for documenting and discussing 44 episodes of a fortnightly &quot;Media &amp; Democracy&quot; series of 29:00 mm:ss podcasts syndicated for the [https://pacificanetwork.org/stations-2/ Pacifica Radio Network] featuring the opinions of leading experts on the increase in political polarization and violence and what those experts think should be done about this. 

I've just posted another chapter to [[Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. I hope you will agree that this book can make a positive contribution to Wikibooks and to [[w:Jimmy Wales|Jimbo Wales]]' [[w:Wikipedia:Prime objective|Prime Directive]] to create &quot;a world in which every single person on the planet is given free access to the sum of all human knowledge.&quot; Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 01:19, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Thank you and I understand this, but I am asking why you think this material is more suitable at Wikibooks rather than at Wikiversity. From what I can see, Wikiversity seems like the more appropriate home for it given our [[Wikibooks:WIW|scope]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:59, 9 February 2026 (UTC)

::{{re|Kittycataclysm}} 

::&quot;Media Literacy and You&quot; is textbook to support both self study and classes on media literacy. 

::I have been posting content to Wikiversity since 2014 and have not encountered support there for books. A search just now turned up a hint of a book on Wikiversity, but I could not easily find anything on how to do it, etc.  

::I think this &quot;Media Literacy and You&quot; project would lose the vast majority of its potential if it were not on Wikibooks. 

::??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:22, 9 February 2026 (UTC)

{{outdent}}

{{re|Kittycataclysm}} 
Will you please help me with the protocols of creating a book on Wikiversity? 

1. I have found documentation that claims that Wikiversity supports such. However, the documentation seems incomplete, potentially out of date, etc. For example, I could not see how to follow the instructions for [[Wikiversity:Help:Books#Step 1: Enable the &quot;Book creator&quot; tool]]. So I posted a question to [[Wikiversity:Help talk:Books]]. 

2. What do you suggest I do next? 

:I can create an article on Wikiversity titled, &quot;Media Literacy and You&quot;, and port everything I've posted to Wikibooks there, then replace the pages on Wikibooks with redirects to [[Wikiversity:Media Literacy and You]], [[Wikiversity:Media Literacy and You/Introduction]], and [[Wikiversity:Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. 

:If you think that's the best way to build this book project, great. It would actually be easier for me, because there would be less translation between what I already have on Wikiversity and a version for Wikibooks. (Also, Wikiversity supports &lt;nowiki&gt;{{cite Q|...}}&lt;/nowiki&gt;, which I have used extensively for years.) 

:Thanks for your help. [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 13:26, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Unfortunately, I am not familiar with the exact workings of Wikiversity, so I can't be much help there. My personal recommendation is that you ask there for help on how best to structure your materials to match the WV requirements. If you'd like some additional opinions/insight, please feel free to also check in at the [[Wikibooks:Reading room/General|reading room]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:22, 10 February 2026 (UTC)

::{{re|Kittycataclysm}} I believe I have finished migrating all of ''Media Literacy and You'' to Wikiversity and replacing the parts of it on Wikibooks with redirects. Comments? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 17:32, 10 February 2026 (UTC)

== Thank you!  ==

Heya, thanks for reviewing my stuff! Just to note, the first lesson page was done and so that'll need moving. If you want to discuss anything with me, I am easily reachable on Discord @ xiluosi233. I can explain philosophy, approach, and so on from my teaching experience if you want anything regarding that. [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:48, 17 February 2026 (UTC)

:It appears [[An Introduction to the Han Script]] was moved wrong - should it not be [[General Literary Chinese from Scratch/An Introduction to the Han Script]]? [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:52, 17 February 2026 (UTC)
::@[[User:Shira the Mogul|Shira the Mogul]] good catch! I accidentally removed more of the title than intended. I've fixed this now. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:18, 18 February 2026 (UTC)

== A test request ==

Just to see whether a recent Luna update turned out as intended, could you briefly revert your [[User:Kittycataclysm/lunaoptions.json|Luna preferences page]] to the first revision? Since you don't appear to have any custom preferences in the first place, I don't think there should be any conflicts. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 01:49, 30 March 2026 (UTC)

:Done! But, it seems to have perhaps auto-updated again immediately afterwards. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:39, 10 April 2026 (UTC)

== Linking ==
Hi,&lt;br&gt;
For my edification, why is a link from [[Cookbook:nettle|nettle]] to [[w:Urtica_dioica|Urtica dioica]] not appropriate? The Wikipedia article has more information &amp; seems relevant.&lt;br&gt;
Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 01:53, 24 April 2026 (UTC)

:@[[User:PeterEasthope|PeterEasthope]] good question! Wikibooks discourages outlinking, since books should be self-contained units. Instead of linking to [[w:Urtica dioica]], the correct approach would be to flesh out the actual chapter here at Wikibooks. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:34, 24 April 2026 (UTC)
::Should all material in the Wikipedia article about Urtica dioica relevant to cooking be duplicated into the nettle article in the cookbook? Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 02:30, 2 May 2026 (UTC)
:::@[[User:PeterEasthope|PeterEasthope]] you could do that, although you should only include information that is sourced. However, I recommend that you wait, because I am coincidentally working on the page right now and fleshing it out significantly. I should publish today. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:40, 2 May 2026 (UTC)
::::The nettle page is better now. Thanks.
::::I still wonder, given that the link to ''The Complete Guide to Edible Wild Plants, ...'' is permitted, why not a link to the botanically oriented page in Wikipedia. What if someone reads the Cookbook article and is interested in the toxin for example? Seems that non-Wikimedia references are more privileged than Wikimedia references.
::::Also, by chance, just noticed the [[w:Nettle_soup|Nettle soup]] article in Wikipedia. Better in the Cookbook?
::::Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 19:10, 5 May 2026 (UTC)
:::::Another good question. The reason those books are linked is because they are reputable and topical sources for the subject matter (nettles as used in cooking from an instructional perspective), and the links are part of the citations—this makes it different from a simple outlink to a Wikipedia page. Wikipedia pages should also not be cited themselves as sources. Regarding nettle soup, I don't think it makes sense to have that as a standalone page here in the cookbook due to its encyclopedic tone, and I don't see any recipes there. Does this make sense? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:21, 6 May 2026 (UTC)
::::::Somewhat. Certainly a recipe wouldn't be incongruous in a cookbook. Still seems unhelpful that relevant information in Wikipedia is inaccessible from a Wikibook. In effect there's a &quot;Berlin Wall&quot; between two Wikimedia projects. Would a &quot;See also&quot; section be permissible?
::::::Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 14:00, 7 May 2026 (UTC)

== You may be an eligible candidate for the U4C election ==

&lt;div lang=&quot;en&quot; dir=&quot;ltr&quot; class=&quot;mw-content-ltr&quot;&gt;
Greetings,

The [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee|Universal Code of Conduct Coordinating Committee (U4C)]] seeks candidates for the 2026 election. The U4C is the global committee responsible for overseeing enforcement of the [[foundation:Special:MyLanguage/Policy:Universal Code of Conduct|Universal Code of Conduct]]. Elections are held annually, if elected a committee member serves for two years.

This year the U4C requires candidates to hold administrator rights on at least one wiki, which is why you are being contacted as you appear to hold this right. There are other requirements, such as candidates must be at least 18 years old and may not be employed by the Wikimedia Foundation or other related chapters and affiliates. You can find more information in the [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026#Call_for_Candidates|call for candidates on Meta-wiki]]. Additionally, the committee's working language is English; some ability to communicate in English is required.

The election opens on 18 May, if you are eligible and interested you have until 10 May to submit your candidacy. There will week between for candidates to answer questions from the community. Voting takes place privately in [[m:Special:MyLanguage/SecurePoll|SecurePoll]], successful candidates must receive at least 60% support. More information is available on [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026|the 2026 Elections page]], including timelines and other candidacy information. If you read over the material and consider yourself qualified, please consider submitting your name to run for the committee. If you think someone else in your community might be interested and qualified, please encourage them to run.

In partnership with the U4C -- [[m:User:Keegan (WMF)|Keegan (WMF)]] ([[m:User_talk:Keegan (WMF)|talk]]) 18:32, 28 April 2026 (UTC) &lt;/div&gt;
&lt;!-- Message sent by User:Keegan (WMF)@metawiki using the list at https://meta.wikimedia.org/w/index.php?title=User:Keegan_(WMF)/test&amp;oldid=30471751 --&gt;

== Undeletion request ==

Hello,


I am writing to request an undeletion of the page Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad. You stated you are a frequent visitor of the Lentis page and are thus familiar with it. This page was part of a class assignment and was in progress at the time of deletion. The work deleted is what we will be graded on for our class, so we would appreciate the restoration. [[User:Yqj3km|Yqj3km]] ([[User talk:Yqj3km|discuss]] • [[Special:Contributions/Yqj3km|contribs]]) 19:36, 4 May 2026 (UTC)

:@[[User:Yqj3km|Yqj3km]] see my response below regarding undeletion. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 May 2026 (UTC)

== Undeletion request ==

About the page on Lentis called Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad: I, too, request undeletion, please. If the authors made any msitakes, the fault is 100 percent mine, for failing to guide them correctly. Like all chapters in this book, this team's chapter is a class assignment. I will be interested also in the reason for deletion so that I can guide authors better. I want to help my students be constructive contributors. Many thanks!

[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 20:03, 4 May 2026 (UTC)

:Hi @[[User:Norton|Norton]] and thanks for the ping! I deleted it because it was not titled/filed correctly, so I didn't realize it was part of [[Lentis]]. I have undeleted it and moved it to [[Lentis/Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:14, 4 May 2026 (UTC)
::Many, many thanks, @[[User:Kittycataclysm|Kittycataclysm]]! I am very grateful as always for everything you do for Wikibooks!
::[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 22:27, 4 May 2026 (UTC)

== Log in issues ==

Hi, messaging you as you seem to be the most active admin at the moment. I can't log in (as posted at  &lt;bdi&gt;[[Wikibooks:Reading room/Administrative Assistance]] and also on my WP page at&lt;/bdi&gt; [[w:User_talk:Xania]]). Seems to be an issue with extra security for admins? I am asked to use my authenticator app (which I can't as I have never set it up for Wikibooks) or a recovery code (which I don't have). Any idea what I should do in this situation? Xania [[Special:Contributions/&amp;#126;2026-28255-89|&amp;#126;2026-28255-89]] ([[User talk:&amp;#126;2026-28255-89|talk]]) 18:21, 10 May 2026 (UTC)

:Apologies for missing this yesterday! It seems like we have a few people working on it over in the reading room, and I'll keep track there. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:37, 11 May 2026 (UTC)

== Splitting pages ==
FYI, I untagged [[Art Print Production Methods]] as for splitting: the page is rather small with its 20 KB and does not need splitting, in my view. Ideally, there would be an operationalized, fairly detailed policy on the matter, but I do not know of one. Single-page books are in [[:Category:One-page books]]. --[[User:Dan Polansky|Dan Polansky]] ([[User talk:Dan Polansky|discuss]] • [[Special:Contributions/Dan Polansky|contribs]]) 04:45, 20 May 2026 (UTC)

== Slander ==

Your tag is slanderous and very easily proven wrong.[https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654455] Given you likely didn't bother to look at the edit history, I would remind you that your given reason that you think it was AI is because you see the chapter is &quot;numbered&quot;. That however was 100% my own personal decision after I reviewed my work and thought to myself that I later wrote in the introduction that there is a first to fourth chapter. However I thought to myself that the readers would not be easily made aware of what is meant by first to fourth as I didn't number them - so is why I dedicated an entire edit to make it less ambiguous  [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654328]. I should not have to be falsely penalized because I wanted to be more considerate and ensure better clarity. I do however request AI to help me figure out coding like this - [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654329] as I don't know how to link. But I intentionally take great efforts to not rely on AI to write that book and find your wrongful presumptions troubling. [[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 06:00, 15 July 2026 (UTC)

:@[[User:JaredMcKenzie|JaredMcKenzie]] thank you for clarifying! I flagged it for review because it matched a common pattern we see associated with LLM use here. If that is not the case, then nothing needs to happen in that respect; however, you will likely want to fix the lists so that they are correctly formatted in the Wikitext and not hard-written—let me know if you have any questions about that. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:14, 16 July 2026 (UTC)</text>
      <sha1>by1qs4r6xoh61avps8vqt1tog12ozvz</sha1>
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! colspan=&quot;3&quot; |Talk Page Archives
|-
|[[User talk:Kittycataclysm/Archive 2022|2022]]
|[[User talk:Kittycataclysm/Archive 2023|2023]]
|[[User talk:Kittycataclysm/Archive 2024|2024]]

|}

== That IP range calculator ==

Following [[phab:T381138|T381138]], I have now become the maintainer of the IP range calculator you like. You can find it [[toolforge:ftools/general/ip-range-calc.html|here]]. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 23:10, 9 January 2025 (UTC)

:Thank you for the heads-up! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:56, 10 January 2025 (UTC)

== A merge and unmerge from two years ago ==

I was browsing through the history merge log when I saw that you merged [[Cookbook:Chicken Bog]] into [[Cookbook:Chicken Bog I]], and then promptly reverted it. What happened here exactly? Could I correct it? [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 15:55, 10 January 2025 (UTC)

:Good question! I can't remember what I was trying to do, but it looks like I didn't succeed at what I wanted based on the log comment. You're just trying to history merge to get [[Cookbook:Chicken Bog I]] to have continuity of history? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:35, 10 January 2025 (UTC)
::I think I figured out your mistake: it outright moved the revisions from the first page to the second, rather than copying them. This would have caused the other two [[Cookbook:Chicken Bog]] pages to have incomplete histories. I think the only solution would be to XML import the pre-April 2023 revisions from the first page to the other three, and I'm not sure if that's the best idea, and I am technically unable to do so. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 16:49, 10 January 2025 (UTC)

== Undeletion request ==

I wouldn't be surprised if you expected this, but I'd like to ask you to undelete the subpages of [[Rotorcraft Fundamentals]] you just deleted with the summary &quot;Use of copyrighted work without permission. Please read Terms of Use: page needs to be imported for attribution&quot;, so that I can do that. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 19:54, 14 January 2025 (UTC)

:Done! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:57, 14 January 2025 (UTC)
::Upon further investigation, this might actually be a rare case where an [[WB:UT|unmerged transwiki]] is ''preferred'' (this is part of why I stopped calling them &quot;bad transwikis&quot;), since only a small portion of the Wikipedia article (with over 2,000 revisions) was copied over. Importation is generally only needed if the ''majority'' of the page is copied across wikis. I'll just leave a null edit providing attribution and add {{tlx|Copied}}. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 21:19, 14 January 2025 (UTC)

== Reusing [[Cookbook:8 Desserts in 1 Pan]] on wikiHow ==

Hi, I am a user on wikiHow, see [[wikihow:User:Xeverything11]]. I would like to create a new recipe on wikiHow. I wanted to let us know if I can give permission to reuse your contributions to this recipe from Wikibooks to wikiHow. I (as a copyright holder) created this recipe on Wikibooks, but you contributed to this recipe.

If not, I'll use the revision before you contributed since I was the only author. 

Wikibooks uses CC-BY-SA 4.0 while wikiHow uses CC-BY-NC-SA 3.0, which both licenses are incompatible due to ShareAlike conditions.

Thanks [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 08:27, 15 January 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] I'm personally fine with this as long as proper attribution is given back to the original recipe page here. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:52, 20 January 2025 (UTC)
::I adapted this [[wikihow:Make-8-Desserts-in-1-Pan|recipe]] on wikiHow with attribution, and got a Rising Star (an achievement used for best new articles on wikiHow). Thank you! [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 19:49, 24 January 2025 (UTC)

== Wikibooks community ==

Hi, @[[User:Kittycataclysm|Kittycataclysm]]!

I am trying to contribute more to English Wikibooks. My main contributions will focus on the Cookbook, especially on Indonesian recipes. Do you have a community group where we can discuss and share ideas together?

I am looking forward to join. Thank you!

[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 08:47, 16 January 2025 (UTC)

:@[[User:Raflinoer32|Raflinoer32]] Sorry I missed this, and welcome! Are you asking about a Cookbook-specific area for discussion? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:39, 20 January 2025 (UTC)
::Yes. Do you know place for this?
::Thank you 
::[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 09:41, 21 January 2025 (UTC)
:::Honestly, there's not a centralized Cookbook-specific discussion space, especially since there aren't currently a ton of active contributors. Some people ask questions at [[Cookbook talk:Table of Contents]]. I'm currently the most consistently active and involved Cookbook editor, so feel free to ask me questions! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:46, 22 January 2025 (UTC)

== Congratulations! ==

[[File:Admin T-shirt.svg|thumb|You get this now.]]
You are now a permanent administrator. Welcome to the team (I am entitled to say this because I technically got the extension a few hours before you did)!{{FBDB}} [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 10:33, 29 January 2025 (UTC)

:Thanks :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:29, 29 January 2025 (UTC)

== Is there a way to contact a Steward on WikiBooks? ==

Hi {{PAGENAME}},
Is there a way to contact a Steward on WB? I tried to find who the active Stewards are here  at [[Special:ActiveUsers?username=&amp;groups%5B%5D=steward&amp;wpFormIdentifier=specialactiveusers]] but nothing shows up.

The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the [[Wikimania-wiki]], but I just visited the [[wikimania 2014 wiki]] and could not  find this backward link. I tried to ask about this  on the [[Wikimania 2014 main-page talk]] but disovered that the Stewards have protected it. 

Is there a way  wikibookians can communicate with Stewards at WB? Thanks in advance for answering this non-urgent question, and apologies for all the red-links which I can bluify if needed. Cheers [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 16:37, 7 February 2025 (UTC)

:@[[User:Ottawahitech|Ottawahitech]] You can ask this on somewhere like [[metawiki:Steward requests/Miscellaneous]]. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 17:01, 7 February 2025 (UTC)
&lt;s&gt;:@[[User:Ottawahitech|Ottawahitech]] seconding what Leaderboard said—we no longer have any active stewards at enWB.&lt;/s&gt; Had a brain fade there and mixed up stewards with bureaucrats. Yes, meta is the place for this. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:15, 7 February 2025 (UTC)
::@Kittycataclysm,@[[User:Leaderboard|Leaderboard]], or anyone else:
::Some wikibookians prefer for various reasons to post only at wb. I myself am indef-blocked at  META so could not participate at [[metawiki:Steward requests/Miscellaneous]] even if I waned to.
::Since [[Wikimania]] is a topic of interest to all members of the [[wikimedia movement]] why can't wikibookians talk to thier elected representatives here? [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:56, 7 February 2025 (UTC)
:::@[[User:Ottawahitech|Ottawahitech]] I can check with the blocking admin to see if they'd be willing to unblock you, if you'd like. The reason things like these are done at Meta is that Meta is a cross-project coordination platform - stewards ''cannot'' be expected to watch every project after all. Now you could message any steward here on Wikibooks if you really wanted to, but that is not normally a good idea. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 02:26, 8 February 2025 (UTC)
::::Wikimania is the annual conference celebrating all the free knowledge projects hosted by the Wikimedia Foundation (WMF).  It is a wikimedia initiative which is meant to help all of our projects (including wikibooks), gain more readership, educate more wiki-editors, foster better communications, and much more.  The wmf has been hosting  a Wikimania-wiki dedicated to each Wikimania annual event since 2004. These wikis contain a wealth of information, but can  benefit from wiki-improvements, starting from spelling and grammar errors that detract from their to appeal to the general membership. It would be nice if Stewards paid more attention to it.
::::@[[User:Leaderboard|Leaderboard]], I truly appreciate your offer, but  I posted this here not in order to get someone to advocate for one unblocking at META. As I said earlier:
::::* &quot;Some wikibookians prefer for various reasons to post only at wb&quot;
::::* &quot;The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the Wikimania-wiki, but I just visited the wikimania 2014 wiki and could not find this backward link. I tried to ask about this on the Wikimania 2014 main-page talk but disovered that the Stewards have protected it&quot; 
::::I would much rather see more wikimedia members question blocking in general at META. One cannot run such large movement of people from different backgrounds and nationalities simply by silencing minorities  IMIO. [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:12, 8 February 2025 (UTC)

== [[Crystal ball]] ==

That page appears to be a mixture of isolated paragraphs from [[w:Crystal ball|Crystal ball]], hence my tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 03:04, 9 February 2025 (UTC)

:Yep, that seems correct! I also queried it simply because it does not seem suitable for inclusion at all. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:09, 9 February 2025 (UTC)

== Question about an edit suggestion ==

Hi Kittycataclysm,

Thanks for the great work you do as an admin! I wanted to clarify a suggestion you made on a recently published page I’m working on. You recommended splitting it into smaller sections—would you suggest creating separate pages for these sections, or would a higher-level header for some topics be sufficient?

Any specific recommendations you have would be greatly appreciated!

Here’s the link to the page I’m referring to: [[Funding and Finance of Transportation Projects in the United States of America]]

Thank you! [[User:Svrmustafa|Svrmustafa]] ([[User talk:Svrmustafa|discuss]] • [[Special:Contributions/Svrmustafa|contribs]]) 18:19, 18 February 2025 (UTC)

:Hi @[[User:Svrmustafa|Svrmustafa]], and thanks for asking! Splitting refers to creating new pages, each with a smaller amount of content. The main page should then contain a table of contents, and each page can contain a navigation template for easier navigation. I'll create the table of contents based on the current work and move some content to one of those pages as an example for you; then, you can do the rest. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:26, 19 February 2025 (UTC)
::Following up on this—I noticed that you use the term &quot;paper&quot;. However, technically Wikibooks hosts books not papers, so you should probably change this wording. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:38, 19 February 2025 (UTC)
== Talkback ==
{{Talkback|Cookbook talk:Chilli Crab|Recipe Questions}} [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 09:54, 19 February 2025 (UTC)

:@[[User:Kittycataclysm|Kittycataclysm]] I also made [[Cookbook:Prata|this]] [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:15, 19 February 2025 (UTC)

== Hello ==

Can you look at my latest recipe? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 00:10, 28 February 2025 (UTC)

:I saw it! It needs a few corrections, which I'll note. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:23, 28 February 2025 (UTC)
::@[[User:Kittycataclysm|Kittycataclysm]] How do you write recipe summary, correct headers [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 06:04, 28 February 2025 (UTC)
:::Please see [[Cookbook:Policy/Recipe template]]. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:08, 28 February 2025 (UTC)
::::ok [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 02:33, 1 March 2025 (UTC)

== Cookbook ==

Hi there, Kittycataclysm. I wandered over here from Wikipedia, and I'm quite enamoured with this cookbook. I noticed you seem to be the one maintaining it, and I thought I'd reach out. Can I really just start cranking out recipes from public domain cookbooks and my family recipes? It's that simple? I was also wondering about the featured recipes section. There's not very many in there, and I imagine there's not very many folks around to do reviews compared to GAR on Wikipedia. How do you handle content review? Thanks. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:51, 1 March 2025 (UTC)

:Hi @[[User:MediaKyle|MediaKyle]] and welcome! For some context, the Cookbook has been around since the very beginning of Wikibooks, but it had gotten into a bit of disarray over the course of about two decades by the time I found it. I started the long process of overhauling, standardizing, and expanding it just over four years ago—I finished standardizing the recipe formatting and quality a while back and am currently working my way through the ingredient pages before moving on to equipment, techniques, and cuisines. You can absolutely add any public domain recipes as well as your own recipes—they just need to conform to the [[Cookbook:Policy/Recipe template|recipe template]] and [[Cookbook:Policy|Cookbook policy overall]]. It's even better if you've made the recipe and can contribute a nice picture and specific guidance/instructions/notes! Please feel free to ask me any questions. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:27, 1 March 2025 (UTC)
::Oh, and regarding the featured recipes section, I actually haven't gotten around to looking into that yet—there's been a lot to do! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:28, 1 March 2025 (UTC)
::That's great, thanks a lot for your response. This is just delightful. Maybe content review is something that we could collaborate on. There's a lot of recipes in here and it would be nice to know which ones are the best. Question for you, [[:Category:Brown sauces]] is really bothering me. How can I move that to Brown sauce recipes? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:29, 1 March 2025 (UTC)
:::Good catch on that category! It seems like it was created two decades ago and never got corrected—feel free to recategorize those recipes. Thank you also for introducing the hideprefix parameter to the category trees—I didn't realize that was an option, and it reduces the visual clutter! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:38, 1 March 2025 (UTC)
::::My pleasure! As I continue to look at the categories, this is actually worse than I thought. We have both [[:Category:Sauce recipes]] and [[:Category:Recipes for condiments]] and I suspect that's just the beginning. I want to go through and categorize everything properly, but the bones aren't even there... How long do I have to be here before it'll let me create and move around categories? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:40, 1 March 2025 (UTC)
:::::Regarding the categories, the category overhauling is in progress, since I address the category when I overhaul the associated page. The variation in titling is actually somewhat deliberate—I started changing it from &quot;____ recipes&quot; in certain cases to solve a particular categorization problem. Sometimes, there is an item that is used in recipes as an ingredient but for which there are also recipes. For example, [[:Category:Recipes for bread]] versus [[:Category:Recipes using bread]]. The different naming scheme is necessary to properly delineate the categories, and I'm working on implementing it a bit more consistently as I go. While you're still getting started, it would be great if you could check with me when something looks odd or out of place—that way I can take a look and weigh in on whether that's normal or not and maybe provide some context. Just off the top of my head, I think you will have to wait for autoreview status to make move changes. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:56, 1 March 2025 (UTC)
::::::I see what you're saying, I've been trying to wrap my head around that. Maybe it would be beneficial to try to put together some sort of a Cookbook MOS regarding category structure? It's kind of all over the place right now. Using your bread example, would it perhaps make more sense to have [[:Category:Bread recipes]] and [[:Category:Recipes using bread]]? There would be no ambiguity with just those two categories, but when you add the extra [[:Category:Recipes for bread]], that's when things start getting a little whacky. What do you think? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:05, 1 March 2025 (UTC)
:::::::Either that or get rid of [[:Category:Bread recipes]] and keep the other two. But one of these categories gotta go, I reckon. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:07, 1 March 2025 (UTC)
::::::::I see you already had the same thought as me. I think all categories should include &quot;for&quot; or &quot;using&quot;. Take for example, [[:Category:Recipes for pancakes]] as opposed to [[:Category:Pancake recipes]]. Well obviously there's no recipes using pancakes. But for something like [[:Category:Recipes for gravy]], there may also be a need for [[:Category:Recipes using gravy]]. The lack of consistency in this regard means the only way to achieve consistency across the categories is by changing them over to that format. Sorry for clogging up your talk page! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:18, 1 March 2025 (UTC)
:::::::::Same heads-up as below—migrating this over to [[Cookbook talk:Table of Contents]] —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:10, 4 March 2025 (UTC)
:Also, on [[Cookbook:Table of Contents]], could you please add a wikilink for [[Cookbook:Breakfast]], and maybe add cooknav to the top for seamless navigation between all the top level articles? Can't edit that article yet. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:47, 1 March 2025 (UTC)

== More Table of Content Edits ==

Hello again. I've been going through everything and this is my list of suggestions for edits to the table of contents. Unfortunately there's not much else I can do for now, because without autoconfirmed my ability to change anything is very limited. I was going to ask for someone to check off the confirmed box for me at RfP but I can't post there either, so I guess I'll be back in four days.

* Fix Bread wikilink
* Remove &quot;Creaming&quot; from techniques, redirected to Mixing
* [[Cookbook:History of Food and Cooking]] points to redirect, needs capitalized
* [[Cookbook:Low-Carb]] points to redirect, needs capitalized
* [[Cookbook:Cuisine of the Mediterranean]] to [[Cookbook:Mediterranean Cuisine]] for parity
* Remove the S from the cuisine wikilinks on ToC, currently redirecting
* Create [[:Category:Lunch recipes]], wikilink to ToC
* Wikilink [[Cookbook:Dessert]] under Meals
* Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category
* Create [[Cookbook:East Asian Cuisine]] so I can add the recipes from [[:Category:East Asian recipes]] to it; currently is a redlink on the ToC
* Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;
* Appendix and Equipment sections switch places

Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:46, 1 March 2025 (UTC)

:I took the liberty of doing it myself in my userspace. You can just copy it over from [[User:MediaKyle/sandbox]]. Figured I'd save you the trouble of trying to figure out what I'm talking about. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 14:15, 1 March 2025 (UTC)
:Circling back to this! It seems like your suggestions are getting at a couple different things. I'll try to go through them point-by-point below:
:* {{xt|Fix Bread wikilink}} {{done}}
:* {{xt|Remove &quot;Creaming&quot; from techniques, redirected to Mixing}} see below comments on TOC.
:* {{xt|Cookbook:History of Food and Cooking points to redirect, needs capitalized}} {{not done}} for now because I don't fully understand the urgency and I want to triage/prioritize things for you, but please feel free to make this change yourself once you can!
:* {{xt|Cookbook:Low-Carb points to redirect, needs capitalized}} {{not done}} for same reason as above.
:* {{xt|Cookbook:Cuisine of the Mediterranean to Cookbook:Mediterranean Cuisine for parity}} {{not done}} for now just because we do have a lot of cuisine pages that follow the form &quot;Cuisine of ____&quot;. It could be good to standardize, and I had been planning to do that once I got around to the cuisines.
:* {{xt|Remove the S from the cuisine wikilinks on ToC, currently redirecting}} {{not done}} for same reason as other redirects
:* {{xt|Create Category:Lunch recipes, wikilink to ToC}} Not quite sure what you mean here, and I didn't see what it corresponded to in your linked sandbox page
:* {{xt|Wikilink Cookbook:Dessert under Meals}} {{done}}
:* {{xt|Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category}} I'm not sure about this—brunch is in many places considered a separate entity, and I don't necessarily think it would cause confusion. But, overall it's hard to determine whether it should have its own page and TOC link because I haven't actually gotten around to evaluating the meal pages and what role they should play. See also the TOC notes below.
:* {{xt|Create Cookbook:East Asian Cuisine so I can add the recipes from Category:East Asian recipes to it; currently is a redlink on the ToC}} {{done}} for now; however, I'm not sure yet whether it will ultimately make sense to keep that as a content page. I think content pages should be reasonably focused, and it may not be the best to have a cuisine page that is so broad. This is something I planned to consider once I made my way around the overhauling the cuisines.
:* {{xt|Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;}} The reason I made it &quot;Introductory Matter&quot; instead of &quot;Introduction&quot; is because there's already a chapter itself titled &quot;Introduction&quot;—it felt odd to have the entire section titled that as well. Happy to discuss other header options (e.g. &quot;Front Matter&quot;, which is a generally accepted book term)
:* {{xt|Appendix and Equipment sections switch places}} see below comments on TOC.
:* '''Comments on the TOC:''' So, I think a fundamental issue with the current TOC is that it somewhat arbitrarily picks and chooses individual pages to link. It also sometimes direct-links to categories and sometimes to content pages, which I don't think we should do. Because the cookbook is so expansive, it's been established that manual indices intending to capture detail in large areas don't really make sense and quickly get bulky and out-of-date. This is why categorytree is such a useful tool! After thinking on it for a while and making some small tweaks, I think I'd ultimately like to overhaul the TOC and come to a solution that keeps a few broad headers/links to the small handful of the primary content pages while perhaps stashing away more detailed and self-updating lists in a collapsible way to reduce clutter but allow for customizable user navigation. Much to think about, and I'll probably workshop some things on the side to see how they feel.
:Let me know if I've misunderstood anything! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:24, 3 March 2025 (UTC)
::Thanks for the notes! Here's my thoughts:
::* On the Cuisine titling, it actually seems like [[Cookbook:Cuisine of the Mediterranean]] and [[Cookbook:East Asian cuisines]] are the only ones that don't follow the naming scheme, i.e. &quot;[[Cookbook:African Cuisine]]&quot;, and I think that shorter titles are preferable where it makes sense.
::* On your note about East Asian Cuisine, I actually had the same thought after going through the cuisine pages. Having three separate pages for different kinds of Asian cuisine does seem a little silly, doesn't it? Do you think it might be better to combine all of them under one &quot;Asian Cuisine&quot;, but put the different locales under separate headers?
::* On Brunch - I honestly think there's way too much ambiguity around what exactly constitutes as &quot;brunch&quot; to keep that in. I feel as though the term brunch more applies to the time you're eating, rather than the kind of food. I think it would be easier to keep meals that include commonly accepted breakfast foods in the Breakfast category, and things that don't fit neatly into that, into the Lunch category. This would prevent any dilemmas in the future where we can't decide whether something is breakfast or brunch.
::* You're right that it looks a little awkward to have the header as Introduction when there's a page called introduction. I still think that to say &quot;Introductory Matter&quot;, or &quot;Front Matter&quot; as you mentioned, is a little long-winded and reflects a more academic tone than needed for a cookbook. Upon further reflection, I think maybe rather than worrying about the header at this point, we should perhaps think about trying to compile all of those short introductory type pages into one comprehensive introductory page. Then we likely won't even need a header for it on the ToC.
::* The ToC is definitely a bit cluttered, and it bothers me too that there's a real lack of consistency across whether the wikilinks lead to a page or a category. I'm not sure how I would feel about cutting away too much of the navigation from it, though, because just about every page on there does have a reason to be there, it's just that they're not presented very nicely. Some of it can certainly get nested or combined though. I'll play around with it over the next few days in my sandbox as well and let you know if I come up with anything.
::* As an aside, the first thing on my to-do list once my autoconfirmed comes through is to start subcategorizing all of the recipes so that they're all nicely sorted in the category trees. When you have a chance, I'd love to hear your thoughts on what we should use as the standard naming for categories. Once we determine this, I think we can also take the liberty of updating the cookbook MoS to reflect it.
::Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:33, 3 March 2025 (UTC)
:::Note: After writing this, I realized what you were getting at about slashing away some of the subpages. Maybe we can come up with a system where all of those subpages are under their main subpage rather than on the ToC. For example, all the Cuisines are under [[Cookbook:Cuisines]], all techniques under [[Cookbook:Cooking Techniques]], to keep the subpages off the main ToC. Also, I wonder if maybe we should try to make a centralized discussion for this somewhere, in case anyone else wants to join in at some point? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:45, 3 March 2025 (UTC)
::::Heads-up: to make it easier to keep track of these and since I think they deserve their own discussions, I'm going to gradually migrate them over individually to [[Cookbook talk:Table of Contents]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:52, 4 March 2025 (UTC)
:::::Good idea. Can you remove the semi-protection from that talk page? I see no reason why it should be protected. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:23, 4 March 2025 (UTC)

== Cookbook ToC ==

Hi [[User:Kittycataclysm|Kittycataclysm]]. I was just wondering why you didn't respond to my above message, and started a separate sandbox for the ToC instead? It seems as though you don't really want to collaborate. It would be nice if we could work on this together. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 22:43, 2 March 2025 (UTC)

:@[[User:MediaKyle|MediaKyle]] thanks for the ping! I'm sorry you feel like I don't want to collaborate—the opposite is true, and please understand that this is good-faith editing. The reason I haven't responded to the above points is mostly since you've been modifying a bunch of content and adding suggestions lately, and I've been working my way through these while continuing with my routine contributions and real life as well—things happen a little more slowly here than on other projects, and I'm the one person dedicated to the cookbook right now. The reason I created that sandbox was because I saw [[Wikibooks:Reading room/General#Modernize the shelves|your comment]] at the reading room and wanted to play around and think about your suggestion without touching the actual TOC. You're right that it's not the best, and it's been something I've been thinking about for a bit now. Please understand also that it can be overwhelming when a new editor unfamiliar with the Cookbook begins making a high volume of edits and suggestions without having much experience with it or its history—this isn't to say that you don't have good ideas or things worth contributing. In fact, you have already made a few helpful changes, as I've mentioned. I just want to do this properly and take the time to evaluate your suggestions together with the current efforts that are underway, and that can take a bit. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:03, 2 March 2025 (UTC)
::Thanks for getting back to me. While I may be new to Wikibooks, I'm certainly not new to MediaWiki, and I've been working with small wiki projects for a number of years. Perhaps it's been a misunderstanding to some degree, but I've found my reception here to be unusually unwelcoming. The way to do this properly, as you said, would be to have discussions and form consensus. Yesterday, when you reached out to me about adding hideroot to the pages, I gave you my rationale and was more than happy to have a discussion about it, but you did not reply. I noticed a similar situation happened with [https://en.wikibooks.org/wiki/User_talk:Ottawahitech#Category_sorting Ottawahitech], regarding category sorting. I'm aware that you're the main person looking after the cookbook right now, which is why I reached out to you right from the get go.
::I understand why you would want to create your own sandbox to play around with options for the ToC, but I'm sure you can understand why it would draw my attention that you would do this without implementing any of the wikilink fixes I mentioned, or making an attempt to discuss it further. This came across to me as not wanting my help.
::I invite you to check out my page on Wikipedia. I've made contributions across quite a wide area of topics there, as well as the other Wikimedia projects, and this is the first time I've encountered any sort of resistance to my contributions. I think Wikibooks has enormous potential, and I'm very excited to contribute to helping it grow. On most projects, this would be something to be encouraged. I don't feel like &quot;I'm sorry that you feel that way&quot; was really an appropriate response. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:59, 2 March 2025 (UTC)
:::I think you're right that this has been a mix of misunderstanding and miscommunication, and I think I can understand how things came across as unwelcoming! For whatever it's worth, I absolutely plan on circling back to the various discussions at hand (I have all the relevant pages open to return to), but it seems like the order I did things made it seem like I was ignoring you (if I'm understanding correctly). I am pretty busy, so sometimes items on my to-do list do get lost/shunted or it takes me a bit to get around to something—please don't hesitate to give me a ping if it seems like I'm taking a while to get back to something. Looking forward to more collaboration! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:49, 3 March 2025 (UTC)
::::I'm glad you can understand where I'm coming from. To clarify, my intent is not to try to rush you, or to try to push you to make changes that you don't agree with. It's really easy to misinterpret things over the Internet, and I think a short message can go a long way. I apologize if I've caused you any undue stress by coming into the cookbook and unleashing a flurry of alterations, but do rest assured that I'm not married to any of my changes, I'm always open for discussion, and I want to see the cookbook improve just like you do. The great thing about wikis is that no change is permanent. I think we'll have it in tip-top shape in no time! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:19, 3 March 2025 (UTC)

== [[Cookbook:Polish Doughnuts (Paczki)]] ==

Do you see any reason not to just add this to Featured Recipes? At least we know this one works, and it seems like this is now one of the few recipes to have a picture that actually aligns with the recipe used. I was thinking later on we'll come up with a content review system where a couple editors will actually try the recipes nominated for FR, but in the absence of that I'd just add it to the list. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 12:25, 4 March 2025 (UTC)

:I'm fine with adding it to the featured recipes. You're right that we'll want to come up with a good system for this going forward, though it's lower down on my personal priority list at moment. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 March 2025 (UTC)

== [[Cookbook:Cream Cheese American Buttercream]] ==

Hi! I am a wikiHow user and I am planning to adapt this recipe to wikiHow. Since you contributed to this recipe, I wanted to know if I can get permission to reuse your contributions to this recipe. Thanks. [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 21:41, 4 March 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] that's fine with me as long as proper attribution and linking back to the original recipe page here are included at the top. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:28, 4 March 2025 (UTC)

== [[A Companion to Our Literary Journey]] ==

Hi! I feel that we have started to outline the scope in a clearer and more precise way and that’s the work we are going to do with the students this and for the next years, adding more sections and content. Do you think that would be enough? [[User:Ferdi2005|Ferdi2005]] ([[User talk:Ferdi2005|discuss]] • [[Special:Contributions/Ferdi2005|contribs]]) 22:43, 6 March 2025 (UTC)

:Hi @[[User:Ferdi2005|Ferdi2005]]! Yes, this seems to be reasonably outlined. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:51, 7 March 2025 (UTC)

== Exercising care with copyright ==

When deleting a page as a copyright violation, it is important that you '''do not quote any content from the deleted page'''. If you do, then your log entry is itself a copyright violation. I have redacted a recent deletion that you performed because of this. If you want to make sure that none of your past deletions have been problematic for this reason, you can [[quarry:query/90444|run this SQL query]] to get a list of every deletion that could be eligible for redaction. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 18:32, 21 March 2025 (UTC)

:Hi @[[User:JJPMaster|JJPMaster]] and thank you for the message. In the most recent instance that I think you're referencing, I do not see any material in the edit summary that posed a significant risk—I don't believe the few listed words would be a copyright concern. However, I do understand your concern! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:31, 21 March 2025 (UTC)

== Splitting Pages ==

Hi I have recently made the book on the [[History of the Nawabs of Bengal]] and you gave a notice on how you believe it should be split into smaller bits. As I am still new to wikibooks I don't know how to do this. Can you please assist me on renaming the page so I can split the page into multiple pages? @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 19:47, 29 March 2025 (UTC)

:@[[User:Greatswrd|Greatswrd]]: You did it. I've removed the tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 22:44, 29 March 2025 (UTC)
:Like @[[User:JJPMaster|JJPMaster]] said, you're all set! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:53, 29 March 2025 (UTC)
::Thanks! @[[User:JJPMaster|JJPMaster]] @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 10:24, 30 March 2025 (UTC)

== Minecraft book ==

Is it good creating pages like this, [[Minecraft#Husk]]? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 12:43, 9 May 2025 (UTC)

:@[[User:Cactusisme|Cactusisme]] what do you mean? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:18, 10 May 2025 (UTC)
::are we allowed to create pages like that? like for every mob [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:02, 11 May 2025 (UTC)
:::To be honest, I don't think the structure and formatting of the book is very good. Several of the mob pages, for example, have very little information and aren't particularly helpful on their own. If I were working on it, I would restructure the book. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 14:09, 11 May 2025 (UTC)
::::I am planning to do that. [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 04:19, 12 May 2025 (UTC)

== Request to Review Adjusted User Page (XoriantTeam) ==

Hello [[User:Kittycataclysm|Kittycataclysm]],

I hope you're well. I noticed that my user page ([[User:XoriantTeam]]) was recently deleted for appearing promotional or inappropriate for Wikibooks. Thank you for keeping the community standards in check.

I’ve since revised the content with closer attention to neutrality and compliance with Wikibooks guidelines. My intent is to participate constructively, especially in areas related to digital engineering and educational content creation.

If possible, I’d appreciate your help reviewing the revised version. I'm happy to share it or upload it as a file if there’s a preferred method.

Please let me know how best to proceed. I welcome any suggestions and will gladly make further adjustments.

Best regards,  

XoriantTeam [[User:XoriantTeam|XoriantTeam]] ([[User talk:XoriantTeam|discuss]] • [[Special:Contributions/XoriantTeam|contribs]]) 11:02, 15 May 2025 (UTC)

:Hi there—you can publish an updated user page, but I'd caution you against talking about your company. Keep it limited to your involvement with Wikibooks. You may contribute productively here, but further promotional materials are grounds for an indefinite block. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 12:30, 15 May 2025 (UTC)

== Planning to use AWB to update categories on the cookbook ==

Hello. I noticed in recent changes that you were moving some categories using HotCat (e.g. moving Category:Chile recipes to Category:Recipes using chile), which can be time-consuming. Therefore, I plan to help you with moving the cookbook categories by adding myself to enabledusers and enabledbots in [[Wikibooks:AutoWikiBrowser/CheckPageJSON]]. Would this be fine if I assist you and to add myself to the check page? I am familiar with using AWB after testing on a non-Wikimedia project. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:42, 8 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—thank you for the tip! I just installed JWB, so this should make my mass cat changes much faster. Thanks again! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:11, 8 June 2025 (UTC)
:: Thank you for the information. Also, is it okay if I change (for example) [[:Category:Vinegar recipes]] to [[:Category:Recipes using vinegar]] (I can redirect the former category to the latter), given that we should move {{tq|Category:[ingredient] recipes}} to {{tq|Category:Recipes using [ingredient]}} for consistency? [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:57, 8 June 2025 (UTC)
:::Sure thing—go ahead! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:53, 8 June 2025 (UTC)

== Tool for even faster category changes ==

See [[:c:Help:Gadget-Cat-a-lot#As_your_user_gadget]]. I just [https://en.wikibooks.org/w/index.php?title=User:Koavf/common.js&amp;action=history installed it] and used it dozens of times in a click. Let me know if you need any help. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:36, 19 June 2025 (UTC)

:@[[User:Koavf|Koavf]] Thanks! I'm having a little trouble activating it, but I'll keep trying. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:54, 19 June 2025 (UTC)
::A lot of times, a purge will do the trick. See [[:mw:Purge]]. Usually just &lt;kbd&gt;Ctrl+Shift+R&lt;/kbd&gt; once or twice. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:55, 19 June 2025 (UTC)
:::Took several purges, but we're set now! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:16, 19 June 2025 (UTC)

== Advice on when I should run for adminship ==

Hi, I hope you are doing well. I am asking for some advice on when I should run for enwikibooks adminship, given the following below:

Currently, I am doing some optimizations for dark mode on this project, and some of the message box/MediaWiki interface/template pages might be outdated, fully protected, or can use a little help using mw-parser-output. These unfortunately might hinder the process of updating these pages/templates for Vector 2022's dark mode.&lt;br&gt;
Additionally, I have a solid expertise with edit filters, as I have requested some administrators to update deprecated filter variables, switching filters from warn and disallow to disallow only, and I can also monitor the filter log for potential false positives (from local or global filters).

A fellow English Wikibooks administrator also said to me that they are willing to support me in a few months when I run for adminship, as I am generally trusted.

I hold two advanced global permissions, and I hold an edit filter helper permission on the English Wikipedia, to be sure. Thank you for your consideration. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 01:02, 23 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—good question! I agree that you are a trusted user, and I think it would be reasonable for you to run for adminship, especially given our need to fix up technical aspects of the project. If you don't plan to commit to Wikibooks long-term (i.e. you have some projects you'd like to take a few months to complete and then be done), you can always request temporary adminship. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:30, 23 June 2025 (UTC)
:: Thank you for your feedback, but I also plan to monitor for vandalism/spam, and to commit to reduce the administrative assistance reading room backlog, should I be elected for adminship (and I forgot to mention those). Anyway, regarding your feedback, I might run by August or even July, given that I've lately started contributing more often to Wikibooks. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:29, 23 June 2025 (UTC)
::: [[User:Kittycataclysm|Kittycataclysm]], I am pinging you one more time to see if you have read my response above yours. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:34, 26 June 2025 (UTC)
::::Hi @[[User:Codename Noreste|Codename Noreste]]! I'm not sure what you mean—was there an additional question you had? Everything you've outlined seems quite reasonable. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:26, 26 June 2025 (UTC)
::::: Apologies for the confusion, I don't have any questions to ask. I was clarifying that I can help with implementing edit requests and to block obvious vandals and spammers, aside from the skills I mentioned earlier. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:32, 26 June 2025 (UTC)

== how is it you feel able to interfere in my sandbox? ==

you deleted a page in my sandbox that was my way of providing my response to a request from an OpenSCAD dev team leader for a couple of text blurbs for use on a web page of the OpenSCAD site.

now that you have deleted my page i have to recreate the texts from a screenshot to be able to offer the suggestions, which i will 

This kind of high handed treatment is what keeps me from being a wiki-anything contributor .. If it is Wiki policy to interfere in the documentation of an open source project because it is hosted on Wikibooks then i will take up the task of moving our online docs to a site where you cannot interfere.
--
[[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 21:56, 29 June 2025 (UTC)

:Hi @[[User:VulcanWikiEdit|VulcanWikiEdit]]—thanks for bringing this to my attention. I now understand that this was intended to be in your user namespace—I've undeleted it and moved it to the correct namespace for you. Let me know if anything else comes up! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:05, 30 June 2025 (UTC)
::ah .. err .. umm .. well that is a gentle answer to my ire. Thanks for being so gracious [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:29, 30 June 2025 (UTC)
::and .. isn't my sandbox in my namespace by default? [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:30, 30 June 2025 (UTC)
:::No worries—it looks like you didn't add the prefix &quot;User:&quot; before writing out the full page titles, so the pages you created were technically in the project's Main space with the official published materials. Going forward, you can just double-check that the page title starts with &quot;'''User:'''VulcanWikiEdit/sandbox&quot;, and that should keep everything in the right place! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:36, 30 June 2025 (UTC)
::::BTW .. i love the play on cat lover name [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 15:35, 1 July 2025 (UTC)
:::::Thank you! That's very kind. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:46, 1 July 2025 (UTC)

== Regarding the user Codename Tameirao ==

Could this be Matthew again (the Unicode LTA)? I believe it might be him based on his usage of edit summaries, and his usual edits to [[Unicode/Versions]]. I just blocked his recent account, and then I protected and stabilized that Unicode book. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 23:51, 12 August 2025 (UTC)

:I suspect you're right! That seems like a reasonable course of action. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:56, 13 August 2025 (UTC)
:: I recently encountered another possible LTA, see [[Special:Contributions/~2025-55706-6]] (as well as [[Unicode/Roadmap Blocks]]). I can email you more details if you want. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 16:30, 9 September 2025 (UTC)
:::I think this is the same LTA, yes! I've protected [[Unicode/Roadmap Blocks]], but I think it would be a good idea if we could automate this monitoring somewhat using the edit filter. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:07, 9 September 2025 (UTC)
:::: I don't think that was Matthew, as he typically uses edit summaries. The deleted page was not protected, as it was protected before you deleted it; I salted it from creation for one year. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 20:22, 9 September 2025 (UTC)
::::: You might want to look at [[Special:Contributions/Freddy Fazbearing Others]]. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:18, 26 October 2025 (UTC)
::::::Thank you! I went ahead and blocked them. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:54, 28 October 2025 (UTC)

== IP block exempt  ==

Hi Kitty,
I currently have IP block exemption on enwiki, Commons and Wikidata as I use VPNs connected to my internet security software. Can you please grant me the right on wikibooks. I have a strong password and use two factor authentication. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 10:51, 22 August 2025 (UTC)

:Hi @[[User:TarnishedPath|TarnishedPath]]! This doesn't sound unreasonable to me, but I think it would be good if you requested at [[Wikibooks:Requests for permissions]] so we can have a discussion—I have not granted this right before. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:50, 23 August 2025 (UTC)
::Kitty, thanks for pointing me in the right direction. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:25, 23 August 2025 (UTC)
::See [[Wikibooks:Requests_for_permissions#TarnishedPath_(discuss_·_contribs_·_count_·_logs_·_block_log_·_rfp_·_rights)_(IP_Block_Exemption)]] ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:35, 23 August 2025 (UTC)
== You've got mail! ==
{{You've got mail|sig=&lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 00:20, 6 September 2025 (UTC)}}

:Thank you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:06, 6 September 2025 (UTC)

== Are you able to import? ==

I made a few requests over at https://en.wikibooks.org/wiki/Wikibooks:Requests_for_import . [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 22:32, 4 October 2025 (UTC)
: [[User:2005-Fan|2005-Fan]], I'll go ahead and start the imports. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:29, 5 October 2025 (UTC)
::Thank you for your help [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 16:51, 5 October 2025 (UTC)
::: My apologies for not doing this sooner, because some database error appears when I am trying to mass import. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 23:39, 5 October 2025 (UTC)
::::I also tried to make this import earlier and ran into issues with the software. I was hoping it was a temporary bug, but it seems to be persisting. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:01, 6 October 2025 (UTC)
:::::This seems like I should get involved. {{working}}... [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 13:11, 6 October 2025 (UTC)
:::::: I believe there are five pages that have massive page histories they fail to import here. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:13, 6 October 2025 (UTC)
:::::::I backed up the XMLs of them locally but im unsure how much that'd do. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 15:18, 6 October 2025 (UTC)
::::::::Just became an importer. The reason is prob understandable but I cannot upload the XML file to here locally. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 17:23, 10 October 2025 (UTC)

== About the category parameter in the recipe summary template ==

When it uses a &quot;recipe by type&quot; category, should it use a &quot;[type/food] recipes&quot; name or &quot;Recipes for [type/food]&quot;?

I recently operated JWB to change from [[:Category:Dessert recipes]] to [[:Category:Recipes for dessert]] in multiple Cookbook recipes, and from what I've said before, I've changed to ''Recipes for dessert'' in the category parameter of Cookbook recipes. Hope you don't mind that this was over more than 250 changes (not counting the recent category changes after moving some recipe categories). Thanks. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 02:07, 27 October 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—those JWB changes you made seem fine to me! I'm not quite sure what you're asking in your first sentence, though. Assuming I understand correctly: in general, I think the default format should be whatever the actual category name is. BUT if there is a redirect, it ultimately shouldn't matter too much. And, because I'm not convinced of the utility of that infobox parameter in the first place (thinking of removing it), I'm not hugely concerned about it for the time being. Does this help? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:21, 27 October 2025 (UTC)
:: Probably, but I will say the following below (for my first sentence) to clarify:
:: On the &lt;code&gt;|category =&lt;/code&gt; parameter, when placing a recipe category name, should it either be {{tq|Sandwich recipes}} or {{tq|Recipes for sandwiches}}? I hope this clears the confusion. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:39, 27 October 2025 (UTC)

== Please no more Unicode LTA ==

Please don't block me again. I promise I will edit Unicode stuff and add correct information. [[Special:Contributions/&amp;#126;2025-30839-28|&amp;#126;2025-30839-28]] ([[User talk:&amp;#126;2025-30839-28|talk]]) 20:54, 1 November 2025 (UTC)
:&lt;small&gt;I am a bit out of the loop, so correct me if I'm wrong - I'm assuming here&lt;/small&gt; I think the point is that they want you to ''not'' edit the Unicode stuff? Also hi kitty, it's been a ... very long time.. &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:13, 5 November 2025 (UTC)
::Ok so apparently not as long as I thought, but it feels like I've been away for at least a year lol &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:23, 5 November 2025 (UTC)
:::Nice to see you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:41, 5 November 2025 (UTC)

== Administrator and reviewer user right combinations are not needed anymore ==

Given that administrators can review edits in addition to reviewers, I would suggest for you (and other administrators) to kindly remove the reviewer permission from (own) accounts. What I'm saying is that if one holds administrator and reviewer permissions together, they can remove the reviewer permission from their own account and retain their administrator permission. Thanks. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:06, 11 November 2025 (UTC)

:Gotcha—is there a reason it's bad for one user to have both these rights? If so, I can remove my reviewer right. Otherwise, it seems fairly harmless? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:26, 11 November 2025 (UTC)
:: The thing is, administrators have the &lt;code&gt;review&lt;/code&gt; user right, as well as some permissions in the reviewer user group in the administrator toolset. That means that having the reviewer user group together with the admin user group is redundant. Hope this explains it. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 19:59, 11 November 2025 (UTC)
::: @[[User:Kittycataclysm|Kittycataclysm]] &lt;s&gt;I'll do this tomorrow morning, as well as to remove autoreviewed user permissions from users who are reviewers.&lt;/s&gt; ({{doing}}) [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:24, 12 November 2025 (UTC)
: I have removed the autoreviewed user permission from users who are reviewers. As for administrators, I will do so later today. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:40, 13 November 2025 (UTC)

== Nesting in Open Book of Ecovillages and Eco Communities  ==

Hi Kittycataclysm,

I am editor of wikipedia since 2004. We have the habit if we have a concern using the talk page to clarify the case. I am not sure to delete meaningful content without previous notification and doing major redirection without agreeing the main contributor(s) is an adequate admin act and sign of good manner of host (see [[W:Wikipedia:Etiquette|Wikipedia:Etiquette]].)

Yes, It will be not an average book but above the regular. This is the exact case: ''&quot;this may be appropriate, such as with large textbooks that contain subsections with a lot of content.&quot;'' ''for to establish good structural and stylistic practices''

I have a data management certification. If you asking it will have 4 nest level on strict purpose. If you saw the introduction of the [[Open Book of Ecovillages and Eco Communities]] is/will be a global collection making effective collaboration over borders and continents. One structured + categorized(!) page for each community willing to show up. The Postal addresses has also same or larger deepness, this is unavoidable (Country/Postal Code/Location/Street/House/floor/door). Here will looks like: '''Eco-comm/Continent/Regio code/Community name'''

The goal of this system to open bridge + experience highway  for the communities using the same permaculture technics what collected parallelly in [[Open Book of Permaculture]]. That is also part of this knowledge base please dont do simplification steps on that without discussion.

I am kindly asking to revert your edits in this book.

After that I will put a notification template  about 
 &quot;This book is under construction with major changes. Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History. Common clarifications/ guides are on the primary talk page.&quot;


Thanks: [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 02:22, 12 November 2025 (UTC)

:Hi @[[User:Rodrigo|Rodrigo]], and thank you both for your contributions and for reaching out! Yes, I did make the following changes to [[Open Book of Ecovillages and Eco Communities]]:
:* I moved the pages from the [[Eco-comm]] namespace to the [[Open Book of Ecovillages and Eco Communities]] namespace, since the table of contents and pages for a given book should be under that book's namespace.
:* I removed the links to Wikipedia that were on [[Open Book of Ecovillages and Eco Communities]], since outlinking has been discouraged at en.Wikibooks as a matter of practice. Compilations of links may not fall into WB scope as an instructional text, and [[Wikibooks:Requests for deletion/Piano Solo Music: An Encyclopedia|there is precedent for deleting them]]. But, I do see that the tool I used didn't just remove links to enWP, so I will restore the prior revision and ping the tool developer.
:* I flagged it as needing denesting—you're right that nested entries can sometimes be appropriate. In this case, I was primarily flagging for a denest because the table of contents needs to be moved onto the main page, and it shouldn't have hidden navigation within the nested portions.
:Could you clarify which of these edits you do not agree with so I can make sure they are individually addressed? As an aside, it could be helpful to create a [[Help:Local manuals of style|local manual of style]] for the book in order to clearly outline the expectations. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:59, 12 November 2025 (UTC)
::My main concern not about moving and flagging but '''deleting''' [[Eco-comm]] against [[Wikibooks:Deletion policy]] and not mentioning in the clarification even after my notification. Should I note all administrators [[Wikibooks:Please do not bite the newcomers]] - or will they do speedy deleting one by one until I make them individually addressed?
:::The &lt;u&gt; local manual of style&lt;/u&gt; development is ongoing together with the sample pages.
::'''MAIN PAGE'''
::The '''Main page''' and '''Namespace''' is the [[Eco-comm]]. The '''Full Title''' or '''Cover''' is [[Open Book of Ecovillages and Eco Communities]]. Because of the high level of nesting the below extra-long-full-text-title to be avoided the Cover page is a redirection with preface/intro etc.
::'''NESTING '''
:::Featured book with 3 level nesting: [[Social and Cultural Foundations of American Education/Educational Change/Theory]]
:::5 level nesting example: [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]]
::'''Categories''' The [[:Category:Eco-comm]] will let the users make practical sub-categories e.g. [[:Category:Eco-comm/Project/numundo]] [[:Category:Eco-comm/]]
:::
::[[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 03:44, 18 November 2025 (UTC)
:::Thank you for elaborating! I'm unfortunately not sure what you mean about deleting [[Eco-comm]]—are you referring to the fact that I moved it without leaving a redirect? Regarding the nesting, I do honestly think those other books you linked should have their navigation denested since I find their format difficult to parse, and they have some navigation issues. Looping in some other active admins (@[[User:Leaderboard|Leaderboard]] @[[User:MarcGarver|MarcGarver]] @[[User:JJPMaster|JJPMaster]] @[[User:Codename Noreste|Codename Noreste]] (@[[User:SHB2000|SHB2000]]) so they can get eyes on this and voice anything they think is important. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 04:12, 18 November 2025 (UTC)
::::It makes no sense to have some crazy abbreviation as a &quot;main page&quot; or &quot;namespace&quot; (whatever that means in this context) for a book in order to allow it to be deep nested. Nobody needs to type the whole name of the nesting because that's what navigation templates do, and it is a simple matter to override the page title. I also take issue with the statement, above, &quot;Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History.&quot; Anybody can edit, and nobody gets to own and control any work. Taken together, this complaint looks like a case of attempting to assert ownership and to operate against the normal practices of Wikibooks. As such, I am completely aligned with the changes made. [[User:MarcGarver|MarcGarver]] ([[User talk:MarcGarver|discuss]] • [[Special:Contributions/MarcGarver|contribs]]) 12:49, 18 November 2025 (UTC)
:::::That. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 14:59, 18 November 2025 (UTC)
::::Thanks @[[User:MarcGarver|MarcGarver]]@[[User:Leaderboard|Leaderboard]] for the contribution, btw the [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]] also looks crazy long, is'nt it? Lets continue in the [[Wikibooks:Reading_room/General]] keeping this page for personal messages. [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 23:07, 20 November 2025 (UTC)

== Deletions of Wikibook subpages ==

Hello @[[User:Kittycataclysm|Kittycataclysm]],

regarding the [[Thesis Writing Guide]] subpage deletions, should I just recreate them when I keep working on them or was there an automatic deletion that we could undo? This document will grow, but really slowly.

Best,
Tim [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 11:37, 16 December 2025 (UTC)

:Hi @[[User:TimBorgNetzWerk|TimBorgNetzWerk]]! Since there was so little content on the deleted pages, my recommendation would just be for you to gradually recreate the chapters as you go. Does that make sense? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:54, 17 December 2025 (UTC)
::Makes sense, not my ideal solution, but also not far from it :) The end result will be the same, the in-between will just feel a little bit weird from time to time.
::Thank you for taking time to curate and quality-control Wikibooks - wishing wonderful holidays and a happy new year! [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 20:43, 17 December 2025 (UTC)
:::Thank you, and happy holidays to you as well :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:13, 17 December 2025 (UTC)

== help with &quot;Media Literacy and You&quot; == 

{{re|Kittycataclysm}} What do I need to do to get a quality review of ''[[Media Literacy and You]]'', or whatever is needed to remove &lt;nowiki&gt;{{Qr-em|not clear how this is to be structured as a book}}&lt;/nowiki&gt;? 

I ask, because you added that flag just over 2 hours after I created it. I later found that I had accidentally created it as an anonymous user. I've since started using my standard Wikiname, and I tried to respond to the requests both by creating a discussion on the &quot;Discussion&quot; page associated with that book and by upgrading the content. 

The upgrades included adding the &quot;Introduction&quot; chapter by revising an article on Wikiversity that convinced me to start this Wikibook. I have other articles that I plan to rewrite to create 9 of the remaining 11 chapters in the current table of contents, as indicated in this table of contents. 

??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:23, 8 February 2026 (UTC)

:Hi @[[User:DavidMCEddy|DavidMCEddy]]! I removed the query flag, since this is clearly not a test page. I do have concerns about the suitability of this book for Wikibooks, since it seems to be more in line with essays and original research/analysis (which are [[Wikibooks:WIW|out of scope here]]). Wikiversity seems like a very suitable place for them—is there a specific reason you want to move them here? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:24, 8 February 2026 (UTC)

::{{re|Kittycataclysm}} 
::This book is intended to accelerate the diffusion of [[w:Media literacy|media literacy]] by making it easier for humans to (a) access training materials and (b) connect with research on the most important issues that concern them and (c) discuss those issues with others who may believe differently in a nonthreatening context that encourages dialogue and a shared search for what can honestly be said about any particular issue. This is an extension of &quot;The wisdom of polarized crowds&quot; discussed in [[Wikipedia:Reliability of Wikipedia]]. 

::I don't know about you, but I'm frightened by the collapse of nuclear arms control agreements since the year 2000, by global warming, by the threats of the Trump administration to invade Canada and Greenland, etc. If this book project is successful, it will make a material contribution to reversing these trends -- unless this kind of dialogue is [[v:Responding to a nuclear attack|interrupted by a nuclear war]]. 

=== Who is DavidMCEddy ===

::I'm a [[w:Vietnam veteran|Vietnam-era veteran]] with a PhD in statistics and a publication record for which [https://www.researchgate.net/profile/Spencer-Graves-3 ReserchGate has found over 1,200 academic publications that have cited my work.] Since  [https://xtools.wmcloud.org/ec/en.wikipedia.org/DavidMCEddy 2010 I have logged]
*  6,000+ edits in each of Wikipedia and Wikiversity, 
*  1,000+ in Wikimedia Commons, 
* 30,000+ in Wikidata, and 
* almost 1,000 in other Wikimedia Foundation projects like Wikiquote and edits to the Spanish, French and German Wikipedias. 

This includes dozens of research reports posted to Wikiversity under [[v:Category:Freedom and abundance]] and 44 posts under [[v:Category:Media reform to improve democracy]] that provide a platform for documenting and discussing 44 episodes of a fortnightly &quot;Media &amp; Democracy&quot; series of 29:00 mm:ss podcasts syndicated for the [https://pacificanetwork.org/stations-2/ Pacifica Radio Network] featuring the opinions of leading experts on the increase in political polarization and violence and what those experts think should be done about this. 

I've just posted another chapter to [[Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. I hope you will agree that this book can make a positive contribution to Wikibooks and to [[w:Jimmy Wales|Jimbo Wales]]' [[w:Wikipedia:Prime objective|Prime Directive]] to create &quot;a world in which every single person on the planet is given free access to the sum of all human knowledge.&quot; Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 01:19, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Thank you and I understand this, but I am asking why you think this material is more suitable at Wikibooks rather than at Wikiversity. From what I can see, Wikiversity seems like the more appropriate home for it given our [[Wikibooks:WIW|scope]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:59, 9 February 2026 (UTC)

::{{re|Kittycataclysm}} 

::&quot;Media Literacy and You&quot; is textbook to support both self study and classes on media literacy. 

::I have been posting content to Wikiversity since 2014 and have not encountered support there for books. A search just now turned up a hint of a book on Wikiversity, but I could not easily find anything on how to do it, etc.  

::I think this &quot;Media Literacy and You&quot; project would lose the vast majority of its potential if it were not on Wikibooks. 

::??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:22, 9 February 2026 (UTC)

{{outdent}}

{{re|Kittycataclysm}} 
Will you please help me with the protocols of creating a book on Wikiversity? 

1. I have found documentation that claims that Wikiversity supports such. However, the documentation seems incomplete, potentially out of date, etc. For example, I could not see how to follow the instructions for [[Wikiversity:Help:Books#Step 1: Enable the &quot;Book creator&quot; tool]]. So I posted a question to [[Wikiversity:Help talk:Books]]. 

2. What do you suggest I do next? 

:I can create an article on Wikiversity titled, &quot;Media Literacy and You&quot;, and port everything I've posted to Wikibooks there, then replace the pages on Wikibooks with redirects to [[Wikiversity:Media Literacy and You]], [[Wikiversity:Media Literacy and You/Introduction]], and [[Wikiversity:Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. 

:If you think that's the best way to build this book project, great. It would actually be easier for me, because there would be less translation between what I already have on Wikiversity and a version for Wikibooks. (Also, Wikiversity supports &lt;nowiki&gt;{{cite Q|...}}&lt;/nowiki&gt;, which I have used extensively for years.) 

:Thanks for your help. [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 13:26, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Unfortunately, I am not familiar with the exact workings of Wikiversity, so I can't be much help there. My personal recommendation is that you ask there for help on how best to structure your materials to match the WV requirements. If you'd like some additional opinions/insight, please feel free to also check in at the [[Wikibooks:Reading room/General|reading room]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:22, 10 February 2026 (UTC)

::{{re|Kittycataclysm}} I believe I have finished migrating all of ''Media Literacy and You'' to Wikiversity and replacing the parts of it on Wikibooks with redirects. Comments? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 17:32, 10 February 2026 (UTC)

== Thank you!  ==

Heya, thanks for reviewing my stuff! Just to note, the first lesson page was done and so that'll need moving. If you want to discuss anything with me, I am easily reachable on Discord @ xiluosi233. I can explain philosophy, approach, and so on from my teaching experience if you want anything regarding that. [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:48, 17 February 2026 (UTC)

:It appears [[An Introduction to the Han Script]] was moved wrong - should it not be [[General Literary Chinese from Scratch/An Introduction to the Han Script]]? [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:52, 17 February 2026 (UTC)
::@[[User:Shira the Mogul|Shira the Mogul]] good catch! I accidentally removed more of the title than intended. I've fixed this now. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:18, 18 February 2026 (UTC)

== A test request ==

Just to see whether a recent Luna update turned out as intended, could you briefly revert your [[User:Kittycataclysm/lunaoptions.json|Luna preferences page]] to the first revision? Since you don't appear to have any custom preferences in the first place, I don't think there should be any conflicts. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 01:49, 30 March 2026 (UTC)

:Done! But, it seems to have perhaps auto-updated again immediately afterwards. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:39, 10 April 2026 (UTC)

== Linking ==
Hi,&lt;br&gt;
For my edification, why is a link from [[Cookbook:nettle|nettle]] to [[w:Urtica_dioica|Urtica dioica]] not appropriate? The Wikipedia article has more information &amp; seems relevant.&lt;br&gt;
Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 01:53, 24 April 2026 (UTC)

:@[[User:PeterEasthope|PeterEasthope]] good question! Wikibooks discourages outlinking, since books should be self-contained units. Instead of linking to [[w:Urtica dioica]], the correct approach would be to flesh out the actual chapter here at Wikibooks. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:34, 24 April 2026 (UTC)
::Should all material in the Wikipedia article about Urtica dioica relevant to cooking be duplicated into the nettle article in the cookbook? Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 02:30, 2 May 2026 (UTC)
:::@[[User:PeterEasthope|PeterEasthope]] you could do that, although you should only include information that is sourced. However, I recommend that you wait, because I am coincidentally working on the page right now and fleshing it out significantly. I should publish today. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:40, 2 May 2026 (UTC)
::::The nettle page is better now. Thanks.
::::I still wonder, given that the link to ''The Complete Guide to Edible Wild Plants, ...'' is permitted, why not a link to the botanically oriented page in Wikipedia. What if someone reads the Cookbook article and is interested in the toxin for example? Seems that non-Wikimedia references are more privileged than Wikimedia references.
::::Also, by chance, just noticed the [[w:Nettle_soup|Nettle soup]] article in Wikipedia. Better in the Cookbook?
::::Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 19:10, 5 May 2026 (UTC)
:::::Another good question. The reason those books are linked is because they are reputable and topical sources for the subject matter (nettles as used in cooking from an instructional perspective), and the links are part of the citations—this makes it different from a simple outlink to a Wikipedia page. Wikipedia pages should also not be cited themselves as sources. Regarding nettle soup, I don't think it makes sense to have that as a standalone page here in the cookbook due to its encyclopedic tone, and I don't see any recipes there. Does this make sense? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:21, 6 May 2026 (UTC)
::::::Somewhat. Certainly a recipe wouldn't be incongruous in a cookbook. Still seems unhelpful that relevant information in Wikipedia is inaccessible from a Wikibook. In effect there's a &quot;Berlin Wall&quot; between two Wikimedia projects. Would a &quot;See also&quot; section be permissible?
::::::Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 14:00, 7 May 2026 (UTC)

== You may be an eligible candidate for the U4C election ==

&lt;div lang=&quot;en&quot; dir=&quot;ltr&quot; class=&quot;mw-content-ltr&quot;&gt;
Greetings,

The [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee|Universal Code of Conduct Coordinating Committee (U4C)]] seeks candidates for the 2026 election. The U4C is the global committee responsible for overseeing enforcement of the [[foundation:Special:MyLanguage/Policy:Universal Code of Conduct|Universal Code of Conduct]]. Elections are held annually, if elected a committee member serves for two years.

This year the U4C requires candidates to hold administrator rights on at least one wiki, which is why you are being contacted as you appear to hold this right. There are other requirements, such as candidates must be at least 18 years old and may not be employed by the Wikimedia Foundation or other related chapters and affiliates. You can find more information in the [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026#Call_for_Candidates|call for candidates on Meta-wiki]]. Additionally, the committee's working language is English; some ability to communicate in English is required.

The election opens on 18 May, if you are eligible and interested you have until 10 May to submit your candidacy. There will week between for candidates to answer questions from the community. Voting takes place privately in [[m:Special:MyLanguage/SecurePoll|SecurePoll]], successful candidates must receive at least 60% support. More information is available on [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026|the 2026 Elections page]], including timelines and other candidacy information. If you read over the material and consider yourself qualified, please consider submitting your name to run for the committee. If you think someone else in your community might be interested and qualified, please encourage them to run.

In partnership with the U4C -- [[m:User:Keegan (WMF)|Keegan (WMF)]] ([[m:User_talk:Keegan (WMF)|talk]]) 18:32, 28 April 2026 (UTC) &lt;/div&gt;
&lt;!-- Message sent by User:Keegan (WMF)@metawiki using the list at https://meta.wikimedia.org/w/index.php?title=User:Keegan_(WMF)/test&amp;oldid=30471751 --&gt;

== Undeletion request ==

Hello,


I am writing to request an undeletion of the page Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad. You stated you are a frequent visitor of the Lentis page and are thus familiar with it. This page was part of a class assignment and was in progress at the time of deletion. The work deleted is what we will be graded on for our class, so we would appreciate the restoration. [[User:Yqj3km|Yqj3km]] ([[User talk:Yqj3km|discuss]] • [[Special:Contributions/Yqj3km|contribs]]) 19:36, 4 May 2026 (UTC)

:@[[User:Yqj3km|Yqj3km]] see my response below regarding undeletion. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 May 2026 (UTC)

== Undeletion request ==

About the page on Lentis called Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad: I, too, request undeletion, please. If the authors made any msitakes, the fault is 100 percent mine, for failing to guide them correctly. Like all chapters in this book, this team's chapter is a class assignment. I will be interested also in the reason for deletion so that I can guide authors better. I want to help my students be constructive contributors. Many thanks!

[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 20:03, 4 May 2026 (UTC)

:Hi @[[User:Norton|Norton]] and thanks for the ping! I deleted it because it was not titled/filed correctly, so I didn't realize it was part of [[Lentis]]. I have undeleted it and moved it to [[Lentis/Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:14, 4 May 2026 (UTC)
::Many, many thanks, @[[User:Kittycataclysm|Kittycataclysm]]! I am very grateful as always for everything you do for Wikibooks!
::[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 22:27, 4 May 2026 (UTC)

== Log in issues ==

Hi, messaging you as you seem to be the most active admin at the moment. I can't log in (as posted at  &lt;bdi&gt;[[Wikibooks:Reading room/Administrative Assistance]] and also on my WP page at&lt;/bdi&gt; [[w:User_talk:Xania]]). Seems to be an issue with extra security for admins? I am asked to use my authenticator app (which I can't as I have never set it up for Wikibooks) or a recovery code (which I don't have). Any idea what I should do in this situation? Xania [[Special:Contributions/&amp;#126;2026-28255-89|&amp;#126;2026-28255-89]] ([[User talk:&amp;#126;2026-28255-89|talk]]) 18:21, 10 May 2026 (UTC)

:Apologies for missing this yesterday! It seems like we have a few people working on it over in the reading room, and I'll keep track there. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:37, 11 May 2026 (UTC)

== Splitting pages ==
FYI, I untagged [[Art Print Production Methods]] as for splitting: the page is rather small with its 20 KB and does not need splitting, in my view. Ideally, there would be an operationalized, fairly detailed policy on the matter, but I do not know of one. Single-page books are in [[:Category:One-page books]]. --[[User:Dan Polansky|Dan Polansky]] ([[User talk:Dan Polansky|discuss]] • [[Special:Contributions/Dan Polansky|contribs]]) 04:45, 20 May 2026 (UTC)

== Slander ==

Your tag is slanderous and very easily proven wrong.[https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654455] Given you likely didn't bother to look at the edit history, I would remind you that your given reason that you think it was AI is because you see the chapter is &quot;numbered&quot;. That however was 100% my own personal decision after I reviewed my work and thought to myself that I later wrote in the introduction that there is a first to fourth chapter. However I thought to myself that the readers would not be easily made aware of what is meant by first to fourth as I didn't number them - so is why I dedicated an entire edit to make it less ambiguous  [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654328]. I should not have to be falsely penalized because I wanted to be more considerate and ensure better clarity. I do however request AI to help me figure out coding like this - [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654329] as I don't know how to link. But I intentionally take great efforts to not rely on AI to write that book and find your wrongful presumptions troubling. [[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 06:00, 15 July 2026 (UTC)

:@[[User:JaredMcKenzie|JaredMcKenzie]] thank you for clarifying! I flagged it for review because it matched a common pattern we see associated with LLM use here. If that is not the case, then nothing needs to happen in that respect; however, you will likely want to fix the lists so that they are correctly formatted in the Wikitext and not hard-written—let me know if you have any questions about that. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:14, 16 July 2026 (UTC)
::Yeah, I don't really understand what you mean by &quot;correctly formatted&quot; list. I assume you are referring to chapter 4 - (Fourth reading)? What exactly is wrong with it? Could you go and demonstrate what fixing that looks like? I believe I would just quickly learn by seeing what you mean and hopefully know what to do in future. [[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 18:35, 16 July 2026 (UTC)</text>
      <sha1>ogx3l0vna5cgrrkscun6nshity99qm9</sha1>
    </revision>
    <revision>
      <id>4654725</id>
      <parentid>4654724</parentid>
      <timestamp>2026-07-16T18:36:02Z</timestamp>
      <contributor>
        <username>JaredMcKenzie</username>
        <id>3528493</id>
      </contributor>
      <comment>/* Slander */ Typo.</comment>
      <origin>4654725</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="96175" sha1="124cfqhsvfb2xz91dnz0ke34p51xr8d" xml:space="preserve">{| class=&quot;wikitable&quot;
|+
! colspan=&quot;3&quot; |Talk Page Archives
|-
|[[User talk:Kittycataclysm/Archive 2022|2022]]
|[[User talk:Kittycataclysm/Archive 2023|2023]]
|[[User talk:Kittycataclysm/Archive 2024|2024]]

|}

== That IP range calculator ==

Following [[phab:T381138|T381138]], I have now become the maintainer of the IP range calculator you like. You can find it [[toolforge:ftools/general/ip-range-calc.html|here]]. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 23:10, 9 January 2025 (UTC)

:Thank you for the heads-up! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:56, 10 January 2025 (UTC)

== A merge and unmerge from two years ago ==

I was browsing through the history merge log when I saw that you merged [[Cookbook:Chicken Bog]] into [[Cookbook:Chicken Bog I]], and then promptly reverted it. What happened here exactly? Could I correct it? [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 15:55, 10 January 2025 (UTC)

:Good question! I can't remember what I was trying to do, but it looks like I didn't succeed at what I wanted based on the log comment. You're just trying to history merge to get [[Cookbook:Chicken Bog I]] to have continuity of history? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:35, 10 January 2025 (UTC)
::I think I figured out your mistake: it outright moved the revisions from the first page to the second, rather than copying them. This would have caused the other two [[Cookbook:Chicken Bog]] pages to have incomplete histories. I think the only solution would be to XML import the pre-April 2023 revisions from the first page to the other three, and I'm not sure if that's the best idea, and I am technically unable to do so. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 16:49, 10 January 2025 (UTC)

== Undeletion request ==

I wouldn't be surprised if you expected this, but I'd like to ask you to undelete the subpages of [[Rotorcraft Fundamentals]] you just deleted with the summary &quot;Use of copyrighted work without permission. Please read Terms of Use: page needs to be imported for attribution&quot;, so that I can do that. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 19:54, 14 January 2025 (UTC)

:Done! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:57, 14 January 2025 (UTC)
::Upon further investigation, this might actually be a rare case where an [[WB:UT|unmerged transwiki]] is ''preferred'' (this is part of why I stopped calling them &quot;bad transwikis&quot;), since only a small portion of the Wikipedia article (with over 2,000 revisions) was copied over. Importation is generally only needed if the ''majority'' of the page is copied across wikis. I'll just leave a null edit providing attribution and add {{tlx|Copied}}. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 21:19, 14 January 2025 (UTC)

== Reusing [[Cookbook:8 Desserts in 1 Pan]] on wikiHow ==

Hi, I am a user on wikiHow, see [[wikihow:User:Xeverything11]]. I would like to create a new recipe on wikiHow. I wanted to let us know if I can give permission to reuse your contributions to this recipe from Wikibooks to wikiHow. I (as a copyright holder) created this recipe on Wikibooks, but you contributed to this recipe.

If not, I'll use the revision before you contributed since I was the only author. 

Wikibooks uses CC-BY-SA 4.0 while wikiHow uses CC-BY-NC-SA 3.0, which both licenses are incompatible due to ShareAlike conditions.

Thanks [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 08:27, 15 January 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] I'm personally fine with this as long as proper attribution is given back to the original recipe page here. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:52, 20 January 2025 (UTC)
::I adapted this [[wikihow:Make-8-Desserts-in-1-Pan|recipe]] on wikiHow with attribution, and got a Rising Star (an achievement used for best new articles on wikiHow). Thank you! [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 19:49, 24 January 2025 (UTC)

== Wikibooks community ==

Hi, @[[User:Kittycataclysm|Kittycataclysm]]!

I am trying to contribute more to English Wikibooks. My main contributions will focus on the Cookbook, especially on Indonesian recipes. Do you have a community group where we can discuss and share ideas together?

I am looking forward to join. Thank you!

[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 08:47, 16 January 2025 (UTC)

:@[[User:Raflinoer32|Raflinoer32]] Sorry I missed this, and welcome! Are you asking about a Cookbook-specific area for discussion? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:39, 20 January 2025 (UTC)
::Yes. Do you know place for this?
::Thank you 
::[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 09:41, 21 January 2025 (UTC)
:::Honestly, there's not a centralized Cookbook-specific discussion space, especially since there aren't currently a ton of active contributors. Some people ask questions at [[Cookbook talk:Table of Contents]]. I'm currently the most consistently active and involved Cookbook editor, so feel free to ask me questions! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:46, 22 January 2025 (UTC)

== Congratulations! ==

[[File:Admin T-shirt.svg|thumb|You get this now.]]
You are now a permanent administrator. Welcome to the team (I am entitled to say this because I technically got the extension a few hours before you did)!{{FBDB}} [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 10:33, 29 January 2025 (UTC)

:Thanks :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:29, 29 January 2025 (UTC)

== Is there a way to contact a Steward on WikiBooks? ==

Hi {{PAGENAME}},
Is there a way to contact a Steward on WB? I tried to find who the active Stewards are here  at [[Special:ActiveUsers?username=&amp;groups%5B%5D=steward&amp;wpFormIdentifier=specialactiveusers]] but nothing shows up.

The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the [[Wikimania-wiki]], but I just visited the [[wikimania 2014 wiki]] and could not  find this backward link. I tried to ask about this  on the [[Wikimania 2014 main-page talk]] but disovered that the Stewards have protected it. 

Is there a way  wikibookians can communicate with Stewards at WB? Thanks in advance for answering this non-urgent question, and apologies for all the red-links which I can bluify if needed. Cheers [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 16:37, 7 February 2025 (UTC)

:@[[User:Ottawahitech|Ottawahitech]] You can ask this on somewhere like [[metawiki:Steward requests/Miscellaneous]]. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 17:01, 7 February 2025 (UTC)
&lt;s&gt;:@[[User:Ottawahitech|Ottawahitech]] seconding what Leaderboard said—we no longer have any active stewards at enWB.&lt;/s&gt; Had a brain fade there and mixed up stewards with bureaucrats. Yes, meta is the place for this. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:15, 7 February 2025 (UTC)
::@Kittycataclysm,@[[User:Leaderboard|Leaderboard]], or anyone else:
::Some wikibookians prefer for various reasons to post only at wb. I myself am indef-blocked at  META so could not participate at [[metawiki:Steward requests/Miscellaneous]] even if I waned to.
::Since [[Wikimania]] is a topic of interest to all members of the [[wikimedia movement]] why can't wikibookians talk to thier elected representatives here? [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:56, 7 February 2025 (UTC)
:::@[[User:Ottawahitech|Ottawahitech]] I can check with the blocking admin to see if they'd be willing to unblock you, if you'd like. The reason things like these are done at Meta is that Meta is a cross-project coordination platform - stewards ''cannot'' be expected to watch every project after all. Now you could message any steward here on Wikibooks if you really wanted to, but that is not normally a good idea. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 02:26, 8 February 2025 (UTC)
::::Wikimania is the annual conference celebrating all the free knowledge projects hosted by the Wikimedia Foundation (WMF).  It is a wikimedia initiative which is meant to help all of our projects (including wikibooks), gain more readership, educate more wiki-editors, foster better communications, and much more.  The wmf has been hosting  a Wikimania-wiki dedicated to each Wikimania annual event since 2004. These wikis contain a wealth of information, but can  benefit from wiki-improvements, starting from spelling and grammar errors that detract from their to appeal to the general membership. It would be nice if Stewards paid more attention to it.
::::@[[User:Leaderboard|Leaderboard]], I truly appreciate your offer, but  I posted this here not in order to get someone to advocate for one unblocking at META. As I said earlier:
::::* &quot;Some wikibookians prefer for various reasons to post only at wb&quot;
::::* &quot;The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the Wikimania-wiki, but I just visited the wikimania 2014 wiki and could not find this backward link. I tried to ask about this on the Wikimania 2014 main-page talk but disovered that the Stewards have protected it&quot; 
::::I would much rather see more wikimedia members question blocking in general at META. One cannot run such large movement of people from different backgrounds and nationalities simply by silencing minorities  IMIO. [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:12, 8 February 2025 (UTC)

== [[Crystal ball]] ==

That page appears to be a mixture of isolated paragraphs from [[w:Crystal ball|Crystal ball]], hence my tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 03:04, 9 February 2025 (UTC)

:Yep, that seems correct! I also queried it simply because it does not seem suitable for inclusion at all. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:09, 9 February 2025 (UTC)

== Question about an edit suggestion ==

Hi Kittycataclysm,

Thanks for the great work you do as an admin! I wanted to clarify a suggestion you made on a recently published page I’m working on. You recommended splitting it into smaller sections—would you suggest creating separate pages for these sections, or would a higher-level header for some topics be sufficient?

Any specific recommendations you have would be greatly appreciated!

Here’s the link to the page I’m referring to: [[Funding and Finance of Transportation Projects in the United States of America]]

Thank you! [[User:Svrmustafa|Svrmustafa]] ([[User talk:Svrmustafa|discuss]] • [[Special:Contributions/Svrmustafa|contribs]]) 18:19, 18 February 2025 (UTC)

:Hi @[[User:Svrmustafa|Svrmustafa]], and thanks for asking! Splitting refers to creating new pages, each with a smaller amount of content. The main page should then contain a table of contents, and each page can contain a navigation template for easier navigation. I'll create the table of contents based on the current work and move some content to one of those pages as an example for you; then, you can do the rest. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:26, 19 February 2025 (UTC)
::Following up on this—I noticed that you use the term &quot;paper&quot;. However, technically Wikibooks hosts books not papers, so you should probably change this wording. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:38, 19 February 2025 (UTC)
== Talkback ==
{{Talkback|Cookbook talk:Chilli Crab|Recipe Questions}} [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 09:54, 19 February 2025 (UTC)

:@[[User:Kittycataclysm|Kittycataclysm]] I also made [[Cookbook:Prata|this]] [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:15, 19 February 2025 (UTC)

== Hello ==

Can you look at my latest recipe? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 00:10, 28 February 2025 (UTC)

:I saw it! It needs a few corrections, which I'll note. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:23, 28 February 2025 (UTC)
::@[[User:Kittycataclysm|Kittycataclysm]] How do you write recipe summary, correct headers [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 06:04, 28 February 2025 (UTC)
:::Please see [[Cookbook:Policy/Recipe template]]. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:08, 28 February 2025 (UTC)
::::ok [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 02:33, 1 March 2025 (UTC)

== Cookbook ==

Hi there, Kittycataclysm. I wandered over here from Wikipedia, and I'm quite enamoured with this cookbook. I noticed you seem to be the one maintaining it, and I thought I'd reach out. Can I really just start cranking out recipes from public domain cookbooks and my family recipes? It's that simple? I was also wondering about the featured recipes section. There's not very many in there, and I imagine there's not very many folks around to do reviews compared to GAR on Wikipedia. How do you handle content review? Thanks. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:51, 1 March 2025 (UTC)

:Hi @[[User:MediaKyle|MediaKyle]] and welcome! For some context, the Cookbook has been around since the very beginning of Wikibooks, but it had gotten into a bit of disarray over the course of about two decades by the time I found it. I started the long process of overhauling, standardizing, and expanding it just over four years ago—I finished standardizing the recipe formatting and quality a while back and am currently working my way through the ingredient pages before moving on to equipment, techniques, and cuisines. You can absolutely add any public domain recipes as well as your own recipes—they just need to conform to the [[Cookbook:Policy/Recipe template|recipe template]] and [[Cookbook:Policy|Cookbook policy overall]]. It's even better if you've made the recipe and can contribute a nice picture and specific guidance/instructions/notes! Please feel free to ask me any questions. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:27, 1 March 2025 (UTC)
::Oh, and regarding the featured recipes section, I actually haven't gotten around to looking into that yet—there's been a lot to do! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:28, 1 March 2025 (UTC)
::That's great, thanks a lot for your response. This is just delightful. Maybe content review is something that we could collaborate on. There's a lot of recipes in here and it would be nice to know which ones are the best. Question for you, [[:Category:Brown sauces]] is really bothering me. How can I move that to Brown sauce recipes? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:29, 1 March 2025 (UTC)
:::Good catch on that category! It seems like it was created two decades ago and never got corrected—feel free to recategorize those recipes. Thank you also for introducing the hideprefix parameter to the category trees—I didn't realize that was an option, and it reduces the visual clutter! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:38, 1 March 2025 (UTC)
::::My pleasure! As I continue to look at the categories, this is actually worse than I thought. We have both [[:Category:Sauce recipes]] and [[:Category:Recipes for condiments]] and I suspect that's just the beginning. I want to go through and categorize everything properly, but the bones aren't even there... How long do I have to be here before it'll let me create and move around categories? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:40, 1 March 2025 (UTC)
:::::Regarding the categories, the category overhauling is in progress, since I address the category when I overhaul the associated page. The variation in titling is actually somewhat deliberate—I started changing it from &quot;____ recipes&quot; in certain cases to solve a particular categorization problem. Sometimes, there is an item that is used in recipes as an ingredient but for which there are also recipes. For example, [[:Category:Recipes for bread]] versus [[:Category:Recipes using bread]]. The different naming scheme is necessary to properly delineate the categories, and I'm working on implementing it a bit more consistently as I go. While you're still getting started, it would be great if you could check with me when something looks odd or out of place—that way I can take a look and weigh in on whether that's normal or not and maybe provide some context. Just off the top of my head, I think you will have to wait for autoreview status to make move changes. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:56, 1 March 2025 (UTC)
::::::I see what you're saying, I've been trying to wrap my head around that. Maybe it would be beneficial to try to put together some sort of a Cookbook MOS regarding category structure? It's kind of all over the place right now. Using your bread example, would it perhaps make more sense to have [[:Category:Bread recipes]] and [[:Category:Recipes using bread]]? There would be no ambiguity with just those two categories, but when you add the extra [[:Category:Recipes for bread]], that's when things start getting a little whacky. What do you think? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:05, 1 March 2025 (UTC)
:::::::Either that or get rid of [[:Category:Bread recipes]] and keep the other two. But one of these categories gotta go, I reckon. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:07, 1 March 2025 (UTC)
::::::::I see you already had the same thought as me. I think all categories should include &quot;for&quot; or &quot;using&quot;. Take for example, [[:Category:Recipes for pancakes]] as opposed to [[:Category:Pancake recipes]]. Well obviously there's no recipes using pancakes. But for something like [[:Category:Recipes for gravy]], there may also be a need for [[:Category:Recipes using gravy]]. The lack of consistency in this regard means the only way to achieve consistency across the categories is by changing them over to that format. Sorry for clogging up your talk page! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:18, 1 March 2025 (UTC)
:::::::::Same heads-up as below—migrating this over to [[Cookbook talk:Table of Contents]] —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:10, 4 March 2025 (UTC)
:Also, on [[Cookbook:Table of Contents]], could you please add a wikilink for [[Cookbook:Breakfast]], and maybe add cooknav to the top for seamless navigation between all the top level articles? Can't edit that article yet. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:47, 1 March 2025 (UTC)

== More Table of Content Edits ==

Hello again. I've been going through everything and this is my list of suggestions for edits to the table of contents. Unfortunately there's not much else I can do for now, because without autoconfirmed my ability to change anything is very limited. I was going to ask for someone to check off the confirmed box for me at RfP but I can't post there either, so I guess I'll be back in four days.

* Fix Bread wikilink
* Remove &quot;Creaming&quot; from techniques, redirected to Mixing
* [[Cookbook:History of Food and Cooking]] points to redirect, needs capitalized
* [[Cookbook:Low-Carb]] points to redirect, needs capitalized
* [[Cookbook:Cuisine of the Mediterranean]] to [[Cookbook:Mediterranean Cuisine]] for parity
* Remove the S from the cuisine wikilinks on ToC, currently redirecting
* Create [[:Category:Lunch recipes]], wikilink to ToC
* Wikilink [[Cookbook:Dessert]] under Meals
* Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category
* Create [[Cookbook:East Asian Cuisine]] so I can add the recipes from [[:Category:East Asian recipes]] to it; currently is a redlink on the ToC
* Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;
* Appendix and Equipment sections switch places

Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:46, 1 March 2025 (UTC)

:I took the liberty of doing it myself in my userspace. You can just copy it over from [[User:MediaKyle/sandbox]]. Figured I'd save you the trouble of trying to figure out what I'm talking about. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 14:15, 1 March 2025 (UTC)
:Circling back to this! It seems like your suggestions are getting at a couple different things. I'll try to go through them point-by-point below:
:* {{xt|Fix Bread wikilink}} {{done}}
:* {{xt|Remove &quot;Creaming&quot; from techniques, redirected to Mixing}} see below comments on TOC.
:* {{xt|Cookbook:History of Food and Cooking points to redirect, needs capitalized}} {{not done}} for now because I don't fully understand the urgency and I want to triage/prioritize things for you, but please feel free to make this change yourself once you can!
:* {{xt|Cookbook:Low-Carb points to redirect, needs capitalized}} {{not done}} for same reason as above.
:* {{xt|Cookbook:Cuisine of the Mediterranean to Cookbook:Mediterranean Cuisine for parity}} {{not done}} for now just because we do have a lot of cuisine pages that follow the form &quot;Cuisine of ____&quot;. It could be good to standardize, and I had been planning to do that once I got around to the cuisines.
:* {{xt|Remove the S from the cuisine wikilinks on ToC, currently redirecting}} {{not done}} for same reason as other redirects
:* {{xt|Create Category:Lunch recipes, wikilink to ToC}} Not quite sure what you mean here, and I didn't see what it corresponded to in your linked sandbox page
:* {{xt|Wikilink Cookbook:Dessert under Meals}} {{done}}
:* {{xt|Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category}} I'm not sure about this—brunch is in many places considered a separate entity, and I don't necessarily think it would cause confusion. But, overall it's hard to determine whether it should have its own page and TOC link because I haven't actually gotten around to evaluating the meal pages and what role they should play. See also the TOC notes below.
:* {{xt|Create Cookbook:East Asian Cuisine so I can add the recipes from Category:East Asian recipes to it; currently is a redlink on the ToC}} {{done}} for now; however, I'm not sure yet whether it will ultimately make sense to keep that as a content page. I think content pages should be reasonably focused, and it may not be the best to have a cuisine page that is so broad. This is something I planned to consider once I made my way around the overhauling the cuisines.
:* {{xt|Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;}} The reason I made it &quot;Introductory Matter&quot; instead of &quot;Introduction&quot; is because there's already a chapter itself titled &quot;Introduction&quot;—it felt odd to have the entire section titled that as well. Happy to discuss other header options (e.g. &quot;Front Matter&quot;, which is a generally accepted book term)
:* {{xt|Appendix and Equipment sections switch places}} see below comments on TOC.
:* '''Comments on the TOC:''' So, I think a fundamental issue with the current TOC is that it somewhat arbitrarily picks and chooses individual pages to link. It also sometimes direct-links to categories and sometimes to content pages, which I don't think we should do. Because the cookbook is so expansive, it's been established that manual indices intending to capture detail in large areas don't really make sense and quickly get bulky and out-of-date. This is why categorytree is such a useful tool! After thinking on it for a while and making some small tweaks, I think I'd ultimately like to overhaul the TOC and come to a solution that keeps a few broad headers/links to the small handful of the primary content pages while perhaps stashing away more detailed and self-updating lists in a collapsible way to reduce clutter but allow for customizable user navigation. Much to think about, and I'll probably workshop some things on the side to see how they feel.
:Let me know if I've misunderstood anything! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:24, 3 March 2025 (UTC)
::Thanks for the notes! Here's my thoughts:
::* On the Cuisine titling, it actually seems like [[Cookbook:Cuisine of the Mediterranean]] and [[Cookbook:East Asian cuisines]] are the only ones that don't follow the naming scheme, i.e. &quot;[[Cookbook:African Cuisine]]&quot;, and I think that shorter titles are preferable where it makes sense.
::* On your note about East Asian Cuisine, I actually had the same thought after going through the cuisine pages. Having three separate pages for different kinds of Asian cuisine does seem a little silly, doesn't it? Do you think it might be better to combine all of them under one &quot;Asian Cuisine&quot;, but put the different locales under separate headers?
::* On Brunch - I honestly think there's way too much ambiguity around what exactly constitutes as &quot;brunch&quot; to keep that in. I feel as though the term brunch more applies to the time you're eating, rather than the kind of food. I think it would be easier to keep meals that include commonly accepted breakfast foods in the Breakfast category, and things that don't fit neatly into that, into the Lunch category. This would prevent any dilemmas in the future where we can't decide whether something is breakfast or brunch.
::* You're right that it looks a little awkward to have the header as Introduction when there's a page called introduction. I still think that to say &quot;Introductory Matter&quot;, or &quot;Front Matter&quot; as you mentioned, is a little long-winded and reflects a more academic tone than needed for a cookbook. Upon further reflection, I think maybe rather than worrying about the header at this point, we should perhaps think about trying to compile all of those short introductory type pages into one comprehensive introductory page. Then we likely won't even need a header for it on the ToC.
::* The ToC is definitely a bit cluttered, and it bothers me too that there's a real lack of consistency across whether the wikilinks lead to a page or a category. I'm not sure how I would feel about cutting away too much of the navigation from it, though, because just about every page on there does have a reason to be there, it's just that they're not presented very nicely. Some of it can certainly get nested or combined though. I'll play around with it over the next few days in my sandbox as well and let you know if I come up with anything.
::* As an aside, the first thing on my to-do list once my autoconfirmed comes through is to start subcategorizing all of the recipes so that they're all nicely sorted in the category trees. When you have a chance, I'd love to hear your thoughts on what we should use as the standard naming for categories. Once we determine this, I think we can also take the liberty of updating the cookbook MoS to reflect it.
::Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:33, 3 March 2025 (UTC)
:::Note: After writing this, I realized what you were getting at about slashing away some of the subpages. Maybe we can come up with a system where all of those subpages are under their main subpage rather than on the ToC. For example, all the Cuisines are under [[Cookbook:Cuisines]], all techniques under [[Cookbook:Cooking Techniques]], to keep the subpages off the main ToC. Also, I wonder if maybe we should try to make a centralized discussion for this somewhere, in case anyone else wants to join in at some point? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:45, 3 March 2025 (UTC)
::::Heads-up: to make it easier to keep track of these and since I think they deserve their own discussions, I'm going to gradually migrate them over individually to [[Cookbook talk:Table of Contents]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:52, 4 March 2025 (UTC)
:::::Good idea. Can you remove the semi-protection from that talk page? I see no reason why it should be protected. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:23, 4 March 2025 (UTC)

== Cookbook ToC ==

Hi [[User:Kittycataclysm|Kittycataclysm]]. I was just wondering why you didn't respond to my above message, and started a separate sandbox for the ToC instead? It seems as though you don't really want to collaborate. It would be nice if we could work on this together. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 22:43, 2 March 2025 (UTC)

:@[[User:MediaKyle|MediaKyle]] thanks for the ping! I'm sorry you feel like I don't want to collaborate—the opposite is true, and please understand that this is good-faith editing. The reason I haven't responded to the above points is mostly since you've been modifying a bunch of content and adding suggestions lately, and I've been working my way through these while continuing with my routine contributions and real life as well—things happen a little more slowly here than on other projects, and I'm the one person dedicated to the cookbook right now. The reason I created that sandbox was because I saw [[Wikibooks:Reading room/General#Modernize the shelves|your comment]] at the reading room and wanted to play around and think about your suggestion without touching the actual TOC. You're right that it's not the best, and it's been something I've been thinking about for a bit now. Please understand also that it can be overwhelming when a new editor unfamiliar with the Cookbook begins making a high volume of edits and suggestions without having much experience with it or its history—this isn't to say that you don't have good ideas or things worth contributing. In fact, you have already made a few helpful changes, as I've mentioned. I just want to do this properly and take the time to evaluate your suggestions together with the current efforts that are underway, and that can take a bit. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:03, 2 March 2025 (UTC)
::Thanks for getting back to me. While I may be new to Wikibooks, I'm certainly not new to MediaWiki, and I've been working with small wiki projects for a number of years. Perhaps it's been a misunderstanding to some degree, but I've found my reception here to be unusually unwelcoming. The way to do this properly, as you said, would be to have discussions and form consensus. Yesterday, when you reached out to me about adding hideroot to the pages, I gave you my rationale and was more than happy to have a discussion about it, but you did not reply. I noticed a similar situation happened with [https://en.wikibooks.org/wiki/User_talk:Ottawahitech#Category_sorting Ottawahitech], regarding category sorting. I'm aware that you're the main person looking after the cookbook right now, which is why I reached out to you right from the get go.
::I understand why you would want to create your own sandbox to play around with options for the ToC, but I'm sure you can understand why it would draw my attention that you would do this without implementing any of the wikilink fixes I mentioned, or making an attempt to discuss it further. This came across to me as not wanting my help.
::I invite you to check out my page on Wikipedia. I've made contributions across quite a wide area of topics there, as well as the other Wikimedia projects, and this is the first time I've encountered any sort of resistance to my contributions. I think Wikibooks has enormous potential, and I'm very excited to contribute to helping it grow. On most projects, this would be something to be encouraged. I don't feel like &quot;I'm sorry that you feel that way&quot; was really an appropriate response. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:59, 2 March 2025 (UTC)
:::I think you're right that this has been a mix of misunderstanding and miscommunication, and I think I can understand how things came across as unwelcoming! For whatever it's worth, I absolutely plan on circling back to the various discussions at hand (I have all the relevant pages open to return to), but it seems like the order I did things made it seem like I was ignoring you (if I'm understanding correctly). I am pretty busy, so sometimes items on my to-do list do get lost/shunted or it takes me a bit to get around to something—please don't hesitate to give me a ping if it seems like I'm taking a while to get back to something. Looking forward to more collaboration! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:49, 3 March 2025 (UTC)
::::I'm glad you can understand where I'm coming from. To clarify, my intent is not to try to rush you, or to try to push you to make changes that you don't agree with. It's really easy to misinterpret things over the Internet, and I think a short message can go a long way. I apologize if I've caused you any undue stress by coming into the cookbook and unleashing a flurry of alterations, but do rest assured that I'm not married to any of my changes, I'm always open for discussion, and I want to see the cookbook improve just like you do. The great thing about wikis is that no change is permanent. I think we'll have it in tip-top shape in no time! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:19, 3 March 2025 (UTC)

== [[Cookbook:Polish Doughnuts (Paczki)]] ==

Do you see any reason not to just add this to Featured Recipes? At least we know this one works, and it seems like this is now one of the few recipes to have a picture that actually aligns with the recipe used. I was thinking later on we'll come up with a content review system where a couple editors will actually try the recipes nominated for FR, but in the absence of that I'd just add it to the list. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 12:25, 4 March 2025 (UTC)

:I'm fine with adding it to the featured recipes. You're right that we'll want to come up with a good system for this going forward, though it's lower down on my personal priority list at moment. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 March 2025 (UTC)

== [[Cookbook:Cream Cheese American Buttercream]] ==

Hi! I am a wikiHow user and I am planning to adapt this recipe to wikiHow. Since you contributed to this recipe, I wanted to know if I can get permission to reuse your contributions to this recipe. Thanks. [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 21:41, 4 March 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] that's fine with me as long as proper attribution and linking back to the original recipe page here are included at the top. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:28, 4 March 2025 (UTC)

== [[A Companion to Our Literary Journey]] ==

Hi! I feel that we have started to outline the scope in a clearer and more precise way and that’s the work we are going to do with the students this and for the next years, adding more sections and content. Do you think that would be enough? [[User:Ferdi2005|Ferdi2005]] ([[User talk:Ferdi2005|discuss]] • [[Special:Contributions/Ferdi2005|contribs]]) 22:43, 6 March 2025 (UTC)

:Hi @[[User:Ferdi2005|Ferdi2005]]! Yes, this seems to be reasonably outlined. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:51, 7 March 2025 (UTC)

== Exercising care with copyright ==

When deleting a page as a copyright violation, it is important that you '''do not quote any content from the deleted page'''. If you do, then your log entry is itself a copyright violation. I have redacted a recent deletion that you performed because of this. If you want to make sure that none of your past deletions have been problematic for this reason, you can [[quarry:query/90444|run this SQL query]] to get a list of every deletion that could be eligible for redaction. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 18:32, 21 March 2025 (UTC)

:Hi @[[User:JJPMaster|JJPMaster]] and thank you for the message. In the most recent instance that I think you're referencing, I do not see any material in the edit summary that posed a significant risk—I don't believe the few listed words would be a copyright concern. However, I do understand your concern! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:31, 21 March 2025 (UTC)

== Splitting Pages ==

Hi I have recently made the book on the [[History of the Nawabs of Bengal]] and you gave a notice on how you believe it should be split into smaller bits. As I am still new to wikibooks I don't know how to do this. Can you please assist me on renaming the page so I can split the page into multiple pages? @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 19:47, 29 March 2025 (UTC)

:@[[User:Greatswrd|Greatswrd]]: You did it. I've removed the tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 22:44, 29 March 2025 (UTC)
:Like @[[User:JJPMaster|JJPMaster]] said, you're all set! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:53, 29 March 2025 (UTC)
::Thanks! @[[User:JJPMaster|JJPMaster]] @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 10:24, 30 March 2025 (UTC)

== Minecraft book ==

Is it good creating pages like this, [[Minecraft#Husk]]? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 12:43, 9 May 2025 (UTC)

:@[[User:Cactusisme|Cactusisme]] what do you mean? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:18, 10 May 2025 (UTC)
::are we allowed to create pages like that? like for every mob [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:02, 11 May 2025 (UTC)
:::To be honest, I don't think the structure and formatting of the book is very good. Several of the mob pages, for example, have very little information and aren't particularly helpful on their own. If I were working on it, I would restructure the book. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 14:09, 11 May 2025 (UTC)
::::I am planning to do that. [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 04:19, 12 May 2025 (UTC)

== Request to Review Adjusted User Page (XoriantTeam) ==

Hello [[User:Kittycataclysm|Kittycataclysm]],

I hope you're well. I noticed that my user page ([[User:XoriantTeam]]) was recently deleted for appearing promotional or inappropriate for Wikibooks. Thank you for keeping the community standards in check.

I’ve since revised the content with closer attention to neutrality and compliance with Wikibooks guidelines. My intent is to participate constructively, especially in areas related to digital engineering and educational content creation.

If possible, I’d appreciate your help reviewing the revised version. I'm happy to share it or upload it as a file if there’s a preferred method.

Please let me know how best to proceed. I welcome any suggestions and will gladly make further adjustments.

Best regards,  

XoriantTeam [[User:XoriantTeam|XoriantTeam]] ([[User talk:XoriantTeam|discuss]] • [[Special:Contributions/XoriantTeam|contribs]]) 11:02, 15 May 2025 (UTC)

:Hi there—you can publish an updated user page, but I'd caution you against talking about your company. Keep it limited to your involvement with Wikibooks. You may contribute productively here, but further promotional materials are grounds for an indefinite block. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 12:30, 15 May 2025 (UTC)

== Planning to use AWB to update categories on the cookbook ==

Hello. I noticed in recent changes that you were moving some categories using HotCat (e.g. moving Category:Chile recipes to Category:Recipes using chile), which can be time-consuming. Therefore, I plan to help you with moving the cookbook categories by adding myself to enabledusers and enabledbots in [[Wikibooks:AutoWikiBrowser/CheckPageJSON]]. Would this be fine if I assist you and to add myself to the check page? I am familiar with using AWB after testing on a non-Wikimedia project. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:42, 8 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—thank you for the tip! I just installed JWB, so this should make my mass cat changes much faster. Thanks again! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:11, 8 June 2025 (UTC)
:: Thank you for the information. Also, is it okay if I change (for example) [[:Category:Vinegar recipes]] to [[:Category:Recipes using vinegar]] (I can redirect the former category to the latter), given that we should move {{tq|Category:[ingredient] recipes}} to {{tq|Category:Recipes using [ingredient]}} for consistency? [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:57, 8 June 2025 (UTC)
:::Sure thing—go ahead! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:53, 8 June 2025 (UTC)

== Tool for even faster category changes ==

See [[:c:Help:Gadget-Cat-a-lot#As_your_user_gadget]]. I just [https://en.wikibooks.org/w/index.php?title=User:Koavf/common.js&amp;action=history installed it] and used it dozens of times in a click. Let me know if you need any help. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:36, 19 June 2025 (UTC)

:@[[User:Koavf|Koavf]] Thanks! I'm having a little trouble activating it, but I'll keep trying. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:54, 19 June 2025 (UTC)
::A lot of times, a purge will do the trick. See [[:mw:Purge]]. Usually just &lt;kbd&gt;Ctrl+Shift+R&lt;/kbd&gt; once or twice. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:55, 19 June 2025 (UTC)
:::Took several purges, but we're set now! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:16, 19 June 2025 (UTC)

== Advice on when I should run for adminship ==

Hi, I hope you are doing well. I am asking for some advice on when I should run for enwikibooks adminship, given the following below:

Currently, I am doing some optimizations for dark mode on this project, and some of the message box/MediaWiki interface/template pages might be outdated, fully protected, or can use a little help using mw-parser-output. These unfortunately might hinder the process of updating these pages/templates for Vector 2022's dark mode.&lt;br&gt;
Additionally, I have a solid expertise with edit filters, as I have requested some administrators to update deprecated filter variables, switching filters from warn and disallow to disallow only, and I can also monitor the filter log for potential false positives (from local or global filters).

A fellow English Wikibooks administrator also said to me that they are willing to support me in a few months when I run for adminship, as I am generally trusted.

I hold two advanced global permissions, and I hold an edit filter helper permission on the English Wikipedia, to be sure. Thank you for your consideration. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 01:02, 23 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—good question! I agree that you are a trusted user, and I think it would be reasonable for you to run for adminship, especially given our need to fix up technical aspects of the project. If you don't plan to commit to Wikibooks long-term (i.e. you have some projects you'd like to take a few months to complete and then be done), you can always request temporary adminship. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:30, 23 June 2025 (UTC)
:: Thank you for your feedback, but I also plan to monitor for vandalism/spam, and to commit to reduce the administrative assistance reading room backlog, should I be elected for adminship (and I forgot to mention those). Anyway, regarding your feedback, I might run by August or even July, given that I've lately started contributing more often to Wikibooks. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:29, 23 June 2025 (UTC)
::: [[User:Kittycataclysm|Kittycataclysm]], I am pinging you one more time to see if you have read my response above yours. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:34, 26 June 2025 (UTC)
::::Hi @[[User:Codename Noreste|Codename Noreste]]! I'm not sure what you mean—was there an additional question you had? Everything you've outlined seems quite reasonable. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:26, 26 June 2025 (UTC)
::::: Apologies for the confusion, I don't have any questions to ask. I was clarifying that I can help with implementing edit requests and to block obvious vandals and spammers, aside from the skills I mentioned earlier. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:32, 26 June 2025 (UTC)

== how is it you feel able to interfere in my sandbox? ==

you deleted a page in my sandbox that was my way of providing my response to a request from an OpenSCAD dev team leader for a couple of text blurbs for use on a web page of the OpenSCAD site.

now that you have deleted my page i have to recreate the texts from a screenshot to be able to offer the suggestions, which i will 

This kind of high handed treatment is what keeps me from being a wiki-anything contributor .. If it is Wiki policy to interfere in the documentation of an open source project because it is hosted on Wikibooks then i will take up the task of moving our online docs to a site where you cannot interfere.
--
[[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 21:56, 29 June 2025 (UTC)

:Hi @[[User:VulcanWikiEdit|VulcanWikiEdit]]—thanks for bringing this to my attention. I now understand that this was intended to be in your user namespace—I've undeleted it and moved it to the correct namespace for you. Let me know if anything else comes up! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:05, 30 June 2025 (UTC)
::ah .. err .. umm .. well that is a gentle answer to my ire. Thanks for being so gracious [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:29, 30 June 2025 (UTC)
::and .. isn't my sandbox in my namespace by default? [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:30, 30 June 2025 (UTC)
:::No worries—it looks like you didn't add the prefix &quot;User:&quot; before writing out the full page titles, so the pages you created were technically in the project's Main space with the official published materials. Going forward, you can just double-check that the page title starts with &quot;'''User:'''VulcanWikiEdit/sandbox&quot;, and that should keep everything in the right place! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:36, 30 June 2025 (UTC)
::::BTW .. i love the play on cat lover name [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 15:35, 1 July 2025 (UTC)
:::::Thank you! That's very kind. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:46, 1 July 2025 (UTC)

== Regarding the user Codename Tameirao ==

Could this be Matthew again (the Unicode LTA)? I believe it might be him based on his usage of edit summaries, and his usual edits to [[Unicode/Versions]]. I just blocked his recent account, and then I protected and stabilized that Unicode book. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 23:51, 12 August 2025 (UTC)

:I suspect you're right! That seems like a reasonable course of action. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:56, 13 August 2025 (UTC)
:: I recently encountered another possible LTA, see [[Special:Contributions/~2025-55706-6]] (as well as [[Unicode/Roadmap Blocks]]). I can email you more details if you want. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 16:30, 9 September 2025 (UTC)
:::I think this is the same LTA, yes! I've protected [[Unicode/Roadmap Blocks]], but I think it would be a good idea if we could automate this monitoring somewhat using the edit filter. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:07, 9 September 2025 (UTC)
:::: I don't think that was Matthew, as he typically uses edit summaries. The deleted page was not protected, as it was protected before you deleted it; I salted it from creation for one year. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 20:22, 9 September 2025 (UTC)
::::: You might want to look at [[Special:Contributions/Freddy Fazbearing Others]]. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:18, 26 October 2025 (UTC)
::::::Thank you! I went ahead and blocked them. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:54, 28 October 2025 (UTC)

== IP block exempt  ==

Hi Kitty,
I currently have IP block exemption on enwiki, Commons and Wikidata as I use VPNs connected to my internet security software. Can you please grant me the right on wikibooks. I have a strong password and use two factor authentication. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 10:51, 22 August 2025 (UTC)

:Hi @[[User:TarnishedPath|TarnishedPath]]! This doesn't sound unreasonable to me, but I think it would be good if you requested at [[Wikibooks:Requests for permissions]] so we can have a discussion—I have not granted this right before. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:50, 23 August 2025 (UTC)
::Kitty, thanks for pointing me in the right direction. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:25, 23 August 2025 (UTC)
::See [[Wikibooks:Requests_for_permissions#TarnishedPath_(discuss_·_contribs_·_count_·_logs_·_block_log_·_rfp_·_rights)_(IP_Block_Exemption)]] ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:35, 23 August 2025 (UTC)
== You've got mail! ==
{{You've got mail|sig=&lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 00:20, 6 September 2025 (UTC)}}

:Thank you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:06, 6 September 2025 (UTC)

== Are you able to import? ==

I made a few requests over at https://en.wikibooks.org/wiki/Wikibooks:Requests_for_import . [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 22:32, 4 October 2025 (UTC)
: [[User:2005-Fan|2005-Fan]], I'll go ahead and start the imports. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:29, 5 October 2025 (UTC)
::Thank you for your help [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 16:51, 5 October 2025 (UTC)
::: My apologies for not doing this sooner, because some database error appears when I am trying to mass import. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 23:39, 5 October 2025 (UTC)
::::I also tried to make this import earlier and ran into issues with the software. I was hoping it was a temporary bug, but it seems to be persisting. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:01, 6 October 2025 (UTC)
:::::This seems like I should get involved. {{working}}... [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 13:11, 6 October 2025 (UTC)
:::::: I believe there are five pages that have massive page histories they fail to import here. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:13, 6 October 2025 (UTC)
:::::::I backed up the XMLs of them locally but im unsure how much that'd do. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 15:18, 6 October 2025 (UTC)
::::::::Just became an importer. The reason is prob understandable but I cannot upload the XML file to here locally. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 17:23, 10 October 2025 (UTC)

== About the category parameter in the recipe summary template ==

When it uses a &quot;recipe by type&quot; category, should it use a &quot;[type/food] recipes&quot; name or &quot;Recipes for [type/food]&quot;?

I recently operated JWB to change from [[:Category:Dessert recipes]] to [[:Category:Recipes for dessert]] in multiple Cookbook recipes, and from what I've said before, I've changed to ''Recipes for dessert'' in the category parameter of Cookbook recipes. Hope you don't mind that this was over more than 250 changes (not counting the recent category changes after moving some recipe categories). Thanks. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 02:07, 27 October 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—those JWB changes you made seem fine to me! I'm not quite sure what you're asking in your first sentence, though. Assuming I understand correctly: in general, I think the default format should be whatever the actual category name is. BUT if there is a redirect, it ultimately shouldn't matter too much. And, because I'm not convinced of the utility of that infobox parameter in the first place (thinking of removing it), I'm not hugely concerned about it for the time being. Does this help? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:21, 27 October 2025 (UTC)
:: Probably, but I will say the following below (for my first sentence) to clarify:
:: On the &lt;code&gt;|category =&lt;/code&gt; parameter, when placing a recipe category name, should it either be {{tq|Sandwich recipes}} or {{tq|Recipes for sandwiches}}? I hope this clears the confusion. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:39, 27 October 2025 (UTC)

== Please no more Unicode LTA ==

Please don't block me again. I promise I will edit Unicode stuff and add correct information. [[Special:Contributions/&amp;#126;2025-30839-28|&amp;#126;2025-30839-28]] ([[User talk:&amp;#126;2025-30839-28|talk]]) 20:54, 1 November 2025 (UTC)
:&lt;small&gt;I am a bit out of the loop, so correct me if I'm wrong - I'm assuming here&lt;/small&gt; I think the point is that they want you to ''not'' edit the Unicode stuff? Also hi kitty, it's been a ... very long time.. &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:13, 5 November 2025 (UTC)
::Ok so apparently not as long as I thought, but it feels like I've been away for at least a year lol &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:23, 5 November 2025 (UTC)
:::Nice to see you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:41, 5 November 2025 (UTC)

== Administrator and reviewer user right combinations are not needed anymore ==

Given that administrators can review edits in addition to reviewers, I would suggest for you (and other administrators) to kindly remove the reviewer permission from (own) accounts. What I'm saying is that if one holds administrator and reviewer permissions together, they can remove the reviewer permission from their own account and retain their administrator permission. Thanks. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:06, 11 November 2025 (UTC)

:Gotcha—is there a reason it's bad for one user to have both these rights? If so, I can remove my reviewer right. Otherwise, it seems fairly harmless? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:26, 11 November 2025 (UTC)
:: The thing is, administrators have the &lt;code&gt;review&lt;/code&gt; user right, as well as some permissions in the reviewer user group in the administrator toolset. That means that having the reviewer user group together with the admin user group is redundant. Hope this explains it. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 19:59, 11 November 2025 (UTC)
::: @[[User:Kittycataclysm|Kittycataclysm]] &lt;s&gt;I'll do this tomorrow morning, as well as to remove autoreviewed user permissions from users who are reviewers.&lt;/s&gt; ({{doing}}) [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:24, 12 November 2025 (UTC)
: I have removed the autoreviewed user permission from users who are reviewers. As for administrators, I will do so later today. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:40, 13 November 2025 (UTC)

== Nesting in Open Book of Ecovillages and Eco Communities  ==

Hi Kittycataclysm,

I am editor of wikipedia since 2004. We have the habit if we have a concern using the talk page to clarify the case. I am not sure to delete meaningful content without previous notification and doing major redirection without agreeing the main contributor(s) is an adequate admin act and sign of good manner of host (see [[W:Wikipedia:Etiquette|Wikipedia:Etiquette]].)

Yes, It will be not an average book but above the regular. This is the exact case: ''&quot;this may be appropriate, such as with large textbooks that contain subsections with a lot of content.&quot;'' ''for to establish good structural and stylistic practices''

I have a data management certification. If you asking it will have 4 nest level on strict purpose. If you saw the introduction of the [[Open Book of Ecovillages and Eco Communities]] is/will be a global collection making effective collaboration over borders and continents. One structured + categorized(!) page for each community willing to show up. The Postal addresses has also same or larger deepness, this is unavoidable (Country/Postal Code/Location/Street/House/floor/door). Here will looks like: '''Eco-comm/Continent/Regio code/Community name'''

The goal of this system to open bridge + experience highway  for the communities using the same permaculture technics what collected parallelly in [[Open Book of Permaculture]]. That is also part of this knowledge base please dont do simplification steps on that without discussion.

I am kindly asking to revert your edits in this book.

After that I will put a notification template  about 
 &quot;This book is under construction with major changes. Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History. Common clarifications/ guides are on the primary talk page.&quot;


Thanks: [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 02:22, 12 November 2025 (UTC)

:Hi @[[User:Rodrigo|Rodrigo]], and thank you both for your contributions and for reaching out! Yes, I did make the following changes to [[Open Book of Ecovillages and Eco Communities]]:
:* I moved the pages from the [[Eco-comm]] namespace to the [[Open Book of Ecovillages and Eco Communities]] namespace, since the table of contents and pages for a given book should be under that book's namespace.
:* I removed the links to Wikipedia that were on [[Open Book of Ecovillages and Eco Communities]], since outlinking has been discouraged at en.Wikibooks as a matter of practice. Compilations of links may not fall into WB scope as an instructional text, and [[Wikibooks:Requests for deletion/Piano Solo Music: An Encyclopedia|there is precedent for deleting them]]. But, I do see that the tool I used didn't just remove links to enWP, so I will restore the prior revision and ping the tool developer.
:* I flagged it as needing denesting—you're right that nested entries can sometimes be appropriate. In this case, I was primarily flagging for a denest because the table of contents needs to be moved onto the main page, and it shouldn't have hidden navigation within the nested portions.
:Could you clarify which of these edits you do not agree with so I can make sure they are individually addressed? As an aside, it could be helpful to create a [[Help:Local manuals of style|local manual of style]] for the book in order to clearly outline the expectations. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:59, 12 November 2025 (UTC)
::My main concern not about moving and flagging but '''deleting''' [[Eco-comm]] against [[Wikibooks:Deletion policy]] and not mentioning in the clarification even after my notification. Should I note all administrators [[Wikibooks:Please do not bite the newcomers]] - or will they do speedy deleting one by one until I make them individually addressed?
:::The &lt;u&gt; local manual of style&lt;/u&gt; development is ongoing together with the sample pages.
::'''MAIN PAGE'''
::The '''Main page''' and '''Namespace''' is the [[Eco-comm]]. The '''Full Title''' or '''Cover''' is [[Open Book of Ecovillages and Eco Communities]]. Because of the high level of nesting the below extra-long-full-text-title to be avoided the Cover page is a redirection with preface/intro etc.
::'''NESTING '''
:::Featured book with 3 level nesting: [[Social and Cultural Foundations of American Education/Educational Change/Theory]]
:::5 level nesting example: [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]]
::'''Categories''' The [[:Category:Eco-comm]] will let the users make practical sub-categories e.g. [[:Category:Eco-comm/Project/numundo]] [[:Category:Eco-comm/]]
:::
::[[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 03:44, 18 November 2025 (UTC)
:::Thank you for elaborating! I'm unfortunately not sure what you mean about deleting [[Eco-comm]]—are you referring to the fact that I moved it without leaving a redirect? Regarding the nesting, I do honestly think those other books you linked should have their navigation denested since I find their format difficult to parse, and they have some navigation issues. Looping in some other active admins (@[[User:Leaderboard|Leaderboard]] @[[User:MarcGarver|MarcGarver]] @[[User:JJPMaster|JJPMaster]] @[[User:Codename Noreste|Codename Noreste]] (@[[User:SHB2000|SHB2000]]) so they can get eyes on this and voice anything they think is important. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 04:12, 18 November 2025 (UTC)
::::It makes no sense to have some crazy abbreviation as a &quot;main page&quot; or &quot;namespace&quot; (whatever that means in this context) for a book in order to allow it to be deep nested. Nobody needs to type the whole name of the nesting because that's what navigation templates do, and it is a simple matter to override the page title. I also take issue with the statement, above, &quot;Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History.&quot; Anybody can edit, and nobody gets to own and control any work. Taken together, this complaint looks like a case of attempting to assert ownership and to operate against the normal practices of Wikibooks. As such, I am completely aligned with the changes made. [[User:MarcGarver|MarcGarver]] ([[User talk:MarcGarver|discuss]] • [[Special:Contributions/MarcGarver|contribs]]) 12:49, 18 November 2025 (UTC)
:::::That. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 14:59, 18 November 2025 (UTC)
::::Thanks @[[User:MarcGarver|MarcGarver]]@[[User:Leaderboard|Leaderboard]] for the contribution, btw the [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]] also looks crazy long, is'nt it? Lets continue in the [[Wikibooks:Reading_room/General]] keeping this page for personal messages. [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 23:07, 20 November 2025 (UTC)

== Deletions of Wikibook subpages ==

Hello @[[User:Kittycataclysm|Kittycataclysm]],

regarding the [[Thesis Writing Guide]] subpage deletions, should I just recreate them when I keep working on them or was there an automatic deletion that we could undo? This document will grow, but really slowly.

Best,
Tim [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 11:37, 16 December 2025 (UTC)

:Hi @[[User:TimBorgNetzWerk|TimBorgNetzWerk]]! Since there was so little content on the deleted pages, my recommendation would just be for you to gradually recreate the chapters as you go. Does that make sense? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:54, 17 December 2025 (UTC)
::Makes sense, not my ideal solution, but also not far from it :) The end result will be the same, the in-between will just feel a little bit weird from time to time.
::Thank you for taking time to curate and quality-control Wikibooks - wishing wonderful holidays and a happy new year! [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 20:43, 17 December 2025 (UTC)
:::Thank you, and happy holidays to you as well :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:13, 17 December 2025 (UTC)

== help with &quot;Media Literacy and You&quot; == 

{{re|Kittycataclysm}} What do I need to do to get a quality review of ''[[Media Literacy and You]]'', or whatever is needed to remove &lt;nowiki&gt;{{Qr-em|not clear how this is to be structured as a book}}&lt;/nowiki&gt;? 

I ask, because you added that flag just over 2 hours after I created it. I later found that I had accidentally created it as an anonymous user. I've since started using my standard Wikiname, and I tried to respond to the requests both by creating a discussion on the &quot;Discussion&quot; page associated with that book and by upgrading the content. 

The upgrades included adding the &quot;Introduction&quot; chapter by revising an article on Wikiversity that convinced me to start this Wikibook. I have other articles that I plan to rewrite to create 9 of the remaining 11 chapters in the current table of contents, as indicated in this table of contents. 

??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:23, 8 February 2026 (UTC)

:Hi @[[User:DavidMCEddy|DavidMCEddy]]! I removed the query flag, since this is clearly not a test page. I do have concerns about the suitability of this book for Wikibooks, since it seems to be more in line with essays and original research/analysis (which are [[Wikibooks:WIW|out of scope here]]). Wikiversity seems like a very suitable place for them—is there a specific reason you want to move them here? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:24, 8 February 2026 (UTC)

::{{re|Kittycataclysm}} 
::This book is intended to accelerate the diffusion of [[w:Media literacy|media literacy]] by making it easier for humans to (a) access training materials and (b) connect with research on the most important issues that concern them and (c) discuss those issues with others who may believe differently in a nonthreatening context that encourages dialogue and a shared search for what can honestly be said about any particular issue. This is an extension of &quot;The wisdom of polarized crowds&quot; discussed in [[Wikipedia:Reliability of Wikipedia]]. 

::I don't know about you, but I'm frightened by the collapse of nuclear arms control agreements since the year 2000, by global warming, by the threats of the Trump administration to invade Canada and Greenland, etc. If this book project is successful, it will make a material contribution to reversing these trends -- unless this kind of dialogue is [[v:Responding to a nuclear attack|interrupted by a nuclear war]]. 

=== Who is DavidMCEddy ===

::I'm a [[w:Vietnam veteran|Vietnam-era veteran]] with a PhD in statistics and a publication record for which [https://www.researchgate.net/profile/Spencer-Graves-3 ReserchGate has found over 1,200 academic publications that have cited my work.] Since  [https://xtools.wmcloud.org/ec/en.wikipedia.org/DavidMCEddy 2010 I have logged]
*  6,000+ edits in each of Wikipedia and Wikiversity, 
*  1,000+ in Wikimedia Commons, 
* 30,000+ in Wikidata, and 
* almost 1,000 in other Wikimedia Foundation projects like Wikiquote and edits to the Spanish, French and German Wikipedias. 

This includes dozens of research reports posted to Wikiversity under [[v:Category:Freedom and abundance]] and 44 posts under [[v:Category:Media reform to improve democracy]] that provide a platform for documenting and discussing 44 episodes of a fortnightly &quot;Media &amp; Democracy&quot; series of 29:00 mm:ss podcasts syndicated for the [https://pacificanetwork.org/stations-2/ Pacifica Radio Network] featuring the opinions of leading experts on the increase in political polarization and violence and what those experts think should be done about this. 

I've just posted another chapter to [[Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. I hope you will agree that this book can make a positive contribution to Wikibooks and to [[w:Jimmy Wales|Jimbo Wales]]' [[w:Wikipedia:Prime objective|Prime Directive]] to create &quot;a world in which every single person on the planet is given free access to the sum of all human knowledge.&quot; Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 01:19, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Thank you and I understand this, but I am asking why you think this material is more suitable at Wikibooks rather than at Wikiversity. From what I can see, Wikiversity seems like the more appropriate home for it given our [[Wikibooks:WIW|scope]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:59, 9 February 2026 (UTC)

::{{re|Kittycataclysm}} 

::&quot;Media Literacy and You&quot; is textbook to support both self study and classes on media literacy. 

::I have been posting content to Wikiversity since 2014 and have not encountered support there for books. A search just now turned up a hint of a book on Wikiversity, but I could not easily find anything on how to do it, etc.  

::I think this &quot;Media Literacy and You&quot; project would lose the vast majority of its potential if it were not on Wikibooks. 

::??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:22, 9 February 2026 (UTC)

{{outdent}}

{{re|Kittycataclysm}} 
Will you please help me with the protocols of creating a book on Wikiversity? 

1. I have found documentation that claims that Wikiversity supports such. However, the documentation seems incomplete, potentially out of date, etc. For example, I could not see how to follow the instructions for [[Wikiversity:Help:Books#Step 1: Enable the &quot;Book creator&quot; tool]]. So I posted a question to [[Wikiversity:Help talk:Books]]. 

2. What do you suggest I do next? 

:I can create an article on Wikiversity titled, &quot;Media Literacy and You&quot;, and port everything I've posted to Wikibooks there, then replace the pages on Wikibooks with redirects to [[Wikiversity:Media Literacy and You]], [[Wikiversity:Media Literacy and You/Introduction]], and [[Wikiversity:Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. 

:If you think that's the best way to build this book project, great. It would actually be easier for me, because there would be less translation between what I already have on Wikiversity and a version for Wikibooks. (Also, Wikiversity supports &lt;nowiki&gt;{{cite Q|...}}&lt;/nowiki&gt;, which I have used extensively for years.) 

:Thanks for your help. [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 13:26, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Unfortunately, I am not familiar with the exact workings of Wikiversity, so I can't be much help there. My personal recommendation is that you ask there for help on how best to structure your materials to match the WV requirements. If you'd like some additional opinions/insight, please feel free to also check in at the [[Wikibooks:Reading room/General|reading room]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:22, 10 February 2026 (UTC)

::{{re|Kittycataclysm}} I believe I have finished migrating all of ''Media Literacy and You'' to Wikiversity and replacing the parts of it on Wikibooks with redirects. Comments? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 17:32, 10 February 2026 (UTC)

== Thank you!  ==

Heya, thanks for reviewing my stuff! Just to note, the first lesson page was done and so that'll need moving. If you want to discuss anything with me, I am easily reachable on Discord @ xiluosi233. I can explain philosophy, approach, and so on from my teaching experience if you want anything regarding that. [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:48, 17 February 2026 (UTC)

:It appears [[An Introduction to the Han Script]] was moved wrong - should it not be [[General Literary Chinese from Scratch/An Introduction to the Han Script]]? [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:52, 17 February 2026 (UTC)
::@[[User:Shira the Mogul|Shira the Mogul]] good catch! I accidentally removed more of the title than intended. I've fixed this now. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:18, 18 February 2026 (UTC)

== A test request ==

Just to see whether a recent Luna update turned out as intended, could you briefly revert your [[User:Kittycataclysm/lunaoptions.json|Luna preferences page]] to the first revision? Since you don't appear to have any custom preferences in the first place, I don't think there should be any conflicts. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 01:49, 30 March 2026 (UTC)

:Done! But, it seems to have perhaps auto-updated again immediately afterwards. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:39, 10 April 2026 (UTC)

== Linking ==
Hi,&lt;br&gt;
For my edification, why is a link from [[Cookbook:nettle|nettle]] to [[w:Urtica_dioica|Urtica dioica]] not appropriate? The Wikipedia article has more information &amp; seems relevant.&lt;br&gt;
Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 01:53, 24 April 2026 (UTC)

:@[[User:PeterEasthope|PeterEasthope]] good question! Wikibooks discourages outlinking, since books should be self-contained units. Instead of linking to [[w:Urtica dioica]], the correct approach would be to flesh out the actual chapter here at Wikibooks. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:34, 24 April 2026 (UTC)
::Should all material in the Wikipedia article about Urtica dioica relevant to cooking be duplicated into the nettle article in the cookbook? Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 02:30, 2 May 2026 (UTC)
:::@[[User:PeterEasthope|PeterEasthope]] you could do that, although you should only include information that is sourced. However, I recommend that you wait, because I am coincidentally working on the page right now and fleshing it out significantly. I should publish today. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:40, 2 May 2026 (UTC)
::::The nettle page is better now. Thanks.
::::I still wonder, given that the link to ''The Complete Guide to Edible Wild Plants, ...'' is permitted, why not a link to the botanically oriented page in Wikipedia. What if someone reads the Cookbook article and is interested in the toxin for example? Seems that non-Wikimedia references are more privileged than Wikimedia references.
::::Also, by chance, just noticed the [[w:Nettle_soup|Nettle soup]] article in Wikipedia. Better in the Cookbook?
::::Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 19:10, 5 May 2026 (UTC)
:::::Another good question. The reason those books are linked is because they are reputable and topical sources for the subject matter (nettles as used in cooking from an instructional perspective), and the links are part of the citations—this makes it different from a simple outlink to a Wikipedia page. Wikipedia pages should also not be cited themselves as sources. Regarding nettle soup, I don't think it makes sense to have that as a standalone page here in the cookbook due to its encyclopedic tone, and I don't see any recipes there. Does this make sense? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:21, 6 May 2026 (UTC)
::::::Somewhat. Certainly a recipe wouldn't be incongruous in a cookbook. Still seems unhelpful that relevant information in Wikipedia is inaccessible from a Wikibook. In effect there's a &quot;Berlin Wall&quot; between two Wikimedia projects. Would a &quot;See also&quot; section be permissible?
::::::Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 14:00, 7 May 2026 (UTC)

== You may be an eligible candidate for the U4C election ==

&lt;div lang=&quot;en&quot; dir=&quot;ltr&quot; class=&quot;mw-content-ltr&quot;&gt;
Greetings,

The [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee|Universal Code of Conduct Coordinating Committee (U4C)]] seeks candidates for the 2026 election. The U4C is the global committee responsible for overseeing enforcement of the [[foundation:Special:MyLanguage/Policy:Universal Code of Conduct|Universal Code of Conduct]]. Elections are held annually, if elected a committee member serves for two years.

This year the U4C requires candidates to hold administrator rights on at least one wiki, which is why you are being contacted as you appear to hold this right. There are other requirements, such as candidates must be at least 18 years old and may not be employed by the Wikimedia Foundation or other related chapters and affiliates. You can find more information in the [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026#Call_for_Candidates|call for candidates on Meta-wiki]]. Additionally, the committee's working language is English; some ability to communicate in English is required.

The election opens on 18 May, if you are eligible and interested you have until 10 May to submit your candidacy. There will week between for candidates to answer questions from the community. Voting takes place privately in [[m:Special:MyLanguage/SecurePoll|SecurePoll]], successful candidates must receive at least 60% support. More information is available on [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026|the 2026 Elections page]], including timelines and other candidacy information. If you read over the material and consider yourself qualified, please consider submitting your name to run for the committee. If you think someone else in your community might be interested and qualified, please encourage them to run.

In partnership with the U4C -- [[m:User:Keegan (WMF)|Keegan (WMF)]] ([[m:User_talk:Keegan (WMF)|talk]]) 18:32, 28 April 2026 (UTC) &lt;/div&gt;
&lt;!-- Message sent by User:Keegan (WMF)@metawiki using the list at https://meta.wikimedia.org/w/index.php?title=User:Keegan_(WMF)/test&amp;oldid=30471751 --&gt;

== Undeletion request ==

Hello,


I am writing to request an undeletion of the page Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad. You stated you are a frequent visitor of the Lentis page and are thus familiar with it. This page was part of a class assignment and was in progress at the time of deletion. The work deleted is what we will be graded on for our class, so we would appreciate the restoration. [[User:Yqj3km|Yqj3km]] ([[User talk:Yqj3km|discuss]] • [[Special:Contributions/Yqj3km|contribs]]) 19:36, 4 May 2026 (UTC)

:@[[User:Yqj3km|Yqj3km]] see my response below regarding undeletion. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 May 2026 (UTC)

== Undeletion request ==

About the page on Lentis called Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad: I, too, request undeletion, please. If the authors made any msitakes, the fault is 100 percent mine, for failing to guide them correctly. Like all chapters in this book, this team's chapter is a class assignment. I will be interested also in the reason for deletion so that I can guide authors better. I want to help my students be constructive contributors. Many thanks!

[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 20:03, 4 May 2026 (UTC)

:Hi @[[User:Norton|Norton]] and thanks for the ping! I deleted it because it was not titled/filed correctly, so I didn't realize it was part of [[Lentis]]. I have undeleted it and moved it to [[Lentis/Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:14, 4 May 2026 (UTC)
::Many, many thanks, @[[User:Kittycataclysm|Kittycataclysm]]! I am very grateful as always for everything you do for Wikibooks!
::[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 22:27, 4 May 2026 (UTC)

== Log in issues ==

Hi, messaging you as you seem to be the most active admin at the moment. I can't log in (as posted at  &lt;bdi&gt;[[Wikibooks:Reading room/Administrative Assistance]] and also on my WP page at&lt;/bdi&gt; [[w:User_talk:Xania]]). Seems to be an issue with extra security for admins? I am asked to use my authenticator app (which I can't as I have never set it up for Wikibooks) or a recovery code (which I don't have). Any idea what I should do in this situation? Xania [[Special:Contributions/&amp;#126;2026-28255-89|&amp;#126;2026-28255-89]] ([[User talk:&amp;#126;2026-28255-89|talk]]) 18:21, 10 May 2026 (UTC)

:Apologies for missing this yesterday! It seems like we have a few people working on it over in the reading room, and I'll keep track there. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:37, 11 May 2026 (UTC)

== Splitting pages ==
FYI, I untagged [[Art Print Production Methods]] as for splitting: the page is rather small with its 20 KB and does not need splitting, in my view. Ideally, there would be an operationalized, fairly detailed policy on the matter, but I do not know of one. Single-page books are in [[:Category:One-page books]]. --[[User:Dan Polansky|Dan Polansky]] ([[User talk:Dan Polansky|discuss]] • [[Special:Contributions/Dan Polansky|contribs]]) 04:45, 20 May 2026 (UTC)

== Slander ==

Your tag is slanderous and very easily proven wrong.[https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654455] Given you likely didn't bother to look at the edit history, I would remind you that your given reason that you think it was AI is because you see the chapter is &quot;numbered&quot;. That however was 100% my own personal decision after I reviewed my work and thought to myself that I later wrote in the introduction that there is a first to fourth chapter. However I thought to myself that the readers would not be easily made aware of what is meant by first to fourth as I didn't number them - so is why I dedicated an entire edit to make it less ambiguous  [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654328]. I should not have to be falsely penalized because I wanted to be more considerate and ensure better clarity. I do however request AI to help me figure out coding like this - [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654329] as I don't know how to link. But I intentionally take great efforts to not rely on AI to write that book and find your wrongful presumptions troubling. [[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 06:00, 15 July 2026 (UTC)

:@[[User:JaredMcKenzie|JaredMcKenzie]] thank you for clarifying! I flagged it for review because it matched a common pattern we see associated with LLM use here. If that is not the case, then nothing needs to happen in that respect; however, you will likely want to fix the lists so that they are correctly formatted in the Wikitext and not hard-written—let me know if you have any questions about that. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:14, 16 July 2026 (UTC)
::Yeah, I don't really understand what you mean by &quot;correctly formatted&quot; list. I assume you are referring to chapter 4 - (''Further reading'')? What exactly is wrong with it? Could you go and demonstrate what fixing that looks like? I believe I would just quickly learn by seeing what you mean and hopefully know what to do in future. [[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 18:35, 16 July 2026 (UTC)</text>
      <sha1>124cfqhsvfb2xz91dnz0ke34p51xr8d</sha1>
    </revision>
    <revision>
      <id>4654739</id>
      <parentid>4654725</parentid>
      <timestamp>2026-07-16T19:27:30Z</timestamp>
      <contributor>
        <username>JaredMcKenzie</username>
        <id>3528493</id>
      </contributor>
      <comment>/* Slander */ Update; I think I understand.</comment>
      <origin>4654739</origin>
      <model>wikitext</model>
      <format>text/x-wiki</format>
      <text bytes="96254" sha1="7ibjfr347eaoz1blro1dgmh5ifl31hd" xml:space="preserve">{| class=&quot;wikitable&quot;
|+
! colspan=&quot;3&quot; |Talk Page Archives
|-
|[[User talk:Kittycataclysm/Archive 2022|2022]]
|[[User talk:Kittycataclysm/Archive 2023|2023]]
|[[User talk:Kittycataclysm/Archive 2024|2024]]

|}

== That IP range calculator ==

Following [[phab:T381138|T381138]], I have now become the maintainer of the IP range calculator you like. You can find it [[toolforge:ftools/general/ip-range-calc.html|here]]. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 23:10, 9 January 2025 (UTC)

:Thank you for the heads-up! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:56, 10 January 2025 (UTC)

== A merge and unmerge from two years ago ==

I was browsing through the history merge log when I saw that you merged [[Cookbook:Chicken Bog]] into [[Cookbook:Chicken Bog I]], and then promptly reverted it. What happened here exactly? Could I correct it? [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 15:55, 10 January 2025 (UTC)

:Good question! I can't remember what I was trying to do, but it looks like I didn't succeed at what I wanted based on the log comment. You're just trying to history merge to get [[Cookbook:Chicken Bog I]] to have continuity of history? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:35, 10 January 2025 (UTC)
::I think I figured out your mistake: it outright moved the revisions from the first page to the second, rather than copying them. This would have caused the other two [[Cookbook:Chicken Bog]] pages to have incomplete histories. I think the only solution would be to XML import the pre-April 2023 revisions from the first page to the other three, and I'm not sure if that's the best idea, and I am technically unable to do so. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 16:49, 10 January 2025 (UTC)

== Undeletion request ==

I wouldn't be surprised if you expected this, but I'd like to ask you to undelete the subpages of [[Rotorcraft Fundamentals]] you just deleted with the summary &quot;Use of copyrighted work without permission. Please read Terms of Use: page needs to be imported for attribution&quot;, so that I can do that. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 19:54, 14 January 2025 (UTC)

:Done! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:57, 14 January 2025 (UTC)
::Upon further investigation, this might actually be a rare case where an [[WB:UT|unmerged transwiki]] is ''preferred'' (this is part of why I stopped calling them &quot;bad transwikis&quot;), since only a small portion of the Wikipedia article (with over 2,000 revisions) was copied over. Importation is generally only needed if the ''majority'' of the page is copied across wikis. I'll just leave a null edit providing attribution and add {{tlx|Copied}}. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 21:19, 14 January 2025 (UTC)

== Reusing [[Cookbook:8 Desserts in 1 Pan]] on wikiHow ==

Hi, I am a user on wikiHow, see [[wikihow:User:Xeverything11]]. I would like to create a new recipe on wikiHow. I wanted to let us know if I can give permission to reuse your contributions to this recipe from Wikibooks to wikiHow. I (as a copyright holder) created this recipe on Wikibooks, but you contributed to this recipe.

If not, I'll use the revision before you contributed since I was the only author. 

Wikibooks uses CC-BY-SA 4.0 while wikiHow uses CC-BY-NC-SA 3.0, which both licenses are incompatible due to ShareAlike conditions.

Thanks [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 08:27, 15 January 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] I'm personally fine with this as long as proper attribution is given back to the original recipe page here. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:52, 20 January 2025 (UTC)
::I adapted this [[wikihow:Make-8-Desserts-in-1-Pan|recipe]] on wikiHow with attribution, and got a Rising Star (an achievement used for best new articles on wikiHow). Thank you! [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 19:49, 24 January 2025 (UTC)

== Wikibooks community ==

Hi, @[[User:Kittycataclysm|Kittycataclysm]]!

I am trying to contribute more to English Wikibooks. My main contributions will focus on the Cookbook, especially on Indonesian recipes. Do you have a community group where we can discuss and share ideas together?

I am looking forward to join. Thank you!

[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 08:47, 16 January 2025 (UTC)

:@[[User:Raflinoer32|Raflinoer32]] Sorry I missed this, and welcome! Are you asking about a Cookbook-specific area for discussion? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:39, 20 January 2025 (UTC)
::Yes. Do you know place for this?
::Thank you 
::[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 09:41, 21 January 2025 (UTC)
:::Honestly, there's not a centralized Cookbook-specific discussion space, especially since there aren't currently a ton of active contributors. Some people ask questions at [[Cookbook talk:Table of Contents]]. I'm currently the most consistently active and involved Cookbook editor, so feel free to ask me questions! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:46, 22 January 2025 (UTC)

== Congratulations! ==

[[File:Admin T-shirt.svg|thumb|You get this now.]]
You are now a permanent administrator. Welcome to the team (I am entitled to say this because I technically got the extension a few hours before you did)!{{FBDB}} [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 10:33, 29 January 2025 (UTC)

:Thanks :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:29, 29 January 2025 (UTC)

== Is there a way to contact a Steward on WikiBooks? ==

Hi {{PAGENAME}},
Is there a way to contact a Steward on WB? I tried to find who the active Stewards are here  at [[Special:ActiveUsers?username=&amp;groups%5B%5D=steward&amp;wpFormIdentifier=specialactiveusers]] but nothing shows up.

The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the [[Wikimania-wiki]], but I just visited the [[wikimania 2014 wiki]] and could not  find this backward link. I tried to ask about this  on the [[Wikimania 2014 main-page talk]] but disovered that the Stewards have protected it. 

Is there a way  wikibookians can communicate with Stewards at WB? Thanks in advance for answering this non-urgent question, and apologies for all the red-links which I can bluify if needed. Cheers [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 16:37, 7 February 2025 (UTC)

:@[[User:Ottawahitech|Ottawahitech]] You can ask this on somewhere like [[metawiki:Steward requests/Miscellaneous]]. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 17:01, 7 February 2025 (UTC)
&lt;s&gt;:@[[User:Ottawahitech|Ottawahitech]] seconding what Leaderboard said—we no longer have any active stewards at enWB.&lt;/s&gt; Had a brain fade there and mixed up stewards with bureaucrats. Yes, meta is the place for this. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:15, 7 February 2025 (UTC)
::@Kittycataclysm,@[[User:Leaderboard|Leaderboard]], or anyone else:
::Some wikibookians prefer for various reasons to post only at wb. I myself am indef-blocked at  META so could not participate at [[metawiki:Steward requests/Miscellaneous]] even if I waned to.
::Since [[Wikimania]] is a topic of interest to all members of the [[wikimedia movement]] why can't wikibookians talk to thier elected representatives here? [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:56, 7 February 2025 (UTC)
:::@[[User:Ottawahitech|Ottawahitech]] I can check with the blocking admin to see if they'd be willing to unblock you, if you'd like. The reason things like these are done at Meta is that Meta is a cross-project coordination platform - stewards ''cannot'' be expected to watch every project after all. Now you could message any steward here on Wikibooks if you really wanted to, but that is not normally a good idea. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 02:26, 8 February 2025 (UTC)
::::Wikimania is the annual conference celebrating all the free knowledge projects hosted by the Wikimedia Foundation (WMF).  It is a wikimedia initiative which is meant to help all of our projects (including wikibooks), gain more readership, educate more wiki-editors, foster better communications, and much more.  The wmf has been hosting  a Wikimania-wiki dedicated to each Wikimania annual event since 2004. These wikis contain a wealth of information, but can  benefit from wiki-improvements, starting from spelling and grammar errors that detract from their to appeal to the general membership. It would be nice if Stewards paid more attention to it.
::::@[[User:Leaderboard|Leaderboard]], I truly appreciate your offer, but  I posted this here not in order to get someone to advocate for one unblocking at META. As I said earlier:
::::* &quot;Some wikibookians prefer for various reasons to post only at wb&quot;
::::* &quot;The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the Wikimania-wiki, but I just visited the wikimania 2014 wiki and could not find this backward link. I tried to ask about this on the Wikimania 2014 main-page talk but disovered that the Stewards have protected it&quot; 
::::I would much rather see more wikimedia members question blocking in general at META. One cannot run such large movement of people from different backgrounds and nationalities simply by silencing minorities  IMIO. [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:12, 8 February 2025 (UTC)

== [[Crystal ball]] ==

That page appears to be a mixture of isolated paragraphs from [[w:Crystal ball|Crystal ball]], hence my tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 03:04, 9 February 2025 (UTC)

:Yep, that seems correct! I also queried it simply because it does not seem suitable for inclusion at all. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:09, 9 February 2025 (UTC)

== Question about an edit suggestion ==

Hi Kittycataclysm,

Thanks for the great work you do as an admin! I wanted to clarify a suggestion you made on a recently published page I’m working on. You recommended splitting it into smaller sections—would you suggest creating separate pages for these sections, or would a higher-level header for some topics be sufficient?

Any specific recommendations you have would be greatly appreciated!

Here’s the link to the page I’m referring to: [[Funding and Finance of Transportation Projects in the United States of America]]

Thank you! [[User:Svrmustafa|Svrmustafa]] ([[User talk:Svrmustafa|discuss]] • [[Special:Contributions/Svrmustafa|contribs]]) 18:19, 18 February 2025 (UTC)

:Hi @[[User:Svrmustafa|Svrmustafa]], and thanks for asking! Splitting refers to creating new pages, each with a smaller amount of content. The main page should then contain a table of contents, and each page can contain a navigation template for easier navigation. I'll create the table of contents based on the current work and move some content to one of those pages as an example for you; then, you can do the rest. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:26, 19 February 2025 (UTC)
::Following up on this—I noticed that you use the term &quot;paper&quot;. However, technically Wikibooks hosts books not papers, so you should probably change this wording. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:38, 19 February 2025 (UTC)
== Talkback ==
{{Talkback|Cookbook talk:Chilli Crab|Recipe Questions}} [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 09:54, 19 February 2025 (UTC)

:@[[User:Kittycataclysm|Kittycataclysm]] I also made [[Cookbook:Prata|this]] [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:15, 19 February 2025 (UTC)

== Hello ==

Can you look at my latest recipe? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 00:10, 28 February 2025 (UTC)

:I saw it! It needs a few corrections, which I'll note. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:23, 28 February 2025 (UTC)
::@[[User:Kittycataclysm|Kittycataclysm]] How do you write recipe summary, correct headers [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 06:04, 28 February 2025 (UTC)
:::Please see [[Cookbook:Policy/Recipe template]]. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:08, 28 February 2025 (UTC)
::::ok [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 02:33, 1 March 2025 (UTC)

== Cookbook ==

Hi there, Kittycataclysm. I wandered over here from Wikipedia, and I'm quite enamoured with this cookbook. I noticed you seem to be the one maintaining it, and I thought I'd reach out. Can I really just start cranking out recipes from public domain cookbooks and my family recipes? It's that simple? I was also wondering about the featured recipes section. There's not very many in there, and I imagine there's not very many folks around to do reviews compared to GAR on Wikipedia. How do you handle content review? Thanks. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:51, 1 March 2025 (UTC)

:Hi @[[User:MediaKyle|MediaKyle]] and welcome! For some context, the Cookbook has been around since the very beginning of Wikibooks, but it had gotten into a bit of disarray over the course of about two decades by the time I found it. I started the long process of overhauling, standardizing, and expanding it just over four years ago—I finished standardizing the recipe formatting and quality a while back and am currently working my way through the ingredient pages before moving on to equipment, techniques, and cuisines. You can absolutely add any public domain recipes as well as your own recipes—they just need to conform to the [[Cookbook:Policy/Recipe template|recipe template]] and [[Cookbook:Policy|Cookbook policy overall]]. It's even better if you've made the recipe and can contribute a nice picture and specific guidance/instructions/notes! Please feel free to ask me any questions. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:27, 1 March 2025 (UTC)
::Oh, and regarding the featured recipes section, I actually haven't gotten around to looking into that yet—there's been a lot to do! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:28, 1 March 2025 (UTC)
::That's great, thanks a lot for your response. This is just delightful. Maybe content review is something that we could collaborate on. There's a lot of recipes in here and it would be nice to know which ones are the best. Question for you, [[:Category:Brown sauces]] is really bothering me. How can I move that to Brown sauce recipes? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:29, 1 March 2025 (UTC)
:::Good catch on that category! It seems like it was created two decades ago and never got corrected—feel free to recategorize those recipes. Thank you also for introducing the hideprefix parameter to the category trees—I didn't realize that was an option, and it reduces the visual clutter! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:38, 1 March 2025 (UTC)
::::My pleasure! As I continue to look at the categories, this is actually worse than I thought. We have both [[:Category:Sauce recipes]] and [[:Category:Recipes for condiments]] and I suspect that's just the beginning. I want to go through and categorize everything properly, but the bones aren't even there... How long do I have to be here before it'll let me create and move around categories? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:40, 1 March 2025 (UTC)
:::::Regarding the categories, the category overhauling is in progress, since I address the category when I overhaul the associated page. The variation in titling is actually somewhat deliberate—I started changing it from &quot;____ recipes&quot; in certain cases to solve a particular categorization problem. Sometimes, there is an item that is used in recipes as an ingredient but for which there are also recipes. For example, [[:Category:Recipes for bread]] versus [[:Category:Recipes using bread]]. The different naming scheme is necessary to properly delineate the categories, and I'm working on implementing it a bit more consistently as I go. While you're still getting started, it would be great if you could check with me when something looks odd or out of place—that way I can take a look and weigh in on whether that's normal or not and maybe provide some context. Just off the top of my head, I think you will have to wait for autoreview status to make move changes. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:56, 1 March 2025 (UTC)
::::::I see what you're saying, I've been trying to wrap my head around that. Maybe it would be beneficial to try to put together some sort of a Cookbook MOS regarding category structure? It's kind of all over the place right now. Using your bread example, would it perhaps make more sense to have [[:Category:Bread recipes]] and [[:Category:Recipes using bread]]? There would be no ambiguity with just those two categories, but when you add the extra [[:Category:Recipes for bread]], that's when things start getting a little whacky. What do you think? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:05, 1 March 2025 (UTC)
:::::::Either that or get rid of [[:Category:Bread recipes]] and keep the other two. But one of these categories gotta go, I reckon. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:07, 1 March 2025 (UTC)
::::::::I see you already had the same thought as me. I think all categories should include &quot;for&quot; or &quot;using&quot;. Take for example, [[:Category:Recipes for pancakes]] as opposed to [[:Category:Pancake recipes]]. Well obviously there's no recipes using pancakes. But for something like [[:Category:Recipes for gravy]], there may also be a need for [[:Category:Recipes using gravy]]. The lack of consistency in this regard means the only way to achieve consistency across the categories is by changing them over to that format. Sorry for clogging up your talk page! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:18, 1 March 2025 (UTC)
:::::::::Same heads-up as below—migrating this over to [[Cookbook talk:Table of Contents]] —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:10, 4 March 2025 (UTC)
:Also, on [[Cookbook:Table of Contents]], could you please add a wikilink for [[Cookbook:Breakfast]], and maybe add cooknav to the top for seamless navigation between all the top level articles? Can't edit that article yet. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:47, 1 March 2025 (UTC)

== More Table of Content Edits ==

Hello again. I've been going through everything and this is my list of suggestions for edits to the table of contents. Unfortunately there's not much else I can do for now, because without autoconfirmed my ability to change anything is very limited. I was going to ask for someone to check off the confirmed box for me at RfP but I can't post there either, so I guess I'll be back in four days.

* Fix Bread wikilink
* Remove &quot;Creaming&quot; from techniques, redirected to Mixing
* [[Cookbook:History of Food and Cooking]] points to redirect, needs capitalized
* [[Cookbook:Low-Carb]] points to redirect, needs capitalized
* [[Cookbook:Cuisine of the Mediterranean]] to [[Cookbook:Mediterranean Cuisine]] for parity
* Remove the S from the cuisine wikilinks on ToC, currently redirecting
* Create [[:Category:Lunch recipes]], wikilink to ToC
* Wikilink [[Cookbook:Dessert]] under Meals
* Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category
* Create [[Cookbook:East Asian Cuisine]] so I can add the recipes from [[:Category:East Asian recipes]] to it; currently is a redlink on the ToC
* Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;
* Appendix and Equipment sections switch places

Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:46, 1 March 2025 (UTC)

:I took the liberty of doing it myself in my userspace. You can just copy it over from [[User:MediaKyle/sandbox]]. Figured I'd save you the trouble of trying to figure out what I'm talking about. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 14:15, 1 March 2025 (UTC)
:Circling back to this! It seems like your suggestions are getting at a couple different things. I'll try to go through them point-by-point below:
:* {{xt|Fix Bread wikilink}} {{done}}
:* {{xt|Remove &quot;Creaming&quot; from techniques, redirected to Mixing}} see below comments on TOC.
:* {{xt|Cookbook:History of Food and Cooking points to redirect, needs capitalized}} {{not done}} for now because I don't fully understand the urgency and I want to triage/prioritize things for you, but please feel free to make this change yourself once you can!
:* {{xt|Cookbook:Low-Carb points to redirect, needs capitalized}} {{not done}} for same reason as above.
:* {{xt|Cookbook:Cuisine of the Mediterranean to Cookbook:Mediterranean Cuisine for parity}} {{not done}} for now just because we do have a lot of cuisine pages that follow the form &quot;Cuisine of ____&quot;. It could be good to standardize, and I had been planning to do that once I got around to the cuisines.
:* {{xt|Remove the S from the cuisine wikilinks on ToC, currently redirecting}} {{not done}} for same reason as other redirects
:* {{xt|Create Category:Lunch recipes, wikilink to ToC}} Not quite sure what you mean here, and I didn't see what it corresponded to in your linked sandbox page
:* {{xt|Wikilink Cookbook:Dessert under Meals}} {{done}}
:* {{xt|Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category}} I'm not sure about this—brunch is in many places considered a separate entity, and I don't necessarily think it would cause confusion. But, overall it's hard to determine whether it should have its own page and TOC link because I haven't actually gotten around to evaluating the meal pages and what role they should play. See also the TOC notes below.
:* {{xt|Create Cookbook:East Asian Cuisine so I can add the recipes from Category:East Asian recipes to it; currently is a redlink on the ToC}} {{done}} for now; however, I'm not sure yet whether it will ultimately make sense to keep that as a content page. I think content pages should be reasonably focused, and it may not be the best to have a cuisine page that is so broad. This is something I planned to consider once I made my way around the overhauling the cuisines.
:* {{xt|Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;}} The reason I made it &quot;Introductory Matter&quot; instead of &quot;Introduction&quot; is because there's already a chapter itself titled &quot;Introduction&quot;—it felt odd to have the entire section titled that as well. Happy to discuss other header options (e.g. &quot;Front Matter&quot;, which is a generally accepted book term)
:* {{xt|Appendix and Equipment sections switch places}} see below comments on TOC.
:* '''Comments on the TOC:''' So, I think a fundamental issue with the current TOC is that it somewhat arbitrarily picks and chooses individual pages to link. It also sometimes direct-links to categories and sometimes to content pages, which I don't think we should do. Because the cookbook is so expansive, it's been established that manual indices intending to capture detail in large areas don't really make sense and quickly get bulky and out-of-date. This is why categorytree is such a useful tool! After thinking on it for a while and making some small tweaks, I think I'd ultimately like to overhaul the TOC and come to a solution that keeps a few broad headers/links to the small handful of the primary content pages while perhaps stashing away more detailed and self-updating lists in a collapsible way to reduce clutter but allow for customizable user navigation. Much to think about, and I'll probably workshop some things on the side to see how they feel.
:Let me know if I've misunderstood anything! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:24, 3 March 2025 (UTC)
::Thanks for the notes! Here's my thoughts:
::* On the Cuisine titling, it actually seems like [[Cookbook:Cuisine of the Mediterranean]] and [[Cookbook:East Asian cuisines]] are the only ones that don't follow the naming scheme, i.e. &quot;[[Cookbook:African Cuisine]]&quot;, and I think that shorter titles are preferable where it makes sense.
::* On your note about East Asian Cuisine, I actually had the same thought after going through the cuisine pages. Having three separate pages for different kinds of Asian cuisine does seem a little silly, doesn't it? Do you think it might be better to combine all of them under one &quot;Asian Cuisine&quot;, but put the different locales under separate headers?
::* On Brunch - I honestly think there's way too much ambiguity around what exactly constitutes as &quot;brunch&quot; to keep that in. I feel as though the term brunch more applies to the time you're eating, rather than the kind of food. I think it would be easier to keep meals that include commonly accepted breakfast foods in the Breakfast category, and things that don't fit neatly into that, into the Lunch category. This would prevent any dilemmas in the future where we can't decide whether something is breakfast or brunch.
::* You're right that it looks a little awkward to have the header as Introduction when there's a page called introduction. I still think that to say &quot;Introductory Matter&quot;, or &quot;Front Matter&quot; as you mentioned, is a little long-winded and reflects a more academic tone than needed for a cookbook. Upon further reflection, I think maybe rather than worrying about the header at this point, we should perhaps think about trying to compile all of those short introductory type pages into one comprehensive introductory page. Then we likely won't even need a header for it on the ToC.
::* The ToC is definitely a bit cluttered, and it bothers me too that there's a real lack of consistency across whether the wikilinks lead to a page or a category. I'm not sure how I would feel about cutting away too much of the navigation from it, though, because just about every page on there does have a reason to be there, it's just that they're not presented very nicely. Some of it can certainly get nested or combined though. I'll play around with it over the next few days in my sandbox as well and let you know if I come up with anything.
::* As an aside, the first thing on my to-do list once my autoconfirmed comes through is to start subcategorizing all of the recipes so that they're all nicely sorted in the category trees. When you have a chance, I'd love to hear your thoughts on what we should use as the standard naming for categories. Once we determine this, I think we can also take the liberty of updating the cookbook MoS to reflect it.
::Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:33, 3 March 2025 (UTC)
:::Note: After writing this, I realized what you were getting at about slashing away some of the subpages. Maybe we can come up with a system where all of those subpages are under their main subpage rather than on the ToC. For example, all the Cuisines are under [[Cookbook:Cuisines]], all techniques under [[Cookbook:Cooking Techniques]], to keep the subpages off the main ToC. Also, I wonder if maybe we should try to make a centralized discussion for this somewhere, in case anyone else wants to join in at some point? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:45, 3 March 2025 (UTC)
::::Heads-up: to make it easier to keep track of these and since I think they deserve their own discussions, I'm going to gradually migrate them over individually to [[Cookbook talk:Table of Contents]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:52, 4 March 2025 (UTC)
:::::Good idea. Can you remove the semi-protection from that talk page? I see no reason why it should be protected. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:23, 4 March 2025 (UTC)

== Cookbook ToC ==

Hi [[User:Kittycataclysm|Kittycataclysm]]. I was just wondering why you didn't respond to my above message, and started a separate sandbox for the ToC instead? It seems as though you don't really want to collaborate. It would be nice if we could work on this together. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 22:43, 2 March 2025 (UTC)

:@[[User:MediaKyle|MediaKyle]] thanks for the ping! I'm sorry you feel like I don't want to collaborate—the opposite is true, and please understand that this is good-faith editing. The reason I haven't responded to the above points is mostly since you've been modifying a bunch of content and adding suggestions lately, and I've been working my way through these while continuing with my routine contributions and real life as well—things happen a little more slowly here than on other projects, and I'm the one person dedicated to the cookbook right now. The reason I created that sandbox was because I saw [[Wikibooks:Reading room/General#Modernize the shelves|your comment]] at the reading room and wanted to play around and think about your suggestion without touching the actual TOC. You're right that it's not the best, and it's been something I've been thinking about for a bit now. Please understand also that it can be overwhelming when a new editor unfamiliar with the Cookbook begins making a high volume of edits and suggestions without having much experience with it or its history—this isn't to say that you don't have good ideas or things worth contributing. In fact, you have already made a few helpful changes, as I've mentioned. I just want to do this properly and take the time to evaluate your suggestions together with the current efforts that are underway, and that can take a bit. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:03, 2 March 2025 (UTC)
::Thanks for getting back to me. While I may be new to Wikibooks, I'm certainly not new to MediaWiki, and I've been working with small wiki projects for a number of years. Perhaps it's been a misunderstanding to some degree, but I've found my reception here to be unusually unwelcoming. The way to do this properly, as you said, would be to have discussions and form consensus. Yesterday, when you reached out to me about adding hideroot to the pages, I gave you my rationale and was more than happy to have a discussion about it, but you did not reply. I noticed a similar situation happened with [https://en.wikibooks.org/wiki/User_talk:Ottawahitech#Category_sorting Ottawahitech], regarding category sorting. I'm aware that you're the main person looking after the cookbook right now, which is why I reached out to you right from the get go.
::I understand why you would want to create your own sandbox to play around with options for the ToC, but I'm sure you can understand why it would draw my attention that you would do this without implementing any of the wikilink fixes I mentioned, or making an attempt to discuss it further. This came across to me as not wanting my help.
::I invite you to check out my page on Wikipedia. I've made contributions across quite a wide area of topics there, as well as the other Wikimedia projects, and this is the first time I've encountered any sort of resistance to my contributions. I think Wikibooks has enormous potential, and I'm very excited to contribute to helping it grow. On most projects, this would be something to be encouraged. I don't feel like &quot;I'm sorry that you feel that way&quot; was really an appropriate response. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:59, 2 March 2025 (UTC)
:::I think you're right that this has been a mix of misunderstanding and miscommunication, and I think I can understand how things came across as unwelcoming! For whatever it's worth, I absolutely plan on circling back to the various discussions at hand (I have all the relevant pages open to return to), but it seems like the order I did things made it seem like I was ignoring you (if I'm understanding correctly). I am pretty busy, so sometimes items on my to-do list do get lost/shunted or it takes me a bit to get around to something—please don't hesitate to give me a ping if it seems like I'm taking a while to get back to something. Looking forward to more collaboration! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:49, 3 March 2025 (UTC)
::::I'm glad you can understand where I'm coming from. To clarify, my intent is not to try to rush you, or to try to push you to make changes that you don't agree with. It's really easy to misinterpret things over the Internet, and I think a short message can go a long way. I apologize if I've caused you any undue stress by coming into the cookbook and unleashing a flurry of alterations, but do rest assured that I'm not married to any of my changes, I'm always open for discussion, and I want to see the cookbook improve just like you do. The great thing about wikis is that no change is permanent. I think we'll have it in tip-top shape in no time! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:19, 3 March 2025 (UTC)

== [[Cookbook:Polish Doughnuts (Paczki)]] ==

Do you see any reason not to just add this to Featured Recipes? At least we know this one works, and it seems like this is now one of the few recipes to have a picture that actually aligns with the recipe used. I was thinking later on we'll come up with a content review system where a couple editors will actually try the recipes nominated for FR, but in the absence of that I'd just add it to the list. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 12:25, 4 March 2025 (UTC)

:I'm fine with adding it to the featured recipes. You're right that we'll want to come up with a good system for this going forward, though it's lower down on my personal priority list at moment. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 March 2025 (UTC)

== [[Cookbook:Cream Cheese American Buttercream]] ==

Hi! I am a wikiHow user and I am planning to adapt this recipe to wikiHow. Since you contributed to this recipe, I wanted to know if I can get permission to reuse your contributions to this recipe. Thanks. [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 21:41, 4 March 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] that's fine with me as long as proper attribution and linking back to the original recipe page here are included at the top. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:28, 4 March 2025 (UTC)

== [[A Companion to Our Literary Journey]] ==

Hi! I feel that we have started to outline the scope in a clearer and more precise way and that’s the work we are going to do with the students this and for the next years, adding more sections and content. Do you think that would be enough? [[User:Ferdi2005|Ferdi2005]] ([[User talk:Ferdi2005|discuss]] • [[Special:Contributions/Ferdi2005|contribs]]) 22:43, 6 March 2025 (UTC)

:Hi @[[User:Ferdi2005|Ferdi2005]]! Yes, this seems to be reasonably outlined. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:51, 7 March 2025 (UTC)

== Exercising care with copyright ==

When deleting a page as a copyright violation, it is important that you '''do not quote any content from the deleted page'''. If you do, then your log entry is itself a copyright violation. I have redacted a recent deletion that you performed because of this. If you want to make sure that none of your past deletions have been problematic for this reason, you can [[quarry:query/90444|run this SQL query]] to get a list of every deletion that could be eligible for redaction. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 18:32, 21 March 2025 (UTC)

:Hi @[[User:JJPMaster|JJPMaster]] and thank you for the message. In the most recent instance that I think you're referencing, I do not see any material in the edit summary that posed a significant risk—I don't believe the few listed words would be a copyright concern. However, I do understand your concern! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:31, 21 March 2025 (UTC)

== Splitting Pages ==

Hi I have recently made the book on the [[History of the Nawabs of Bengal]] and you gave a notice on how you believe it should be split into smaller bits. As I am still new to wikibooks I don't know how to do this. Can you please assist me on renaming the page so I can split the page into multiple pages? @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 19:47, 29 March 2025 (UTC)

:@[[User:Greatswrd|Greatswrd]]: You did it. I've removed the tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 22:44, 29 March 2025 (UTC)
:Like @[[User:JJPMaster|JJPMaster]] said, you're all set! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:53, 29 March 2025 (UTC)
::Thanks! @[[User:JJPMaster|JJPMaster]] @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 10:24, 30 March 2025 (UTC)

== Minecraft book ==

Is it good creating pages like this, [[Minecraft#Husk]]? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 12:43, 9 May 2025 (UTC)

:@[[User:Cactusisme|Cactusisme]] what do you mean? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:18, 10 May 2025 (UTC)
::are we allowed to create pages like that? like for every mob [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:02, 11 May 2025 (UTC)
:::To be honest, I don't think the structure and formatting of the book is very good. Several of the mob pages, for example, have very little information and aren't particularly helpful on their own. If I were working on it, I would restructure the book. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 14:09, 11 May 2025 (UTC)
::::I am planning to do that. [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 04:19, 12 May 2025 (UTC)

== Request to Review Adjusted User Page (XoriantTeam) ==

Hello [[User:Kittycataclysm|Kittycataclysm]],

I hope you're well. I noticed that my user page ([[User:XoriantTeam]]) was recently deleted for appearing promotional or inappropriate for Wikibooks. Thank you for keeping the community standards in check.

I’ve since revised the content with closer attention to neutrality and compliance with Wikibooks guidelines. My intent is to participate constructively, especially in areas related to digital engineering and educational content creation.

If possible, I’d appreciate your help reviewing the revised version. I'm happy to share it or upload it as a file if there’s a preferred method.

Please let me know how best to proceed. I welcome any suggestions and will gladly make further adjustments.

Best regards,  

XoriantTeam [[User:XoriantTeam|XoriantTeam]] ([[User talk:XoriantTeam|discuss]] • [[Special:Contributions/XoriantTeam|contribs]]) 11:02, 15 May 2025 (UTC)

:Hi there—you can publish an updated user page, but I'd caution you against talking about your company. Keep it limited to your involvement with Wikibooks. You may contribute productively here, but further promotional materials are grounds for an indefinite block. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 12:30, 15 May 2025 (UTC)

== Planning to use AWB to update categories on the cookbook ==

Hello. I noticed in recent changes that you were moving some categories using HotCat (e.g. moving Category:Chile recipes to Category:Recipes using chile), which can be time-consuming. Therefore, I plan to help you with moving the cookbook categories by adding myself to enabledusers and enabledbots in [[Wikibooks:AutoWikiBrowser/CheckPageJSON]]. Would this be fine if I assist you and to add myself to the check page? I am familiar with using AWB after testing on a non-Wikimedia project. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:42, 8 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—thank you for the tip! I just installed JWB, so this should make my mass cat changes much faster. Thanks again! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:11, 8 June 2025 (UTC)
:: Thank you for the information. Also, is it okay if I change (for example) [[:Category:Vinegar recipes]] to [[:Category:Recipes using vinegar]] (I can redirect the former category to the latter), given that we should move {{tq|Category:[ingredient] recipes}} to {{tq|Category:Recipes using [ingredient]}} for consistency? [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:57, 8 June 2025 (UTC)
:::Sure thing—go ahead! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:53, 8 June 2025 (UTC)

== Tool for even faster category changes ==

See [[:c:Help:Gadget-Cat-a-lot#As_your_user_gadget]]. I just [https://en.wikibooks.org/w/index.php?title=User:Koavf/common.js&amp;action=history installed it] and used it dozens of times in a click. Let me know if you need any help. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:36, 19 June 2025 (UTC)

:@[[User:Koavf|Koavf]] Thanks! I'm having a little trouble activating it, but I'll keep trying. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:54, 19 June 2025 (UTC)
::A lot of times, a purge will do the trick. See [[:mw:Purge]]. Usually just &lt;kbd&gt;Ctrl+Shift+R&lt;/kbd&gt; once or twice. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:55, 19 June 2025 (UTC)
:::Took several purges, but we're set now! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:16, 19 June 2025 (UTC)

== Advice on when I should run for adminship ==

Hi, I hope you are doing well. I am asking for some advice on when I should run for enwikibooks adminship, given the following below:

Currently, I am doing some optimizations for dark mode on this project, and some of the message box/MediaWiki interface/template pages might be outdated, fully protected, or can use a little help using mw-parser-output. These unfortunately might hinder the process of updating these pages/templates for Vector 2022's dark mode.&lt;br&gt;
Additionally, I have a solid expertise with edit filters, as I have requested some administrators to update deprecated filter variables, switching filters from warn and disallow to disallow only, and I can also monitor the filter log for potential false positives (from local or global filters).

A fellow English Wikibooks administrator also said to me that they are willing to support me in a few months when I run for adminship, as I am generally trusted.

I hold two advanced global permissions, and I hold an edit filter helper permission on the English Wikipedia, to be sure. Thank you for your consideration. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 01:02, 23 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—good question! I agree that you are a trusted user, and I think it would be reasonable for you to run for adminship, especially given our need to fix up technical aspects of the project. If you don't plan to commit to Wikibooks long-term (i.e. you have some projects you'd like to take a few months to complete and then be done), you can always request temporary adminship. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:30, 23 June 2025 (UTC)
:: Thank you for your feedback, but I also plan to monitor for vandalism/spam, and to commit to reduce the administrative assistance reading room backlog, should I be elected for adminship (and I forgot to mention those). Anyway, regarding your feedback, I might run by August or even July, given that I've lately started contributing more often to Wikibooks. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:29, 23 June 2025 (UTC)
::: [[User:Kittycataclysm|Kittycataclysm]], I am pinging you one more time to see if you have read my response above yours. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:34, 26 June 2025 (UTC)
::::Hi @[[User:Codename Noreste|Codename Noreste]]! I'm not sure what you mean—was there an additional question you had? Everything you've outlined seems quite reasonable. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:26, 26 June 2025 (UTC)
::::: Apologies for the confusion, I don't have any questions to ask. I was clarifying that I can help with implementing edit requests and to block obvious vandals and spammers, aside from the skills I mentioned earlier. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:32, 26 June 2025 (UTC)

== how is it you feel able to interfere in my sandbox? ==

you deleted a page in my sandbox that was my way of providing my response to a request from an OpenSCAD dev team leader for a couple of text blurbs for use on a web page of the OpenSCAD site.

now that you have deleted my page i have to recreate the texts from a screenshot to be able to offer the suggestions, which i will 

This kind of high handed treatment is what keeps me from being a wiki-anything contributor .. If it is Wiki policy to interfere in the documentation of an open source project because it is hosted on Wikibooks then i will take up the task of moving our online docs to a site where you cannot interfere.
--
[[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 21:56, 29 June 2025 (UTC)

:Hi @[[User:VulcanWikiEdit|VulcanWikiEdit]]—thanks for bringing this to my attention. I now understand that this was intended to be in your user namespace—I've undeleted it and moved it to the correct namespace for you. Let me know if anything else comes up! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:05, 30 June 2025 (UTC)
::ah .. err .. umm .. well that is a gentle answer to my ire. Thanks for being so gracious [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:29, 30 June 2025 (UTC)
::and .. isn't my sandbox in my namespace by default? [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:30, 30 June 2025 (UTC)
:::No worries—it looks like you didn't add the prefix &quot;User:&quot; before writing out the full page titles, so the pages you created were technically in the project's Main space with the official published materials. Going forward, you can just double-check that the page title starts with &quot;'''User:'''VulcanWikiEdit/sandbox&quot;, and that should keep everything in the right place! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:36, 30 June 2025 (UTC)
::::BTW .. i love the play on cat lover name [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 15:35, 1 July 2025 (UTC)
:::::Thank you! That's very kind. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:46, 1 July 2025 (UTC)

== Regarding the user Codename Tameirao ==

Could this be Matthew again (the Unicode LTA)? I believe it might be him based on his usage of edit summaries, and his usual edits to [[Unicode/Versions]]. I just blocked his recent account, and then I protected and stabilized that Unicode book. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 23:51, 12 August 2025 (UTC)

:I suspect you're right! That seems like a reasonable course of action. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:56, 13 August 2025 (UTC)
:: I recently encountered another possible LTA, see [[Special:Contributions/~2025-55706-6]] (as well as [[Unicode/Roadmap Blocks]]). I can email you more details if you want. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 16:30, 9 September 2025 (UTC)
:::I think this is the same LTA, yes! I've protected [[Unicode/Roadmap Blocks]], but I think it would be a good idea if we could automate this monitoring somewhat using the edit filter. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:07, 9 September 2025 (UTC)
:::: I don't think that was Matthew, as he typically uses edit summaries. The deleted page was not protected, as it was protected before you deleted it; I salted it from creation for one year. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 20:22, 9 September 2025 (UTC)
::::: You might want to look at [[Special:Contributions/Freddy Fazbearing Others]]. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:18, 26 October 2025 (UTC)
::::::Thank you! I went ahead and blocked them. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:54, 28 October 2025 (UTC)

== IP block exempt  ==

Hi Kitty,
I currently have IP block exemption on enwiki, Commons and Wikidata as I use VPNs connected to my internet security software. Can you please grant me the right on wikibooks. I have a strong password and use two factor authentication. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 10:51, 22 August 2025 (UTC)

:Hi @[[User:TarnishedPath|TarnishedPath]]! This doesn't sound unreasonable to me, but I think it would be good if you requested at [[Wikibooks:Requests for permissions]] so we can have a discussion—I have not granted this right before. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:50, 23 August 2025 (UTC)
::Kitty, thanks for pointing me in the right direction. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:25, 23 August 2025 (UTC)
::See [[Wikibooks:Requests_for_permissions#TarnishedPath_(discuss_·_contribs_·_count_·_logs_·_block_log_·_rfp_·_rights)_(IP_Block_Exemption)]] ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:35, 23 August 2025 (UTC)
== You've got mail! ==
{{You've got mail|sig=&lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 00:20, 6 September 2025 (UTC)}}

:Thank you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:06, 6 September 2025 (UTC)

== Are you able to import? ==

I made a few requests over at https://en.wikibooks.org/wiki/Wikibooks:Requests_for_import . [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 22:32, 4 October 2025 (UTC)
: [[User:2005-Fan|2005-Fan]], I'll go ahead and start the imports. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:29, 5 October 2025 (UTC)
::Thank you for your help [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 16:51, 5 October 2025 (UTC)
::: My apologies for not doing this sooner, because some database error appears when I am trying to mass import. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 23:39, 5 October 2025 (UTC)
::::I also tried to make this import earlier and ran into issues with the software. I was hoping it was a temporary bug, but it seems to be persisting. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:01, 6 October 2025 (UTC)
:::::This seems like I should get involved. {{working}}... [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 13:11, 6 October 2025 (UTC)
:::::: I believe there are five pages that have massive page histories they fail to import here. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:13, 6 October 2025 (UTC)
:::::::I backed up the XMLs of them locally but im unsure how much that'd do. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 15:18, 6 October 2025 (UTC)
::::::::Just became an importer. The reason is prob understandable but I cannot upload the XML file to here locally. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 17:23, 10 October 2025 (UTC)

== About the category parameter in the recipe summary template ==

When it uses a &quot;recipe by type&quot; category, should it use a &quot;[type/food] recipes&quot; name or &quot;Recipes for [type/food]&quot;?

I recently operated JWB to change from [[:Category:Dessert recipes]] to [[:Category:Recipes for dessert]] in multiple Cookbook recipes, and from what I've said before, I've changed to ''Recipes for dessert'' in the category parameter of Cookbook recipes. Hope you don't mind that this was over more than 250 changes (not counting the recent category changes after moving some recipe categories). Thanks. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 02:07, 27 October 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—those JWB changes you made seem fine to me! I'm not quite sure what you're asking in your first sentence, though. Assuming I understand correctly: in general, I think the default format should be whatever the actual category name is. BUT if there is a redirect, it ultimately shouldn't matter too much. And, because I'm not convinced of the utility of that infobox parameter in the first place (thinking of removing it), I'm not hugely concerned about it for the time being. Does this help? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:21, 27 October 2025 (UTC)
:: Probably, but I will say the following below (for my first sentence) to clarify:
:: On the &lt;code&gt;|category =&lt;/code&gt; parameter, when placing a recipe category name, should it either be {{tq|Sandwich recipes}} or {{tq|Recipes for sandwiches}}? I hope this clears the confusion. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:39, 27 October 2025 (UTC)

== Please no more Unicode LTA ==

Please don't block me again. I promise I will edit Unicode stuff and add correct information. [[Special:Contributions/&amp;#126;2025-30839-28|&amp;#126;2025-30839-28]] ([[User talk:&amp;#126;2025-30839-28|talk]]) 20:54, 1 November 2025 (UTC)
:&lt;small&gt;I am a bit out of the loop, so correct me if I'm wrong - I'm assuming here&lt;/small&gt; I think the point is that they want you to ''not'' edit the Unicode stuff? Also hi kitty, it's been a ... very long time.. &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:13, 5 November 2025 (UTC)
::Ok so apparently not as long as I thought, but it feels like I've been away for at least a year lol &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:23, 5 November 2025 (UTC)
:::Nice to see you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:41, 5 November 2025 (UTC)

== Administrator and reviewer user right combinations are not needed anymore ==

Given that administrators can review edits in addition to reviewers, I would suggest for you (and other administrators) to kindly remove the reviewer permission from (own) accounts. What I'm saying is that if one holds administrator and reviewer permissions together, they can remove the reviewer permission from their own account and retain their administrator permission. Thanks. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:06, 11 November 2025 (UTC)

:Gotcha—is there a reason it's bad for one user to have both these rights? If so, I can remove my reviewer right. Otherwise, it seems fairly harmless? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:26, 11 November 2025 (UTC)
:: The thing is, administrators have the &lt;code&gt;review&lt;/code&gt; user right, as well as some permissions in the reviewer user group in the administrator toolset. That means that having the reviewer user group together with the admin user group is redundant. Hope this explains it. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 19:59, 11 November 2025 (UTC)
::: @[[User:Kittycataclysm|Kittycataclysm]] &lt;s&gt;I'll do this tomorrow morning, as well as to remove autoreviewed user permissions from users who are reviewers.&lt;/s&gt; ({{doing}}) [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:24, 12 November 2025 (UTC)
: I have removed the autoreviewed user permission from users who are reviewers. As for administrators, I will do so later today. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:40, 13 November 2025 (UTC)

== Nesting in Open Book of Ecovillages and Eco Communities  ==

Hi Kittycataclysm,

I am editor of wikipedia since 2004. We have the habit if we have a concern using the talk page to clarify the case. I am not sure to delete meaningful content without previous notification and doing major redirection without agreeing the main contributor(s) is an adequate admin act and sign of good manner of host (see [[W:Wikipedia:Etiquette|Wikipedia:Etiquette]].)

Yes, It will be not an average book but above the regular. This is the exact case: ''&quot;this may be appropriate, such as with large textbooks that contain subsections with a lot of content.&quot;'' ''for to establish good structural and stylistic practices''

I have a data management certification. If you asking it will have 4 nest level on strict purpose. If you saw the introduction of the [[Open Book of Ecovillages and Eco Communities]] is/will be a global collection making effective collaboration over borders and continents. One structured + categorized(!) page for each community willing to show up. The Postal addresses has also same or larger deepness, this is unavoidable (Country/Postal Code/Location/Street/House/floor/door). Here will looks like: '''Eco-comm/Continent/Regio code/Community name'''

The goal of this system to open bridge + experience highway  for the communities using the same permaculture technics what collected parallelly in [[Open Book of Permaculture]]. That is also part of this knowledge base please dont do simplification steps on that without discussion.

I am kindly asking to revert your edits in this book.

After that I will put a notification template  about 
 &quot;This book is under construction with major changes. Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History. Common clarifications/ guides are on the primary talk page.&quot;


Thanks: [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 02:22, 12 November 2025 (UTC)

:Hi @[[User:Rodrigo|Rodrigo]], and thank you both for your contributions and for reaching out! Yes, I did make the following changes to [[Open Book of Ecovillages and Eco Communities]]:
:* I moved the pages from the [[Eco-comm]] namespace to the [[Open Book of Ecovillages and Eco Communities]] namespace, since the table of contents and pages for a given book should be under that book's namespace.
:* I removed the links to Wikipedia that were on [[Open Book of Ecovillages and Eco Communities]], since outlinking has been discouraged at en.Wikibooks as a matter of practice. Compilations of links may not fall into WB scope as an instructional text, and [[Wikibooks:Requests for deletion/Piano Solo Music: An Encyclopedia|there is precedent for deleting them]]. But, I do see that the tool I used didn't just remove links to enWP, so I will restore the prior revision and ping the tool developer.
:* I flagged it as needing denesting—you're right that nested entries can sometimes be appropriate. In this case, I was primarily flagging for a denest because the table of contents needs to be moved onto the main page, and it shouldn't have hidden navigation within the nested portions.
:Could you clarify which of these edits you do not agree with so I can make sure they are individually addressed? As an aside, it could be helpful to create a [[Help:Local manuals of style|local manual of style]] for the book in order to clearly outline the expectations. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:59, 12 November 2025 (UTC)
::My main concern not about moving and flagging but '''deleting''' [[Eco-comm]] against [[Wikibooks:Deletion policy]] and not mentioning in the clarification even after my notification. Should I note all administrators [[Wikibooks:Please do not bite the newcomers]] - or will they do speedy deleting one by one until I make them individually addressed?
:::The &lt;u&gt; local manual of style&lt;/u&gt; development is ongoing together with the sample pages.
::'''MAIN PAGE'''
::The '''Main page''' and '''Namespace''' is the [[Eco-comm]]. The '''Full Title''' or '''Cover''' is [[Open Book of Ecovillages and Eco Communities]]. Because of the high level of nesting the below extra-long-full-text-title to be avoided the Cover page is a redirection with preface/intro etc.
::'''NESTING '''
:::Featured book with 3 level nesting: [[Social and Cultural Foundations of American Education/Educational Change/Theory]]
:::5 level nesting example: [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]]
::'''Categories''' The [[:Category:Eco-comm]] will let the users make practical sub-categories e.g. [[:Category:Eco-comm/Project/numundo]] [[:Category:Eco-comm/]]
:::
::[[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 03:44, 18 November 2025 (UTC)
:::Thank you for elaborating! I'm unfortunately not sure what you mean about deleting [[Eco-comm]]—are you referring to the fact that I moved it without leaving a redirect? Regarding the nesting, I do honestly think those other books you linked should have their navigation denested since I find their format difficult to parse, and they have some navigation issues. Looping in some other active admins (@[[User:Leaderboard|Leaderboard]] @[[User:MarcGarver|MarcGarver]] @[[User:JJPMaster|JJPMaster]] @[[User:Codename Noreste|Codename Noreste]] (@[[User:SHB2000|SHB2000]]) so they can get eyes on this and voice anything they think is important. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 04:12, 18 November 2025 (UTC)
::::It makes no sense to have some crazy abbreviation as a &quot;main page&quot; or &quot;namespace&quot; (whatever that means in this context) for a book in order to allow it to be deep nested. Nobody needs to type the whole name of the nesting because that's what navigation templates do, and it is a simple matter to override the page title. I also take issue with the statement, above, &quot;Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History.&quot; Anybody can edit, and nobody gets to own and control any work. Taken together, this complaint looks like a case of attempting to assert ownership and to operate against the normal practices of Wikibooks. As such, I am completely aligned with the changes made. [[User:MarcGarver|MarcGarver]] ([[User talk:MarcGarver|discuss]] • [[Special:Contributions/MarcGarver|contribs]]) 12:49, 18 November 2025 (UTC)
:::::That. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 14:59, 18 November 2025 (UTC)
::::Thanks @[[User:MarcGarver|MarcGarver]]@[[User:Leaderboard|Leaderboard]] for the contribution, btw the [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]] also looks crazy long, is'nt it? Lets continue in the [[Wikibooks:Reading_room/General]] keeping this page for personal messages. [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 23:07, 20 November 2025 (UTC)

== Deletions of Wikibook subpages ==

Hello @[[User:Kittycataclysm|Kittycataclysm]],

regarding the [[Thesis Writing Guide]] subpage deletions, should I just recreate them when I keep working on them or was there an automatic deletion that we could undo? This document will grow, but really slowly.

Best,
Tim [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 11:37, 16 December 2025 (UTC)

:Hi @[[User:TimBorgNetzWerk|TimBorgNetzWerk]]! Since there was so little content on the deleted pages, my recommendation would just be for you to gradually recreate the chapters as you go. Does that make sense? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:54, 17 December 2025 (UTC)
::Makes sense, not my ideal solution, but also not far from it :) The end result will be the same, the in-between will just feel a little bit weird from time to time.
::Thank you for taking time to curate and quality-control Wikibooks - wishing wonderful holidays and a happy new year! [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 20:43, 17 December 2025 (UTC)
:::Thank you, and happy holidays to you as well :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:13, 17 December 2025 (UTC)

== help with &quot;Media Literacy and You&quot; == 

{{re|Kittycataclysm}} What do I need to do to get a quality review of ''[[Media Literacy and You]]'', or whatever is needed to remove &lt;nowiki&gt;{{Qr-em|not clear how this is to be structured as a book}}&lt;/nowiki&gt;? 

I ask, because you added that flag just over 2 hours after I created it. I later found that I had accidentally created it as an anonymous user. I've since started using my standard Wikiname, and I tried to respond to the requests both by creating a discussion on the &quot;Discussion&quot; page associated with that book and by upgrading the content. 

The upgrades included adding the &quot;Introduction&quot; chapter by revising an article on Wikiversity that convinced me to start this Wikibook. I have other articles that I plan to rewrite to create 9 of the remaining 11 chapters in the current table of contents, as indicated in this table of contents. 

??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:23, 8 February 2026 (UTC)

:Hi @[[User:DavidMCEddy|DavidMCEddy]]! I removed the query flag, since this is clearly not a test page. I do have concerns about the suitability of this book for Wikibooks, since it seems to be more in line with essays and original research/analysis (which are [[Wikibooks:WIW|out of scope here]]). Wikiversity seems like a very suitable place for them—is there a specific reason you want to move them here? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:24, 8 February 2026 (UTC)

::{{re|Kittycataclysm}} 
::This book is intended to accelerate the diffusion of [[w:Media literacy|media literacy]] by making it easier for humans to (a) access training materials and (b) connect with research on the most important issues that concern them and (c) discuss those issues with others who may believe differently in a nonthreatening context that encourages dialogue and a shared search for what can honestly be said about any particular issue. This is an extension of &quot;The wisdom of polarized crowds&quot; discussed in [[Wikipedia:Reliability of Wikipedia]]. 

::I don't know about you, but I'm frightened by the collapse of nuclear arms control agreements since the year 2000, by global warming, by the threats of the Trump administration to invade Canada and Greenland, etc. If this book project is successful, it will make a material contribution to reversing these trends -- unless this kind of dialogue is [[v:Responding to a nuclear attack|interrupted by a nuclear war]]. 

=== Who is DavidMCEddy ===

::I'm a [[w:Vietnam veteran|Vietnam-era veteran]] with a PhD in statistics and a publication record for which [https://www.researchgate.net/profile/Spencer-Graves-3 ReserchGate has found over 1,200 academic publications that have cited my work.] Since  [https://xtools.wmcloud.org/ec/en.wikipedia.org/DavidMCEddy 2010 I have logged]
*  6,000+ edits in each of Wikipedia and Wikiversity, 
*  1,000+ in Wikimedia Commons, 
* 30,000+ in Wikidata, and 
* almost 1,000 in other Wikimedia Foundation projects like Wikiquote and edits to the Spanish, French and German Wikipedias. 

This includes dozens of research reports posted to Wikiversity under [[v:Category:Freedom and abundance]] and 44 posts under [[v:Category:Media reform to improve democracy]] that provide a platform for documenting and discussing 44 episodes of a fortnightly &quot;Media &amp; Democracy&quot; series of 29:00 mm:ss podcasts syndicated for the [https://pacificanetwork.org/stations-2/ Pacifica Radio Network] featuring the opinions of leading experts on the increase in political polarization and violence and what those experts think should be done about this. 

I've just posted another chapter to [[Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. I hope you will agree that this book can make a positive contribution to Wikibooks and to [[w:Jimmy Wales|Jimbo Wales]]' [[w:Wikipedia:Prime objective|Prime Directive]] to create &quot;a world in which every single person on the planet is given free access to the sum of all human knowledge.&quot; Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 01:19, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Thank you and I understand this, but I am asking why you think this material is more suitable at Wikibooks rather than at Wikiversity. From what I can see, Wikiversity seems like the more appropriate home for it given our [[Wikibooks:WIW|scope]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:59, 9 February 2026 (UTC)

::{{re|Kittycataclysm}} 

::&quot;Media Literacy and You&quot; is textbook to support both self study and classes on media literacy. 

::I have been posting content to Wikiversity since 2014 and have not encountered support there for books. A search just now turned up a hint of a book on Wikiversity, but I could not easily find anything on how to do it, etc.  

::I think this &quot;Media Literacy and You&quot; project would lose the vast majority of its potential if it were not on Wikibooks. 

::??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:22, 9 February 2026 (UTC)

{{outdent}}

{{re|Kittycataclysm}} 
Will you please help me with the protocols of creating a book on Wikiversity? 

1. I have found documentation that claims that Wikiversity supports such. However, the documentation seems incomplete, potentially out of date, etc. For example, I could not see how to follow the instructions for [[Wikiversity:Help:Books#Step 1: Enable the &quot;Book creator&quot; tool]]. So I posted a question to [[Wikiversity:Help talk:Books]]. 

2. What do you suggest I do next? 

:I can create an article on Wikiversity titled, &quot;Media Literacy and You&quot;, and port everything I've posted to Wikibooks there, then replace the pages on Wikibooks with redirects to [[Wikiversity:Media Literacy and You]], [[Wikiversity:Media Literacy and You/Introduction]], and [[Wikiversity:Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. 

:If you think that's the best way to build this book project, great. It would actually be easier for me, because there would be less translation between what I already have on Wikiversity and a version for Wikibooks. (Also, Wikiversity supports &lt;nowiki&gt;{{cite Q|...}}&lt;/nowiki&gt;, which I have used extensively for years.) 

:Thanks for your help. [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 13:26, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Unfortunately, I am not familiar with the exact workings of Wikiversity, so I can't be much help there. My personal recommendation is that you ask there for help on how best to structure your materials to match the WV requirements. If you'd like some additional opinions/insight, please feel free to also check in at the [[Wikibooks:Reading room/General|reading room]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:22, 10 February 2026 (UTC)

::{{re|Kittycataclysm}} I believe I have finished migrating all of ''Media Literacy and You'' to Wikiversity and replacing the parts of it on Wikibooks with redirects. Comments? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 17:32, 10 February 2026 (UTC)

== Thank you!  ==

Heya, thanks for reviewing my stuff! Just to note, the first lesson page was done and so that'll need moving. If you want to discuss anything with me, I am easily reachable on Discord @ xiluosi233. I can explain philosophy, approach, and so on from my teaching experience if you want anything regarding that. [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:48, 17 February 2026 (UTC)

:It appears [[An Introduction to the Han Script]] was moved wrong - should it not be [[General Literary Chinese from Scratch/An Introduction to the Han Script]]? [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:52, 17 February 2026 (UTC)
::@[[User:Shira the Mogul|Shira the Mogul]] good catch! I accidentally removed more of the title than intended. I've fixed this now. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:18, 18 February 2026 (UTC)

== A test request ==

Just to see whether a recent Luna update turned out as intended, could you briefly revert your [[User:Kittycataclysm/lunaoptions.json|Luna preferences page]] to the first revision? Since you don't appear to have any custom preferences in the first place, I don't think there should be any conflicts. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 01:49, 30 March 2026 (UTC)

:Done! But, it seems to have perhaps auto-updated again immediately afterwards. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:39, 10 April 2026 (UTC)

== Linking ==
Hi,&lt;br&gt;
For my edification, why is a link from [[Cookbook:nettle|nettle]] to [[w:Urtica_dioica|Urtica dioica]] not appropriate? The Wikipedia article has more information &amp; seems relevant.&lt;br&gt;
Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 01:53, 24 April 2026 (UTC)

:@[[User:PeterEasthope|PeterEasthope]] good question! Wikibooks discourages outlinking, since books should be self-contained units. Instead of linking to [[w:Urtica dioica]], the correct approach would be to flesh out the actual chapter here at Wikibooks. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:34, 24 April 2026 (UTC)
::Should all material in the Wikipedia article about Urtica dioica relevant to cooking be duplicated into the nettle article in the cookbook? Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 02:30, 2 May 2026 (UTC)
:::@[[User:PeterEasthope|PeterEasthope]] you could do that, although you should only include information that is sourced. However, I recommend that you wait, because I am coincidentally working on the page right now and fleshing it out significantly. I should publish today. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:40, 2 May 2026 (UTC)
::::The nettle page is better now. Thanks.
::::I still wonder, given that the link to ''The Complete Guide to Edible Wild Plants, ...'' is permitted, why not a link to the botanically oriented page in Wikipedia. What if someone reads the Cookbook article and is interested in the toxin for example? Seems that non-Wikimedia references are more privileged than Wikimedia references.
::::Also, by chance, just noticed the [[w:Nettle_soup|Nettle soup]] article in Wikipedia. Better in the Cookbook?
::::Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 19:10, 5 May 2026 (UTC)
:::::Another good question. The reason those books are linked is because they are reputable and topical sources for the subject matter (nettles as used in cooking from an instructional perspective), and the links are part of the citations—this makes it different from a simple outlink to a Wikipedia page. Wikipedia pages should also not be cited themselves as sources. Regarding nettle soup, I don't think it makes sense to have that as a standalone page here in the cookbook due to its encyclopedic tone, and I don't see any recipes there. Does this make sense? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:21, 6 May 2026 (UTC)
::::::Somewhat. Certainly a recipe wouldn't be incongruous in a cookbook. Still seems unhelpful that relevant information in Wikipedia is inaccessible from a Wikibook. In effect there's a &quot;Berlin Wall&quot; between two Wikimedia projects. Would a &quot;See also&quot; section be permissible?
::::::Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 14:00, 7 May 2026 (UTC)

== You may be an eligible candidate for the U4C election ==

&lt;div lang=&quot;en&quot; dir=&quot;ltr&quot; class=&quot;mw-content-ltr&quot;&gt;
Greetings,

The [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee|Universal Code of Conduct Coordinating Committee (U4C)]] seeks candidates for the 2026 election. The U4C is the global committee responsible for overseeing enforcement of the [[foundation:Special:MyLanguage/Policy:Universal Code of Conduct|Universal Code of Conduct]]. Elections are held annually, if elected a committee member serves for two years.

This year the U4C requires candidates to hold administrator rights on at least one wiki, which is why you are being contacted as you appear to hold this right. There are other requirements, such as candidates must be at least 18 years old and may not be employed by the Wikimedia Foundation or other related chapters and affiliates. You can find more information in the [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026#Call_for_Candidates|call for candidates on Meta-wiki]]. Additionally, the committee's working language is English; some ability to communicate in English is required.

The election opens on 18 May, if you are eligible and interested you have until 10 May to submit your candidacy. There will week between for candidates to answer questions from the community. Voting takes place privately in [[m:Special:MyLanguage/SecurePoll|SecurePoll]], successful candidates must receive at least 60% support. More information is available on [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026|the 2026 Elections page]], including timelines and other candidacy information. If you read over the material and consider yourself qualified, please consider submitting your name to run for the committee. If you think someone else in your community might be interested and qualified, please encourage them to run.

In partnership with the U4C -- [[m:User:Keegan (WMF)|Keegan (WMF)]] ([[m:User_talk:Keegan (WMF)|talk]]) 18:32, 28 April 2026 (UTC) &lt;/div&gt;
&lt;!-- Message sent by User:Keegan (WMF)@metawiki using the list at https://meta.wikimedia.org/w/index.php?title=User:Keegan_(WMF)/test&amp;oldid=30471751 --&gt;

== Undeletion request ==

Hello,


I am writing to request an undeletion of the page Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad. You stated you are a frequent visitor of the Lentis page and are thus familiar with it. This page was part of a class assignment and was in progress at the time of deletion. The work deleted is what we will be graded on for our class, so we would appreciate the restoration. [[User:Yqj3km|Yqj3km]] ([[User talk:Yqj3km|discuss]] • [[Special:Contributions/Yqj3km|contribs]]) 19:36, 4 May 2026 (UTC)

:@[[User:Yqj3km|Yqj3km]] see my response below regarding undeletion. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 May 2026 (UTC)

== Undeletion request ==

About the page on Lentis called Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad: I, too, request undeletion, please. If the authors made any msitakes, the fault is 100 percent mine, for failing to guide them correctly. Like all chapters in this book, this team's chapter is a class assignment. I will be interested also in the reason for deletion so that I can guide authors better. I want to help my students be constructive contributors. Many thanks!

[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 20:03, 4 May 2026 (UTC)

:Hi @[[User:Norton|Norton]] and thanks for the ping! I deleted it because it was not titled/filed correctly, so I didn't realize it was part of [[Lentis]]. I have undeleted it and moved it to [[Lentis/Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:14, 4 May 2026 (UTC)
::Many, many thanks, @[[User:Kittycataclysm|Kittycataclysm]]! I am very grateful as always for everything you do for Wikibooks!
::[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 22:27, 4 May 2026 (UTC)

== Log in issues ==

Hi, messaging you as you seem to be the most active admin at the moment. I can't log in (as posted at  &lt;bdi&gt;[[Wikibooks:Reading room/Administrative Assistance]] and also on my WP page at&lt;/bdi&gt; [[w:User_talk:Xania]]). Seems to be an issue with extra security for admins? I am asked to use my authenticator app (which I can't as I have never set it up for Wikibooks) or a recovery code (which I don't have). Any idea what I should do in this situation? Xania [[Special:Contributions/&amp;#126;2026-28255-89|&amp;#126;2026-28255-89]] ([[User talk:&amp;#126;2026-28255-89|talk]]) 18:21, 10 May 2026 (UTC)

:Apologies for missing this yesterday! It seems like we have a few people working on it over in the reading room, and I'll keep track there. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:37, 11 May 2026 (UTC)

== Splitting pages ==
FYI, I untagged [[Art Print Production Methods]] as for splitting: the page is rather small with its 20 KB and does not need splitting, in my view. Ideally, there would be an operationalized, fairly detailed policy on the matter, but I do not know of one. Single-page books are in [[:Category:One-page books]]. --[[User:Dan Polansky|Dan Polansky]] ([[User talk:Dan Polansky|discuss]] • [[Special:Contributions/Dan Polansky|contribs]]) 04:45, 20 May 2026 (UTC)

== Slander ==

Your tag is slanderous and very easily proven wrong.[https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654455] Given you likely didn't bother to look at the edit history, I would remind you that your given reason that you think it was AI is because you see the chapter is &quot;numbered&quot;. That however was 100% my own personal decision after I reviewed my work and thought to myself that I later wrote in the introduction that there is a first to fourth chapter. However I thought to myself that the readers would not be easily made aware of what is meant by first to fourth as I didn't number them - so is why I dedicated an entire edit to make it less ambiguous  [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654328]. I should not have to be falsely penalized because I wanted to be more considerate and ensure better clarity. I do however request AI to help me figure out coding like this - [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654329] as I don't know how to link. But I intentionally take great efforts to not rely on AI to write that book and find your wrongful presumptions troubling. [[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 06:00, 15 July 2026 (UTC)

:@[[User:JaredMcKenzie|JaredMcKenzie]] thank you for clarifying! I flagged it for review because it matched a common pattern we see associated with LLM use here. If that is not the case, then nothing needs to happen in that respect; however, you will likely want to fix the lists so that they are correctly formatted in the Wikitext and not hard-written—let me know if you have any questions about that. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:14, 16 July 2026 (UTC)
::Yeah, I don't instantly understand what you mean by &quot;correctly formatted&quot; list. At first, I assumed you were referring to chapter 4 - (''Further reading'')? But I think I know what you mean. I made this edit here [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654738] to align with how I see wikibooks typically do lists. Did I fix it? If not, feel free to clarify.[[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 18:35, 16 July 2026 (UTC)</text>
      <sha1>7ibjfr347eaoz1blro1dgmh5ifl31hd</sha1>
    </revision>
    <revision>
      <id>4654765</id>
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        <username>JaredMcKenzie</username>
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|+
! colspan=&quot;3&quot; |Talk Page Archives
|-
|[[User talk:Kittycataclysm/Archive 2022|2022]]
|[[User talk:Kittycataclysm/Archive 2023|2023]]
|[[User talk:Kittycataclysm/Archive 2024|2024]]

|}

== That IP range calculator ==

Following [[phab:T381138|T381138]], I have now become the maintainer of the IP range calculator you like. You can find it [[toolforge:ftools/general/ip-range-calc.html|here]]. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 23:10, 9 January 2025 (UTC)

:Thank you for the heads-up! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:56, 10 January 2025 (UTC)

== A merge and unmerge from two years ago ==

I was browsing through the history merge log when I saw that you merged [[Cookbook:Chicken Bog]] into [[Cookbook:Chicken Bog I]], and then promptly reverted it. What happened here exactly? Could I correct it? [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 15:55, 10 January 2025 (UTC)

:Good question! I can't remember what I was trying to do, but it looks like I didn't succeed at what I wanted based on the log comment. You're just trying to history merge to get [[Cookbook:Chicken Bog I]] to have continuity of history? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:35, 10 January 2025 (UTC)
::I think I figured out your mistake: it outright moved the revisions from the first page to the second, rather than copying them. This would have caused the other two [[Cookbook:Chicken Bog]] pages to have incomplete histories. I think the only solution would be to XML import the pre-April 2023 revisions from the first page to the other three, and I'm not sure if that's the best idea, and I am technically unable to do so. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 16:49, 10 January 2025 (UTC)

== Undeletion request ==

I wouldn't be surprised if you expected this, but I'd like to ask you to undelete the subpages of [[Rotorcraft Fundamentals]] you just deleted with the summary &quot;Use of copyrighted work without permission. Please read Terms of Use: page needs to be imported for attribution&quot;, so that I can do that. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 19:54, 14 January 2025 (UTC)

:Done! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:57, 14 January 2025 (UTC)
::Upon further investigation, this might actually be a rare case where an [[WB:UT|unmerged transwiki]] is ''preferred'' (this is part of why I stopped calling them &quot;bad transwikis&quot;), since only a small portion of the Wikipedia article (with over 2,000 revisions) was copied over. Importation is generally only needed if the ''majority'' of the page is copied across wikis. I'll just leave a null edit providing attribution and add {{tlx|Copied}}. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 21:19, 14 January 2025 (UTC)

== Reusing [[Cookbook:8 Desserts in 1 Pan]] on wikiHow ==

Hi, I am a user on wikiHow, see [[wikihow:User:Xeverything11]]. I would like to create a new recipe on wikiHow. I wanted to let us know if I can give permission to reuse your contributions to this recipe from Wikibooks to wikiHow. I (as a copyright holder) created this recipe on Wikibooks, but you contributed to this recipe.

If not, I'll use the revision before you contributed since I was the only author. 

Wikibooks uses CC-BY-SA 4.0 while wikiHow uses CC-BY-NC-SA 3.0, which both licenses are incompatible due to ShareAlike conditions.

Thanks [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 08:27, 15 January 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] I'm personally fine with this as long as proper attribution is given back to the original recipe page here. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:52, 20 January 2025 (UTC)
::I adapted this [[wikihow:Make-8-Desserts-in-1-Pan|recipe]] on wikiHow with attribution, and got a Rising Star (an achievement used for best new articles on wikiHow). Thank you! [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 19:49, 24 January 2025 (UTC)

== Wikibooks community ==

Hi, @[[User:Kittycataclysm|Kittycataclysm]]!

I am trying to contribute more to English Wikibooks. My main contributions will focus on the Cookbook, especially on Indonesian recipes. Do you have a community group where we can discuss and share ideas together?

I am looking forward to join. Thank you!

[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 08:47, 16 January 2025 (UTC)

:@[[User:Raflinoer32|Raflinoer32]] Sorry I missed this, and welcome! Are you asking about a Cookbook-specific area for discussion? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:39, 20 January 2025 (UTC)
::Yes. Do you know place for this?
::Thank you 
::[[User:Raflinoer32|Raflinoer32]] ([[User talk:Raflinoer32|discuss]] • [[Special:Contributions/Raflinoer32|contribs]]) 09:41, 21 January 2025 (UTC)
:::Honestly, there's not a centralized Cookbook-specific discussion space, especially since there aren't currently a ton of active contributors. Some people ask questions at [[Cookbook talk:Table of Contents]]. I'm currently the most consistently active and involved Cookbook editor, so feel free to ask me questions! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:46, 22 January 2025 (UTC)

== Congratulations! ==

[[File:Admin T-shirt.svg|thumb|You get this now.]]
You are now a permanent administrator. Welcome to the team (I am entitled to say this because I technically got the extension a few hours before you did)!{{FBDB}} [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 10:33, 29 January 2025 (UTC)

:Thanks :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:29, 29 January 2025 (UTC)

== Is there a way to contact a Steward on WikiBooks? ==

Hi {{PAGENAME}},
Is there a way to contact a Steward on WB? I tried to find who the active Stewards are here  at [[Special:ActiveUsers?username=&amp;groups%5B%5D=steward&amp;wpFormIdentifier=specialactiveusers]] but nothing shows up.

The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the [[Wikimania-wiki]], but I just visited the [[wikimania 2014 wiki]] and could not  find this backward link. I tried to ask about this  on the [[Wikimania 2014 main-page talk]] but disovered that the Stewards have protected it. 

Is there a way  wikibookians can communicate with Stewards at WB? Thanks in advance for answering this non-urgent question, and apologies for all the red-links which I can bluify if needed. Cheers [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 16:37, 7 February 2025 (UTC)

:@[[User:Ottawahitech|Ottawahitech]] You can ask this on somewhere like [[metawiki:Steward requests/Miscellaneous]]. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 17:01, 7 February 2025 (UTC)
&lt;s&gt;:@[[User:Ottawahitech|Ottawahitech]] seconding what Leaderboard said—we no longer have any active stewards at enWB.&lt;/s&gt; Had a brain fade there and mixed up stewards with bureaucrats. Yes, meta is the place for this. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:15, 7 February 2025 (UTC)
::@Kittycataclysm,@[[User:Leaderboard|Leaderboard]], or anyone else:
::Some wikibookians prefer for various reasons to post only at wb. I myself am indef-blocked at  META so could not participate at [[metawiki:Steward requests/Miscellaneous]] even if I waned to.
::Since [[Wikimania]] is a topic of interest to all members of the [[wikimedia movement]] why can't wikibookians talk to thier elected representatives here? [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:56, 7 February 2025 (UTC)
:::@[[User:Ottawahitech|Ottawahitech]] I can check with the blocking admin to see if they'd be willing to unblock you, if you'd like. The reason things like these are done at Meta is that Meta is a cross-project coordination platform - stewards ''cannot'' be expected to watch every project after all. Now you could message any steward here on Wikibooks if you really wanted to, but that is not normally a good idea. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 02:26, 8 February 2025 (UTC)
::::Wikimania is the annual conference celebrating all the free knowledge projects hosted by the Wikimedia Foundation (WMF).  It is a wikimedia initiative which is meant to help all of our projects (including wikibooks), gain more readership, educate more wiki-editors, foster better communications, and much more.  The wmf has been hosting  a Wikimania-wiki dedicated to each Wikimania annual event since 2004. These wikis contain a wealth of information, but can  benefit from wiki-improvements, starting from spelling and grammar errors that detract from their to appeal to the general membership. It would be nice if Stewards paid more attention to it.
::::@[[User:Leaderboard|Leaderboard]], I truly appreciate your offer, but  I posted this here not in order to get someone to advocate for one unblocking at META. As I said earlier:
::::* &quot;Some wikibookians prefer for various reasons to post only at wb&quot;
::::* &quot;The reason I am asking is that I believe that all individual Wikimania-wikis should have a backward link to the Wikimania-wiki, but I just visited the wikimania 2014 wiki and could not find this backward link. I tried to ask about this on the Wikimania 2014 main-page talk but disovered that the Stewards have protected it&quot; 
::::I would much rather see more wikimedia members question blocking in general at META. One cannot run such large movement of people from different backgrounds and nationalities simply by silencing minorities  IMIO. [[User:Ottawahitech|Ottawahitech]] ([[User talk:Ottawahitech|discuss]] • [[Special:Contributions/Ottawahitech|contribs]]) 20:12, 8 February 2025 (UTC)

== [[Crystal ball]] ==

That page appears to be a mixture of isolated paragraphs from [[w:Crystal ball|Crystal ball]], hence my tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 03:04, 9 February 2025 (UTC)

:Yep, that seems correct! I also queried it simply because it does not seem suitable for inclusion at all. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:09, 9 February 2025 (UTC)

== Question about an edit suggestion ==

Hi Kittycataclysm,

Thanks for the great work you do as an admin! I wanted to clarify a suggestion you made on a recently published page I’m working on. You recommended splitting it into smaller sections—would you suggest creating separate pages for these sections, or would a higher-level header for some topics be sufficient?

Any specific recommendations you have would be greatly appreciated!

Here’s the link to the page I’m referring to: [[Funding and Finance of Transportation Projects in the United States of America]]

Thank you! [[User:Svrmustafa|Svrmustafa]] ([[User talk:Svrmustafa|discuss]] • [[Special:Contributions/Svrmustafa|contribs]]) 18:19, 18 February 2025 (UTC)

:Hi @[[User:Svrmustafa|Svrmustafa]], and thanks for asking! Splitting refers to creating new pages, each with a smaller amount of content. The main page should then contain a table of contents, and each page can contain a navigation template for easier navigation. I'll create the table of contents based on the current work and move some content to one of those pages as an example for you; then, you can do the rest. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:26, 19 February 2025 (UTC)
::Following up on this—I noticed that you use the term &quot;paper&quot;. However, technically Wikibooks hosts books not papers, so you should probably change this wording. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:38, 19 February 2025 (UTC)
== Talkback ==
{{Talkback|Cookbook talk:Chilli Crab|Recipe Questions}} [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 09:54, 19 February 2025 (UTC)

:@[[User:Kittycataclysm|Kittycataclysm]] I also made [[Cookbook:Prata|this]] [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:15, 19 February 2025 (UTC)

== Hello ==

Can you look at my latest recipe? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 00:10, 28 February 2025 (UTC)

:I saw it! It needs a few corrections, which I'll note. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:23, 28 February 2025 (UTC)
::@[[User:Kittycataclysm|Kittycataclysm]] How do you write recipe summary, correct headers [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 06:04, 28 February 2025 (UTC)
:::Please see [[Cookbook:Policy/Recipe template]]. What's the origin of the recipe? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:08, 28 February 2025 (UTC)
::::ok [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 02:33, 1 March 2025 (UTC)

== Cookbook ==

Hi there, Kittycataclysm. I wandered over here from Wikipedia, and I'm quite enamoured with this cookbook. I noticed you seem to be the one maintaining it, and I thought I'd reach out. Can I really just start cranking out recipes from public domain cookbooks and my family recipes? It's that simple? I was also wondering about the featured recipes section. There's not very many in there, and I imagine there's not very many folks around to do reviews compared to GAR on Wikipedia. How do you handle content review? Thanks. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:51, 1 March 2025 (UTC)

:Hi @[[User:MediaKyle|MediaKyle]] and welcome! For some context, the Cookbook has been around since the very beginning of Wikibooks, but it had gotten into a bit of disarray over the course of about two decades by the time I found it. I started the long process of overhauling, standardizing, and expanding it just over four years ago—I finished standardizing the recipe formatting and quality a while back and am currently working my way through the ingredient pages before moving on to equipment, techniques, and cuisines. You can absolutely add any public domain recipes as well as your own recipes—they just need to conform to the [[Cookbook:Policy/Recipe template|recipe template]] and [[Cookbook:Policy|Cookbook policy overall]]. It's even better if you've made the recipe and can contribute a nice picture and specific guidance/instructions/notes! Please feel free to ask me any questions. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:27, 1 March 2025 (UTC)
::Oh, and regarding the featured recipes section, I actually haven't gotten around to looking into that yet—there's been a lot to do! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:28, 1 March 2025 (UTC)
::That's great, thanks a lot for your response. This is just delightful. Maybe content review is something that we could collaborate on. There's a lot of recipes in here and it would be nice to know which ones are the best. Question for you, [[:Category:Brown sauces]] is really bothering me. How can I move that to Brown sauce recipes? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:29, 1 March 2025 (UTC)
:::Good catch on that category! It seems like it was created two decades ago and never got corrected—feel free to recategorize those recipes. Thank you also for introducing the hideprefix parameter to the category trees—I didn't realize that was an option, and it reduces the visual clutter! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:38, 1 March 2025 (UTC)
::::My pleasure! As I continue to look at the categories, this is actually worse than I thought. We have both [[:Category:Sauce recipes]] and [[:Category:Recipes for condiments]] and I suspect that's just the beginning. I want to go through and categorize everything properly, but the bones aren't even there... How long do I have to be here before it'll let me create and move around categories? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:40, 1 March 2025 (UTC)
:::::Regarding the categories, the category overhauling is in progress, since I address the category when I overhaul the associated page. The variation in titling is actually somewhat deliberate—I started changing it from &quot;____ recipes&quot; in certain cases to solve a particular categorization problem. Sometimes, there is an item that is used in recipes as an ingredient but for which there are also recipes. For example, [[:Category:Recipes for bread]] versus [[:Category:Recipes using bread]]. The different naming scheme is necessary to properly delineate the categories, and I'm working on implementing it a bit more consistently as I go. While you're still getting started, it would be great if you could check with me when something looks odd or out of place—that way I can take a look and weigh in on whether that's normal or not and maybe provide some context. Just off the top of my head, I think you will have to wait for autoreview status to make move changes. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:56, 1 March 2025 (UTC)
::::::I see what you're saying, I've been trying to wrap my head around that. Maybe it would be beneficial to try to put together some sort of a Cookbook MOS regarding category structure? It's kind of all over the place right now. Using your bread example, would it perhaps make more sense to have [[:Category:Bread recipes]] and [[:Category:Recipes using bread]]? There would be no ambiguity with just those two categories, but when you add the extra [[:Category:Recipes for bread]], that's when things start getting a little whacky. What do you think? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:05, 1 March 2025 (UTC)
:::::::Either that or get rid of [[:Category:Bread recipes]] and keep the other two. But one of these categories gotta go, I reckon. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:07, 1 March 2025 (UTC)
::::::::I see you already had the same thought as me. I think all categories should include &quot;for&quot; or &quot;using&quot;. Take for example, [[:Category:Recipes for pancakes]] as opposed to [[:Category:Pancake recipes]]. Well obviously there's no recipes using pancakes. But for something like [[:Category:Recipes for gravy]], there may also be a need for [[:Category:Recipes using gravy]]. The lack of consistency in this regard means the only way to achieve consistency across the categories is by changing them over to that format. Sorry for clogging up your talk page! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 03:18, 1 March 2025 (UTC)
:::::::::Same heads-up as below—migrating this over to [[Cookbook talk:Table of Contents]] —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:10, 4 March 2025 (UTC)
:Also, on [[Cookbook:Table of Contents]], could you please add a wikilink for [[Cookbook:Breakfast]], and maybe add cooknav to the top for seamless navigation between all the top level articles? Can't edit that article yet. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 02:47, 1 March 2025 (UTC)

== More Table of Content Edits ==

Hello again. I've been going through everything and this is my list of suggestions for edits to the table of contents. Unfortunately there's not much else I can do for now, because without autoconfirmed my ability to change anything is very limited. I was going to ask for someone to check off the confirmed box for me at RfP but I can't post there either, so I guess I'll be back in four days.

* Fix Bread wikilink
* Remove &quot;Creaming&quot; from techniques, redirected to Mixing
* [[Cookbook:History of Food and Cooking]] points to redirect, needs capitalized
* [[Cookbook:Low-Carb]] points to redirect, needs capitalized
* [[Cookbook:Cuisine of the Mediterranean]] to [[Cookbook:Mediterranean Cuisine]] for parity
* Remove the S from the cuisine wikilinks on ToC, currently redirecting
* Create [[:Category:Lunch recipes]], wikilink to ToC
* Wikilink [[Cookbook:Dessert]] under Meals
* Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category
* Create [[Cookbook:East Asian Cuisine]] so I can add the recipes from [[:Category:East Asian recipes]] to it; currently is a redlink on the ToC
* Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;
* Appendix and Equipment sections switch places

Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:46, 1 March 2025 (UTC)

:I took the liberty of doing it myself in my userspace. You can just copy it over from [[User:MediaKyle/sandbox]]. Figured I'd save you the trouble of trying to figure out what I'm talking about. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 14:15, 1 March 2025 (UTC)
:Circling back to this! It seems like your suggestions are getting at a couple different things. I'll try to go through them point-by-point below:
:* {{xt|Fix Bread wikilink}} {{done}}
:* {{xt|Remove &quot;Creaming&quot; from techniques, redirected to Mixing}} see below comments on TOC.
:* {{xt|Cookbook:History of Food and Cooking points to redirect, needs capitalized}} {{not done}} for now because I don't fully understand the urgency and I want to triage/prioritize things for you, but please feel free to make this change yourself once you can!
:* {{xt|Cookbook:Low-Carb points to redirect, needs capitalized}} {{not done}} for same reason as above.
:* {{xt|Cookbook:Cuisine of the Mediterranean to Cookbook:Mediterranean Cuisine for parity}} {{not done}} for now just because we do have a lot of cuisine pages that follow the form &quot;Cuisine of ____&quot;. It could be good to standardize, and I had been planning to do that once I got around to the cuisines.
:* {{xt|Remove the S from the cuisine wikilinks on ToC, currently redirecting}} {{not done}} for same reason as other redirects
:* {{xt|Create Category:Lunch recipes, wikilink to ToC}} Not quite sure what you mean here, and I didn't see what it corresponded to in your linked sandbox page
:* {{xt|Wikilink Cookbook:Dessert under Meals}} {{done}}
:* {{xt|Get rid of &quot;Brunch&quot;; will just be confusing alongside a breakfast and lunch category}} I'm not sure about this—brunch is in many places considered a separate entity, and I don't necessarily think it would cause confusion. But, overall it's hard to determine whether it should have its own page and TOC link because I haven't actually gotten around to evaluating the meal pages and what role they should play. See also the TOC notes below.
:* {{xt|Create Cookbook:East Asian Cuisine so I can add the recipes from Category:East Asian recipes to it; currently is a redlink on the ToC}} {{done}} for now; however, I'm not sure yet whether it will ultimately make sense to keep that as a content page. I think content pages should be reasonably focused, and it may not be the best to have a cuisine page that is so broad. This is something I planned to consider once I made my way around the overhauling the cuisines.
:* {{xt|Change &quot;Introductory Matter&quot; header to just &quot;Introduction&quot;}} The reason I made it &quot;Introductory Matter&quot; instead of &quot;Introduction&quot; is because there's already a chapter itself titled &quot;Introduction&quot;—it felt odd to have the entire section titled that as well. Happy to discuss other header options (e.g. &quot;Front Matter&quot;, which is a generally accepted book term)
:* {{xt|Appendix and Equipment sections switch places}} see below comments on TOC.
:* '''Comments on the TOC:''' So, I think a fundamental issue with the current TOC is that it somewhat arbitrarily picks and chooses individual pages to link. It also sometimes direct-links to categories and sometimes to content pages, which I don't think we should do. Because the cookbook is so expansive, it's been established that manual indices intending to capture detail in large areas don't really make sense and quickly get bulky and out-of-date. This is why categorytree is such a useful tool! After thinking on it for a while and making some small tweaks, I think I'd ultimately like to overhaul the TOC and come to a solution that keeps a few broad headers/links to the small handful of the primary content pages while perhaps stashing away more detailed and self-updating lists in a collapsible way to reduce clutter but allow for customizable user navigation. Much to think about, and I'll probably workshop some things on the side to see how they feel.
:Let me know if I've misunderstood anything! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 03:24, 3 March 2025 (UTC)
::Thanks for the notes! Here's my thoughts:
::* On the Cuisine titling, it actually seems like [[Cookbook:Cuisine of the Mediterranean]] and [[Cookbook:East Asian cuisines]] are the only ones that don't follow the naming scheme, i.e. &quot;[[Cookbook:African Cuisine]]&quot;, and I think that shorter titles are preferable where it makes sense.
::* On your note about East Asian Cuisine, I actually had the same thought after going through the cuisine pages. Having three separate pages for different kinds of Asian cuisine does seem a little silly, doesn't it? Do you think it might be better to combine all of them under one &quot;Asian Cuisine&quot;, but put the different locales under separate headers?
::* On Brunch - I honestly think there's way too much ambiguity around what exactly constitutes as &quot;brunch&quot; to keep that in. I feel as though the term brunch more applies to the time you're eating, rather than the kind of food. I think it would be easier to keep meals that include commonly accepted breakfast foods in the Breakfast category, and things that don't fit neatly into that, into the Lunch category. This would prevent any dilemmas in the future where we can't decide whether something is breakfast or brunch.
::* You're right that it looks a little awkward to have the header as Introduction when there's a page called introduction. I still think that to say &quot;Introductory Matter&quot;, or &quot;Front Matter&quot; as you mentioned, is a little long-winded and reflects a more academic tone than needed for a cookbook. Upon further reflection, I think maybe rather than worrying about the header at this point, we should perhaps think about trying to compile all of those short introductory type pages into one comprehensive introductory page. Then we likely won't even need a header for it on the ToC.
::* The ToC is definitely a bit cluttered, and it bothers me too that there's a real lack of consistency across whether the wikilinks lead to a page or a category. I'm not sure how I would feel about cutting away too much of the navigation from it, though, because just about every page on there does have a reason to be there, it's just that they're not presented very nicely. Some of it can certainly get nested or combined though. I'll play around with it over the next few days in my sandbox as well and let you know if I come up with anything.
::* As an aside, the first thing on my to-do list once my autoconfirmed comes through is to start subcategorizing all of the recipes so that they're all nicely sorted in the category trees. When you have a chance, I'd love to hear your thoughts on what we should use as the standard naming for categories. Once we determine this, I think we can also take the liberty of updating the cookbook MoS to reflect it.
::Cheers, [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:33, 3 March 2025 (UTC)
:::Note: After writing this, I realized what you were getting at about slashing away some of the subpages. Maybe we can come up with a system where all of those subpages are under their main subpage rather than on the ToC. For example, all the Cuisines are under [[Cookbook:Cuisines]], all techniques under [[Cookbook:Cooking Techniques]], to keep the subpages off the main ToC. Also, I wonder if maybe we should try to make a centralized discussion for this somewhere, in case anyone else wants to join in at some point? [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 11:45, 3 March 2025 (UTC)
::::Heads-up: to make it easier to keep track of these and since I think they deserve their own discussions, I'm going to gradually migrate them over individually to [[Cookbook talk:Table of Contents]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:52, 4 March 2025 (UTC)
:::::Good idea. Can you remove the semi-protection from that talk page? I see no reason why it should be protected. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:23, 4 March 2025 (UTC)

== Cookbook ToC ==

Hi [[User:Kittycataclysm|Kittycataclysm]]. I was just wondering why you didn't respond to my above message, and started a separate sandbox for the ToC instead? It seems as though you don't really want to collaborate. It would be nice if we could work on this together. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 22:43, 2 March 2025 (UTC)

:@[[User:MediaKyle|MediaKyle]] thanks for the ping! I'm sorry you feel like I don't want to collaborate—the opposite is true, and please understand that this is good-faith editing. The reason I haven't responded to the above points is mostly since you've been modifying a bunch of content and adding suggestions lately, and I've been working my way through these while continuing with my routine contributions and real life as well—things happen a little more slowly here than on other projects, and I'm the one person dedicated to the cookbook right now. The reason I created that sandbox was because I saw [[Wikibooks:Reading room/General#Modernize the shelves|your comment]] at the reading room and wanted to play around and think about your suggestion without touching the actual TOC. You're right that it's not the best, and it's been something I've been thinking about for a bit now. Please understand also that it can be overwhelming when a new editor unfamiliar with the Cookbook begins making a high volume of edits and suggestions without having much experience with it or its history—this isn't to say that you don't have good ideas or things worth contributing. In fact, you have already made a few helpful changes, as I've mentioned. I just want to do this properly and take the time to evaluate your suggestions together with the current efforts that are underway, and that can take a bit. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:03, 2 March 2025 (UTC)
::Thanks for getting back to me. While I may be new to Wikibooks, I'm certainly not new to MediaWiki, and I've been working with small wiki projects for a number of years. Perhaps it's been a misunderstanding to some degree, but I've found my reception here to be unusually unwelcoming. The way to do this properly, as you said, would be to have discussions and form consensus. Yesterday, when you reached out to me about adding hideroot to the pages, I gave you my rationale and was more than happy to have a discussion about it, but you did not reply. I noticed a similar situation happened with [https://en.wikibooks.org/wiki/User_talk:Ottawahitech#Category_sorting Ottawahitech], regarding category sorting. I'm aware that you're the main person looking after the cookbook right now, which is why I reached out to you right from the get go.
::I understand why you would want to create your own sandbox to play around with options for the ToC, but I'm sure you can understand why it would draw my attention that you would do this without implementing any of the wikilink fixes I mentioned, or making an attempt to discuss it further. This came across to me as not wanting my help.
::I invite you to check out my page on Wikipedia. I've made contributions across quite a wide area of topics there, as well as the other Wikimedia projects, and this is the first time I've encountered any sort of resistance to my contributions. I think Wikibooks has enormous potential, and I'm very excited to contribute to helping it grow. On most projects, this would be something to be encouraged. I don't feel like &quot;I'm sorry that you feel that way&quot; was really an appropriate response. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 23:59, 2 March 2025 (UTC)
:::I think you're right that this has been a mix of misunderstanding and miscommunication, and I think I can understand how things came across as unwelcoming! For whatever it's worth, I absolutely plan on circling back to the various discussions at hand (I have all the relevant pages open to return to), but it seems like the order I did things made it seem like I was ignoring you (if I'm understanding correctly). I am pretty busy, so sometimes items on my to-do list do get lost/shunted or it takes me a bit to get around to something—please don't hesitate to give me a ping if it seems like I'm taking a while to get back to something. Looking forward to more collaboration! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:49, 3 March 2025 (UTC)
::::I'm glad you can understand where I'm coming from. To clarify, my intent is not to try to rush you, or to try to push you to make changes that you don't agree with. It's really easy to misinterpret things over the Internet, and I think a short message can go a long way. I apologize if I've caused you any undue stress by coming into the cookbook and unleashing a flurry of alterations, but do rest assured that I'm not married to any of my changes, I'm always open for discussion, and I want to see the cookbook improve just like you do. The great thing about wikis is that no change is permanent. I think we'll have it in tip-top shape in no time! [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 01:19, 3 March 2025 (UTC)

== [[Cookbook:Polish Doughnuts (Paczki)]] ==

Do you see any reason not to just add this to Featured Recipes? At least we know this one works, and it seems like this is now one of the few recipes to have a picture that actually aligns with the recipe used. I was thinking later on we'll come up with a content review system where a couple editors will actually try the recipes nominated for FR, but in the absence of that I'd just add it to the list. [[User:MediaKyle|MediaKyle]] ([[User talk:MediaKyle|discuss]] • [[Special:Contributions/MediaKyle|contribs]]) 12:25, 4 March 2025 (UTC)

:I'm fine with adding it to the featured recipes. You're right that we'll want to come up with a good system for this going forward, though it's lower down on my personal priority list at moment. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 March 2025 (UTC)

== [[Cookbook:Cream Cheese American Buttercream]] ==

Hi! I am a wikiHow user and I am planning to adapt this recipe to wikiHow. Since you contributed to this recipe, I wanted to know if I can get permission to reuse your contributions to this recipe. Thanks. [[User:Xeverything11|Xeverything11]] ([[User talk:Xeverything11|discuss]] • [[Special:Contributions/Xeverything11|contribs]]) 21:41, 4 March 2025 (UTC)

:@[[User:Xeverything11|Xeverything11]] that's fine with me as long as proper attribution and linking back to the original recipe page here are included at the top. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:28, 4 March 2025 (UTC)

== [[A Companion to Our Literary Journey]] ==

Hi! I feel that we have started to outline the scope in a clearer and more precise way and that’s the work we are going to do with the students this and for the next years, adding more sections and content. Do you think that would be enough? [[User:Ferdi2005|Ferdi2005]] ([[User talk:Ferdi2005|discuss]] • [[Special:Contributions/Ferdi2005|contribs]]) 22:43, 6 March 2025 (UTC)

:Hi @[[User:Ferdi2005|Ferdi2005]]! Yes, this seems to be reasonably outlined. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:51, 7 March 2025 (UTC)

== Exercising care with copyright ==

When deleting a page as a copyright violation, it is important that you '''do not quote any content from the deleted page'''. If you do, then your log entry is itself a copyright violation. I have redacted a recent deletion that you performed because of this. If you want to make sure that none of your past deletions have been problematic for this reason, you can [[quarry:query/90444|run this SQL query]] to get a list of every deletion that could be eligible for redaction. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 18:32, 21 March 2025 (UTC)

:Hi @[[User:JJPMaster|JJPMaster]] and thank you for the message. In the most recent instance that I think you're referencing, I do not see any material in the edit summary that posed a significant risk—I don't believe the few listed words would be a copyright concern. However, I do understand your concern! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:31, 21 March 2025 (UTC)

== Splitting Pages ==

Hi I have recently made the book on the [[History of the Nawabs of Bengal]] and you gave a notice on how you believe it should be split into smaller bits. As I am still new to wikibooks I don't know how to do this. Can you please assist me on renaming the page so I can split the page into multiple pages? @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 19:47, 29 March 2025 (UTC)

:@[[User:Greatswrd|Greatswrd]]: You did it. I've removed the tag. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 22:44, 29 March 2025 (UTC)
:Like @[[User:JJPMaster|JJPMaster]] said, you're all set! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:53, 29 March 2025 (UTC)
::Thanks! @[[User:JJPMaster|JJPMaster]] @[[User:Kittycataclysm|Kittycataclysm]] [[User:Greatswrd|Greatswrd]] ([[User talk:Greatswrd|discuss]] • [[Special:Contributions/Greatswrd|contribs]]) 10:24, 30 March 2025 (UTC)

== Minecraft book ==

Is it good creating pages like this, [[Minecraft#Husk]]? [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 12:43, 9 May 2025 (UTC)

:@[[User:Cactusisme|Cactusisme]] what do you mean? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:18, 10 May 2025 (UTC)
::are we allowed to create pages like that? like for every mob [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 10:02, 11 May 2025 (UTC)
:::To be honest, I don't think the structure and formatting of the book is very good. Several of the mob pages, for example, have very little information and aren't particularly helpful on their own. If I were working on it, I would restructure the book. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 14:09, 11 May 2025 (UTC)
::::I am planning to do that. [[User:Cactusisme|Cactusisme]] ([[User talk:Cactusisme|discuss]] • [[Special:Contributions/Cactusisme|contribs]]) 04:19, 12 May 2025 (UTC)

== Request to Review Adjusted User Page (XoriantTeam) ==

Hello [[User:Kittycataclysm|Kittycataclysm]],

I hope you're well. I noticed that my user page ([[User:XoriantTeam]]) was recently deleted for appearing promotional or inappropriate for Wikibooks. Thank you for keeping the community standards in check.

I’ve since revised the content with closer attention to neutrality and compliance with Wikibooks guidelines. My intent is to participate constructively, especially in areas related to digital engineering and educational content creation.

If possible, I’d appreciate your help reviewing the revised version. I'm happy to share it or upload it as a file if there’s a preferred method.

Please let me know how best to proceed. I welcome any suggestions and will gladly make further adjustments.

Best regards,  

XoriantTeam [[User:XoriantTeam|XoriantTeam]] ([[User talk:XoriantTeam|discuss]] • [[Special:Contributions/XoriantTeam|contribs]]) 11:02, 15 May 2025 (UTC)

:Hi there—you can publish an updated user page, but I'd caution you against talking about your company. Keep it limited to your involvement with Wikibooks. You may contribute productively here, but further promotional materials are grounds for an indefinite block. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 12:30, 15 May 2025 (UTC)

== Planning to use AWB to update categories on the cookbook ==

Hello. I noticed in recent changes that you were moving some categories using HotCat (e.g. moving Category:Chile recipes to Category:Recipes using chile), which can be time-consuming. Therefore, I plan to help you with moving the cookbook categories by adding myself to enabledusers and enabledbots in [[Wikibooks:AutoWikiBrowser/CheckPageJSON]]. Would this be fine if I assist you and to add myself to the check page? I am familiar with using AWB after testing on a non-Wikimedia project. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:42, 8 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—thank you for the tip! I just installed JWB, so this should make my mass cat changes much faster. Thanks again! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:11, 8 June 2025 (UTC)
:: Thank you for the information. Also, is it okay if I change (for example) [[:Category:Vinegar recipes]] to [[:Category:Recipes using vinegar]] (I can redirect the former category to the latter), given that we should move {{tq|Category:[ingredient] recipes}} to {{tq|Category:Recipes using [ingredient]}} for consistency? [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:57, 8 June 2025 (UTC)
:::Sure thing—go ahead! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:53, 8 June 2025 (UTC)

== Tool for even faster category changes ==

See [[:c:Help:Gadget-Cat-a-lot#As_your_user_gadget]]. I just [https://en.wikibooks.org/w/index.php?title=User:Koavf/common.js&amp;action=history installed it] and used it dozens of times in a click. Let me know if you need any help. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:36, 19 June 2025 (UTC)

:@[[User:Koavf|Koavf]] Thanks! I'm having a little trouble activating it, but I'll keep trying. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:54, 19 June 2025 (UTC)
::A lot of times, a purge will do the trick. See [[:mw:Purge]]. Usually just &lt;kbd&gt;Ctrl+Shift+R&lt;/kbd&gt; once or twice. —[[User:Koavf|Justin (&lt;span style=&quot;color:grey&quot;&gt;ko'''a'''vf&lt;/span&gt;)]]&lt;span style=&quot;color:red&quot;&gt;❤[[User talk:Koavf|T]]☮[[Special:Contributions/Koavf|C]]☺[[Special:Emailuser/Koavf|M]]☯&lt;/span&gt; 00:55, 19 June 2025 (UTC)
:::Took several purges, but we're set now! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:16, 19 June 2025 (UTC)

== Advice on when I should run for adminship ==

Hi, I hope you are doing well. I am asking for some advice on when I should run for enwikibooks adminship, given the following below:

Currently, I am doing some optimizations for dark mode on this project, and some of the message box/MediaWiki interface/template pages might be outdated, fully protected, or can use a little help using mw-parser-output. These unfortunately might hinder the process of updating these pages/templates for Vector 2022's dark mode.&lt;br&gt;
Additionally, I have a solid expertise with edit filters, as I have requested some administrators to update deprecated filter variables, switching filters from warn and disallow to disallow only, and I can also monitor the filter log for potential false positives (from local or global filters).

A fellow English Wikibooks administrator also said to me that they are willing to support me in a few months when I run for adminship, as I am generally trusted.

I hold two advanced global permissions, and I hold an edit filter helper permission on the English Wikipedia, to be sure. Thank you for your consideration. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 01:02, 23 June 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—good question! I agree that you are a trusted user, and I think it would be reasonable for you to run for adminship, especially given our need to fix up technical aspects of the project. If you don't plan to commit to Wikibooks long-term (i.e. you have some projects you'd like to take a few months to complete and then be done), you can always request temporary adminship. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:30, 23 June 2025 (UTC)
:: Thank you for your feedback, but I also plan to monitor for vandalism/spam, and to commit to reduce the administrative assistance reading room backlog, should I be elected for adminship (and I forgot to mention those). Anyway, regarding your feedback, I might run by August or even July, given that I've lately started contributing more often to Wikibooks. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:29, 23 June 2025 (UTC)
::: [[User:Kittycataclysm|Kittycataclysm]], I am pinging you one more time to see if you have read my response above yours. Thank you. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:34, 26 June 2025 (UTC)
::::Hi @[[User:Codename Noreste|Codename Noreste]]! I'm not sure what you mean—was there an additional question you had? Everything you've outlined seems quite reasonable. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:26, 26 June 2025 (UTC)
::::: Apologies for the confusion, I don't have any questions to ask. I was clarifying that I can help with implementing edit requests and to block obvious vandals and spammers, aside from the skills I mentioned earlier. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:32, 26 June 2025 (UTC)

== how is it you feel able to interfere in my sandbox? ==

you deleted a page in my sandbox that was my way of providing my response to a request from an OpenSCAD dev team leader for a couple of text blurbs for use on a web page of the OpenSCAD site.

now that you have deleted my page i have to recreate the texts from a screenshot to be able to offer the suggestions, which i will 

This kind of high handed treatment is what keeps me from being a wiki-anything contributor .. If it is Wiki policy to interfere in the documentation of an open source project because it is hosted on Wikibooks then i will take up the task of moving our online docs to a site where you cannot interfere.
--
[[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 21:56, 29 June 2025 (UTC)

:Hi @[[User:VulcanWikiEdit|VulcanWikiEdit]]—thanks for bringing this to my attention. I now understand that this was intended to be in your user namespace—I've undeleted it and moved it to the correct namespace for you. Let me know if anything else comes up! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:05, 30 June 2025 (UTC)
::ah .. err .. umm .. well that is a gentle answer to my ire. Thanks for being so gracious [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:29, 30 June 2025 (UTC)
::and .. isn't my sandbox in my namespace by default? [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 20:30, 30 June 2025 (UTC)
:::No worries—it looks like you didn't add the prefix &quot;User:&quot; before writing out the full page titles, so the pages you created were technically in the project's Main space with the official published materials. Going forward, you can just double-check that the page title starts with &quot;'''User:'''VulcanWikiEdit/sandbox&quot;, and that should keep everything in the right place! Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:36, 30 June 2025 (UTC)
::::BTW .. i love the play on cat lover name [[User:VulcanWikiEdit|VulcanWikiEdit]] ([[User talk:VulcanWikiEdit|discuss]] • [[Special:Contributions/VulcanWikiEdit|contribs]]) 15:35, 1 July 2025 (UTC)
:::::Thank you! That's very kind. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:46, 1 July 2025 (UTC)

== Regarding the user Codename Tameirao ==

Could this be Matthew again (the Unicode LTA)? I believe it might be him based on his usage of edit summaries, and his usual edits to [[Unicode/Versions]]. I just blocked his recent account, and then I protected and stabilized that Unicode book. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 23:51, 12 August 2025 (UTC)

:I suspect you're right! That seems like a reasonable course of action. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:56, 13 August 2025 (UTC)
:: I recently encountered another possible LTA, see [[Special:Contributions/~2025-55706-6]] (as well as [[Unicode/Roadmap Blocks]]). I can email you more details if you want. &lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 16:30, 9 September 2025 (UTC)
:::I think this is the same LTA, yes! I've protected [[Unicode/Roadmap Blocks]], but I think it would be a good idea if we could automate this monitoring somewhat using the edit filter. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:07, 9 September 2025 (UTC)
:::: I don't think that was Matthew, as he typically uses edit summaries. The deleted page was not protected, as it was protected before you deleted it; I salted it from creation for one year. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 20:22, 9 September 2025 (UTC)
::::: You might want to look at [[Special:Contributions/Freddy Fazbearing Others]]. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 04:18, 26 October 2025 (UTC)
::::::Thank you! I went ahead and blocked them. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:54, 28 October 2025 (UTC)

== IP block exempt  ==

Hi Kitty,
I currently have IP block exemption on enwiki, Commons and Wikidata as I use VPNs connected to my internet security software. Can you please grant me the right on wikibooks. I have a strong password and use two factor authentication. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 10:51, 22 August 2025 (UTC)

:Hi @[[User:TarnishedPath|TarnishedPath]]! This doesn't sound unreasonable to me, but I think it would be good if you requested at [[Wikibooks:Requests for permissions]] so we can have a discussion—I have not granted this right before. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:50, 23 August 2025 (UTC)
::Kitty, thanks for pointing me in the right direction. ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:25, 23 August 2025 (UTC)
::See [[Wikibooks:Requests_for_permissions#TarnishedPath_(discuss_·_contribs_·_count_·_logs_·_block_log_·_rfp_·_rights)_(IP_Block_Exemption)]] ''[[User:TarnishedPath|&lt;b style=&quot;color:#ff0000;&quot;&gt;Tar&lt;/b&gt;&lt;b style=&quot;color:#ff7070;&quot;&gt;nis&lt;/b&gt;&lt;b style=&quot;color:#ffa0a0;&quot;&gt;hed&lt;/b&gt;&lt;b style=&quot;color:#420000;&quot;&gt;Path&lt;/b&gt;]]''&lt;sup&gt;[[User talk:TarnishedPath|&lt;b style=&quot;color:#bd4004;&quot;&gt;talk&lt;/b&gt;]]&lt;/sup&gt; 03:35, 23 August 2025 (UTC)
== You've got mail! ==
{{You've got mail|sig=&lt;span style=&quot;font-family:Verdana&quot;&gt;[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;'''''Codename Noreste'''''&lt;/span&gt;]] ([[User talk:Codename Noreste|&lt;span style=&quot;color:#A1000E&quot;&gt;talk&lt;/span&gt;]])&lt;/span&gt; 00:20, 6 September 2025 (UTC)}}

:Thank you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:06, 6 September 2025 (UTC)

== Are you able to import? ==

I made a few requests over at https://en.wikibooks.org/wiki/Wikibooks:Requests_for_import . [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 22:32, 4 October 2025 (UTC)
: [[User:2005-Fan|2005-Fan]], I'll go ahead and start the imports. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:29, 5 October 2025 (UTC)
::Thank you for your help [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 16:51, 5 October 2025 (UTC)
::: My apologies for not doing this sooner, because some database error appears when I am trying to mass import. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 23:39, 5 October 2025 (UTC)
::::I also tried to make this import earlier and ran into issues with the software. I was hoping it was a temporary bug, but it seems to be persisting. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:01, 6 October 2025 (UTC)
:::::This seems like I should get involved. {{working}}... [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 13:11, 6 October 2025 (UTC)
:::::: I believe there are five pages that have massive page histories they fail to import here. [[User:Codename Noreste|Codename Noreste]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 15:13, 6 October 2025 (UTC)
:::::::I backed up the XMLs of them locally but im unsure how much that'd do. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 15:18, 6 October 2025 (UTC)
::::::::Just became an importer. The reason is prob understandable but I cannot upload the XML file to here locally. [[User:2005-Fan|2005-Fan]] ([[User talk:2005-Fan|discuss]] • [[Special:Contributions/2005-Fan|contribs]]) 17:23, 10 October 2025 (UTC)

== About the category parameter in the recipe summary template ==

When it uses a &quot;recipe by type&quot; category, should it use a &quot;[type/food] recipes&quot; name or &quot;Recipes for [type/food]&quot;?

I recently operated JWB to change from [[:Category:Dessert recipes]] to [[:Category:Recipes for dessert]] in multiple Cookbook recipes, and from what I've said before, I've changed to ''Recipes for dessert'' in the category parameter of Cookbook recipes. Hope you don't mind that this was over more than 250 changes (not counting the recent category changes after moving some recipe categories). Thanks. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 02:07, 27 October 2025 (UTC)

:Hi @[[User:Codename Noreste|Codename Noreste]]—those JWB changes you made seem fine to me! I'm not quite sure what you're asking in your first sentence, though. Assuming I understand correctly: in general, I think the default format should be whatever the actual category name is. BUT if there is a redirect, it ultimately shouldn't matter too much. And, because I'm not convinced of the utility of that infobox parameter in the first place (thinking of removing it), I'm not hugely concerned about it for the time being. Does this help? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:21, 27 October 2025 (UTC)
:: Probably, but I will say the following below (for my first sentence) to clarify:
:: On the &lt;code&gt;|category =&lt;/code&gt; parameter, when placing a recipe category name, should it either be {{tq|Sandwich recipes}} or {{tq|Recipes for sandwiches}}? I hope this clears the confusion. '''[[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]]''' ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 18:39, 27 October 2025 (UTC)

== Please no more Unicode LTA ==

Please don't block me again. I promise I will edit Unicode stuff and add correct information. [[Special:Contributions/&amp;#126;2025-30839-28|&amp;#126;2025-30839-28]] ([[User talk:&amp;#126;2025-30839-28|talk]]) 20:54, 1 November 2025 (UTC)
:&lt;small&gt;I am a bit out of the loop, so correct me if I'm wrong - I'm assuming here&lt;/small&gt; I think the point is that they want you to ''not'' edit the Unicode stuff? Also hi kitty, it's been a ... very long time.. &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:13, 5 November 2025 (UTC)
::Ok so apparently not as long as I thought, but it feels like I've been away for at least a year lol &lt;sup&gt;&amp;#8212; [[User:L10nM4st3r|&lt;span style=&quot;color:#c71300&quot;&gt;L10nM4st3r&lt;/span&gt;]]&lt;/sup&gt; / &lt;sub&gt;[[User talk:L10nM4st3r|&lt;span style=&quot;color:#ce3f00&quot;&gt;'''ROAR''' at me!&lt;/span&gt;]]&lt;/sub&gt; 01:23, 5 November 2025 (UTC)
:::Nice to see you! —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:41, 5 November 2025 (UTC)

== Administrator and reviewer user right combinations are not needed anymore ==

Given that administrators can review edits in addition to reviewers, I would suggest for you (and other administrators) to kindly remove the reviewer permission from (own) accounts. What I'm saying is that if one holds administrator and reviewer permissions together, they can remove the reviewer permission from their own account and retain their administrator permission. Thanks. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 16:06, 11 November 2025 (UTC)

:Gotcha—is there a reason it's bad for one user to have both these rights? If so, I can remove my reviewer right. Otherwise, it seems fairly harmless? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:26, 11 November 2025 (UTC)
:: The thing is, administrators have the &lt;code&gt;review&lt;/code&gt; user right, as well as some permissions in the reviewer user group in the administrator toolset. That means that having the reviewer user group together with the admin user group is redundant. Hope this explains it. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 19:59, 11 November 2025 (UTC)
::: @[[User:Kittycataclysm|Kittycataclysm]] &lt;s&gt;I'll do this tomorrow morning, as well as to remove autoreviewed user permissions from users who are reviewers.&lt;/s&gt; ({{doing}}) [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:24, 12 November 2025 (UTC)
: I have removed the autoreviewed user permission from users who are reviewers. As for administrators, I will do so later today. [[User:Codename Noreste|&lt;span style=&quot;color:#0024FF&quot;&gt;Codename Noreste&lt;/span&gt;]] ([[User talk:Codename Noreste|discuss]] • [[Special:Contributions/Codename Noreste|contribs]]) 03:40, 13 November 2025 (UTC)

== Nesting in Open Book of Ecovillages and Eco Communities  ==

Hi Kittycataclysm,

I am editor of wikipedia since 2004. We have the habit if we have a concern using the talk page to clarify the case. I am not sure to delete meaningful content without previous notification and doing major redirection without agreeing the main contributor(s) is an adequate admin act and sign of good manner of host (see [[W:Wikipedia:Etiquette|Wikipedia:Etiquette]].)

Yes, It will be not an average book but above the regular. This is the exact case: ''&quot;this may be appropriate, such as with large textbooks that contain subsections with a lot of content.&quot;'' ''for to establish good structural and stylistic practices''

I have a data management certification. If you asking it will have 4 nest level on strict purpose. If you saw the introduction of the [[Open Book of Ecovillages and Eco Communities]] is/will be a global collection making effective collaboration over borders and continents. One structured + categorized(!) page for each community willing to show up. The Postal addresses has also same or larger deepness, this is unavoidable (Country/Postal Code/Location/Street/House/floor/door). Here will looks like: '''Eco-comm/Continent/Regio code/Community name'''

The goal of this system to open bridge + experience highway  for the communities using the same permaculture technics what collected parallelly in [[Open Book of Permaculture]]. That is also part of this knowledge base please dont do simplification steps on that without discussion.

I am kindly asking to revert your edits in this book.

After that I will put a notification template  about 
 &quot;This book is under construction with major changes. Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History. Common clarifications/ guides are on the primary talk page.&quot;


Thanks: [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 02:22, 12 November 2025 (UTC)

:Hi @[[User:Rodrigo|Rodrigo]], and thank you both for your contributions and for reaching out! Yes, I did make the following changes to [[Open Book of Ecovillages and Eco Communities]]:
:* I moved the pages from the [[Eco-comm]] namespace to the [[Open Book of Ecovillages and Eco Communities]] namespace, since the table of contents and pages for a given book should be under that book's namespace.
:* I removed the links to Wikipedia that were on [[Open Book of Ecovillages and Eco Communities]], since outlinking has been discouraged at en.Wikibooks as a matter of practice. Compilations of links may not fall into WB scope as an instructional text, and [[Wikibooks:Requests for deletion/Piano Solo Music: An Encyclopedia|there is precedent for deleting them]]. But, I do see that the tool I used didn't just remove links to enWP, so I will restore the prior revision and ping the tool developer.
:* I flagged it as needing denesting—you're right that nested entries can sometimes be appropriate. In this case, I was primarily flagging for a denest because the table of contents needs to be moved onto the main page, and it shouldn't have hidden navigation within the nested portions.
:Could you clarify which of these edits you do not agree with so I can make sure they are individually addressed? As an aside, it could be helpful to create a [[Help:Local manuals of style|local manual of style]] for the book in order to clearly outline the expectations. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:59, 12 November 2025 (UTC)
::My main concern not about moving and flagging but '''deleting''' [[Eco-comm]] against [[Wikibooks:Deletion policy]] and not mentioning in the clarification even after my notification. Should I note all administrators [[Wikibooks:Please do not bite the newcomers]] - or will they do speedy deleting one by one until I make them individually addressed?
:::The &lt;u&gt; local manual of style&lt;/u&gt; development is ongoing together with the sample pages.
::'''MAIN PAGE'''
::The '''Main page''' and '''Namespace''' is the [[Eco-comm]]. The '''Full Title''' or '''Cover''' is [[Open Book of Ecovillages and Eco Communities]]. Because of the high level of nesting the below extra-long-full-text-title to be avoided the Cover page is a redirection with preface/intro etc.
::'''NESTING '''
:::Featured book with 3 level nesting: [[Social and Cultural Foundations of American Education/Educational Change/Theory]]
:::5 level nesting example: [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]]
::'''Categories''' The [[:Category:Eco-comm]] will let the users make practical sub-categories e.g. [[:Category:Eco-comm/Project/numundo]] [[:Category:Eco-comm/]]
:::
::[[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 03:44, 18 November 2025 (UTC)
:::Thank you for elaborating! I'm unfortunately not sure what you mean about deleting [[Eco-comm]]—are you referring to the fact that I moved it without leaving a redirect? Regarding the nesting, I do honestly think those other books you linked should have their navigation denested since I find their format difficult to parse, and they have some navigation issues. Looping in some other active admins (@[[User:Leaderboard|Leaderboard]] @[[User:MarcGarver|MarcGarver]] @[[User:JJPMaster|JJPMaster]] @[[User:Codename Noreste|Codename Noreste]] (@[[User:SHB2000|SHB2000]]) so they can get eyes on this and voice anything they think is important. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 04:12, 18 November 2025 (UTC)
::::It makes no sense to have some crazy abbreviation as a &quot;main page&quot; or &quot;namespace&quot; (whatever that means in this context) for a book in order to allow it to be deep nested. Nobody needs to type the whole name of the nesting because that's what navigation templates do, and it is a simple matter to override the page title. I also take issue with the statement, above, &quot;Before contributing, please discuss and align your work with at least one of the main contributors listed in the Page History.&quot; Anybody can edit, and nobody gets to own and control any work. Taken together, this complaint looks like a case of attempting to assert ownership and to operate against the normal practices of Wikibooks. As such, I am completely aligned with the changes made. [[User:MarcGarver|MarcGarver]] ([[User talk:MarcGarver|discuss]] • [[Special:Contributions/MarcGarver|contribs]]) 12:49, 18 November 2025 (UTC)
:::::That. [[User:Leaderboard|Leaderboard]] ([[User talk:Leaderboard|discuss]] • [[Special:Contributions/Leaderboard|contribs]]) 14:59, 18 November 2025 (UTC)
::::Thanks @[[User:MarcGarver|MarcGarver]]@[[User:Leaderboard|Leaderboard]] for the contribution, btw the [[Development Cooperation Handbook/Designing and Executing Projects/Communication Management/Communication Planning/Develop a Conflict Management Strategy]] also looks crazy long, is'nt it? Lets continue in the [[Wikibooks:Reading_room/General]] keeping this page for personal messages. [[User:Rodrigo|Rodrigo]] ([[User talk:Rodrigo|discuss]] • [[Special:Contributions/Rodrigo|contribs]]) 23:07, 20 November 2025 (UTC)

== Deletions of Wikibook subpages ==

Hello @[[User:Kittycataclysm|Kittycataclysm]],

regarding the [[Thesis Writing Guide]] subpage deletions, should I just recreate them when I keep working on them or was there an automatic deletion that we could undo? This document will grow, but really slowly.

Best,
Tim [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 11:37, 16 December 2025 (UTC)

:Hi @[[User:TimBorgNetzWerk|TimBorgNetzWerk]]! Since there was so little content on the deleted pages, my recommendation would just be for you to gradually recreate the chapters as you go. Does that make sense? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 19:54, 17 December 2025 (UTC)
::Makes sense, not my ideal solution, but also not far from it :) The end result will be the same, the in-between will just feel a little bit weird from time to time.
::Thank you for taking time to curate and quality-control Wikibooks - wishing wonderful holidays and a happy new year! [[User:TimBorgNetzWerk|TimBorgNetzWerk]] ([[User talk:TimBorgNetzWerk|discuss]] • [[Special:Contributions/TimBorgNetzWerk|contribs]]) 20:43, 17 December 2025 (UTC)
:::Thank you, and happy holidays to you as well :) —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 23:13, 17 December 2025 (UTC)

== help with &quot;Media Literacy and You&quot; == 

{{re|Kittycataclysm}} What do I need to do to get a quality review of ''[[Media Literacy and You]]'', or whatever is needed to remove &lt;nowiki&gt;{{Qr-em|not clear how this is to be structured as a book}}&lt;/nowiki&gt;? 

I ask, because you added that flag just over 2 hours after I created it. I later found that I had accidentally created it as an anonymous user. I've since started using my standard Wikiname, and I tried to respond to the requests both by creating a discussion on the &quot;Discussion&quot; page associated with that book and by upgrading the content. 

The upgrades included adding the &quot;Introduction&quot; chapter by revising an article on Wikiversity that convinced me to start this Wikibook. I have other articles that I plan to rewrite to create 9 of the remaining 11 chapters in the current table of contents, as indicated in this table of contents. 

??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:23, 8 February 2026 (UTC)

:Hi @[[User:DavidMCEddy|DavidMCEddy]]! I removed the query flag, since this is clearly not a test page. I do have concerns about the suitability of this book for Wikibooks, since it seems to be more in line with essays and original research/analysis (which are [[Wikibooks:WIW|out of scope here]]). Wikiversity seems like a very suitable place for them—is there a specific reason you want to move them here? Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:24, 8 February 2026 (UTC)

::{{re|Kittycataclysm}} 
::This book is intended to accelerate the diffusion of [[w:Media literacy|media literacy]] by making it easier for humans to (a) access training materials and (b) connect with research on the most important issues that concern them and (c) discuss those issues with others who may believe differently in a nonthreatening context that encourages dialogue and a shared search for what can honestly be said about any particular issue. This is an extension of &quot;The wisdom of polarized crowds&quot; discussed in [[Wikipedia:Reliability of Wikipedia]]. 

::I don't know about you, but I'm frightened by the collapse of nuclear arms control agreements since the year 2000, by global warming, by the threats of the Trump administration to invade Canada and Greenland, etc. If this book project is successful, it will make a material contribution to reversing these trends -- unless this kind of dialogue is [[v:Responding to a nuclear attack|interrupted by a nuclear war]]. 

=== Who is DavidMCEddy ===

::I'm a [[w:Vietnam veteran|Vietnam-era veteran]] with a PhD in statistics and a publication record for which [https://www.researchgate.net/profile/Spencer-Graves-3 ReserchGate has found over 1,200 academic publications that have cited my work.] Since  [https://xtools.wmcloud.org/ec/en.wikipedia.org/DavidMCEddy 2010 I have logged]
*  6,000+ edits in each of Wikipedia and Wikiversity, 
*  1,000+ in Wikimedia Commons, 
* 30,000+ in Wikidata, and 
* almost 1,000 in other Wikimedia Foundation projects like Wikiquote and edits to the Spanish, French and German Wikipedias. 

This includes dozens of research reports posted to Wikiversity under [[v:Category:Freedom and abundance]] and 44 posts under [[v:Category:Media reform to improve democracy]] that provide a platform for documenting and discussing 44 episodes of a fortnightly &quot;Media &amp; Democracy&quot; series of 29:00 mm:ss podcasts syndicated for the [https://pacificanetwork.org/stations-2/ Pacifica Radio Network] featuring the opinions of leading experts on the increase in political polarization and violence and what those experts think should be done about this. 

I've just posted another chapter to [[Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. I hope you will agree that this book can make a positive contribution to Wikibooks and to [[w:Jimmy Wales|Jimbo Wales]]' [[w:Wikipedia:Prime objective|Prime Directive]] to create &quot;a world in which every single person on the planet is given free access to the sum of all human knowledge.&quot; Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 01:19, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Thank you and I understand this, but I am asking why you think this material is more suitable at Wikibooks rather than at Wikiversity. From what I can see, Wikiversity seems like the more appropriate home for it given our [[Wikibooks:WIW|scope]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:59, 9 February 2026 (UTC)

::{{re|Kittycataclysm}} 

::&quot;Media Literacy and You&quot; is textbook to support both self study and classes on media literacy. 

::I have been posting content to Wikiversity since 2014 and have not encountered support there for books. A search just now turned up a hint of a book on Wikiversity, but I could not easily find anything on how to do it, etc.  

::I think this &quot;Media Literacy and You&quot; project would lose the vast majority of its potential if it were not on Wikibooks. 

::??? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 02:22, 9 February 2026 (UTC)

{{outdent}}

{{re|Kittycataclysm}} 
Will you please help me with the protocols of creating a book on Wikiversity? 

1. I have found documentation that claims that Wikiversity supports such. However, the documentation seems incomplete, potentially out of date, etc. For example, I could not see how to follow the instructions for [[Wikiversity:Help:Books#Step 1: Enable the &quot;Book creator&quot; tool]]. So I posted a question to [[Wikiversity:Help talk:Books]]. 

2. What do you suggest I do next? 

:I can create an article on Wikiversity titled, &quot;Media Literacy and You&quot;, and port everything I've posted to Wikibooks there, then replace the pages on Wikibooks with redirects to [[Wikiversity:Media Literacy and You]], [[Wikiversity:Media Literacy and You/Introduction]], and [[Wikiversity:Media Literacy and You/The impact of the media on political economy since the time of the Pharaohs]]. 

:If you think that's the best way to build this book project, great. It would actually be easier for me, because there would be less translation between what I already have on Wikiversity and a version for Wikibooks. (Also, Wikiversity supports &lt;nowiki&gt;{{cite Q|...}}&lt;/nowiki&gt;, which I have used extensively for years.) 

:Thanks for your help. [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 13:26, 9 February 2026 (UTC)

:@[[User:DavidMCEddy|DavidMCEddy]] Unfortunately, I am not familiar with the exact workings of Wikiversity, so I can't be much help there. My personal recommendation is that you ask there for help on how best to structure your materials to match the WV requirements. If you'd like some additional opinions/insight, please feel free to also check in at the [[Wikibooks:Reading room/General|reading room]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 02:22, 10 February 2026 (UTC)

::{{re|Kittycataclysm}} I believe I have finished migrating all of ''Media Literacy and You'' to Wikiversity and replacing the parts of it on Wikibooks with redirects. Comments? Thanks, [[User:DavidMCEddy|DavidMCEddy]] ([[User talk:DavidMCEddy|discuss]] • [[Special:Contributions/DavidMCEddy|contribs]]) 17:32, 10 February 2026 (UTC)

== Thank you!  ==

Heya, thanks for reviewing my stuff! Just to note, the first lesson page was done and so that'll need moving. If you want to discuss anything with me, I am easily reachable on Discord @ xiluosi233. I can explain philosophy, approach, and so on from my teaching experience if you want anything regarding that. [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:48, 17 February 2026 (UTC)

:It appears [[An Introduction to the Han Script]] was moved wrong - should it not be [[General Literary Chinese from Scratch/An Introduction to the Han Script]]? [[User:Shira the Mogul|Shira the Mogul]] ([[User talk:Shira the Mogul|discuss]] • [[Special:Contributions/Shira the Mogul|contribs]]) 19:52, 17 February 2026 (UTC)
::@[[User:Shira the Mogul|Shira the Mogul]] good catch! I accidentally removed more of the title than intended. I've fixed this now. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 13:18, 18 February 2026 (UTC)

== A test request ==

Just to see whether a recent Luna update turned out as intended, could you briefly revert your [[User:Kittycataclysm/lunaoptions.json|Luna preferences page]] to the first revision? Since you don't appear to have any custom preferences in the first place, I don't think there should be any conflicts. [[User:JJPMaster|JJP]]&lt;sub&gt;[[User talk:JJPMaster|Mas]]&lt;sub&gt;[[Special:Contributions/JJPMaster|ter]]&lt;/sub&gt;&lt;/sub&gt; ([[wikt:she|she]]/[[wikt:they|they]]) 01:49, 30 March 2026 (UTC)

:Done! But, it seems to have perhaps auto-updated again immediately afterwards. —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 15:39, 10 April 2026 (UTC)

== Linking ==
Hi,&lt;br&gt;
For my edification, why is a link from [[Cookbook:nettle|nettle]] to [[w:Urtica_dioica|Urtica dioica]] not appropriate? The Wikipedia article has more information &amp; seems relevant.&lt;br&gt;
Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 01:53, 24 April 2026 (UTC)

:@[[User:PeterEasthope|PeterEasthope]] good question! Wikibooks discourages outlinking, since books should be self-contained units. Instead of linking to [[w:Urtica dioica]], the correct approach would be to flesh out the actual chapter here at Wikibooks. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 17:34, 24 April 2026 (UTC)
::Should all material in the Wikipedia article about Urtica dioica relevant to cooking be duplicated into the nettle article in the cookbook? Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 02:30, 2 May 2026 (UTC)
:::@[[User:PeterEasthope|PeterEasthope]] you could do that, although you should only include information that is sourced. However, I recommend that you wait, because I am coincidentally working on the page right now and fleshing it out significantly. I should publish today. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 21:40, 2 May 2026 (UTC)
::::The nettle page is better now. Thanks.
::::I still wonder, given that the link to ''The Complete Guide to Edible Wild Plants, ...'' is permitted, why not a link to the botanically oriented page in Wikipedia. What if someone reads the Cookbook article and is interested in the toxin for example? Seems that non-Wikimedia references are more privileged than Wikimedia references.
::::Also, by chance, just noticed the [[w:Nettle_soup|Nettle soup]] article in Wikipedia. Better in the Cookbook?
::::Thx, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 19:10, 5 May 2026 (UTC)
:::::Another good question. The reason those books are linked is because they are reputable and topical sources for the subject matter (nettles as used in cooking from an instructional perspective), and the links are part of the citations—this makes it different from a simple outlink to a Wikipedia page. Wikipedia pages should also not be cited themselves as sources. Regarding nettle soup, I don't think it makes sense to have that as a standalone page here in the cookbook due to its encyclopedic tone, and I don't see any recipes there. Does this make sense? —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 00:21, 6 May 2026 (UTC)
::::::Somewhat. Certainly a recipe wouldn't be incongruous in a cookbook. Still seems unhelpful that relevant information in Wikipedia is inaccessible from a Wikibook. In effect there's a &quot;Berlin Wall&quot; between two Wikimedia projects. Would a &quot;See also&quot; section be permissible?
::::::Thanks, ... [[User:PeterEasthope|PeterEasthope]] ([[User talk:PeterEasthope|discuss]] • [[Special:Contributions/PeterEasthope|contribs]]) 14:00, 7 May 2026 (UTC)

== You may be an eligible candidate for the U4C election ==

&lt;div lang=&quot;en&quot; dir=&quot;ltr&quot; class=&quot;mw-content-ltr&quot;&gt;
Greetings,

The [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee|Universal Code of Conduct Coordinating Committee (U4C)]] seeks candidates for the 2026 election. The U4C is the global committee responsible for overseeing enforcement of the [[foundation:Special:MyLanguage/Policy:Universal Code of Conduct|Universal Code of Conduct]]. Elections are held annually, if elected a committee member serves for two years.

This year the U4C requires candidates to hold administrator rights on at least one wiki, which is why you are being contacted as you appear to hold this right. There are other requirements, such as candidates must be at least 18 years old and may not be employed by the Wikimedia Foundation or other related chapters and affiliates. You can find more information in the [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026#Call_for_Candidates|call for candidates on Meta-wiki]]. Additionally, the committee's working language is English; some ability to communicate in English is required.

The election opens on 18 May, if you are eligible and interested you have until 10 May to submit your candidacy. There will week between for candidates to answer questions from the community. Voting takes place privately in [[m:Special:MyLanguage/SecurePoll|SecurePoll]], successful candidates must receive at least 60% support. More information is available on [[m:Special:MyLanguage/Universal_Code_of_Conduct/Coordinating_Committee/Election/2026|the 2026 Elections page]], including timelines and other candidacy information. If you read over the material and consider yourself qualified, please consider submitting your name to run for the committee. If you think someone else in your community might be interested and qualified, please encourage them to run.

In partnership with the U4C -- [[m:User:Keegan (WMF)|Keegan (WMF)]] ([[m:User_talk:Keegan (WMF)|talk]]) 18:32, 28 April 2026 (UTC) &lt;/div&gt;
&lt;!-- Message sent by User:Keegan (WMF)@metawiki using the list at https://meta.wikimedia.org/w/index.php?title=User:Keegan_(WMF)/test&amp;oldid=30471751 --&gt;

== Undeletion request ==

Hello,


I am writing to request an undeletion of the page Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad. You stated you are a frequent visitor of the Lentis page and are thus familiar with it. This page was part of a class assignment and was in progress at the time of deletion. The work deleted is what we will be graded on for our class, so we would appreciate the restoration. [[User:Yqj3km|Yqj3km]] ([[User talk:Yqj3km|discuss]] • [[Special:Contributions/Yqj3km|contribs]]) 19:36, 4 May 2026 (UTC)

:@[[User:Yqj3km|Yqj3km]] see my response below regarding undeletion. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:15, 4 May 2026 (UTC)

== Undeletion request ==

About the page on Lentis called Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad: I, too, request undeletion, please. If the authors made any msitakes, the fault is 100 percent mine, for failing to guide them correctly. Like all chapters in this book, this team's chapter is a class assignment. I will be interested also in the reason for deletion so that I can guide authors better. I want to help my students be constructive contributors. Many thanks!

[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 20:03, 4 May 2026 (UTC)

:Hi @[[User:Norton|Norton]] and thanks for the ping! I deleted it because it was not titled/filed correctly, so I didn't realize it was part of [[Lentis]]. I have undeleted it and moved it to [[Lentis/Saumya Pandya Thakkar, Shakuntala Pandya and the Pedestrians of Ahmedabad]]. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 22:14, 4 May 2026 (UTC)
::Many, many thanks, @[[User:Kittycataclysm|Kittycataclysm]]! I am very grateful as always for everything you do for Wikibooks!
::[[User:Norton|Norton]] ([[User talk:Norton|discuss]] • [[Special:Contributions/Norton|contribs]]) 22:27, 4 May 2026 (UTC)

== Log in issues ==

Hi, messaging you as you seem to be the most active admin at the moment. I can't log in (as posted at  &lt;bdi&gt;[[Wikibooks:Reading room/Administrative Assistance]] and also on my WP page at&lt;/bdi&gt; [[w:User_talk:Xania]]). Seems to be an issue with extra security for admins? I am asked to use my authenticator app (which I can't as I have never set it up for Wikibooks) or a recovery code (which I don't have). Any idea what I should do in this situation? Xania [[Special:Contributions/&amp;#126;2026-28255-89|&amp;#126;2026-28255-89]] ([[User talk:&amp;#126;2026-28255-89|talk]]) 18:21, 10 May 2026 (UTC)

:Apologies for missing this yesterday! It seems like we have a few people working on it over in the reading room, and I'll keep track there. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 16:37, 11 May 2026 (UTC)

== Splitting pages ==
FYI, I untagged [[Art Print Production Methods]] as for splitting: the page is rather small with its 20 KB and does not need splitting, in my view. Ideally, there would be an operationalized, fairly detailed policy on the matter, but I do not know of one. Single-page books are in [[:Category:One-page books]]. --[[User:Dan Polansky|Dan Polansky]] ([[User talk:Dan Polansky|discuss]] • [[Special:Contributions/Dan Polansky|contribs]]) 04:45, 20 May 2026 (UTC)

== &lt;s&gt;Slander&lt;/s&gt; ==

&lt;S&gt;Your tag is slanderous and very easily proven wrong.&lt;/s&gt;[https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654455] Given you likely didn't bother to look at the edit history, I would remind you that your given reason that you think it was AI is because you see the chapter is &quot;numbered&quot;. That however was 100% my own personal decision after I reviewed my work and thought to myself that I later wrote in the introduction that there is a first to fourth chapter. However I thought to myself that the readers would not be easily made aware of what is meant by first to fourth as I didn't number them - so is why I dedicated an entire edit to make it less ambiguous  [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654328]. I should not have to be falsely penalized because I wanted to be more considerate and ensure better clarity. I do however request AI to help me figure out coding like this - [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654329] as I don't know how to link. But I intentionally take great efforts to not rely on AI to write that book and find your wrongful presumptions troubling. [[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 06:00, 15 July 2026 (UTC)

:@[[User:JaredMcKenzie|JaredMcKenzie]] thank you for clarifying! I flagged it for review because it matched a common pattern we see associated with LLM use here. If that is not the case, then nothing needs to happen in that respect; however, you will likely want to fix the lists so that they are correctly formatted in the Wikitext and not hard-written—let me know if you have any questions about that. Cheers —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 18:14, 16 July 2026 (UTC)
::Yeah, I don't instantly understand what you mean by &quot;correctly formatted&quot; list. At first, I assumed you were referring to chapter 4 - (''Further reading'')? But I think I know what you mean. I made this edit here [https://en.wikibooks.org/w/index.php?title=Five_Rules_for_Meaningful_Living&amp;diff=prev&amp;oldid=4654738] to align with how I see wikibooks typically do lists. Did I fix it? If not, feel free to clarify.[[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 18:35, 16 July 2026 (UTC)
::I thought about how I responded earlier. Even tho I still disagree, I probably shouldn't have used such a tone. I imagine admins like yourself do a lot of work overseeing wiki and the project owes a lot to you guys. So I take back my harsh words, and I hope we're good.[[User:JaredMcKenzie|JaredMcKenzie]] ([[User talk:JaredMcKenzie|discuss]] • [[Special:Contributions/JaredMcKenzie|contribs]]) 03:38, 17 July 2026 (UTC)</text>
      <sha1>onlhplgyl4ql4r3d3539l0ojx5dnkid</sha1>
    </revision>
  </page>
  <page>
    <title>User:JustTheFacts33/sandbox3</title>
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      <id>4654712</id>
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        <username>JustTheFacts33</username>
        <id>3434282</id>
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      <comment>/* Current factories */</comment>
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      <text bytes="137784" sha1="t4gelubr885161380l6bhniq8gb0ubn" xml:space="preserve">{{user sandbox}}
{{tmbox|type=notice|text=This is a sandbox page, a place for experimenting with Wikibooks.}}

This is a history of Chrysler factories that are being or have been used to produce cars, vans, SUVs, trucks, and automobile components. 

For '''Chrysler brand''' only: Plant code in 1955-1957 was not indicated if it was made in the home plant in Michigan but if it was made in a different plant, then it was indicated by a letter in the 4th position of the serial number.

For '''cars''': Plant code in 1958 was not indicated if it was made in the home plant in Michigan but if it was made in a different plant, then it was indicated by a letter in the 4th position of the serial number. Plant code was the number in the 4th position of the 10-digit serial number for 1959-1965. Plant code was the number in the 7th position of the 13-digit serial number for 1966-1967. Plant code was the letter in the 7th position of the 13-digit serial number for 1968-1980.

Canadian-built cars had the plant code as the number in the 5th position of the 11-digit serial number for 1965.

For '''trucks''': The first digit of the 7-digit sequence number (4th position overall of the 10-digit serial number) indicated which plant built the truck for 1967-1968. Plant code was the number in the 4th position of the 10-digit serial number for 1969. Plant code was the letter in the 7th position of the 13-digit serial number for 1970-1980.

Canadian-built models used a different system for VINs until 1968, when Chrysler of Canada adopted the same system as the US. Plant code for trucks was the number in the 5th position of the 10-digit serial number for 1961-1967.

All models from 1981 on have the plant code in the 11th position as per standardized VIN regulations.

For '''AMC passenger cars from 1966-1967''': Plant code is indicated by the letter in the 3rd position of the 13-digit vehicle number. If the 3rd letter is a K, then it was made in Kenosha, WI. If the 3rd letter is a B, then it was made in Brampton, ON, Canada. [Note: Some early 1966 models used the 1965-style serial numbers.]

For '''AMC passenger cars from 1968 through 1980''': Plant code is indicated by the 8th digit (the first of the sequential serial number) of the 13-digit vehicle number. 1-6 is Kenosha, WI and 7-9 is Brampton, ON, Canada.

For '''Canadian-built Jeeps built by AMC Canada for 1979-1980''': Plant code is indicated by the 8th digit (the first of the sequential serial number) of the 13-digit vehicle number. It was made in Canada if it's either an 8 (1979) or a 7 (1980). All other Jeeps from 1980 and earlier were made in Toledo. 

All models from 1981 on have the plant code in the 11th position as per standardized VIN regulations.

==Current factories== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Current Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| D (1968-),&lt;br&gt; 4 (1966-1967)
| [[w:Belvidere Assembly|Belvidere Assembly]] 
| [[w:Belvidere, Illinois|Belvidere, Illinois]]
| [[w:United States|United States]]
| 1965
| Feb. 2023
| 
| Located at 3000 West Chrysler Drive. '''Belvidere Satellite Stamping Plant''' adjoins the main assembly plant. Began production on July 7, 1965. The first vehicle produced was a 1966 Plymouth Fury four-door. In 1972, the Chrysler Town and Country station wagon was added to the Belvidere plant. In 1977, the plant was converted to build front-wheel drive subcompacts. Production of the Dodge Omni and Plymouth Horizon began on December 5, 1977. All L-body derivatives were made at Belvidere through 1987. In 1987, Belvidere was converted to build Chrysler's midsize, fwd C-body sedans. Belvidere then switched back to building small cars and began production of the Neon on November 10, 1993. Belvidere built the last Plymouth, a silver 2001 Neon LX on June 28, 2001. Neon production ended in September 2005. Dodge Caliber began production in January 2006, followed by Jeep Compass in June 2006 and Jeep Patriot in December 2006. Caliber ended production on December 19, 2011. Dodge Dart began production on April 30, 2012, and ended on October 4, 2016. Compass and Patriot production ended on December 23, 2016. Jeep Cherokee production began on June 1, 2017 and ended on February 28, 2023. Belvidere was then idled. &lt;br&gt; Past models: [[w:Plymouth Fury|Plymouth Fury]] (1966-1974), [[w:Plymouth Gran Fury#1975–1977|Plymouth Gran Fury]] (1975-1977), [[w:Dodge Monaco|Dodge Monaco]] (1966-1976), [[w:Dodge Royal Monaco#1977 (Royal Monaco)|Dodge Royal Monaco]] (1977), [[w:Dodge Polara|Dodge Polara]] (1966-1973), [[w:Chrysler Newport|Chrysler Newport]] (1977), [[w:Chrysler Town &amp; Country|Chrysler Town &amp; Country]] (1973-1977), [[w:Dodge Omni|Dodge Omni]] (1978-1987), [[w:Plymouth Horizon|Plymouth Horizon]] (1978-1987), [[w:Dodge Omni 024|Dodge Omni 024]] (1979-1980), [[w:Plymouth Horizon TC3|Plymouth Horizon TC3]] (1979-1980), [[w:Dodge Omni 024|Dodge 024]] (1981-1982), [[w:Plymouth Horizon TC3|Plymouth TC3]] (1981-1982), [[w:Dodge Charger (1981)|Dodge Charger]] (1983-1987), [[w:Plymouth Turismo|Plymouth Turismo]] (1983-1987), [[w:Dodge Rampage|Dodge Rampage]] (1982-1984),  [[w:Plymouth Scamp|Plymouth Scamp]] (1983), [[w:Dodge Dynasty|Dodge Dynasty]] (1988-1993), [[w:Chrysler Dynasty|Chrysler Dynasty]] (Canada: 1988-1993), [[w:Chrysler New Yorker#1988–1993|Chrysler New Yorker]] (1988-1993), [[w:Chrysler New Yorker Fifth Avenue#1990–1993: New Yorker Fifth Avenue|Chrysler New Yorker Fifth Avenue]] (1990-1993), [[w:Chrysler Imperial#1990–1993|Chrysler Imperial]] (1990-1993), [[w:Dodge Neon|Dodge Neon]] (1995-2005), [[w:Plymouth Neon|Plymouth Neon]] (1995-2001), Chrysler Neon (Canada: 2000-02),&lt;br&gt; Dodge SX 2.0 (Canada: 2003-05),&lt;br&gt; [[w:Dodge Caliber|Dodge Caliber]] (2007-2012), [[w:Jeep Compass#First generation (MK49; 2006)|Jeep Compass]] (2007-2017), [[w:Jeep Patriot|Jeep Patriot]] (2007-2017), [[w:Dodge Dart (PF)|Dodge Dart]] (2013-2016), [[w:Jeep Cherokee (KL)|Jeep Cherokee]] (2017-2023)
|-
| H (1989-),&lt;br&gt; A (1988)
| [[w:Brampton Assembly|Brampton Assembly]] (Formerly Bramalea Assembly)
| [[w:Brampton|Brampton]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1987
| Dec. 2023
| 
| Located at 2000 Williams Parkway East. Factory was built by AMC and Renault. The plant was acquired by Chrysler as part of its takeover of AMC. Began production on September 28, 1987. Plant was originally known as Bramalea Assembly. Plant was renamed Brampton Assembly in 1992 after Chrysler closed and sold the old AMC plant on Kennedy Road in Brampton. The attached '''Brampton Satellite Stamping Plant''' was added in December 1991 and was built for the launch of the Chrysler LH platform. On December 17, 1991, Eagle Premier and Dodge Monaco production ended. Production of the Chrysler LH platform cars began in June 1992. Production switched to the rear-wheel drive Chrysler LX platform cars in January 2004. The Chrysler 300 was also built for export to mainland Europe as the Lancia Thema from 2011-2014. Production ended on December 22, 2023 and the plant was idled. Last vehicle off the line was a Pitch-Black 2023 Dodge Challenger Demon 170. 7,147,888 vehicles were produced through 2023.&lt;br&gt; Past models: [[w:Eagle Premier|Eagle Premier]] (1988-1992), [[w:Dodge Monaco#Fifth generation (1990–1992)|Dodge Monaco]] (1990-1992),&lt;br&gt; [[w:Dodge Intrepid|Dodge Intrepid]] (1993-2004),&lt;br&gt; [[w:Chrysler Intrepid|Chrysler Intrepid]] (Canada: 1993-2004),&lt;br&gt; [[w:Chrysler Concorde|Chrysler Concorde]] (1993-2004),&lt;br&gt; [[w:Eagle Vision|Eagle Vision]] (1993-1997),&lt;br&gt; [[w:Chrysler New Yorker#1994–1996|Chrysler New Yorker]] (1994-1996),&lt;br&gt; [[w:Chrysler LHS|Chrysler LHS]] (1994-1997, 1999-2001),&lt;br&gt; [[w:Chrysler 300M|Chrysler 300M]] (1999-2004),&lt;br&gt; [[w:Chrysler 300|Chrysler 300]] (2005-2023),&lt;br&gt; [[w:Dodge Magnum#Chrysler LX platform (2005–2008)|Dodge Magnum]] (2005-2008),&lt;br&gt; [[w:Dodge Charger (2006)|Dodge Charger]] (2006-2023),&lt;br&gt; [[w:Dodge Challenger (2008)|Dodge Challenger]] (2008-2023),&lt;br&gt; [[w:Lancia Thema#Second generation (2011–2014)|Lancia Thema]] (For export: 2011-2014)
|-
| C
| [[w:Jefferson North Assembly|Detroit Assembly Complex – Jefferson]] / Jefferson North Assembly Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1992
| 
| [[w:Jeep Grand Cherokee|Jeep Grand Cherokee]] (1993-), [[w:Dodge Durango#WD|Dodge Durango]] (2011-)
| Located at 2101 Conner Street. Jefferson North replaced the previous Jefferson Assembly plant that closed in 1990 and was demolished in 1991. Jefferson North is across the street from the old Jefferson Assembly plant, on the north side of Jefferson Ave. Jefferson North was built on the site of Chrysler's old Kercheval Avenue Body Plant, which, in 1955, had been connected to the old Jefferson Assembly plant by a bridge crossing over Jefferson Ave. The Jefferson North plant site also absorbed what had been the axle plant and service parts buildings of the old [[w:Hudson Motor Car Company|Hudson]] plant, which were located at Connor St. and Vernor Hwy. The main Hudson plant is now the parking lot on the corner of Jefferson Ave. and Connor St. After 2017, the Jefferson North plant complex also absorbed the site of the former Budd Co. body- &amp; parts-making plant at Connor St. and Charlevoix Avenue, which had previously belonged to the Liberty Motor Car Co. The Budd plant extended north on Connor from Charlevoix most of the way to Mack Ave. Since the nearby Mack Ave. Assembly Plant began operations in 2021, the 2 plants have operated as the Detroit Assembly Complex. Jefferson North began production on January 14, 1992 with the original Grand Cherokee (ZJ). The 2nd gen. Grand Cherokee began production on July 17, 1998. The 3rd gen. Grand Cherokee began production on July 26, 2004 followed by the Jeep Commander on July 18, 2005. The 4th gen. Grand Cherokee began production on May 10, 2010 followed by the Dodge Durango on December 14, 2010. The 5th gen. Grand Cherokee began production in May 2022. The 4xe plug-in hybrid version of the Grand Cherokee began production at Jefferson North in March 2023. On Aug. 13, 2013, Jefferson North built its 5 millionth vehicle, a silver 2014 Grand Cherokee Overland. On May 25, 2016, Jefferson North built its 6 millionth vehicle, a Granite Crystal (silvery gray) 2016 Grand Cherokee 75th anniversary Edition.&lt;br&gt; Past models:&lt;br&gt; [[w:Jeep Grand Cherokee (ZJ)#Grand Wagoneer (1993)|Jeep Grand Wagoneer (ZJ)]] (1993), [[w:Jeep Commander (XK)|Jeep Commander]] (2006-2010),&lt;br&gt; [[w:Jeep Grand Cherokee (WK2)#Grand Cherokee WK (2022)|Jeep Grand Cherokee WK]] (2022)&lt;br&gt; [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee 4xe]] (2023-2025)
|-
| 8
| [[w:Detroit Assembly Complex – Mack|Detroit Assembly Complex – Mack]] / Mack Ave. Assembly Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 2021
| 
| [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee L]] (2021-), [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee]] (2022-)
| Located at 4000 St. Jean Avenue. The Mack Avenue Assembly Plant is built on the site of the former Mack Ave. Engine Plants I &amp; II, the New Mack Assembly Plant, &amp; the Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. The two plants that comprised the former Mack Avenue Engine Complex were converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North plants have operated as the Detroit Assembly Complex since 2021. Production began in March 2021 with the 3-row Grand Cherokee L. The 2-row Grand Cherokee followed in the fall of 2021. The 4xe plug-in hybrid version of the Grand Cherokee began production at Mack Ave. in August 2022. &lt;br&gt; Past models: [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee 4xe]] (2022-2025)
|-
|
| [[w:Dundee Engine Plant|Dundee Engine Plant]] (Formerly [[W:Global Engine Manufacturing Alliance|GEMA]]) 
| [[w:Dundee, Michigan|Dundee, Michigan]]
| [[w:United States|United States]]
| 2005
| 
| [[w:Prince engine#1.6-litre turbocharged (PSA)|1.6L turbo PSA/BMW Prince EP6CDTX Hybrid I4]],&lt;br&gt; [[w:FCA Global Medium Engine|2.0L turbo Hurricane4 EVO I4 (GME-T4 EVO)]],&lt;br&gt; Engine components
| Located at 5800 North Ann Arbor Road. Plant was originally part of the the Global Engine Manufacturing Alliance, a 3-way engine manufacturing joint venture between DaimlerChrysler, Mitsubishi, and Hyundai. The North Plant launched in October 2005, followed by the South Plant in November 2006. The plant began with production of the I4 World Gasoline Engine, which was developed by the Global Engine Alliance, a 3-way engine development joint venture between DaimlerChrysler, Mitsubishi, and Hyundai. Originally, the plant was envisioned as supplying engines to Mitsubishi and Hyundai as well as Chrysler however the plant only ever supplied engines to Chrysler. Mitsubishi and Hyundai each set up engine production at their own engine plants. On August 31, 2009, Chrysler bought Mitsubishi’s and Hyundai’s stakes in the group and now wholly owns both the Global Engine Manufacturing Alliance and its primary engine-building plant in Dundee, Michigan. In January 2012, the plant was renamed Dundee Engine Plant. Production of the Fiat 1.4-liter FIRE I4 engine began in November 2010. The Tigershark engine, an evolution of the World engine, began production in 2012 for the 2.0L and in May 2013 for the 2.4L. Tigershark engine production ended on March 16, 2023. In November 2019, the Pentastar V6 began production at Dundee, moving from the Mack Ave. Engine Plant in Detroit, which was to be converted into a vehicle assembly plant. The Pentastar V6 ended production at Dundee on August 18, 2023. In 2025, Dundee began making a North American-spec version of the European-developed Prince engine for the 2026 Jeep Cherokee Hybrid. &lt;br&gt; Past engines: [[w:World Gasoline Engine|1.8L/2.0L/2.4L/2.4L Turbo I4 World Gasoline Engine]], [[w:World Gasoline Engine#Tigershark|2.0L/2.4L I4 Tigershark Engine]], [[w:FIRE engine|Fiat 1.4L/1.4L Turbo FIRE MultiAir I4 engine]], [[w:Chrysler Pentastar engine|Chrysler 3.6L Pentastar V6 engine]] 
|-
| 
| Etobicoke Casting Plant
| [[w:Etobicoke|Etobicoke District]], [[w:Toronto|Toronto]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1964
| 
| Aluminum die castings, Engine and Transmission Components
| Located at 15 Brown's Line. Etobicoke used to be a separate city but became part of Toronto in 1998. Factory was originally built in 1942 by the Canadian government and operated by Alcan Aluminum, which used it to make molds for military aircraft parts during World War II. It produced precision aircraft parts and other high quality aluminum castings. The aluminum foundry was purchased by Chrysler in April 1964 from Alcan Aluminum. The plant was expanded in 1965 and 1998. Etobicoke Casting is making oil pans for the 1.6 liter turbo I4 in the 2026 Jeep Cherokee.
|-
|
| [[w:Indiana Transmission#Indiana Transmission I|Indiana Transmission Plant I]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1998
| 
| [[w:ZF 9HP transmission|948TE 9-speed auto.]] transmission, Gear machining and final assembly of electric drive modules
| Located at 3660 North U.S. Highway 931. RFE transmission production ended in January 2025. More than 8 million RFE transmissions were produced at Indiana Transmission Plant I. Production of the nine-speed transmission began in May 2013. The 9-speed is built under license from [[w:ZF Friedrichshafen|ZF]]. &lt;br&gt; Past transmissions:&lt;br&gt; [[w:Chrysler RFE transmission|Chrysler RFE 4-/5-/6-speed auto. trans.]]
|-
|
| [[w:Kokomo Casting|Kokomo Casting Plant]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1965
| 
| Aluminum parts for automotive components, transmission and transaxle cases; engine block castings
| Located at 1001 East Boulevard. Kokomo Casting is the world’s largest die-cast facility. Plant was expanded in 1969, 1986, 1995 and 1997. Over 18 million four-speed transmission cases were made at Kokomo Casting from 1988 through July 2014. Kokomo Casting started making nine-speed transmission cases in 2013. Kokomo Casting is making engine blocks for the 1.6 liter turbo I4 in the 2026 Jeep Cherokee. Kokomo Casting is making gearbox covers for the electric drive modules made at the Indiana Transmission Plant. 
|-
|
| [[w:Kokomo Engine Plant|Kokomo Engine Plant]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 2022 (as Kokomo Engine)
| 
| [[w:FCA Global Medium Engine|2.0L turbo GME-T4 I4]]
| Located at 3360 North U.S. Highway 931. Plant was previously known as Indiana Transmission Plant II, which built automatic transmissions and transmission components from 2003-2019, when it was idled. Starting in 2020, the plant was converted to engine production. Engine production began in late February 2022. 
|-
|
| [[w:Kokomo Transmission|Kokomo Transmission Plant]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1956
| 
| [[w:ZF 8HP transmission|850RE]] 8-speed auto. transmission,&lt;br&gt; [[w:ZF 8HP transmission|880RE]] 8-speed auto. transmission,&lt;br&gt; Machining of engine block castings and transmission components,&lt;br&gt; Machined components for the &lt;br&gt; 9-speed auto. transmission
| Located at 2401 South Reed Road. On October 9, 2020, Kokomo Transmission built its last 41TE 4-speed auto. transmission, assembling more than 17 million 4-speed auto. transmissions since production began in 1988. Kokomo Transmission began building 6-speed auto. transmissions in 2006. Production of the eight-speed automatic transmission began in September 2012. The 8-speed is built under license from [[w:ZF Friedrichshafen|ZF]]. On August 8, 2023, Kokomo Transmission built its 6 millionth 8-speed transmission. Kokomo Transmission is machining gearbox covers for the electric drive modules made at the Indiana Transmission Plant. &lt;br&gt; Past transmissions: &lt;br&gt;[[w:TorqueFlite|TorqueFlite 3-/4-speed auto. trans.]],&lt;br&gt; [[w:Ultradrive|Ultradrive (TE/AE/LE/RLE/TES/TEA)&lt;br&gt; 4-/6-speed auto. trans.]],&lt;br&gt; [[w:ZF 8HP transmission|845RE]] 8-speed auto. transmission,&lt;br&gt; SI-EVT trans. (eFlite) for Pacifica Hybrid
|-
| 
| [[w:Saltillo Engine Plant#South Engine Plant|Saltillo North Engine Plant]] 
| [[w:Ramos Arizpe|Ramos Arizpe]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 1981
| 
| [[w:Chrysler Hemi engine#Third generation: 2003–present|5.7L/6.4L/6.2L supercharged Hemi V8]], [[w:Stellantis Hurricane engine|Chrysler 3.0L twin-turbo Hurricane GME-T6 I6]]
|  Production began on May 8, 1981. Hemi V8 production began in June 2002 with the 5.7L. Production of the supercharged 6.2L Hellcat Hemi V8 began in the third quarter of 2014. Tigershark I4 production began in the first quarter of 2014. &lt;br&gt; Past engines: [[w:Chrysler 2.2 &amp; 2.5 engine|2.2L, 2.5L &quot;K-car&quot; I4 engine]], [[w:Chrysler 1.8, 2.0 &amp; 2.4 engine|2.0L, 2.4L, 2.4L Turbo I4 &quot;Neon engine&quot;]],&lt;br&gt; [[w:World Gasoline Engine#2.4_2|2.4L Tigershark I4 engine]], [[w:Chrysler Hemi engine#6.1|6.1L Hemi V8]]
|-
| 
| [[w:Saltillo Engine Plant#South Engine Plant|Saltillo South Engine Plant]] 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 2010
| 
| [[w:Chrysler Pentastar engine|Chrysler 3.6L Pentastar V6 engine]]
| Plant opened on October 29, 2010. The plant has produced over 6 million Pentastar V6 engines. &lt;br&gt; Past engines: Chrysler 3.6L Pentastar V6 engine (EH3) for Pacifica Plug-in Hybrid
|-
| 
| Saltillo Stamping Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 1997
| 
| Stampings and assemblies including Body panels
| Part of the Saltillo Truck Assembly Complex.
|-
| G
| Saltillo Truck Assembly Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 1995
| 
| [[w:Ram Heavy Duty (fifth generation)|Ram HD pickup &amp; chassis cab]] (2019-)
|  Production began in 1995. As of 2025, also known as Saltillo Truck Heavy Duty Plant. &lt;br&gt; Past models:&lt;br&gt; [[w:Dodge Ram|Dodge Ram pickup]] (1995-2012),&lt;br&gt; [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 pickup]] (2013-2018),&lt;br&gt; [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 Classic pickup]] (2019-2023),&lt;br&gt; [[w:Ram pickup#Fourth generation (2009; DS)|Ram HD pickup &amp; chassis cab]] (2013-2018), [[w:Sterling Bullet|Sterling Truck Bullet]] (2008-2009)
|-
| 4
| Saltillo Truck Extension Assembly Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 2025
| 
| [[w:Ram 1500 (DT)|Ram 1500]] (DT) (2025-)
| Also known as Saltillo Truck Light Duty Plant. 2 new buildings were constructed for the new light duty plant. Production began in May 2025. Initially, production was for export but production for the domestic Mexican market began in February 2026. The plant also includes a seat assembly line, the first Stellantis plant in North America to integrate this process into its own production chain.
|-
| E
| Saltillo Van Assembly Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 2013
| 
| [[w:Ram ProMaster|Ram ProMaster]] (2014-),&lt;br&gt; [[w:Ram ProMaster#E-Ducato and Ram ProMaster EV (2024)|Ram ProMaster EV]] (2024-)
| Production started in July 2013. &lt;br&gt; Past models: [[w:Fiat Ducato|Fiat Ducato]] (Export to Brazil/Argentina: 2018-2022)
|-
| N
| [[w:Sterling Heights Assembly|Sterling Heights Assembly Plant]] 
| [[w:Sterling Heights, Michigan|Sterling Heights, Michigan]]
| [[w:United States|United States]]
| 1984
| 
| [[w:Ram 1500 (DT)|Ram 1500]] (DT) (2019-)
| Located at 38111 Van Dyke Ave. The plant was originally built by the US Navy as a jet engine plant in 1953. It was called Naval Industrial Reserve Aircraft Plant and was owned by the US Navy. When the jet engine project was cancelled, the plant was transferred to the US Army, which contracted with Chrysler to build missiles at the plant, which was now known as the Michigan Ordinance Missile Plant. Chrysler began production of the PGM-11 Redstone missile at the Sterling Heights plant on September 27, 1954. The final Redstone was built in 1961. Chrysler also built the PGM-19 Jupiter missile at Sterling Heights from 1958-December 1960. Chrysler also built the first stage of the Saturn I rocket at the Sterling Heights plant. Chrysler vacated the Michigan Army Missile Plant at the end of 1969. Meanwhile, LTV Corp. (previously Ling-Temco-Vought) built the MGM-52 Lance missile at the Sterling Heights plant. The Army turned the plant over to the state of Michigan, which was then sold it to Volkswagen in 1980. VW converted the plant to automotive production and intended to make the Jetta there but VW's US sales declined and VW never ended up building anything there. VW then sold the plant to Chrysler in 1983. Chrysler LeBaron GTS and Dodge Lancer production began in September 1984 and ended on April 7, 1989. Shadow and Sundance production began on August 25, 1986 and ended on March 9, 1994. The Dodge Daytona was also moved from St. Louis to Sterling Heights in 1991 and was produced there through February 26, 1993. Chrysler then built a succession of midsize cars at Sterling Heights from June 1994. During Chrysler's bankruptcy in 2009, Sterling Heights Assembly was initially left behind in &quot;old Chrysler&quot; and was supposed to close by December 2010 but during 2010, &quot;new Chrysler&quot; changed its mind and bought the plant from &quot;old Chrysler&quot; for $20 million. The 2011 Chrysler 200 and Dodge Avenger sedans began production on December 6, 2010 followed by the Chrysler 200 Convertible in February 2011. The Chrysler 200 Convertible was also built for export to Europe as the Lancia Flavia from March 2012. The 2nd gen. Chrysler 200 sedan began production on March 14, 2014 and ended on December 2, 2016. The plant was then idled for a lengthy retooling to build body-on-frame pickups and began production of the new generation DT-series Ram 1500 in March 2018. &lt;br&gt; Past models: [[w:Dodge Lancer#1985–1989: Lancer|Dodge Lancer]] (1985-1989), [[w:Chrysler LeBaron#1985–1989 LeBaron GTS|Chrysler LeBaron GTS (H-body)]] (1985-1989), [[w:Plymouth Sundance|Plymouth Sundance]] (1987-1994), [[w:Dodge Shadow|Dodge Shadow]] (1987-1994), [[w:Dodge Daytona|Dodge Daytona]] (1992-1993), [[w:Chrysler Daytona|Chrysler Daytona]] (Canada: 1992-1993), [[w:Chrysler Cirrus|Chrysler Cirrus]] (1995-2000), [[w:Dodge Stratus|Dodge Stratus]] sedan (1995-2006), [[w:Plymouth Breeze|Plymouth Breeze]] (1996-2000), [[w:Chrysler Sebring|Chrysler Sebring]] sedan (2001-2010), [[w:Chrysler Sebring|Chrysler Sebring]]  convertible (2001-2006, 2008-2010), [[w:Dodge Avenger#Dodge Avenger sedan (2008–2014)|Dodge Avenger]] sedan (2008-2014), [[w:Chrysler 200|Chrysler 200]] sedan (2011-2017), [[w:Chrysler 200|Chrysler 200]] convertible (2011-2014), [[w:Chrysler 200#Lancia Flavia|Lancia Flavia]] (For export: 2012-2014)  
|-
| 
| Sterling Stamping Plant
| [[w:Sterling Heights, Michigan|Sterling Heights, Michigan]]
| [[w:United States|United States]]
| 1965
| 
| Stampings and assemblies including hoods, roofs, liftgates, side apertures, fenders, and floorpans
| Located at 35777 Van Dyke Ave. This plant is a separate facility but is located next door to the Sterling Heights Assembly Plant. Sterling Stamping is the largest stamping plant in the world. Sterling Stamping supplies stampings to many Chrysler assembly plants, not only Sterling Heights Assembly. The first stampings were produced in January 1965. 
|-
| W
| [[w:Toledo Complex|Toledo Assembly Complex - Toledo North Assembly Plant]] 
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 2001
| 
| [[w:Jeep Wrangler (JL)|Jeep Wrangler (JL)]] (2018-)
| Located at 4400 Chrysler Drive. Toledo North first built the Jeep Liberty, which began in April 2001. Dodge Nitro production began in August 2006 and ended on December 16, 2011. The 2nd gen. Jeep Liberty began production in July 2007. Jeep Liberty ended production on August 16, 2012. Toledo North then closed for retooling to build the all-new 2014 Cherokee. The Jeep Cherokee began production at Toledo North on June 24, 2013 and ended on April 6, 2017. The Cherokee was then moved to Belvidere Assembly. Toledo North was then retooled to build the Jeep Wrangler, which began on November 15th, 2017. The 4xe plug-in hybrid version of the Wrangler began production in December 2020. &lt;br&gt; Past models: [[w:Jeep Liberty|Jeep Liberty]] (2002-2012), [[w:Dodge Nitro|Dodge Nitro]] (2007-2011),&lt;br&gt; [[w:Jeep Cherokee (KL)|Jeep Cherokee]] (2014-2017),&lt;br&gt; [[w:Jeep Wrangler (JL)|Jeep Wrangler 4xe (JL)]] (2021-2025)
|-
| L
| [[w:Toledo Complex|Toledo Assembly Complex - Toledo Supplier Park Plant]] (South plant)
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 2001
| 
| [[w:Jeep Gladiator (JT)|Jeep Gladiator]] (2020-)
| Located along Stickney Ave. The Toledo Supplier Park Plant is built on the site of the former Stickney Ave. plant that became part of Chrysler in 1987 as part of the acquisition of AMC. That plant was acquired by Kaiser Jeep in 1964 from Autolite and was built in 1942. The Toledo Supplier Park Plant includes body and chassis operations in partnership with Kuka and Hyundai Mobis, respectively. The paint shop was originally run in partnership with Magna but Chrysler took over the paint operation in the first quarter of 2011. The Toledo Supplier Park Plant began Wrangler production in August 2006. Wrangler production ended on April 27, 2018. Gladiator pickup production began in March 2019. &lt;br&gt; Past models:&lt;br&gt; [[w:Jeep Wrangler (JK)|Jeep Wrangler (JK)]] (2007-2017),&lt;br&gt; [[w:Jeep Wrangler (JK)#2018 model year update|Jeep Wrangler JK]] (2018)
|-
| 
| [[w:Toledo Machining|Toledo Machining Plant]] 
| [[w:Perrysburg, Ohio|Perrysburg, Ohio]]
| [[w:United States|United States]]
| 1966
| 
| Steering Columns,&lt;br&gt; Torque Converters for 8-spd. rwd and 9-spd. fwd auto. transmissions
| Located at 8000 Chrysler Drive. Production began in 1966 and the plant was expanded in 1969. &lt;br&gt; Past products: Power Electronics module for Wrangler 4xe PHEV
|-
| T,&lt;br&gt; V (1985 only)
| [[w:Toluca Car Assembly|Toluca Car Assembly]] 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| 1968
| 
| [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass (MP)]] (2017-), [[w:Jeep Wagoneer S|Jeep Wagoneer S EV]]&lt;br&gt; (2024-2025, 2027-),&lt;br&gt; [[w:Jeep Cherokee (KM)|Jeep Cherokee (KM)]] (2026-), [[w:Jeep Recon|Jeep Recon EV]] (2026-)
| Originally part of Fabricas Automex, Chrysler's affiliate in Mexico. In 1968, Fabricas Automex was 45% owned by Chrysler. In December 1971, Chrysler increased its stake to 90.5% and changed the Mexican company's name to Chrysler de Mexico. Chrysler later bought another 8.8% stake, taking its total to 99.3%. Began production on December 9, 1968. An adjacent supplier park was opened in 2007. Journey production began in early 2008. PT Cruiser production ended on July 9, 2010. Fiat 500 production began in December 2010. Journey production ended in December 2020. Jeep Compass production began on January 16, 2017. &lt;br&gt; Past models: &lt;br&gt;  Mexico only: Dodge Dart (rwd), Dodge Dart K, Dodge Dart E, Chrysler Valiant Volaré (rwd), Chrysler Valiant Volaré K, Chrysler Valiant Volaré E, [[w:Dodge Magnum#First generation|Dodge Magnum]] [rwd] (1981-1982), [[w:Dodge Magnum#Second generation|Dodge Magnum 400/Magnum]] [fwd] (1983-1988), [[w:Chrysler Phantom|Chrysler Phantom]], [[w:Chrysler Shadow|Chrysler Shadow]], [[w:Chrysler Spirit|Chrysler Spirit]] &lt;br&gt; Export to US: [[w:Dodge Aries|Dodge Aries]] (1984-1989), [[w:Plymouth Reliant|Plymouth Reliant]] (1984-1989), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron coupe]] (1987-1989, 1992), [[w:Dodge Shadow|Dodge Shadow]] (1988, 1991-1994), [[w:Plymouth Sundance|Plymouth Sundance]] (1988, 1992-1994), [[w:Chrysler LeBaron#Third generation sedan (1990–1994)|Chrysler LeBaron sedan]] (1990-1994), [[w:Dodge Spirit|Dodge Spirit]] (1991-1995), [[w:Plymouth Acclaim|Plymouth Acclaim]] (1991-1995), [[w:Dodge Neon#First generation (1994)|Dodge Neon]] (1995-1999), [[w:Plymouth Neon#First generation (1994)|Plymouth Neon]] (1995-1999), [[w:Chrysler Sebring#Convertible (1996–2000)|Chrysler Sebring Convertible]] (1996-2000), [[w:Chrysler PT Cruiser|Chrysler PT Cruiser]] (2001-10), [[w:Dodge Journey|Dodge Journey]] (2009-2020),&lt;br&gt; [[w:Fiat 500 (2007)|Fiat 500]] (2012-2019), [[w:Fiat 500 (2007)#Fiat 500e (2013)|Fiat 500e]] (2013-2019)&lt;br&gt; Export to Brazil/Europe/Australia:&lt;br&gt; [[w:Fiat Freemont|Fiat Freemont]] (2011-2016)
|-
| 
| Toluca Stamping Plant 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| 1994
| 
| Stampings and assemblies including Body panels
| Part of the Toluca Assembly Complex.
|-
| 
| [[w:Trenton Engine Complex|Trenton Engine South Plant]] 
| [[w:Trenton, Michigan|Trenton, Michigan]]
| [[w:United States|United States]]
| 2010
| 
| [[w:Chrysler Pentastar engine|Chrysler Pentastar V6 engine]]
| Located at 2300 Van Horn Road. Production began in March 2010 with the 3.6L Pentastar V6. In 2022, Trenton South was upgraded with a flexible engine line that could build both the Classic and Upgrade versions of the 3.6L Pentastar V6. By the end of 2022, Pentastar Upgrade engine production moved from Trenton North to Trenton South and the older North plant ended production.
|-
| 
| Warren Stamping Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1949
| 
| Stampings and assemblies including roofs, tailgates, side apertures, fenders, and floorpans
| Located at 22800 Mound Road. This plant is a separate facility but is located next door to the Warren Truck Assembly Plant. The plant was expanded in 1952, 1964, 1965, and 1986. Warren Stamping supplies stampings to many Chrysler assembly plants, not only Warren Truck Assembly.
|-
| S (1970-), 1 (1967-1969),&lt;br&gt; 2 (For A-series)
| Warren Truck Assembly Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1938
| 
| [[w:Jeep Wagoneer (WS)|Jeep Grand Wagoneer]] (2022-), [[w:Jeep Wagoneer (WS)|Jeep Grand Wagoneer L]] (2023-)
| Located at 21500 Mound Road. Formerly known as the Dodge City Truck Plant. Also referred to as Warren Truck #1 in the 1970's when there were 2 other truck plants nearby. Began production in October 1938. The Mitsubishi Raider began production in September 2005 and ended on June 11, 2009. Dodge Dakota production ended on August 23, 2011. Full-size Jeep SUV production began in 2021. Ram 1500 Classic production ended in October 2024, ending production of Dodge/Ram trucks at Warren after 86 years. &lt;br&gt; Past models:&lt;br&gt; [[w:Dodge T-, V-, W-Series|Dodge T-, V-, W-Series]] (1939-1947), Dodge military trucks, [[w:Dodge Power Wagon#Civilian 1-ton Power Wagon &quot;Military-Type&quot;, Flat Fender Style&quot; (1945-1978)|Dodge Power Wagon]] (1946-1968), [[w:Dodge B series#Pickup truck|Dodge B series]] (1948-1953),&lt;br&gt; [[w:Dodge C series|Dodge C series]] (1954-1960),&lt;br&gt; [[w:Dodge Town Panel and Town Wagon|Dodge Town Panel/Town Wagon]] (1954-66), [[w:Dodge D series|Dodge D/W series]] (1961-1980), [[w:Dodge Ram|Dodge Ram pickup]] (1981-2012), [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 pickup]] (2013-2018), [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 Classic pickup]] (2019-24), [[w:Dodge Ramcharger|Dodge Ramcharger]] (1977-1978, 1981-1985), [[w:Plymouth Trailduster|Plymouth Trailduster]] (1977-1978, 1981), [[w:Dodge M-series chassis|Dodge M-series chassis]] (1968-1979),&lt;br&gt; [[w:Dodge A100|Dodge A100/A108]] (1964-1970),&lt;br&gt; [[w:Dodge Dakota|Dodge Dakota]] (1987-2011),&lt;br&gt; [[w:Mitsubishi Raider|Mitsubishi Raider]] (2006-2009),&lt;br&gt; [[w:Jeep Wagoneer (WS)|Jeep Wagoneer]] (2022-2025),&lt;br&gt; [[w:Jeep Wagoneer (WS)|Jeep Wagoneer L]] (2023-2025),&lt;br&gt; [[w:Fargo Trucks|Fargo Trucks]] (For export)
|-
| R (1968-),&lt;br&gt; 9 (1959-1967)
| [[w:Windsor Assembly|Windsor Assembly]] 
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1929
| 
| [[w:Chrysler Pacifica (minivan)|Chrysler Pacifica (minivan)]] (2017-), [[w:Chrysler Voyager#Sixth generation (2020–present)|Chrysler Voyager]] (2020-2026), Chrysler Grand Caravan (Canada: 2021-),&lt;br&gt; [[w:Dodge Charger (2024)|Dodge Charger]] (2024-)
| Located at 2199 Chrysler Centre. Today's Windsor Assembly Plant was originally Windsor Plant 3 or Windsor Car Assembly Plant. Before the 1965 US-Canada Auto Pact, Windsor Assembly made most of the cars sold by Chrysler Canada, including some unique-to-Canada variations. On June 10, 1983, Windsor ended rwd car production and was converted to build fwd minivans. Windsor began building minivans on October 7, 1983. For the first 2 generations of Chrysler minivans, Windsor only built the SWB models. For the 3rd generation, Windsor built both SWB and LWB models. For the 4th generation, Windsor only built LWB models. The minivan-based Pacifica SUV began production in January 2003 and  ended production on November 23, 2007. Production of the VW Routan began in August 2008. Production of the Ram C/V began on August 31, 2011, and ended in early 2015. Pacifica minivan production began on February 29, 2016 followed by the PHEV version on December 1, 2016. Town &amp; Country production ended on March 21, 2016 while Dodge Grand Caravan production ended on August 21, 2020. Production of the electric Charger Daytona began in December 2024 followed by the gas-powered Charger Sixpack in December 2025. &lt;br&gt; Past models: [[w:Chrysler Imperial|Chrysler Imperial]] (1929-1937) [https://www.web.imperialclub.info/registry/vin_decode.htm#1931-54], [[w:Dodge Kingsway|Dodge Kingsway]] (Canada: 1940-41, 1951-52), [[w:Dodge Regent|Dodge Regent]] (Canada: 1951-1959), [[w:Dodge Crusader|Dodge Crusader]] (Canada: 1951-1958), [[w:Dodge Mayfair|Dodge Mayfair]] (Canada: 1953-1959), [[w:Dodge Viscount|Dodge Viscount]] (Canada: 1959), [[w:Dodge Custom Royal|Dodge Custom Royal]] (1959), [[w:Dodge Dart|Dodge Dart (full-size)]] (1961), [[w:DeSoto Firedome|DeSoto Firedome]] (1959), [[w:Chrysler Windsor|Chrysler Windsor]] (1957-1966), [[w:Chrysler Saratoga|Chrysler Saratoga]] (1959-1963), [[w:Chrysler 300 non-letter series|Chrysler Saratoga 300]] (1964-1965), [[w:Chrysler Newport#1961–1964|Chrysler Newport]] (1961-1963), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1963-64, 1966), [[w:Plymouth Savoy|Plymouth Savoy]] (1959-1964), [[w:Plymouth Fury|Plymouth Fury]] (1959-1970), [[w:Dodge Polara|Dodge Polara]] (1960, 1964-1969), Dodge 220 (Canada: 1963), [[w:Dodge 330|Dodge 330]] (1963-1965), [[w:Dodge 440|Dodge 440]] (1963-1964), [[w:Dodge Monaco|Dodge Monaco]] (1967-1968), [[w:Plymouth Valiant#Canada (1960–1966)|Valiant]] (Canada: 1960-1966), [[w:Plymouth Barracuda#First generation (1964–1966)|Valiant Barracuda]] (Canada: 1964-1965), [[w:Plymouth Valiant|Plymouth Valiant]] (1970-1974), [[w:Plymouth Duster|Plymouth Duster]] (1970), [[w:Dodge Dart|Dodge Dart (compact)]] (1966, 1970-1975), [[w:Plymouth Satellite#Third generation (1971–1974)|Plymouth Satellite]] (1972-1974),  [[w:Plymouth GTX|Plymouth GTX]] (1971), [[w:Plymouth Road Runner#Second generation (1971–1974)|Plymouth Road Runner]] (1971-1974), [[w:Dodge Charger (1966)#Fourth generation|Dodge Charger]] (1975-1978), [[w:Dodge Magnum#US and Canada (1978–1979)|Dodge Magnum]] (1978-1979), [[w:Chrysler Cordoba|Chrysler Cordoba]] (1975-1983), [[w:Dodge Mirada|Dodge Mirada]] (1980-1983), [[w:Imperial (automobile)#Sixth generation (1981–1983)|Imperial]] (1981-1983), [[w:Chrysler Newport#1979–1981|Chrysler Newport]] (1979), [[w:Dodge Diplomat|Dodge Diplomat]] (1981-1983), [[w:Plymouth Gran Fury#1982–1989|Plymouth Gran Fury]] (1982-83), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle]] (Canada: 1981-1982), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle Salon]] (Canada: 1983), [[w:Chrysler LeBaron#First generation (1977–1981)|Chrysler LeBaron]] (1981), [[w:Chrysler New Yorker#1982|Chrysler New Yorker]] (1982), [[w:Chrysler Fifth Avenue#1982–1989: The M-body years|Chrysler New Yorker Fifth Avenue]] (1983), [[w:Plymouth Voyager|Plymouth Voyager]] (1984-'00), [[w:Plymouth Voyager|Plymouth Grand Voyager]] (1996-2000), [[w:Dodge Caravan|Dodge Caravan]] (1984-2000), [[w:Dodge Caravan|Dodge Grand Caravan]] (1996-2020), [[w:Chrysler Town &amp; Country (minivan)|Chrysler Town &amp; Country]] (2001-2016), [[w:Chrysler Voyager|Chrysler Voyager]] (2000), [[w:Chrysler Voyager|Chrysler Grand Voyager]] (2000), [[w:Chrysler minivans (S)#Cargo van|Dodge Mini Ram Van]] (1984-1988), [[w:Chrysler minivans (RT)#2011 revision|Ram C/V]] (2012-2015), [[w:Volkswagen Routan|Volkswagen Routan]] (2009-14), [[w:Chrysler Voyager#Lancia Voyager|Lancia Voyager]] (For export: 2012-2015), [[w:Chrysler Pacifica (crossover)|Chrysler Pacifica (SUV)]] (2004-2008)
|-
| 
| CpK Interior Products, Inc. - Belleville Operations
| [[w:Belleville, Ontario|Belleville]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 2010 (became part of Chrysler)
| 
| Components for Automotive Interiors
| Located at 134 River Rd. Formed in 2010 as a subsidiary of Chrysler through the buyout of 3 Collins and Aikman plants in Canada after  Collins and Aikman went bankrupt.
|-
| 
| CpK Interior Products, Inc. - Guelph Operations
| [[w:Guelph|Guelph]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 2010 (became part of Chrysler)
| 
| Components for Automotive Interiors
| Located at 500 Laird Rd. Formed in 2010 as a subsidiary of Chrysler through the buyout of 3 Collins and Aikman plants in Canada after  Collins and Aikman went bankrupt.
|-
| 
| CpK Interior Products, Inc. -&lt;br&gt; Port Hope Operations
| [[w:Port Hope, Ontario|Port Hope]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 2010 (became part of Chrysler)
| 
| Components for Automotive Interiors
| Located at 128 Peter St. Formed in 2010 as a subsidiary of Chrysler through the buyout of 3 Collins and Aikman plants in Canada after  Collins and Aikman went bankrupt.
|-
| 4
| Arab American Vehicles Company (AAV)
| [[w:Cairo|Cairo]]
| [[w:Egypt|Egypt]]
| 1978 (production began) &lt;br&gt; 1987 (became part of Chrysler)
| 
| [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee L]] (2025-), [[w:Citroën C4#Third generation (C41; 2020)|Citroën C4X]] (2025-)
| Arab American Vehicles Company is a joint venture between the [[w:Arab Organization for Industrialization|Arab Organization for Industrialization]], which holds 51%, and Stellantis, which holds the other 49%. AAV was originally established in 1977 as a joint venture  with [[w:American Motors Corporation|AMC]] to produce Jeeps. Production began in 1978. It became part of Chrysler when Chrysler bought AMC in 1987. It continued to be a part of subsequent corporate entities DaimlerChrysler, Chrysler LLC, Chrysler Group LLC, [[w:Fiat Chrysler Automobiles|FCA]], and [[w:Stellantis|Stellantis]]. Production of the Jeep J8, a light military vehicle based on the JK Wrangler, began on November 13, 2008. Jeep Grand Cherokee L production began in September 2024. Citroen C4X production began in April 2025. AAV has also produced vehicles for other automakers including Toyota. Toyota Fortuner SUV production began in April 2012. &lt;br&gt; Past models: Jeep CJ6, Jeep Wagoneer (SJ), Jeep AM720 military vehicle, [[w:Jeep Wrangler (YJ)|Jeep Wrangler (YJ)]], [[w:Jeep Wrangler (TJ)|Jeep TJL]], [[w:Jeep Wrangler (JK)#Military Jeep J8 (2007–present)|Jeep J8]] (2008-2019),  [[w:Jeep Cherokee (XJ)|Jeep Cherokee (XJ)]], [[w:Jeep Liberty (KJ)|Jeep Cherokee (KJ)]], [[w:Jeep Liberty (KK)|Jeep Cherokee (KK)]], [[w:Jeep Grand Cherokee (WK2)|Jeep Grand Cherokee (WK2)]]
|}

==Current non-Chrysler FCA/Stellantis Factories Making Chrysler Group Vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Current Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| Y (700),&lt;br&gt; 9 (ProMaster Rapid),&lt;br&gt; 3 (Vision)
| Betim Plant
| [[w:Betim|Betim]], [[w:Minas Gerais|Minas Gerais]]
| [[w:Brazil|Brazil]]
| 1973
| 
| [[w:RAM 700|RAM 700]] (2015-),&lt;br&gt; [[w:ProMaster Rapid|Ram V700 Rapid]] (Peru)&lt;br&gt; Related models:&lt;br&gt; [[w:Fiat Strada|Fiat Strada]] ('99-),&lt;br&gt; [[w:Fiat Fiorino#Latin America (2013–present)|Fiat Fiorino]] ('14-)
| Fiat plant. &lt;br&gt; Past Chrysler Group models:&lt;br&gt; [[w:Dodge Vision|Dodge Vision]] (Mexico: 2015-2018),&lt;br&gt; [[w:ProMaster Rapid|Ram ProMaster Rapid]] (Mexico: '18-'24)
|-
| U
| Cordoba Plant
| [[w:Córdoba, Argentina|Córdoba]], [[w:Córdoba Province, Argentina|Córdoba Province]]
| [[w:Argentina|Argentina]]
| 1995
| 
| [[w:Peugeot Landtrek|Ram Dakota]] (2026-)
| Fiat plant.
|-
| F
| [[w:FCA India Automobiles|FCA India Automobiles Private Limited]]
| [[w:Ranjangaon|Ranjangaon]], [[w:Pune district|Pune district]], [[w:Maharashtra|Maharashtra]]
| [[w:India|India]]
| 1997
| 
| [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass]],&lt;br&gt; [[w:Jeep Wrangler (JL)|Jeep Wrangler (JL)]],&lt;br&gt; [[w:Jeep Meridian|Jeep Meridian/Commander]],&lt;br&gt; [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee]]
| Originally established as a 50/50 joint venture between Fiat and [[w:Tata Motors|Tata Motors]] called Fiat India Automobiles Private Limited. On June 1, 2017, Jeep Compass production began in India, the first Jeep built in India under its own brand. The JL-series Wrangler began to be assembled in India in 2021. The Jeep Meridian began production in May 2022. The Meridian is also exported to Japan as the Commander. The Jeep Grand Cherokee began assembly in India in November 2022. 
|-
| K
| Goiana Plant
| [[w:Goiana|Goiana]], [[w:Pernambuco|Pernambuco]]
| [[w:Brazil|Brazil]]
| 2015
|
| [[w:Jeep Renegade|Jeep Renegade]], [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass]],&lt;br&gt; [[w:Jeep Commander (2022)|Jeep Commander]], [[w:Ram Rampage|Ram Rampage]]&lt;br&gt; Related models: [[w:Fiat Toro|Fiat Toro]]
| [[w:Fiat Chrysler Automobiles|FCA]] plant. Production at Goiana began with the Jeep Renegade in February 2015. &lt;br&gt; Past Chrysler Group models: [[w:Ram 1000|Ram 1000]]
|-
| P
| Melfi Plant (formerly SATA = Società Automobilistica Tecnologie Avanzate [Advanced Technologies Automotive Company])
| [[w:Melfi|Melfi]], [[w:Province of Potenza|Province of Potenza]]
| [[w:Italy|Italy]]
| 1993
|
| [[w:Jeep Compass#Third generation (J4U; 2025)|Jeep Compass (J4U)]]&lt;br&gt; (Europe: '26-)
| Fiat plant. Jeep production began at Melfi in 2014 with the Renegade. Renegade production at Melfi ended on October 17, 2025. Production of the 3rd gen. Compass began on October 29, 2025. &lt;br&gt; Past Chrysler Group models:&lt;br&gt; [[w:Jeep Renegade|Jeep Renegade]] (US/Can.: '15-'23, Europe: '15-'25),&lt;br&gt; [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass (MP)]] (Europe: '20-'25) &lt;br&gt; Related models:&lt;br&gt; [[w:Fiat 500X|Fiat 500X]] (US/Can.: '16-'23,&lt;br&gt; Europe: '15-'24)
|-
| B
| Porto Real Plant
| [[w:Porto Real|Porto Real]], [[w:Rio de Janeiro (state)|Rio de Janeiro state]]
| [[w:Brazil|Brazil]]
| 2000
|
| [[w:Jeep Avenger|Jeep Avenger]]
| PSA plant. The Jeep Avenger is the first Jeep to be made in a former PSA plant. 
|-
| U (2027-), 6 (2015-2022)
| [[w:Tofaş|Tofaş]]
| [[w:Bursa|Bursa]]
| [[w:Turkey|Turkey]]
| 1971
|
| [[w:Citroën Jumpy#Ram ProMaster City|Ram ProMaster City]] (2027-)
| Originally a Fiat joint venture, it is now 37.8% owned by Stellantis, 37.8% owned by [[w:Koç Holding|Koç Holding]], and 24.3% publicly traded on the Istanbul Stock Exchange. &lt;br&gt; Past Chrysler Group models: &lt;br&gt; [[w:Fiat Doblò#Ram ProMaster City|Ram ProMaster City]] (2015-2022),&lt;br&gt; [[w:Chrysler Neon#Third generation (2016)|Dodge Neon]]&lt;br&gt; (Mexico &amp; Middle East: 2017-2020),&lt;br&gt; [[w:Fiat Fiorino#Europe (2007–2024)|Ram V700 City]] (Chile: 2018-2023)
|-
| J,&lt;br&gt; 5 (Ypsilon)
| Tychy Plant
| [[w:Tychy|Tychy]], [[w:Silesian Voivodeship|Silesian Voivodeship]]
| [[w:Poland|Poland]]
| 1975
|
| [[w:Jeep Avenger|Jeep Avenger]]
| Fiat plant. Production began in September 1975 when the plant was owned by Polish automaker [[w:Fabryka Samochodów Małolitrażowych|FSM]], which built Fiat-based models. Fiat took over FSM in 1992. Fiat subsequently became [[w:Fiat Chrysler Automobiles|FCA]] and then Stellantis. Jeep Avenger production began on January 31, 2023. &lt;br&gt; Past Chrysler Group models:&lt;br&gt; [[w:Chrysler Ypsilon|Chrysler Ypsilon]] (UK/Ireland/Japan)
|}

==Current partner factories making Chrysler Group vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Current Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 1
| GAC Hangzhou plant
| [[w:Hangzhou|Hangzhou]], [[w:Zhejiang|Zhejiang]]
| [[w:China|China]]
| 2021 (production began for Chrysler)
|
| [[w:Trumpchi GS5#Dodge Journey|Dodge Journey]] (Mexico: 2022-)
| [[w:GAC Group|GAC]] plant. 
|-
| 3
| GAC Yichang plant
| [[w:Yichang|Yichang]], [[w:Hubei|Hubei]]
| [[w:China|China]]
| 2024 (production began for Chrysler)
|
| [[w:Dodge Attitude#Fourth generation (2025)|Dodge Attitude]] (Mexico: 2025-)
| [[w:GAC Group|GAC]] plant. 
|-
| 5
| Shenzhen Baoneng Motor Co., Ltd.
| [[w:Shenzhen|Shenzhen]], [[w:Guangdong|Guangdong]]
| [[w:China|China]]
| 2024 (production began for Chrysler)
|
| [[w:Peugeot Landtrek|Ram 1200]] (Mexico: 2025-)
| [[w:Baoneng Group#Automotive business|Shenzhen Baoneng Motor Co., Ltd.]] plant. 
|}

==Former factories== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Closed
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
|
| Ajax Trim plant
| [[w:Ajax, Ontario|Ajax]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1953, 1964 (became part of Chrysler)
| 2003
| Automotive Soft Trim Components, Seat Cushion and Seatback Covers, Foam-in-place Covers
| Built in 1953 by Canadian Automotive Trim. Purchased by Chrysler in 1964. Closed by December 2003.
|-
| J (1989-1992),&lt;br&gt; B (1981-1988),&lt;br&gt; 7-8 (1966-1980),&lt;br&gt; T (1958-1966) 
| [[w:Brampton Assembly (AMC)|AMC Brampton Assembly]]
| [[w:Brampton|Brampton]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]] 
| 1961,&lt;br&gt; 1987 (became part of Chrysler)
| 1992
| [[w:Jeep Wrangler (YJ)|Jeep Wrangler (YJ)]] (1987-92), [[w:Jeep CJ#CJ-5|Jeep CJ-5]] (1979-1980),&lt;br&gt; [[w:Jeep CJ#CJ-7|Jeep CJ-7]] (1979-1980),&lt;br&gt; [[w:AMC Eagle|AMC Eagle]] (1981-1987), [[w:AMC Eagle|Eagle Wagon]] (1988), [[w:AMC Concord|AMC Concord]] (1978, 1981-1983), [[w:AMC Spirit|AMC Spirit]] (1983), [[w:AMC Hornet|AMC Hornet]] (1970-77), [[w:AMC Gremlin|AMC Gremlin]] (1970-1978),&lt;br&gt; [[w:AMC Rebel|AMC Rebel]] (1968-1970), [[w:Rambler Rebel#Fifth generation|Rambler Rebel]] (1967), [[w:Rambler Classic|Rambler Classic]] (1961-1966),&lt;br&gt; [[w:AMC Ambassador|AMC Ambassador]] (1966-1968), [[w:AMC Ambassador|Rambler Ambassador]] ('63-'65), [[w:Rambler American|Rambler American]] (1962-68), [[w:Rambler American|AMC Rambler]] (1969)
| [[w:American Motors Corporation|AMC]] plant. Became part of Chrysler in the 1987 buyout of AMC. Located at at the corner of Kennedy Road South and Steeles Avenue East. Production began on January 26, 1961 with the Rambler Classic. This was the last plant to produce AMC vehicles. Eagle Wagon (formerly AMC Eagle) ended production on December 11, 1987. Production ended in April 1992 and Jeep Wrangler production was moved to Toledo, OH. Buildings on the west side of the plant were demolished in 2005 and buildings on the east side were demolished in 2007. A Lowe's and a Wal-Mart now occupy some of the former plant site.
|-
| 7
| [[w:Beijing Jeep|Beijing Jeep]]/&lt;br&gt;Beijing Benz-DaimlerChrysler Automotive Co Ltd.
| [[w:Beijing|Beijing]]
| [[w:China|China]]
| 1985 (prod. began),&lt;br&gt; 1987 (became part of Chrysler)
| 2009 (Non-Mercedes prod. ended)
| [[w:Jeep Cherokee (XJ)|Jeep BJ2021/BJ7250/2500/2700 (XJ)]], [[w:Jeep Grand Cherokee (WJ)|Jeep 4000/4700 (WJ)]], [[w:Chrysler 300#First generation (2005)|Chrysler 300]],&lt;br&gt; [[w:Chrysler Sebring#Third generation (JS; 2007)|Chrysler Sebring sedan]]&lt;br&gt;Other models built:&lt;br&gt; [[w:Mitsubishi Pajero Sport#First generation (K80/K90/PA/PA II; 1996)|Mitsubishi Pajero Sport]], [[w:Mitsubishi Outlander#First generation (CU/ZE/ZF; 2001)|Mitsubishi Outlander]],&lt;br&gt; [[w:Mercedes-Benz E-Class (W211)|Mercedes-Benz E-Class (W211)]], [[w:Mercedes-Benz C-Class (W204)|Mercedes-Benz C-Class (W204)]]
| Originally established on May 5, 1983 as a 50/50 joint venture between [[w:American Motors Corporation|AMC]] and [[w:BAIC Group|BAIC]] called Beijing Jeep Corp. Production began on Sept. 26, 1985. In 1987, Chrysler Corp. took over AMC and its 50% stake in Beijing Jeep. Mitsubishi SUVs were added to Beijing Jeep's production in 2003 with the Pajero Sport, followed by the Outlander in 2004. In 2004, Beijing Jeep was renamed Beijing Benz-DaimlerChrysler Automotive Co Ltd., following the creation of DaimlerChrysler in 1998. Mercedes-Benz production began in 2005. Chrysler brand sedan production began in 2006 with the 300, followed by the Sebring in 2007. After DaimlerChrysler broke up in 2007, production for the Chrysler Group ended in 2009. The joint venture company was then renamed Beijing Benz in 2010 and Chrysler was removed from the venture which Daimler kept for itself to produce Mercedes-Benz models.
|-
| 3
| Campo Largo Assembly
| [[w:Campo Largo, Paraná|Campo Largo]], [[w:Paraná (state)|Paraná (state)]]
| [[w:Brazil|Brazil]]
| 1998
| 2001
| [[w:Dodge Dakota#Second generation (1997–2004)|Dodge Dakota]]
| Plant built vehicles in cooperation with suppliers.
|-
| V
| [[w:Conner Avenue Assembly|Conner Avenue Assembly]] 
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1996
| 2017
| [[w:Dodge Viper|Dodge Viper]] &lt;br&gt; GTS: '96, &lt;br&gt; All models: &lt;br&gt; '97-'06, '08-'10, '13-'17, [[w:Plymouth Prowler|Plymouth Prowler]]&lt;br&gt; ('97, '99-'01),&lt;br&gt; [[w:Chrysler Prowler|Chrysler Prowler]] ('01-'02),&lt;br&gt; [[w:Viper engine|8.0L/8.3L/8.4L aluminum &lt;br&gt; Viper V10 engine]] &lt;br&gt;(5/01-2017)
| Actually located at 20000 Connor Street. The plant was originally built in 1966 to make spark plugs by Champion. After Champion was bought by Cooper Industries in 1990, the plant was closed. It remained empty until Chrysler bought it in 1995. Viper production was moved to the Connor Avenue plant from the New Mack plant beginning with the GTS coupe for 1996, followed by the RT/10 roadster for 1997. Prowler production began in May 1997 and ended on February 15, 2002. Production of the Viper's aluminum V10 engine was moved to Connor Avenue, where it was built alongside the Viper itself, in May 2001 from the Mound Road Engine Plant, which closed in 2002. Viper production ended on July 2, 2010 and the plant was dormant until production restarted in December 2012. Production ended on Aug. 31, 2017. In 2018, the plant was renamed Connor Center, a meeting and display space that will showcase Chrysler’s concept and historic vehicle collection.
|-
| 2
| Cordoba Assembly
| [[w:Córdoba, Argentina|Córdoba]], [[w:Córdoba Province, Argentina|Córdoba Province]]
| [[w:Argentina|Argentina]]
| 1997
| 2001
| [[w:Jeep Grand Cherokee (ZJ)|Jeep Grand Cherokee (ZJ)]] (1997-1998), [[w:Jeep Grand Cherokee (WJ)|Jeep Grand Cherokee (WJ)]] (1999-2001), [[w:Jeep Cherokee (XJ)|Jeep Cherokee (XJ)]] (1998-01)
| Opened in the 2nd quarter of 1997, building the Jeep Grand Cherokee. Jeep Cherokee production was added in 1998. 
|-
|E
| [[w:Diamond-Star Motors|Diamond-Star Motors/Mitsubishi Motors Manufacturing America/Mitsubishi Motors North America Manufacturing Division]]
| [[w:Normal, Illinois|Normal, Illinois]]
| [[w:United States|United States]]
| 1988
| 2005 (end of Chrysler production)/&lt;br&gt; 2015 (end of Mitsubishi production)
| [[w:Plymouth Laser|Plymouth Laser]] (1990-1994),&lt;br&gt; [[w:Eagle Talon|Eagle Talon]] (1990-1998),&lt;br&gt; [[w:Eagle Summit#First generation (1989–1992)|Eagle Summit 4-d]] (1991-1992),&lt;br&gt; [[w:Dodge Avenger#Dodge Avenger Coupe (1995–2000)|Dodge Avenger]] (1995-2000),&lt;br&gt; [[w:Dodge Stratus#Stratus coupe (2001–2005)|Dodge Stratus Coupe]]&lt;br&gt; (2001-2005),&lt;br&gt; [[w:Chrysler Sebring|Chrysler Sebring Coupe]]&lt;br&gt; (1995-2005),&lt;br&gt;  [[w:Mitsubishi Eclipse|Mitsubishi Eclipse]] (1990-2012),&lt;br&gt; [[w:Mitsubishi Mirage#Third generation (1987)|Mirage sedan]] (1991-1992),&lt;br&gt; [[w:Mitsubishi Galant|Galant]] (1994-2012),&lt;br&gt; [[w:Mitsubishi Endeavor|Endeavor]] (2004-2011),&lt;br&gt; [[w:Mitsubishi ASX#First generation (GA; 2010)|Outlander Sport/RVR]] (2013-15)
| Originally established as Diamond-Star Motors, a 50/50 joint venture between Chrysler and Mitsubishi which assembled both Chrysler and Mitsubishi vehicles. Production began in September 1988. In October 1991, Chrysler sold its 50% stake in the plant to Mitsubishi but production for Chrysler continued under contract. On May 24, 1993, production of the Mitsubishi Galant began at the Diamond-Star plant. In July 1995, the plant was renamed Mitsubishi Motors Manufacturing America. In January 2002, the plant was renamed Mitsubishi Motors North America Manufacturing Division. In January 2003, production of the Mitsubishi Endeavor began, the first SUV built at the Mitsubishi plant. In February 2005, production of vehicles for Chrysler ended. All further production was only of Mitsubishi-branded vehicles. In mid-2012, the plant began producing the Mitsubishi Outlander Sport. The Outlander Sport is sold as the RVR in Canada. On November 30, 2015, vehicle production ended. The Mitsubishi plant produced 3,283,549 vehicles. The plant continued to produce replacement parts until May 2016, when the plant closed completely. In June 2016, the plant was sold to liquidation firm Maynards Industries. In January 2017, EV startup [[w:Rivian|Rivian Automotive]] bought the former Mitsubishi plant. Rivian began production at the Normal, IL plant in September 2021 with the [[w:Rivian R1T|R1T]] electric pickup.
|-
| U
| [[w:Eurostar Automobilwerk|Eurostar]] - Chrysler Graz Assembly
| [[w:Graz|Graz]], [[w:Styria|Styria]]
| [[w:Austria|Austria]]
| 1991
| 2002
| [[w:Chrysler Voyager#Fourth generation (2001–2007)|Chrysler Voyager/Grand Voyager]] (1992-2002), [[w:Chrysler PT Cruiser|Chrysler PT Cruiser]] (2002)
| Originally, a 50/50 joint venture between Chrysler and Steyr-Daimler-Puch founded in 1990. The Eurostar plant is next to the Steyr Fahrzeugtechnik plant solely owned by Steyr-Daimler-Puch. Production of the Chrysler Voyager and Grand Voyager minivans began in October 1991. This was the 2nd generation Chrysler minivan. The 3rd generation began production on September 25, 1995. In 1996, production of right-hand drive minivans began. The 4th generation began production in January 2001. Production of the PT Cruiser began in July 2001 on the same line as the Voyager minivans. In 1999, DaimlerChrysler bought the 50% stake in Eurostar held by Steyr-Daimler-Puch Fahrzeugtechnik, now majority owned by Magna International, making Eurostar a subsidiary of DaimlerChrysler. DaimlerChrysler sold 100% of Eurostar to Magna Steyr in July 2002. PT Cruiser production in Austria ended and was consolidated in Toluca, Mexico. Production of the Chrysler Voyager and Grand Voyager minivans moved next door to the main Magna Steyr plant for 2003. Magna International had acquired a majority holding of 66.8% in Steyr-Daimler-Puch in 1998 and acquired the rest by 2002 when it was renamed Magna Steyr. 
|-
| 3 (1959),&lt;br&gt; E (1958)
| Evansville Assembly
| [[w:Evansville, Indiana|Evansville, Indiana]]
| [[w:United States|United States]]
| 1919, 1928 (became part of Chrysler)
| 1959 
| Graham Brothers trucks (through 1932),&lt;br&gt; Dodge Brothers trucks &lt;br&gt; (through 1932),&lt;br&gt; Plymouth cars (1936-1958),&lt;br&gt; Dodge cars (1937-1938),&lt;br&gt; [[w:Plymouth Savoy|Plymouth Savoy]] (1959), [[w:Plymouth Belvedere|Plymouth Belvedere]] (1959), [[w:Plymouth Fury|Plymouth Fury]] (1959)
| Located at 1625 N. Garvin St. Built in 1919 by Graham Brothers Truck Company to build trucks. In 1925, Dodge Brothers bought a controlling 51% stake in Graham Brothers and then bought the rest in 1926, completely merging the 2 companies. This gave Dodge Brothers plants in Evansville, IN and Stockton, CA. Dodge Brothers was bought by the Chrysler Corporation on July 31, 1928. At that point, trucks with a Dodge Brothers nameplate were rated as a half-ton; larger rated trucks were sold under the Graham Brothers name. On January 1, 1929, the Graham Brothers brand was eliminated, and all trucks produced became Dodge trucks. In 1932, Chrysler closed the Evansville plant due to the Great Depression. In 1935, as the economy improved, Chrysler reopened the Evansville plant and renovated and expanded it. It began building Plymouth cars for 1936. Dodge cars were also built for 1937 and 1938. During World War II, the plant became the Evansville Ordinance Plant, which produced more than 3.26 billion ammunition  cartridges - about 96% of all the .45 automatic ammunition produced for all the armed forces. The Evansville Ordinance Plant also rebuilt 1,600 Sherman tanks and 4,000 military trucks. After the war ended, Plymouth car production resumed. However, in the early 1950s, during the Korean War, the Evansville plant retooled and dedicated about a third of its space and manpower to building 60-foot aluminum hulls for Grumman  UF-1 Albatross air-sea rescue planes for the Navy and Coast Guard. Evansville built its 1 millionth Plymouth in March 1953. The plant was closed in 1959 and was replaced by the larger, more modern St. Louis plant in Fenton, MO, which had access to more railroad lines for shipping than Evansville did. 
|-
| 
| Evansville Stamping
| [[w:Evansville, Indiana|Evansville, Indiana]]
| [[w:United States|United States]]
| 1935, 1953 (became part of Chrysler)
| 1959 
| Body panel stampings
| Opened by Briggs Manufacturing Company when Chrysler reopened Evansville Assembly in 1935 to build Plymouth cars. One of the plants Chrysler acquired from Briggs Manufacturing in 1953. Made body panels for the nearby Evansville Assembly plant. Closed when Evansville Assembly closed in 1959.
|-
| A
| [[w:GAC Fiat Chrysler|GAC Fiat Chrysler]]: Changsha plant
| [[w:Changsha|Changsha]], [[w:Hunan|Hunan province]]
| [[w:China|China]]
| 2012 (Fiat prod. began),&lt;br&gt; 2015 (prod. began for Chrysler)
| 2022
| [[w:Jeep Cherokee (KL)|Jeep Cherokee (K4)]],&lt;br&gt; [[w:Jeep Grand Commander|Jeep Grand Commander/&lt;br&gt;Commander (K8)]]&lt;br&gt;Other models built:&lt;br&gt; [[w:Fiat Viaggio|Fiat Viaggio]], [[w:Fiat Ottimo|Fiat Ottimo]]
| Originally established in 2010 as a 50/50 joint venture between [[w:Fiat S.p.A.|Fiat]] and [[w:GAC Group|GAC]] called GAC Fiat Automobiles Co., Ltd. Fiat production began with the Viaggio sedan in 2012, followed by the Ottimo hatchback in 2014. In January 2015, GAC Fiat was renamed GAC Fiat Chrysler Automobiles Co., Ltd. to reflect the creation of [[w:Fiat Chrysler Automobiles|Fiat Chrysler Automobiles]] in 2014 and the inclusion of Chrysler in the joint venture, which would now also produce Jeeps. In October 2015, Jeep Cherokee production began, followed by the Grand Commander in 2018. The Jeep Commander was a 2-row version of the 3-row Grand Commander. In 2022, all production ended and the joint venture was terminated.
|-
| B
| [[w:GAC Fiat Chrysler|GAC Fiat Chrysler]]: Guangzhou plant
| [[w:Guangzhou|Guangzhou]], [[w:Guangdong|Guangdong province]]
| [[w:China|China]]
| 2016
| 2022
| [[w:Jeep Renegade|Jeep Renegade (BQ)]],&lt;br&gt; [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass (M4/553)]]
| Originally established in 2010 as a 50/50 joint venture between [[w:Fiat S.p.A.|Fiat]] and [[w:GAC Group|GAC]] called GAC Fiat Automobiles Co., Ltd. In January 2015, GAC Fiat was renamed GAC Fiat Chrysler Automobiles Co., Ltd. to reflect the creation of [[w:Fiat Chrysler Automobiles|Fiat Chrysler Automobiles]] in 2014 and the inclusion of Chrysler in the joint venture, which would now also produce Jeeps. A 2nd plant was opened in Guangzhou in 2016 building the Jeep Renegade, followed by the Compass. In 2022, all production ended and the joint venture was terminated.
|-
| B (1968-1980),&lt;br&gt; 2 (1960-1967),&lt;br&gt; 2 (1959)
| [[w:Dodge Main|Hamtramck Assembly (Dodge Main)]]
| [[w:Hamtramck, Michigan|Hamtramck, Michigan]]
| [[w:United States|United States]]
| 1911,&lt;br&gt; 1928 (became part of Chrysler)
| 1980 
| Dodge (1914-1958),&lt;br&gt; [[w:Dodge Coronet#Fourth generation (1957–1959)|Dodge Coronet]] (1959),&lt;br&gt; [[w:Dodge Royal#Third generation (1957–1959)|Dodge Royal]] (1959),&lt;br&gt; [[w:Dodge Custom Royal|Dodge Custom Royal]] (1959), [[w:DeSoto Firesweep|DeSoto Firesweep]] (1957-1959),&lt;br&gt; [[w:Dodge Matador|Dodge Matador]] (1960),&lt;br&gt; [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962),&lt;br&gt; [[w:Dodge Polara|Dodge Polara]] (1960-1964),&lt;br&gt; [[w:Dodge 330|Dodge 330]] (1963-1964),&lt;br&gt; [[w:Dodge 440|Dodge 440]] (1963-1964),&lt;br&gt; [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1975), [[w:Plymouth Duster|Plymouth Duster]] (1970-1975), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1969, 1972-1975), [[w:Dodge_Dart#1971|Dodge Dart Demon]] (1971-1972),&lt;br&gt; [[w:Dodge Charger (1966)|Dodge Charger]] (1967-1969), [[w:Dodge Charger Daytona#First generation (1969)|Dodge Charger Daytona]] ('69), [[w:Plymouth Barracuda|Plymouth Barracuda]] (1964-74), [[w:Dodge Challenger (1970)|Dodge Challenger]] (1970-1974), [[w:Dodge Aspen|Dodge Aspen]] (1976-1980), [[w:Plymouth Volaré|Plymouth Volaré]] (1976-1980),&lt;br&gt; Engines, Foundry
| Located at 7900 Joseph Campau Ave. This plant predated Dodge being part of Chrysler Corp. On November 4, 1914, the first Dodge Brothers passenger car was produced at the Hamtramck plant. Prior to that, Dodge Brothers made components for other automakers, primarily Ford. The Hamtramck plant was fully vertically integrated, capable of building almost every part needed to build a complete car. Dodge Brothers was bought by the Chrysler Corporation on July 31, 1928. Even after the Chrysler takeover, Hamtramck remained Dodge's home plant. From the early 1950s, various operations were automated or moved to other plants and Hamtramck became more of an assembly plant by the early 1960s. Closed January 4, 1980. Last vehicle built was a Silver Metallic 1980 Dodge Aspen R/T 2-door. 13,943,221 vehicles were produced at the plant. Demolished in 1981. Replaced by the General Motors Detroit/Hamtramck Assembly Plant (Factory Zero), which opened in 1985. 
|-
| 
| [[w:Highland Park Chrysler Plant|Highland Park Plant]]
| [[w:Highland Park, Michigan|Highland Park, Michigan]]
| [[w:United States|United States]]
| 1909,&lt;br&gt; 1925 (became part of Chrysler)
| 1960s (end of manufacturing)
| Maxwell cars (1910-1925), Chrysler Series 50 (1926-27), Chrysler Series 52 (1928), Plymouth Model Q (1929), Chrysler Series 60 (1927), Chrysler Series 62 (1928), DeSoto Series K (1929-1930), DeSoto Series CK (1930), DeSoto Series CF (1930), Fargo Trucks (1928-1930) &lt;br&gt; Parts including fluid coupling and torque converter for [[w:Fluid Drive|Fluid Drive]]
| Located at at 12000 Chrysler Service Drive (formerly Chrysler Drive). Originally, this was [[w:Maxwell Motor Company|Maxwell Motor Company]]'s main plant. However, before Maxwell Motor Co.'s formation, parts of the site was used by several car and truck manufacturers: Grabowsky Power Wagon Company used 1 building, Brush Runabout Co. used another building, and Gray Motor Co. owned another building. Gray only used the western 1/3 of the building so they leased the middle third to Alden- Sampson Truck Co. and the eastern third to Maxwell-Briscoe Motor Co. All these companies, along with several others, combined under the [[w:United States Motor Company|United States Motor Company]] in 1910. In 1913, United States Motor Company collapsed and Maxwell was the only surviving part. The U.S. Motor Co. assets were purchased by Walter Flanders, who reorganized the company as the Maxwell Motor Co. Maxwell hired Walter P. Chrysler to turn the company around in 1921 after its finances deteriorated in the post-World War I recession in 1920. In early 1921, Maxwell Motor Co. was liquidated and replaced by Maxwell Motor Corp. with Walter P. Chrysler as Chairman. On December 7, 1922, Maxwell took over the bankrupt Chalmers including its Jefferson Ave. plant. Chrysler brand cars began to be produced in 1924 at the Jefferson Ave. plant. Chalmers was discontinued in late 1923 with the last cars being 1924 models. Maxwell production ended in May 1925 at Highland Park. Maxwell Motor Corp. was reorganized into the Chrysler Corporation on June 6, 1925. The 1925 Maxwell was reworked into an entry-level, 4-cylinder Chrysler model for 1926-1928 built at Highland Park and was then reworked again into the first Plymouth in 1928, also built at Highland Park. Plymouth production was moved to the new Lynch Road Assembly plant in 1929 and DeSoto production also moved to the new Lynch Road Assembly plant in 1931. Highland Park still built parts but it no longer built vehicles. Highland Park was used more for design,  engineering, and management and served as Chrysler Corporation's headquarters through 1996. During the 1990's, Chrysler moved to its current headquarters at the Chrysler Technology Center in Auburn Hills. Much of the site has been demolished though Chrysler still has a small presence at the site with the FCA Detroit Office Warehouse. Other parts of the site are now occupied by several automotive suppliers including Magna, Valeo, Mobis, Avancez, and Yanfeng.
|-
|
| [[w:Indiana Transmission#Indiana Transmission Plant II|Indiana Transmission Plant II]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 2003 (as Indiana Transmission Plant II)
| 2019 (as Indiana Transmission Plant II)
| [[w:W5A580|Mercedes W5A580 (A580) &lt;br&gt; 5-speed auto. trans.]], Transmission components
| Located at 3360 North U.S. Highway 931. Plant was originally known as Indiana Transmission Plant II, which built automatic transmissions and transmission components from 2003-2019, when it was idled. Production began in November 2003. 5-speed auto. trans. production ended in August 2018 while production of components for the 8-speed auto. transmission ended in the fall of 2019. Starting in 2020, the plant was converted to engine production and is now known as Kokomo Engine Plant. Engine production began in late February 2022. 
|-
|
| Indianapolis Electrical Plant
| [[w:Indianapolis|Indianapolis]], [[w:Indiana|Indiana]]
| [[w:United States|United States]]
| 1953
| 1988
| Transmission plant: [[w:Chrysler PowerFlite transmission|Chrysler PowerFlite 2-speed auto. transmission]] &lt;br&gt; Electrical Plant: Alternators, distributors, starters, power steering units, voltage regulators, windshield wiper motors, and other electrical parts for cars
| Located at 2900 Shadeland Ave. Began making transmissions in 1953. In January 1959, Chrysler housed its new Electrical Division at the Shadeland Avenue plant, replacing transmission production. Became part of Chrysler's Acustar components subsidiary in 1987. Production ended on November 30, 1988 but shipping and other activities continued until March 1989 when the factory closed. Certain portions have been demolished and improvements were made to the remainder, which is now the Shadeland Business Center. 
|-
|
| [[w:Indianapolis Foundry|Indianapolis Foundry]] - Naomi Street plant
| [[w:Indianapolis|Indianapolis]], [[w:Indiana|Indiana]]
| [[w:United States|United States]]
| 1946 (became part of Chrysler)
| 1970's
| Engine blocks
| Located at 1535 Naomi Street. Purchased from American Foundry Company in 1946. Operated as a subsidiary of Chrysler Corp. called American Foundry Co. until 1959, when it was merged into Chrysler Corp. Kept operating even after the Tibbs Ave. plant was launched. This location is now Wilco Gutter Supply. 
|-
|
| [[w:Indianapolis Foundry|Indianapolis Foundry]] - Tibbs Avenue plant
| [[w:Indianapolis|Indianapolis]], [[w:Indiana|Indiana]]
| [[w:United States|United States]]
| 1950 
| 2005
| Engine heads and blocks and other components
| Located at 1100 S. Tibbs Avenue. Operated as a subsidiary of Chrysler Corp. called American Foundry Co. until 1959, when it was merged into Chrysler Corp. Production ended on September 30, 2005 and the facility closed. Demolished in 2006. 
|-
| C (1968-1990),&lt;br&gt; 3 (1960-1967),&lt;br&gt; 1 (1959)
| [[w:Detroit Assembly Complex – Jefferson#Jefferson Avenue Assembly|Jefferson Avenue Assembly]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1908,&lt;br&gt; 1925 (became part of Chrysler)
| 1990
| [[w:Chrysler Six|Chrysler Series 70 (B-70)]] (1924-1925), [[w:Chrysler Six|Chrysler Series 70 (G-70)]] (1926-1927), [[w:Chrysler Six|Chrysler Series 72]] (1928), [[w:Chrysler Royal|Chrysler Royal]] (1933, 1937-1950), DeSoto SD (1933), Chrysler Airflow (1934-1937), Chrysler Airstream (1935-36), [[w:Chrysler (brand)|Chrysler brand]] (1937-1958), Desoto Airflow (1934-1936), DeSoto Airstream (1935-1936), [[w:Chrysler Imperial|Chrysler Imperial]] (1926-1942, 1946-1954), [[w:Imperial (automobile)|Imperial]] (1955-1958, 1962-1975), [[w:Chrysler 300 letter series|Chrysler 300 letter series]] (1959-1965), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1959-1978), [[w:Chrysler Saratoga|Chrysler Saratoga]] (1959-1960), [[w:Chrysler Windsor|Chrysler Windsor]] (1959-1961), [[w:Chrysler Newport|Chrysler Newport]] (1961-1978), [[w:Chrysler 300 non-letter series|Chrysler 300 Sport Series]] (1962-1971), [[w:Chrysler Town &amp; Country|Chrysler Town &amp; Country]] (1968-1972), [[w:DeSoto Firedome|DeSoto Firedome]] (1959), [[w:DeSoto Fireflite|DeSoto Fireflite]] (1959-1960), [[w:DeSoto Adventurer|DeSoto Adventurer]] (1959-1960), [[w:DeSoto (automobile)#1961|DeSoto]] (1961), [[w:Dodge Matador|Dodge Matador]] (1960), [[w:Dodge Polara|Dodge Polara]] (1965-1966), [[w:Dodge D series|Dodge D/W series]] (1979-1980), [[w:Dodge Ramcharger|Dodge Ramcharger]] (1979-1980), [[w:Plymouth Trailduster|Plymouth Trailduster]] (1979-1980), [[w:Dodge Aries|Dodge Aries]] (1981-1989), [[w:Plymouth Reliant|Plymouth Reliant]] (1981-1989), [[w:Dodge 400|Dodge 400]] 4-d (1982-1983), [[w:Chrysler LeBaron|Chrysler LeBaron]] 4-d (1982-1984), [[w:Chrysler New Yorker#1983–1988|Chrysler New Yorker (E-body)]] (1983-1987), [[w:Chrysler New Yorker#1983–1988|Chrysler New Yorker Turbo (E-body)]] (1988), [[w:Dodge 600|Dodge 600]] 4-d (1983-1988), [[w:Chrysler E-Class|Chrysler E-Class]] (1983-1984), [[w:Plymouth Caravelle|Plymouth Caravelle]] (US: 1985-1988), [[w:Plymouth Caravelle|Plymouth Caravelle]] 4-d (Canada: 1983-1988), [[w:Dodge Omni|Dodge Omni]] (1989-1990), [[w:Plymouth Horizon|Plymouth Horizon]] (1989-1990),&lt;br&gt; Engines
| Located at 12200 East Jefferson Ave. Plant was originally opened by [[w:Chalmers Automobile|Chalmers Motor Co.]]. After falling on hard times, Chalmers agreed in 1917 to build cars for [[w:Maxwell Motor Company|Maxwell Motor Co.]] at the Jefferson Ave. plant in Detroit. In exchange, Chalmers cars would be sold through Maxwell dealers. After having its own financial problems, Maxwell stopped producing cars at the Chalmers plant in 1921. Maxwell hired Walter P. Chrysler to turn the company around in 1921. In early 1921, Maxwell Motor Co. was liquidated and replaced by Maxwell Motor Corp. with Walter P. Chrysler as Chairman. On December 7, 1922, Maxwell took over the bankrupt Chalmers including the Jefferson Ave. plant. Chrysler brand cars began to be produced in 1924. Chalmers was discontinued in late 1923 with the last cars being 1924 models. Maxwell production ended in May 1925. Maxwell Motor Corp. was reorganized into the Chrysler Corporation on June 6, 1925. The 1925 Maxwell was reworked into an entry-level, 4-cylinder Chrysler model for 1926-1928 and was then reworked again into the first Plymouth in 1928. The Jefferson Ave. plant was the home plant of the Chrysler brand through 1978. It was also the home plant for the spin-off Imperial brand except for 1959-1961, when Imperial had its own exclusive plant on Warren Ave. in Dearborn. By the time it ended production on February 2, 1990, Jefferson Ave. Assembly had built 8,310,107 vehicles. Demolished in 1991. Replaced by the Jefferson North plant built across Jefferson Ave. from the old plant, where the Kercheval Body Plant used to be. The Jefferson North plant opened in January 1992.
|-
| W (1987-1989 Chrysler M-body) &lt;br&gt;&lt;br&gt; [K for 1981-1983 AMC and 1983-1987 Renault],&lt;br&gt; 0-6 (1966-1980 AMC)
| Kenosha I Assembly
| [[w:Kenosha, Wisconsin|Kenosha, Wisconsin]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 1988
| [[w:Chrysler Fifth Avenue#1982–1989: The M-body years|Chrysler Fifth Avenue]]&lt;br&gt; (1987-1989),&lt;br&gt; [[w:Dodge Diplomat#Second generation (1980)|Dodge Diplomat]] (1987-1989), [[w:Plymouth Gran Fury#1982–1989|Plymouth Gran Fury]] (1987-89), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle Salon]] (Canada: 1987-1989)
| This was the Kenosha Main Plant of [[w:American Motors Corporation|AMC]]. The Kenosha plant was the oldest still operating automobile factory in the world when it ended vehicle production in December 1988. It first built automobiles in 1902 for the Thomas B. Jeffery Company under the Rambler brand. The factory was purchased in 1900 from the Sterling Bicycle Co., which built it in 1895. In 1914, the Thomas B. Jeffery Company rebranded its vehicles under the Jeffery brand. In 1916, the Thomas B. Jeffery Company was bought by Charles Nash and renamed Nash Motors. Kenosha produced Nash vehicles from 1917-1957. Kenosha also produced Nash's entry-level Lafayette brand from 1934-1936. After Nash merged with Hudson to form American Motors in 1954, Kenosha also produced Hudson vehicles from 1955-1957. Kenosha then produced vehicles under the Rambler brand for AMC from 1958-1968 and under the AMC brand from 1966-1983. Kenosha also produced the Alliance for AMC shareholder Renault for 1983-1987 along with the Encore for 1984-1986 and the GTA for 1987. Chrysler signed a deal with AMC in September 1986 to utilize surplus capacity at AMC's Kenosha plant to build Chrysler's trio of rwd M-body sedans beginning in February 1987. Chrysler did not have any capacity left in its own plants to continue building the M-body sedans. The St. Louis North plant that had been building the M-body sedans had been converted to build the extended length minivans. This deal led to Chrysler's acquisition of AMC, announced in March 1987. Became part of Chrysler in the 1987 buyout of AMC. Vehicle production ended in December 1988 and the M-bodies were discontinued. The site continued building engines until 2010. The plant has since been demolished.
|-
| Y
| Kenosha II Assembly
| [[w:Kenosha, Wisconsin|Kenosha, Wisconsin]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 1988
| [[w:Dodge Omni|Dodge Omni]] (1988-1989), [[w:Plymouth Horizon|Plymouth Horizon]] (1988-1989)
| This was the Kenosha Lakefront Plant of [[w:American Motors Corporation|AMC]], located on the shore of Lake Michigan. This property was originally a Simmons mattress manufacturing plant from 1870 to 1960. AMC bought it in 1960 to manufacture and paint auto bodies. Became part of Chrysler in the 1987 buyout of AMC. In September 1987, production of the Dodge Omni and Plymouth Horizon began. Production was moved to Kenosha from Chrysler's Belvidere, IL plant, which was being converted to build Chrysler's C-body sedans (Dynasty/New Yorker). Closed in December 1988. Omni &amp; Horizon production then moved to the Jefferson Ave. plant in Detroit. Demolished in 1990. In 1994, the City of Kenosha purchased the property for $1. The property was subsequently cleaned up and redeveloped into the HarborPark area, which includes a park and open space, a public museum, residential housing, and a marina. 
|-
| 
| [[w:Kenosha Engine|Kenosha Engine Plant]]
| [[w:Kenosha, Wisconsin|Kenosha, Wisconsin]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 2010
| [[w:AMC straight-4 engine|AMC straight-4 engine]],&lt;br&gt; [[w:AMC straight-6 engine|AMC straight-6 engine]],&lt;br&gt; [[w:AMC V8 engine|AMC V8 engine]],&lt;br&gt; [[w:Chrysler LH engine|Chrysler 2.7L DOHC V6]], [[w:Chrysler SOHC V6 engine#3.5|Chrysler 3.5L SOHC V6]]
| Located at 5555 30th Avenue. Became part of Chrysler in the 1987 buyout of AMC. Vehicle production ended in December 1988 at the adjacent assembly plant but the site continued building engines until 2010. After the Chrysler buyout, the plant kept building the AMC 5.9L V8 for the SJ Jeep Grand Wagoneer through 1991, the AMC 2.5L I4 through 2002 for Jeeps and the Dodge Dakota, the AMC 4.2L I6 through 1990 for the Jeep Wrangler, and the AMC 4.0L I6 through 2006 for various Jeeps ('06 Wrangler was the last to use the 4.0L). Chrysler started building its own 2.7L V6 at Kenosha in 1997 and its own 3.5L V6 in 2003. Engine production ended in October 2010 and the plant closed. Demolished in 2012-2013.
|-
|
| Kercheval Body Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1920,&lt;br&gt; 1925 (became part of Chrysler)
| 1990
| Automobile Bodies
| Located at 12265 E Jefferson Ave., across Jefferson Ave. from Chrysler's Jefferson Ave. Assembly Plant, which had originally been the Chalmers plant. The assembly plant was on the south side of Jefferson Ave. while the body plant was on the north side. The plant was called Kercheval because the north side of the plant was bordered by Kercheval Ave. The plant was built in 1920 by Wadsworth Manufacturing Co. to replace a previous plant on the same site that burned down in 1919. That fire had also damaged the Chalmers plant across the street. In November 1920, Wadsworth Manufacturing was sold to American Motor Body Co., a division of the American Can Co. On July 1, 1923, American Motor Body Co. became American Motor Body Corp., run by Charles M. Schwab. On September 4, 1925, Chrysler Corp. bought the Detroit plant of the American Motor Body Corp. to quickly increase its manufacturing capacity. In 1955, Kercheval Body Plant was connected to the Jefferson Assembly plant by a bridge crossing over Jefferson Ave. Previously, bodies made at Kercheval had to be transported by truck across Jefferson Ave. to the assembly plant. The plant closed in Feb. 1990, at the same time the Jefferson Ave. Assembly Plant closed. The Kercheval plant was demolished and Chrysler built the new Jefferson North Assembly Plant on the site of the former Kercheval Body Plant, on the north side of Jefferson Ave. 
|-
|
| Kokomo - Home Ave. plant
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1937
| 1969
| Manual Transmissions (1937-1955), Aluminum die casting (1955-1969)
| Located at 1105 S. Home Ave. Chrysler bought this plant in 1937. This was Chrysler's first plant in Kokomo. It had previously belonged to the [[w:Haynes Automobile Company|Haynes Automobile Co.]], which went out of business in 1925. The plant had been dormant since then. 5,124,211 manual transmissions were built here from 1937-1955. Transmission production then shifted to a new plant about a mile southeast on South Reed Road. The Home Ave. plant then became an aluminum die casting plant until 1969, when that operation shifted to the new Kokomo Casting plant on East Boulevard. Chrysler subsequently sold this plant. The facility was last used by Warren's Auto Parts, an auto salvage yard, which closed in 2020 after nearly 50 years. It is currently empty though still standing as of 2025. 
|-
| M
| [[w:Lago Alberto Assembly|Lago Alberto Assembly]]
| [[w:Nuevo Polanco|Nuevo Polanco district]], [[w:Miguel Hidalgo, Mexico City|Miguel Hidalgo borough]], [[w:Mexico City|Mexico City]]
| [[w:Mexico|Mexico]]
| 1938
| 2002
| &lt;br&gt; Past models: &lt;br&gt;  Mexico only: Dodge Savoy, Dodge Dart, Dodge 330, Dodge 440, Chrysler Valiant (1963-1969), Valiant Barracuda (1965-1969), Dodge Coronet, [[w:Dodge Ram|Dodge Ram pickup]] (1981-02), [[w:Dodge Ramcharger#Second generation (1981–1993)|Dodge Ramcharger]] (1986-96), [[w:Dodge Ramcharger#Third generation (1999–2001)|Dodge Ramcharger]] (1999-01) &lt;br&gt; Export to US:&lt;br&gt; [[w:Dodge Ramcharger#Second generation (1981–1993)|Dodge Ramcharger]] (1986-93), [[w:Dodge Ram#First generation (1981; D/W)|Dodge Ram pickup]] (1990-93), [[w:Dodge Ram#Second generation (1994; BR/BE)|Dodge Ram pickup]] (1994-02)
| Located at 320 Lago Alberto Street. Originally part of Fabricas Automex, Chrysler's affiliate in Mexico. In 1968, Fabricas Automex was 45% owned by Chrysler. In December 1971, Chrysler increased its stake to 90.5% and changed the Mexican company's name to Chrysler de Mexico. Chrysler later bought another 8.8% stake, taking its total to 99.3%. Lago Alberto began exporting to the US with the 1986 Dodge Ramcharger, sourced exclusively from Mexico. The Lago Alberto plant was closed in 2002 and Mexican pickup production was consolidated in the newer, more modern Saltillo plant. 
|-
| E (1968-1971),&lt;br&gt; 5 (1960-1967),&lt;br&gt; 4 (1959),&lt;br&gt; L (1958),&lt;br&gt; L (1955-1957 Chrysler brand)
| [[w:Los Angeles (Maywood) Assembly|Los Angeles (Maywood) Assembly]]
| [[w:Commerce, California|City of Commerce, California]]
| [[w:United States|United States]]
| 1932
| 1971
| Plymouth (1946-1958), Dodge (1946-1953, 1955-1958), [[w:Dodge Power Wagon#Civilian 1-ton Power Wagon &quot;Military-Type&quot;, Flat Fender Style&quot; (1945-1978)|Dodge Power Wagon]] (1946-1949), DeSoto Deluxe/Custom (1948-1952), DeSoto Powermaster Six (1953-1954), DeSoto Firedome (1952-57), DeSoto Fireflite (1955-1957), DeSoto Firesweep (1957-1958), Chrysler Windsor (1948-1958), Chrysler Royal (1949-1950), Chrysler Saratoga (1951-1952, 1957-1958), Chrysler New Yorker (1953-1958), [[w:Chrysler Windsor|Chrysler Windsor]] (1959-1960), [[w:Chrysler Saratoga|Chrysler Saratoga]] (1959-1960), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1959-60), [[w:DeSoto Firesweep|DeSoto Firesweep]] (1959), [[w:Dodge Coronet#Fourth generation (1957–1959)|Dodge Coronet]] (1957-1959), [[w:Dodge Custom Royal|Dodge Custom Royal]] (1958-1959), [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962), [[w:Dodge 330|Dodge 330]] (1963-1964), [[w:Dodge 440|Dodge 440]] (1963-1964), [[w:Dodge Polara|Dodge Polara]] (1960-1964), [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (1959), [[w:Plymouth Fury|Plymouth Fury]] (1958-1964), [[w:Plymouth Suburban|Plymouth Suburban wagon]] (1959-1961), [[w:Plymouth Savoy|Plymouth Savoy]] (1958-1959, 1963-1964), [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1971), [[w:Plymouth Duster|Plymouth Duster]] (1970-1971), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1971), [[w:Dodge Dart#1971|Dodge Dart Demon]] (1971), [[w:Plymouth Barracuda|Plymouth Barracuda]] (1964-1966, 1970), [[w:Dodge Challenger (1970)|Dodge Challenger]] (1970), [[w:Plymouth Belvedere#Intermediate series|Plymouth Belvedere]] (1965-70), [[w:Plymouth Satellite|Plymouth Satellite]] (1965-1971), [[w:Plymouth GTX|Plymouth GTX]] (1967-1971), [[w:Plymouth Road Runner|Plymouth Road Runner]] (1968-1971), [[w:Dodge Coronet|Dodge Coronet]] (1965-1971), [[w:Dodge Charger (1966)|Dodge Charger]] (1971), [[w:Dodge Super Bee|Dodge Super Bee]] (1968-1971)
| Located at 5800 South Eastern Avenue and Slauson Avenue in Maywood, now part of City of Commerce. Across the street from the [[w:Maywood Assembly|Ford Maywood Assembly plant (Los Angeles Assembly plant No. 1)]]. 
|-
| A (1968-1981),&lt;br&gt; 1 (1960-1967),&lt;br&gt; 6 (1959)
| [[w:Lynch Road Assembly|Lynch Road Assembly]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1929
| 1981
| Plymouth (1929-1958), DeSoto (1931-1932), [[w:Plymouth Savoy|Plymouth Savoy]] (1959-64), [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (59-61), [[w:Plymouth Fury|Plymouth Fury]] (1959-1964), [[w:Plymouth Suburban|Plymouth Suburban wagon]] (59-61), [[w:Plymouth Belvedere#Intermediate series|Plymouth Belvedere]] (62-70), [[w:Plymouth Satellite|Plymouth Satellite]] (1965-1970, 1973-1974), [[w:Plymouth Fury#Seventh generation (1975–1978)|Plymouth Fury]] (1975-1978), [[w:Plymouth GTX|Plymouth GTX]] (1967-1970), [[w:Plymouth Road Runner|Plymouth Road Runner]] (1968-1970, 1973, 1975), [[w:Plymouth Superbird|Plymouth Road Runner Superbird]] (1970), [[w:Dodge Coronet|Dodge Coronet]] (1965-1976), [[w:Dodge Monaco#Fourth generation (1977–1978)|Dodge Monaco]] (1977-1978), [[w:Dodge Charger (1966)#1966|Dodge Charger]] (1966), [[w:Dodge Charger (1966)#Third generation|Dodge Charger]] (1971-1974), [[w:Dodge Super Bee|Dodge Super Bee]] (1968-1971),  [[w:Chrysler Newport#1979–1981|Chrysler Newport]] (1979-81), [[w:Chrysler New Yorker#1979–1981|Chrysler New Yorker]] (79-81), [[w:Dodge St. Regis|Dodge St. Regis]] (1979-81), [[w:Plymouth Gran Fury#1980–1981|Plymouth Gran Fury]] (80-81),&lt;br&gt; Engines
| Located at 6334 Lynch Road. This was originally Plymouth's home plant. At the time it opened in 1929, Lynch Road was the largest single story auto plant in the world. DeSoto production was transferred from Highland Park to Lynch Road in 1931. In June 1932, DeSoto production was moved to the Jefferson Ave. plant when the DeSoto brand moved up in the brand hierarchy to between Dodge and Chrysler. Previously, DeSoto was between Plymouth and Dodge. During World War II, Lynch Road made tank transmissions, truck parts, and uranium enrichment diffusers for the Oak Ridge Gaseous Diffusion Plant in Oak Ridge, TN to produce enriched uranium for the atomic bomb. For 1965, Lynch Road began to focus on production of Plymouth and Dodge intermediate models. For 1979, Lynch Road was switched to build Chrysler's R-body full-size cars for all 3 Chrysler car brands. Production ended on April 3, 1981 and the factory closed. Last car produced was a white Plymouth Gran Fury police car. 
|-
| 
| [[w:Detroit Assembly Complex – Mack|Mack Ave. Engine Plant I]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1998
| 2019
| [[w:Chrysler PowerTech engine#4.7|4.7L PowerTech SOHC V8]],&lt;br&gt; [[w:Chrysler Pentastar engine|3.0L/3.2L/3.6L Pentastar V6]]
| Located at 4000 St. Jean Avenue. Mack Ave. Engine Plant I was built on the site of the former New Mack Assembly Plant and the Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. The first engine was built in 1998. 4.7L V8 engine production ended in April 2013. Pentastar V6 engine production ended in 2019. The 2 engine plants were subsequently converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North Assembly plants have operated as the Detroit Assembly Complex since 2021.
|-
| 
| [[w:Detroit Assembly Complex – Mack|Mack Ave. Engine Plant II]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 2000
| 2012
| [[w:Chrysler PowerTech engine#3.7 EKG|3.7L PowerTech SOHC 90° V6]]
| Located at 4500 St. Jean Avenue. Mack Ave. Engine Plant II was built next to the Mack Ave. Engine Plant I, which had been built on the site of the former New Mack Assembly Plant and the Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. The first engine was built in November 2000. Production ended in September 2012. The 2 engine plants were subsequently converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North Assembly plants have operated as the Detroit Assembly Complex since 2021.
|-
|
| Mack Ave. Stamping Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953 (became part of Chrysler)
| 1979
| Stampings
| Chrysler acquired the Mack Ave. Stamping Plant from Briggs Manufacturing Company in 1953. The plant was originally built in 1916 by the Michigan Stamping Company, which was taken over by Briggs Manufacturing in 1923. The plant was closed in 1979 and the site was basically abandoned. The city of Detroit bought the plant site in 1982 but was unable to find a purchaser or afford environmental remediation for the site and returned it to Chrysler. In 1990, Chrysler began cleanup and demolition of the old plant and built a new factory on the site, which became the New Mack Assembly Plant. The site later became the Mack Ave. Engine Complex and later, the Mack Ave. Assembly Plant, which is now part of the Detroit Assembly Complex.
|-
| 
| McGraw Stamping/McGraw Glass Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 19?
| 2003
| Oil pans, valve covers, and other small stampings,&lt;br&gt; Automotive Glass (1960-)
| Located at 9400 McGraw Ave. Was around the corner and behind the Wyoming Ave. DeSoto/Export plant. Originally, a stamping plant. In 1960, switched to making automotive glass. Used Safeguard brand. Glass was DOT# 21. Demolished. 
|-
|
| [[w:Mound Road Engine|Mound Road Engine Plant]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953 (became part of Chrysler)
| 2002
| [[w:Chrysler A engine|Chrysler A V8 engine]],&lt;br&gt; [[w:Chrysler LA engine|Chrysler LA V8 engine]],&lt;br&gt; [[w:Chrysler LA engine#239 V6|3.9L 90° V6 engine]],&lt;br&gt; [[w:Chrysler LA engine#Magnum 8.0 L V10|8.0L iron Magnum V10 engine]],&lt;br&gt; [[w:Viper engine|8.0L aluminum Viper V10 engine]] (1992-5/01)
| Located at 20300 Mound Road. One of the plants Chrysler acquired from Briggs Manufacturing Company in 1953. Chrysler used the plant to produce aircraft parts from 1953-1954 and then transferred the plant to Plymouth in 1954 to build its new A-series V8 engine for 1956 model year cars. Converted into an engine plant and enlarged by 71,000 sq. ft., it began building V8 engines for Plymouth in July 1955. Dodge later used the A engine from 1959 in the US in cars and trucks and Chrysler used the A engine from 1960 in the US. The plant was closed in 2002 and demolished in 2003. The land was then paved over and is now used as a storage lot for vehicles produced at the nearby Warren Truck Assembly Plant. Warren Truck Assembly is just to the north of where Mound Road Engine was. Mt. Elliott Tool and Die was located immediately to the south of the Mound Road Engine Plant on Outer Drive East.
|-
|
| [[w:Mount Elliott Tool and Die|Mount Elliott Tool and Die]]/Outer Drive Manufacturing Technology Center/Outer Drive Stamping
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1938, 1953 (became part of Chrysler)
| 2018
| Stamping Dies, Checking Fixtures, Stamping Fixtures 
| Located at 3675 Outer Drive East. Built in 1938 by Briggs Manufacturing Company. One of the plants Chrysler acquired from Briggs Manufacturing in 1953. Chrysler renamed it Outer Drive Stamping. Stamping operations ended in 1983 and operations from the closed Vernor Tool &amp; Die plant were moved here. The plant was then renamed Outer Drive Manufacturing Technology Center. The plant now did tool and die work as well as pilot plant operations and engineering for new stamping technologies. Once the Chrysler Technology Center in Auburn Hills was built, Pilot Operations and Advanced Stamping Manufacturing Engineering moved there and the plant was renamed Mount Elliott Tool and Die. Operations at the plant ended in 2018 and the plant was sold to German automotive supplier Laepple Automotive in 2024. Laepple Automotive is producing stamped body parts at the plant. 
|-
| V
| [[w:Detroit Assembly Complex – Mack|New Mack Assembly Plant]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1992
| 1995
| [[w:Dodge Viper|Dodge Viper RT/10]] (1992-96)
| Located at 4000 St. Jean Avenue. The New Mack Assembly Plant is built on the site of the former Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. Viper production began in May 1992 at the New Mack Assembly Plant. After ending production in 1995, New Mack Assembly was converted into the Mack Ave. Engine Plant I. A new addition was then built to create Mack Ave. Engine Plant II. The 2 engine plants were subsequently converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North Assembly plants have operated as the Detroit Assembly Complex since 2021. 
|-
| F (1968-2009),&lt;br&gt; 6 (1960-1967),&lt;br&gt; 5 (1959),&lt;br&gt; N (1958)
| [[w:Newark Assembly|Newark Assembly]]
| [[w:Newark, Delaware|Newark, Delaware]]
| [[w:United States|United States]]
| 1951,&lt;br&gt; 1957 (Automotive prod.)
| 2008
| Plymouth (1957-1958), Dodge (1958), [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (1958-1959, 1961), [[w:Plymouth Fury|Plymouth Fury]] (1959-1974), [[w:Plymouth Savoy|Plymouth Savoy]] (1959-1964), [[w:Dodge Coronet#Fourth generation (1957–1959)|Dodge Coronet]] (1958-1959), [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962), [[w:Dodge Polara|Dodge Polara]] (1960-1966), [[w:Dodge Monaco|Dodge Monaco]] (1965-1966, 1968), [[w:Chrysler Newport|Chrysler Newport]] (1965-1970), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1965-70), [[w:Chrysler Town &amp; Country (1941–1988)|Chrysler Town &amp; Country]] (1966-1967), [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1964, 1974-1976), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1964, 1974-76), [[w:Dodge Aspen|Dodge Aspen]] (1976-1980), [[w:Plymouth Volare|Plymouth Volare]] (1976-1980), [[w:Chrysler LeBaron#First generation (1977–1981)|Chrysler LeBaron (M-body)]] (1979-1980), [[w:Plymouth Reliant|Plymouth Reliant]] sedan &amp; wagon (1981-1988), [[w:Dodge Aries|Dodge Aries]] sedan &amp; wagon (1981-1988), [[w:Chrysler LeBaron#Second generation (1982–1988)|Chrysler LeBaron (K-body)]] (sedan: 1984-1988, wagon: 1982-1988), [[w:Plymouth Acclaim|Plymouth Acclaim]] (1989-1995), [[w:Dodge Spirit|Dodge Spirit]] (1989-1995), [[w:Chrysler LeBaron#Third generation sedan (1990–1994)|Chrysler LeBaron Sedan (A-body)]] (1990, 1993-1994), [[w:Chrysler Saratoga#1989–1995|Chrysler Saratoga]] (For export: 1990-1992), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron coupe (J-body)]] (1992-1993), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron convertible (J-body)]] (1992-1995), [[w:Dodge Intrepid#First generation (1993–1997)|Dodge Intrepid]] (1994-1996), [[w:Chrysler Intrepid#First generation (1993–1997)|Chrysler Intrepid]] (Canada: 1994-1995), [[w:Chrysler Concorde#First generation (1993–1997)|Chrysler Concorde]] (1995-1996), [[w:Dodge Durango#First generation (DN; 1998)|Dodge Durango (DN)]] (1998-2003), [[w:Dodge Durango#Second generation (HB; 2004)|Dodge Durango (HB)]] (2004-2009), [[w:Chrysler Aspen|Chrysler Aspen]] (2007-2009) 
| Chrysler began construction of the Delaware Tank Plant in January 1951 to build [[w:M48 Patton|M48 Patton]] tanks. Production began in April 1952. Production ended in May 1961 and the Tank Plant was closed in October 1961. Low rate initial production of the [[w:M60 tank|M60 tank]] was also done at the Newark plant in 1959 before production was moved to the [[w:Detroit Arsenal (Warren, Michigan)|Detroit Arsenal Tank Plant]] in Warren, MI in 1960. Conversion to automotive production began in 1956. Production of Plymouth and Dodge cars began on April 30, 1957. Production ended on December 19, 2008. Sold to the University of Delaware on October 24, 2009. Most of the plant was demolished in 2010-2011 except for the Administration Building near the front of the complex. The site is now the Science, Technology, and Advanced Research (STAR) campus. The old Chrysler Administration Building has been redesigned and is now being used by the College of Health Sciences. 
|-
| K
| [[w:Pillette Road Truck Assembly|Pillette Road Truck Assembly]]
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1976
| 2003
| [[w:Dodge Sportsman|Dodge Tradesman/Sportsman]] (1976-1980),&lt;br&gt; [[w:Dodge Ram Van|Dodge Ram Van]] (1981-2003), [[w:Dodge Ram Wagon|Dodge Ram Wagon]] (1981-'02), [[w:Plymouth Voyager#Full-size van (AB; 1974–1983)|Plymouth Voyager]] (1976-1983)
| Located at 2935 Pillette Road. Was originally Windsor Plant 6. The Pillette Road plant was located less than a mile away from Chryslers' main plant complex in Windsor. Production began in January 1976. Production ended on June 12, 2003. 2,309,399 units were built. Demolished in 2004. Part of the site is now the Grand Central Business Park. Another part was a logistics center serving Chrysler's Windsor Assembly Plant and operated by Syncreon. The Syncreon Automotive Windsor site closed in October 2022. The parts sorting and sequencing work done there was now going to be done in-house at Chrysler's Windsor Assembly Plant. 
|-
| 
| [[w:Los Angeles (Maywood) Assembly#San Leandro Assembly|San Leandro Assembly]]
| [[w:San Leandro, California|San Leandro, California]]
| [[w:United States|United States]]
| 1948
| 1954
| Plymouth (1949-1954),&lt;br&gt; Dodge (1949-1954),&lt;br&gt; [[w:Dodge Power Wagon#Civilian 1-ton Power Wagon &quot;Military-Type&quot;, Flat Fender Style&quot; (1945-1978)|Dodge Power Wagon]] (1950-1954)
| Located at 1933 Davis St. Plant was originally run by Dodge Division. In 1953, San Leandro began to make its own car bodies instead of sourcing bodies from Detroit and only doing final assembly locally. Closed in 1954 when Chrysler consolidated West Coast auto production at the Los Angeles plant. Used by International Harvester to build heavy-duty trucks from 1963 to 1975, replacing an earlier plant in Emeryville.  Now the Westgate Center, a shopping mall, and Gate510, a hub for entrepreneurs. 
|-
| B (1996-2009),&lt;br&gt; G (1968-1991),&lt;br&gt; 7 (1960-1967),&lt;br&gt; 8 (1959)
| [[w:Saint Louis Assembly|St. Louis I Assembly]] - South plant
| [[w:Fenton, Missouri|Fenton, Missouri]]
| [[w:United States|United States]]
| 1959
| 2008
| [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (1960), [[w:Plymouth Fury|Plymouth Fury]] (1960-1964), [[w:Plymouth Savoy|Plymouth Savoy]] (1960-1964), [[w:Plymouth Suburban|Plymouth Suburban wagon]] (1961), [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962), [[w:Dodge 330|Dodge 330]] (1963-1964), [[w:Dodge 440|Dodge 440]] (1963-1964), [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1965, 1976), [[w:Plymouth Duster|Plymouth Duster]] (1973-1976), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1965, 1973-1976), [[w:Plymouth Barracuda|Plymouth Barracuda]] (1964-1965),&lt;br&gt; [[w:Plymouth Belvedere#Intermediate series|Plymouth Belvedere]] (1965-1970), [[w:Plymouth Satellite|Plymouth Satellite]] (1965-1974), [[w:Plymouth GTX|Plymouth GTX]] (1967-1971), [[w:Plymouth Road Runner|Plymouth Road Runner]] (1968-75), [[w:Plymouth Fury#Seventh generation (1975–1978)|Plymouth Fury]] (1975-1976), [[w:Dodge Coronet|Dodge Coronet]] (1965-1973, 75), [[w:Dodge Charger (1966)|Dodge Charger]] (1968-1974), [[w:Dodge Super Bee|Dodge Super Bee]] (1968-1971), [[w:Dodge Diplomat|Dodge Diplomat]] (1977-1981), [[w:Chrysler LeBaron#First generation (1977–1981)|Chrysler LeBaron (M-body)]] (1977-1981), [[w:Plymouth Caravelle|Plymouth Caravelle (M-body)]] (Canada: 1978-1981), [[w:Plymouth Reliant|Plymouth Reliant]] 2-d (1982-1986), [[w:Dodge Aries|Dodge Aries]] 2-d (1982-1986), [[w:Dodge 400|Dodge 400]] 2-d &amp; convertible (1982-1983), [[w:Dodge 600|Dodge 600]] 2-d &amp; convertible (1984-1986), [[w:Plymouth Caravelle|Plymouth Caravelle]] 2-d (Canada: 1983-1986), [[w:Chrysler LeBaron#Second generation (1982–1988)|Chrysler LeBaron (K-body)]] (2-d &amp; convertible: 1982-1986), [[w:Chrysler Executive|Chrysler Executive]] (1983-1986), [[w:Dodge Daytona|Dodge Daytona]] (1984-1991), [[w:Chrysler Daytona|Chrysler Daytona]] (Canada: 1984-1991), [[w:Dodge Daytona#Chrysler Laser|Chrysler Laser]] (1984-1986), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron coupe/convertible (J-body)]] (1987-1991), [[w:Plymouth Voyager|Plymouth Voyager]] (1996-2000), [[w:Plymouth Voyager|Plymouth Grand Voyager]] (1996-2000), [[w:Dodge Caravan|Dodge Caravan]] (1996-2007), [[w:Dodge Caravan|Dodge Grand Caravan]] (1996-2009), [[w:Chrysler Voyager|Chrysler Voyager]] (2001-2003), [[w:Chrysler Voyager|Chrysler Grand Voyager]] (2000), [[w:Chrysler Town &amp; Country (minivan)|Chrysler Town &amp; Country]] (1996-2001, 2004-2007)
| Located at 1001 N. Hwy Dr. All 1970 Dodge Chargers were made here. St. Louis South was idled in 1991. The Dodge Daytona was moved to Sterling Heights and the J-body Chrysler LeBaron was moved to Newark, DE. St. Louis South was reopened in 1995 to build minivans, which were moved from the St. Louis North plant. For the 3rd generation, St. Louis South built both SWB and LWB models. For the 4th generation, St. Louis South built all SWB models but also built some LWB models. Closed on October 31, 2008. Demolished in 2011. Site was sold in 2014 and is now the Fenton Logistics Park.
|-
| J (1996-2009),&lt;br&gt; X (1973-1995),&lt;br&gt; U (1970-1972),&lt;br&gt; 7 (1967-1969)
| [[w:Saint Louis Assembly|St. Louis II Assembly]] - North plant / Missouri Truck Assembly Plant
| [[w:Fenton, Missouri|Fenton, Missouri]]
| [[w:United States|United States]]
| 1966
| 2009
| [[w:Dodge D series|Dodge D/W series]] (1967-1973), [[w:Dodge Ramcharger|Dodge Ramcharger]] (1974-1977), [[w:Plymouth Trail Duster|Plymouth Trail Duster]] (1974-76), [[w:Dodge Sportsman|Dodge Tradesman/Sportsman]] (1971-1980), [[w:Plymouth Voyager#Full-size van (AB; 1974–1983)|Plymouth Voyager]] (1975-1976, 1980),&lt;br&gt; [[w:Plymouth Gran Fury#1982–1989|Plymouth Gran Fury]] (1984-1987), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle Salon]] (Canada: 1984-1987), [[w:Dodge Diplomat|Dodge Diplomat]] (1984-1987), [[w:Chrysler Fifth Avenue#1982–1989: The M-body years|Chrysler Fifth Avenue]] ('84-'87), [[w:Plymouth Voyager|Plymouth Grand Voyager]] (1987-1995), [[w:Dodge Caravan|Dodge Grand Caravan]] (1987-1995), [[w:Chrysler minivans (S)#Cargo van|Dodge Extended Mini Ram Van]] (1987-1988), [[w:Chrysler Town &amp; Country (minivan)|Chrysler Town &amp; Country]] (1990-1995),&lt;br&gt; [[w:Dodge Ram|Dodge Ram pickup]] (1996-'09)
| Originally opened to build trucks as the Missouri Truck Assembly Plant. In 1980, the plant was idled. Plant was reopened in 1983 to build the rwd, M-body sedans, which were moved from Windsor, ON, Canada so that Windsor could be converted to build minivans. Plant was renamed St. Louis II Assembly. During 1987, the M-body sedans were moved to AMC's plant in Kenosha, WI so that St. Louis North could be converted to build the new LWB minivans. For the first 2 generations of Chrysler minivans, St. Louis North only built the LWB models. For 1996, minivan production moved to St. Louis South and the North plant was converted to build full-size pickups. Closed on July 10, 2009. Demolished in 2011. Site was sold in 2014 and is now the Fenton Logistics Park.
|-
| J (1970-1978),&lt;br&gt; 6 (1968-1969),&lt;br&gt; 9 (1961-1967)
| Tecumseh Road Truck Assembly / Windsor Truck Assembly Plant
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1916,&lt;br&gt; 1925 (became part of Chrysler)
| 1978
| Maxwell (1924-1925),&lt;br&gt; Chrysler (1924-1929),&lt;br&gt; Dodge Trucks (1931-1960), &lt;br&gt; Dodge D-Series Trucks: &lt;br&gt; D100 (1961), D200 (1964), W200 (1965), W100 (1966), D100/W100 (1967), D200 (1970), D500 (1968),&lt;br&gt; D500/D600/D700/D800 &lt;br&gt; medium-duty trucks (1970-1972), D500/D600/W600/D700/D800 medium-duty trucks (1974-1977),&lt;br&gt; D100 (1978),&lt;br&gt; Fargo Trucks (1936-1972)
| Located at 300 Tecumseh Road East. Was originally Windsor Plant 1. Became part of Chrysler upon its founding in 1925. Was previously a Maxwell-Chalmers plant and was originally Maxwell's Canadian plant from 1916. Switched to building trucks in 1931 after Plant 3 opened in 1929. Closed in 1978. Became the Imperial Quality Assurance Centre from 1980-1983, doing extra quality control on the 1981-1983 Imperial built at the Windsor Assembly Plant (the car plant - Plant 3) about 1.5 miles east of Plant 1. The Imperial Quality Assurance Centre closed in 1983 when the Imperial was discontinued. Subsequently demolished. Is now the Plaza 300 shopping mall.
|-
|
| Tipton Transmission Plant
| [[w:Tipton, Indiana|Tipton, Indiana]]
| [[w:United States|United States]]
| 2014
| 2023
| [[w:ZF 9HP transmission|948TE 9-speed auto.]] transmission, SI-EVT transmission
| Located at 5880 W. State Road 28. Originally, the plant was supposed to be a [[w:Getrag|Getrag]] plant focused on supplying Chrysler with dual-clutch transmissions. Chrysler withdrew from the deal in 2008 after a dispute over financing and sued Getrag. The 80% completed facility then sat dormant until Chrysler Group purchased the facility in February 2013 and completed construction. Production began in April 2014 with the ZF-designed 9-speed auto. transmission, built under license from ZF. Production ended in June 2023 and 9-speed production was consolidated into Indiana Transmission Plant I in Kokomo, IN. The SI-EVT transmission for the Pacifica Hybrid was moved to Kokomo Transmission Plant. Sold to IRH Manufacturing LLC in September 2024 to make solar cells.
|-
| L (1989-2001),&lt;br&gt; T (1981-1988)
| [[w:Toledo Complex#Parkway|Toledo Assembly #1 Plant]] - Jeep Parkway plant
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 2001 (ended final assembly), 2006 (ended body assembly)
| [[w:Jeep Cherokee (XJ)|Jeep Cherokee (XJ)]] (1984-01), [[w:Jeep Cherokee (XJ)#Wagoneer|Jeep Wagoneer (XJ)]] (1984-90), [[w:Jeep Comanche|Jeep Comanche]] (1986-1992),&lt;br&gt; Bodies for vehicles made at Stickney Ave. plant &lt;br&gt; 
Models only made before Chrysler takeover: Willys Aero (1952-1955), Kaiser Manhattan (1954-1955), Jeep CJ (1946-1986), Jeep DJ, Jeep Jeepster (1948-1950), Jeep Jeepster Commando (1967-1971), Jeep Commando (1972-1973), Willys Jeep Station Wagon (1946-1964), Willys Jeep Truck (1947-1965), Jeep Gladiator (SJ) (1963-1971), Jeep J-series pickup, Jeep Wagoneer [SJ] (1963-1981), Jeep Cherokee [SJ] (1974-1981), Jeep Forward Control [FC] (1957-1965), Jeep FJ Fleetvan (1961-1975), Military Jeeps
| Located at 1000 Jeep Parkway. The John North Willys-owned Overland Automobile Co. purchased the plant in 1909 from Pope-Toledo, another early automaker. Overland Automobile Co. became Willys-Overland in 1912. Began building Jeeps in the 1940s. This was the original Jeep assembly plant. Willys-Overland was bought by Kaiser in 1953. Kaiser then sold its Willow Run plant in Ypsilanti, MI to GM and moved its production to the Willys plant in Toledo, OH. Kaiser and Willys production in the US ended in 1955 and Toledo focused on Jeep production going forward. Kaiser Jeep was sold to AMC in 1970. Became part of Chrysler in the 1987 buyout of AMC. Final assembly ended in 2001 when the XJ Cherokee ended production but painted body production continued until June 30, 2006, when the TJ Wrangler ended production. Production of the replacement JK Wrangler moved to the new Toledo Supplier Park plant a few miles away.  The Administration Building, used from 1915 through 1974, was imploded on April 14, 1979. A third of the plant was demolished in 2002 after final assembly ended including the Jeep Museum. The remainder was demolished in 2006-2007 after body production ended. One of the three large brick smokestacks was preserved and was dedicated in 2013 to the plant's history and workforce. A bronze plaque was mounted next to the smokestack, which still says &quot;Overland&quot; on it. Over 11 million vehicles were produced at the site, including military Jeeps during World War II. The site was sold to the Toledo-Lucas County Port Authority in 2010. The site has been redeveloped into the Overland Industrial Park. Dana Inc. and Detroit Manufacturing Systems are among the tenants in the Overland Industrial Park and those plants supply the current Jeep plants elsewhere in Toledo. All-Phase Electric Supply Co. is another tenant. 
|-
| P (1989-2006),&lt;br&gt; T (1981-1988)
| [[w:Toledo Complex#Stickney|Toledo Assembly #2 Plant]] - Jeep Stickney Ave. plant
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 2006 
| [[w:Jeep Wagoneer (SJ)#1984: SJ and XJ|Jeep Grand Wagoneer (SJ)]]&lt;br&gt; (1984-1991),&lt;br&gt; [[w:Jeep Wrangler (YJ)|Jeep Wrangler (YJ)]] (1993-95), [[w:Jeep Wrangler (TJ)|Jeep Wrangler (TJ)]] (1997-06)
Models only made before Chrysler takeover:&lt;br&gt; Jeep Wagoneer [SJ] (1981-1983), Jeep Cherokee [SJ] (1981-1983)
| Located at 4000 Stickney Ave. Originally opened in 1942 by the Electric Auto-Lite Co., a maker of spark plugs. Sold to Kaiser-Jeep in 1964, which used it as a machining and engine plant until 1981, when AMC converted it for vehicle production. AMC had taken over Kaiser Jeep in 1970. AMC built the SJ Wagoneer and Cherokee at the Stickney Ave. plant. Body assembly was done at an SJ- or later,  Wrangler-specific body shop at the Parkway plant while final assembly was at the Stickney Ave. plant. Became part of Chrysler in the 1987 buyout of AMC. Production ended in 2006 with the end of the TJ Wrangler. Production of the replacement JK Wrangler moved to the new Toledo Supplier Park plant built on the site of the old Stickney Ave. plant. 
|-
| W (1994-1996)
| [[w:Toledo Complex#Stickney|Toledo Assembly #3 Plant]] - Jeep Stickney Ave. plant
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 1993
| 1996 
| [[w:Dodge Dakota#First generation (1987–1996)|Dodge Dakota]] (1994-1996)
| Body assembly was done at a Dakota-specific body shop at the Parkway plant while final assembly was at the Stickney Ave. plant.
|-
|
| Toluca Engine Plant 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| ?
| 2002
| [[w:Chrysler Slant-6 engine|Chrysler Slant-6 engine]], [[w:Chrysler LA engine|Chrysler LA V8 engine]]
| Closed in 2002
|-
|
| Toluca Transmission Plant 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| ?
| 2001
| Automatic Transmissions for fwd cars
| Closed in 2001
|-
| 
| [[w:Trenton Engine Complex|Trenton Engine North Plant]] 
| [[w:Trenton, Michigan|Trenton, Michigan]]
| [[w:United States|United States]]
| 1952
| 2022
| [[w:Chrysler B engine|Chrysler B V8 engine]],&lt;br&gt; [[w:Chrysler B engine#RB engines|Chrysler RB V8 engine]],&lt;br&gt; [[w:Chrysler Slant-6 engine|Chrysler Slant-6 engine]],&lt;br&gt; [[w:Volkswagen EA827 engine#1.7|VW 1.7L EA827 I4 engine]] (adding Chrysler parts to already built VW engines made in W. Germany),&lt;br&gt; [[w:Chrysler 2.2 &amp; 2.5 engine|2.2L/2.5L &quot;K-car&quot; I4 engine]], [[w:Chrysler 1.8, 2.0 &amp; 2.4 engine|1.8L, 2.0L I4 &quot;Neon engine&quot;]], [[w:Chrysler 3.3 &amp; 3.8 engines|3.3L/3.8L OHV V6]], [[w:Chrysler SOHC V6 engine|3.5L/3.2L/4.0L SOHC V6]], [[w:Chrysler Pentastar engine|3.2L/3.6L Pentastar V6 engine]], [[w:World Gasoline Engine#2.4_2|2.4L Tigershark I4]],&lt;br&gt; Engine components,&lt;br&gt; Air raid sirens
| Located at 2000 Van Horn Road. Trenton North began production in fall 1952 and was expanded in 1964, 1967, 1969, 1976, and 1977. At first, Trenton North began by making water pumps and air raid sirens but engines quickly followed. Trenton Engine North was Chrysler’s first dedicated engine factory in the US, separate from the assembly plants. On September 29, 1978, V8 production ended. Trenton North added Chrysler parts such as the intake and exhaust manifolds, water pump, ignition system and other major parts to already built VW 1.7L EA827 I4 engines imported from Salzgitter, W. Germany for use in the Omni/Horizon. Production of the 3.5L V6 moved to Kenosha Engine in 2003. Trenton North was idled in May 2011 when the 3.8 V6 ended production following the end of 3.3 &amp; 4.0 V6 engine production in 2010. Chrysler then announced in June 2011 it would use a fifth of the plant to make components for the Pentastar V6 being made at Trenton South. In January 2012, Trenton North began producing the 3.6L Pentastar V6 engine. Chrysler then installed a flexible production line that could build both the Pentastar V6 and the Tigershark I4. In May 2013, Trenton began producing the 3.2L Pentastar V6. Tigershark I4 production began late in 3rd quarter 2013. By the end of 2022, Pentastar Upgrade engine production moved from Trenton North to Trenton South and the older North plant ended production. Trenton North has been repurposed for warehousing and other non-manufacturing opportunities. 
|-
|
| [[w:Tritec engine|Tritec Motors Ltda.]] 
| [[w:Campo Largo, Paraná|Campo Largo, Paraná]] 
| [[w:Brazil|Brazil]]
| 2000
| 2007
| [[w:Tritec engine|1.4L/1.6L/1.6L supercharged &lt;br&gt; Tritec I4 engine]] 
| Originally established in 1997 as a 50/50 joint venture between Chrysler and [[w:BMW|BMW]] to jointly develop the Tritec 4-cylinder engine and build it at a newly built, jointly owned plant in Brazil. At the time, BMW owned the [[w:Rover Group|Rover Group]], which was developing a new generation of the Mini and Rover worked with Chrysler to develop the Tritec engine that would power the new Mini. In 1998, Chrysler merged with Daimler-Benz, forming DaimlerChrysler. Production of the new engine began in January 2000. BMW broke up and sold off the Rover Group in 2000 but it retained the rights to the new generation Mini then under development and the 50% stake in Tritec Motors. BMW used all 3 versions of the engine in the new generation [[w:Mini Hatch#First generation (R50/52/53; 2001)|MINI]]. Chrysler used the normally aspirated 1.6L version of the engine in non-North American market versions of the [[w:Chrysler Neon#Second generation (2000)|Neon]] and the [[w:Chrysler PT Cruiser|PT Cruiser]]. The normally aspirated 1.6L engine was also supplied to Chinese automakers [[w:Chery|Chery]] and [[w:Lifan Group|Lifan]]. Tritec engine production ended in June 2007. On July 11, 2007, BMW sold its 50% stake in Tritec Motors to [[w:Chrysler#1998–2007: DaimlerChrysler|DaimlerChrysler]]'s Chrysler Group. BMW did not use the Tritec engine in any subsequent models. BMW jointly developed with [[w:PSA Group|PSA Peugeot Citroën]] a new engine called [[w:Prince engine|Prince]] for the [[w:Mini Hatch#Second generation (R56/57; 2006)|next generation Mini]], which launched as a 3-d hatch for 2007 and as a convertible for 2009. In March 2008, the plant and the rights to the engine design were sold to [[w:Fiat|Fiat]], which then updated the engine into the [[w:Fiat E.torQ engine|E.torQ engine]]. The E.torQ engine was offered in the same 1.6L displacement as the Tritec and was also enlarged to 1.7L (1747 cc), though the 1.7L was referred to as a 1.8L. The E.torQ engine was produced in the same plant as the Tritec engine by Fiat from 2010-2023. Became part of [[w:Fiat Chrysler Automobiles|Fiat Chrysler Automobiles]] upon its founding in 2014. Then became part of [[w:Stellantis|Stellantis]] upon its founding in 2021 along with Fiat and Chrysler. Ironically, the E.torQ engine also ended up powering certain Chrysler Group models outside the US and Canada. It was used in the South American/European/Australian market Jeep Renegade and the Mexican and Middle East market 2017-2020 Dodge Neon, which was a rebadged Fiat Tipo made in Turkey. It was also used in the Mexican market Dodge Vision and Ram 700 and the South American market Ram 1000. The plant was closed in 2023, following the end of E.torQ engine production.
|-
|
| [[w:Twinsburg Stamping|Twinsburg Stamping]]
| [[w:Twinsburg, Ohio|Twinsburg, Ohio]]
| [[w:United States|United States]]
| 1957
| 2010
| Stampings and assemblies
| Located at 2000 East Aurora Road. Opened in August 1957. Closed July 31, 2010. Sold in 2011. Demolished in 2012-2013. Now the Cornerstone Business Park.
|-
|
| Vernor Tool &amp; Die plant (South plant)
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953
| 1983
| Tooling &amp; Dies
| Located at 12026 E Vernor Highway. Operations moved to Mount Elliott Tool and Die. The former location seems to have been swallowed up by the Jefferson North Assembly plant.
|-
|
| Vernor Trim plant (North plant)
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953
| 1970's
| Trim
| Located at 12025 E Vernor Highway. The former location seems to have been swallowed up by the Jefferson North Assembly plant.
|-
| 4 (1960-1961),&lt;br&gt; 7 (1959)
| Warren Avenue Plant
| [[w:Dearborn, Michigan|Dearborn, Michigan]]
| [[w:United States|United States]]
| 1927,&lt;br&gt; 1950 (opened as part of Chrysler)
| 1960s
| DeSoto bodies (1950-1958), DeSoto engines &lt;br&gt; (1951-1958),&lt;br&gt; [[w:Imperial (automobile)#Second generation (1957–1966)|Imperial]] (1959-1961)
| Located at 8505 West Warren Avenue. This was previously the factory of Paige and Graham-Paige. Chrysler leased half the plant in 1941 to use for military production. Chrysler produced aircraft components for the [[w:Martin B-26 Marauder|B-26 Marauder]] (nose and center fuselage sections) and the [[w:Boeing B-29 Superfortress|B-29 Superfortress]] (the pressurized nose section, wing leading edges, and engine cowlings). The B-29 had a nose so large that trenches had to be dug in the floor and some of the bracing for the plant’s roof girders had to be removed to accommodate the aircraft. Chrysler bought the plant in 1947. Began building bodies for DeSoto in August 1950. Engine production began in 1951. Production of the Imperial brand moved here from the Jefferson Ave. plant in Detroit for 1959 in an attempt to give the Imperial brand its own, exclusive factory however sales weren't high enough to support its own plant so Imperial production moved back to the Jefferson Ave. plant in Detroit for 1962. Production of small parts followed for a few years as did export operations. The plant was later sold. Most of the plant has seen been demolished but the front building facing on Warren Ave. is still there and is now used as Corporate HQ by Shatila Food Products. The DeSoto logo, featuring a stylized image of Hernando de Soto, can still be seen at the top of the building above the front door. 
|-
| T (1970-), 2 (1966-1969),&lt;br&gt; 
| Warren Truck #2 Assembly Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1966
| 1975
| Dodge heavy-duty trucks
| Located at 6600 East 9 Mile Road, at the corner of Sherwood Ave and East 9 Mile Road. Closed in 1975 when Dodge exited the heavy-duty truck market. Site now belongs to Sundance Beverage Co., the parent of Everfresh Juice Co.
|-
| V (1971-1979)
| Warren Truck (Compact) #3 Assembly Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1970
| 1979
| [[w:Dodge Sportsman|Dodge Tradesman/Sportsman]] (1971-1979),&lt;br&gt;[[w:Plymouth Voyager#Full-size van (AB; 1974–1983)|Plymouth Voyager]] (1974-1979)
| Was located at 22000 Hoover Road between Toepfer Road and East 9 Mile Road however this address is no longer used. It's now 21900 Hoover Road. The property was purchased in 1937 by Divco (Detroit Industrial Vehicle Company), which opened a new factory on the site in 1939 to build delivery trucks. Divco's headquarters were also at this location but moved to Richmond, IN after Divco bought Wayne Works, Inc. in 1956. In 1968, delivery truck production was moved to Delaware, OH and in 1969, the factory was sold to Chrysler. Chrysler started building the new 1971 model &lt;br&gt; B-series vans there in 1970. Production seems to have ended in 1979. The buildings still seem intact as of 2025. Midwest Freight Systems and Sherwood Truck Repair occupy the site now.
|-
| 
| Windsor Engine Plant
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1938
| 1980
| [[w:Chrysler flathead engine#Straight-6|Chrysler flathead inline 6]],&lt;br&gt; [[w:Chrysler Slant-6 engine|Chrysler Slant-6 engine]], &lt;br&gt;[[w:Chrysler A engine|Chrysler A V8 engine]],&lt;br&gt; [[w:Chrysler LA engine|Chrysler LA V8 engine]]
| Was originally Windsor Plant 2. Located just to the south of Windsor Plant 3, the current minivan factory. Closed in August 1980. Built over 8 million engines. Windsor Assembly Plant (Plant 3) expanded onto the site of the old engine plant when it was being renovated for minivan production. 
|- 
|
| [[w:Detroit Assembly#LaSalle Factory/DeSoto Factory|Wyoming Ave. Assembly (DeSoto Wyoming Ave. plant)]] / Wyoming Export Plant
| [[w:Detroit|Detroit]], [[w:Michigan|Michigan]]
| United States
| 1936
| 1958 (Vehicle prod.),&lt;br&gt; 1980 (export operations)
| [[w:DeSoto (automobile)|DeSoto]] (1937-1958),&lt;br&gt; CKD Export (1960-1980)
| Located at 6000 Wyoming Avenue. Originally built to produce Liberty aircraft engines in World War I, opening in 1917. In 1919, was taken over by Saxon Motor Co., owned by Hugh Chalmers of Chalmers Motor Co. GM bought the plant in 1926 and built the LaSalle there from 1927-1933. GM sold Wyoming Assembly to Chrysler in 1934, which then used it to build its DeSoto brand. Became DeSoto's home plant. During World War II, Chrysler built wing center sections for the [[w:Curtiss SB2C Helldiver|Curtiss SB2C Helldiver]] at the Wyoming Ave. plant. For 1959, DeSoto's models other than the Dodge-based Firesweep were moved to Chrysler's Jefferson Ave. plant in Detroit. The Dodge-based Firesweep was already built at the Dodge plant in Hamtramck. This was done so that bodies and final assembly would be done in either a single facility or a pair of connected facilities. This was part of Chrysler's move to unibody construction for 1960 for all cars except Imperial. After the DeSoto brand was discontinued in late 1960, became Wyoming Export plant which was used to prepare vehicles for export. Plant closed in 1980. Plant was demolished in 1992. Site is now occupied by Comprehensive Logistics Inc.
|}

==Non-Chrysler FCA/Stellantis Factories Previously Making Chrysler Group Vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 1
| [[w:Fiat Cassino Plant|Cassino Plant]]
| [[w:Piedimonte San Germano|Piedimonte San Germano]], [[w:Province of Frosinone|Province of Frosinone]]
| [[w:Italy|Italy]]
| 1972
| 
| Past Chrysler Group models: [[w:Lancia Delta#|Chrysler Delta]] (UK/Ireland)
| Fiat plant. 
|-
| 3
| [[w:Alfa Romeo Pomigliano d'Arco plant|Pomigliano d'Arco plant]] (Giambattista Vico plant)
| [[w:Pomigliano d'Arco|Pomigliano d'Arco]], [[w:Metropolitan City of Naples|Metropolitan City of Naples]]
| [[w:Italy|Italy]]
| 1972
|
| Past Chrysler Group models: [[w:Dodge Hornet|Dodge Hornet]] (2023-2025). Related models:&lt;br&gt; [[w:Alfa Romeo Tonale|Alfa Romeo Tonale]] (2023-)
| Originally, an Alfa Romeo plant. Oriiginally owned by Construction Industry Neapolitan Vehicles Alfa Romeo - Alfasud S.p.A., a joint venture between Alfa Romeo (88%), Finmeccanica (10%), and IRI (2%). In 1982, Alfasud S.p.A. was renamed Inca Investments. Alfa Romeo was taken over by Fiat in 1986. Fiat merged with Chrysler to form Fiat Chrysler Automobiles (FCA) in 2014. FCA merged with PSA Group to form Stellantis in 2021. 
|}

==Non-Chrysler Group DaimlerChrysler/Daimler AG Factories Previously Making Chrysler Group Vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 5
| Mercedes-Benz Plant Düsseldorf
| [[w:Düsseldorf|Düsseldorf]], [[w:North Rhine-Westphalia|North Rhine-Westphalia]]
| [[w:Germany|Germany]]
| 1962
|
| [[w:Dodge Sprinter|Dodge Sprinter]] (2003-2009)
| Mercedes-Benz Plant. 
|-
| 9
| Mercedes-Benz Plant Ludwigsfelde
| [[w:Ludwigsfelde|Ludwigsfelde]], [[w:Brandenburg|Brandenburg]]
| [[w:Germany|Germany]]
| 1991 (Mercedes prod. began)
|
| [[w:Dodge Sprinter#Second generation (2006–2018, NCV3)|Dodge Sprinter]] chassis cab (2007-2009)
| Mercedes-Benz Plant. Originally established in 1936 by Daimler-Benz to make airplane engines. The plant was bombed by the US in 1945. After the war ended, what remained of the factory was dismantled and taken to the Soviet Union as reparations. On February 1, 1991, Mercedes-Benz took a 25% stake in the Ludwigsfelde plant, which had previously belonged to East German truckmaker VEB Automobilwerke. It became a 100% owned subsidiary of Mercedes-Benz on January 1, 1994. Sprinter production began in 2006. 
|}

==Former partner factories== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Prod. for Chrysler began
! style=&quot;width:10px;&quot;|Prod. for Chrysler ended
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 6
| [[w:China Motor Corporation|China Motor Corporation]]
| [[w:Yangmei District|Yangmei District]], [[w:Taoyuan, Taiwan|Taoyuan]]
| [[w:Taiwan|Taiwan]]
| 2006
| 2007
| [[w:Chrysler Town &amp; Country (minivan)#Fourth generation (2001–2007)|Chrysler Town &amp; Country]]&lt;br&gt; (Taiwan: 2006-2007),&lt;br&gt; [[w:Dodge 1000|Dodge 1000]] (Mexico: 2007-'10)
| China Motor Corporation plant. Built for Chrysler under license by China Motor Corporation of Taiwan. Production began April 18, 2006. 
|-
|
| [[w:Carrozzeria Ghia|Carrozzeria Ghia]] 
| [[w:Turin|Turin]]
| [[w:Italy|Italy]]
| 1957
| 1965
| [[w:Imperial (automobile)#Imperial Crown (1955–1965)|Imperial Crown Limousine]] (1957-1965) modified, painted limousine bodies and interiors
| 132 Imperial Crown Limousines were built by Ghia under contract for Chrysler between 1957 and 1965. The 1957-1959 models were based on modified 2-door hardtops with the more rigid chassis from the convertible. The 1960-1965 models were based on 4-door models. Ghia lengthened the frame and modified the bodywork and interiors to create the limousines. After producion ended in 1965, Ghia sold the tooling to Barreiros of Spain, which built another 10 Imperial Crown Limousines. Barreiros had been 35% owned by Chrysler since 1963. That was increased to 77% in 1967 and 100% in 1969.  
|-
| U
| [[w:Hyundai Motor Company|Hyundai Motor Co.]] - [[w:List of Hyundai Motor Company manufacturing facilities#Ulsan Plant|Ulsan plant]]
| [[w:Ulsan|Ulsan]]
| [[w:South Korea|South Korea]]
| 2000
| 2014
| Mexico only: &lt;br&gt; [[w:Dodge Atos|Dodge Atos]] (2001-2012),&lt;br&gt;  [[w:Dodge Verna|Dodge Verna]] (2004-06),&lt;br&gt;  [[w:Dodge Attitude#First generation (MC; 2006)|Dodge Attitude (MC)]] (2007-'11), [[w:Dodge Attitude#Second generation (RB; 2011)|Dodge Attitude (RB)]] (2012-'14), [[w:Dodge H100|Dodge H100 truck]],&lt;br&gt; [[w:Hyundai Starex#Second generation (TQ; 2007)|Dodge H100 Van/Wagon]]
| Rebadged Hyundai models sold as Dodges in Mexico. 
|-
| 
| [[w:Hyundai Motor India|Hyundai Motor India]]
| [[w:Chennai|Chennai]], [[w:Tamil Nadu|Tamil Nadu]]
| [[w:India|India]]
| 2011
| 2014
| Mexico only: &lt;br&gt; [[w:Dodge i10|Dodge i10]] (2012-2014)
| Rebadged Hyundai model sold as a Dodge in Mexico. 
|-
| X
| [[w:Karmann|Karmann Osnabrück Assembly]]
| [[w:Osnabrück|Osnabrück]], [[w:Lower Saxony|Lower Saxony]]
| [[w:Germany|Germany]]
| 2003
| 2007
| [[w:Chrysler Crossfire|Chrysler Crossfire]] (2004-2008)
| Karmann plant. Built under contract for Chrysler. 
|-
| Y
| [[w:Magna Steyr|Magna Steyr]] / Steyr-Daimler-Puch - Chrysler Steyr Assembly
| [[w:Graz|Graz]], [[w:Styria|Styria]]
| [[w:Austria|Austria]]
| 1994
| 2010
| [[w:Jeep Grand Cherokee|Jeep Grand Cherokee]]&lt;br&gt; (1995-2010),&lt;br&gt; [[w:Jeep Commander (XK)|Jeep Commander]] (2006-2010), [[w:Chrysler Voyager#Fourth generation (2001–2007)|Chrysler Voyager/Grand Voyager]] (2003-2007),&lt;br&gt; [[w:Chrysler 300#First generation (2005)|Chrysler 300C/300C Touring]] (2005-2010)
| Originally, a Steyr-Daimler-Puch plant. Magna International acquired a majority holding of 66.8% in Steyr-Daimler-Puch in 1998 and acquired the rest by 2002 when it was renamed Magna Steyr. Production of the Chrysler Voyager and Grand Voyager minivans moved from the Eurostar plant  next door to the main Magna Steyr plant for 2003. Chrysler minivan production in Austria ended on November 30, 2007. Built under contract for Chrysler. 
|-
| B
| [[w:Maserati|Maserati]] - [[w:Innocenti|Innocenti]] plant
| [[w:Lambrate|Lambrate district]], [[w:Milan|Milan]]
| [[w:Italy|Italy]]
| 1988
| 1990
| [[w:Chrysler TC by Maserati|Chrysler TC by Maserati]]&lt;br&gt; (1989-1991)
| Developed jointly by Chrysler and Maserati, the TC was built in Italy by Maserati at the Innocenti plant in Milan. Maserati and Innocenti were both owned by DeTomaso at the time. Chrysler bought a 5% stake in Maserati in 1984 and increased its stake to 15.6% in 1986. Production ended in 1990 due to low sales.
|-
| U
| Mitsubishi - Mizushima plant (Line 1)
| [[w:Kurashiki|Kurashiki]], [[w:Okayama Prefecture|Okayama Prefecture]] 
| [[w:Japan|Japan]]
| 1970s
| 1996
| [[w:Plymouth Champ|Plymouth Champ]] (1981-1982), [[w:Plymouth Colt|Plymouth Colt]] (1983-1994), [[w:Dodge Colt|Dodge Colt]] (1981-1994), [[w:Dodge Colt|Dodge/Plymouth Colt]]&lt;br&gt; (Canada only: 1995),&lt;br&gt; [[w:Eagle Summit|Eagle Summit]]&lt;br&gt; (4-d: 1989-1990, 1993-1996,&lt;br&gt; 3-d: 1991-1992, 2-d: 1993-96), [[w:Mitsubishi RVR#North America|Plymouth Colt Vista]] (1993-94), [[w:Mitsubishi RVR#North America|Eagle Summit Wagon]] (1993-96)
| Mitsubishi Motors plant.
|-
| Z
| Mitsubishi - Okazaki plant
| [[w:Okazaki, Aichi|Okazaki]], [[w:Aichi Prefecture|Aichi Prefecture]] 
| [[w:Japan|Japan]]
| 1983
| 1996
| [[w:Plymouth Conquest|Plymouth Conquest]] (1984-86), [[w:Dodge Conquest|Dodge Conquest]] (1984-1986), [[w:Chrysler Conquest|Chrysler Conquest]] (1987-1989), [[w:Dodge Colt Vista#Colt Vista|Dodge Colt Vista]] (1984-1991), [[w:Plymouth Colt Vista#Colt Vista|Plymouth Colt Vista]] (1984-91), [[w:Mitsubishi RVR#North America|Plymouth Colt Vista]] (1992-94), [[w:Mitsubishi RVR#North America|Eagle Summit Wagon]] (1992-96) [[w:Eagle Vista#Vista Wagon|Eagle Vista Wagon]]&lt;br&gt; (Canada: 1989-1991)
| Mitsubishi Motors plant.
|-
| Y (Line 1)&lt;br&gt;/&lt;br /&gt;P (Line 2)
| Mitsubishi - &lt;br&gt; Ooe plant &lt;br&gt; a.k.a. &lt;br&gt; Nagoya #1&lt;br&gt;/&lt;br&gt;Nagoya #2
| Ooe-cho, [[w:Minato-ku, Nagoya|Minato ward]], [[w:Nagoya|Nagoya]], [[w:Aichi Prefecture|Aichi Prefecture]] 
| [[w:Japan|Japan]]
| 1970s
| 1996
| VIN code Y:&lt;br&gt; [[w:Plymouth Sapporo|Plymouth Sapporo]] (1981-1983), [[w:Dodge Challenger#Second generation (1978–1983)|Dodge Challenger]] (1981-1983), [[w:Plymouth Arrow Truck#Chrysler variants|Plymouth Arrow Truck]] ('81-'82), [[w:Dodge Ram 50|Dodge Ram 50]] (1981-1984), [[w:Dodge Stealth|Dodge Stealth]] (1991-1996)
VIN code P:&lt;br&gt; [[w:Dodge Ram 50|Dodge Ram 50]] (1985-1986), [[w:Dodge Ram 50#North America|Dodge Ram 50]] (1987-1993)
| Mitsubishi Motors plant. Closed in 2001. Sold to Mitsubishi Heavy Industries and now used by its Aircraft, Defense &amp; Space Business Area.
|-
| J
| Mitsubishi -  Toyo Koki/Pajero Manufacturing Co., Ltd. plant
| [[w:Sakahogi, Gifu|Sakahogi]], [[w:Gifu Prefecture|Gifu Prefecture]] 
| [[w:Japan|Japan]]
| 1986
| 1989
| [[w:Dodge Raider|Dodge Raider]] (1987-1989)
|  Originally, a Toyo Koki Co. Ltd. plant. Opened in 1976. Built vehicles under contract for Mitsubishi. Mitsubishi Motors owned 35% of Toyo Koki and increased its stake to a majority in March 1995. The plant was then renamed Pajero Manufacturing Co., Ltd. in July 1995. In March 2003, Mitsubishi bought all the remaining shares in Pajero Manufacturing Co., Ltd., making it a wholly owned subsidiary. Closed in 2021. Sold to Daio Paper in 2022.
|-
| H (Attitude), 9 (1200)
| [[w:Mitsubishi Motors (Thailand)|Mitsubishi Motors Thailand]]
| [[w:Laem Chabang|Laem Chabang]], [[w:Chonburi province|Chonburi province]]
| [[w:Thailand|Thailand]]
| 2014
| 2024
| [[w:Dodge Attitude#Third generation (A10; 2015)|Dodge Attitude]]&lt;br&gt; (Mexico: 2015-2024),&lt;br&gt; [[w:Mitsubishi Triton#Fifth generation (KJ/KK/KL; 2014)|Ram 1200]]&lt;br&gt; (Middle East: 2017-2019)
| Mitsubishi Motors plant.  
|-
| ?
| [[w:MMC Automotriz|MMC Automotriz]]
| [[w:Barcelona, Venezuela|Barcelona]], [[w:Anzoátegui|Anzoátegui state]]
| [[w:Venezuela|Venezuela]]
| 2002
| 2009
| [[w:Dodge Brisa|Dodge Brisa]]&lt;br&gt; ([[w:Hyundai Accent#First generation (X3; 1994)|2002-2005]]), ([[w:Hyundai Getz|2006-2009]])
| MMC Automotriz plant. Originally, MMC Automotriz was 49% owned by Consorcio Inversionista Fabril S.A. (CIF) of Venezuela and 42% owned by Nissho Iwai Corp. The remaining 9% of the company was owned by the Japan International Development Organization Ltd., a partnership between the government-financed Overseas Economic Cooperation Fund and 98 private companies. Nissho Iwai merged with Nichimen Corp. in 2004 to form Sojitz Corp. Sojitz later increased its stake in MMC Automotriz to 98%, with the other 2% still held by CIF. MMC Automotriz was sold to the the Sylca Group (also known as Yammine Group) in 2015. MMC Automotriz produced Mitsubishi vehicles and from 1996-2012, also produced Hyundai vehicles. The Dodge Brisa was produced for DaimlerChrysler as part of its cooperation with [[w:Hyundai Motor Company|Hyundai]]. MMC Automotriz also produced Mitsubishi Fuso trucks. 
|-
| G
| [[w:Mitsubishi Motors (Thailand)|MMC Sittipol Co., Ltd.]]
| [[w:Laem Chabang|Laem Chabang]], [[w:Chonburi province|Chonburi province]]
| [[w:Thailand|Thailand]]
| 1988
| 1992
| [[w:Plymouth Colt#Fifth generation (1985–1988)|Plymouth Colt 100]]&lt;br&gt; (Canada: 1988-1992),&lt;br&gt; [[w:Dodge Colt#Fifth generation (1985–1988)|Dodge Colt 100]]&lt;br&gt; (Canada: 1988-1992),&lt;br&gt; [[w:Eagle Vista|Eagle Vista]] (Canada: 1988-92)
| Mitsubishi Motors plant. MMC Sittipol is the predecessor company of Mitsubishi Motors (Thailand). These were the first vehicle exports from Thailand. 
|-
| 2
| [[w:Renault|Renault]] - [[w:Maubeuge Construction Automobile|Maubeuge plant]]
| [[w:Maubeuge|Maubeuge]]
| [[w:France|France]]
| 1987
| 1989
| [[w:Renault Medallion|Renault Medallion]] (1988),&lt;br&gt; [[w:Eagle Medallion|Eagle Medallion]] (1989)
| Renault plant. The Medallion was sold through Chrysler's Jeep-Eagle dealer network as a legacy of Chrysler's takeover of AMC from Renault.
|-
| 8,&lt;br&gt; 0
| [[w:Soueast|Soueast]]
| [[w:Fuzhou|Fuzhou]], [[w:Fujian|Fujian province]]
| [[w:China|China]]
| 2008
| 2010
| [[w:Chrysler Voyager#Fourth generation (2001–2007)|Chrysler Voyager]],&lt;br&gt; [[w:Dodge Caravan#Fourth generation (2001–2007)|Dodge Caravan]]
| South East (Fujian) Motor Co., Ltd. plant. Built for Chrysler under license by South East (Fujian) Motor Co., Ltd.
|}</text>
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    <revision>
      <id>4654714</id>
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        <id>3434282</id>
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{{tmbox|type=notice|text=This is a sandbox page, a place for experimenting with Wikibooks.}}

This is a history of Chrysler factories that are being or have been used to produce cars, vans, SUVs, trucks, and automobile components. 

For '''Chrysler brand''' only: Plant code in 1955-1957 was not indicated if it was made in the home plant in Michigan but if it was made in a different plant, then it was indicated by a letter in the 4th position of the serial number.

For '''cars''': Plant code in 1958 was not indicated if it was made in the home plant in Michigan but if it was made in a different plant, then it was indicated by a letter in the 4th position of the serial number. Plant code was the number in the 4th position of the 10-digit serial number for 1959-1965. Plant code was the number in the 7th position of the 13-digit serial number for 1966-1967. Plant code was the letter in the 7th position of the 13-digit serial number for 1968-1980.

Canadian-built cars had the plant code as the number in the 5th position of the 11-digit serial number for 1965.

For '''trucks''': The first digit of the 7-digit sequence number (4th position overall of the 10-digit serial number) indicated which plant built the truck for 1967-1968. Plant code was the number in the 4th position of the 10-digit serial number for 1969. Plant code was the letter in the 7th position of the 13-digit serial number for 1970-1980.

Canadian-built models used a different system for VINs until 1968, when Chrysler of Canada adopted the same system as the US. Plant code for trucks was the number in the 5th position of the 10-digit serial number for 1961-1967.

All models from 1981 on have the plant code in the 11th position as per standardized VIN regulations.

For '''AMC passenger cars from 1966-1967''': Plant code is indicated by the letter in the 3rd position of the 13-digit vehicle number. If the 3rd letter is a K, then it was made in Kenosha, WI. If the 3rd letter is a B, then it was made in Brampton, ON, Canada. [Note: Some early 1966 models used the 1965-style serial numbers.]

For '''AMC passenger cars from 1968 through 1980''': Plant code is indicated by the 8th digit (the first of the sequential serial number) of the 13-digit vehicle number. 1-6 is Kenosha, WI and 7-9 is Brampton, ON, Canada.

For '''Canadian-built Jeeps built by AMC Canada for 1979-1980''': Plant code is indicated by the 8th digit (the first of the sequential serial number) of the 13-digit vehicle number. It was made in Canada if it's either an 8 (1979) or a 7 (1980). All other Jeeps from 1980 and earlier were made in Toledo. 

All models from 1981 on have the plant code in the 11th position as per standardized VIN regulations.

==Current factories== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Current Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| D (1968-),&lt;br&gt; 4 (1966-1967)
| [[w:Belvidere Assembly|Belvidere Assembly]] 
| [[w:Belvidere, Illinois|Belvidere, Illinois]]
| [[w:United States|United States]]
| 1965
| Feb. 2023
| 
| Located at 3000 West Chrysler Drive. '''Belvidere Satellite Stamping Plant''' adjoins the main assembly plant. Began production on July 7, 1965. The first vehicle produced was a 1966 Plymouth Fury four-door. In 1972, the Chrysler Town and Country station wagon was added to the Belvidere plant. In 1977, the plant was converted to build front-wheel drive subcompacts. Production of the Dodge Omni and Plymouth Horizon began on December 5, 1977. All L-body derivatives were made at Belvidere through 1987. In 1987, Belvidere was converted to build Chrysler's midsize, fwd C-body sedans. Belvidere then switched back to building small cars and began production of the Neon on November 10, 1993. Belvidere built the last Plymouth, a silver 2001 Neon LX on June 28, 2001. Neon production ended in September 2005. Dodge Caliber began production in January 2006, followed by Jeep Compass in June 2006 and Jeep Patriot in December 2006. Caliber ended production on December 19, 2011. Dodge Dart began production on April 30, 2012, and ended on October 4, 2016. Compass and Patriot production ended on December 23, 2016. Jeep Cherokee production began on June 1, 2017 and ended on February 28, 2023. Belvidere was then idled. &lt;br&gt; Past models: [[w:Plymouth Fury|Plymouth Fury]] (1966-1974), [[w:Plymouth Gran Fury#1975–1977|Plymouth Gran Fury]] (1975-1977), [[w:Dodge Monaco|Dodge Monaco]] (1966-1976), [[w:Dodge Royal Monaco#1977 (Royal Monaco)|Dodge Royal Monaco]] (1977), [[w:Dodge Polara|Dodge Polara]] (1966-1973), [[w:Chrysler Newport|Chrysler Newport]] (1977), [[w:Chrysler Town &amp; Country|Chrysler Town &amp; Country]] (1973-1977), [[w:Dodge Omni|Dodge Omni]] (1978-1987), [[w:Plymouth Horizon|Plymouth Horizon]] (1978-1987), [[w:Dodge Omni 024|Dodge Omni 024]] (1979-1980), [[w:Plymouth Horizon TC3|Plymouth Horizon TC3]] (1979-1980), [[w:Dodge Omni 024|Dodge 024]] (1981-1982), [[w:Plymouth Horizon TC3|Plymouth TC3]] (1981-1982), [[w:Dodge Charger (1981)|Dodge Charger]] (1983-1987), [[w:Plymouth Turismo|Plymouth Turismo]] (1983-1987), [[w:Dodge Rampage|Dodge Rampage]] (1982-1984),  [[w:Plymouth Scamp|Plymouth Scamp]] (1983), [[w:Dodge Dynasty|Dodge Dynasty]] (1988-1993), [[w:Chrysler Dynasty|Chrysler Dynasty]] (Canada: 1988-1993), [[w:Chrysler New Yorker#1988–1993|Chrysler New Yorker]] (1988-1993), [[w:Chrysler New Yorker Fifth Avenue#1990–1993: New Yorker Fifth Avenue|Chrysler New Yorker Fifth Avenue]] (1990-1993), [[w:Chrysler Imperial#1990–1993|Chrysler Imperial]] (1990-1993), [[w:Dodge Neon|Dodge Neon]] (1995-2005), [[w:Plymouth Neon|Plymouth Neon]] (1995-2001), Chrysler Neon (Canada: 2000-02),&lt;br&gt; Dodge SX 2.0 (Canada: 2003-05),&lt;br&gt; [[w:Dodge Caliber|Dodge Caliber]] (2007-2012), [[w:Jeep Compass#First generation (MK49; 2006)|Jeep Compass]] (2007-2017), [[w:Jeep Patriot|Jeep Patriot]] (2007-2017), [[w:Dodge Dart (PF)|Dodge Dart]] (2013-2016), [[w:Jeep Cherokee (KL)|Jeep Cherokee]] (2017-2023)
|-
| H (1989-),&lt;br&gt; A (1988)
| [[w:Brampton Assembly|Brampton Assembly]] (Formerly Bramalea Assembly)
| [[w:Brampton|Brampton]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1987
| Dec. 2023
| 
| Located at 2000 Williams Parkway East. Factory was built by AMC and Renault. The plant was acquired by Chrysler as part of its takeover of AMC. Began production on September 28, 1987. Plant was originally known as Bramalea Assembly. Plant was renamed Brampton Assembly in 1992 after Chrysler closed and sold the old AMC plant on Kennedy Road in Brampton. The attached '''Brampton Satellite Stamping Plant''' was added in December 1991 and was built for the launch of the Chrysler LH platform. On December 17, 1991, Eagle Premier and Dodge Monaco production ended. Production of the Chrysler LH platform cars began in June 1992. Production switched to the rear-wheel drive Chrysler LX platform cars in January 2004. The Chrysler 300 was also built for export to mainland Europe as the Lancia Thema from 2011-2014. Production ended on December 22, 2023 and the plant was idled. Last vehicle off the line was a Pitch-Black 2023 Dodge Challenger Demon 170. 7,147,888 vehicles were produced through 2023.&lt;br&gt; Past models: [[w:Eagle Premier|Eagle Premier]] (1988-1992), [[w:Dodge Monaco#Fifth generation (1990–1992)|Dodge Monaco]] (1990-1992),&lt;br&gt; [[w:Dodge Intrepid|Dodge Intrepid]] (1993-2004),&lt;br&gt; [[w:Chrysler Intrepid|Chrysler Intrepid]] (Canada: 1993-2004),&lt;br&gt; [[w:Chrysler Concorde|Chrysler Concorde]] (1993-2004),&lt;br&gt; [[w:Eagle Vision|Eagle Vision]] (1993-1997),&lt;br&gt; [[w:Chrysler New Yorker#1994–1996|Chrysler New Yorker]] (1994-1996),&lt;br&gt; [[w:Chrysler LHS|Chrysler LHS]] (1994-1997, 1999-2001),&lt;br&gt; [[w:Chrysler 300M|Chrysler 300M]] (1999-2004),&lt;br&gt; [[w:Chrysler 300|Chrysler 300]] (2005-2023),&lt;br&gt; [[w:Dodge Magnum#Chrysler LX platform (2005–2008)|Dodge Magnum]] (2005-2008),&lt;br&gt; [[w:Dodge Charger (2006)|Dodge Charger]] (2006-2023),&lt;br&gt; [[w:Dodge Challenger (2008)|Dodge Challenger]] (2008-2023),&lt;br&gt; [[w:Lancia Thema#Second generation (2011–2014)|Lancia Thema]] (For export: 2011-2014)
|-
| C
| [[w:Jefferson North Assembly|Detroit Assembly Complex – Jefferson]] / Jefferson North Assembly Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1992
| 
| [[w:Jeep Grand Cherokee|Jeep Grand Cherokee]] (1993-), [[w:Dodge Durango#WD|Dodge Durango]] (2011-)
| Located at 2101 Conner Street. Jefferson North replaced the previous Jefferson Assembly plant that closed in 1990 and was demolished in 1991. Jefferson North is across the street from the old Jefferson Assembly plant, on the north side of Jefferson Ave. Jefferson North was built on the site of Chrysler's old Kercheval Avenue Body Plant, which, in 1955, had been connected to the old Jefferson Assembly plant by a bridge crossing over Jefferson Ave. The Jefferson North plant site also absorbed what had been the axle plant and service parts buildings of the old [[w:Hudson Motor Car Company|Hudson]] plant, which were located at Connor St. and Vernor Hwy. The main Hudson plant is now the parking lot on the corner of Jefferson Ave. and Connor St. After 2017, the Jefferson North plant complex also absorbed the site of the former Budd Co. body- &amp; parts-making plant at Connor St. and Charlevoix Avenue, which had previously belonged to the Liberty Motor Car Co. The Budd plant extended north on Connor from Charlevoix most of the way to Mack Ave. Since the nearby Mack Ave. Assembly Plant began operations in 2021, the 2 plants have operated as the Detroit Assembly Complex. Jefferson North began production on January 14, 1992 with the original Grand Cherokee (ZJ). The 2nd gen. Grand Cherokee began production on July 17, 1998. The 3rd gen. Grand Cherokee began production on July 26, 2004 followed by the Jeep Commander on July 18, 2005. The 4th gen. Grand Cherokee began production on May 10, 2010 followed by the Dodge Durango on December 14, 2010. The 5th gen. Grand Cherokee began production in May 2022. The 4xe plug-in hybrid version of the Grand Cherokee began production at Jefferson North in March 2023. On Aug. 13, 2013, Jefferson North built its 5 millionth vehicle, a silver 2014 Grand Cherokee Overland. On May 25, 2016, Jefferson North built its 6 millionth vehicle, a Granite Crystal (silvery gray) 2016 Grand Cherokee 75th anniversary Edition.&lt;br&gt; Past models:&lt;br&gt; [[w:Jeep Grand Cherokee (ZJ)#Grand Wagoneer (1993)|Jeep Grand Wagoneer (ZJ)]] (1993),&lt;br&gt; [[w:Jeep Commander (XK)|Jeep Commander]] (2006-2010),&lt;br&gt; [[w:Jeep Grand Cherokee (WK2)#Grand Cherokee WK (2022)|Jeep Grand Cherokee WK]] (2022)&lt;br&gt; [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee 4xe]] (2023-2025)
|-
| 8
| [[w:Detroit Assembly Complex – Mack|Detroit Assembly Complex – Mack]] / Mack Ave. Assembly Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 2021
| 
| [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee L]] (2021-), [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee]] (2022-)
| Located at 4000 St. Jean Avenue. The Mack Avenue Assembly Plant is built on the site of the former Mack Ave. Engine Plants I &amp; II, the New Mack Assembly Plant, &amp; the Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. The two plants that comprised the former Mack Avenue Engine Complex were converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North plants have operated as the Detroit Assembly Complex since 2021. Production began in March 2021 with the 3-row Grand Cherokee L. The 2-row Grand Cherokee followed in the fall of 2021. The 4xe plug-in hybrid version of the Grand Cherokee began production at Mack Ave. in August 2022. &lt;br&gt; Past models: [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee 4xe]] (2022-2025)
|-
|
| [[w:Dundee Engine Plant|Dundee Engine Plant]] (Formerly [[W:Global Engine Manufacturing Alliance|GEMA]]) 
| [[w:Dundee, Michigan|Dundee, Michigan]]
| [[w:United States|United States]]
| 2005
| 
| [[w:Prince engine#1.6-litre turbocharged (PSA)|1.6L turbo PSA/BMW Prince EP6CDTX Hybrid I4]],&lt;br&gt; [[w:FCA Global Medium Engine|2.0L turbo Hurricane4 EVO I4 (GME-T4 EVO)]],&lt;br&gt; Engine components
| Located at 5800 North Ann Arbor Road. Plant was originally part of the the Global Engine Manufacturing Alliance, a 3-way engine manufacturing joint venture between DaimlerChrysler, Mitsubishi, and Hyundai. The North Plant launched in October 2005, followed by the South Plant in November 2006. The plant began with production of the I4 World Gasoline Engine, which was developed by the Global Engine Alliance, a 3-way engine development joint venture between DaimlerChrysler, Mitsubishi, and Hyundai. Originally, the plant was envisioned as supplying engines to Mitsubishi and Hyundai as well as Chrysler however the plant only ever supplied engines to Chrysler. Mitsubishi and Hyundai each set up engine production at their own engine plants. On August 31, 2009, Chrysler bought Mitsubishi’s and Hyundai’s stakes in the group and now wholly owns both the Global Engine Manufacturing Alliance and its primary engine-building plant in Dundee, Michigan. In January 2012, the plant was renamed Dundee Engine Plant. Production of the Fiat 1.4-liter FIRE I4 engine began in November 2010. The Tigershark engine, an evolution of the World engine, began production in 2012 for the 2.0L and in May 2013 for the 2.4L. Tigershark engine production ended on March 16, 2023. In November 2019, the Pentastar V6 began production at Dundee, moving from the Mack Ave. Engine Plant in Detroit, which was to be converted into a vehicle assembly plant. The Pentastar V6 ended production at Dundee on August 18, 2023. In 2025, Dundee began making a North American-spec version of the European-developed Prince engine for the 2026 Jeep Cherokee Hybrid. &lt;br&gt; Past engines: [[w:World Gasoline Engine|1.8L/2.0L/2.4L/2.4L Turbo I4 World Gasoline Engine]], [[w:World Gasoline Engine#Tigershark|2.0L/2.4L I4 Tigershark Engine]], [[w:FIRE engine|Fiat 1.4L/1.4L Turbo FIRE MultiAir I4 engine]], [[w:Chrysler Pentastar engine|Chrysler 3.6L Pentastar V6 engine]] 
|-
| 
| Etobicoke Casting Plant
| [[w:Etobicoke|Etobicoke District]], [[w:Toronto|Toronto]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1964
| 
| Aluminum die castings, Engine and Transmission Components
| Located at 15 Brown's Line. Etobicoke used to be a separate city but became part of Toronto in 1998. Factory was originally built in 1942 by the Canadian government and operated by Alcan Aluminum, which used it to make molds for military aircraft parts during World War II. It produced precision aircraft parts and other high quality aluminum castings. The aluminum foundry was purchased by Chrysler in April 1964 from Alcan Aluminum. The plant was expanded in 1965 and 1998. Etobicoke Casting is making oil pans for the 1.6 liter turbo I4 in the 2026 Jeep Cherokee.
|-
|
| [[w:Indiana Transmission#Indiana Transmission I|Indiana Transmission Plant I]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1998
| 
| [[w:ZF 9HP transmission|948TE 9-speed auto.]] transmission, Gear machining and final assembly of electric drive modules
| Located at 3660 North U.S. Highway 931. RFE transmission production ended in January 2025. More than 8 million RFE transmissions were produced at Indiana Transmission Plant I. Production of the nine-speed transmission began in May 2013. The 9-speed is built under license from [[w:ZF Friedrichshafen|ZF]]. &lt;br&gt; Past transmissions:&lt;br&gt; [[w:Chrysler RFE transmission|Chrysler RFE 4-/5-/6-speed auto. trans.]]
|-
|
| [[w:Kokomo Casting|Kokomo Casting Plant]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1965
| 
| Aluminum parts for automotive components, transmission and transaxle cases; engine block castings
| Located at 1001 East Boulevard. Kokomo Casting is the world’s largest die-cast facility. Plant was expanded in 1969, 1986, 1995 and 1997. Over 18 million four-speed transmission cases were made at Kokomo Casting from 1988 through July 2014. Kokomo Casting started making nine-speed transmission cases in 2013. Kokomo Casting is making engine blocks for the 1.6 liter turbo I4 in the 2026 Jeep Cherokee. Kokomo Casting is making gearbox covers for the electric drive modules made at the Indiana Transmission Plant. 
|-
|
| [[w:Kokomo Engine Plant|Kokomo Engine Plant]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 2022 (as Kokomo Engine)
| 
| [[w:FCA Global Medium Engine|2.0L turbo GME-T4 I4]]
| Located at 3360 North U.S. Highway 931. Plant was previously known as Indiana Transmission Plant II, which built automatic transmissions and transmission components from 2003-2019, when it was idled. Starting in 2020, the plant was converted to engine production. Engine production began in late February 2022. 
|-
|
| [[w:Kokomo Transmission|Kokomo Transmission Plant]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1956
| 
| [[w:ZF 8HP transmission|850RE]] 8-speed auto. transmission,&lt;br&gt; [[w:ZF 8HP transmission|880RE]] 8-speed auto. transmission,&lt;br&gt; Machining of engine block castings and transmission components,&lt;br&gt; Machined components for the &lt;br&gt; 9-speed auto. transmission
| Located at 2401 South Reed Road. On October 9, 2020, Kokomo Transmission built its last 41TE 4-speed auto. transmission, assembling more than 17 million 4-speed auto. transmissions since production began in 1988. Kokomo Transmission began building 6-speed auto. transmissions in 2006. Production of the eight-speed automatic transmission began in September 2012. The 8-speed is built under license from [[w:ZF Friedrichshafen|ZF]]. On August 8, 2023, Kokomo Transmission built its 6 millionth 8-speed transmission. Kokomo Transmission is machining gearbox covers for the electric drive modules made at the Indiana Transmission Plant. &lt;br&gt; Past transmissions: &lt;br&gt;[[w:TorqueFlite|TorqueFlite 3-/4-speed auto. trans.]],&lt;br&gt; [[w:Ultradrive|Ultradrive (TE/AE/LE/RLE/TES/TEA)&lt;br&gt; 4-/6-speed auto. trans.]],&lt;br&gt; [[w:ZF 8HP transmission|845RE]] 8-speed auto. transmission,&lt;br&gt; SI-EVT trans. (eFlite) for Pacifica Hybrid
|-
| 
| [[w:Saltillo Engine Plant#South Engine Plant|Saltillo North Engine Plant]] 
| [[w:Ramos Arizpe|Ramos Arizpe]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 1981
| 
| [[w:Chrysler Hemi engine#Third generation: 2003–present|5.7L/6.4L/6.2L supercharged Hemi V8]], [[w:Stellantis Hurricane engine|Chrysler 3.0L twin-turbo Hurricane GME-T6 I6]]
|  Production began on May 8, 1981. Hemi V8 production began in June 2002 with the 5.7L. Production of the supercharged 6.2L Hellcat Hemi V8 began in the third quarter of 2014. Tigershark I4 production began in the first quarter of 2014. &lt;br&gt; Past engines: [[w:Chrysler 2.2 &amp; 2.5 engine|2.2L, 2.5L &quot;K-car&quot; I4 engine]], [[w:Chrysler 1.8, 2.0 &amp; 2.4 engine|2.0L, 2.4L, 2.4L Turbo I4 &quot;Neon engine&quot;]],&lt;br&gt; [[w:World Gasoline Engine#2.4_2|2.4L Tigershark I4 engine]], [[w:Chrysler Hemi engine#6.1|6.1L Hemi V8]]
|-
| 
| [[w:Saltillo Engine Plant#South Engine Plant|Saltillo South Engine Plant]] 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 2010
| 
| [[w:Chrysler Pentastar engine|Chrysler 3.6L Pentastar V6 engine]]
| Plant opened on October 29, 2010. The plant has produced over 6 million Pentastar V6 engines. &lt;br&gt; Past engines: Chrysler 3.6L Pentastar V6 engine (EH3) for Pacifica Plug-in Hybrid
|-
| 
| Saltillo Stamping Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 1997
| 
| Stampings and assemblies including Body panels
| Part of the Saltillo Truck Assembly Complex.
|-
| G
| Saltillo Truck Assembly Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 1995
| 
| [[w:Ram Heavy Duty (fifth generation)|Ram HD pickup &amp; chassis cab]] (2019-)
|  Production began in 1995. As of 2025, also known as Saltillo Truck Heavy Duty Plant. &lt;br&gt; Past models:&lt;br&gt; [[w:Dodge Ram|Dodge Ram pickup]] (1995-2012),&lt;br&gt; [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 pickup]] (2013-2018),&lt;br&gt; [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 Classic pickup]] (2019-2023),&lt;br&gt; [[w:Ram pickup#Fourth generation (2009; DS)|Ram HD pickup &amp; chassis cab]] (2013-2018), [[w:Sterling Bullet|Sterling Truck Bullet]] (2008-2009)
|-
| 4
| Saltillo Truck Extension Assembly Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 2025
| 
| [[w:Ram 1500 (DT)|Ram 1500]] (DT) (2025-)
| Also known as Saltillo Truck Light Duty Plant. 2 new buildings were constructed for the new light duty plant. Production began in May 2025. Initially, production was for export but production for the domestic Mexican market began in February 2026. The plant also includes a seat assembly line, the first Stellantis plant in North America to integrate this process into its own production chain.
|-
| E
| Saltillo Van Assembly Plant 
| [[w:Saltillo|Saltillo]], [[w:Coahuila|Coahuila]]
| [[w:Mexico|Mexico]]
| 2013
| 
| [[w:Ram ProMaster|Ram ProMaster]] (2014-),&lt;br&gt; [[w:Ram ProMaster#E-Ducato and Ram ProMaster EV (2024)|Ram ProMaster EV]] (2024-)
| Production started in July 2013. &lt;br&gt; Past models: [[w:Fiat Ducato|Fiat Ducato]] (Export to Brazil/Argentina: 2018-2022)
|-
| N
| [[w:Sterling Heights Assembly|Sterling Heights Assembly Plant]] 
| [[w:Sterling Heights, Michigan|Sterling Heights, Michigan]]
| [[w:United States|United States]]
| 1984
| 
| [[w:Ram 1500 (DT)|Ram 1500]] (DT) (2019-)
| Located at 38111 Van Dyke Ave. The plant was originally built by the US Navy as a jet engine plant in 1953. It was called Naval Industrial Reserve Aircraft Plant and was owned by the US Navy. When the jet engine project was cancelled, the plant was transferred to the US Army, which contracted with Chrysler to build missiles at the plant, which was now known as the Michigan Ordinance Missile Plant. Chrysler began production of the PGM-11 Redstone missile at the Sterling Heights plant on September 27, 1954. The final Redstone was built in 1961. Chrysler also built the PGM-19 Jupiter missile at Sterling Heights from 1958-December 1960. Chrysler also built the first stage of the Saturn I rocket at the Sterling Heights plant. Chrysler vacated the Michigan Army Missile Plant at the end of 1969. Meanwhile, LTV Corp. (previously Ling-Temco-Vought) built the MGM-52 Lance missile at the Sterling Heights plant. The Army turned the plant over to the state of Michigan, which was then sold it to Volkswagen in 1980. VW converted the plant to automotive production and intended to make the Jetta there but VW's US sales declined and VW never ended up building anything there. VW then sold the plant to Chrysler in 1983. Chrysler LeBaron GTS and Dodge Lancer production began in September 1984 and ended on April 7, 1989. Shadow and Sundance production began on August 25, 1986 and ended on March 9, 1994. The Dodge Daytona was also moved from St. Louis to Sterling Heights in 1991 and was produced there through February 26, 1993. Chrysler then built a succession of midsize cars at Sterling Heights from June 1994. During Chrysler's bankruptcy in 2009, Sterling Heights Assembly was initially left behind in &quot;old Chrysler&quot; and was supposed to close by December 2010 but during 2010, &quot;new Chrysler&quot; changed its mind and bought the plant from &quot;old Chrysler&quot; for $20 million. The 2011 Chrysler 200 and Dodge Avenger sedans began production on December 6, 2010 followed by the Chrysler 200 Convertible in February 2011. The Chrysler 200 Convertible was also built for export to Europe as the Lancia Flavia from March 2012. The 2nd gen. Chrysler 200 sedan began production on March 14, 2014 and ended on December 2, 2016. The plant was then idled for a lengthy retooling to build body-on-frame pickups and began production of the new generation DT-series Ram 1500 in March 2018. &lt;br&gt; Past models: [[w:Dodge Lancer#1985–1989: Lancer|Dodge Lancer]] (1985-1989), [[w:Chrysler LeBaron#1985–1989 LeBaron GTS|Chrysler LeBaron GTS (H-body)]] (1985-1989), [[w:Plymouth Sundance|Plymouth Sundance]] (1987-1994), [[w:Dodge Shadow|Dodge Shadow]] (1987-1994), [[w:Dodge Daytona|Dodge Daytona]] (1992-1993), [[w:Chrysler Daytona|Chrysler Daytona]] (Canada: 1992-1993), [[w:Chrysler Cirrus|Chrysler Cirrus]] (1995-2000), [[w:Dodge Stratus|Dodge Stratus]] sedan (1995-2006), [[w:Plymouth Breeze|Plymouth Breeze]] (1996-2000), [[w:Chrysler Sebring|Chrysler Sebring]] sedan (2001-2010), [[w:Chrysler Sebring|Chrysler Sebring]]  convertible (2001-2006, 2008-2010), [[w:Dodge Avenger#Dodge Avenger sedan (2008–2014)|Dodge Avenger]] sedan (2008-2014), [[w:Chrysler 200|Chrysler 200]] sedan (2011-2017), [[w:Chrysler 200|Chrysler 200]] convertible (2011-2014), [[w:Chrysler 200#Lancia Flavia|Lancia Flavia]] (For export: 2012-2014)  
|-
| 
| Sterling Stamping Plant
| [[w:Sterling Heights, Michigan|Sterling Heights, Michigan]]
| [[w:United States|United States]]
| 1965
| 
| Stampings and assemblies including hoods, roofs, liftgates, side apertures, fenders, and floorpans
| Located at 35777 Van Dyke Ave. This plant is a separate facility but is located next door to the Sterling Heights Assembly Plant. Sterling Stamping is the largest stamping plant in the world. Sterling Stamping supplies stampings to many Chrysler assembly plants, not only Sterling Heights Assembly. The first stampings were produced in January 1965. 
|-
| W
| [[w:Toledo Complex|Toledo Assembly Complex - Toledo North Assembly Plant]] 
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 2001
| 
| [[w:Jeep Wrangler (JL)|Jeep Wrangler (JL)]] (2018-)
| Located at 4400 Chrysler Drive. Toledo North first built the Jeep Liberty, which began in April 2001. Dodge Nitro production began in August 2006 and ended on December 16, 2011. The 2nd gen. Jeep Liberty began production in July 2007. Jeep Liberty ended production on August 16, 2012. Toledo North then closed for retooling to build the all-new 2014 Cherokee. The Jeep Cherokee began production at Toledo North on June 24, 2013 and ended on April 6, 2017. The Cherokee was then moved to Belvidere Assembly. Toledo North was then retooled to build the Jeep Wrangler, which began on November 15th, 2017. The 4xe plug-in hybrid version of the Wrangler began production in December 2020. &lt;br&gt; Past models: [[w:Jeep Liberty|Jeep Liberty]] (2002-2012), [[w:Dodge Nitro|Dodge Nitro]] (2007-2011),&lt;br&gt; [[w:Jeep Cherokee (KL)|Jeep Cherokee]] (2014-2017),&lt;br&gt; [[w:Jeep Wrangler (JL)|Jeep Wrangler 4xe (JL)]] (2021-2025)
|-
| L
| [[w:Toledo Complex|Toledo Assembly Complex - Toledo Supplier Park Plant]] (South plant)
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 2001
| 
| [[w:Jeep Gladiator (JT)|Jeep Gladiator]] (2020-)
| Located along Stickney Ave. The Toledo Supplier Park Plant is built on the site of the former Stickney Ave. plant that became part of Chrysler in 1987 as part of the acquisition of AMC. That plant was acquired by Kaiser Jeep in 1964 from Autolite and was built in 1942. The Toledo Supplier Park Plant includes body and chassis operations in partnership with Kuka and Hyundai Mobis, respectively. The paint shop was originally run in partnership with Magna but Chrysler took over the paint operation in the first quarter of 2011. The Toledo Supplier Park Plant began Wrangler production in August 2006. Wrangler production ended on April 27, 2018. Gladiator pickup production began in March 2019. &lt;br&gt; Past models:&lt;br&gt; [[w:Jeep Wrangler (JK)|Jeep Wrangler (JK)]] (2007-2017),&lt;br&gt; [[w:Jeep Wrangler (JK)#2018 model year update|Jeep Wrangler JK]] (2018)
|-
| 
| [[w:Toledo Machining|Toledo Machining Plant]] 
| [[w:Perrysburg, Ohio|Perrysburg, Ohio]]
| [[w:United States|United States]]
| 1966
| 
| Steering Columns,&lt;br&gt; Torque Converters for 8-spd. rwd and 9-spd. fwd auto. transmissions
| Located at 8000 Chrysler Drive. Production began in 1966 and the plant was expanded in 1969. &lt;br&gt; Past products: Power Electronics module for Wrangler 4xe PHEV
|-
| T,&lt;br&gt; V (1985 only)
| [[w:Toluca Car Assembly|Toluca Car Assembly]] 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| 1968
| 
| [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass (MP)]] (2017-), [[w:Jeep Wagoneer S|Jeep Wagoneer S EV]]&lt;br&gt; (2024-2025, 2027-),&lt;br&gt; [[w:Jeep Cherokee (KM)|Jeep Cherokee (KM)]] (2026-), [[w:Jeep Recon|Jeep Recon EV]] (2026-)
| Originally part of Fabricas Automex, Chrysler's affiliate in Mexico. In 1968, Fabricas Automex was 45% owned by Chrysler. In December 1971, Chrysler increased its stake to 90.5% and changed the Mexican company's name to Chrysler de Mexico. Chrysler later bought another 8.8% stake, taking its total to 99.3%. Began production on December 9, 1968. An adjacent supplier park was opened in 2007. Journey production began in early 2008. PT Cruiser production ended on July 9, 2010. Fiat 500 production began in December 2010. Journey production ended in December 2020. Jeep Compass production began on January 16, 2017. &lt;br&gt; Past models: &lt;br&gt;  Mexico only: Dodge Dart (rwd), Dodge Dart K, Dodge Dart E, Chrysler Valiant Volaré (rwd), Chrysler Valiant Volaré K, Chrysler Valiant Volaré E, [[w:Dodge Magnum#First generation|Dodge Magnum]] [rwd] (1981-1982), [[w:Dodge Magnum#Second generation|Dodge Magnum 400/Magnum]] [fwd] (1983-1988), [[w:Chrysler Phantom|Chrysler Phantom]], [[w:Chrysler Shadow|Chrysler Shadow]], [[w:Chrysler Spirit|Chrysler Spirit]] &lt;br&gt; Export to US: [[w:Dodge Aries|Dodge Aries]] (1984-1989), [[w:Plymouth Reliant|Plymouth Reliant]] (1984-1989), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron coupe]] (1987-1989, 1992), [[w:Dodge Shadow|Dodge Shadow]] (1988, 1991-1994), [[w:Plymouth Sundance|Plymouth Sundance]] (1988, 1992-1994), [[w:Chrysler LeBaron#Third generation sedan (1990–1994)|Chrysler LeBaron sedan]] (1990-1994), [[w:Dodge Spirit|Dodge Spirit]] (1991-1995), [[w:Plymouth Acclaim|Plymouth Acclaim]] (1991-1995), [[w:Dodge Neon#First generation (1994)|Dodge Neon]] (1995-1999), [[w:Plymouth Neon#First generation (1994)|Plymouth Neon]] (1995-1999), [[w:Chrysler Sebring#Convertible (1996–2000)|Chrysler Sebring Convertible]] (1996-2000), [[w:Chrysler PT Cruiser|Chrysler PT Cruiser]] (2001-10), [[w:Dodge Journey|Dodge Journey]] (2009-2020),&lt;br&gt; [[w:Fiat 500 (2007)|Fiat 500]] (2012-2019), [[w:Fiat 500 (2007)#Fiat 500e (2013)|Fiat 500e]] (2013-2019)&lt;br&gt; Export to Brazil/Europe/Australia:&lt;br&gt; [[w:Fiat Freemont|Fiat Freemont]] (2011-2016)
|-
| 
| Toluca Stamping Plant 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| 1994
| 
| Stampings and assemblies including Body panels
| Part of the Toluca Assembly Complex.
|-
| 
| [[w:Trenton Engine Complex|Trenton Engine South Plant]] 
| [[w:Trenton, Michigan|Trenton, Michigan]]
| [[w:United States|United States]]
| 2010
| 
| [[w:Chrysler Pentastar engine|Chrysler Pentastar V6 engine]]
| Located at 2300 Van Horn Road. Production began in March 2010 with the 3.6L Pentastar V6. In 2022, Trenton South was upgraded with a flexible engine line that could build both the Classic and Upgrade versions of the 3.6L Pentastar V6. By the end of 2022, Pentastar Upgrade engine production moved from Trenton North to Trenton South and the older North plant ended production.
|-
| 
| Warren Stamping Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1949
| 
| Stampings and assemblies including roofs, tailgates, side apertures, fenders, and floorpans
| Located at 22800 Mound Road. This plant is a separate facility but is located next door to the Warren Truck Assembly Plant. The plant was expanded in 1952, 1964, 1965, and 1986. Warren Stamping supplies stampings to many Chrysler assembly plants, not only Warren Truck Assembly.
|-
| S (1970-), 1 (1967-1969),&lt;br&gt; 2 (For A-series)
| Warren Truck Assembly Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1938
| 
| [[w:Jeep Wagoneer (WS)|Jeep Grand Wagoneer]] (2022-), [[w:Jeep Wagoneer (WS)|Jeep Grand Wagoneer L]] (2023-)
| Located at 21500 Mound Road. Formerly known as the Dodge City Truck Plant. Also referred to as Warren Truck #1 in the 1970's when there were 2 other truck plants nearby. Began production in October 1938. The Mitsubishi Raider began production in September 2005 and ended on June 11, 2009. Dodge Dakota production ended on August 23, 2011. Full-size Jeep SUV production began in 2021. Ram 1500 Classic production ended in October 2024, ending production of Dodge/Ram trucks at Warren after 86 years. &lt;br&gt; Past models:&lt;br&gt; [[w:Dodge T-, V-, W-Series|Dodge T-, V-, W-Series]] (1939-1947), Dodge military trucks, [[w:Dodge Power Wagon#Civilian 1-ton Power Wagon &quot;Military-Type&quot;, Flat Fender Style&quot; (1945-1978)|Dodge Power Wagon]] (1946-1968), [[w:Dodge B series#Pickup truck|Dodge B series]] (1948-1953),&lt;br&gt; [[w:Dodge C series|Dodge C series]] (1954-1960),&lt;br&gt; [[w:Dodge Town Panel and Town Wagon|Dodge Town Panel/Town Wagon]] (1954-66), [[w:Dodge D series|Dodge D/W series]] (1961-1980), [[w:Dodge Ram|Dodge Ram pickup]] (1981-2012), [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 pickup]] (2013-2018), [[w:Ram pickup#Fourth generation (2009; DS)|Ram 1500 Classic pickup]] (2019-24), [[w:Dodge Ramcharger|Dodge Ramcharger]] (1977-1978, 1981-1985), [[w:Plymouth Trailduster|Plymouth Trailduster]] (1977-1978, 1981), [[w:Dodge M-series chassis|Dodge M-series chassis]] (1968-1979),&lt;br&gt; [[w:Dodge A100|Dodge A100/A108]] (1964-1970),&lt;br&gt; [[w:Dodge Dakota|Dodge Dakota]] (1987-2011),&lt;br&gt; [[w:Mitsubishi Raider|Mitsubishi Raider]] (2006-2009),&lt;br&gt; [[w:Jeep Wagoneer (WS)|Jeep Wagoneer]] (2022-2025),&lt;br&gt; [[w:Jeep Wagoneer (WS)|Jeep Wagoneer L]] (2023-2025),&lt;br&gt; [[w:Fargo Trucks|Fargo Trucks]] (For export)
|-
| R (1968-),&lt;br&gt; 9 (1959-1967)
| [[w:Windsor Assembly|Windsor Assembly]] 
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1929
| 
| [[w:Chrysler Pacifica (minivan)|Chrysler Pacifica (minivan)]] (2017-), [[w:Chrysler Voyager#Sixth generation (2020–present)|Chrysler Voyager]] (2020-2026), Chrysler Grand Caravan (Canada: 2021-),&lt;br&gt; [[w:Dodge Charger (2024)|Dodge Charger]] (2024-)
| Located at 2199 Chrysler Centre. Today's Windsor Assembly Plant was originally Windsor Plant 3 or Windsor Car Assembly Plant. Before the 1965 US-Canada Auto Pact, Windsor Assembly made most of the cars sold by Chrysler Canada, including some unique-to-Canada variations. On June 10, 1983, Windsor ended rwd car production and was converted to build fwd minivans. Windsor began building minivans on October 7, 1983. For the first 2 generations of Chrysler minivans, Windsor only built the SWB models. For the 3rd generation, Windsor built both SWB and LWB models. For the 4th generation, Windsor only built LWB models. The minivan-based Pacifica SUV began production in January 2003 and  ended production on November 23, 2007. Production of the VW Routan began in August 2008. Production of the Ram C/V began on August 31, 2011, and ended in early 2015. Pacifica minivan production began on February 29, 2016 followed by the PHEV version on December 1, 2016. Town &amp; Country production ended on March 21, 2016 while Dodge Grand Caravan production ended on August 21, 2020. Production of the electric Charger Daytona began in December 2024 followed by the gas-powered Charger Sixpack in December 2025. &lt;br&gt; Past models: [[w:Chrysler Imperial|Chrysler Imperial]] (1929-1937) [https://www.web.imperialclub.info/registry/vin_decode.htm#1931-54], [[w:Dodge Kingsway|Dodge Kingsway]] (Canada: 1940-41, 1951-52), [[w:Dodge Regent|Dodge Regent]] (Canada: 1951-1959), [[w:Dodge Crusader|Dodge Crusader]] (Canada: 1951-1958), [[w:Dodge Mayfair|Dodge Mayfair]] (Canada: 1953-1959), [[w:Dodge Viscount|Dodge Viscount]] (Canada: 1959), [[w:Dodge Custom Royal|Dodge Custom Royal]] (1959), [[w:Dodge Dart|Dodge Dart (full-size)]] (1961), [[w:DeSoto Firedome|DeSoto Firedome]] (1959), [[w:Chrysler Windsor|Chrysler Windsor]] (1957-1966), [[w:Chrysler Saratoga|Chrysler Saratoga]] (1959-1963), [[w:Chrysler 300 non-letter series|Chrysler Saratoga 300]] (1964-1965), [[w:Chrysler Newport#1961–1964|Chrysler Newport]] (1961-1963), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1963-64, 1966), [[w:Plymouth Savoy|Plymouth Savoy]] (1959-1964), [[w:Plymouth Fury|Plymouth Fury]] (1959-1970), [[w:Dodge Polara|Dodge Polara]] (1960, 1964-1969), Dodge 220 (Canada: 1963), [[w:Dodge 330|Dodge 330]] (1963-1965), [[w:Dodge 440|Dodge 440]] (1963-1964), [[w:Dodge Monaco|Dodge Monaco]] (1967-1968), [[w:Plymouth Valiant#Canada (1960–1966)|Valiant]] (Canada: 1960-1966), [[w:Plymouth Barracuda#First generation (1964–1966)|Valiant Barracuda]] (Canada: 1964-1965), [[w:Plymouth Valiant|Plymouth Valiant]] (1970-1974), [[w:Plymouth Duster|Plymouth Duster]] (1970), [[w:Dodge Dart|Dodge Dart (compact)]] (1966, 1970-1975), [[w:Plymouth Satellite#Third generation (1971–1974)|Plymouth Satellite]] (1972-1974),  [[w:Plymouth GTX|Plymouth GTX]] (1971), [[w:Plymouth Road Runner#Second generation (1971–1974)|Plymouth Road Runner]] (1971-1974), [[w:Dodge Charger (1966)#Fourth generation|Dodge Charger]] (1975-1978), [[w:Dodge Magnum#US and Canada (1978–1979)|Dodge Magnum]] (1978-1979), [[w:Chrysler Cordoba|Chrysler Cordoba]] (1975-1983), [[w:Dodge Mirada|Dodge Mirada]] (1980-1983), [[w:Imperial (automobile)#Sixth generation (1981–1983)|Imperial]] (1981-1983), [[w:Chrysler Newport#1979–1981|Chrysler Newport]] (1979), [[w:Dodge Diplomat|Dodge Diplomat]] (1981-1983), [[w:Plymouth Gran Fury#1982–1989|Plymouth Gran Fury]] (1982-83), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle]] (Canada: 1981-1982), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle Salon]] (Canada: 1983), [[w:Chrysler LeBaron#First generation (1977–1981)|Chrysler LeBaron]] (1981), [[w:Chrysler New Yorker#1982|Chrysler New Yorker]] (1982), [[w:Chrysler Fifth Avenue#1982–1989: The M-body years|Chrysler New Yorker Fifth Avenue]] (1983), [[w:Plymouth Voyager|Plymouth Voyager]] (1984-'00), [[w:Plymouth Voyager|Plymouth Grand Voyager]] (1996-2000), [[w:Dodge Caravan|Dodge Caravan]] (1984-2000), [[w:Dodge Caravan|Dodge Grand Caravan]] (1996-2020), [[w:Chrysler Town &amp; Country (minivan)|Chrysler Town &amp; Country]] (2001-2016), [[w:Chrysler Voyager|Chrysler Voyager]] (2000), [[w:Chrysler Voyager|Chrysler Grand Voyager]] (2000), [[w:Chrysler minivans (S)#Cargo van|Dodge Mini Ram Van]] (1984-1988), [[w:Chrysler minivans (RT)#2011 revision|Ram C/V]] (2012-2015), [[w:Volkswagen Routan|Volkswagen Routan]] (2009-14), [[w:Chrysler Voyager#Lancia Voyager|Lancia Voyager]] (For export: 2012-2015), [[w:Chrysler Pacifica (crossover)|Chrysler Pacifica (SUV)]] (2004-2008)
|-
| 
| CpK Interior Products, Inc. - Belleville Operations
| [[w:Belleville, Ontario|Belleville]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 2010 (became part of Chrysler)
| 
| Components for Automotive Interiors
| Located at 134 River Rd. Formed in 2010 as a subsidiary of Chrysler through the buyout of 3 Collins and Aikman plants in Canada after  Collins and Aikman went bankrupt.
|-
| 
| CpK Interior Products, Inc. - Guelph Operations
| [[w:Guelph|Guelph]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 2010 (became part of Chrysler)
| 
| Components for Automotive Interiors
| Located at 500 Laird Rd. Formed in 2010 as a subsidiary of Chrysler through the buyout of 3 Collins and Aikman plants in Canada after  Collins and Aikman went bankrupt.
|-
| 
| CpK Interior Products, Inc. -&lt;br&gt; Port Hope Operations
| [[w:Port Hope, Ontario|Port Hope]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 2010 (became part of Chrysler)
| 
| Components for Automotive Interiors
| Located at 128 Peter St. Formed in 2010 as a subsidiary of Chrysler through the buyout of 3 Collins and Aikman plants in Canada after  Collins and Aikman went bankrupt.
|-
| 4
| Arab American Vehicles Company (AAV)
| [[w:Cairo|Cairo]]
| [[w:Egypt|Egypt]]
| 1978 (production began) &lt;br&gt; 1987 (became part of Chrysler)
| 
| [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee L]] (2025-), [[w:Citroën C4#Third generation (C41; 2020)|Citroën C4X]] (2025-)
| Arab American Vehicles Company is a joint venture between the [[w:Arab Organization for Industrialization|Arab Organization for Industrialization]], which holds 51%, and Stellantis, which holds the other 49%. AAV was originally established in 1977 as a joint venture  with [[w:American Motors Corporation|AMC]] to produce Jeeps. Production began in 1978. It became part of Chrysler when Chrysler bought AMC in 1987. It continued to be a part of subsequent corporate entities DaimlerChrysler, Chrysler LLC, Chrysler Group LLC, [[w:Fiat Chrysler Automobiles|FCA]], and [[w:Stellantis|Stellantis]]. Production of the Jeep J8, a light military vehicle based on the JK Wrangler, began on November 13, 2008. Jeep Grand Cherokee L production began in September 2024. Citroen C4X production began in April 2025. AAV has also produced vehicles for other automakers including Toyota. Toyota Fortuner SUV production began in April 2012. &lt;br&gt; Past models: Jeep CJ6, Jeep Wagoneer (SJ), Jeep AM720 military vehicle, [[w:Jeep Wrangler (YJ)|Jeep Wrangler (YJ)]], [[w:Jeep Wrangler (TJ)|Jeep TJL]], [[w:Jeep Wrangler (JK)#Military Jeep J8 (2007–present)|Jeep J8]] (2008-2019),  [[w:Jeep Cherokee (XJ)|Jeep Cherokee (XJ)]], [[w:Jeep Liberty (KJ)|Jeep Cherokee (KJ)]], [[w:Jeep Liberty (KK)|Jeep Cherokee (KK)]], [[w:Jeep Grand Cherokee (WK2)|Jeep Grand Cherokee (WK2)]]
|}

==Current non-Chrysler FCA/Stellantis Factories Making Chrysler Group Vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Current Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| Y (700),&lt;br&gt; 9 (ProMaster Rapid),&lt;br&gt; 3 (Vision)
| Betim Plant
| [[w:Betim|Betim]], [[w:Minas Gerais|Minas Gerais]]
| [[w:Brazil|Brazil]]
| 1973
| 
| [[w:RAM 700|RAM 700]] (2015-),&lt;br&gt; [[w:ProMaster Rapid|Ram V700 Rapid]] (Peru)&lt;br&gt; Related models:&lt;br&gt; [[w:Fiat Strada|Fiat Strada]] ('99-),&lt;br&gt; [[w:Fiat Fiorino#Latin America (2013–present)|Fiat Fiorino]] ('14-)
| Fiat plant. &lt;br&gt; Past Chrysler Group models:&lt;br&gt; [[w:Dodge Vision|Dodge Vision]] (Mexico: 2015-2018),&lt;br&gt; [[w:ProMaster Rapid|Ram ProMaster Rapid]] (Mexico: '18-'24)
|-
| U
| Cordoba Plant
| [[w:Córdoba, Argentina|Córdoba]], [[w:Córdoba Province, Argentina|Córdoba Province]]
| [[w:Argentina|Argentina]]
| 1995
| 
| [[w:Peugeot Landtrek|Ram Dakota]] (2026-)
| Fiat plant.
|-
| F
| [[w:FCA India Automobiles|FCA India Automobiles Private Limited]]
| [[w:Ranjangaon|Ranjangaon]], [[w:Pune district|Pune district]], [[w:Maharashtra|Maharashtra]]
| [[w:India|India]]
| 1997
| 
| [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass]],&lt;br&gt; [[w:Jeep Wrangler (JL)|Jeep Wrangler (JL)]],&lt;br&gt; [[w:Jeep Meridian|Jeep Meridian/Commander]],&lt;br&gt; [[w:Jeep Grand Cherokee#Fifth generation (WL; 2021)|Jeep Grand Cherokee]]
| Originally established as a 50/50 joint venture between Fiat and [[w:Tata Motors|Tata Motors]] called Fiat India Automobiles Private Limited. On June 1, 2017, Jeep Compass production began in India, the first Jeep built in India under its own brand. The JL-series Wrangler began to be assembled in India in 2021. The Jeep Meridian began production in May 2022. The Meridian is also exported to Japan as the Commander. The Jeep Grand Cherokee began assembly in India in November 2022. 
|-
| K
| Goiana Plant
| [[w:Goiana|Goiana]], [[w:Pernambuco|Pernambuco]]
| [[w:Brazil|Brazil]]
| 2015
|
| [[w:Jeep Renegade|Jeep Renegade]], [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass]],&lt;br&gt; [[w:Jeep Commander (2022)|Jeep Commander]], [[w:Ram Rampage|Ram Rampage]]&lt;br&gt; Related models: [[w:Fiat Toro|Fiat Toro]]
| [[w:Fiat Chrysler Automobiles|FCA]] plant. Production at Goiana began with the Jeep Renegade in February 2015. &lt;br&gt; Past Chrysler Group models: [[w:Ram 1000|Ram 1000]]
|-
| P
| Melfi Plant (formerly SATA = Società Automobilistica Tecnologie Avanzate [Advanced Technologies Automotive Company])
| [[w:Melfi|Melfi]], [[w:Province of Potenza|Province of Potenza]]
| [[w:Italy|Italy]]
| 1993
|
| [[w:Jeep Compass#Third generation (J4U; 2025)|Jeep Compass (J4U)]]&lt;br&gt; (Europe: '26-)
| Fiat plant. Jeep production began at Melfi in 2014 with the Renegade. Renegade production at Melfi ended on October 17, 2025. Production of the 3rd gen. Compass began on October 29, 2025. &lt;br&gt; Past Chrysler Group models:&lt;br&gt; [[w:Jeep Renegade|Jeep Renegade]] (US/Can.: '15-'23, Europe: '15-'25),&lt;br&gt; [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass (MP)]] (Europe: '20-'25) &lt;br&gt; Related models:&lt;br&gt; [[w:Fiat 500X|Fiat 500X]] (US/Can.: '16-'23,&lt;br&gt; Europe: '15-'24)
|-
| B
| Porto Real Plant
| [[w:Porto Real|Porto Real]], [[w:Rio de Janeiro (state)|Rio de Janeiro state]]
| [[w:Brazil|Brazil]]
| 2000
|
| [[w:Jeep Avenger|Jeep Avenger]]
| PSA plant. The Jeep Avenger is the first Jeep to be made in a former PSA plant. 
|-
| U (2027-), 6 (2015-2022)
| [[w:Tofaş|Tofaş]]
| [[w:Bursa|Bursa]]
| [[w:Turkey|Turkey]]
| 1971
|
| [[w:Citroën Jumpy#Ram ProMaster City|Ram ProMaster City]] (2027-)
| Originally a Fiat joint venture, it is now 37.8% owned by Stellantis, 37.8% owned by [[w:Koç Holding|Koç Holding]], and 24.3% publicly traded on the Istanbul Stock Exchange. &lt;br&gt; Past Chrysler Group models: &lt;br&gt; [[w:Fiat Doblò#Ram ProMaster City|Ram ProMaster City]] (2015-2022),&lt;br&gt; [[w:Chrysler Neon#Third generation (2016)|Dodge Neon]]&lt;br&gt; (Mexico &amp; Middle East: 2017-2020),&lt;br&gt; [[w:Fiat Fiorino#Europe (2007–2024)|Ram V700 City]] (Chile: 2018-2023)
|-
| J,&lt;br&gt; 5 (Ypsilon)
| Tychy Plant
| [[w:Tychy|Tychy]], [[w:Silesian Voivodeship|Silesian Voivodeship]]
| [[w:Poland|Poland]]
| 1975
|
| [[w:Jeep Avenger|Jeep Avenger]]
| Fiat plant. Production began in September 1975 when the plant was owned by Polish automaker [[w:Fabryka Samochodów Małolitrażowych|FSM]], which built Fiat-based models. Fiat took over FSM in 1992. Fiat subsequently became [[w:Fiat Chrysler Automobiles|FCA]] and then Stellantis. Jeep Avenger production began on January 31, 2023. &lt;br&gt; Past Chrysler Group models:&lt;br&gt; [[w:Chrysler Ypsilon|Chrysler Ypsilon]] (UK/Ireland/Japan)
|}

==Current partner factories making Chrysler Group vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Current Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 1
| GAC Hangzhou plant
| [[w:Hangzhou|Hangzhou]], [[w:Zhejiang|Zhejiang]]
| [[w:China|China]]
| 2021 (production began for Chrysler)
|
| [[w:Trumpchi GS5#Dodge Journey|Dodge Journey]] (Mexico: 2022-)
| [[w:GAC Group|GAC]] plant. 
|-
| 3
| GAC Yichang plant
| [[w:Yichang|Yichang]], [[w:Hubei|Hubei]]
| [[w:China|China]]
| 2024 (production began for Chrysler)
|
| [[w:Dodge Attitude#Fourth generation (2025)|Dodge Attitude]] (Mexico: 2025-)
| [[w:GAC Group|GAC]] plant. 
|-
| 5
| Shenzhen Baoneng Motor Co., Ltd.
| [[w:Shenzhen|Shenzhen]], [[w:Guangdong|Guangdong]]
| [[w:China|China]]
| 2024 (production began for Chrysler)
|
| [[w:Peugeot Landtrek|Ram 1200]] (Mexico: 2025-)
| [[w:Baoneng Group#Automotive business|Shenzhen Baoneng Motor Co., Ltd.]] plant. 
|}

==Former factories== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Closed
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
|
| Ajax Trim plant
| [[w:Ajax, Ontario|Ajax]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1953, 1964 (became part of Chrysler)
| 2003
| Automotive Soft Trim Components, Seat Cushion and Seatback Covers, Foam-in-place Covers
| Built in 1953 by Canadian Automotive Trim. Purchased by Chrysler in 1964. Closed by December 2003.
|-
| J (1989-1992),&lt;br&gt; B (1981-1988),&lt;br&gt; 7-8 (1966-1980),&lt;br&gt; T (1958-1966) 
| [[w:Brampton Assembly (AMC)|AMC Brampton Assembly]]
| [[w:Brampton|Brampton]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]] 
| 1961,&lt;br&gt; 1987 (became part of Chrysler)
| 1992
| [[w:Jeep Wrangler (YJ)|Jeep Wrangler (YJ)]] (1987-92), [[w:Jeep CJ#CJ-5|Jeep CJ-5]] (1979-1980),&lt;br&gt; [[w:Jeep CJ#CJ-7|Jeep CJ-7]] (1979-1980),&lt;br&gt; [[w:AMC Eagle|AMC Eagle]] (1981-1987), [[w:AMC Eagle|Eagle Wagon]] (1988), [[w:AMC Concord|AMC Concord]] (1978, 1981-1983), [[w:AMC Spirit|AMC Spirit]] (1983), [[w:AMC Hornet|AMC Hornet]] (1970-77), [[w:AMC Gremlin|AMC Gremlin]] (1970-1978),&lt;br&gt; [[w:AMC Rebel|AMC Rebel]] (1968-1970), [[w:Rambler Rebel#Fifth generation|Rambler Rebel]] (1967), [[w:Rambler Classic|Rambler Classic]] (1961-1966),&lt;br&gt; [[w:AMC Ambassador|AMC Ambassador]] (1966-1968), [[w:AMC Ambassador|Rambler Ambassador]] ('63-'65), [[w:Rambler American|Rambler American]] (1962-68), [[w:Rambler American|AMC Rambler]] (1969)
| [[w:American Motors Corporation|AMC]] plant. Became part of Chrysler in the 1987 buyout of AMC. Located at at the corner of Kennedy Road South and Steeles Avenue East. Production began on January 26, 1961 with the Rambler Classic. This was the last plant to produce AMC vehicles. Eagle Wagon (formerly AMC Eagle) ended production on December 11, 1987. Production ended in April 1992 and Jeep Wrangler production was moved to Toledo, OH. Buildings on the west side of the plant were demolished in 2005 and buildings on the east side were demolished in 2007. A Lowe's and a Wal-Mart now occupy some of the former plant site.
|-
| 7
| [[w:Beijing Jeep|Beijing Jeep]]/&lt;br&gt;Beijing Benz-DaimlerChrysler Automotive Co Ltd.
| [[w:Beijing|Beijing]]
| [[w:China|China]]
| 1985 (prod. began),&lt;br&gt; 1987 (became part of Chrysler)
| 2009 (Non-Mercedes prod. ended)
| [[w:Jeep Cherokee (XJ)|Jeep BJ2021/BJ7250/2500/2700 (XJ)]], [[w:Jeep Grand Cherokee (WJ)|Jeep 4000/4700 (WJ)]], [[w:Chrysler 300#First generation (2005)|Chrysler 300]],&lt;br&gt; [[w:Chrysler Sebring#Third generation (JS; 2007)|Chrysler Sebring sedan]]&lt;br&gt;Other models built:&lt;br&gt; [[w:Mitsubishi Pajero Sport#First generation (K80/K90/PA/PA II; 1996)|Mitsubishi Pajero Sport]], [[w:Mitsubishi Outlander#First generation (CU/ZE/ZF; 2001)|Mitsubishi Outlander]],&lt;br&gt; [[w:Mercedes-Benz E-Class (W211)|Mercedes-Benz E-Class (W211)]], [[w:Mercedes-Benz C-Class (W204)|Mercedes-Benz C-Class (W204)]]
| Originally established on May 5, 1983 as a 50/50 joint venture between [[w:American Motors Corporation|AMC]] and [[w:BAIC Group|BAIC]] called Beijing Jeep Corp. Production began on Sept. 26, 1985. In 1987, Chrysler Corp. took over AMC and its 50% stake in Beijing Jeep. Mitsubishi SUVs were added to Beijing Jeep's production in 2003 with the Pajero Sport, followed by the Outlander in 2004. In 2004, Beijing Jeep was renamed Beijing Benz-DaimlerChrysler Automotive Co Ltd., following the creation of DaimlerChrysler in 1998. Mercedes-Benz production began in 2005. Chrysler brand sedan production began in 2006 with the 300, followed by the Sebring in 2007. After DaimlerChrysler broke up in 2007, production for the Chrysler Group ended in 2009. The joint venture company was then renamed Beijing Benz in 2010 and Chrysler was removed from the venture which Daimler kept for itself to produce Mercedes-Benz models.
|-
| 3
| Campo Largo Assembly
| [[w:Campo Largo, Paraná|Campo Largo]], [[w:Paraná (state)|Paraná (state)]]
| [[w:Brazil|Brazil]]
| 1998
| 2001
| [[w:Dodge Dakota#Second generation (1997–2004)|Dodge Dakota]]
| Plant built vehicles in cooperation with suppliers.
|-
| V
| [[w:Conner Avenue Assembly|Conner Avenue Assembly]] 
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1996
| 2017
| [[w:Dodge Viper|Dodge Viper]] &lt;br&gt; GTS: '96, &lt;br&gt; All models: &lt;br&gt; '97-'06, '08-'10, '13-'17, [[w:Plymouth Prowler|Plymouth Prowler]]&lt;br&gt; ('97, '99-'01),&lt;br&gt; [[w:Chrysler Prowler|Chrysler Prowler]] ('01-'02),&lt;br&gt; [[w:Viper engine|8.0L/8.3L/8.4L aluminum &lt;br&gt; Viper V10 engine]] &lt;br&gt;(5/01-2017)
| Actually located at 20000 Connor Street. The plant was originally built in 1966 to make spark plugs by Champion. After Champion was bought by Cooper Industries in 1990, the plant was closed. It remained empty until Chrysler bought it in 1995. Viper production was moved to the Connor Avenue plant from the New Mack plant beginning with the GTS coupe for 1996, followed by the RT/10 roadster for 1997. Prowler production began in May 1997 and ended on February 15, 2002. Production of the Viper's aluminum V10 engine was moved to Connor Avenue, where it was built alongside the Viper itself, in May 2001 from the Mound Road Engine Plant, which closed in 2002. Viper production ended on July 2, 2010 and the plant was dormant until production restarted in December 2012. Production ended on Aug. 31, 2017. In 2018, the plant was renamed Connor Center, a meeting and display space that will showcase Chrysler’s concept and historic vehicle collection.
|-
| 2
| Cordoba Assembly
| [[w:Córdoba, Argentina|Córdoba]], [[w:Córdoba Province, Argentina|Córdoba Province]]
| [[w:Argentina|Argentina]]
| 1997
| 2001
| [[w:Jeep Grand Cherokee (ZJ)|Jeep Grand Cherokee (ZJ)]] (1997-1998), [[w:Jeep Grand Cherokee (WJ)|Jeep Grand Cherokee (WJ)]] (1999-2001), [[w:Jeep Cherokee (XJ)|Jeep Cherokee (XJ)]] (1998-01)
| Opened in the 2nd quarter of 1997, building the Jeep Grand Cherokee. Jeep Cherokee production was added in 1998. 
|-
|E
| [[w:Diamond-Star Motors|Diamond-Star Motors/Mitsubishi Motors Manufacturing America/Mitsubishi Motors North America Manufacturing Division]]
| [[w:Normal, Illinois|Normal, Illinois]]
| [[w:United States|United States]]
| 1988
| 2005 (end of Chrysler production)/&lt;br&gt; 2015 (end of Mitsubishi production)
| [[w:Plymouth Laser|Plymouth Laser]] (1990-1994),&lt;br&gt; [[w:Eagle Talon|Eagle Talon]] (1990-1998),&lt;br&gt; [[w:Eagle Summit#First generation (1989–1992)|Eagle Summit 4-d]] (1991-1992),&lt;br&gt; [[w:Dodge Avenger#Dodge Avenger Coupe (1995–2000)|Dodge Avenger]] (1995-2000),&lt;br&gt; [[w:Dodge Stratus#Stratus coupe (2001–2005)|Dodge Stratus Coupe]]&lt;br&gt; (2001-2005),&lt;br&gt; [[w:Chrysler Sebring|Chrysler Sebring Coupe]]&lt;br&gt; (1995-2005),&lt;br&gt;  [[w:Mitsubishi Eclipse|Mitsubishi Eclipse]] (1990-2012),&lt;br&gt; [[w:Mitsubishi Mirage#Third generation (1987)|Mirage sedan]] (1991-1992),&lt;br&gt; [[w:Mitsubishi Galant|Galant]] (1994-2012),&lt;br&gt; [[w:Mitsubishi Endeavor|Endeavor]] (2004-2011),&lt;br&gt; [[w:Mitsubishi ASX#First generation (GA; 2010)|Outlander Sport/RVR]] (2013-15)
| Originally established as Diamond-Star Motors, a 50/50 joint venture between Chrysler and Mitsubishi which assembled both Chrysler and Mitsubishi vehicles. Production began in September 1988. In October 1991, Chrysler sold its 50% stake in the plant to Mitsubishi but production for Chrysler continued under contract. On May 24, 1993, production of the Mitsubishi Galant began at the Diamond-Star plant. In July 1995, the plant was renamed Mitsubishi Motors Manufacturing America. In January 2002, the plant was renamed Mitsubishi Motors North America Manufacturing Division. In January 2003, production of the Mitsubishi Endeavor began, the first SUV built at the Mitsubishi plant. In February 2005, production of vehicles for Chrysler ended. All further production was only of Mitsubishi-branded vehicles. In mid-2012, the plant began producing the Mitsubishi Outlander Sport. The Outlander Sport is sold as the RVR in Canada. On November 30, 2015, vehicle production ended. The Mitsubishi plant produced 3,283,549 vehicles. The plant continued to produce replacement parts until May 2016, when the plant closed completely. In June 2016, the plant was sold to liquidation firm Maynards Industries. In January 2017, EV startup [[w:Rivian|Rivian Automotive]] bought the former Mitsubishi plant. Rivian began production at the Normal, IL plant in September 2021 with the [[w:Rivian R1T|R1T]] electric pickup.
|-
| U
| [[w:Eurostar Automobilwerk|Eurostar]] - Chrysler Graz Assembly
| [[w:Graz|Graz]], [[w:Styria|Styria]]
| [[w:Austria|Austria]]
| 1991
| 2002
| [[w:Chrysler Voyager#Fourth generation (2001–2007)|Chrysler Voyager/Grand Voyager]] (1992-2002), [[w:Chrysler PT Cruiser|Chrysler PT Cruiser]] (2002)
| Originally, a 50/50 joint venture between Chrysler and Steyr-Daimler-Puch founded in 1990. The Eurostar plant is next to the Steyr Fahrzeugtechnik plant solely owned by Steyr-Daimler-Puch. Production of the Chrysler Voyager and Grand Voyager minivans began in October 1991. This was the 2nd generation Chrysler minivan. The 3rd generation began production on September 25, 1995. In 1996, production of right-hand drive minivans began. The 4th generation began production in January 2001. Production of the PT Cruiser began in July 2001 on the same line as the Voyager minivans. In 1999, DaimlerChrysler bought the 50% stake in Eurostar held by Steyr-Daimler-Puch Fahrzeugtechnik, now majority owned by Magna International, making Eurostar a subsidiary of DaimlerChrysler. DaimlerChrysler sold 100% of Eurostar to Magna Steyr in July 2002. PT Cruiser production in Austria ended and was consolidated in Toluca, Mexico. Production of the Chrysler Voyager and Grand Voyager minivans moved next door to the main Magna Steyr plant for 2003. Magna International had acquired a majority holding of 66.8% in Steyr-Daimler-Puch in 1998 and acquired the rest by 2002 when it was renamed Magna Steyr. 
|-
| 3 (1959),&lt;br&gt; E (1958)
| Evansville Assembly
| [[w:Evansville, Indiana|Evansville, Indiana]]
| [[w:United States|United States]]
| 1919, 1928 (became part of Chrysler)
| 1959 
| Graham Brothers trucks (through 1932),&lt;br&gt; Dodge Brothers trucks &lt;br&gt; (through 1932),&lt;br&gt; Plymouth cars (1936-1958),&lt;br&gt; Dodge cars (1937-1938),&lt;br&gt; [[w:Plymouth Savoy|Plymouth Savoy]] (1959), [[w:Plymouth Belvedere|Plymouth Belvedere]] (1959), [[w:Plymouth Fury|Plymouth Fury]] (1959)
| Located at 1625 N. Garvin St. Built in 1919 by Graham Brothers Truck Company to build trucks. In 1925, Dodge Brothers bought a controlling 51% stake in Graham Brothers and then bought the rest in 1926, completely merging the 2 companies. This gave Dodge Brothers plants in Evansville, IN and Stockton, CA. Dodge Brothers was bought by the Chrysler Corporation on July 31, 1928. At that point, trucks with a Dodge Brothers nameplate were rated as a half-ton; larger rated trucks were sold under the Graham Brothers name. On January 1, 1929, the Graham Brothers brand was eliminated, and all trucks produced became Dodge trucks. In 1932, Chrysler closed the Evansville plant due to the Great Depression. In 1935, as the economy improved, Chrysler reopened the Evansville plant and renovated and expanded it. It began building Plymouth cars for 1936. Dodge cars were also built for 1937 and 1938. During World War II, the plant became the Evansville Ordinance Plant, which produced more than 3.26 billion ammunition  cartridges - about 96% of all the .45 automatic ammunition produced for all the armed forces. The Evansville Ordinance Plant also rebuilt 1,600 Sherman tanks and 4,000 military trucks. After the war ended, Plymouth car production resumed. However, in the early 1950s, during the Korean War, the Evansville plant retooled and dedicated about a third of its space and manpower to building 60-foot aluminum hulls for Grumman  UF-1 Albatross air-sea rescue planes for the Navy and Coast Guard. Evansville built its 1 millionth Plymouth in March 1953. The plant was closed in 1959 and was replaced by the larger, more modern St. Louis plant in Fenton, MO, which had access to more railroad lines for shipping than Evansville did. 
|-
| 
| Evansville Stamping
| [[w:Evansville, Indiana|Evansville, Indiana]]
| [[w:United States|United States]]
| 1935, 1953 (became part of Chrysler)
| 1959 
| Body panel stampings
| Opened by Briggs Manufacturing Company when Chrysler reopened Evansville Assembly in 1935 to build Plymouth cars. One of the plants Chrysler acquired from Briggs Manufacturing in 1953. Made body panels for the nearby Evansville Assembly plant. Closed when Evansville Assembly closed in 1959.
|-
| A
| [[w:GAC Fiat Chrysler|GAC Fiat Chrysler]]: Changsha plant
| [[w:Changsha|Changsha]], [[w:Hunan|Hunan province]]
| [[w:China|China]]
| 2012 (Fiat prod. began),&lt;br&gt; 2015 (prod. began for Chrysler)
| 2022
| [[w:Jeep Cherokee (KL)|Jeep Cherokee (K4)]],&lt;br&gt; [[w:Jeep Grand Commander|Jeep Grand Commander/&lt;br&gt;Commander (K8)]]&lt;br&gt;Other models built:&lt;br&gt; [[w:Fiat Viaggio|Fiat Viaggio]], [[w:Fiat Ottimo|Fiat Ottimo]]
| Originally established in 2010 as a 50/50 joint venture between [[w:Fiat S.p.A.|Fiat]] and [[w:GAC Group|GAC]] called GAC Fiat Automobiles Co., Ltd. Fiat production began with the Viaggio sedan in 2012, followed by the Ottimo hatchback in 2014. In January 2015, GAC Fiat was renamed GAC Fiat Chrysler Automobiles Co., Ltd. to reflect the creation of [[w:Fiat Chrysler Automobiles|Fiat Chrysler Automobiles]] in 2014 and the inclusion of Chrysler in the joint venture, which would now also produce Jeeps. In October 2015, Jeep Cherokee production began, followed by the Grand Commander in 2018. The Jeep Commander was a 2-row version of the 3-row Grand Commander. In 2022, all production ended and the joint venture was terminated.
|-
| B
| [[w:GAC Fiat Chrysler|GAC Fiat Chrysler]]: Guangzhou plant
| [[w:Guangzhou|Guangzhou]], [[w:Guangdong|Guangdong province]]
| [[w:China|China]]
| 2016
| 2022
| [[w:Jeep Renegade|Jeep Renegade (BQ)]],&lt;br&gt; [[w:Jeep Compass#Second generation (MP/552; 2016)|Jeep Compass (M4/553)]]
| Originally established in 2010 as a 50/50 joint venture between [[w:Fiat S.p.A.|Fiat]] and [[w:GAC Group|GAC]] called GAC Fiat Automobiles Co., Ltd. In January 2015, GAC Fiat was renamed GAC Fiat Chrysler Automobiles Co., Ltd. to reflect the creation of [[w:Fiat Chrysler Automobiles|Fiat Chrysler Automobiles]] in 2014 and the inclusion of Chrysler in the joint venture, which would now also produce Jeeps. A 2nd plant was opened in Guangzhou in 2016 building the Jeep Renegade, followed by the Compass. In 2022, all production ended and the joint venture was terminated.
|-
| B (1968-1980),&lt;br&gt; 2 (1960-1967),&lt;br&gt; 2 (1959)
| [[w:Dodge Main|Hamtramck Assembly (Dodge Main)]]
| [[w:Hamtramck, Michigan|Hamtramck, Michigan]]
| [[w:United States|United States]]
| 1911,&lt;br&gt; 1928 (became part of Chrysler)
| 1980 
| Dodge (1914-1958),&lt;br&gt; [[w:Dodge Coronet#Fourth generation (1957–1959)|Dodge Coronet]] (1959),&lt;br&gt; [[w:Dodge Royal#Third generation (1957–1959)|Dodge Royal]] (1959),&lt;br&gt; [[w:Dodge Custom Royal|Dodge Custom Royal]] (1959), [[w:DeSoto Firesweep|DeSoto Firesweep]] (1957-1959),&lt;br&gt; [[w:Dodge Matador|Dodge Matador]] (1960),&lt;br&gt; [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962),&lt;br&gt; [[w:Dodge Polara|Dodge Polara]] (1960-1964),&lt;br&gt; [[w:Dodge 330|Dodge 330]] (1963-1964),&lt;br&gt; [[w:Dodge 440|Dodge 440]] (1963-1964),&lt;br&gt; [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1975), [[w:Plymouth Duster|Plymouth Duster]] (1970-1975), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1969, 1972-1975), [[w:Dodge_Dart#1971|Dodge Dart Demon]] (1971-1972),&lt;br&gt; [[w:Dodge Charger (1966)|Dodge Charger]] (1967-1969), [[w:Dodge Charger Daytona#First generation (1969)|Dodge Charger Daytona]] ('69), [[w:Plymouth Barracuda|Plymouth Barracuda]] (1964-74), [[w:Dodge Challenger (1970)|Dodge Challenger]] (1970-1974), [[w:Dodge Aspen|Dodge Aspen]] (1976-1980), [[w:Plymouth Volaré|Plymouth Volaré]] (1976-1980),&lt;br&gt; Engines, Foundry
| Located at 7900 Joseph Campau Ave. This plant predated Dodge being part of Chrysler Corp. On November 4, 1914, the first Dodge Brothers passenger car was produced at the Hamtramck plant. Prior to that, Dodge Brothers made components for other automakers, primarily Ford. The Hamtramck plant was fully vertically integrated, capable of building almost every part needed to build a complete car. Dodge Brothers was bought by the Chrysler Corporation on July 31, 1928. Even after the Chrysler takeover, Hamtramck remained Dodge's home plant. From the early 1950s, various operations were automated or moved to other plants and Hamtramck became more of an assembly plant by the early 1960s. Closed January 4, 1980. Last vehicle built was a Silver Metallic 1980 Dodge Aspen R/T 2-door. 13,943,221 vehicles were produced at the plant. Demolished in 1981. Replaced by the General Motors Detroit/Hamtramck Assembly Plant (Factory Zero), which opened in 1985. 
|-
| 
| [[w:Highland Park Chrysler Plant|Highland Park Plant]]
| [[w:Highland Park, Michigan|Highland Park, Michigan]]
| [[w:United States|United States]]
| 1909,&lt;br&gt; 1925 (became part of Chrysler)
| 1960s (end of manufacturing)
| Maxwell cars (1910-1925), Chrysler Series 50 (1926-27), Chrysler Series 52 (1928), Plymouth Model Q (1929), Chrysler Series 60 (1927), Chrysler Series 62 (1928), DeSoto Series K (1929-1930), DeSoto Series CK (1930), DeSoto Series CF (1930), Fargo Trucks (1928-1930) &lt;br&gt; Parts including fluid coupling and torque converter for [[w:Fluid Drive|Fluid Drive]]
| Located at at 12000 Chrysler Service Drive (formerly Chrysler Drive). Originally, this was [[w:Maxwell Motor Company|Maxwell Motor Company]]'s main plant. However, before Maxwell Motor Co.'s formation, parts of the site was used by several car and truck manufacturers: Grabowsky Power Wagon Company used 1 building, Brush Runabout Co. used another building, and Gray Motor Co. owned another building. Gray only used the western 1/3 of the building so they leased the middle third to Alden- Sampson Truck Co. and the eastern third to Maxwell-Briscoe Motor Co. All these companies, along with several others, combined under the [[w:United States Motor Company|United States Motor Company]] in 1910. In 1913, United States Motor Company collapsed and Maxwell was the only surviving part. The U.S. Motor Co. assets were purchased by Walter Flanders, who reorganized the company as the Maxwell Motor Co. Maxwell hired Walter P. Chrysler to turn the company around in 1921 after its finances deteriorated in the post-World War I recession in 1920. In early 1921, Maxwell Motor Co. was liquidated and replaced by Maxwell Motor Corp. with Walter P. Chrysler as Chairman. On December 7, 1922, Maxwell took over the bankrupt Chalmers including its Jefferson Ave. plant. Chrysler brand cars began to be produced in 1924 at the Jefferson Ave. plant. Chalmers was discontinued in late 1923 with the last cars being 1924 models. Maxwell production ended in May 1925 at Highland Park. Maxwell Motor Corp. was reorganized into the Chrysler Corporation on June 6, 1925. The 1925 Maxwell was reworked into an entry-level, 4-cylinder Chrysler model for 1926-1928 built at Highland Park and was then reworked again into the first Plymouth in 1928, also built at Highland Park. Plymouth production was moved to the new Lynch Road Assembly plant in 1929 and DeSoto production also moved to the new Lynch Road Assembly plant in 1931. Highland Park still built parts but it no longer built vehicles. Highland Park was used more for design,  engineering, and management and served as Chrysler Corporation's headquarters through 1996. During the 1990's, Chrysler moved to its current headquarters at the Chrysler Technology Center in Auburn Hills. Much of the site has been demolished though Chrysler still has a small presence at the site with the FCA Detroit Office Warehouse. Other parts of the site are now occupied by several automotive suppliers including Magna, Valeo, Mobis, Avancez, and Yanfeng.
|-
|
| [[w:Indiana Transmission#Indiana Transmission Plant II|Indiana Transmission Plant II]]
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 2003 (as Indiana Transmission Plant II)
| 2019 (as Indiana Transmission Plant II)
| [[w:W5A580|Mercedes W5A580 (A580) &lt;br&gt; 5-speed auto. trans.]], Transmission components
| Located at 3360 North U.S. Highway 931. Plant was originally known as Indiana Transmission Plant II, which built automatic transmissions and transmission components from 2003-2019, when it was idled. Production began in November 2003. 5-speed auto. trans. production ended in August 2018 while production of components for the 8-speed auto. transmission ended in the fall of 2019. Starting in 2020, the plant was converted to engine production and is now known as Kokomo Engine Plant. Engine production began in late February 2022. 
|-
|
| Indianapolis Electrical Plant
| [[w:Indianapolis|Indianapolis]], [[w:Indiana|Indiana]]
| [[w:United States|United States]]
| 1953
| 1988
| Transmission plant: [[w:Chrysler PowerFlite transmission|Chrysler PowerFlite 2-speed auto. transmission]] &lt;br&gt; Electrical Plant: Alternators, distributors, starters, power steering units, voltage regulators, windshield wiper motors, and other electrical parts for cars
| Located at 2900 Shadeland Ave. Began making transmissions in 1953. In January 1959, Chrysler housed its new Electrical Division at the Shadeland Avenue plant, replacing transmission production. Became part of Chrysler's Acustar components subsidiary in 1987. Production ended on November 30, 1988 but shipping and other activities continued until March 1989 when the factory closed. Certain portions have been demolished and improvements were made to the remainder, which is now the Shadeland Business Center. 
|-
|
| [[w:Indianapolis Foundry|Indianapolis Foundry]] - Naomi Street plant
| [[w:Indianapolis|Indianapolis]], [[w:Indiana|Indiana]]
| [[w:United States|United States]]
| 1946 (became part of Chrysler)
| 1970's
| Engine blocks
| Located at 1535 Naomi Street. Purchased from American Foundry Company in 1946. Operated as a subsidiary of Chrysler Corp. called American Foundry Co. until 1959, when it was merged into Chrysler Corp. Kept operating even after the Tibbs Ave. plant was launched. This location is now Wilco Gutter Supply. 
|-
|
| [[w:Indianapolis Foundry|Indianapolis Foundry]] - Tibbs Avenue plant
| [[w:Indianapolis|Indianapolis]], [[w:Indiana|Indiana]]
| [[w:United States|United States]]
| 1950 
| 2005
| Engine heads and blocks and other components
| Located at 1100 S. Tibbs Avenue. Operated as a subsidiary of Chrysler Corp. called American Foundry Co. until 1959, when it was merged into Chrysler Corp. Production ended on September 30, 2005 and the facility closed. Demolished in 2006. 
|-
| C (1968-1990),&lt;br&gt; 3 (1960-1967),&lt;br&gt; 1 (1959)
| [[w:Detroit Assembly Complex – Jefferson#Jefferson Avenue Assembly|Jefferson Avenue Assembly]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1908,&lt;br&gt; 1925 (became part of Chrysler)
| 1990
| [[w:Chrysler Six|Chrysler Series 70 (B-70)]] (1924-1925), [[w:Chrysler Six|Chrysler Series 70 (G-70)]] (1926-1927), [[w:Chrysler Six|Chrysler Series 72]] (1928), [[w:Chrysler Royal|Chrysler Royal]] (1933, 1937-1950), DeSoto SD (1933), Chrysler Airflow (1934-1937), Chrysler Airstream (1935-36), [[w:Chrysler (brand)|Chrysler brand]] (1937-1958), Desoto Airflow (1934-1936), DeSoto Airstream (1935-1936), [[w:Chrysler Imperial|Chrysler Imperial]] (1926-1942, 1946-1954), [[w:Imperial (automobile)|Imperial]] (1955-1958, 1962-1975), [[w:Chrysler 300 letter series|Chrysler 300 letter series]] (1959-1965), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1959-1978), [[w:Chrysler Saratoga|Chrysler Saratoga]] (1959-1960), [[w:Chrysler Windsor|Chrysler Windsor]] (1959-1961), [[w:Chrysler Newport|Chrysler Newport]] (1961-1978), [[w:Chrysler 300 non-letter series|Chrysler 300 Sport Series]] (1962-1971), [[w:Chrysler Town &amp; Country|Chrysler Town &amp; Country]] (1968-1972), [[w:DeSoto Firedome|DeSoto Firedome]] (1959), [[w:DeSoto Fireflite|DeSoto Fireflite]] (1959-1960), [[w:DeSoto Adventurer|DeSoto Adventurer]] (1959-1960), [[w:DeSoto (automobile)#1961|DeSoto]] (1961), [[w:Dodge Matador|Dodge Matador]] (1960), [[w:Dodge Polara|Dodge Polara]] (1965-1966), [[w:Dodge D series|Dodge D/W series]] (1979-1980), [[w:Dodge Ramcharger|Dodge Ramcharger]] (1979-1980), [[w:Plymouth Trailduster|Plymouth Trailduster]] (1979-1980), [[w:Dodge Aries|Dodge Aries]] (1981-1989), [[w:Plymouth Reliant|Plymouth Reliant]] (1981-1989), [[w:Dodge 400|Dodge 400]] 4-d (1982-1983), [[w:Chrysler LeBaron|Chrysler LeBaron]] 4-d (1982-1984), [[w:Chrysler New Yorker#1983–1988|Chrysler New Yorker (E-body)]] (1983-1987), [[w:Chrysler New Yorker#1983–1988|Chrysler New Yorker Turbo (E-body)]] (1988), [[w:Dodge 600|Dodge 600]] 4-d (1983-1988), [[w:Chrysler E-Class|Chrysler E-Class]] (1983-1984), [[w:Plymouth Caravelle|Plymouth Caravelle]] (US: 1985-1988), [[w:Plymouth Caravelle|Plymouth Caravelle]] 4-d (Canada: 1983-1988), [[w:Dodge Omni|Dodge Omni]] (1989-1990), [[w:Plymouth Horizon|Plymouth Horizon]] (1989-1990),&lt;br&gt; Engines
| Located at 12200 East Jefferson Ave. Plant was originally opened by [[w:Chalmers Automobile|Chalmers Motor Co.]]. After falling on hard times, Chalmers agreed in 1917 to build cars for [[w:Maxwell Motor Company|Maxwell Motor Co.]] at the Jefferson Ave. plant in Detroit. In exchange, Chalmers cars would be sold through Maxwell dealers. After having its own financial problems, Maxwell stopped producing cars at the Chalmers plant in 1921. Maxwell hired Walter P. Chrysler to turn the company around in 1921. In early 1921, Maxwell Motor Co. was liquidated and replaced by Maxwell Motor Corp. with Walter P. Chrysler as Chairman. On December 7, 1922, Maxwell took over the bankrupt Chalmers including the Jefferson Ave. plant. Chrysler brand cars began to be produced in 1924. Chalmers was discontinued in late 1923 with the last cars being 1924 models. Maxwell production ended in May 1925. Maxwell Motor Corp. was reorganized into the Chrysler Corporation on June 6, 1925. The 1925 Maxwell was reworked into an entry-level, 4-cylinder Chrysler model for 1926-1928 and was then reworked again into the first Plymouth in 1928. The Jefferson Ave. plant was the home plant of the Chrysler brand through 1978. It was also the home plant for the spin-off Imperial brand except for 1959-1961, when Imperial had its own exclusive plant on Warren Ave. in Dearborn. By the time it ended production on February 2, 1990, Jefferson Ave. Assembly had built 8,310,107 vehicles. Demolished in 1991. Replaced by the Jefferson North plant built across Jefferson Ave. from the old plant, where the Kercheval Body Plant used to be. The Jefferson North plant opened in January 1992.
|-
| W (1987-1989 Chrysler M-body) &lt;br&gt;&lt;br&gt; [K for 1981-1983 AMC and 1983-1987 Renault],&lt;br&gt; 0-6 (1966-1980 AMC)
| Kenosha I Assembly
| [[w:Kenosha, Wisconsin|Kenosha, Wisconsin]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 1988
| [[w:Chrysler Fifth Avenue#1982–1989: The M-body years|Chrysler Fifth Avenue]]&lt;br&gt; (1987-1989),&lt;br&gt; [[w:Dodge Diplomat#Second generation (1980)|Dodge Diplomat]] (1987-1989), [[w:Plymouth Gran Fury#1982–1989|Plymouth Gran Fury]] (1987-89), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle Salon]] (Canada: 1987-1989)
| This was the Kenosha Main Plant of [[w:American Motors Corporation|AMC]]. The Kenosha plant was the oldest still operating automobile factory in the world when it ended vehicle production in December 1988. It first built automobiles in 1902 for the Thomas B. Jeffery Company under the Rambler brand. The factory was purchased in 1900 from the Sterling Bicycle Co., which built it in 1895. In 1914, the Thomas B. Jeffery Company rebranded its vehicles under the Jeffery brand. In 1916, the Thomas B. Jeffery Company was bought by Charles Nash and renamed Nash Motors. Kenosha produced Nash vehicles from 1917-1957. Kenosha also produced Nash's entry-level Lafayette brand from 1934-1936. After Nash merged with Hudson to form American Motors in 1954, Kenosha also produced Hudson vehicles from 1955-1957. Kenosha then produced vehicles under the Rambler brand for AMC from 1958-1968 and under the AMC brand from 1966-1983. Kenosha also produced the Alliance for AMC shareholder Renault for 1983-1987 along with the Encore for 1984-1986 and the GTA for 1987. Chrysler signed a deal with AMC in September 1986 to utilize surplus capacity at AMC's Kenosha plant to build Chrysler's trio of rwd M-body sedans beginning in February 1987. Chrysler did not have any capacity left in its own plants to continue building the M-body sedans. The St. Louis North plant that had been building the M-body sedans had been converted to build the extended length minivans. This deal led to Chrysler's acquisition of AMC, announced in March 1987. Became part of Chrysler in the 1987 buyout of AMC. Vehicle production ended in December 1988 and the M-bodies were discontinued. The site continued building engines until 2010. The plant has since been demolished.
|-
| Y
| Kenosha II Assembly
| [[w:Kenosha, Wisconsin|Kenosha, Wisconsin]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 1988
| [[w:Dodge Omni|Dodge Omni]] (1988-1989), [[w:Plymouth Horizon|Plymouth Horizon]] (1988-1989)
| This was the Kenosha Lakefront Plant of [[w:American Motors Corporation|AMC]], located on the shore of Lake Michigan. This property was originally a Simmons mattress manufacturing plant from 1870 to 1960. AMC bought it in 1960 to manufacture and paint auto bodies. Became part of Chrysler in the 1987 buyout of AMC. In September 1987, production of the Dodge Omni and Plymouth Horizon began. Production was moved to Kenosha from Chrysler's Belvidere, IL plant, which was being converted to build Chrysler's C-body sedans (Dynasty/New Yorker). Closed in December 1988. Omni &amp; Horizon production then moved to the Jefferson Ave. plant in Detroit. Demolished in 1990. In 1994, the City of Kenosha purchased the property for $1. The property was subsequently cleaned up and redeveloped into the HarborPark area, which includes a park and open space, a public museum, residential housing, and a marina. 
|-
| 
| [[w:Kenosha Engine|Kenosha Engine Plant]]
| [[w:Kenosha, Wisconsin|Kenosha, Wisconsin]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 2010
| [[w:AMC straight-4 engine|AMC straight-4 engine]],&lt;br&gt; [[w:AMC straight-6 engine|AMC straight-6 engine]],&lt;br&gt; [[w:AMC V8 engine|AMC V8 engine]],&lt;br&gt; [[w:Chrysler LH engine|Chrysler 2.7L DOHC V6]], [[w:Chrysler SOHC V6 engine#3.5|Chrysler 3.5L SOHC V6]]
| Located at 5555 30th Avenue. Became part of Chrysler in the 1987 buyout of AMC. Vehicle production ended in December 1988 at the adjacent assembly plant but the site continued building engines until 2010. After the Chrysler buyout, the plant kept building the AMC 5.9L V8 for the SJ Jeep Grand Wagoneer through 1991, the AMC 2.5L I4 through 2002 for Jeeps and the Dodge Dakota, the AMC 4.2L I6 through 1990 for the Jeep Wrangler, and the AMC 4.0L I6 through 2006 for various Jeeps ('06 Wrangler was the last to use the 4.0L). Chrysler started building its own 2.7L V6 at Kenosha in 1997 and its own 3.5L V6 in 2003. Engine production ended in October 2010 and the plant closed. Demolished in 2012-2013.
|-
|
| Kercheval Body Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1920,&lt;br&gt; 1925 (became part of Chrysler)
| 1990
| Automobile Bodies
| Located at 12265 E Jefferson Ave., across Jefferson Ave. from Chrysler's Jefferson Ave. Assembly Plant, which had originally been the Chalmers plant. The assembly plant was on the south side of Jefferson Ave. while the body plant was on the north side. The plant was called Kercheval because the north side of the plant was bordered by Kercheval Ave. The plant was built in 1920 by Wadsworth Manufacturing Co. to replace a previous plant on the same site that burned down in 1919. That fire had also damaged the Chalmers plant across the street. In November 1920, Wadsworth Manufacturing was sold to American Motor Body Co., a division of the American Can Co. On July 1, 1923, American Motor Body Co. became American Motor Body Corp., run by Charles M. Schwab. On September 4, 1925, Chrysler Corp. bought the Detroit plant of the American Motor Body Corp. to quickly increase its manufacturing capacity. In 1955, Kercheval Body Plant was connected to the Jefferson Assembly plant by a bridge crossing over Jefferson Ave. Previously, bodies made at Kercheval had to be transported by truck across Jefferson Ave. to the assembly plant. The plant closed in Feb. 1990, at the same time the Jefferson Ave. Assembly Plant closed. The Kercheval plant was demolished and Chrysler built the new Jefferson North Assembly Plant on the site of the former Kercheval Body Plant, on the north side of Jefferson Ave. 
|-
|
| Kokomo - Home Ave. plant
| [[w:Kokomo, Indiana|Kokomo, Indiana]]
| [[w:United States|United States]]
| 1937
| 1969
| Manual Transmissions (1937-1955), Aluminum die casting (1955-1969)
| Located at 1105 S. Home Ave. Chrysler bought this plant in 1937. This was Chrysler's first plant in Kokomo. It had previously belonged to the [[w:Haynes Automobile Company|Haynes Automobile Co.]], which went out of business in 1925. The plant had been dormant since then. 5,124,211 manual transmissions were built here from 1937-1955. Transmission production then shifted to a new plant about a mile southeast on South Reed Road. The Home Ave. plant then became an aluminum die casting plant until 1969, when that operation shifted to the new Kokomo Casting plant on East Boulevard. Chrysler subsequently sold this plant. The facility was last used by Warren's Auto Parts, an auto salvage yard, which closed in 2020 after nearly 50 years. It is currently empty though still standing as of 2025. 
|-
| M
| [[w:Lago Alberto Assembly|Lago Alberto Assembly]]
| [[w:Nuevo Polanco|Nuevo Polanco district]], [[w:Miguel Hidalgo, Mexico City|Miguel Hidalgo borough]], [[w:Mexico City|Mexico City]]
| [[w:Mexico|Mexico]]
| 1938
| 2002
| &lt;br&gt; Past models: &lt;br&gt;  Mexico only: Dodge Savoy, Dodge Dart, Dodge 330, Dodge 440, Chrysler Valiant (1963-1969), Valiant Barracuda (1965-1969), Dodge Coronet, [[w:Dodge Ram|Dodge Ram pickup]] (1981-02), [[w:Dodge Ramcharger#Second generation (1981–1993)|Dodge Ramcharger]] (1986-96), [[w:Dodge Ramcharger#Third generation (1999–2001)|Dodge Ramcharger]] (1999-01) &lt;br&gt; Export to US:&lt;br&gt; [[w:Dodge Ramcharger#Second generation (1981–1993)|Dodge Ramcharger]] (1986-93), [[w:Dodge Ram#First generation (1981; D/W)|Dodge Ram pickup]] (1990-93), [[w:Dodge Ram#Second generation (1994; BR/BE)|Dodge Ram pickup]] (1994-02)
| Located at 320 Lago Alberto Street. Originally part of Fabricas Automex, Chrysler's affiliate in Mexico. In 1968, Fabricas Automex was 45% owned by Chrysler. In December 1971, Chrysler increased its stake to 90.5% and changed the Mexican company's name to Chrysler de Mexico. Chrysler later bought another 8.8% stake, taking its total to 99.3%. Lago Alberto began exporting to the US with the 1986 Dodge Ramcharger, sourced exclusively from Mexico. The Lago Alberto plant was closed in 2002 and Mexican pickup production was consolidated in the newer, more modern Saltillo plant. 
|-
| E (1968-1971),&lt;br&gt; 5 (1960-1967),&lt;br&gt; 4 (1959),&lt;br&gt; L (1958),&lt;br&gt; L (1955-1957 Chrysler brand)
| [[w:Los Angeles (Maywood) Assembly|Los Angeles (Maywood) Assembly]]
| [[w:Commerce, California|City of Commerce, California]]
| [[w:United States|United States]]
| 1932
| 1971
| Plymouth (1946-1958), Dodge (1946-1953, 1955-1958), [[w:Dodge Power Wagon#Civilian 1-ton Power Wagon &quot;Military-Type&quot;, Flat Fender Style&quot; (1945-1978)|Dodge Power Wagon]] (1946-1949), DeSoto Deluxe/Custom (1948-1952), DeSoto Powermaster Six (1953-1954), DeSoto Firedome (1952-57), DeSoto Fireflite (1955-1957), DeSoto Firesweep (1957-1958), Chrysler Windsor (1948-1958), Chrysler Royal (1949-1950), Chrysler Saratoga (1951-1952, 1957-1958), Chrysler New Yorker (1953-1958), [[w:Chrysler Windsor|Chrysler Windsor]] (1959-1960), [[w:Chrysler Saratoga|Chrysler Saratoga]] (1959-1960), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1959-60), [[w:DeSoto Firesweep|DeSoto Firesweep]] (1959), [[w:Dodge Coronet#Fourth generation (1957–1959)|Dodge Coronet]] (1957-1959), [[w:Dodge Custom Royal|Dodge Custom Royal]] (1958-1959), [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962), [[w:Dodge 330|Dodge 330]] (1963-1964), [[w:Dodge 440|Dodge 440]] (1963-1964), [[w:Dodge Polara|Dodge Polara]] (1960-1964), [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (1959), [[w:Plymouth Fury|Plymouth Fury]] (1958-1964), [[w:Plymouth Suburban|Plymouth Suburban wagon]] (1959-1961), [[w:Plymouth Savoy|Plymouth Savoy]] (1958-1959, 1963-1964), [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1971), [[w:Plymouth Duster|Plymouth Duster]] (1970-1971), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1971), [[w:Dodge Dart#1971|Dodge Dart Demon]] (1971), [[w:Plymouth Barracuda|Plymouth Barracuda]] (1964-1966, 1970), [[w:Dodge Challenger (1970)|Dodge Challenger]] (1970), [[w:Plymouth Belvedere#Intermediate series|Plymouth Belvedere]] (1965-70), [[w:Plymouth Satellite|Plymouth Satellite]] (1965-1971), [[w:Plymouth GTX|Plymouth GTX]] (1967-1971), [[w:Plymouth Road Runner|Plymouth Road Runner]] (1968-1971), [[w:Dodge Coronet|Dodge Coronet]] (1965-1971), [[w:Dodge Charger (1966)|Dodge Charger]] (1971), [[w:Dodge Super Bee|Dodge Super Bee]] (1968-1971)
| Located at 5800 South Eastern Avenue and Slauson Avenue in Maywood, now part of City of Commerce. Across the street from the [[w:Maywood Assembly|Ford Maywood Assembly plant (Los Angeles Assembly plant No. 1)]]. 
|-
| A (1968-1981),&lt;br&gt; 1 (1960-1967),&lt;br&gt; 6 (1959)
| [[w:Lynch Road Assembly|Lynch Road Assembly]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1929
| 1981
| Plymouth (1929-1958), DeSoto (1931-1932), [[w:Plymouth Savoy|Plymouth Savoy]] (1959-64), [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (59-61), [[w:Plymouth Fury|Plymouth Fury]] (1959-1964), [[w:Plymouth Suburban|Plymouth Suburban wagon]] (59-61), [[w:Plymouth Belvedere#Intermediate series|Plymouth Belvedere]] (62-70), [[w:Plymouth Satellite|Plymouth Satellite]] (1965-1970, 1973-1974), [[w:Plymouth Fury#Seventh generation (1975–1978)|Plymouth Fury]] (1975-1978), [[w:Plymouth GTX|Plymouth GTX]] (1967-1970), [[w:Plymouth Road Runner|Plymouth Road Runner]] (1968-1970, 1973, 1975), [[w:Plymouth Superbird|Plymouth Road Runner Superbird]] (1970), [[w:Dodge Coronet|Dodge Coronet]] (1965-1976), [[w:Dodge Monaco#Fourth generation (1977–1978)|Dodge Monaco]] (1977-1978), [[w:Dodge Charger (1966)#1966|Dodge Charger]] (1966), [[w:Dodge Charger (1966)#Third generation|Dodge Charger]] (1971-1974), [[w:Dodge Super Bee|Dodge Super Bee]] (1968-1971),  [[w:Chrysler Newport#1979–1981|Chrysler Newport]] (1979-81), [[w:Chrysler New Yorker#1979–1981|Chrysler New Yorker]] (79-81), [[w:Dodge St. Regis|Dodge St. Regis]] (1979-81), [[w:Plymouth Gran Fury#1980–1981|Plymouth Gran Fury]] (80-81),&lt;br&gt; Engines
| Located at 6334 Lynch Road. This was originally Plymouth's home plant. At the time it opened in 1929, Lynch Road was the largest single story auto plant in the world. DeSoto production was transferred from Highland Park to Lynch Road in 1931. In June 1932, DeSoto production was moved to the Jefferson Ave. plant when the DeSoto brand moved up in the brand hierarchy to between Dodge and Chrysler. Previously, DeSoto was between Plymouth and Dodge. During World War II, Lynch Road made tank transmissions, truck parts, and uranium enrichment diffusers for the Oak Ridge Gaseous Diffusion Plant in Oak Ridge, TN to produce enriched uranium for the atomic bomb. For 1965, Lynch Road began to focus on production of Plymouth and Dodge intermediate models. For 1979, Lynch Road was switched to build Chrysler's R-body full-size cars for all 3 Chrysler car brands. Production ended on April 3, 1981 and the factory closed. Last car produced was a white Plymouth Gran Fury police car. 
|-
| 
| [[w:Detroit Assembly Complex – Mack|Mack Ave. Engine Plant I]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1998
| 2019
| [[w:Chrysler PowerTech engine#4.7|4.7L PowerTech SOHC V8]],&lt;br&gt; [[w:Chrysler Pentastar engine|3.0L/3.2L/3.6L Pentastar V6]]
| Located at 4000 St. Jean Avenue. Mack Ave. Engine Plant I was built on the site of the former New Mack Assembly Plant and the Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. The first engine was built in 1998. 4.7L V8 engine production ended in April 2013. Pentastar V6 engine production ended in 2019. The 2 engine plants were subsequently converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North Assembly plants have operated as the Detroit Assembly Complex since 2021.
|-
| 
| [[w:Detroit Assembly Complex – Mack|Mack Ave. Engine Plant II]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 2000
| 2012
| [[w:Chrysler PowerTech engine#3.7 EKG|3.7L PowerTech SOHC 90° V6]]
| Located at 4500 St. Jean Avenue. Mack Ave. Engine Plant II was built next to the Mack Ave. Engine Plant I, which had been built on the site of the former New Mack Assembly Plant and the Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. The first engine was built in November 2000. Production ended in September 2012. The 2 engine plants were subsequently converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North Assembly plants have operated as the Detroit Assembly Complex since 2021.
|-
|
| Mack Ave. Stamping Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953 (became part of Chrysler)
| 1979
| Stampings
| Chrysler acquired the Mack Ave. Stamping Plant from Briggs Manufacturing Company in 1953. The plant was originally built in 1916 by the Michigan Stamping Company, which was taken over by Briggs Manufacturing in 1923. The plant was closed in 1979 and the site was basically abandoned. The city of Detroit bought the plant site in 1982 but was unable to find a purchaser or afford environmental remediation for the site and returned it to Chrysler. In 1990, Chrysler began cleanup and demolition of the old plant and built a new factory on the site, which became the New Mack Assembly Plant. The site later became the Mack Ave. Engine Complex and later, the Mack Ave. Assembly Plant, which is now part of the Detroit Assembly Complex.
|-
| 
| McGraw Stamping/McGraw Glass Plant
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 19?
| 2003
| Oil pans, valve covers, and other small stampings,&lt;br&gt; Automotive Glass (1960-)
| Located at 9400 McGraw Ave. Was around the corner and behind the Wyoming Ave. DeSoto/Export plant. Originally, a stamping plant. In 1960, switched to making automotive glass. Used Safeguard brand. Glass was DOT# 21. Demolished. 
|-
|
| [[w:Mound Road Engine|Mound Road Engine Plant]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953 (became part of Chrysler)
| 2002
| [[w:Chrysler A engine|Chrysler A V8 engine]],&lt;br&gt; [[w:Chrysler LA engine|Chrysler LA V8 engine]],&lt;br&gt; [[w:Chrysler LA engine#239 V6|3.9L 90° V6 engine]],&lt;br&gt; [[w:Chrysler LA engine#Magnum 8.0 L V10|8.0L iron Magnum V10 engine]],&lt;br&gt; [[w:Viper engine|8.0L aluminum Viper V10 engine]] (1992-5/01)
| Located at 20300 Mound Road. One of the plants Chrysler acquired from Briggs Manufacturing Company in 1953. Chrysler used the plant to produce aircraft parts from 1953-1954 and then transferred the plant to Plymouth in 1954 to build its new A-series V8 engine for 1956 model year cars. Converted into an engine plant and enlarged by 71,000 sq. ft., it began building V8 engines for Plymouth in July 1955. Dodge later used the A engine from 1959 in the US in cars and trucks and Chrysler used the A engine from 1960 in the US. The plant was closed in 2002 and demolished in 2003. The land was then paved over and is now used as a storage lot for vehicles produced at the nearby Warren Truck Assembly Plant. Warren Truck Assembly is just to the north of where Mound Road Engine was. Mt. Elliott Tool and Die was located immediately to the south of the Mound Road Engine Plant on Outer Drive East.
|-
|
| [[w:Mount Elliott Tool and Die|Mount Elliott Tool and Die]]/Outer Drive Manufacturing Technology Center/Outer Drive Stamping
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1938, 1953 (became part of Chrysler)
| 2018
| Stamping Dies, Checking Fixtures, Stamping Fixtures 
| Located at 3675 Outer Drive East. Built in 1938 by Briggs Manufacturing Company. One of the plants Chrysler acquired from Briggs Manufacturing in 1953. Chrysler renamed it Outer Drive Stamping. Stamping operations ended in 1983 and operations from the closed Vernor Tool &amp; Die plant were moved here. The plant was then renamed Outer Drive Manufacturing Technology Center. The plant now did tool and die work as well as pilot plant operations and engineering for new stamping technologies. Once the Chrysler Technology Center in Auburn Hills was built, Pilot Operations and Advanced Stamping Manufacturing Engineering moved there and the plant was renamed Mount Elliott Tool and Die. Operations at the plant ended in 2018 and the plant was sold to German automotive supplier Laepple Automotive in 2024. Laepple Automotive is producing stamped body parts at the plant. 
|-
| V
| [[w:Detroit Assembly Complex – Mack|New Mack Assembly Plant]]
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1992
| 1995
| [[w:Dodge Viper|Dodge Viper RT/10]] (1992-96)
| Located at 4000 St. Jean Avenue. The New Mack Assembly Plant is built on the site of the former Mack Ave. Stamping Plant that Chrysler acquired from Briggs Manufacturing Company in 1953. Viper production began in May 1992 at the New Mack Assembly Plant. After ending production in 1995, New Mack Assembly was converted into the Mack Ave. Engine Plant I. A new addition was then built to create Mack Ave. Engine Plant II. The 2 engine plants were subsequently converted into a single vehicle assembly plant and a new paint shop was built to create the Mack Ave. Assembly Plant. The Mack Ave. and the Jefferson North Assembly plants have operated as the Detroit Assembly Complex since 2021. 
|-
| F (1968-2009),&lt;br&gt; 6 (1960-1967),&lt;br&gt; 5 (1959),&lt;br&gt; N (1958)
| [[w:Newark Assembly|Newark Assembly]]
| [[w:Newark, Delaware|Newark, Delaware]]
| [[w:United States|United States]]
| 1951,&lt;br&gt; 1957 (Automotive prod.)
| 2008
| Plymouth (1957-1958), Dodge (1958), [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (1958-1959, 1961), [[w:Plymouth Fury|Plymouth Fury]] (1959-1974), [[w:Plymouth Savoy|Plymouth Savoy]] (1959-1964), [[w:Dodge Coronet#Fourth generation (1957–1959)|Dodge Coronet]] (1958-1959), [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962), [[w:Dodge Polara|Dodge Polara]] (1960-1966), [[w:Dodge Monaco|Dodge Monaco]] (1965-1966, 1968), [[w:Chrysler Newport|Chrysler Newport]] (1965-1970), [[w:Chrysler New Yorker|Chrysler New Yorker]] (1965-70), [[w:Chrysler Town &amp; Country (1941–1988)|Chrysler Town &amp; Country]] (1966-1967), [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1964, 1974-1976), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1964, 1974-76), [[w:Dodge Aspen|Dodge Aspen]] (1976-1980), [[w:Plymouth Volare|Plymouth Volare]] (1976-1980), [[w:Chrysler LeBaron#First generation (1977–1981)|Chrysler LeBaron (M-body)]] (1979-1980), [[w:Plymouth Reliant|Plymouth Reliant]] sedan &amp; wagon (1981-1988), [[w:Dodge Aries|Dodge Aries]] sedan &amp; wagon (1981-1988), [[w:Chrysler LeBaron#Second generation (1982–1988)|Chrysler LeBaron (K-body)]] (sedan: 1984-1988, wagon: 1982-1988), [[w:Plymouth Acclaim|Plymouth Acclaim]] (1989-1995), [[w:Dodge Spirit|Dodge Spirit]] (1989-1995), [[w:Chrysler LeBaron#Third generation sedan (1990–1994)|Chrysler LeBaron Sedan (A-body)]] (1990, 1993-1994), [[w:Chrysler Saratoga#1989–1995|Chrysler Saratoga]] (For export: 1990-1992), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron coupe (J-body)]] (1992-1993), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron convertible (J-body)]] (1992-1995), [[w:Dodge Intrepid#First generation (1993–1997)|Dodge Intrepid]] (1994-1996), [[w:Chrysler Intrepid#First generation (1993–1997)|Chrysler Intrepid]] (Canada: 1994-1995), [[w:Chrysler Concorde#First generation (1993–1997)|Chrysler Concorde]] (1995-1996), [[w:Dodge Durango#First generation (DN; 1998)|Dodge Durango (DN)]] (1998-2003), [[w:Dodge Durango#Second generation (HB; 2004)|Dodge Durango (HB)]] (2004-2009), [[w:Chrysler Aspen|Chrysler Aspen]] (2007-2009) 
| Chrysler began construction of the Delaware Tank Plant in January 1951 to build [[w:M48 Patton|M48 Patton]] tanks. Production began in April 1952. Production ended in May 1961 and the Tank Plant was closed in October 1961. Low rate initial production of the [[w:M60 tank|M60 tank]] was also done at the Newark plant in 1959 before production was moved to the [[w:Detroit Arsenal (Warren, Michigan)|Detroit Arsenal Tank Plant]] in Warren, MI in 1960. Conversion to automotive production began in 1956. Production of Plymouth and Dodge cars began on April 30, 1957. Production ended on December 19, 2008. Sold to the University of Delaware on October 24, 2009. Most of the plant was demolished in 2010-2011 except for the Administration Building near the front of the complex. The site is now the Science, Technology, and Advanced Research (STAR) campus. The old Chrysler Administration Building has been redesigned and is now being used by the College of Health Sciences. 
|-
| K
| [[w:Pillette Road Truck Assembly|Pillette Road Truck Assembly]]
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1976
| 2003
| [[w:Dodge Sportsman|Dodge Tradesman/Sportsman]] (1976-1980),&lt;br&gt; [[w:Dodge Ram Van|Dodge Ram Van]] (1981-2003), [[w:Dodge Ram Wagon|Dodge Ram Wagon]] (1981-'02), [[w:Plymouth Voyager#Full-size van (AB; 1974–1983)|Plymouth Voyager]] (1976-1983)
| Located at 2935 Pillette Road. Was originally Windsor Plant 6. The Pillette Road plant was located less than a mile away from Chryslers' main plant complex in Windsor. Production began in January 1976. Production ended on June 12, 2003. 2,309,399 units were built. Demolished in 2004. Part of the site is now the Grand Central Business Park. Another part was a logistics center serving Chrysler's Windsor Assembly Plant and operated by Syncreon. The Syncreon Automotive Windsor site closed in October 2022. The parts sorting and sequencing work done there was now going to be done in-house at Chrysler's Windsor Assembly Plant. 
|-
| 
| [[w:Los Angeles (Maywood) Assembly#San Leandro Assembly|San Leandro Assembly]]
| [[w:San Leandro, California|San Leandro, California]]
| [[w:United States|United States]]
| 1948
| 1954
| Plymouth (1949-1954),&lt;br&gt; Dodge (1949-1954),&lt;br&gt; [[w:Dodge Power Wagon#Civilian 1-ton Power Wagon &quot;Military-Type&quot;, Flat Fender Style&quot; (1945-1978)|Dodge Power Wagon]] (1950-1954)
| Located at 1933 Davis St. Plant was originally run by Dodge Division. In 1953, San Leandro began to make its own car bodies instead of sourcing bodies from Detroit and only doing final assembly locally. Closed in 1954 when Chrysler consolidated West Coast auto production at the Los Angeles plant. Used by International Harvester to build heavy-duty trucks from 1963 to 1975, replacing an earlier plant in Emeryville.  Now the Westgate Center, a shopping mall, and Gate510, a hub for entrepreneurs. 
|-
| B (1996-2009),&lt;br&gt; G (1968-1991),&lt;br&gt; 7 (1960-1967),&lt;br&gt; 8 (1959)
| [[w:Saint Louis Assembly|St. Louis I Assembly]] - South plant
| [[w:Fenton, Missouri|Fenton, Missouri]]
| [[w:United States|United States]]
| 1959
| 2008
| [[w:Plymouth Belvedere#Full-size series|Plymouth Belvedere]] (1960), [[w:Plymouth Fury|Plymouth Fury]] (1960-1964), [[w:Plymouth Savoy|Plymouth Savoy]] (1960-1964), [[w:Plymouth Suburban|Plymouth Suburban wagon]] (1961), [[w:Dodge Dart|Dodge Dart (full-size)]] (1960-1962), [[w:Dodge 330|Dodge 330]] (1963-1964), [[w:Dodge 440|Dodge 440]] (1963-1964), [[w:Plymouth Valiant#First generation (1960–1962)|Valiant]] (1960), [[w:Plymouth Valiant|Plymouth Valiant]] (1961-1965, 1976), [[w:Plymouth Duster|Plymouth Duster]] (1973-1976), [[w:Dodge Lancer#1961–1962: Lancer|Dodge Lancer]] (1961-1962), [[w:Dodge Dart|Dodge Dart (compact)]] (1963-1965, 1973-1976), [[w:Plymouth Barracuda|Plymouth Barracuda]] (1964-1965),&lt;br&gt; [[w:Plymouth Belvedere#Intermediate series|Plymouth Belvedere]] (1965-1970), [[w:Plymouth Satellite|Plymouth Satellite]] (1965-1974), [[w:Plymouth GTX|Plymouth GTX]] (1967-1971), [[w:Plymouth Road Runner|Plymouth Road Runner]] (1968-75), [[w:Plymouth Fury#Seventh generation (1975–1978)|Plymouth Fury]] (1975-1976), [[w:Dodge Coronet|Dodge Coronet]] (1965-1973, 75), [[w:Dodge Charger (1966)|Dodge Charger]] (1968-1974), [[w:Dodge Super Bee|Dodge Super Bee]] (1968-1971), [[w:Dodge Diplomat|Dodge Diplomat]] (1977-1981), [[w:Chrysler LeBaron#First generation (1977–1981)|Chrysler LeBaron (M-body)]] (1977-1981), [[w:Plymouth Caravelle|Plymouth Caravelle (M-body)]] (Canada: 1978-1981), [[w:Plymouth Reliant|Plymouth Reliant]] 2-d (1982-1986), [[w:Dodge Aries|Dodge Aries]] 2-d (1982-1986), [[w:Dodge 400|Dodge 400]] 2-d &amp; convertible (1982-1983), [[w:Dodge 600|Dodge 600]] 2-d &amp; convertible (1984-1986), [[w:Plymouth Caravelle|Plymouth Caravelle]] 2-d (Canada: 1983-1986), [[w:Chrysler LeBaron#Second generation (1982–1988)|Chrysler LeBaron (K-body)]] (2-d &amp; convertible: 1982-1986), [[w:Chrysler Executive|Chrysler Executive]] (1983-1986), [[w:Dodge Daytona|Dodge Daytona]] (1984-1991), [[w:Chrysler Daytona|Chrysler Daytona]] (Canada: 1984-1991), [[w:Dodge Daytona#Chrysler Laser|Chrysler Laser]] (1984-1986), [[w:Chrysler LeBaron#Third generation coupe/convertible (1987–1995)|Chrysler LeBaron coupe/convertible (J-body)]] (1987-1991), [[w:Plymouth Voyager|Plymouth Voyager]] (1996-2000), [[w:Plymouth Voyager|Plymouth Grand Voyager]] (1996-2000), [[w:Dodge Caravan|Dodge Caravan]] (1996-2007), [[w:Dodge Caravan|Dodge Grand Caravan]] (1996-2009), [[w:Chrysler Voyager|Chrysler Voyager]] (2001-2003), [[w:Chrysler Voyager|Chrysler Grand Voyager]] (2000), [[w:Chrysler Town &amp; Country (minivan)|Chrysler Town &amp; Country]] (1996-2001, 2004-2007)
| Located at 1001 N. Hwy Dr. All 1970 Dodge Chargers were made here. St. Louis South was idled in 1991. The Dodge Daytona was moved to Sterling Heights and the J-body Chrysler LeBaron was moved to Newark, DE. St. Louis South was reopened in 1995 to build minivans, which were moved from the St. Louis North plant. For the 3rd generation, St. Louis South built both SWB and LWB models. For the 4th generation, St. Louis South built all SWB models but also built some LWB models. Closed on October 31, 2008. Demolished in 2011. Site was sold in 2014 and is now the Fenton Logistics Park.
|-
| J (1996-2009),&lt;br&gt; X (1973-1995),&lt;br&gt; U (1970-1972),&lt;br&gt; 7 (1967-1969)
| [[w:Saint Louis Assembly|St. Louis II Assembly]] - North plant / Missouri Truck Assembly Plant
| [[w:Fenton, Missouri|Fenton, Missouri]]
| [[w:United States|United States]]
| 1966
| 2009
| [[w:Dodge D series|Dodge D/W series]] (1967-1973), [[w:Dodge Ramcharger|Dodge Ramcharger]] (1974-1977), [[w:Plymouth Trail Duster|Plymouth Trail Duster]] (1974-76), [[w:Dodge Sportsman|Dodge Tradesman/Sportsman]] (1971-1980), [[w:Plymouth Voyager#Full-size van (AB; 1974–1983)|Plymouth Voyager]] (1975-1976, 1980),&lt;br&gt; [[w:Plymouth Gran Fury#1982–1989|Plymouth Gran Fury]] (1984-1987), [[w:Plymouth Caravelle#Canada|Plymouth Caravelle Salon]] (Canada: 1984-1987), [[w:Dodge Diplomat|Dodge Diplomat]] (1984-1987), [[w:Chrysler Fifth Avenue#1982–1989: The M-body years|Chrysler Fifth Avenue]] ('84-'87), [[w:Plymouth Voyager|Plymouth Grand Voyager]] (1987-1995), [[w:Dodge Caravan|Dodge Grand Caravan]] (1987-1995), [[w:Chrysler minivans (S)#Cargo van|Dodge Extended Mini Ram Van]] (1987-1988), [[w:Chrysler Town &amp; Country (minivan)|Chrysler Town &amp; Country]] (1990-1995),&lt;br&gt; [[w:Dodge Ram|Dodge Ram pickup]] (1996-'09)
| Originally opened to build trucks as the Missouri Truck Assembly Plant. In 1980, the plant was idled. Plant was reopened in 1983 to build the rwd, M-body sedans, which were moved from Windsor, ON, Canada so that Windsor could be converted to build minivans. Plant was renamed St. Louis II Assembly. During 1987, the M-body sedans were moved to AMC's plant in Kenosha, WI so that St. Louis North could be converted to build the new LWB minivans. For the first 2 generations of Chrysler minivans, St. Louis North only built the LWB models. For 1996, minivan production moved to St. Louis South and the North plant was converted to build full-size pickups. Closed on July 10, 2009. Demolished in 2011. Site was sold in 2014 and is now the Fenton Logistics Park.
|-
| J (1970-1978),&lt;br&gt; 6 (1968-1969),&lt;br&gt; 9 (1961-1967)
| Tecumseh Road Truck Assembly / Windsor Truck Assembly Plant
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1916,&lt;br&gt; 1925 (became part of Chrysler)
| 1978
| Maxwell (1924-1925),&lt;br&gt; Chrysler (1924-1929),&lt;br&gt; Dodge Trucks (1931-1960), &lt;br&gt; Dodge D-Series Trucks: &lt;br&gt; D100 (1961), D200 (1964), W200 (1965), W100 (1966), D100/W100 (1967), D200 (1970), D500 (1968),&lt;br&gt; D500/D600/D700/D800 &lt;br&gt; medium-duty trucks (1970-1972), D500/D600/W600/D700/D800 medium-duty trucks (1974-1977),&lt;br&gt; D100 (1978),&lt;br&gt; Fargo Trucks (1936-1972)
| Located at 300 Tecumseh Road East. Was originally Windsor Plant 1. Became part of Chrysler upon its founding in 1925. Was previously a Maxwell-Chalmers plant and was originally Maxwell's Canadian plant from 1916. Switched to building trucks in 1931 after Plant 3 opened in 1929. Closed in 1978. Became the Imperial Quality Assurance Centre from 1980-1983, doing extra quality control on the 1981-1983 Imperial built at the Windsor Assembly Plant (the car plant - Plant 3) about 1.5 miles east of Plant 1. The Imperial Quality Assurance Centre closed in 1983 when the Imperial was discontinued. Subsequently demolished. Is now the Plaza 300 shopping mall.
|-
|
| Tipton Transmission Plant
| [[w:Tipton, Indiana|Tipton, Indiana]]
| [[w:United States|United States]]
| 2014
| 2023
| [[w:ZF 9HP transmission|948TE 9-speed auto.]] transmission, SI-EVT transmission
| Located at 5880 W. State Road 28. Originally, the plant was supposed to be a [[w:Getrag|Getrag]] plant focused on supplying Chrysler with dual-clutch transmissions. Chrysler withdrew from the deal in 2008 after a dispute over financing and sued Getrag. The 80% completed facility then sat dormant until Chrysler Group purchased the facility in February 2013 and completed construction. Production began in April 2014 with the ZF-designed 9-speed auto. transmission, built under license from ZF. Production ended in June 2023 and 9-speed production was consolidated into Indiana Transmission Plant I in Kokomo, IN. The SI-EVT transmission for the Pacifica Hybrid was moved to Kokomo Transmission Plant. Sold to IRH Manufacturing LLC in September 2024 to make solar cells.
|-
| L (1989-2001),&lt;br&gt; T (1981-1988)
| [[w:Toledo Complex#Parkway|Toledo Assembly #1 Plant]] - Jeep Parkway plant
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 2001 (ended final assembly), 2006 (ended body assembly)
| [[w:Jeep Cherokee (XJ)|Jeep Cherokee (XJ)]] (1984-01), [[w:Jeep Cherokee (XJ)#Wagoneer|Jeep Wagoneer (XJ)]] (1984-90), [[w:Jeep Comanche|Jeep Comanche]] (1986-1992),&lt;br&gt; Bodies for vehicles made at Stickney Ave. plant &lt;br&gt; 
Models only made before Chrysler takeover: Willys Aero (1952-1955), Kaiser Manhattan (1954-1955), Jeep CJ (1946-1986), Jeep DJ, Jeep Jeepster (1948-1950), Jeep Jeepster Commando (1967-1971), Jeep Commando (1972-1973), Willys Jeep Station Wagon (1946-1964), Willys Jeep Truck (1947-1965), Jeep Gladiator (SJ) (1963-1971), Jeep J-series pickup, Jeep Wagoneer [SJ] (1963-1981), Jeep Cherokee [SJ] (1974-1981), Jeep Forward Control [FC] (1957-1965), Jeep FJ Fleetvan (1961-1975), Military Jeeps
| Located at 1000 Jeep Parkway. The John North Willys-owned Overland Automobile Co. purchased the plant in 1909 from Pope-Toledo, another early automaker. Overland Automobile Co. became Willys-Overland in 1912. Began building Jeeps in the 1940s. This was the original Jeep assembly plant. Willys-Overland was bought by Kaiser in 1953. Kaiser then sold its Willow Run plant in Ypsilanti, MI to GM and moved its production to the Willys plant in Toledo, OH. Kaiser and Willys production in the US ended in 1955 and Toledo focused on Jeep production going forward. Kaiser Jeep was sold to AMC in 1970. Became part of Chrysler in the 1987 buyout of AMC. Final assembly ended in 2001 when the XJ Cherokee ended production but painted body production continued until June 30, 2006, when the TJ Wrangler ended production. Production of the replacement JK Wrangler moved to the new Toledo Supplier Park plant a few miles away.  The Administration Building, used from 1915 through 1974, was imploded on April 14, 1979. A third of the plant was demolished in 2002 after final assembly ended including the Jeep Museum. The remainder was demolished in 2006-2007 after body production ended. One of the three large brick smokestacks was preserved and was dedicated in 2013 to the plant's history and workforce. A bronze plaque was mounted next to the smokestack, which still says &quot;Overland&quot; on it. Over 11 million vehicles were produced at the site, including military Jeeps during World War II. The site was sold to the Toledo-Lucas County Port Authority in 2010. The site has been redeveloped into the Overland Industrial Park. Dana Inc. and Detroit Manufacturing Systems are among the tenants in the Overland Industrial Park and those plants supply the current Jeep plants elsewhere in Toledo. All-Phase Electric Supply Co. is another tenant. 
|-
| P (1989-2006),&lt;br&gt; T (1981-1988)
| [[w:Toledo Complex#Stickney|Toledo Assembly #2 Plant]] - Jeep Stickney Ave. plant
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 1987 (became part of Chrysler)
| 2006 
| [[w:Jeep Wagoneer (SJ)#1984: SJ and XJ|Jeep Grand Wagoneer (SJ)]]&lt;br&gt; (1984-1991),&lt;br&gt; [[w:Jeep Wrangler (YJ)|Jeep Wrangler (YJ)]] (1993-95), [[w:Jeep Wrangler (TJ)|Jeep Wrangler (TJ)]] (1997-06)
Models only made before Chrysler takeover:&lt;br&gt; Jeep Wagoneer [SJ] (1981-1983), Jeep Cherokee [SJ] (1981-1983)
| Located at 4000 Stickney Ave. Originally opened in 1942 by the Electric Auto-Lite Co., a maker of spark plugs. Sold to Kaiser-Jeep in 1964, which used it as a machining and engine plant until 1981, when AMC converted it for vehicle production. AMC had taken over Kaiser Jeep in 1970. AMC built the SJ Wagoneer and Cherokee at the Stickney Ave. plant. Body assembly was done at an SJ- or later,  Wrangler-specific body shop at the Parkway plant while final assembly was at the Stickney Ave. plant. Became part of Chrysler in the 1987 buyout of AMC. Production ended in 2006 with the end of the TJ Wrangler. Production of the replacement JK Wrangler moved to the new Toledo Supplier Park plant built on the site of the old Stickney Ave. plant. 
|-
| W (1994-1996)
| [[w:Toledo Complex#Stickney|Toledo Assembly #3 Plant]] - Jeep Stickney Ave. plant
| [[w:Toledo, Ohio|Toledo, Ohio]]
| [[w:United States|United States]]
| 1993
| 1996 
| [[w:Dodge Dakota#First generation (1987–1996)|Dodge Dakota]] (1994-1996)
| Body assembly was done at a Dakota-specific body shop at the Parkway plant while final assembly was at the Stickney Ave. plant.
|-
|
| Toluca Engine Plant 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| ?
| 2002
| [[w:Chrysler Slant-6 engine|Chrysler Slant-6 engine]], [[w:Chrysler LA engine|Chrysler LA V8 engine]]
| Closed in 2002
|-
|
| Toluca Transmission Plant 
| [[w:Toluca|Toluca]], [[w:State of Mexico|State of Mexico]]
| [[w:Mexico|Mexico]]
| ?
| 2001
| Automatic Transmissions for fwd cars
| Closed in 2001
|-
| 
| [[w:Trenton Engine Complex|Trenton Engine North Plant]] 
| [[w:Trenton, Michigan|Trenton, Michigan]]
| [[w:United States|United States]]
| 1952
| 2022
| [[w:Chrysler B engine|Chrysler B V8 engine]],&lt;br&gt; [[w:Chrysler B engine#RB engines|Chrysler RB V8 engine]],&lt;br&gt; [[w:Chrysler Slant-6 engine|Chrysler Slant-6 engine]],&lt;br&gt; [[w:Volkswagen EA827 engine#1.7|VW 1.7L EA827 I4 engine]] (adding Chrysler parts to already built VW engines made in W. Germany),&lt;br&gt; [[w:Chrysler 2.2 &amp; 2.5 engine|2.2L/2.5L &quot;K-car&quot; I4 engine]], [[w:Chrysler 1.8, 2.0 &amp; 2.4 engine|1.8L, 2.0L I4 &quot;Neon engine&quot;]], [[w:Chrysler 3.3 &amp; 3.8 engines|3.3L/3.8L OHV V6]], [[w:Chrysler SOHC V6 engine|3.5L/3.2L/4.0L SOHC V6]], [[w:Chrysler Pentastar engine|3.2L/3.6L Pentastar V6 engine]], [[w:World Gasoline Engine#2.4_2|2.4L Tigershark I4]],&lt;br&gt; Engine components,&lt;br&gt; Air raid sirens
| Located at 2000 Van Horn Road. Trenton North began production in fall 1952 and was expanded in 1964, 1967, 1969, 1976, and 1977. At first, Trenton North began by making water pumps and air raid sirens but engines quickly followed. Trenton Engine North was Chrysler’s first dedicated engine factory in the US, separate from the assembly plants. On September 29, 1978, V8 production ended. Trenton North added Chrysler parts such as the intake and exhaust manifolds, water pump, ignition system and other major parts to already built VW 1.7L EA827 I4 engines imported from Salzgitter, W. Germany for use in the Omni/Horizon. Production of the 3.5L V6 moved to Kenosha Engine in 2003. Trenton North was idled in May 2011 when the 3.8 V6 ended production following the end of 3.3 &amp; 4.0 V6 engine production in 2010. Chrysler then announced in June 2011 it would use a fifth of the plant to make components for the Pentastar V6 being made at Trenton South. In January 2012, Trenton North began producing the 3.6L Pentastar V6 engine. Chrysler then installed a flexible production line that could build both the Pentastar V6 and the Tigershark I4. In May 2013, Trenton began producing the 3.2L Pentastar V6. Tigershark I4 production began late in 3rd quarter 2013. By the end of 2022, Pentastar Upgrade engine production moved from Trenton North to Trenton South and the older North plant ended production. Trenton North has been repurposed for warehousing and other non-manufacturing opportunities. 
|-
|
| [[w:Tritec engine|Tritec Motors Ltda.]] 
| [[w:Campo Largo, Paraná|Campo Largo, Paraná]] 
| [[w:Brazil|Brazil]]
| 2000
| 2007
| [[w:Tritec engine|1.4L/1.6L/1.6L supercharged &lt;br&gt; Tritec I4 engine]] 
| Originally established in 1997 as a 50/50 joint venture between Chrysler and [[w:BMW|BMW]] to jointly develop the Tritec 4-cylinder engine and build it at a newly built, jointly owned plant in Brazil. At the time, BMW owned the [[w:Rover Group|Rover Group]], which was developing a new generation of the Mini and Rover worked with Chrysler to develop the Tritec engine that would power the new Mini. In 1998, Chrysler merged with Daimler-Benz, forming DaimlerChrysler. Production of the new engine began in January 2000. BMW broke up and sold off the Rover Group in 2000 but it retained the rights to the new generation Mini then under development and the 50% stake in Tritec Motors. BMW used all 3 versions of the engine in the new generation [[w:Mini Hatch#First generation (R50/52/53; 2001)|MINI]]. Chrysler used the normally aspirated 1.6L version of the engine in non-North American market versions of the [[w:Chrysler Neon#Second generation (2000)|Neon]] and the [[w:Chrysler PT Cruiser|PT Cruiser]]. The normally aspirated 1.6L engine was also supplied to Chinese automakers [[w:Chery|Chery]] and [[w:Lifan Group|Lifan]]. Tritec engine production ended in June 2007. On July 11, 2007, BMW sold its 50% stake in Tritec Motors to [[w:Chrysler#1998–2007: DaimlerChrysler|DaimlerChrysler]]'s Chrysler Group. BMW did not use the Tritec engine in any subsequent models. BMW jointly developed with [[w:PSA Group|PSA Peugeot Citroën]] a new engine called [[w:Prince engine|Prince]] for the [[w:Mini Hatch#Second generation (R56/57; 2006)|next generation Mini]], which launched as a 3-d hatch for 2007 and as a convertible for 2009. In March 2008, the plant and the rights to the engine design were sold to [[w:Fiat|Fiat]], which then updated the engine into the [[w:Fiat E.torQ engine|E.torQ engine]]. The E.torQ engine was offered in the same 1.6L displacement as the Tritec and was also enlarged to 1.7L (1747 cc), though the 1.7L was referred to as a 1.8L. The E.torQ engine was produced in the same plant as the Tritec engine by Fiat from 2010-2023. Became part of [[w:Fiat Chrysler Automobiles|Fiat Chrysler Automobiles]] upon its founding in 2014. Then became part of [[w:Stellantis|Stellantis]] upon its founding in 2021 along with Fiat and Chrysler. Ironically, the E.torQ engine also ended up powering certain Chrysler Group models outside the US and Canada. It was used in the South American/European/Australian market Jeep Renegade and the Mexican and Middle East market 2017-2020 Dodge Neon, which was a rebadged Fiat Tipo made in Turkey. It was also used in the Mexican market Dodge Vision and Ram 700 and the South American market Ram 1000. The plant was closed in 2023, following the end of E.torQ engine production.
|-
|
| [[w:Twinsburg Stamping|Twinsburg Stamping]]
| [[w:Twinsburg, Ohio|Twinsburg, Ohio]]
| [[w:United States|United States]]
| 1957
| 2010
| Stampings and assemblies
| Located at 2000 East Aurora Road. Opened in August 1957. Closed July 31, 2010. Sold in 2011. Demolished in 2012-2013. Now the Cornerstone Business Park.
|-
|
| Vernor Tool &amp; Die plant (South plant)
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953
| 1983
| Tooling &amp; Dies
| Located at 12026 E Vernor Highway. Operations moved to Mount Elliott Tool and Die. The former location seems to have been swallowed up by the Jefferson North Assembly plant.
|-
|
| Vernor Trim plant (North plant)
| [[w:Detroit, Michigan|Detroit, Michigan]]
| [[w:United States|United States]]
| 1953
| 1970's
| Trim
| Located at 12025 E Vernor Highway. The former location seems to have been swallowed up by the Jefferson North Assembly plant.
|-
| 4 (1960-1961),&lt;br&gt; 7 (1959)
| Warren Avenue Plant
| [[w:Dearborn, Michigan|Dearborn, Michigan]]
| [[w:United States|United States]]
| 1927,&lt;br&gt; 1950 (opened as part of Chrysler)
| 1960s
| DeSoto bodies (1950-1958), DeSoto engines &lt;br&gt; (1951-1958),&lt;br&gt; [[w:Imperial (automobile)#Second generation (1957–1966)|Imperial]] (1959-1961)
| Located at 8505 West Warren Avenue. This was previously the factory of Paige and Graham-Paige. Chrysler leased half the plant in 1941 to use for military production. Chrysler produced aircraft components for the [[w:Martin B-26 Marauder|B-26 Marauder]] (nose and center fuselage sections) and the [[w:Boeing B-29 Superfortress|B-29 Superfortress]] (the pressurized nose section, wing leading edges, and engine cowlings). The B-29 had a nose so large that trenches had to be dug in the floor and some of the bracing for the plant’s roof girders had to be removed to accommodate the aircraft. Chrysler bought the plant in 1947. Began building bodies for DeSoto in August 1950. Engine production began in 1951. Production of the Imperial brand moved here from the Jefferson Ave. plant in Detroit for 1959 in an attempt to give the Imperial brand its own, exclusive factory however sales weren't high enough to support its own plant so Imperial production moved back to the Jefferson Ave. plant in Detroit for 1962. Production of small parts followed for a few years as did export operations. The plant was later sold. Most of the plant has seen been demolished but the front building facing on Warren Ave. is still there and is now used as Corporate HQ by Shatila Food Products. The DeSoto logo, featuring a stylized image of Hernando de Soto, can still be seen at the top of the building above the front door. 
|-
| T (1970-), 2 (1966-1969),&lt;br&gt; 
| Warren Truck #2 Assembly Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1966
| 1975
| Dodge heavy-duty trucks
| Located at 6600 East 9 Mile Road, at the corner of Sherwood Ave and East 9 Mile Road. Closed in 1975 when Dodge exited the heavy-duty truck market. Site now belongs to Sundance Beverage Co., the parent of Everfresh Juice Co.
|-
| V (1971-1979)
| Warren Truck (Compact) #3 Assembly Plant
| [[w:Warren, Michigan|Warren, Michigan]]
| [[w:United States|United States]]
| 1970
| 1979
| [[w:Dodge Sportsman|Dodge Tradesman/Sportsman]] (1971-1979),&lt;br&gt;[[w:Plymouth Voyager#Full-size van (AB; 1974–1983)|Plymouth Voyager]] (1974-1979)
| Was located at 22000 Hoover Road between Toepfer Road and East 9 Mile Road however this address is no longer used. It's now 21900 Hoover Road. The property was purchased in 1937 by Divco (Detroit Industrial Vehicle Company), which opened a new factory on the site in 1939 to build delivery trucks. Divco's headquarters were also at this location but moved to Richmond, IN after Divco bought Wayne Works, Inc. in 1956. In 1968, delivery truck production was moved to Delaware, OH and in 1969, the factory was sold to Chrysler. Chrysler started building the new 1971 model &lt;br&gt; B-series vans there in 1970. Production seems to have ended in 1979. The buildings still seem intact as of 2025. Midwest Freight Systems and Sherwood Truck Repair occupy the site now.
|-
| 
| Windsor Engine Plant
| [[w:Windsor, Ontario|Windsor]], [[w:Ontario|Ontario]]
| [[w:Canada|Canada]]
| 1938
| 1980
| [[w:Chrysler flathead engine#Straight-6|Chrysler flathead inline 6]],&lt;br&gt; [[w:Chrysler Slant-6 engine|Chrysler Slant-6 engine]], &lt;br&gt;[[w:Chrysler A engine|Chrysler A V8 engine]],&lt;br&gt; [[w:Chrysler LA engine|Chrysler LA V8 engine]]
| Was originally Windsor Plant 2. Located just to the south of Windsor Plant 3, the current minivan factory. Closed in August 1980. Built over 8 million engines. Windsor Assembly Plant (Plant 3) expanded onto the site of the old engine plant when it was being renovated for minivan production. 
|- 
|
| [[w:Detroit Assembly#LaSalle Factory/DeSoto Factory|Wyoming Ave. Assembly (DeSoto Wyoming Ave. plant)]] / Wyoming Export Plant
| [[w:Detroit|Detroit]], [[w:Michigan|Michigan]]
| United States
| 1936
| 1958 (Vehicle prod.),&lt;br&gt; 1980 (export operations)
| [[w:DeSoto (automobile)|DeSoto]] (1937-1958),&lt;br&gt; CKD Export (1960-1980)
| Located at 6000 Wyoming Avenue. Originally built to produce Liberty aircraft engines in World War I, opening in 1917. In 1919, was taken over by Saxon Motor Co., owned by Hugh Chalmers of Chalmers Motor Co. GM bought the plant in 1926 and built the LaSalle there from 1927-1933. GM sold Wyoming Assembly to Chrysler in 1934, which then used it to build its DeSoto brand. Became DeSoto's home plant. During World War II, Chrysler built wing center sections for the [[w:Curtiss SB2C Helldiver|Curtiss SB2C Helldiver]] at the Wyoming Ave. plant. For 1959, DeSoto's models other than the Dodge-based Firesweep were moved to Chrysler's Jefferson Ave. plant in Detroit. The Dodge-based Firesweep was already built at the Dodge plant in Hamtramck. This was done so that bodies and final assembly would be done in either a single facility or a pair of connected facilities. This was part of Chrysler's move to unibody construction for 1960 for all cars except Imperial. After the DeSoto brand was discontinued in late 1960, became Wyoming Export plant which was used to prepare vehicles for export. Plant closed in 1980. Plant was demolished in 1992. Site is now occupied by Comprehensive Logistics Inc.
|}

==Non-Chrysler FCA/Stellantis Factories Previously Making Chrysler Group Vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 1
| [[w:Fiat Cassino Plant|Cassino Plant]]
| [[w:Piedimonte San Germano|Piedimonte San Germano]], [[w:Province of Frosinone|Province of Frosinone]]
| [[w:Italy|Italy]]
| 1972
| 
| Past Chrysler Group models: [[w:Lancia Delta#|Chrysler Delta]] (UK/Ireland)
| Fiat plant. 
|-
| 3
| [[w:Alfa Romeo Pomigliano d'Arco plant|Pomigliano d'Arco plant]] (Giambattista Vico plant)
| [[w:Pomigliano d'Arco|Pomigliano d'Arco]], [[w:Metropolitan City of Naples|Metropolitan City of Naples]]
| [[w:Italy|Italy]]
| 1972
|
| Past Chrysler Group models: [[w:Dodge Hornet|Dodge Hornet]] (2023-2025). Related models:&lt;br&gt; [[w:Alfa Romeo Tonale|Alfa Romeo Tonale]] (2023-)
| Originally, an Alfa Romeo plant. Oriiginally owned by Construction Industry Neapolitan Vehicles Alfa Romeo - Alfasud S.p.A., a joint venture between Alfa Romeo (88%), Finmeccanica (10%), and IRI (2%). In 1982, Alfasud S.p.A. was renamed Inca Investments. Alfa Romeo was taken over by Fiat in 1986. Fiat merged with Chrysler to form Fiat Chrysler Automobiles (FCA) in 2014. FCA merged with PSA Group to form Stellantis in 2021. 
|}

==Non-Chrysler Group DaimlerChrysler/Daimler AG Factories Previously Making Chrysler Group Vehicles== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Opened
! style=&quot;width:10px;&quot;|Idled
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 5
| Mercedes-Benz Plant Düsseldorf
| [[w:Düsseldorf|Düsseldorf]], [[w:North Rhine-Westphalia|North Rhine-Westphalia]]
| [[w:Germany|Germany]]
| 1962
|
| [[w:Dodge Sprinter|Dodge Sprinter]] (2003-2009)
| Mercedes-Benz Plant. 
|-
| 9
| Mercedes-Benz Plant Ludwigsfelde
| [[w:Ludwigsfelde|Ludwigsfelde]], [[w:Brandenburg|Brandenburg]]
| [[w:Germany|Germany]]
| 1991 (Mercedes prod. began)
|
| [[w:Dodge Sprinter#Second generation (2006–2018, NCV3)|Dodge Sprinter]] chassis cab (2007-2009)
| Mercedes-Benz Plant. Originally established in 1936 by Daimler-Benz to make airplane engines. The plant was bombed by the US in 1945. After the war ended, what remained of the factory was dismantled and taken to the Soviet Union as reparations. On February 1, 1991, Mercedes-Benz took a 25% stake in the Ludwigsfelde plant, which had previously belonged to East German truckmaker VEB Automobilwerke. It became a 100% owned subsidiary of Mercedes-Benz on January 1, 1994. Sprinter production began in 2006. 
|}

==Former partner factories== 
{| class=&quot;wikitable sortable&quot;
! style=&quot;width:60px;&quot;|VIN
! style=&quot;width:100px;&quot;|Name
! style=&quot;width:80px;&quot;|City/state
! style=&quot;width:80px;&quot;|Country
! style=&quot;width:10px;&quot;|Prod. for Chrysler began
! style=&quot;width:10px;&quot;|Prod. for Chrysler ended
! style=&quot;width:260px;&quot;|Products
! style=&quot;width:370px;&quot; class=&quot;unsortable&quot;|Comments
|-
| 6
| [[w:China Motor Corporation|China Motor Corporation]]
| [[w:Yangmei District|Yangmei District]], [[w:Taoyuan, Taiwan|Taoyuan]]
| [[w:Taiwan|Taiwan]]
| 2006
| 2007
| [[w:Chrysler Town &amp; Country (minivan)#Fourth generation (2001–2007)|Chrysler Town &amp; Country]]&lt;br&gt; (Taiwan: 2006-2007),&lt;br&gt; [[w:Dodge 1000|Dodge 1000]] (Mexico: 2007-'10)
| China Motor Corporation plant. Built for Chrysler under license by China Motor Corporation of Taiwan. Production began April 18, 2006. 
|-
|
| [[w:Carrozzeria Ghia|Carrozzeria Ghia]] 
| [[w:Turin|Turin]]
| [[w:Italy|Italy]]
| 1957
| 1965
| [[w:Imperial (automobile)#Imperial Crown (1955–1965)|Imperial Crown Limousine]] (1957-1965) modified, painted limousine bodies and interiors
| 132 Imperial Crown Limousines were built by Ghia under contract for Chrysler between 1957 and 1965. The 1957-1959 models were based on modified 2-door hardtops with the more rigid chassis from the convertible. The 1960-1965 models were based on 4-door models. Ghia lengthened the frame and modified the bodywork and interiors to create the limousines. After producion ended in 1965, Ghia sold the tooling to Barreiros of Spain, which built another 10 Imperial Crown Limousines. Barreiros had been 35% owned by Chrysler since 1963. That was increased to 77% in 1967 and 100% in 1969.  
|-
| U
| [[w:Hyundai Motor Company|Hyundai Motor Co.]] - [[w:List of Hyundai Motor Company manufacturing facilities#Ulsan Plant|Ulsan plant]]
| [[w:Ulsan|Ulsan]]
| [[w:South Korea|South Korea]]
| 2000
| 2014
| Mexico only: &lt;br&gt; [[w:Dodge Atos|Dodge Atos]] (2001-2012),&lt;br&gt;  [[w:Dodge Verna|Dodge Verna]] (2004-06),&lt;br&gt;  [[w:Dodge Attitude#First generation (MC; 2006)|Dodge Attitude (MC)]] (2007-'11), [[w:Dodge Attitude#Second generation (RB; 2011)|Dodge Attitude (RB)]] (2012-'14), [[w:Dodge H100|Dodge H100 truck]],&lt;br&gt; [[w:Hyundai Starex#Second generation (TQ; 2007)|Dodge H100 Van/Wagon]]
| Rebadged Hyundai models sold as Dodges in Mexico. 
|-
| 
| [[w:Hyundai Motor India|Hyundai Motor India]]
| [[w:Chennai|Chennai]], [[w:Tamil Nadu|Tamil Nadu]]
| [[w:India|India]]
| 2011
| 2014
| Mexico only: &lt;br&gt; [[w:Dodge i10|Dodge i10]] (2012-2014)
| Rebadged Hyundai model sold as a Dodge in Mexico. 
|-
| X
| [[w:Karmann|Karmann Osnabrück Assembly]]
| [[w:Osnabrück|Osnabrück]], [[w:Lower Saxony|Lower Saxony]]
| [[w:Germany|Germany]]
| 2003
| 2007
| [[w:Chrysler Crossfire|Chrysler Crossfire]] (2004-2008)
| Karmann plant. Built under contract for Chrysler. 
|-
| Y
| [[w:Magna Steyr|Magna Steyr]] / Steyr-Daimler-Puch - Chrysler Steyr Assembly
| [[w:Graz|Graz]], [[w:Styria|Styria]]
| [[w:Austria|Austria]]
| 1994
| 2010
| [[w:Jeep Grand Cherokee|Jeep Grand Cherokee]]&lt;br&gt; (1995-2010),&lt;br&gt; [[w:Jeep Commander (XK)|Jeep Commander]] (2006-2010), [[w:Chrysler Voyager#Fourth generation (2001–2007)|Chrysler Voyager/Grand Voyager]] (2003-2007),&lt;br&gt; [[w:Chrysler 300#First generation (2005)|Chrysler 300C/300C Touring]] (2005-2010)
| Originally, a Steyr-Daimler-Puch plant. Magna International acquired a majority holding of 66.8% in Steyr-Daimler-Puch in 1998 and acquired the rest by 2002 when it was renamed Magna Steyr. Production of the Chrysler Voyager and Grand Voyager minivans moved from the Eurostar plant  next door to the main Magna Steyr plant for 2003. Chrysler minivan production in Austria ended on November 30, 2007. Built under contract for Chrysler. 
|-
| B
| [[w:Maserati|Maserati]] - [[w:Innocenti|Innocenti]] plant
| [[w:Lambrate|Lambrate district]], [[w:Milan|Milan]]
| [[w:Italy|Italy]]
| 1988
| 1990
| [[w:Chrysler TC by Maserati|Chrysler TC by Maserati]]&lt;br&gt; (1989-1991)
| Developed jointly by Chrysler and Maserati, the TC was built in Italy by Maserati at the Innocenti plant in Milan. Maserati and Innocenti were both owned by DeTomaso at the time. Chrysler bought a 5% stake in Maserati in 1984 and increased its stake to 15.6% in 1986. Production ended in 1990 due to low sales.
|-
| U
| Mitsubishi - Mizushima plant (Line 1)
| [[w:Kurashiki|Kurashiki]], [[w:Okayama Prefecture|Okayama Prefecture]] 
| [[w:Japan|Japan]]
| 1970s
| 1996
| [[w:Plymouth Champ|Plymouth Champ]] (1981-1982), [[w:Plymouth Colt|Plymouth Colt]] (1983-1994), [[w:Dodge Colt|Dodge Colt]] (1981-1994), [[w:Dodge Colt|Dodge/Plymouth Colt]]&lt;br&gt; (Canada only: 1995),&lt;br&gt; [[w:Eagle Summit|Eagle Summit]]&lt;br&gt; (4-d: 1989-1990, 1993-1996,&lt;br&gt; 3-d: 1991-1992, 2-d: 1993-96), [[w:Mitsubishi RVR#North America|Plymouth Colt Vista]] (1993-94), [[w:Mitsubishi RVR#North America|Eagle Summit Wagon]] (1993-96)
| Mitsubishi Motors plant.
|-
| Z
| Mitsubishi - Okazaki plant
| [[w:Okazaki, Aichi|Okazaki]], [[w:Aichi Prefecture|Aichi Prefecture]] 
| [[w:Japan|Japan]]
| 1983
| 1996
| [[w:Plymouth Conquest|Plymouth Conquest]] (1984-86), [[w:Dodge Conquest|Dodge Conquest]] (1984-1986), [[w:Chrysler Conquest|Chrysler Conquest]] (1987-1989), [[w:Dodge Colt Vista#Colt Vista|Dodge Colt Vista]] (1984-1991), [[w:Plymouth Colt Vista#Colt Vista|Plymouth Colt Vista]] (1984-91), [[w:Mitsubishi RVR#North America|Plymouth Colt Vista]] (1992-94), [[w:Mitsubishi RVR#North America|Eagle Summit Wagon]] (1992-96) [[w:Eagle Vista#Vista Wagon|Eagle Vista Wagon]]&lt;br&gt; (Canada: 1989-1991)
| Mitsubishi Motors plant.
|-
| Y (Line 1)&lt;br&gt;/&lt;br /&gt;P (Line 2)
| Mitsubishi - &lt;br&gt; Ooe plant &lt;br&gt; a.k.a. &lt;br&gt; Nagoya #1&lt;br&gt;/&lt;br&gt;Nagoya #2
| Ooe-cho, [[w:Minato-ku, Nagoya|Minato ward]], [[w:Nagoya|Nagoya]], [[w:Aichi Prefecture|Aichi Prefecture]] 
| [[w:Japan|Japan]]
| 1970s
| 1996
| VIN code Y:&lt;br&gt; [[w:Plymouth Sapporo|Plymouth Sapporo]] (1981-1983), [[w:Dodge Challenger#Second generation (1978–1983)|Dodge Challenger]] (1981-1983), [[w:Plymouth Arrow Truck#Chrysler variants|Plymouth Arrow Truck]] ('81-'82), [[w:Dodge Ram 50|Dodge Ram 50]] (1981-1984), [[w:Dodge Stealth|Dodge Stealth]] (1991-1996)
VIN code P:&lt;br&gt; [[w:Dodge Ram 50|Dodge Ram 50]] (1985-1986), [[w:Dodge Ram 50#North America|Dodge Ram 50]] (1987-1993)
| Mitsubishi Motors plant. Closed in 2001. Sold to Mitsubishi Heavy Industries and now used by its Aircraft, Defense &amp; Space Business Area.
|-
| J
| Mitsubishi -  Toyo Koki/Pajero Manufacturing Co., Ltd. plant
| [[w:Sakahogi, Gifu|Sakahogi]], [[w:Gifu Prefecture|Gifu Prefecture]] 
| [[w:Japan|Japan]]
| 1986
| 1989
| [[w:Dodge Raider|Dodge Raider]] (1987-1989)
|  Originally, a Toyo Koki Co. Ltd. plant. Opened in 1976. Built vehicles under contract for Mitsubishi. Mitsubishi Motors owned 35% of Toyo Koki and increased its stake to a majority in March 1995. The plant was then renamed Pajero Manufacturing Co., Ltd. in July 1995. In March 2003, Mitsubishi bought all the remaining shares in Pajero Manufacturing Co., Ltd., making it a wholly owned subsidiary. Closed in 2021. Sold to Daio Paper in 2022.
|-
| H (Attitude), 9 (1200)
| [[w:Mitsubishi Motors (Thailand)|Mitsubishi Motors Thailand]]
| [[w:Laem Chabang|Laem Chabang]], [[w:Chonburi province|Chonburi province]]
| [[w:Thailand|Thailand]]
| 2014
| 2024
| [[w:Dodge Attitude#Third generation (A10; 2015)|Dodge Attitude]]&lt;br&gt; (Mexico: 2015-2024),&lt;br&gt; [[w:Mitsubishi Triton#Fifth generation (KJ/KK/KL; 2014)|Ram 1200]]&lt;br&gt; (Middle East: 2017-2019)
| Mitsubishi Motors plant.  
|-
| ?
| [[w:MMC Automotriz|MMC Automotriz]]
| [[w:Barcelona, Venezuela|Barcelona]], [[w:Anzoátegui|Anzoátegui state]]
| [[w:Venezuela|Venezuela]]
| 2002
| 2009
| [[w:Dodge Brisa|Dodge Brisa]]&lt;br&gt; ([[w:Hyundai Accent#First generation (X3; 1994)|2002-2005]]), ([[w:Hyundai Getz|2006-2009]])
| MMC Automotriz plant. Originally, MMC Automotriz was 49% owned by Consorcio Inversionista Fabril S.A. (CIF) of Venezuela and 42% owned by Nissho Iwai Corp. The remaining 9% of the company was owned by the Japan International Development Organization Ltd., a partnership between the government-financed Overseas Economic Cooperation Fund and 98 private companies. Nissho Iwai merged with Nichimen Corp. in 2004 to form Sojitz Corp. Sojitz later increased its stake in MMC Automotriz to 98%, with the other 2% still held by CIF. MMC Automotriz was sold to the the Sylca Group (also known as Yammine Group) in 2015. MMC Automotriz produced Mitsubishi vehicles and from 1996-2012, also produced Hyundai vehicles. The Dodge Brisa was produced for DaimlerChrysler as part of its cooperation with [[w:Hyundai Motor Company|Hyundai]]. MMC Automotriz also produced Mitsubishi Fuso trucks. 
|-
| G
| [[w:Mitsubishi Motors (Thailand)|MMC Sittipol Co., Ltd.]]
| [[w:Laem Chabang|Laem Chabang]], [[w:Chonburi province|Chonburi province]]
| [[w:Thailand|Thailand]]
| 1988
| 1992
| [[w:Plymouth Colt#Fifth generation (1985–1988)|Plymouth Colt 100]]&lt;br&gt; (Canada: 1988-1992),&lt;br&gt; [[w:Dodge Colt#Fifth generation (1985–1988)|Dodge Colt 100]]&lt;br&gt; (Canada: 1988-1992),&lt;br&gt; [[w:Eagle Vista|Eagle Vista]] (Canada: 1988-92)
| Mitsubishi Motors plant. MMC Sittipol is the predecessor company of Mitsubishi Motors (Thailand). These were the first vehicle exports from Thailand. 
|-
| 2
| [[w:Renault|Renault]] - [[w:Maubeuge Construction Automobile|Maubeuge plant]]
| [[w:Maubeuge|Maubeuge]]
| [[w:France|France]]
| 1987
| 1989
| [[w:Renault Medallion|Renault Medallion]] (1988),&lt;br&gt; [[w:Eagle Medallion|Eagle Medallion]] (1989)
| Renault plant. The Medallion was sold through Chrysler's Jeep-Eagle dealer network as a legacy of Chrysler's takeover of AMC from Renault.
|-
| 8,&lt;br&gt; 0
| [[w:Soueast|Soueast]]
| [[w:Fuzhou|Fuzhou]], [[w:Fujian|Fujian province]]
| [[w:China|China]]
| 2008
| 2010
| [[w:Chrysler Voyager#Fourth generation (2001–2007)|Chrysler Voyager]],&lt;br&gt; [[w:Dodge Caravan#Fourth generation (2001–2007)|Dodge Caravan]]
| South East (Fujian) Motor Co., Ltd. plant. Built for Chrysler under license by South East (Fujian) Motor Co., Ltd.
|}</text>
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  <page>
    <title>Taking Bearings: Artificial Intelligence in Knowledge Platforms and Open, Social Scholarship/Introduction</title>
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      <text bytes="77379" sha1="esdruira6c6194b116v5fzwy2frhn9w" xml:space="preserve">This research scan surveys an emergent and contested terrain: the interlaced developments in artificial intelligence, generative AI, large language models (LLMs) and their predecessors, and the ways these systems are reshaping knowledge production, circulation, and engagement across scholarly and public contexts.

This scan uses artificial intelligence, or AI, as a broad umbrella term for computational systems designed to perform tasks associated with classification, prediction, reasoning, language processing, recommendation, perception, automation, or decision support. It uses generative AI, or genAI, more specifically for systems that generate text, images, code, audio, video, or other outputs in response to prompts, queries, or other inputs. Large language models, or LLMs, are a prominent subset of contemporary genAI systems trained to model and generate language. Because public disclosure often uses these terms interchangeably, this scan uses AI for the broader field and infrastructure, genAI where generative functions are specifically at issue, and LLM where the discussion concerns language-model systems in particular. The wider AI landscape includes technical architectures ranging from symbolic logic and &quot;good old-fashioned AI&quot; (GOFAI), through statistical natural language processing, to contemporary transformer-based genAI models, all situated within institutional and platform economies, cloud infrastructures, and evolving governance regimes (Jones 2023; Anderson 2024). These systems now recalibrate discretion, authority, and visiblity, influencing what is recognized as knowledge, who produces it, and how it moves among diverse publics. 

A brief historical distinction is useful here. AI has not developed through a single technical or ideological pathway. Symbolic approaches, prominent in early AI, treated intelligence as the manipulation of explicit rules, formal representation, and logical structures. Connectionist approaches, by contrast, emphasized distributed pattern recognition across networks of weighted relations. Contemporary deep learning and transformer-based genAI inherit much more from the connectionist tradition, especially its reliance on large datasets, statistical association, and learned representations rather than explicit rules. This inheritance helps explain why contemporary systems can be powerful aids for pattern detection, generation, and transformation, while remaining weak at grounding, verification, and accountable judgement. &quot;Hallucinations&quot;—false responses generated by AI that are especially misleading due to their plausible surfaces—stem from the inherent mathematical design of such systems, which are optimized to generate probable outputs rather than to verify claims within accountable epistemic communities. For fuller historical and critical accounts of these developments, see Jones (2023), Ali et al. (2023), Anderson (2024), and Whiteley (2023).

What emerges from this mapping is a complex phenomenology of entanglement. Generative AI is woven in part from scholarship's own materials—open access literature, research data, metadata schemas, citation networks, community-developed software, and collaborative data infrastructures. These are not the only, or even necessarily the largest, sources on which contemporary systems are trained. But they are unusually authoritative in that they help organize what counts as reliable knowledge, how claims are linked to evidence, how materials are discovered, and how intellectual legitimacy is conferred. The AI systems that now analyze, summarize, and generate scholarly text therefore draw upon knowledge infrastructures whose value has been built over decades by researchers, editors, librarians, publishers, software communities, institutions, and publics.

This recursive relationship positions scholarship as both one of AI's important knowledge substrates and one of its objects of transformation, but the entanglement runs deeper still. Scholarship does not merely feed AI systems; it is increasingly mediated by them. Researchers discover literature through AI-powered recommendation engines, draft manuscripts with generative assistants, and navigate peer review processes augmented by algorithmic triage. Students encounter AI both as subject of study and as tool for learning, while institutions struggle to develop governance frameworks adequate to technologies that evolve faster than policy cycles. The recursive loop—scholarship training AI training scholarship—creates conditions where distinguishing human from machine contribution becomes progressively more difficult, and where the very categories through which we understand authorship, originality, and expertise require renegotiation.

The organizing logic of this collection moves from foundational grounding through INKE-aligned focal points that structure the annotated bibliography itself. It first establishes essential contexts: the histories and theories of AI, including critical perspectives from Science and Technology Studies (STS) and Critical Digital Humanities; accounts of knowledge as relational, plural, and platformed; and the principles of Open Social Scholarship (OSS) as articulated by the Implementing New Knowledge Environments (INKE) Partnership and the Electronic Textual Cultures Lab (ETCL). It then follows three focal threads—&quot;open&quot;, &quot;social&quot;, and &quot;scholarship&quot;—that mark key sites where AI's effects both align with and challenge OSS commitments to accessibility, reciprocity, participatory governance, and public engagement (Arbuckle et al. 2022; El Khatib et al. 2019).

Throughout, the ethos of Open Social Scholarship provides a normative coordinate: a set of principles for interpreting how AI mediates relations among researchers, institutions, communities, and publics. The focus is on how practices, infrastructures, and relations are changing, and how these shifts intersect with OSS values. Which concepts, practices, actors, infrastructures, and frictions are currently reconfiguring the conditions of knowledge and engagement? Where do these movements align with, complicate, or unsettle OSS principles of accessibility, reciprocity, and public value? By attending closely to these dynamics—openness entangled with enclosure, provenance linked to trust, bias in tension with diversity, governance negotiated through participation—a conceptual scaffolding emerges for further analysis and empirical inquiry.

A critical OSS response to AI need not only be defensive. The same systems that threaten enclosure, decontextualization, and epistemic flattening may, under different governance conditions, support broader forms of scholarly engagement: multilingual and plain-language summaries, alternative format outputs, assistive reading and navigation, metadata enrichment, participatory annotation, community translation, and more accessible pathways into specialized research. These possibilities in no way cancel the risks identified throughout this scan. Rather, they clarify the architectural task lying ahead of open, social scholarship: to ask what forms of AI-mediated scholarship can be built under conditions of reciprocity, transparency, care, public value, and shared authority.

== Four Cross-Cutting Tensions ==

The sources assembled here reveal four cross-cutting tensions that structure AI's engagement with scholarship. None admits of simple resolution—each marks a site where choices about AI design and deployment carry real stakes for knowledge production, and where different communities are actively negotiating trade-offs that no technical fix can settle.

'''Operational assistance versus epistemic authority'''. While AI can reduce friction in many workflows, it raises fundamental questions about where judgement, accountability, and interpretive responsibility should reside, and how those boundaries should be renegotiated as tools, practices, and disciplinary norms change. AI excels at standardized tasks—formatting, initial drafts, pattern identification, literature triage—while struggling with the evaluative judgement that gives scholarship its value. The challenge lies in leveraging assistance without ceding authority, using AI capabilities while preserving human responsibility for consequential decisions. When does operational support cross into epistemic territory? How should that boundary be renegotiated as capabilities shift, practices stabilize, and disciplinary communities develop new norms? 

This boundary is historically and institutionally variable. Reference verification, metadata enrichment, formatting, and duplication checks may increasingly be treated as operational tasks. Literature triage, evidence synthesis, translation, and review assistance venture into more contested terrain. Assessments of originality, significance, methodological adequacy, interpretive force, and public consequence continue to require accountable human judgement. The problem of governance is therefore not one of simply drawing a fixed, indelible line once, but to define processes through which scholarly communities can revisit that line over time.

The fluency of AI-generated text can mask the absence of understanding; the appearance of authority can obscure the statistical operations underneath. Sun (2025) emphasizes that models, by definition, are constrained in how they evaluate the novelty of research—they can recognize patterns but cannot evaluate whether patterns matter. This distinction is integral to peer review, research methods, pedagogy, and governance, and each requires clarity about where AI can appropriately assist and where human judgement must remain central.

'''Openness versus enclosure'''. The open infrastructure that has supported equitable access to knowledge is being absorbed into commercial AI systems in ways that may foreclose openness rather than extend it, and the trajectory of this tension will shape whether AI serves broad publics or narrow interests. Open access literature feeds model pretraining: This raises serious concerns about a new enclosure dynamic, in which freely accessible works become inputs for proprietary AI systems that generate commercial value without meaningful reciprocity. Pooley (2024) reveals a troubling symmetry in the underlying asymmetry: both commercial publishers and AI developers extract value from the scholarly commons while returning little to the researchers who create it. The licensing frameworks developed for human readers require substantial adaptation to govern machine consumption, where attribution and context preservation present fundamentally different challenges. Community-sourced data and labour underwrite AI functions, yet the question of whether benefits return to those communities remains contested.

'''Technical capability versus organizational capacity'''. The pace of AI development consistently outstrips the ability of institutions to evaluate, govern, and respond thoughtfully, and the gap between what AI can technically accomplish and what institutions can responsibly deploy constitutes a critical site of intervention.  Building capacity for thoughtful AI adoption requires sustained investment in skills, governance structures, and evaluative frameworks. Weber et al. (2023) identify organizational capabilities as crucial mediators, noting failures often stem from organizational incapacity to manage sociotechnical complexity. Resource-intensive approaches assume capacities—technical staff, governance infrastructure, training budgets, and time for implementation—that are unevenly distributed across institutions and communities. These differences do not map neatly onto institutional size or prestige: large research universities may have more formal infrastructure, but also larger user bases, more complex bureaucracies, and interventions that can become less responsive to local needs. Smaller institutions such as community colleges, public libraries, independent scholarly organizations, and grassroots knowledge projects may face different constraints, including limited staffing, funding, or access to specialized expertise. Across all contexts, institutions are encountering unforeseen complexities for which existing governance structures may be poorly prepared. This tension requires attention to differential institutional positions and the development of governance models that remain humane, adaptable, and scalable across varied contexts. 

'''Efficiency versus process'''. Although AI accelerates tasks, scholarly knowledge earns its credibility through deliberate, iterative processes of review and community validation that efficiency-oriented tools may erode. Pedagogical and scholarly transformations require valuing cognitive work that AI cannot replicate, and education involves developing capacities through practice, not just acquiring outputs. The speed and fluency of AI-generated text can mask the erasure of the deliberative processes—reading, synthesizing, drafting, revising—through which understanding develops. Deng et al. (2025) find that ChatGPT improves student performance while reducing mental effort, raising questions about what learning means when cognitive work is offloaded to machines. The compression of research, writing, and discovery processes may generate outputs while eroding the developmental experiences that scholarly communities value. Process-centered assessment, transparent documentation, and attention to the formative dimensions of intellectual work become crucial responses.

These tensions recur throughout the bibliography's domains. They structure debates about AI in peer review, pedagogy, platform governance, and infrastructure design. Understanding them as ongoing negotiations rather than problems awaiting solution helps position responsible engagement with AI's transformative effects.

== Fundamentals and Ideologies of AI ==
The prominence of generative AI and LLMs is rooted in layered histories. Early symbolic AI attempted to encode knowledge as explicit rules and representations. Statistical natural language processing redirected attention to learning patterns from data. Deep learning, accelerated by transformer architectures and large-scale computation, now underpins models that generate fluent text, code, and images (Jones 2023). Each wave is embedded in institutional settings, funding regimes, and sociotechnical imaginaries that combine benchmark cultures, optimization logics, data abundance, and investor narratives of efficiency and disruption. The concept of &quot;sociotechnical imaginaries&quot; provides crucial analytical purchase for understanding how collective visions shape governance and discourse; as Mao, Richter and Katzenbach (2025) demonstrate, these imaginaries function performatively, actively mobilizing resources, legitimating interventions, and establishing trajectories for development. The figure of &quot;intelligence&quot; functions here as a sociotechnical imaginary: a collective vision that orients research agendas, policy priorities, and public expectations, often sidelining questions of transparency, accountability, and epistemic pluralism.

Understanding contemporary AI requires genealogical attention to its intellectual origins and the sociotechnical imaginaries that have shaped its development. The transition from symbolic AI to statistical learning—from explicit knowledge representation to pattern recognition across massive datasets—represents a fundamental reorientation of assumptions about what counts as intelligence and whose knowledge gets represented. As Jones (2023) argues, the shift toward &quot;empiricist&quot; approaches that capitalize on the &quot;unreasonable effectiveness of data&quot; threatens professions centred on particularity while demonstrating that AI functions as a reflection of human creations including their best and worst traits.

Anderson's (2024) examination of John McCarthy's foundational program reveals AI as philosophical ideology—a vision of perfectly rational abstraction built upon objectivism and scientism that has &quot;come to serve as a blind for increasing techno-corporate control of society.&quot; McCarthy's conception of artificial intelligence as a &quot;stripped down model of human mental engagement without emotional qualities&quot; established patterns that continue to shape the field: the subordination of interpretive judgement to formal optimization, the bracketing of contextual understanding in favor of scalable pattern matching, and the assumption that intelligence admits of decomposition into modular, transferable components. Ali et al. (2023) extend this analysis by situating AI within broader genealogies of industrialization and colonialism, identifying threads of hidden labour, encoded behaviour, and cognitive injustice running through AI's history—positioning AI as the flagship of the Information Age conditioned by the Management Age.

The term &quot;artificial intelligence&quot; itself warrants critical scrutiny. As Whiteley (2023) observes, the phrase anthropomorphizes what is essentially computer-assisted statistical analysis, encouraging expectations and trust that the technology cannot warrant. This terminological slippage—from statistical prediction to &quot;intelligence&quot;—exemplifies how language shapes perception and, through perception, governance. The sources in this bibliography provide conceptual resources for more precise description that preserves space for human agency, critical evaluation, and alternative design pathways.

Critical perspectives from Digital Humanities (DH) and Science, Technology and Society (STS) supply key interpretive tools. They foreground the ways datasets, labels, and evaluation metrics encode values and worldviews; how training regimes replicate archival absences and classification politics; and how the defaults embedded in language, genre, and culture travel into outputs, with particular consequences for marginalized communities. Bender et al. (2021) critically analyze how larger models reproduce hegemonic views: size does not guarantee diversity, because the communities most underrepresented in training data are also those most likely to bear the downstream costs of systems built without them. Automation theory highlights AI as a redistribution of discretion and authority: tasks that once required situated human judgement are delegated to systems that lack context, while accountability structures struggle to keep pace.

Berry (2025) theorizes this moment as &quot;the Inversion&quot; under &quot;computational capitalism&quot; where machine-generated works reshape meaning-making infrastructure, producing &quot;AI slop&quot; that infiltrates information ecosystems with garbled meaning. His concept of &quot;diffusionisation&quot; describes how AI systems dissolve cultural forms into probabilistic vector spaces and reconstitute them through latent space manipulation—a process that transforms the infrastructure of meaning-making itself. This moves beyond mechanical reproduction toward what Berry theorizes as &quot;post-consciousness,&quot; where boundaries between individual and synthetic consciousness become porous. The concept challenges scholars to attend not merely to AI outputs but to how generative systems transform the very grounds upon which experience and meaning are constituted.

Environmental and labour analyses add further layers, tracing the energy-intensive training runs and precarious annotation and moderation work that underpin current capabilities. Klein et al. (2025) argue that AI's statistical enactment of ideology imposes an objectivist European modernist framework upon data, making issues of &quot;bias&quot; unsolvable through technical means alone—even the distinction between &quot;pure&quot; and &quot;toxic&quot; training data reflects ideological commitments. They propose that smaller, purpose-built models developed through genuine interdisciplinary collaboration offer a path forward, one where &quot;technical researchers must recognize the institutional asymmetries&quot; that currently disadvantage humanistic approaches.

Relations with OSS-aligned communities complicate this picture. Open-source software, open datasets, and commons-based peer production have been central to AI's development; influential models rely on openly shared corpora and community-built tools. At the present inflection point, however, pressures toward enclosure are intensifying. Recent work by the Open Source Initiative on open source AI, including its 1.0 Open Source AI Definition, clarifies that releasing model weights alone is not equivalent to full openness. Meaningful openness also depends on access to documentation, code, data information, use rights, and other artifacts needed to understand, modify, and reuse a system. This clarification responds to broader concerns about “openwashing,” in which companies describe AI systems as open while releasing models under restrictive licenses, with incomplete documentation, or without access to key development artifacts. White et al. (2024) similarly develop the Model Openness Framework, establishing a three-tiered classification that shows AI “openness” exists on a spectrum, from minimal weight release to fuller disclosure of training data, intermediate checkpoints, code, documentation, and development practices. Rather than a simple binary between open and closed, the field is experimenting with hybrid forms—open weights under usage constraints, community checkpoints, and permissive yet bounded licenses—that seek to reconcile accessibility with risk management and intellectual property considerations. 

Vake et al. (2025) find the open-source AI community depends on businesses to develop base models—there are few incentives for companies to release openly because doing so risks intellectual property and competitive advantage. This structural dependence raises questions about whether open AI can genuinely serve public interests or will remain subordinated to commercial imperatives. These choices shape not only technical access, but also epistemic legitimacy and the capacity for public oversight, critique, and repair.

== Geographic Diversity in AI Imaginaries ==

The imaginaries circulating around AI vary significantly across geographic and political-economic contexts, challenging narratives of technological inevitability that treat AI development as following a single universal trajectory. Mao, Richter and Katzenbach's (2025) comparative analysis across the United States, China, and Germany reveals heterogeneous and often contradictory imaginaries even within single regulatory regimes. Where US discourse fragments across multiple geographic AI hubs, German imaginaries center on EU policy compliance and regulatory frameworks, while Chinese articulations align tightly with party-state directives that minimize local variation.

Building on the varied sociotechnical imaginaries discussed earlier, Chung (2025) extends this analysis to economically advanced but geographically non-dominant Asian societies—Singapore, Hong Kong, and Taiwan—demonstrating how &quot;techno-developmentalism&quot; produces distinct imaginaries shaped by local political-economic conditions and historical trajectories. These varied articulations challenge the Global North/South binary that structures much AI governance literature, revealing that AI development trajectories remain contingent and shaped by specific political choices rather than following universal technological imperatives.

The imaginaries circulating around AI shape technical design itself. Van Es and Nguyen (2024) demonstrate how ChatGPT's self-representations—82% depicting humanoid forms—strategically cultivate anthropomorphic imaginaries that encourage overlooking ethical and legal challenges. The friendly assistant persona, surrounded by books and radiating futuristic light, constructs a humanoid image of trustworthy intellectual companionship that obscures the statistical operations underneath.

For scholarly communities, these developments necessitate specifically humanities-oriented engagement. Chun and Elkins (2023) argue that humanities-oriented pedagogy offers distinctive resources for this moment, insisting that the most effective AI tools amplify rather than replace human intellectual engagement—a claim developed more fully in the Critical Literacies section below.

== Knowledge Foundations ==

In this framework, knowledge appears as a relational practice rooted in communities, languages, and infrastructures. Three dimensions are especially salient for understanding AI's impact: diversity, mobilization, and platforms.

'''Diversity'''. Epistemic, cultural, linguistic, and methodological plurality are conditions for robust, public-facing scholarship. Models trained predominantly on dominant corpora risk misrecognition and erasure, flattening the diversity that constitutes human knowledge. Arbuckle (2020) articulates diversity as fundamental to legitimate knowledge translation, emphasizing inclusive modes of engagement and participatory approaches that honor varied ways of knowing. In response, approaches such as community governance of data, participatory evaluation, and multilingual modeling work to adapt tools to difference rather than requiring difference to conform to tools. Crompton et al. (2020) address how community governance can safeguard plural representation in data infrastructures like Wikidata, demonstrating that technical systems encode choices about whose knowledge counts and how it gets categorized. The FAIR principles—Findable, Accessible, Interoperable, Reusable—offer a technical framework for data stewardship, while the CARE principles—Collective Benefit, Authority to Control, Responsibility, Ethics—introduce dimensions of sovereignty, consent, and community benefit that are especially important for Indigenous data and other contexts shaped by power asymmetries (Carroll et al. 2020; Carroll et al. 2021).

'''Mobilization'''. Knowledge mobilization concerns how research travels and is taken up across domains: from scholarship to policy, from specialist discourses to public understanding, from the classroom to community settings. Generative tools can accelerate synthesis and enhance accessibility by producing multilingual summaries, plain-language translations, and alternative-format outputs. The same tools can also increase the volume and velocity of decontextualized or misleading claims. Winter (2023) frames policy as a vehicle for mobilization emphasizing provenance and accountability—mechanisms that become ever more crucial when automated systems mediate between research and its publics. Jensen (2023) connects commons-based infrastructures to mobilization pathways, highlighting how interoperability and community practices shape whether knowledge flows toward public benefit or private capture. A central challenge is ensuring that speed does not erode fidelity, and that reach does not come at the expense of context or community consent.

The Canadian HSS Commons exemplifies mobilization infrastructure designed around principles of reciprocity and community responsiveness. Winter et al. (2020) describe how this platform instantiates governance mechanisms, provenance tracking, and dialogic engagement in a Canadian context, offering a concrete model for how digital research communities might align with OSS values. The Commons demonstrates that alternatives to extractive platform models are possible when design priorities center community benefit and participatory governance.

'''Infrastructure and Platforms'''. Repositories, journals, preprint servers, and social scholarly tools form the infrastructural backbone of scholarly communication due to their ubiquity, reliability and invisibility (Plantin et al. 2018). AI-mediated functions such as search, recommendation, summarization, moderation, and peer review reshape relations of production, discoverability, and legitimacy. Turning research outputs into training data for AI technologies creates a process of platformization of digital research infrastructure, in which the research process is commodified and turned into data for publishers and corporations to exploit while excluding the research community from the governance of these infrastructures. Bullard (2023) reveals how metadata shapes these dynamics, demonstrating that descriptive schemas determine what gets found, how it gets categorized, and whose work becomes visible. Goddard (2021) positions persistent identifiers as crucial connective tissue for provenance and interoperability, enabling the traceability that accountability requires. Whether platforms act as commons or proprietary funnels depends on decisions about interoperability, open standards, licensing, and governance. Colbert-Lewis et al. (2024) examine the citation economy as a site of extraction for surveillance publishing, documenting how publishers have transitioned to technology-driven data brokers that monetize researcher behavior alongside research outputs. Seemingly technical or back-end decisions structure how knowledge circulates and who benefits from that circulation.

== Open Social Scholarship Principles ==

Open Social Scholarship, as developed by INKE and ETCL, characterizes scholarship as a public, collaborative practice sustained by open, participatory, and ethically governed infrastructures (Arbuckle et al. 2022; El Khatib et al. 2019). Within this frame, AI is evaluated not solely on technical metrics but on whether it strengthens dialogic exchange, lowers barriers without reproducing harm, and supports reciprocal engagement rather than unilateral extraction. Openness is coupled with care; accessibility with accountability; participation with shared authority. Arbuckle and Maxwell (2019) move beyond open access by emphasizing infrastructure choices and governance as sites where values are enacted—recognizing that technical decisions embed normative commitments about who can participate, on what terms, and toward what ends. Maxwell (2015) argues that &quot;access&quot; alone proves insufficient; usability and community-responsive workflows reposition openness as an ecosystem with embedded care and accountability.

This also gives OSS a constructive role in relation to AI. Rather than approaching AI only as an external threat to be resisted, OSS can help specify what accountable alternatives would require: community-shaped tools, transparent provenance, accessible interfaces, multilingual and multimodal engagement, benefit-sharing where public or community knowledge is used, and governance arrangements that keep interpretive authority distributed rather than concentrated in proprietary systems.

Several principles translate into analytical vantage points for observing AI's effects:

'''Openness with care''' balances access with consent and community control, recognizing that uncontrolled circulation can facilitate extraction when reciprocity is absent (Carroll et al. 2020). Some knowledge requires protection; openness can become extractive when divorced from attention to power asymmetries and community interests.

'''Participation with shared authority''' embeds publics and communities in the design, evaluation, and governance of AI tools, rather than positioning them as passive recipients. Engagement becomes genuine partnership, not consultation that leaves final decisions to technical experts.

'''Accessibility''' is treated as multidimensional, spanning language, different ableness, technical literacy, and the digital divides that structure who can engage with AI-mediated scholarship. True accessibility requires attention to the multiple barriers—linguistic, economic, infrastructural—that shape unequal participation.

'''Reciprocity and benefit-sharing''' acquire particular weight where community-sourced data, scholarship, cultural material or labour underwrite AI functions; the question of whether benefits return to those communities become central. In heterogeneous training-data environments, reciprocity cannot always mean simple one-to-one compensation or attribution. It may also require collective mechanisms: investment in public infrastructure, support for community-governed datasets, licensing arrangements, provenance standards, access rights, audit mechanisms, and benefit-sharing models that recognize the distributed labour through which knowledge systems are built.

'''Infrastructural responsibility''' assigns institutions ongoing obligations to steward provenance, auditability, and accountability across the AI lifecycle—from adoption through monitoring, incident response, and iterative refinement. 

These principles serve as lenses that help clarify where choices around AI align with OSS values and where they introduce new tensions. They support a descriptive, attuned stance that remains open to emerging research, changing practices, and the contested meanings that animate debates over AI's place in scholarship.

== AI and &quot;Open&quot; ==

Openness operates across several registers—access, data, source, science, and social scholarship—and AI interacts differently with each. The recursive relationship between AI and openness demands particular attention: open access literature, open data, open source software, open standards, and community-maintained infrastructures have all contributed to the conditions under which contemporary AI systems became possible. Yet these resources now circulate within systems that often tend toward enclosure, secrecy, and commercial capture. The result is not a simple opposition between open and closed, but a contested field in which openness can serve public knowledge, enable scrutiny, and support community adaptation, while also becoming a reservoir from which private systems extract value without adequate attribution, consent, or reciprocity. 

=== Open Access ===

Open access literature forms one important input into model pretraining, retrieval-augmented generation, summarization, and later synthesis, while a dark shadow has fallen over how works licensed for broad human access are being repurposed for machine processing, private capture, and commercial value extraction. Pooley (2024) critically examines how commercial publishers frame AI companies as &quot;free-riders&quot; while themselves profiting from unpaid scholarly labour, extending &quot;surveillance publishing&quot; into AI domains. His analysis reveals a troubling symmetry: both commercial publishers and AI developers extract value from the scholarly commons while returning little to the researchers who create it. Kember and Brand (2023) document how OA policies may unintentionally contribute to greater consolidation enabling &quot;corporate capture&quot;—a warning that good intentions around openness can produce perverse outcomes when power asymmetries remain unaddressed.

Licensing frameworks and machine-access provisions influence whether open access functions as a commons or a reservoir for extraction. Luth (2025) examines how stakeholders navigate AI training on Creative Commons content, finding compliance often uncertain and highlighting strategies for protecting shared knowledge while sustaining open ecosystems. Smith (2025) analyzes how existing licenses perform in machine learning contexts, noting most were drafted without anticipating large-scale AI training and proposing machine-readable licensing provisions that could clarify terms and enable technical enforcement. These analyses suggest that the licensing frameworks developed for human readers require substantial adaptation to govern machine consumption, where attribution and context preservation present fundamentally different challenges.

AI thus makes open licensing a live infrastructural question rather than a settled legal background condition. Licensors, libraries, funders, publishers, repositories, and scholarly communities will need to clarify how open licenses apply to machine reading, text and data mining, model training, retrieval-augmented generation, and downstream synthetic outputs. The important question here is whether the use of open materials preserves attribution, context, reciprocity and the public purposes for which openness was advanced.

The dual role of open access—as both input to AI development and public good in its own right—underscores the importance of provenance-aware summarization, appropriate attribution, and consent mechanisms that reflect authors' and communities' intentions. When AI models synthesize open access literature, questions of attribution become vexed: whose work is represented in a probabilistic blend? How can communities maintain oversight of how their contributions are used?

=== Open Data ===

Open data, crucial for reproducibility and model improvement, raises issues of privacy, consent, and community sovereignty, especially in relation to sensitive or Indigenous data. The CARE principles complement FAIR by centering collective benefit, authority to control, responsibility, and ethics (Carroll et al. 2020). Carroll et al. (2020) ground these principles in the structural biases and colonization processes producing &quot;epistemicide,&quot; directly addressing tensions between Indigenous Data Sovereignty and AI's voracious data demands. Their framework demonstrates that open data governance constitutes a political practice, where broad data sharing and algorithmic extraction can undermine the rights, consent, and collective interests of communities whose knowledge becomes training material.

Carroll et al. (2021) demonstrate FAIR and CARE operationalized together. Because many scientific datasets contain Indigenous Knowledge, applying CARE principles ensures this data is oriented toward community wellbeing through rigorous provenance tracking and appropriate governance models. Arrangements such as data trusts, tiered access, and purpose-bound licenses illustrate how openness can be conditioned: open to whom, for which purposes, under what accountability terms?

Documentation practices emerge as crucial infrastructure for responsible AI development. Bender and Friedman (2018) propose data statements as critical enabling infrastructure to reduce exclusion and bias in language technologies, arguing that such documentation can prevent misrepresentation and support more ethical system development. Boyd (2021) empirically demonstrates that documentation frameworks increase engineers' ethical sensitivity—through think-aloud sessions, practitioners who received Datasheets identified ethical issues earlier and more frequently. This finding challenges assumptions that openness automatically leads to fairer systems; structured documentation actively shapes how practitioners recognize and respond to potential harms.

=== Open Source ===

Open source dynamics in AI include open weights, permissive licenses, and community checkpoints that support verification, plural innovation, and public-interest development. At the same time, discussions of misuse and dual-use emphasize capability control and risk. White et al. (2024) establish a Model Openness Framework with three-tiered classification, codifying 17 components that expose the requirements for reproducibility and scrutiny. Graduated openness—incremental model releases, safety mitigations, and governance charters—appears as one path toward balancing transparency with harm reduction. The evolution of open models will influence the accessibility of AI to under-resourced institutions, public-interest researchers, and communities seeking to adapt technologies to local contexts.

The Open Source Initiative's Open Source AI Definition 1.0, released in 2024, provides criteria for describing an AI system as &quot;Open Source AI&quot;, including the freedoms to use, study, modify, and share, access to the preferred form for modification, and sufficient information about training data provenance. As a definition rather than a license or implementation practice, it offers a community standard for assessing whether licenses, releases, and documentation practices support genuine openness, including whether &quot;open weights&quot; claims are matched by the artifacts, permissions, and transparency needed to avoid openwashing.

=== Open Science ===

Open science principles encourage reproducible workflows—transparent notebooks, containers, pipelines, and documentation—while AI introduces dependencies that can be opaque and difficult to reproduce. Practices such as open benchmarking, model cards, data cards, and documentation standards aim to make training data, evaluation metrics, and known limitations more visible. The push and pull between speed and scrutiny is pronounced in AI-assisted research: rapid exploration can generate insights, yet robust claims require validation, transparency, and often slower processes.

The tension between efficiency and process manifests acutely in open science contexts. AI can accelerate literature review, code generation, and data analysis, but the compression of these processes may obscure the iterative work through which understanding develops. Open science's emphasis on showing work—through preregistration, open notebooks, and transparent reporting—provides resources for maintaining visibility even as AI augments research workflows.

=== Open Social Scholarship ===

Within open social scholarship, AI is approached as a means to enhance public dialogue and shared inquiry. Examples include co-authorship with non-academic collaborators, explicit attribution of AI assistance, and participatory governance of tools in community-engaged projects (Arbuckle et al. 2022). Alignment with OSS principles is assessed by whether AI-supported practices sustain reciprocity, accessibility, and shared authority in knowledge production, and whether technological mediation amplifies rather than displaces human voice, agency, and accountability.

The feedback relationship—scholarship as training data, AI as scholarly tool—manifests throughout these registers. Open access literature trains models that then summarize open access literature. Peer review norms shape training data that then assists peer review. Pedagogical materials become training data for tools used in teaching. This recursion creates feedback loops whose effects on scholarly practice remain to be fully understood.

== AI and &quot;Social&quot; ==

The &quot;social&quot; dimension concerns the distribution of attention, credibility, and participation within and beyond academia. AI now helps mediate content creation, curation, and moderation, altering these distributions in ways that merit close scrutiny.

=== Platforms and Synthetic Content ===

Platforms hosting synthetic content must contend with provenance and identity. As generated text, images, and deepfake media proliferate, distinguishing among forms of authorship becomes more complex, with direct implications for trust and credibility. Van Es and Nguyen (2024) show that these anthropomorphic imaginaries are not incidental: they are actively constructed through ChatGPT's own self-representations, which consistently project a friendly, humanoid intellectual companion that obscures the statistical operations underneath. Mitra, Cramer, and Gurevich (2024) diagnose &quot;information access&quot; under generative AI as &quot;sociotechnical settlement&quot;—models &quot;intermediate credibility, reshape attention, and re-allocate epistemic authority.&quot; Their framing positions AI-mediated search and synthesis as fundamentally reconfiguring who gets heard, whose claims become visible, and whose expertise counts.

Recommendation systems juggle personalization, diversity, and serendipity, shaping canon formation and the visibility of marginalized voices. Attention economies are being reshaped: some work is surfaced and amplified; other work is obscured, sometimes by design and sometimes as a side effect of algorithmic optimization. Content credentials—cryptographic signatures and rich metadata—attempt to record origin and transformation history, while questions persist about whether such mechanisms can scale to match the velocity of synthetic content production. For scholarly communication, such mechanisms should be treated as part of the infrastructure of citation, preservation, disclosure and accountability; their value depends on whether they can travel across repositories, journals, platforms and public interfaces without being stripped of context.

=== Governance, Moderation, and Policy ===

Leadership, governance, moderation, and policy become iterative and layered rather than singular and top-down. Universities, libraries, journals, and repositories intersect with platform governance in setting norms for AI-assisted authorship, disclosure, review, and engagement. Sartori and Theodorou (2022) view AI as a &quot;magnifying glass&quot; amplifying existing inequities—a framing that clarifies bias as an older problem than the technology and locates responsibility in social structures and institutional choices. Their analysis challenges approaches that treat fairness as achievable through algorithmic adjustment alone, arguing that human control requires institutional mechanisms for contestation that acknowledge AI practice as fundamentally political.

Akter et al. (2021) theorize algorithmic bias as emerging from interacting sources—data bias, method bias, and societal bias—demonstrated through Australia's Robo-Debt scheme, which inherited and amplified existing inequities through automated decision-making. Their framework implicitly contests technological determinism by revealing how managerial choices about data collection priorities, acceptable error rates, and stakeholder consultation shape algorithmic outcomes in ways that exceed engineering decisions.

Jensen et al. (2022) address governance and moderation as platform design commitments aligned with OSS values, showing how choices about community safety and trust shape the kinds of scholarship platforms can support. Transparency reports, appeal procedures, and community-based moderation seek to address harms while preserving legitimate expression. Policy becomes experimental, subject to revision as impacts, unintended consequences, and community norms evolve.

=== Critical Literacies ===

Critical literacies, for both scholars and publics, extend beyond operational proficiency. They involve understanding model limits, recognizing sources of bias, interpreting provenance signals, and practicing verification. Chun and Elkins (2023) position AI's advancement as precipitating interlocking crises demanding pedagogical response grounded in reflective and collaborative meaning-making, explicitly connecting pedagogical design to civic preparation and positioning students as &quot;critically engaged citizens capable of interrogating the social and economic implications of algorithmic mediation.&quot; Zeffiro (2024) reveals how corporate narratives of AI as &quot;democratizing force&quot; obscure differential vulnerabilities while &quot;automating insecurities&quot;—a concept capturing how AI tools institutionalize particular understandings of risk that reflect corporate priorities rather than community needs.

These literacies include skills such as documenting AI use, distinguishing synthesis from source, reading expressions of uncertainty, and maintaining awareness of the gap between fluency and accuracy. The ease with which AI produces confident-sounding text makes discrimination skills more important: fluency does not indicate accuracy, and the appearance of authority can mask the absence of understanding.

=== Global Asymmetries and Epistemic Centralization ===

AI’s geopolitical dimensions draw attention to questions of influence, globalism, and colonization. Training regimes often reproduce global asymmetries in language and corpus composition: English-language and Global North sources dominate, while linguistic and epistemic diversity from other regions receive less representation. Bender et al. (2021) critically analyze how larger models reproduce hegemonic views, noting that the damages associated with large-scale language models—environmental costs, representational harms, concentration of power—are more likely to fall on marginalized populations.

Chung (2025) extends geographic scope to Asia's advanced economies, revealing how techno-developmentalism produces distinct imaginaries shaped by local political-economic conditions. Multilingual models, community-owned datasets, and South–South collaborations seek to counteract epistemic centralization, yet the structural dynamics of extraction without reciprocity remain strong. Arthur et al. (2021) reveal how national policy shapes whether openness reduces or reproduces inequities, showing that structural barriers—funding models, institutional incentives, infrastructure gaps—mediate between stated commitments to openness and their realization in practice.

Debates over determinism, diversity, and justice challenge narratives of technological inevitability. Sartori and Theodorou (2022) extend this analysis to the global scale, emphasizing that adoption choices, design priorities, and evaluation metrics remain matters of collective agency—and that the communities most affected by AI's asymmetries are precisely those least represented in the governance structures that shape them. Justice-oriented evaluation foregrounds the distribution of harms and benefits, rather than focusing solely on aggregate performance: who is helped, who is harmed, and along which axes of power and marginalization?

=== Humanity, Community, Connection, and the Affective Dimensions of AI Mediation ===

Beyond the technical and governance dimensions, AI mediation carries affective and relational aspects that shape scholarly communication in subtle but significant ways. Generative systems influence the tone and velocity of discourse and can intensify polarization or foster connection depending on design choices and deployment contexts. The ability to flood channels with synthetic text or avatars strains existing trust infrastructures, creating new challenges for maintaining the relational fabric of scholarly communities.

Design choices that emphasize care—thoughtful moderation, friction for high-risk actions, community control of spaces—become part of scholarly platform ethics. These choices counter acceleration and decontextualization that undermine deliberation and mutual recognition. The question moves beyond whether AI produces accurate outputs, but whether AI-mediated environments support the kinds of dialogue, disagreement, and collaborative inquiry that scholarship requires. Connection and community constitute values that technical efficiency can erode if left unattended.

Jensen et al. (2022) explore how digital communities of care can be fostered through attention to safety, security, and trust—values that require ongoing cultivation rather than one-time technical implementation. The relational dimensions of scholarship—mentorship, collaboration, peer recognition, collegial support—may be affected by AI mediation in ways that exceed questions of accuracy or efficiency.

=== Environmental and Labour Costs ===

Material costs, both labour and environmental, ground AI capability in ways that often remain invisible. The AI pipeline depends on precarious annotation and moderation labour, often transnational and underpaid. Workers in the Global South perform essential tasks—labeling training data, flagging harmful content, refining model outputs—under conditions that rarely feature in celebratory narratives of AI advancement. This hidden labour connects AI development to broader patterns of extraction and externalization, where the costs of technological systems are displaced onto vulnerable populations.

Energy and water consumption for training and deployment contribute to climate impacts that intersect with environmental justice concerns. Bender et al. (2021) observe that the damages associated with large-scale language models—environmental costs, representational harms, concentration of power—&quot;are more likely to fall on marginalized populations.&quot; The communities least likely to benefit from AI capabilities bear disproportionate burdens from their development.

Disclosure norms, ethical procurement, and commitments to &quot;green AI&quot; bring these dimensions into infrastructural planning rather than treating them as externalities. For institutions committed to sustainability and justice, AI adoption cannot be evaluated solely on functional criteria; the material conditions of AI production become relevant to responsible deployment decisions. This connects AI governance to broader institutional commitments around environmental responsibility and labour ethics.

== AI and &quot;Scholarship&quot; ==

Across the scholarly lifecycle, AI now participates in research, writing, teaching, review, and administration, changing how practice and infrastructure co-evolve. The tension between operational assistance and epistemic authority manifests at each stage.

=== Research Methods and Practice ===

Research methods and practices incorporate LLMs for literature review, coding, data cleaning, translation, and analysis. Key questions concern how assistance is documented, how outputs are validated, and how communities renegotiate the line between exploratory use, operational support, interpretive contribution, and settled scholarly claim. Mehlenbacher, Balbon, and Mehlenbacher (2024) examine &quot;synthetic genres&quot; that push apart definitions of &quot;information&quot; and &quot;knowledge,&quot; suggesting that AI-generated text occupies a novel categorical space requiring new frameworks for evaluation. Bozkurt (2024) addresses authorship implications, proposing the aiTARAS Framework while maintaining that responsibility ultimately belongs to the human author. Maintaining epistemic standards while exploring new efficiencies requires treating AI as a tool supporting thought and analysis, not as a substitute for disciplinary judgement.

Domain-specific norms—interpretive rigor in the humanities, reproducibility in quantitative fields—must shape appropriate use. The question of when AI assistance becomes AI authorship remains contested, with implications for credit, accountability, and the integrity of scholarly claims. Documenting AI use transparently allows readers to assess the epistemic status of outputs and evaluate whether human judgement remains central to the knowledge claims of a given piece.

=== Scholarly Outputs ===

Forms of scholarly output are changing as generative tools support multimodal and interactive work: dynamic narratives, layered visualizations, and synthesis artefacts that draw together diverse sources. Bergstrom and Ruediger (2024) anticipate &quot;discovery, interpretation, and writing services&quot; becoming integrated suites while noting concerns about platform intermediation that could concentrate power over scholarly communication. Authorship, attribution, and preservation practices need to adapt: whose contributions are recognized, how AI assistance is disclosed, and how AI-mediated outputs are archived and made citable. Provenance and disclosure become part of the paratext, informing evaluations of reliability and situating works within ongoing conversations.

=== Teaching and Pedagogy ===

Teaching and pedagogy integrate AI as both subject and instrument. Tan and Maravilla (2024) position AI as &quot;catalyst necessitating pedagogical transformation—shifting from transmission models toward environments where students actively construct knowledge.&quot; This reframing treats AI as an occasion for rethinking educational purposes and methods, emphasizing the human capacities—critical judgement, ethical reflection, creative synthesis—that AI systems cannot replicate.

Deng et al. (2025) meta-analyze 69 studies finding ChatGPT improves performance while reducing mental effort, raising questions about what learning means when cognitive work is offloaded to machines. Their findings suggest that traditional assessment measures require recalibration to capture the thinking processes that educational institutions value. The tension between efficiency and process manifests acutely here: if AI can produce essays, what is being assessed? Process-centered assessment emphasizes transparency, ethical reflection, and the development of critical literacies that enable students to assess model outputs, recognize limitations, and engage thoughtfully with AI-mediated knowledge.

Lee and Palmer (2025) establish prompt engineering as emergent practice mirroring &quot;Socratic dialogue,&quot; suggesting continuities between AI interaction and established pedagogical traditions. Oates and Johnson (2025) demonstrate pedagogical value in making AI outputs &quot;subjects for evaluation rather than endpoints of learning&quot;—an approach that uses AI as material for critical analysis. Berry (2023) warns that uncritical AI reliance risks &quot;algorithmization&quot; of Digital Humanities, where computational methods become defaults that shape questions before they are asked.

=== Service and Peer Review ===

Service and peer review use AI for triage, formatting checks, and detection tasks—identifying duplication, verifying references, smoothing language—while preserving human judgement for evaluations of originality, significance, and methodological rigor. Sun (2025) maps LLM applications in peer review, emphasizing that models &quot;remain fundamentally limited in assessing research novelty&quot;. Hosseini and Horbach (2023) document potential to combat reviewer fatigue while identifying risks when &quot;operational assistance crosses into epistemic territory,&quot; suggesting that the boundary between support and substitution requires careful negotiation. Checco et al. (2021) demonstrate AI can predict outcomes based on &quot;superficial&quot; features while emphasizing &quot;semi-automated&quot; approaches that preserve human judgement for consequential decisions.

The line between operational assistance and epistemic authority runs directly through peer review, but it is better understood as a moving boundary than a fixed division. Tasks such as formatting checks, duplication detection, reference verification, and metadata checks may sit relatively comfortably on the operational side. Literature triage, reviewer matching, summary generation, and consistency checking occupy more contested middle ground. Assessments of novelty, significance, methodological rigor, interpretive adequacy, and contribution to a field require the kind of accountable judgement that remains distinctively human. Clarity about this boundary helps preserve the integrity of peer review while leveraging AI's capacity for routine tasks.

The inverse problem is integrity infrastructure. AI may assist legitimate review workflows, but it can also amplify older forms of scholarly fraud: paper mills, fabricated peer reviews, synthetic citations, citation cartels, manipulated images, and low-quality or fabricated manuscripts designed to pass superficial screening. These problems predate contemporary genAI, but generative systems increase their scale, speed, and plausible fluency. Responsible AI governance in publishing therefore requires attention not only to how reviewers may use AI, but also to how editorial systems detect, document, and respond to AI-amplified threats to the scholarly record. 

=== Research-Related Infrastructures ===

Research-related infrastructures span organizational governance, publishing and communication platforms, workflow systems, and accountability mechanisms. Governance frameworks, risk registers, roles, and capacity-building programs institutionalize stewardship, coordinating policy and practice across libraries, IT, research support, and ethics offices. Wu, Zhang, and Carroll (2024) document Big Ten universities' &quot;multi-unit governance involving information technology, teaching centers, libraries, and research offices&quot;—a distributed model recognizing AI as a cross-sectoral concern requiring coordinated response.

AI also places new pressure on open scholarly infrastructure. Repositories, commons platforms, digital research infrastructures, standards bodies, and open-science advising organizations must decide whether and how to integrate AI-mediated search, metadata generation, summarization, moderation, preservation, and analytics. These decisions affect governance, sustainability, procurement, interoperability, environmental cost, labour, and the degree to which open infrastructures remain accountable to scholarly and public communities rather than becoming dependent on proprietary AI services.

Open infrastructure responses should therefore be assessed against principles such as transparency, community governance, interoperability, portability, auditability, and long-term stewardship. In this context, standards for open infrastructure become AI governance instruments: they shape whether AI functions can be inspected, contested, replaced, or collectively maintained. 

Papagiannidis, Mikalef, and Conboy (2025) differentiate governance practices, revealing tensions &quot;between centralized oversight and distributed expertise.&quot; Institutions must navigate between the efficiency of centralized decision-making and the contextual knowledge held by distributed practitioners who understand how AI affects their specific domains.

Rughiniș et al. (2025) introduce &quot;dual black-boxing&quot; capturing compound accountability challenges when opaque AI systems meet opaque institutional processes. When neither the AI nor the institution is transparent about its decision-making, accountability becomes doubly difficult. Janssen (2025) reframes AI governance as managing &quot;complex adaptive systems characterized by co-evolution and emergent properties,&quot; suggesting that governance frameworks must themselves be adaptive. Weber et al. (2023)—whose findings on organizational capacity are discussed in the cross-cutting tensions above—appear here as a reminder that infrastructure governance is where those abstract tensions become concrete institutional failures.

Publishing and communication infrastructures increasingly integrate AI functions—journal recommendation, reviewer matching, manuscript screening, metadata generation—as part of scholarly workflow systems. Kousha and Thelwall (2024) map AI tool deployment across the publishing pipeline, distinguishing demonstrated capabilities from promotional claims. Their analysis reveals that substantial efficiency improvements are achievable in labour-intensive administrative tasks, while human judgement remains integral to core intellectual evaluations. This distinction—between what AI can assist with operationally and what requires human epistemic judgement—structures responsible integration of AI into publishing infrastructures. Ultimately, however, the success of these infrastructural choices is measured not just by operational efficiency, but by how effectively they mediate knowledge for the diverse publics who rely on them.

== Audiences and Differential Impacts ==

Audiences—scholars, students, practitioners, policymakers, and broader publics—encounter AI-mediated summaries, translations, and recommendations that shape how they access and interpret scholarship. Each audience brings different needs, literacies, and vulnerabilities to these encounters, and AI effects manifest differently across these diverse contexts.

Personalization raises the risk of filter bubbles, where recommendation systems surface content that confirms existing interests and perspectives while obscuring alternatives. Taneja and Tripathi (2020) identify structural tensions inherent in personalization algorithms that enhance user experience while simultaneously constructing echo chambers that systematically exclude novel, dissenting, or interdisciplinary perspectives. For scholarly communication, filter bubbles could reinforce disciplinary silos and impede the cross-fertilization that drives innovation. Audience-aware communication emphasizes context, uncertainty, and reciprocity, recognizing that different audiences need different framings and levels of technical detail.

The accessibility principles outlined earlier apply with particular force here: different audiences face different obstacles. AI can broaden participation and lower barriers—through translation, summarization, and alternative formats—but only when its design and governance prioritize inclusion, fidelity, and the preservation of diverse voices and perspectives. Da Silva Cardoso and Rocio (2025) propose frameworks for integrating AI into academic digital libraries that position librarians as essential partners in system development, emphasizing that understanding the nuanced and context-dependent needs of diverse academic communities requires human expertise that cannot be automated. The question is whether AI mediation grows or shrinks the publics that can engage with scholarship.

The sources reveal how AI effects vary by context in ways that demand attention to differential impacts:

'''Institutional type'''. AI adoption is shaped by uneven institutional capacities, but these differences do not map neatly onto size or prestige. Large research universities may have more formal infrastructure, while also facing larger user bases, more complex bureaucracies, and less responsive or less humane interventions. Smaller institutions, community colleges, public libraries, independent scholarly organizations, and grassroots knowledge projects may face different constraints, including limited staffing, funding, or access to specialized expertise. Equitable AI adoption therefore requires governance models that can adapt across institutional contexts without assuming uniform access to technical capacity, administrative infrastructure, or training resources.

'''Language communities'''. What serves English-language scholarship may disadvantage multilingual communities. Models trained predominantly on English reproduce Anglophone perspectives; multilingual support often lags behind. For scholars working in languages underrepresented in training corpora, AI tools may be less accurate, less helpful, or actively distorting. Linguistic diversity constitutes both an epistemic and an ethical concern: knowledge produced in non-dominant languages risks marginalization when AI systems favor majority languages.

'''Career stage'''. What benefits established researchers may burden early-career scholars differently. Senior researchers with established reputations may more easily navigate AI-mediated environments, using AI assistance to amplify existing authority. Early-career scholars face additional pressures around attribution, originality, and demonstrating independent capability. When AI can generate fluent prose, summarize literatures, and accelerate administrative or writing tasks, how do junior scholars demonstrate the intellectual development that hiring, promotion and grant committees have traditionally valued? Assessment criteria developed for human-only production may require adaptation to remain meaningful in AI-augmented contexts, but such adaptation must avoid intensifying surveillance or creating new burdens of disclosure that fall unevenly on those with the least institutional power. 

AI in the evaluation of researchers deserves separate attention from AI in the peer review of scholarly outputs. Hiring, promotion, tenure, grants, fellowships, and institutional metrics shape careers, disciplines, and access to scholarly futures. If AI-mediated tools are used to screen CVs, rank candidates, summarize dossiers, evaluate productivity, or assess “fit,” their consequences may be especially significant for early-career scholars, contingent faculty, disabled scholars, scholars working in less dominant languages, interdisciplinary researchers, and those whose contributions are not well captured by standard metrics. Governance in this area should require transparency, contestability, human accountability, and careful attention to disparate impact. 

'''Disciplinary context'''. Different disciplines bring different norms, methods, and evaluation criteria to AI engagement. What constitutes appropriate AI assistance in a literature review differs from appropriate assistance in data analysis or creative work. Disciplinary communities are developing varied approaches, and cross-disciplinary dialogue helps surface assumptions and identify best practices that might transfer across contexts.

'''Geographic location'''. Scholars in different regions face different infrastructural realities, regulatory frameworks, and access conditions. AI tools developed primarily for well-resourced contexts may not serve scholars working with limited bandwidth, different privacy regimes, or constrained institutional support. Geographic diversity in AI impacts connects to broader patterns of global inequality in knowledge production and circulation.

Attention to these differential impacts marks responsible AI adoption, requiring ongoing assessment of who benefits, who bears burdens, and how distributions might be made more equitable. Rather than assuming uniform effects, responsible governance monitors for disparate impacts and adjusts policies and tools in response to evidence of inequitable outcomes.

== Phenomena, Relations, and Ongoing Inquiry ==

The sources in this annotated bibliography have been selected to trace several intersecting concerns. Conceptually, works that articulate critical frameworks (STS, data colonialism) offer key tools for understanding AI as a sociotechnical formation. (Anderson 2024; Ali et al. 2023; Bender et al. 2021). Normatively, scholarship on public engagement, participatory infrastructures, reciprocity, and accessibility grounds the discussion in the normative coordinates of open social scholarship (Arbuckle et al. 2022; El Khatib et al. 2019). Infrastructurally, sources on data governance (FAIR and CARE), licensing, repositories, and platforms illuminate how AI is being integrated into the material and organizational substrates of knowledge work (Carroll et al. 2020; White et al. 2024). Methodologically, contributions from anthropology, STS, media studies, information science, and environmental humanities help maintain epistemic plurality and attend to global and intersectional dimensions (Chung 2025; Richter, Katzenbach, and Schäfer 2025). Finally, empirically, studies of peer review, literature searching, pedagogical applications, and governance supply concrete evidence of AI's effects in practice (Sun 2025; Deng et al. 2025; Wu, Zhang, and Carroll 2024).

== Conceptual Mapping ==

The conceptual mapping that orients this bibliography treats concepts, phenomena, and relations as interconnected. This mapping is meant to help readers locate where a given source sits: what it names, what it observes, and what it connects:

'''Concepts''' such as openness, provenance, bias, governance, data sovereignty, participation, reproducibility, labour, sustainability, platformization, multilingualism, accessibility, evaluation, enclosure, commons, personalization, and exposure diversity mark key terms of analysis.

'''Phenomena''' such as pretraining on public corpora, proliferation of synthetic content, recommendation feedback loops, metadata drift, hallucination, hybrid openness models, human-in-the-loop verification, green AI practices, community moderation, content credentials, and retrieval-augmented generation describe observable patterns in the field.

'''Relations''' trace interactions among these elements: openness and enclosure meet through licensing and reciprocity mechanisms; provenance and trust are linked through audit trails and disclosure practices; bias and diversity intersect in dataset governance and evaluation design; governance and participation connect through co-design and community oversight; platformization shapes visibility through algorithmic curation and efforts to foster exposure diversity; labour and sustainability meet in discussions of ethical procurement and environmental accounting; reproducibility pushes against black-boxing through documentation and open benchmarking; multilingualism and accessibility intertwine in translation and community review; evaluation anchors legitimacy by attending to social impact and equity metrics.

== Focused Areas for Further Intervention ==

Several areas emerge from this scan as candidates for shorter, more pragmatic follow-up work. AI-mediated scholarly discovery is already reshaping canon formation, citation patterns and visibility through search engines, recommender systems, citation-context services, discovery platforms and automated synthesis tools. Provenance infrastructure, including content credentials, persistent identifiers, verifiable metadata, and workflow documentation, could strengthen disclosure by making AI involvement more portable, auditable and machine-readable. Smaller, community-built, purpose-specific models offer a constructive path for aligning AI with OSS values where communities can define scope, data governance, evaluation criteria, and benefit-sharing arrangements. 

Integrity infrastructure also requires urgent attention, since paper mills, fabricated reviews, synthetic citations and AI-amplified fraud threaten the trust systems upon which scholarship depends. AI in the evaluation of researchers—hiring, promotion, grants, fellowships, and institutional metrics—deserves treatment distinct from peer review of outputs because its consequence for early-career scholars, equity and disciplinary futures may be especially profound. Parallel interventions on AI and open licensing, and on AI’s effects on open scholarly infrastructure, would clarify how licensors, libraries, funders, digital research infrastructures, advising bodies and standards communities are adapting to machine use of open knowledge.

=== Conditions for Flourishing ===

The question animating this bibliography remains phenomenological: what conditions enable scholarship to flourish? The sources suggest these conditions include:

* '''Diverse participation''' that brings varied perspectives to bear on complex problems
* '''Critical literacy''' that equips scholars and publics to evaluate AI-mediated claims
* '''Transparent processes''' that make choices visible and contestable
* '''Human accountability''' that maintains responsibility for consequential decisions
* '''Infrastructural stewardship''' that ensures technical systems serve public purposes

OSS principles provide the normative coordinates for navigating the cross-cutting tensions this scan has identified—offering a framework to ensure that operational assistance does not usurp epistemic authority, that openness resists extractive enclosure, that technical deployments match organizational capacity, and that efficiency does not erase the deliberative processes of scholarship. Specifically, openness with care balances access with consent and community control. Participation with shared authority embeds publics and communities in design and evaluation. Accessibility spans language, disability, and technical literacy. Reciprocity ensures that where community-sourced data or labour underwrite AI functions, benefits flow back to contributors. Infrastructural responsibility commits institutions to steward provenance, auditability, and accountability across deployment lifecycles.

This mapping does not aim to close debate or fix categories. It sketches a topology of the current field: which nodes are active, where tensions gather, and how shifts in one domain reverberate through others. The annotated bibliography is offered as a baseline &quot;lay of the land&quot; against which ongoing research can be situated, helping scholars and practitioners locate their work within a broader conceptual ecology and identify gaps, alignments, and opportunities for intervention shaped by OSS principles of accessibility, reciprocity, and public value.

These conditions also point towards a positive agenda. AI-mediated scholarship could support forms of access and engagement that have long mattered to OSS: translation across languages and registers, navigation of complex archives, discovery across disciplinary boundaries, support of disabled readers and writers, richer metadata, and new forms of dialogue between specialists and broader publics. Whether such uses weaken or strengthen scholarship depends less on the abstract presence of AI than on the infrastructures, governance processes, and values through which AI is developed and adopted.

The landscape will continue to shift. New capabilities will emerge, governance frameworks will evolve, communities will develop practices and norms through experimentation and deliberation. What this bibliography offers is a documented moment from which change can be measured and assessed. The sources assembled here provide conceptual resources for that ongoing work: frameworks for analysis, evidence of effects, models for governance, and principles for evaluation. The task ahead is to use these resources thoughtfully, maintaining the commitments to accessibility, reciprocity, and public engagement that make scholarship worth pursuing.

{{Navigation|previous=Essential Ideas|next=Essential Contexts}}

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      <text bytes="77379" sha1="rgiqyy9esaag1c6jq6b4dywke450jnt" xml:space="preserve">This research scan surveys an emergent and contested terrain: the interlaced developments in artificial intelligence, generative AI, large language models (LLMs) and their predecessors, and the ways these systems are reshaping knowledge production, circulation, and engagement across scholarly and public contexts.

This scan uses artificial intelligence, or AI, as a broad umbrella term for computational systems designed to perform tasks associated with classification, prediction, reasoning, language processing, recommendation, perception, automation, or decision support. It uses generative AI, or genAI, more specifically for systems that generate text, images, code, audio, video, or other outputs in response to prompts, queries, or other inputs. Large language models, or LLMs, are a prominent subset of contemporary genAI systems trained to model and generate language. Because public disclosure often uses these terms interchangeably, this scan uses AI for the broader field and infrastructure, genAI where generative functions are specifically at issue, and LLM where the discussion concerns language-model systems in particular. The wider AI landscape includes technical architectures ranging from symbolic logic and &quot;good old-fashioned AI&quot; (GOFAI), through statistical natural language processing, to contemporary transformer-based genAI models, all situated within institutional and platform economies, cloud infrastructures, and evolving governance regimes (Jones 2023; Anderson 2024). These systems now recalibrate discretion, authority, and visiblity, influencing what is recognized as knowledge, who produces it, and how it moves among diverse publics. 

A brief historical distinction is useful here. AI has not developed through a single technical or ideological pathway. Symbolic approaches, prominent in early AI, treated intelligence as the manipulation of explicit rules, formal representation, and logical structures. Connectionist approaches, by contrast, emphasized distributed pattern recognition across networks of weighted relations. Contemporary deep learning and transformer-based genAI inherit much more from the connectionist tradition, especially its reliance on large datasets, statistical association, and learned representations rather than explicit rules. This inheritance helps explain why contemporary systems can be powerful aids for pattern detection, generation, and transformation, while remaining weak at grounding, verification, and accountable judgement. &quot;Hallucinations&quot;—false responses generated by AI that are especially misleading due to their plausible surfaces—stem from the inherent mathematical design of such systems, which are optimized to generate probable outputs rather than to verify claims within accountable epistemic communities. For fuller historical and critical accounts of these developments, see Jones (2023), Ali et al. (2023), Anderson (2024), and Whiteley (2023).

What emerges from this mapping is a complex phenomenology of entanglement. Generative AI is woven in part from scholarship's own materials—open access literature, research data, metadata schemas, citation networks, community-developed software, and collaborative data infrastructures. These are not the only, or even necessarily the largest, sources on which contemporary systems are trained. But they are unusually authoritative in that they help organize what counts as reliable knowledge, how claims are linked to evidence, how materials are discovered, and how intellectual legitimacy is conferred. The AI systems that now analyze, summarize, and generate scholarly text therefore draw upon knowledge infrastructures whose value has been built over decades by researchers, editors, librarians, publishers, software communities, institutions, and publics.

This recursive relationship positions scholarship as both one of AI's important knowledge substrates and one of its objects of transformation, but the entanglement runs deeper still. Scholarship does not merely feed AI systems; it is increasingly mediated by them. Researchers discover literature through AI-powered recommendation engines, draft manuscripts with generative assistants, and navigate peer review processes augmented by algorithmic triage. Students encounter AI both as subject of study and as tool for learning, while institutions struggle to develop governance frameworks adequate to technologies that evolve faster than policy cycles. The recursive loop—scholarship training AI training scholarship—creates conditions where distinguishing human from machine contribution becomes progressively more difficult, and where the very categories through which we understand authorship, originality, and expertise require renegotiation.

The organizing logic of this collection moves from foundational grounding through INKE-aligned focal points that structure the annotated bibliography itself. It first establishes essential contexts: the histories and theories of AI, including critical perspectives from Science and Technology Studies (STS) and Critical Digital Humanities; accounts of knowledge as relational, plural, and platformed; and the principles of Open Social Scholarship (OSS) as articulated by the Implementing New Knowledge Environments (INKE) Partnership and the Electronic Textual Cultures Lab (ETCL). It then follows three focal threads—&quot;open&quot;, &quot;social&quot;, and &quot;scholarship&quot;—that mark key sites where AI's effects both align with and challenge OSS commitments to accessibility, reciprocity, participatory governance, and public engagement (Arbuckle et al. 2022; El Khatib et al. 2019).

Throughout, the ethos of Open Social Scholarship provides a normative coordinate: a set of principles for interpreting how AI mediates relations among researchers, institutions, communities, and publics. The focus is on how practices, infrastructures, and relations are changing, and how these shifts intersect with OSS values. Which concepts, practices, actors, infrastructures, and frictions are currently reconfiguring the conditions of knowledge and engagement? Where do these movements align with, complicate, or unsettle OSS principles of accessibility, reciprocity, and public value? By attending closely to these dynamics—openness entangled with enclosure, provenance linked to trust, bias in tension with diversity, governance negotiated through participation—a conceptual scaffolding emerges for further analysis and empirical inquiry.

A critical OSS response to AI need not only be defensive. The same systems that threaten enclosure, decontextualization, and epistemic flattening may, under different governance conditions, support broader forms of scholarly engagement: multilingual and plain-language summaries, alternative format outputs, assistive reading and navigation, metadata enrichment, participatory annotation, community translation, and more accessible pathways into specialized research. These possibilities in no way cancel the risks identified throughout this scan. Rather, they clarify the architectural task lying ahead of open, social scholarship: to ask what forms of AI-mediated scholarship can be built under conditions of reciprocity, transparency, care, public value, and shared authority.

== Four Cross-Cutting Tensions ==

The sources assembled here reveal four cross-cutting tensions that structure AI's engagement with scholarship. None admits of simple resolution—each marks a site where choices about AI design and deployment carry real stakes for knowledge production, and where different communities are actively negotiating trade-offs that no technical fix can settle.

'''Operational assistance versus epistemic authority'''. While AI can reduce friction in many workflows, it raises fundamental questions about where judgement, accountability, and interpretive responsibility should reside, and how those boundaries should be renegotiated as tools, practices, and disciplinary norms change. AI excels at standardized tasks—formatting, initial drafts, pattern identification, literature triage—while struggling with the evaluative judgement that gives scholarship its value. The challenge lies in leveraging assistance without ceding authority, using AI capabilities while preserving human responsibility for consequential decisions. When does operational support cross into epistemic territory? How should that boundary be renegotiated as capabilities shift, practices stabilize, and disciplinary communities develop new norms? 

This boundary is historically and institutionally variable. Reference verification, metadata enrichment, formatting, and duplication checks may increasingly be treated as operational tasks. Literature triage, evidence synthesis, translation, and review assistance venture into more contested terrain. Assessments of originality, significance, methodological adequacy, interpretive force, and public consequence continue to require accountable human judgement. The problem of governance is therefore not one of simply drawing a fixed, indelible line once, but to define processes through which scholarly communities can revisit that line over time.

The fluency of AI-generated text can mask the absence of understanding; the appearance of authority can obscure the statistical operations underneath. Sun (2025) emphasizes that models, by definition, are constrained in how they evaluate the novelty of research—they can recognize patterns but cannot evaluate whether patterns matter. This distinction is integral to peer review, research methods, pedagogy, and governance, and each requires clarity about where AI can appropriately assist and where human judgement must remain central.

'''Openness versus enclosure'''. The open infrastructure that has supported equitable access to knowledge is being absorbed into commercial AI systems in ways that may foreclose openness rather than extend it, and the trajectory of this tension will shape whether AI serves broad publics or narrow interests. Open access literature feeds model pretraining; this raises serious concerns about a new enclosure dynamic, in which freely accessible works become inputs for proprietary AI systems that generate commercial value without meaningful reciprocity. Pooley (2024) reveals a troubling symmetry in the underlying asymmetry: both commercial publishers and AI developers extract value from the scholarly commons while returning little to the researchers who create it. The licensing frameworks developed for human readers require substantial adaptation to govern machine consumption, where attribution and context preservation present fundamentally different challenges. Community-sourced data and labour underwrite AI functions, yet the question of whether benefits return to those communities remains contested.

'''Technical capability versus organizational capacity'''. The pace of AI development consistently outstrips the ability of institutions to evaluate, govern, and respond thoughtfully, and the gap between what AI can technically accomplish and what institutions can responsibly deploy constitutes a critical site of intervention.  Building capacity for thoughtful AI adoption requires sustained investment in skills, governance structures, and evaluative frameworks. Weber et al. (2023) identify organizational capabilities as crucial mediators, noting failures often stem from organizational incapacity to manage sociotechnical complexity. Resource-intensive approaches assume capacities—technical staff, governance infrastructure, training budgets, and time for implementation—that are unevenly distributed across institutions and communities. These differences do not map neatly onto institutional size or prestige: large research universities may have more formal infrastructure, but also larger user bases, more complex bureaucracies, and interventions that can become less responsive to local needs. Smaller institutions such as community colleges, public libraries, independent scholarly organizations, and grassroots knowledge projects may face different constraints, including limited staffing, funding, or access to specialized expertise. Across all contexts, institutions are encountering unforeseen complexities for which existing governance structures may be poorly prepared. This tension requires attention to differential institutional positions and the development of governance models that remain humane, adaptable, and scalable across varied contexts. 

'''Efficiency versus process'''. Although AI accelerates tasks, scholarly knowledge earns its credibility through deliberate, iterative processes of review and community validation that efficiency-oriented tools may erode. Pedagogical and scholarly transformations require valuing cognitive work that AI cannot replicate, and education involves developing capacities through practice, not just acquiring outputs. The speed and fluency of AI-generated text can mask the erasure of the deliberative processes—reading, synthesizing, drafting, revising—through which understanding develops. Deng et al. (2025) find that ChatGPT improves student performance while reducing mental effort, raising questions about what learning means when cognitive work is offloaded to machines. The compression of research, writing, and discovery processes may generate outputs while eroding the developmental experiences that scholarly communities value. Process-centered assessment, transparent documentation, and attention to the formative dimensions of intellectual work become crucial responses.

These tensions recur throughout the bibliography's domains. They structure debates about AI in peer review, pedagogy, platform governance, and infrastructure design. Understanding them as ongoing negotiations rather than problems awaiting solution helps position responsible engagement with AI's transformative effects.

== Fundamentals and Ideologies of AI ==
The prominence of generative AI and LLMs is rooted in layered histories. Early symbolic AI attempted to encode knowledge as explicit rules and representations. Statistical natural language processing redirected attention to learning patterns from data. Deep learning, accelerated by transformer architectures and large-scale computation, now underpins models that generate fluent text, code, and images (Jones 2023). Each wave is embedded in institutional settings, funding regimes, and sociotechnical imaginaries that combine benchmark cultures, optimization logics, data abundance, and investor narratives of efficiency and disruption. The concept of &quot;sociotechnical imaginaries&quot; provides crucial analytical purchase for understanding how collective visions shape governance and discourse; as Mao, Richter and Katzenbach (2025) demonstrate, these imaginaries function performatively, actively mobilizing resources, legitimating interventions, and establishing trajectories for development. The figure of &quot;intelligence&quot; functions here as a sociotechnical imaginary: a collective vision that orients research agendas, policy priorities, and public expectations, often sidelining questions of transparency, accountability, and epistemic pluralism.

Understanding contemporary AI requires genealogical attention to its intellectual origins and the sociotechnical imaginaries that have shaped its development. The transition from symbolic AI to statistical learning—from explicit knowledge representation to pattern recognition across massive datasets—represents a fundamental reorientation of assumptions about what counts as intelligence and whose knowledge gets represented. As Jones (2023) argues, the shift toward &quot;empiricist&quot; approaches that capitalize on the &quot;unreasonable effectiveness of data&quot; threatens professions centred on particularity while demonstrating that AI functions as a reflection of human creations including their best and worst traits.

Anderson's (2024) examination of John McCarthy's foundational program reveals AI as philosophical ideology—a vision of perfectly rational abstraction built upon objectivism and scientism that has &quot;come to serve as a blind for increasing techno-corporate control of society.&quot; McCarthy's conception of artificial intelligence as a &quot;stripped down model of human mental engagement without emotional qualities&quot; established patterns that continue to shape the field: the subordination of interpretive judgement to formal optimization, the bracketing of contextual understanding in favor of scalable pattern matching, and the assumption that intelligence admits of decomposition into modular, transferable components. Ali et al. (2023) extend this analysis by situating AI within broader genealogies of industrialization and colonialism, identifying threads of hidden labour, encoded behaviour, and cognitive injustice running through AI's history—positioning AI as the flagship of the Information Age conditioned by the Management Age.

The term &quot;artificial intelligence&quot; itself warrants critical scrutiny. As Whiteley (2023) observes, the phrase anthropomorphizes what is essentially computer-assisted statistical analysis, encouraging expectations and trust that the technology cannot warrant. This terminological slippage—from statistical prediction to &quot;intelligence&quot;—exemplifies how language shapes perception and, through perception, governance. The sources in this bibliography provide conceptual resources for more precise description that preserves space for human agency, critical evaluation, and alternative design pathways.

Critical perspectives from Digital Humanities (DH) and Science, Technology and Society (STS) supply key interpretive tools. They foreground the ways datasets, labels, and evaluation metrics encode values and worldviews; how training regimes replicate archival absences and classification politics; and how the defaults embedded in language, genre, and culture travel into outputs, with particular consequences for marginalized communities. Bender et al. (2021) critically analyze how larger models reproduce hegemonic views: size does not guarantee diversity, because the communities most underrepresented in training data are also those most likely to bear the downstream costs of systems built without them. Automation theory highlights AI as a redistribution of discretion and authority: tasks that once required situated human judgement are delegated to systems that lack context, while accountability structures struggle to keep pace.

Berry (2025) theorizes this moment as &quot;the Inversion&quot; under &quot;computational capitalism&quot; where machine-generated works reshape meaning-making infrastructure, producing &quot;AI slop&quot; that infiltrates information ecosystems with garbled meaning. His concept of &quot;diffusionisation&quot; describes how AI systems dissolve cultural forms into probabilistic vector spaces and reconstitute them through latent space manipulation—a process that transforms the infrastructure of meaning-making itself. This moves beyond mechanical reproduction toward what Berry theorizes as &quot;post-consciousness,&quot; where boundaries between individual and synthetic consciousness become porous. The concept challenges scholars to attend not merely to AI outputs but to how generative systems transform the very grounds upon which experience and meaning are constituted.

Environmental and labour analyses add further layers, tracing the energy-intensive training runs and precarious annotation and moderation work that underpin current capabilities. Klein et al. (2025) argue that AI's statistical enactment of ideology imposes an objectivist European modernist framework upon data, making issues of &quot;bias&quot; unsolvable through technical means alone—even the distinction between &quot;pure&quot; and &quot;toxic&quot; training data reflects ideological commitments. They propose that smaller, purpose-built models developed through genuine interdisciplinary collaboration offer a path forward, one where &quot;technical researchers must recognize the institutional asymmetries&quot; that currently disadvantage humanistic approaches.

Relations with OSS-aligned communities complicate this picture. Open-source software, open datasets, and commons-based peer production have been central to AI's development; influential models rely on openly shared corpora and community-built tools. At the present inflection point, however, pressures toward enclosure are intensifying. Recent work by the Open Source Initiative on open source AI, including its 1.0 Open Source AI Definition, clarifies that releasing model weights alone is not equivalent to full openness. Meaningful openness also depends on access to documentation, code, data information, use rights, and other artifacts needed to understand, modify, and reuse a system. This clarification responds to broader concerns about “openwashing,” in which companies describe AI systems as open while releasing models under restrictive licenses, with incomplete documentation, or without access to key development artifacts. White et al. (2024) similarly develop the Model Openness Framework, establishing a three-tiered classification that shows AI “openness” exists on a spectrum, from minimal weight release to fuller disclosure of training data, intermediate checkpoints, code, documentation, and development practices. Rather than a simple binary between open and closed, the field is experimenting with hybrid forms—open weights under usage constraints, community checkpoints, and permissive yet bounded licenses—that seek to reconcile accessibility with risk management and intellectual property considerations. 

Vake et al. (2025) find the open-source AI community depends on businesses to develop base models—there are few incentives for companies to release openly because doing so risks intellectual property and competitive advantage. This structural dependence raises questions about whether open AI can genuinely serve public interests or will remain subordinated to commercial imperatives. These choices shape not only technical access, but also epistemic legitimacy and the capacity for public oversight, critique, and repair.

== Geographic Diversity in AI Imaginaries ==

The imaginaries circulating around AI vary significantly across geographic and political-economic contexts, challenging narratives of technological inevitability that treat AI development as following a single universal trajectory. Mao, Richter and Katzenbach's (2025) comparative analysis across the United States, China, and Germany reveals heterogeneous and often contradictory imaginaries even within single regulatory regimes. Where US discourse fragments across multiple geographic AI hubs, German imaginaries center on EU policy compliance and regulatory frameworks, while Chinese articulations align tightly with party-state directives that minimize local variation.

Building on the varied sociotechnical imaginaries discussed earlier, Chung (2025) extends this analysis to economically advanced but geographically non-dominant Asian societies—Singapore, Hong Kong, and Taiwan—demonstrating how &quot;techno-developmentalism&quot; produces distinct imaginaries shaped by local political-economic conditions and historical trajectories. These varied articulations challenge the Global North/South binary that structures much AI governance literature, revealing that AI development trajectories remain contingent and shaped by specific political choices rather than following universal technological imperatives.

The imaginaries circulating around AI shape technical design itself. Van Es and Nguyen (2024) demonstrate how ChatGPT's self-representations—82% depicting humanoid forms—strategically cultivate anthropomorphic imaginaries that encourage overlooking ethical and legal challenges. The friendly assistant persona, surrounded by books and radiating futuristic light, constructs a humanoid image of trustworthy intellectual companionship that obscures the statistical operations underneath.

For scholarly communities, these developments necessitate specifically humanities-oriented engagement. Chun and Elkins (2023) argue that humanities-oriented pedagogy offers distinctive resources for this moment, insisting that the most effective AI tools amplify rather than replace human intellectual engagement—a claim developed more fully in the Critical Literacies section below.

== Knowledge Foundations ==

In this framework, knowledge appears as a relational practice rooted in communities, languages, and infrastructures. Three dimensions are especially salient for understanding AI's impact: diversity, mobilization, and platforms.

'''Diversity'''. Epistemic, cultural, linguistic, and methodological plurality are conditions for robust, public-facing scholarship. Models trained predominantly on dominant corpora risk misrecognition and erasure, flattening the diversity that constitutes human knowledge. Arbuckle (2020) articulates diversity as fundamental to legitimate knowledge translation, emphasizing inclusive modes of engagement and participatory approaches that honor varied ways of knowing. In response, approaches such as community governance of data, participatory evaluation, and multilingual modeling work to adapt tools to difference rather than requiring difference to conform to tools. Crompton et al. (2020) address how community governance can safeguard plural representation in data infrastructures like Wikidata, demonstrating that technical systems encode choices about whose knowledge counts and how it gets categorized. The FAIR principles—Findable, Accessible, Interoperable, Reusable—offer a technical framework for data stewardship, while the CARE principles—Collective Benefit, Authority to Control, Responsibility, Ethics—introduce dimensions of sovereignty, consent, and community benefit that are especially important for Indigenous data and other contexts shaped by power asymmetries (Carroll et al. 2020; Carroll et al. 2021).

'''Mobilization'''. Knowledge mobilization concerns how research travels and is taken up across domains: from scholarship to policy, from specialist discourses to public understanding, from the classroom to community settings. Generative tools can accelerate synthesis and enhance accessibility by producing multilingual summaries, plain-language translations, and alternative-format outputs. The same tools can also increase the volume and velocity of decontextualized or misleading claims. Winter (2023) frames policy as a vehicle for mobilization emphasizing provenance and accountability—mechanisms that become ever more crucial when automated systems mediate between research and its publics. Jensen (2023) connects commons-based infrastructures to mobilization pathways, highlighting how interoperability and community practices shape whether knowledge flows toward public benefit or private capture. A central challenge is ensuring that speed does not erode fidelity, and that reach does not come at the expense of context or community consent.

The Canadian HSS Commons exemplifies mobilization infrastructure designed around principles of reciprocity and community responsiveness. Winter et al. (2020) describe how this platform instantiates governance mechanisms, provenance tracking, and dialogic engagement in a Canadian context, offering a concrete model for how digital research communities might align with OSS values. The Commons demonstrates that alternatives to extractive platform models are possible when design priorities center community benefit and participatory governance.

'''Infrastructure and Platforms'''. Repositories, journals, preprint servers, and social scholarly tools form the infrastructural backbone of scholarly communication due to their ubiquity, reliability and invisibility (Plantin et al. 2018). AI-mediated functions such as search, recommendation, summarization, moderation, and peer review reshape relations of production, discoverability, and legitimacy. Turning research outputs into training data for AI technologies creates a process of platformization of digital research infrastructure, in which the research process is commodified and turned into data for publishers and corporations to exploit while excluding the research community from the governance of these infrastructures. Bullard (2023) reveals how metadata shapes these dynamics, demonstrating that descriptive schemas determine what gets found, how it gets categorized, and whose work becomes visible. Goddard (2021) positions persistent identifiers as crucial connective tissue for provenance and interoperability, enabling the traceability that accountability requires. Whether platforms act as commons or proprietary funnels depends on decisions about interoperability, open standards, licensing, and governance. Colbert-Lewis et al. (2024) examine the citation economy as a site of extraction for surveillance publishing, documenting how publishers have transitioned to technology-driven data brokers that monetize researcher behavior alongside research outputs. Seemingly technical or back-end decisions structure how knowledge circulates and who benefits from that circulation.

== Open Social Scholarship Principles ==

Open Social Scholarship, as developed by INKE and ETCL, characterizes scholarship as a public, collaborative practice sustained by open, participatory, and ethically governed infrastructures (Arbuckle et al. 2022; El Khatib et al. 2019). Within this frame, AI is evaluated not solely on technical metrics but on whether it strengthens dialogic exchange, lowers barriers without reproducing harm, and supports reciprocal engagement rather than unilateral extraction. Openness is coupled with care; accessibility with accountability; participation with shared authority. Arbuckle and Maxwell (2019) move beyond open access by emphasizing infrastructure choices and governance as sites where values are enacted—recognizing that technical decisions embed normative commitments about who can participate, on what terms, and toward what ends. Maxwell (2015) argues that &quot;access&quot; alone proves insufficient; usability and community-responsive workflows reposition openness as an ecosystem with embedded care and accountability.

This also gives OSS a constructive role in relation to AI. Rather than approaching AI only as an external threat to be resisted, OSS can help specify what accountable alternatives would require: community-shaped tools, transparent provenance, accessible interfaces, multilingual and multimodal engagement, benefit-sharing where public or community knowledge is used, and governance arrangements that keep interpretive authority distributed rather than concentrated in proprietary systems.

Several principles translate into analytical vantage points for observing AI's effects:

'''Openness with care''' balances access with consent and community control, recognizing that uncontrolled circulation can facilitate extraction when reciprocity is absent (Carroll et al. 2020). Some knowledge requires protection; openness can become extractive when divorced from attention to power asymmetries and community interests.

'''Participation with shared authority''' embeds publics and communities in the design, evaluation, and governance of AI tools, rather than positioning them as passive recipients. Engagement becomes genuine partnership, not consultation that leaves final decisions to technical experts.

'''Accessibility''' is treated as multidimensional, spanning language, different ableness, technical literacy, and the digital divides that structure who can engage with AI-mediated scholarship. True accessibility requires attention to the multiple barriers—linguistic, economic, infrastructural—that shape unequal participation.

'''Reciprocity and benefit-sharing''' acquire particular weight where community-sourced data, scholarship, cultural material or labour underwrite AI functions; the question of whether benefits return to those communities become central. In heterogeneous training-data environments, reciprocity cannot always mean simple one-to-one compensation or attribution. It may also require collective mechanisms: investment in public infrastructure, support for community-governed datasets, licensing arrangements, provenance standards, access rights, audit mechanisms, and benefit-sharing models that recognize the distributed labour through which knowledge systems are built.

'''Infrastructural responsibility''' assigns institutions ongoing obligations to steward provenance, auditability, and accountability across the AI lifecycle—from adoption through monitoring, incident response, and iterative refinement. 

These principles serve as lenses that help clarify where choices around AI align with OSS values and where they introduce new tensions. They support a descriptive, attuned stance that remains open to emerging research, changing practices, and the contested meanings that animate debates over AI's place in scholarship.

== AI and &quot;Open&quot; ==

Openness operates across several registers—access, data, source, science, and social scholarship—and AI interacts differently with each. The recursive relationship between AI and openness demands particular attention: open access literature, open data, open source software, open standards, and community-maintained infrastructures have all contributed to the conditions under which contemporary AI systems became possible. Yet these resources now circulate within systems that often tend toward enclosure, secrecy, and commercial capture. The result is not a simple opposition between open and closed, but a contested field in which openness can serve public knowledge, enable scrutiny, and support community adaptation, while also becoming a reservoir from which private systems extract value without adequate attribution, consent, or reciprocity. 

=== Open Access ===

Open access literature forms one important input into model pretraining, retrieval-augmented generation, summarization, and later synthesis, while a dark shadow has fallen over how works licensed for broad human access are being repurposed for machine processing, private capture, and commercial value extraction. Pooley (2024) critically examines how commercial publishers frame AI companies as &quot;free-riders&quot; while themselves profiting from unpaid scholarly labour, extending &quot;surveillance publishing&quot; into AI domains. His analysis reveals a troubling symmetry: both commercial publishers and AI developers extract value from the scholarly commons while returning little to the researchers who create it. Kember and Brand (2023) document how OA policies may unintentionally contribute to greater consolidation enabling &quot;corporate capture&quot;—a warning that good intentions around openness can produce perverse outcomes when power asymmetries remain unaddressed.

Licensing frameworks and machine-access provisions influence whether open access functions as a commons or a reservoir for extraction. Luth (2025) examines how stakeholders navigate AI training on Creative Commons content, finding compliance often uncertain and highlighting strategies for protecting shared knowledge while sustaining open ecosystems. Smith (2025) analyzes how existing licenses perform in machine learning contexts, noting most were drafted without anticipating large-scale AI training and proposing machine-readable licensing provisions that could clarify terms and enable technical enforcement. These analyses suggest that the licensing frameworks developed for human readers require substantial adaptation to govern machine consumption, where attribution and context preservation present fundamentally different challenges.

AI thus makes open licensing a live infrastructural question rather than a settled legal background condition. Licensors, libraries, funders, publishers, repositories, and scholarly communities will need to clarify how open licenses apply to machine reading, text and data mining, model training, retrieval-augmented generation, and downstream synthetic outputs. The important question here is whether the use of open materials preserves attribution, context, reciprocity and the public purposes for which openness was advanced.

The dual role of open access—as both input to AI development and public good in its own right—underscores the importance of provenance-aware summarization, appropriate attribution, and consent mechanisms that reflect authors' and communities' intentions. When AI models synthesize open access literature, questions of attribution become vexed: whose work is represented in a probabilistic blend? How can communities maintain oversight of how their contributions are used?

=== Open Data ===

Open data, crucial for reproducibility and model improvement, raises issues of privacy, consent, and community sovereignty, especially in relation to sensitive or Indigenous data. The CARE principles complement FAIR by centering collective benefit, authority to control, responsibility, and ethics (Carroll et al. 2020). Carroll et al. (2020) ground these principles in the structural biases and colonization processes producing &quot;epistemicide,&quot; directly addressing tensions between Indigenous Data Sovereignty and AI's voracious data demands. Their framework demonstrates that open data governance constitutes a political practice, where broad data sharing and algorithmic extraction can undermine the rights, consent, and collective interests of communities whose knowledge becomes training material.

Carroll et al. (2021) demonstrate FAIR and CARE operationalized together. Because many scientific datasets contain Indigenous Knowledge, applying CARE principles ensures this data is oriented toward community wellbeing through rigorous provenance tracking and appropriate governance models. Arrangements such as data trusts, tiered access, and purpose-bound licenses illustrate how openness can be conditioned: open to whom, for which purposes, under what accountability terms?

Documentation practices emerge as crucial infrastructure for responsible AI development. Bender and Friedman (2018) propose data statements as critical enabling infrastructure to reduce exclusion and bias in language technologies, arguing that such documentation can prevent misrepresentation and support more ethical system development. Boyd (2021) empirically demonstrates that documentation frameworks increase engineers' ethical sensitivity—through think-aloud sessions, practitioners who received Datasheets identified ethical issues earlier and more frequently. This finding challenges assumptions that openness automatically leads to fairer systems; structured documentation actively shapes how practitioners recognize and respond to potential harms.

=== Open Source ===

Open source dynamics in AI include open weights, permissive licenses, and community checkpoints that support verification, plural innovation, and public-interest development. At the same time, discussions of misuse and dual-use emphasize capability control and risk. White et al. (2024) establish a Model Openness Framework with three-tiered classification, codifying 17 components that expose the requirements for reproducibility and scrutiny. Graduated openness—incremental model releases, safety mitigations, and governance charters—appears as one path toward balancing transparency with harm reduction. The evolution of open models will influence the accessibility of AI to under-resourced institutions, public-interest researchers, and communities seeking to adapt technologies to local contexts.

The Open Source Initiative's Open Source AI Definition 1.0, released in 2024, provides criteria for describing an AI system as &quot;Open Source AI&quot;, including the freedoms to use, study, modify, and share, access to the preferred form for modification, and sufficient information about training data provenance. As a definition rather than a license or implementation practice, it offers a community standard for assessing whether licenses, releases, and documentation practices support genuine openness, including whether &quot;open weights&quot; claims are matched by the artifacts, permissions, and transparency needed to avoid openwashing.

=== Open Science ===

Open science principles encourage reproducible workflows—transparent notebooks, containers, pipelines, and documentation—while AI introduces dependencies that can be opaque and difficult to reproduce. Practices such as open benchmarking, model cards, data cards, and documentation standards aim to make training data, evaluation metrics, and known limitations more visible. The push and pull between speed and scrutiny is pronounced in AI-assisted research: rapid exploration can generate insights, yet robust claims require validation, transparency, and often slower processes.

The tension between efficiency and process manifests acutely in open science contexts. AI can accelerate literature review, code generation, and data analysis, but the compression of these processes may obscure the iterative work through which understanding develops. Open science's emphasis on showing work—through preregistration, open notebooks, and transparent reporting—provides resources for maintaining visibility even as AI augments research workflows.

=== Open Social Scholarship ===

Within open social scholarship, AI is approached as a means to enhance public dialogue and shared inquiry. Examples include co-authorship with non-academic collaborators, explicit attribution of AI assistance, and participatory governance of tools in community-engaged projects (Arbuckle et al. 2022). Alignment with OSS principles is assessed by whether AI-supported practices sustain reciprocity, accessibility, and shared authority in knowledge production, and whether technological mediation amplifies rather than displaces human voice, agency, and accountability.

The feedback relationship—scholarship as training data, AI as scholarly tool—manifests throughout these registers. Open access literature trains models that then summarize open access literature. Peer review norms shape training data that then assists peer review. Pedagogical materials become training data for tools used in teaching. This recursion creates feedback loops whose effects on scholarly practice remain to be fully understood.

== AI and &quot;Social&quot; ==

The &quot;social&quot; dimension concerns the distribution of attention, credibility, and participation within and beyond academia. AI now helps mediate content creation, curation, and moderation, altering these distributions in ways that merit close scrutiny.

=== Platforms and Synthetic Content ===

Platforms hosting synthetic content must contend with provenance and identity. As generated text, images, and deepfake media proliferate, distinguishing among forms of authorship becomes more complex, with direct implications for trust and credibility. Van Es and Nguyen (2024) show that these anthropomorphic imaginaries are not incidental: they are actively constructed through ChatGPT's own self-representations, which consistently project a friendly, humanoid intellectual companion that obscures the statistical operations underneath. Mitra, Cramer, and Gurevich (2024) diagnose &quot;information access&quot; under generative AI as &quot;sociotechnical settlement&quot;—models &quot;intermediate credibility, reshape attention, and re-allocate epistemic authority.&quot; Their framing positions AI-mediated search and synthesis as fundamentally reconfiguring who gets heard, whose claims become visible, and whose expertise counts.

Recommendation systems juggle personalization, diversity, and serendipity, shaping canon formation and the visibility of marginalized voices. Attention economies are being reshaped: some work is surfaced and amplified; other work is obscured, sometimes by design and sometimes as a side effect of algorithmic optimization. Content credentials—cryptographic signatures and rich metadata—attempt to record origin and transformation history, while questions persist about whether such mechanisms can scale to match the velocity of synthetic content production. For scholarly communication, such mechanisms should be treated as part of the infrastructure of citation, preservation, disclosure and accountability; their value depends on whether they can travel across repositories, journals, platforms and public interfaces without being stripped of context.

=== Governance, Moderation, and Policy ===

Leadership, governance, moderation, and policy become iterative and layered rather than singular and top-down. Universities, libraries, journals, and repositories intersect with platform governance in setting norms for AI-assisted authorship, disclosure, review, and engagement. Sartori and Theodorou (2022) view AI as a &quot;magnifying glass&quot; amplifying existing inequities—a framing that clarifies bias as an older problem than the technology and locates responsibility in social structures and institutional choices. Their analysis challenges approaches that treat fairness as achievable through algorithmic adjustment alone, arguing that human control requires institutional mechanisms for contestation that acknowledge AI practice as fundamentally political.

Akter et al. (2021) theorize algorithmic bias as emerging from interacting sources—data bias, method bias, and societal bias—demonstrated through Australia's Robo-Debt scheme, which inherited and amplified existing inequities through automated decision-making. Their framework implicitly contests technological determinism by revealing how managerial choices about data collection priorities, acceptable error rates, and stakeholder consultation shape algorithmic outcomes in ways that exceed engineering decisions.

Jensen et al. (2022) address governance and moderation as platform design commitments aligned with OSS values, showing how choices about community safety and trust shape the kinds of scholarship platforms can support. Transparency reports, appeal procedures, and community-based moderation seek to address harms while preserving legitimate expression. Policy becomes experimental, subject to revision as impacts, unintended consequences, and community norms evolve.

=== Critical Literacies ===

Critical literacies, for both scholars and publics, extend beyond operational proficiency. They involve understanding model limits, recognizing sources of bias, interpreting provenance signals, and practicing verification. Chun and Elkins (2023) position AI's advancement as precipitating interlocking crises demanding pedagogical response grounded in reflective and collaborative meaning-making, explicitly connecting pedagogical design to civic preparation and positioning students as &quot;critically engaged citizens capable of interrogating the social and economic implications of algorithmic mediation.&quot; Zeffiro (2024) reveals how corporate narratives of AI as &quot;democratizing force&quot; obscure differential vulnerabilities while &quot;automating insecurities&quot;—a concept capturing how AI tools institutionalize particular understandings of risk that reflect corporate priorities rather than community needs.

These literacies include skills such as documenting AI use, distinguishing synthesis from source, reading expressions of uncertainty, and maintaining awareness of the gap between fluency and accuracy. The ease with which AI produces confident-sounding text makes discrimination skills more important: fluency does not indicate accuracy, and the appearance of authority can mask the absence of understanding.

=== Global Asymmetries and Epistemic Centralization ===

AI’s geopolitical dimensions draw attention to questions of influence, globalism, and colonization. Training regimes often reproduce global asymmetries in language and corpus composition: English-language and Global North sources dominate, while linguistic and epistemic diversity from other regions receive less representation. Bender et al. (2021) critically analyze how larger models reproduce hegemonic views, noting that the damages associated with large-scale language models—environmental costs, representational harms, concentration of power—are more likely to fall on marginalized populations.

Chung (2025) extends geographic scope to Asia's advanced economies, revealing how techno-developmentalism produces distinct imaginaries shaped by local political-economic conditions. Multilingual models, community-owned datasets, and South–South collaborations seek to counteract epistemic centralization, yet the structural dynamics of extraction without reciprocity remain strong. Arthur et al. (2021) reveal how national policy shapes whether openness reduces or reproduces inequities, showing that structural barriers—funding models, institutional incentives, infrastructure gaps—mediate between stated commitments to openness and their realization in practice.

Debates over determinism, diversity, and justice challenge narratives of technological inevitability. Sartori and Theodorou (2022) extend this analysis to the global scale, emphasizing that adoption choices, design priorities, and evaluation metrics remain matters of collective agency—and that the communities most affected by AI's asymmetries are precisely those least represented in the governance structures that shape them. Justice-oriented evaluation foregrounds the distribution of harms and benefits, rather than focusing solely on aggregate performance: who is helped, who is harmed, and along which axes of power and marginalization?

=== Humanity, Community, Connection, and the Affective Dimensions of AI Mediation ===

Beyond the technical and governance dimensions, AI mediation carries affective and relational aspects that shape scholarly communication in subtle but significant ways. Generative systems influence the tone and velocity of discourse and can intensify polarization or foster connection depending on design choices and deployment contexts. The ability to flood channels with synthetic text or avatars strains existing trust infrastructures, creating new challenges for maintaining the relational fabric of scholarly communities.

Design choices that emphasize care—thoughtful moderation, friction for high-risk actions, community control of spaces—become part of scholarly platform ethics. These choices counter acceleration and decontextualization that undermine deliberation and mutual recognition. The question moves beyond whether AI produces accurate outputs, but whether AI-mediated environments support the kinds of dialogue, disagreement, and collaborative inquiry that scholarship requires. Connection and community constitute values that technical efficiency can erode if left unattended.

Jensen et al. (2022) explore how digital communities of care can be fostered through attention to safety, security, and trust—values that require ongoing cultivation rather than one-time technical implementation. The relational dimensions of scholarship—mentorship, collaboration, peer recognition, collegial support—may be affected by AI mediation in ways that exceed questions of accuracy or efficiency.

=== Environmental and Labour Costs ===

Material costs, both labour and environmental, ground AI capability in ways that often remain invisible. The AI pipeline depends on precarious annotation and moderation labour, often transnational and underpaid. Workers in the Global South perform essential tasks—labeling training data, flagging harmful content, refining model outputs—under conditions that rarely feature in celebratory narratives of AI advancement. This hidden labour connects AI development to broader patterns of extraction and externalization, where the costs of technological systems are displaced onto vulnerable populations.

Energy and water consumption for training and deployment contribute to climate impacts that intersect with environmental justice concerns. Bender et al. (2021) observe that the damages associated with large-scale language models—environmental costs, representational harms, concentration of power—&quot;are more likely to fall on marginalized populations.&quot; The communities least likely to benefit from AI capabilities bear disproportionate burdens from their development.

Disclosure norms, ethical procurement, and commitments to &quot;green AI&quot; bring these dimensions into infrastructural planning rather than treating them as externalities. For institutions committed to sustainability and justice, AI adoption cannot be evaluated solely on functional criteria; the material conditions of AI production become relevant to responsible deployment decisions. This connects AI governance to broader institutional commitments around environmental responsibility and labour ethics.

== AI and &quot;Scholarship&quot; ==

Across the scholarly lifecycle, AI now participates in research, writing, teaching, review, and administration, changing how practice and infrastructure co-evolve. The tension between operational assistance and epistemic authority manifests at each stage.

=== Research Methods and Practice ===

Research methods and practices incorporate LLMs for literature review, coding, data cleaning, translation, and analysis. Key questions concern how assistance is documented, how outputs are validated, and how communities renegotiate the line between exploratory use, operational support, interpretive contribution, and settled scholarly claim. Mehlenbacher, Balbon, and Mehlenbacher (2024) examine &quot;synthetic genres&quot; that push apart definitions of &quot;information&quot; and &quot;knowledge,&quot; suggesting that AI-generated text occupies a novel categorical space requiring new frameworks for evaluation. Bozkurt (2024) addresses authorship implications, proposing the aiTARAS Framework while maintaining that responsibility ultimately belongs to the human author. Maintaining epistemic standards while exploring new efficiencies requires treating AI as a tool supporting thought and analysis, not as a substitute for disciplinary judgement.

Domain-specific norms—interpretive rigor in the humanities, reproducibility in quantitative fields—must shape appropriate use. The question of when AI assistance becomes AI authorship remains contested, with implications for credit, accountability, and the integrity of scholarly claims. Documenting AI use transparently allows readers to assess the epistemic status of outputs and evaluate whether human judgement remains central to the knowledge claims of a given piece.

=== Scholarly Outputs ===

Forms of scholarly output are changing as generative tools support multimodal and interactive work: dynamic narratives, layered visualizations, and synthesis artefacts that draw together diverse sources. Bergstrom and Ruediger (2024) anticipate &quot;discovery, interpretation, and writing services&quot; becoming integrated suites while noting concerns about platform intermediation that could concentrate power over scholarly communication. Authorship, attribution, and preservation practices need to adapt: whose contributions are recognized, how AI assistance is disclosed, and how AI-mediated outputs are archived and made citable. Provenance and disclosure become part of the paratext, informing evaluations of reliability and situating works within ongoing conversations.

=== Teaching and Pedagogy ===

Teaching and pedagogy integrate AI as both subject and instrument. Tan and Maravilla (2024) position AI as &quot;catalyst necessitating pedagogical transformation—shifting from transmission models toward environments where students actively construct knowledge.&quot; This reframing treats AI as an occasion for rethinking educational purposes and methods, emphasizing the human capacities—critical judgement, ethical reflection, creative synthesis—that AI systems cannot replicate.

Deng et al. (2025) meta-analyze 69 studies finding ChatGPT improves performance while reducing mental effort, raising questions about what learning means when cognitive work is offloaded to machines. Their findings suggest that traditional assessment measures require recalibration to capture the thinking processes that educational institutions value. The tension between efficiency and process manifests acutely here: if AI can produce essays, what is being assessed? Process-centered assessment emphasizes transparency, ethical reflection, and the development of critical literacies that enable students to assess model outputs, recognize limitations, and engage thoughtfully with AI-mediated knowledge.

Lee and Palmer (2025) establish prompt engineering as emergent practice mirroring &quot;Socratic dialogue,&quot; suggesting continuities between AI interaction and established pedagogical traditions. Oates and Johnson (2025) demonstrate pedagogical value in making AI outputs &quot;subjects for evaluation rather than endpoints of learning&quot;—an approach that uses AI as material for critical analysis. Berry (2023) warns that uncritical AI reliance risks &quot;algorithmization&quot; of Digital Humanities, where computational methods become defaults that shape questions before they are asked.

=== Service and Peer Review ===

Service and peer review use AI for triage, formatting checks, and detection tasks—identifying duplication, verifying references, smoothing language—while preserving human judgement for evaluations of originality, significance, and methodological rigor. Sun (2025) maps LLM applications in peer review, emphasizing that models &quot;remain fundamentally limited in assessing research novelty&quot;. Hosseini and Horbach (2023) document potential to combat reviewer fatigue while identifying risks when &quot;operational assistance crosses into epistemic territory,&quot; suggesting that the boundary between support and substitution requires careful negotiation. Checco et al. (2021) demonstrate AI can predict outcomes based on &quot;superficial&quot; features while emphasizing &quot;semi-automated&quot; approaches that preserve human judgement for consequential decisions.

The line between operational assistance and epistemic authority runs directly through peer review, but it is better understood as a moving boundary than a fixed division. Tasks such as formatting checks, duplication detection, reference verification, and metadata checks may sit relatively comfortably on the operational side. Literature triage, reviewer matching, summary generation, and consistency checking occupy more contested middle ground. Assessments of novelty, significance, methodological rigor, interpretive adequacy, and contribution to a field require the kind of accountable judgement that remains distinctively human. Clarity about this boundary helps preserve the integrity of peer review while leveraging AI's capacity for routine tasks.

The inverse problem is integrity infrastructure. AI may assist legitimate review workflows, but it can also amplify older forms of scholarly fraud: paper mills, fabricated peer reviews, synthetic citations, citation cartels, manipulated images, and low-quality or fabricated manuscripts designed to pass superficial screening. These problems predate contemporary genAI, but generative systems increase their scale, speed, and plausible fluency. Responsible AI governance in publishing therefore requires attention not only to how reviewers may use AI, but also to how editorial systems detect, document, and respond to AI-amplified threats to the scholarly record. 

=== Research-Related Infrastructures ===

Research-related infrastructures span organizational governance, publishing and communication platforms, workflow systems, and accountability mechanisms. Governance frameworks, risk registers, roles, and capacity-building programs institutionalize stewardship, coordinating policy and practice across libraries, IT, research support, and ethics offices. Wu, Zhang, and Carroll (2024) document Big Ten universities' &quot;multi-unit governance involving information technology, teaching centers, libraries, and research offices&quot;—a distributed model recognizing AI as a cross-sectoral concern requiring coordinated response.

AI also places new pressure on open scholarly infrastructure. Repositories, commons platforms, digital research infrastructures, standards bodies, and open-science advising organizations must decide whether and how to integrate AI-mediated search, metadata generation, summarization, moderation, preservation, and analytics. These decisions affect governance, sustainability, procurement, interoperability, environmental cost, labour, and the degree to which open infrastructures remain accountable to scholarly and public communities rather than becoming dependent on proprietary AI services.

Open infrastructure responses should therefore be assessed against principles such as transparency, community governance, interoperability, portability, auditability, and long-term stewardship. In this context, standards for open infrastructure become AI governance instruments: they shape whether AI functions can be inspected, contested, replaced, or collectively maintained. 

Papagiannidis, Mikalef, and Conboy (2025) differentiate governance practices, revealing tensions &quot;between centralized oversight and distributed expertise.&quot; Institutions must navigate between the efficiency of centralized decision-making and the contextual knowledge held by distributed practitioners who understand how AI affects their specific domains.

Rughiniș et al. (2025) introduce &quot;dual black-boxing&quot; capturing compound accountability challenges when opaque AI systems meet opaque institutional processes. When neither the AI nor the institution is transparent about its decision-making, accountability becomes doubly difficult. Janssen (2025) reframes AI governance as managing &quot;complex adaptive systems characterized by co-evolution and emergent properties,&quot; suggesting that governance frameworks must themselves be adaptive. Weber et al. (2023)—whose findings on organizational capacity are discussed in the cross-cutting tensions above—appear here as a reminder that infrastructure governance is where those abstract tensions become concrete institutional failures.

Publishing and communication infrastructures increasingly integrate AI functions—journal recommendation, reviewer matching, manuscript screening, metadata generation—as part of scholarly workflow systems. Kousha and Thelwall (2024) map AI tool deployment across the publishing pipeline, distinguishing demonstrated capabilities from promotional claims. Their analysis reveals that substantial efficiency improvements are achievable in labour-intensive administrative tasks, while human judgement remains integral to core intellectual evaluations. This distinction—between what AI can assist with operationally and what requires human epistemic judgement—structures responsible integration of AI into publishing infrastructures. Ultimately, however, the success of these infrastructural choices is measured not just by operational efficiency, but by how effectively they mediate knowledge for the diverse publics who rely on them.

== Audiences and Differential Impacts ==

Audiences—scholars, students, practitioners, policymakers, and broader publics—encounter AI-mediated summaries, translations, and recommendations that shape how they access and interpret scholarship. Each audience brings different needs, literacies, and vulnerabilities to these encounters, and AI effects manifest differently across these diverse contexts.

Personalization raises the risk of filter bubbles, where recommendation systems surface content that confirms existing interests and perspectives while obscuring alternatives. Taneja and Tripathi (2020) identify structural tensions inherent in personalization algorithms that enhance user experience while simultaneously constructing echo chambers that systematically exclude novel, dissenting, or interdisciplinary perspectives. For scholarly communication, filter bubbles could reinforce disciplinary silos and impede the cross-fertilization that drives innovation. Audience-aware communication emphasizes context, uncertainty, and reciprocity, recognizing that different audiences need different framings and levels of technical detail.

The accessibility principles outlined earlier apply with particular force here: different audiences face different obstacles. AI can broaden participation and lower barriers—through translation, summarization, and alternative formats—but only when its design and governance prioritize inclusion, fidelity, and the preservation of diverse voices and perspectives. Da Silva Cardoso and Rocio (2025) propose frameworks for integrating AI into academic digital libraries that position librarians as essential partners in system development, emphasizing that understanding the nuanced and context-dependent needs of diverse academic communities requires human expertise that cannot be automated. The question is whether AI mediation grows or shrinks the publics that can engage with scholarship.

The sources reveal how AI effects vary by context in ways that demand attention to differential impacts:

'''Institutional type'''. AI adoption is shaped by uneven institutional capacities, but these differences do not map neatly onto size or prestige. Large research universities may have more formal infrastructure, while also facing larger user bases, more complex bureaucracies, and less responsive or less humane interventions. Smaller institutions, community colleges, public libraries, independent scholarly organizations, and grassroots knowledge projects may face different constraints, including limited staffing, funding, or access to specialized expertise. Equitable AI adoption therefore requires governance models that can adapt across institutional contexts without assuming uniform access to technical capacity, administrative infrastructure, or training resources.

'''Language communities'''. What serves English-language scholarship may disadvantage multilingual communities. Models trained predominantly on English reproduce Anglophone perspectives; multilingual support often lags behind. For scholars working in languages underrepresented in training corpora, AI tools may be less accurate, less helpful, or actively distorting. Linguistic diversity constitutes both an epistemic and an ethical concern: knowledge produced in non-dominant languages risks marginalization when AI systems favor majority languages.

'''Career stage'''. What benefits established researchers may burden early-career scholars differently. Senior researchers with established reputations may more easily navigate AI-mediated environments, using AI assistance to amplify existing authority. Early-career scholars face additional pressures around attribution, originality, and demonstrating independent capability. When AI can generate fluent prose, summarize literatures, and accelerate administrative or writing tasks, how do junior scholars demonstrate the intellectual development that hiring, promotion and grant committees have traditionally valued? Assessment criteria developed for human-only production may require adaptation to remain meaningful in AI-augmented contexts, but such adaptation must avoid intensifying surveillance or creating new burdens of disclosure that fall unevenly on those with the least institutional power. 

AI in the evaluation of researchers deserves separate attention from AI in the peer review of scholarly outputs. Hiring, promotion, tenure, grants, fellowships, and institutional metrics shape careers, disciplines, and access to scholarly futures. If AI-mediated tools are used to screen CVs, rank candidates, summarize dossiers, evaluate productivity, or assess “fit,” their consequences may be especially significant for early-career scholars, contingent faculty, disabled scholars, scholars working in less dominant languages, interdisciplinary researchers, and those whose contributions are not well captured by standard metrics. Governance in this area should require transparency, contestability, human accountability, and careful attention to disparate impact. 

'''Disciplinary context'''. Different disciplines bring different norms, methods, and evaluation criteria to AI engagement. What constitutes appropriate AI assistance in a literature review differs from appropriate assistance in data analysis or creative work. Disciplinary communities are developing varied approaches, and cross-disciplinary dialogue helps surface assumptions and identify best practices that might transfer across contexts.

'''Geographic location'''. Scholars in different regions face different infrastructural realities, regulatory frameworks, and access conditions. AI tools developed primarily for well-resourced contexts may not serve scholars working with limited bandwidth, different privacy regimes, or constrained institutional support. Geographic diversity in AI impacts connects to broader patterns of global inequality in knowledge production and circulation.

Attention to these differential impacts marks responsible AI adoption, requiring ongoing assessment of who benefits, who bears burdens, and how distributions might be made more equitable. Rather than assuming uniform effects, responsible governance monitors for disparate impacts and adjusts policies and tools in response to evidence of inequitable outcomes.

== Phenomena, Relations, and Ongoing Inquiry ==

The sources in this annotated bibliography have been selected to trace several intersecting concerns. Conceptually, works that articulate critical frameworks (STS, data colonialism) offer key tools for understanding AI as a sociotechnical formation. (Anderson 2024; Ali et al. 2023; Bender et al. 2021). Normatively, scholarship on public engagement, participatory infrastructures, reciprocity, and accessibility grounds the discussion in the normative coordinates of open social scholarship (Arbuckle et al. 2022; El Khatib et al. 2019). Infrastructurally, sources on data governance (FAIR and CARE), licensing, repositories, and platforms illuminate how AI is being integrated into the material and organizational substrates of knowledge work (Carroll et al. 2020; White et al. 2024). Methodologically, contributions from anthropology, STS, media studies, information science, and environmental humanities help maintain epistemic plurality and attend to global and intersectional dimensions (Chung 2025; Richter, Katzenbach, and Schäfer 2025). Finally, empirically, studies of peer review, literature searching, pedagogical applications, and governance supply concrete evidence of AI's effects in practice (Sun 2025; Deng et al. 2025; Wu, Zhang, and Carroll 2024).

== Conceptual Mapping ==

The conceptual mapping that orients this bibliography treats concepts, phenomena, and relations as interconnected. This mapping is meant to help readers locate where a given source sits: what it names, what it observes, and what it connects:

'''Concepts''' such as openness, provenance, bias, governance, data sovereignty, participation, reproducibility, labour, sustainability, platformization, multilingualism, accessibility, evaluation, enclosure, commons, personalization, and exposure diversity mark key terms of analysis.

'''Phenomena''' such as pretraining on public corpora, proliferation of synthetic content, recommendation feedback loops, metadata drift, hallucination, hybrid openness models, human-in-the-loop verification, green AI practices, community moderation, content credentials, and retrieval-augmented generation describe observable patterns in the field.

'''Relations''' trace interactions among these elements: openness and enclosure meet through licensing and reciprocity mechanisms; provenance and trust are linked through audit trails and disclosure practices; bias and diversity intersect in dataset governance and evaluation design; governance and participation connect through co-design and community oversight; platformization shapes visibility through algorithmic curation and efforts to foster exposure diversity; labour and sustainability meet in discussions of ethical procurement and environmental accounting; reproducibility pushes against black-boxing through documentation and open benchmarking; multilingualism and accessibility intertwine in translation and community review; evaluation anchors legitimacy by attending to social impact and equity metrics.

== Focused Areas for Further Intervention ==

Several areas emerge from this scan as candidates for shorter, more pragmatic follow-up work. AI-mediated scholarly discovery is already reshaping canon formation, citation patterns and visibility through search engines, recommender systems, citation-context services, discovery platforms and automated synthesis tools. Provenance infrastructure, including content credentials, persistent identifiers, verifiable metadata, and workflow documentation, could strengthen disclosure by making AI involvement more portable, auditable and machine-readable. Smaller, community-built, purpose-specific models offer a constructive path for aligning AI with OSS values where communities can define scope, data governance, evaluation criteria, and benefit-sharing arrangements. 

Integrity infrastructure also requires urgent attention, since paper mills, fabricated reviews, synthetic citations and AI-amplified fraud threaten the trust systems upon which scholarship depends. AI in the evaluation of researchers—hiring, promotion, grants, fellowships, and institutional metrics—deserves treatment distinct from peer review of outputs because its consequence for early-career scholars, equity and disciplinary futures may be especially profound. Parallel interventions on AI and open licensing, and on AI’s effects on open scholarly infrastructure, would clarify how licensors, libraries, funders, digital research infrastructures, advising bodies and standards communities are adapting to machine use of open knowledge.

=== Conditions for Flourishing ===

The question animating this bibliography remains phenomenological: what conditions enable scholarship to flourish? The sources suggest these conditions include:

* '''Diverse participation''' that brings varied perspectives to bear on complex problems
* '''Critical literacy''' that equips scholars and publics to evaluate AI-mediated claims
* '''Transparent processes''' that make choices visible and contestable
* '''Human accountability''' that maintains responsibility for consequential decisions
* '''Infrastructural stewardship''' that ensures technical systems serve public purposes

OSS principles provide the normative coordinates for navigating the cross-cutting tensions this scan has identified—offering a framework to ensure that operational assistance does not usurp epistemic authority, that openness resists extractive enclosure, that technical deployments match organizational capacity, and that efficiency does not erase the deliberative processes of scholarship. Specifically, openness with care balances access with consent and community control. Participation with shared authority embeds publics and communities in design and evaluation. Accessibility spans language, disability, and technical literacy. Reciprocity ensures that where community-sourced data or labour underwrite AI functions, benefits flow back to contributors. Infrastructural responsibility commits institutions to steward provenance, auditability, and accountability across deployment lifecycles.

This mapping does not aim to close debate or fix categories. It sketches a topology of the current field: which nodes are active, where tensions gather, and how shifts in one domain reverberate through others. The annotated bibliography is offered as a baseline &quot;lay of the land&quot; against which ongoing research can be situated, helping scholars and practitioners locate their work within a broader conceptual ecology and identify gaps, alignments, and opportunities for intervention shaped by OSS principles of accessibility, reciprocity, and public value.

These conditions also point towards a positive agenda. AI-mediated scholarship could support forms of access and engagement that have long mattered to OSS: translation across languages and registers, navigation of complex archives, discovery across disciplinary boundaries, support of disabled readers and writers, richer metadata, and new forms of dialogue between specialists and broader publics. Whether such uses weaken or strengthen scholarship depends less on the abstract presence of AI than on the infrastructures, governance processes, and values through which AI is developed and adopted.

The landscape will continue to shift. New capabilities will emerge, governance frameworks will evolve, communities will develop practices and norms through experimentation and deliberation. What this bibliography offers is a documented moment from which change can be measured and assessed. The sources assembled here provide conceptual resources for that ongoing work: frameworks for analysis, evidence of effects, models for governance, and principles for evaluation. The task ahead is to use these resources thoughtfully, maintaining the commitments to accessibility, reciprocity, and public engagement that make scholarship worth pursuing.

{{Navigation|previous=Essential Ideas|next=Essential Contexts}}

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      <text bytes="470" sha1="mpfsf7uu0egr4w54y98cbu6kydc8gnv" xml:space="preserve">Hi, my name is &quot;一隻北極熊&quot;(Pinyin:Yizhibeijixiong, ''yi-jur-bay-jee-siong'') and I am a student from Taiwan. I am currently learning Russian.

==My Works==
*[[Bopomofo]](near finished!)
*[[Taiwan History]](freshly started)
*I also like to edit the [[Chinese (Mandarin)]] textbook.
&lt;noinclude&gt;{{Userboxtop}}
[[File:Mandarin-fruit-mandarin- language-joke.png|400px]]
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      <timestamp>2026-07-17T04:51:53Z</timestamp>
      <contributor>
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      <origin>4654770</origin>
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      <text bytes="467" sha1="06q44yfhgijfuvvbu67tm485m4vrypr" xml:space="preserve">Hi, my name is &quot;一隻北極熊&quot;(Pinyin:Yizhibeijixiong, ''yi-jur-bay-jee-siong'') and I am a student from Taiwan. I am currently learning Russian.

==My Works==
*[[Bopomofo]] (finished!)
*[[Taiwan History]] (freshly started)
*I also like to edit the [[Chinese (Mandarin)]] textbook.
&lt;noinclude&gt;{{Userboxtop}}
[[File:Mandarin-fruit-mandarin- language-joke.png|400px]]
{{user language|zh|N}}
{{user language|en|N}}
{{user language|ru|1}}
{{Userboxbottom}}
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    <title>Bopomofo</title>
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      <text bytes="1131" sha1="gbi2tdtnug0idc5o89zsurb410mv195" xml:space="preserve">{{New book}}{{Formatting}}__NOTOC__ __NOEDITSECTION__
{| width=&quot;100%&quot; style=&quot; box-shadow:gray 1px 1px 5px; padding:1em; &quot;
|+
|-
| width=&quot;100%&quot; |
&lt;div id=&quot;mf-head&quot;&gt;
&lt;div align=&quot;center&quot; style=&quot;font-size:2.8em; color:; margin:0.4em&quot;&gt;'''Bopomofo Textbook'''&lt;/div&gt;
&lt;div align=&quot;center&quot; style=&quot;font-size:1.2em; color:gray; margin:0.2em;&quot;&gt;'''ㄓㄨˋㄧㄣ ㄈㄨˊ ㄏㄠˋ ㄐㄧㄠˋ ㄎㄜ ㄕㄨ'''
&lt;/div&gt;
&lt;span style=&quot;color:#cc0000;&quot;&gt;'''''Note:'''''&lt;/span&gt; To use this book, your web browser must first be configured to display Bopomofo characters and Chinese characters. Check the three boxes below:
{| border=&quot;1&quot; cellspacing=&quot;0&quot; cellpadding=&quot;6&quot; align=&quot;center&quot;
| style=&quot;background-color:#eeeeee;&quot; | ㄅㄆㄇㄈㄉㄊㄋㄌ
| style=&quot;background-color:#eeeeee;&quot; | 注音符號教科書
| style=&quot;background-color:#eeeeee;&quot; | 注音符号教科书
|}
==Contents==
*[[/Introduction-What is Bopomofo?/]]
*1.[[/Initials/]]
*2.[[/Medials/]]
*3.[[/Finals/]]
*4.[[/Tones/]]
*5.[[/Practice &amp; Application/]]
*[[/Appendix/]]
==Related books==
*[[Pinyin]]
*[[Chinese (Mandarin)]]
{{Shelves|Chinese language}}
{{Status|100%}}
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    <title>Bopomofo/Appendix</title>
    <ns>0</ns>
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      <text bytes="76" sha1="rpm71cssg7fd5ykudytw0s6naw1628n" xml:space="preserve">*[[Bopomofo/List of Bopomofo]]
*[[Bopomofo/Printable version]]


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    <title>Taiwan history/About Taiwan History</title>
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      <timestamp>2026-07-16T16:16:55Z</timestamp>
      <contributor>
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      <text bytes="811" sha1="3apcq85hconwnjc9c9be5xa8cys0xel" xml:space="preserve">[[file:Taiwan NASA Terra MODIS 23791.jpg|thumb|Taiwan]]
'''Taiwan''' (Traditional Chinese:台灣), located on the Pacific ocean, is a country with a complex history. It is a rich mosaic shaped by its indigenous roots, successive waves of colonization, and a modern transformation into a thriving democracy and global technological powerhouse. Learning the Taiwan history can help you understand more about the Taiwanese culture. This book will introduce all of the Taiwanese history, from the Prehistorical Era to the Modern day Taiwan. Have fun learning!

'''Note:''' Not to be confused with ''History of Republic of China'', which is the modern government in Taiwan, started in 1912 in mainland China, and retreated to Taiwan in 1949. This book will be focusing on the island of Taiwan's history.

{{BookCat}}</text>
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      <id>4654762</id>
      <parentid>4654709</parentid>
      <timestamp>2026-07-17T03:31:08Z</timestamp>
      <contributor>
        <username>一隻北極熊</username>
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      <text bytes="823" sha1="r0cnkzj3gnjjf6vhhn3gbhm7ubm54ic" xml:space="preserve">[[file:Taiwan NASA Terra MODIS 23791.jpg|thumb|Taiwan]]
'''Taiwan''' (Traditional Chinese:台灣), is a island located on the Pacific ocean, is a country with a complex history. It is a rich mosaic shaped by its indigenous roots, successive waves of colonization, and a modern transformation into a thriving democracy and global technological powerhouse. Learning the Taiwan history can help you understand more about the Taiwanese culture. This book will introduce all of the Taiwanese history, from the Prehistorical Era to the Modern day Taiwan. Have fun learning!

'''Note:''' Not to be confused with ''History of Republic of China'', which is the modern government in Taiwan, started in 1912 in mainland China, and retreated to Taiwan in 1949. This book will be focusing on the island of Taiwan's history.

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    <title>Chinese (Mandarin)/Lesson 17/Examples</title>
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      <text bytes="1152" sha1="ks9jcgb0ugk4wxca05ibvc8076c64wa" xml:space="preserve">These are the examples of basic heteronyms in Chinese.
{| class=&quot;wikitable sortable&quot;
! Simplified (简)
! Traditional (繁)
! Pinyin 1
! Example 1
! Pinyin 2
! Example 2
|-
| 长
| 長
| cháng
| 长度(length)
| zhǎng
| 长高(Growing taller)
|-
| 行
| 行
| xíng
| 行走(walk)
| háng
| 第一行(first row)
|-
| 得
| 得
| dé
| 得到(get)
| děi
| 总得(must)
|-
| 还
| 還
| hái
| 还要(still need)
| huán
| 还钱(return money)
|-
| 好
| 好
| hǎo
| 好棒(good)
| hào
| 好客(hospitable）
|-
| 乐
| 樂
| lè
| 快乐(happy)
| yuè
| 音乐(music)
|-
| 觉
| 覺
| jué
| 察觉(aware)
| jiào
| 睡觉(sleep)
|-
| 看
| 看
| kàn
| 看书(read book)
| kān
| 看门(look after the house)
|-
| 少
| 少
| shǎo
| 少量(little amount)
| shào
| 少女(young girl)
|-
| 便
| 便
| biàn
| 便利(convenient)
| pián
| 便宜(cheap)
|-
| 重
| 重
| zhòng
| 重物(heavy thing)
| chóng
| 重复(repeat)
|-
| 发
| 發
| fā
| 批发(Wholesale）
| fà
| 头发(hair)
|-
| 调
| 調
| tiáo
| 调味(Seasoning)
| diào
| 声调(tone)
|-
| 切
| 切
| qiē
| 切菜(cut vegetable)
| qiè
| 切记(must remember)
|}

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  <page>
    <title>Vehicle Identification Numbers (VIN codes)/Saab/VIN Codes</title>
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      </contributor>
      <comment>/* Position 11, Production Plant: */</comment>
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      <text bytes="12311" sha1="fyijwq5p1crg2o0t2x5lz5lgp05r6ms" xml:space="preserve">{{Vehicle Identification Numbers (VIN codes)/Warning}}{{clear}}

For Saab 9-2X, see the Subaru VIN page: [[Vehicle Identification Numbers (VIN codes)/Subaru/VIN Codes]]. 
For Saab 9-4X and 9-7X, see the GM VIN page: [[Vehicle Identification Numbers (VIN codes)/GM/VIN Codes]].

===Positions 1–3, World Manufacturer Identifier:===  
* YS3 - Saab passenger car
* YK1 - Saab passenger car made by Valmet in Finland ('81-'83)
* JF4 - Saab passenger car made by Subaru in Japan ('05-'06 9-2X)
* 3G0 - Saab MPV made by GM in Mexico ('11 9-4X)
* 5S3 - Saab MPV made by GM in US ('05-'09 9-7X)

===Positions 4, Model Line:===
* A = 900 (1st gen. - '81-'93, '94 convertible)
* C = 9000 ('86-'98)
* D = 900 (2nd gen. - '94-'98 3-d/5-d, '95-'98 convertible)
* D = 9-3 (1st gen. - '99-'02, '03 convertible)
* E = 9-5 (1st gen. - '99-'09)
* F = 9-3 (2nd gen. - '03-'11 4-d, '04-'11 convertible, '06-'11 wagon)
* G = 9-5 (2nd gen. - '10-'11)

===Positions 5, Series 1981-1986:===
* G = Base model ('81-'83 900)
* S = S 3-d ('81-'83 900)
* E = S 4-d ('81-'83 900)
* M = Base model ('84-'85 900)
* H = S ('84-'85 900)
* T = Turbo ('81-'85 900)
* B = Base model ('86 900)
* C = S ('86 900)
* D = Turbo ('86 900, '86 9000)

===Positions 5, Series/Restraint 1987-2011:===
* R = Base model w/Active (Manual) seat belts ('87-'89 900)
* S = S w/Active (Manual) seat belts ('87-'89 900, '87-'89 9000)
* T = Turbo w/Active (Manual) seat belts ('87-'89 900, '87-'89 9000)
* J = Base model w/Motorized seat belts (Passive Restraint) ('89 900)
* K = S w/Motorized seat belts (Passive Restraint) ('87-'89 900)
* L = Turbo w/Motorized seat belts (Passive Restraint) ('88-'89 900)
* J = Base model w/Active (Manual) seat belts &amp; Driver-side airbag ('90 900)
* K = S w/Active (Manual) seat belts &amp; Driver-side airbag ('89-'90 9000, '90 900)
* K = Models w/normally aspirated engine w/Active (Manual) seat belts &amp; Driver-side airbag ('91-'93 9000, '91-'93 900, '94 900 convertible)
* L = Turbo or CD Turbo (9000) or CD Turbo Griffin Edition ('92 9000) w/Active (Manual) seat belts &amp; Driver-side airbag ('89-'92 9000, '90-'92 900)
* L = Models w/turbocharged engine w/Active (Manual) seat belts &amp; Driver-side airbag ('93 9000, '93 900, '94 900 convertible)
* M = Models w/normally aspirated engine w/Active (Manual) seat belts &amp; Dual front airbags ('94 900 3-d/5-d, '94 9000)
* N = Models w/turbocharged engine w/Active (Manual) seat belts &amp; Dual front airbags ('94 900 3-d/5-d, '94 9000)

* D = 900 S or 9000 CS w/Active (Manual) seat belts &amp; Dual front airbags ('95-'98)
* F = 900 SE or 9000 CSE/CDE w/Active (Manual) seat belts &amp; Dual front airbags ('95-'98)
* H = 9000 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('95-'97)

* B = 9-3 Linear w/Active (Manual) seat belts &amp; Dual front airbags ('03-'05)
* B = 9-3 2.0T w/Active (Manual) seat belts &amp; Dual front airbags ('08-'09)
* B = 9-5 Linear w/Active (Manual) seat belts &amp; Dual front airbags ('02-'05)
* B = 9-5 Griffin Edition w/Active (Manual) seat belts &amp; Dual front airbags ('09)
* D = 9-3 Base model or 9-5 Base model or 9-5 Gary Fisher Edition ('00) w/Active (Manual) seat belts &amp; Dual front airbags ('99-'01)
* D = 9-3 Arc w/Active (Manual) seat belts &amp; Dual front airbags ('03-'05)
* D = 9-3 2.0T w/Active (Manual) seat belts &amp; Dual front airbags ('06-'07)
* D = 9-5 Arc w/Active (Manual) seat belts &amp; Dual front airbags ('02-'05)
* D = 9-5 Standard model 2.3T w/Active (Manual) seat belts &amp; Dual front airbags ('06-'09)
* F = 9-3 SE w/Active (Manual) seat belts &amp; Dual front airbags ('99-'02, '03 convertible)
* F = 9-3 Vector w/Active (Manual) seat belts &amp; Dual front airbags ('03)
* F = 9-5 SE w/Active (Manual) seat belts &amp; Dual front airbags ('99-'01)
* H = 9-3 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('04-'09)
* H = 9-5 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('00-'05)
* H = 9-5 w/Sport Package w/Active (Manual) seat belts &amp; Dual front airbags ('06)
* H = 9-5 w/Aero Package w/Active (Manual) seat belts &amp; Dual front airbags ('07)
* H = 9-5 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('08-'09)
* M = 9-3 Turbo X w/Active (Manual) seat belts &amp; Dual front airbags ('08)
* P = 9-3 Viggen w/Active (Manual) seat belts &amp; Dual front airbags ('99-'02)

* A = 9-3 2.0T 4-d/wagon w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Airbags &amp; Side Curtain Airbags ('10-'11)
* A = 9-3 2.0T convertible made in Sweden w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10-'11)
* C = 9-3 Aero 4-d/wagon w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Airbags &amp; Side Curtain Airbags ('10-'11)
* C = 9-3 Aero convertible made in Sweden w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10-'11)
* D = 9-3X wagon w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Airbags &amp; Side Curtain Airbags ('10-'11)
* E = 9-3 2.0T convertible made in Austria w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10)
* G = 9-3 Aero convertible made in Austria w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10)
* N = 9-5 Turbo4 &amp; Turbo6 w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front and Rear Side Airbags &amp; Side Curtain Airbags ('11)
* R = 9-5 Aero w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front and Rear Side Airbags &amp; Side Curtain Airbags ('10-'11)

===Positions 6, Body Style:===
* 2 = 2-dr. sedan ('85-'86 900)
* 3 = 3-dr. hatchback ('81-'98 900, '99-'02 9-3)
* 4 = 4-dr. sedan ('81-'93 900, '03-'11 9-3, '89-'95 9000, '99-'11 9-5)
* 5 = 5-dr. hatchback ('94-'98 900, '99-'02 9-3, '86-'92 9000)
* 5 = 5-dr. wagon ('99-'09 9-5 wagon/SportCombi, '06-'11 9-3 SportCombi)
* 6 = 5-dr. hatchback ('93-'98 9000)
* 7 = 2-dr. convertible ('86-'98 900, '99-'11 9-3)

===Position 7, Engine 1981-1983:===
*3 = 2.0L SOHC 8-valve fuel injected Saab H engine B201I I4 ('81-'83 900 base model, S)
*4 = 2.0L turbo SOHC 8-valve fuel injected Saab H engine B201S I4 ('81-'83 900 Turbo)

===Positions 7, Transmission 1984-2011:===
* 5 = 5-spd. manual ('84-'93 900, '94 900 convertible, '86-'98 9000)
* 6 = 3-spd. automatic ('84-'93 900, '94 900 convertible)
* 6 = 6-spd. manual ('03-'07 9-3)
* 8 = 4-spd. automatic ('94-'98 900, '99-'02 9-3, '03 9-3 convertible, '86-'98 9000, '99-'01 9-5)
* 9 = 5-spd. automatic ('02-'07 9-5)
* 1 = 6-spd. automatic ('06-'07 9-3 Aero 2.8T)

* 1 = 6-spd. automatic, FWD ('08-'09 9-3 Aero 2.8T)
* 2 = 6-spd. automatic, AWD ('08-'09 9-3 Aero 2.8T, '08 9-3 Turbo X, '09 9-3 2.0T XWD) 
* 5 = 5-spd. manual, FWD ('08-'09 9-5)
* 6 = 6-spd. manual, FWD ('08-'09 9-3)
* 7 = 6-spd. manual, AWD ('08-'09 9-3 Aero 2.8T, '08 9-3 Turbo X, '09 9-3 2.0T XWD)
* 9 = 5-spd. automatic, FWD ('08-'09 9-3 2.0T FWD, '08-'09 9-5)

* A = 6-spd. automatic, FWD ('11 9-5)
* B = 6-spd. automatic, AWD ('10-'11 9-3, '10-'11 9-5)
* C = 5-spd. automatic, FWD ('10-'11 9-3)
* M = 6-spd. manual, FWD ('10-'11 9-3, '11 9-5)
* N = 6-spd. manual, AWD ('10-'11 9-3)

===Position 8, Restraint 1981-1983:===
*S = Active (Manual) seat belts

===Position 8, Engine 1984-2011:===
*A = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B235L I4 ('04-'05 9-5 Arc)
*B = 2.3L DOHC 16-valve Saab H engine B234I I4 &lt;br&gt; (Mid '90 9000 S, '91-'92 9000 Base/S/CD, '93-'94 9000 CS/CSE, '93 9000 CD/CDE, '94-'98 900 S 5-d, '94-'97 900 S 3-d, '95-'98 900 S convertible)
*D = 2.0L DOHC 16-valve Saab H engine B202I I4 ('89-'90 900 base model, '86-'90 900 S, '87-Early '90 9000 S)
*E = 2.1L DOHC 16-valve Saab H engine B212I I4 ('91-'92 900 base model, '91-'93 900 S, '94 900 S Convertible)
*E = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B235E Light-pressure turbo I4 &lt;br&gt; ('99 9-5 2.3T, '00-'01 9-5 2.3T Base model, '00 9-5 Gary Fisher Edition wagon, '02-'05 9-5 Linear)
*G = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B235R high output I4 ('99-'02 9-3 Viggen, '00-'05 9-5 Aero, '06-'09 9-5)
*H = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B205L std. output I4 ('00-'01 9-3 base model)
*J = 2.0L SOHC 8-valve Saab H engine B201I I4 ('84-'88 900 base model, '84-'85 900 S)
*J = 2.8L turbo [[w:Intercooler|IC]] DOHC 24-valve GM High Feature Saab A28NER V6 (RPO code: LAU) ('10-'11 9-5)
*K = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B205R high output I4 ('00-'02 9-3 SE 5-d, '00-'03 9-3 SE convertible)
*L = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B202L I4 &lt;br&gt; ('85-'93 900 Turbo, '85-'91 900 Turbo SPG, '91 900 S.E. Turbo convertible, '94 900 Turbo Convertible, '86-'90 9000 Turbo, '89-'90 9000 CD Turbo)
*M = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B234L std. output I4 &lt;br&gt; ('91-'92 9000 Turbo/CD Turbo, '92 9000 CD Turbo Griffin Edition, '93-'94 9000 CS Turbo, '93-'97 9000 CSE Turbo, '93 9000 CD Turbo, '93-'94 9000 CDE Turbo, &lt;br&gt; '93-'97 9000 Aero w/auto. trans., '98 9000 CSE w/auto. trans.)
*N = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B204L std. output I4 ('98 900 S Turbo 3-d, '94-'98 900 SE Turbo 3-d, '95-'98 900 SE Turbo convertible,&lt;br&gt; '96-'98 900 SE Turbo 5-d, '97 900 SE Turbo Talladega Edition, '99 9-3 base model, SE w/auto. trans., Early '99 9-3 SE w/man. trans.)
*P = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B204R high output I4 (Mid '99 9-3 SE w/man. trans.)
*R = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B234R high output I4 ('93-'97 9000 Aero w/man. trans., '98 9000 CSE w/man. trans.)
*R = 2.8L turbo [[w:Intercooler|IC]] DOHC 24-valve GM High Feature Saab B284R high output V6 &lt;br&gt; ('08-'09 9-3 Aero XWD 4-d/wagon, '08 9-3 Turbo X XWD 4-d/wagon, '09 9-3 Aero FWD convertible)
*R = 2.0L turbo [[w:Intercooler|IC]] Gas/E85 Flex-Fuel (Biopower) DOHC 16-valve Direct injection GM Ecotec Gen II Saab A20NFT I4 (RPO code: LHU) ('11 9-5)
*S = 2.0L turbo SOHC 8-valve Saab H engine B201S I4 ('84 900 Turbo)
*S = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve GM Ecotec Gen I Saab B207L Light-pressure turbo I4 ('03-'05 9-3 Linear)
*T = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B202R high output I4 [185 hp] &lt;br&gt; ('93 900 Turbo 3-d Commemorative Edition, '94 900 Turbo Convertible Commemorative Edition)
*U = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B234E Light-pressure turbo I4 ('95-'97 9000 CS)
*U = 2.8L turbo [[w:Intercooler|IC]] DOHC 24-valve GM High Feature Saab B284L V6 ('06-'08 9-3 Aero FWD)
*V = 2.5L DOHC 24-valve GM/Opel 54° V6 Saab B258I ('94-'97 900 SE V6 5-d, '95-'97 900 SE V6 convertible)
*W = 3.0L DOHC 24-valve GM/Opel 54° V6 Saab B308I ('95-'97 9000 CSE V6, '95 9000 CDE V6)
*Y = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve GM Ecotec Gen I Saab B207R high output I4 ('03 9-3 Arc, Vector, '04-'05 9-3 Arc, Aero, '06-'11 9-3 2.0T)
*Z = 3.0L turbo [[w:Intercooler|IC]] DOHC 24-valve GM/Opel 54° V6 Saab B308E ('99 9-5 V6, '00-'01 9-5 SE, '02-'03 9-5 Arc)

===Position 9, Check Digit===
[[Vehicle Identification Numbers (VIN codes)/Check digit |Check digit]]

===Position 10, Model Year===                      
[[Vehicle Identification Numbers (VIN codes)/Model year|Model year]]

===Position 11, Production Plant:===
* 1:    Trollhattan, Sweden (Line 1: '81-'85 900, Line A: '86-'98 9000, '03-'11 9-3)
* 2:    Trollhattan, Sweden (Line 2: '81-'85 900, Line B: '86-'98 900, '88-'91 9000)
* 2:    Trollhattan, Sweden (Line A: '99-'02 9-3)
* 3:    Arlov, Sweden ('85-'90 900)
* 3:    Trollhattan, Sweden (Line B: '99-'09 9-5)
* 4:    Malmo, Sweden (9000)
* 4:    Trollhattan, Sweden ('10-'11 9-5)
* 5:    Malmo, Sweden ('90-'91 900)
* 6:    Uusikaupunki, Finland (Valmet plant - '81-'84 99, '85-'87 90) N/A in N. America
* 6:    Graz, Austria (Magna Steyr plant: '04-'10 9-3 convertible) 
* 7:    Uusikaupunki, Finland (Valmet plant - '85-'98 900, '99-'03 9-3)
* 8:    Uusikaupunki, Finland (Valmet plant - 9000)
* 9:    Trollhattan, Sweden (Prototype/Pre-production Line)

* G:    Ota, Gunma prefecture, Japan [Subaru plant] ('05-'06 Saab 9-2X w/5-spd. man. trans.)
* H:    Ota, Gunma prefecture, Japan [Subaru plant]  ('05-'06 Saab 9-2X w/4-spd. auto. trans.)

* S:    Ramos Arizpe, Coahuila, Mexico [GM plant] ('11 9-4X)
* 2:    Moraine, Ohio, US [GM plant] ('05-'09 9-7X)

'''Positions 12–17, Serial Number'''

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For Saab 9-2X, see the Subaru VIN page: [[Vehicle Identification Numbers (VIN codes)/Subaru/VIN Codes]]. 
For Saab 9-4X and 9-7X, see the GM VIN page: [[Vehicle Identification Numbers (VIN codes)/GM/VIN Codes]].

===Positions 1–3, World Manufacturer Identifier:===  
* YS3 - Saab passenger car
* YK1 - Saab passenger car made by Valmet in Finland ('81-'83)
* JF4 - Saab passenger car made by Subaru in Japan ('05-'06 9-2X)
* 3G0 - Saab MPV made by GM in Mexico ('11 9-4X)
* 5S3 - Saab MPV made by GM in US ('05-'09 9-7X)

===Positions 4, Model Line:===
* A = 900 (1st gen. - '81-'93, '94 convertible)
* B = 99 ('81-'84), 90 ('85-'87) N/A in N. America
* C = 9000 ('86-'98)
* D = 900 (2nd gen. - '94-'98 3-d/5-d, '95-'98 convertible)
* D = 9-3 (1st gen. - '99-'02, '03 convertible)
* E = 9-5 (1st gen. - '99-'09)
* F = 9-3 (2nd gen. - '03-'11 4-d, '04-'11 convertible, '06-'11 wagon)
* G = 9-5 (2nd gen. - '10-'11)

===Positions 5, Series 1981-1986:===
* G = Base model ('81-'83 900)
* S = S 3-d ('81-'83 900)
* E = S 4-d ('81-'83 900)
* M = Base model ('84-'85 900)
* H = S ('84-'85 900)
* T = Turbo ('81-'85 900)
* B = Base model ('86 900)
* C = S ('86 900)
* D = Turbo ('86 900, '86 9000)

===Positions 5, Series/Restraint 1987-2011:===
* R = Base model w/Active (Manual) seat belts ('87-'89 900)
* S = S w/Active (Manual) seat belts ('87-'89 900, '87-'89 9000)
* T = Turbo w/Active (Manual) seat belts ('87-'89 900, '87-'89 9000)
* J = Base model w/Motorized seat belts (Passive Restraint) ('89 900)
* K = S w/Motorized seat belts (Passive Restraint) ('87-'89 900)
* L = Turbo w/Motorized seat belts (Passive Restraint) ('88-'89 900)
* J = Base model w/Active (Manual) seat belts &amp; Driver-side airbag ('90 900)
* K = S w/Active (Manual) seat belts &amp; Driver-side airbag ('89-'90 9000, '90 900)
* K = Models w/normally aspirated engine w/Active (Manual) seat belts &amp; Driver-side airbag ('91-'93 9000, '91-'93 900, '94 900 convertible)
* L = Turbo or CD Turbo (9000) or CD Turbo Griffin Edition ('92 9000) w/Active (Manual) seat belts &amp; Driver-side airbag ('89-'92 9000, '90-'92 900)
* L = Models w/turbocharged engine w/Active (Manual) seat belts &amp; Driver-side airbag ('93 9000, '93 900, '94 900 convertible)
* M = Models w/normally aspirated engine w/Active (Manual) seat belts &amp; Dual front airbags ('94 900 3-d/5-d, '94 9000)
* N = Models w/turbocharged engine w/Active (Manual) seat belts &amp; Dual front airbags ('94 900 3-d/5-d, '94 9000)

* D = 900 S or 9000 CS w/Active (Manual) seat belts &amp; Dual front airbags ('95-'98)
* F = 900 SE or 9000 CSE/CDE w/Active (Manual) seat belts &amp; Dual front airbags ('95-'98)
* H = 9000 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('95-'97)

* B = 9-3 Linear w/Active (Manual) seat belts &amp; Dual front airbags ('03-'05)
* B = 9-3 2.0T w/Active (Manual) seat belts &amp; Dual front airbags ('08-'09)
* B = 9-5 Linear w/Active (Manual) seat belts &amp; Dual front airbags ('02-'05)
* B = 9-5 Griffin Edition w/Active (Manual) seat belts &amp; Dual front airbags ('09)
* D = 9-3 Base model or 9-5 Base model or 9-5 Gary Fisher Edition ('00) w/Active (Manual) seat belts &amp; Dual front airbags ('99-'01)
* D = 9-3 Arc w/Active (Manual) seat belts &amp; Dual front airbags ('03-'05)
* D = 9-3 2.0T w/Active (Manual) seat belts &amp; Dual front airbags ('06-'07)
* D = 9-5 Arc w/Active (Manual) seat belts &amp; Dual front airbags ('02-'05)
* D = 9-5 Standard model 2.3T w/Active (Manual) seat belts &amp; Dual front airbags ('06-'09)
* F = 9-3 SE w/Active (Manual) seat belts &amp; Dual front airbags ('99-'02, '03 convertible)
* F = 9-3 Vector w/Active (Manual) seat belts &amp; Dual front airbags ('03)
* F = 9-5 SE w/Active (Manual) seat belts &amp; Dual front airbags ('99-'01)
* H = 9-3 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('04-'09)
* H = 9-5 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('00-'05)
* H = 9-5 w/Sport Package w/Active (Manual) seat belts &amp; Dual front airbags ('06)
* H = 9-5 w/Aero Package w/Active (Manual) seat belts &amp; Dual front airbags ('07)
* H = 9-5 Aero w/Active (Manual) seat belts &amp; Dual front airbags ('08-'09)
* M = 9-3 Turbo X w/Active (Manual) seat belts &amp; Dual front airbags ('08)
* P = 9-3 Viggen w/Active (Manual) seat belts &amp; Dual front airbags ('99-'02)

* A = 9-3 2.0T 4-d/wagon w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Airbags &amp; Side Curtain Airbags ('10-'11)
* A = 9-3 2.0T convertible made in Sweden w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10-'11)
* C = 9-3 Aero 4-d/wagon w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Airbags &amp; Side Curtain Airbags ('10-'11)
* C = 9-3 Aero convertible made in Sweden w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10-'11)
* D = 9-3X wagon w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Airbags &amp; Side Curtain Airbags ('10-'11)
* E = 9-3 2.0T convertible made in Austria w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10)
* G = 9-3 Aero convertible made in Austria w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front Side Head/Thorax Airbags ('10)
* N = 9-5 Turbo4 &amp; Turbo6 w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front and Rear Side Airbags &amp; Side Curtain Airbags ('11)
* R = 9-5 Aero w/Active (Manual) seat belts &amp; Dual Front Airbags &amp; Front and Rear Side Airbags &amp; Side Curtain Airbags ('10-'11)

===Positions 6, Body Style:===
* 2 = 2-dr. sedan ('85-'86 900)
* 3 = 3-dr. hatchback ('81-'98 900, '99-'02 9-3)
* 4 = 4-dr. sedan ('81-'93 900, '03-'11 9-3, '89-'95 9000, '99-'11 9-5)
* 5 = 5-dr. hatchback ('94-'98 900, '99-'02 9-3, '86-'92 9000)
* 5 = 5-dr. wagon ('99-'09 9-5 wagon/SportCombi, '06-'11 9-3 SportCombi)
* 6 = 5-dr. hatchback ('93-'98 9000)
* 7 = 2-dr. convertible ('86-'98 900, '99-'11 9-3)

===Position 7, Engine 1981-1983:===
*3 = 2.0L SOHC 8-valve fuel injected Saab H engine B201I I4 ('81-'83 900 base model, S)
*4 = 2.0L turbo SOHC 8-valve fuel injected Saab H engine B201S I4 ('81-'83 900 Turbo)

===Positions 7, Transmission 1984-2011:===
* 5 = 5-spd. manual ('84-'93 900, '94 900 convertible, '86-'98 9000)
* 6 = 3-spd. automatic ('84-'93 900, '94 900 convertible)
* 6 = 6-spd. manual ('03-'07 9-3)
* 8 = 4-spd. automatic ('94-'98 900, '99-'02 9-3, '03 9-3 convertible, '86-'98 9000, '99-'01 9-5)
* 9 = 5-spd. automatic ('02-'07 9-5)
* 1 = 6-spd. automatic ('06-'07 9-3 Aero 2.8T)

* 1 = 6-spd. automatic, FWD ('08-'09 9-3 Aero 2.8T)
* 2 = 6-spd. automatic, AWD ('08-'09 9-3 Aero 2.8T, '08 9-3 Turbo X, '09 9-3 2.0T XWD) 
* 5 = 5-spd. manual, FWD ('08-'09 9-5)
* 6 = 6-spd. manual, FWD ('08-'09 9-3)
* 7 = 6-spd. manual, AWD ('08-'09 9-3 Aero 2.8T, '08 9-3 Turbo X, '09 9-3 2.0T XWD)
* 9 = 5-spd. automatic, FWD ('08-'09 9-3 2.0T FWD, '08-'09 9-5)

* A = 6-spd. automatic, FWD ('11 9-5)
* B = 6-spd. automatic, AWD ('10-'11 9-3, '10-'11 9-5)
* C = 5-spd. automatic, FWD ('10-'11 9-3)
* M = 6-spd. manual, FWD ('10-'11 9-3, '11 9-5)
* N = 6-spd. manual, AWD ('10-'11 9-3)

===Position 8, Restraint 1981-1983:===
*S = Active (Manual) seat belts

===Position 8, Engine 1984-2011:===
*A = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B235L I4 ('04-'05 9-5 Arc)
*B = 2.3L DOHC 16-valve Saab H engine B234I I4 &lt;br&gt; (Mid '90 9000 S, '91-'92 9000 Base/S/CD, '93-'94 9000 CS/CSE, '93 9000 CD/CDE, '94-'98 900 S 5-d, '94-'97 900 S 3-d, '95-'98 900 S convertible)
*D = 2.0L DOHC 16-valve Saab H engine B202I I4 ('89-'90 900 base model, '86-'90 900 S, '87-Early '90 9000 S)
*E = 2.1L DOHC 16-valve Saab H engine B212I I4 ('91-'92 900 base model, '91-'93 900 S, '94 900 S Convertible)
*E = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B235E Light-pressure turbo I4 &lt;br&gt; ('99 9-5 2.3T, '00-'01 9-5 2.3T Base model, '00 9-5 Gary Fisher Edition wagon, '02-'05 9-5 Linear)
*G = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B235R high output I4 ('99-'02 9-3 Viggen, '00-'05 9-5 Aero, '06-'09 9-5)
*H = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B205L std. output I4 ('00-'01 9-3 base model)
*J = 2.0L SOHC 8-valve Saab H engine B201I I4 ('84-'88 900 base model, '84-'85 900 S)
*J = 2.8L turbo [[w:Intercooler|IC]] DOHC 24-valve GM High Feature Saab A28NER V6 (RPO code: LAU) ('10-'11 9-5)
*K = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B205R high output I4 ('00-'02 9-3 SE 5-d, '00-'03 9-3 SE convertible)
*L = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B202L I4 &lt;br&gt; ('85-'93 900 Turbo, '85-'91 900 Turbo SPG, '91 900 S.E. Turbo convertible, '94 900 Turbo Convertible, '86-'90 9000 Turbo, '89-'90 9000 CD Turbo)
*M = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B234L std. output I4 &lt;br&gt; ('91-'92 9000 Turbo/CD Turbo, '92 9000 CD Turbo Griffin Edition, '93-'94 9000 CS Turbo, '93-'97 9000 CSE Turbo, '93 9000 CD Turbo, '93-'94 9000 CDE Turbo, &lt;br&gt; '93-'97 9000 Aero w/auto. trans., '98 9000 CSE w/auto. trans.)
*N = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B204L std. output I4 ('98 900 S Turbo 3-d, '94-'98 900 SE Turbo 3-d, '95-'98 900 SE Turbo convertible,&lt;br&gt; '96-'98 900 SE Turbo 5-d, '97 900 SE Turbo Talladega Edition, '99 9-3 base model, SE w/auto. trans., Early '99 9-3 SE w/man. trans.)
*P = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B204R high output I4 (Mid '99 9-3 SE w/man. trans.)
*R = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B234R high output I4 ('93-'97 9000 Aero w/man. trans., '98 9000 CSE w/man. trans.)
*R = 2.8L turbo [[w:Intercooler|IC]] DOHC 24-valve GM High Feature Saab B284R high output V6 &lt;br&gt; ('08-'09 9-3 Aero XWD 4-d/wagon, '08 9-3 Turbo X XWD 4-d/wagon, '09 9-3 Aero FWD convertible)
*R = 2.0L turbo [[w:Intercooler|IC]] Gas/E85 Flex-Fuel (Biopower) DOHC 16-valve Direct injection GM Ecotec Gen II Saab A20NFT I4 (RPO code: LHU) ('11 9-5)
*S = 2.0L turbo SOHC 8-valve Saab H engine B201S I4 ('84 900 Turbo)
*S = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve GM Ecotec Gen I Saab B207L Light-pressure turbo I4 ('03-'05 9-3 Linear)
*T = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B202R high output I4 [185 hp] &lt;br&gt; ('93 900 Turbo 3-d Commemorative Edition, '94 900 Turbo Convertible Commemorative Edition)
*U = 2.3L turbo [[w:Intercooler|IC]] DOHC 16-valve Saab H engine B234E Light-pressure turbo I4 ('95-'97 9000 CS)
*U = 2.8L turbo [[w:Intercooler|IC]] DOHC 24-valve GM High Feature Saab B284L V6 ('06-'08 9-3 Aero FWD)
*V = 2.5L DOHC 24-valve GM/Opel 54° V6 Saab B258I ('94-'97 900 SE V6 5-d, '95-'97 900 SE V6 convertible)
*W = 3.0L DOHC 24-valve GM/Opel 54° V6 Saab B308I ('95-'97 9000 CSE V6, '95 9000 CDE V6)
*Y = 2.0L turbo [[w:Intercooler|IC]] DOHC 16-valve GM Ecotec Gen I Saab B207R high output I4 ('03 9-3 Arc, Vector, '04-'05 9-3 Arc, Aero, '06-'11 9-3 2.0T)
*Z = 3.0L turbo [[w:Intercooler|IC]] DOHC 24-valve GM/Opel 54° V6 Saab B308E ('99 9-5 V6, '00-'01 9-5 SE, '02-'03 9-5 Arc)

===Position 9, Check Digit===
[[Vehicle Identification Numbers (VIN codes)/Check digit |Check digit]]

===Position 10, Model Year===                      
[[Vehicle Identification Numbers (VIN codes)/Model year|Model year]]

===Position 11, Production Plant:===
* 1:    Trollhattan, Sweden (Line 1: '81-'85 900, Line A: '86-'98 9000, '03-'11 9-3)
* 2:    Trollhattan, Sweden (Line 2: '81-'85 900, Line B: '86-'98 900, '88-'91 9000)
* 2:    Trollhattan, Sweden (Line A: '99-'02 9-3)
* 3:    Arlov, Sweden ('85-'90 900)
* 3:    Trollhattan, Sweden (Line B: '99-'09 9-5)
* 4:    Malmo, Sweden (9000)
* 4:    Trollhattan, Sweden ('10-'11 9-5)
* 5:    Malmo, Sweden ('90-'91 900)
* 6:    Uusikaupunki, Finland (Valmet plant - '81-'84 99, '85-'87 90) N/A in N. America
* 6:    Graz, Austria (Magna Steyr plant: '04-'10 9-3 convertible) 
* 7:    Uusikaupunki, Finland (Valmet plant - '85-'98 900, '99-'03 9-3)
* 8:    Uusikaupunki, Finland (Valmet plant - 9000)
* 9:    Trollhattan, Sweden (Prototype/Pre-production Line)

* G:    Ota, Gunma prefecture, Japan [Subaru plant] ('05-'06 Saab 9-2X w/5-spd. man. trans.)
* H:    Ota, Gunma prefecture, Japan [Subaru plant]  ('05-'06 Saab 9-2X w/4-spd. auto. trans.)

* S:    Ramos Arizpe, Coahuila, Mexico [GM plant] ('11 9-4X)
* 2:    Moraine, Ohio, US [GM plant] ('05-'09 9-7X)

'''Positions 12–17, Serial Number'''

{{BookCat}}</text>
      <sha1>snj0nr8pqiuq3xuj3k83jotshyrcvxs</sha1>
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  <page>
    <title>Taiwan history/Post-war takeover</title>
    <ns>0</ns>
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      <timestamp>2026-07-17T04:57:36Z</timestamp>
      <contributor>
        <username>一隻北極熊</username>
        <id>3609960</id>
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      <text bytes="661" sha1="395x5nzhbqa4dv5udl9dexwrfdz74n9" xml:space="preserve">After the Axis power, including Japan, lost the second world war, Japan returned the Taiwan colony back to China (Republic of China), officially ending the Japanese rule in Taiwan. At the time, most of the Taiwanese are excited for the takeover, however due to many conflicts, it dissapointed them.
[[File:19451025 中國戰區臺灣省受降典禮後 臺灣省警備總司令部全體官兵合影.jpg|thumb|Surrender ceremony in Taipei]]
==Conflicts==
Due to heavy corruption, inflation and the language/culture barrier between the Chinese mainland's army and Taiwanese citizens, these resulted the 228 Incident happened in the year 1947.
{{stub}}

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  <page>
    <title>English in Use/Agreement</title>
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      <text bytes="32566" sha1="okynjrxw5wwsklhip2uvpsxx8bwot8l" xml:space="preserve">'''Agreement''' (also called '''concord''') is the way a word (marked with an &lt;u&gt;underline&lt;/u&gt; in this article) has the form appropriate to the person, number, or gender of the noun or pronoun (written here in '''bold''').&lt;ref&gt;{{cite web |title=Definition of 'agreement' |publisher=Collins Dictionary |url=https://www.collinsdictionary.com/dictionary/english/agreement |access-date=5 April 2026 |language=en}}&lt;/ref&gt;

For example, the sentences &quot;''It exists.''&quot; and &quot;''They exist.''&quot; are grammatically correct, while &quot;''It exist.''&quot; or &quot;''They exists.''&quot; are grammatically incorrect. English grammar requires that the verb and its subject agree in person: the pronoun ''it'' and the verb ''exists'' are singular, whereas the pronoun ''they'' and the verb ''exist'' are plural.

== Subject/Complement–Verb agreement ==
=== Subject–Verb agreement ===
In general, a verb's number is matched to its subject (which normally precedes the verb).{{sfn|Swan|2016|p=205}}

A singular subject takes a singular verb.{{sfn|Hewings|2023|p=80}}{{sfn|ELT|COBUILD|2017|p=36, 42, 49, 51}}&lt;ref name=&quot;grammarbook&quot;&gt;{{cite web |last=Straus |first=Jane |url=https://www.grammarbook.com/grammar/subjectVerbAgree.asp |title=Subject–Verb Agreement |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* '''''The zoo's main attraction''' &lt;u&gt;is&lt;/u&gt; the elephants.''

A plural subject takes a plural verb.{{sfn|Hewings|2023|p=80}}{{sfn|ELT|COBUILD|2017|p=36, 42, 49, 51}}&lt;ref name=&quot;grammarbook&quot; /&gt;
* '''''Elephants''' &lt;u&gt;are&lt;/u&gt; the zoo's main attraction.''

==== Subject after the verb ====
The subject follows the verb in a range of constructions, including certain formal, literary, or emphatic structures as well as using ''here'' and ''there'' at the beginning of a sentence.&lt;ref name=&quot;grammarbook&quot; /&gt;&lt;ref name=&quot;:41&quot;&gt;{{cite web |url=https://dictionary.cambridge.org/grammar/british-grammar/here-and-there |title=Here and there |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Swan|2016|p=57-58}}{{sfn|Hewings|2023|p=80}}{{sfn|Swan|2016|p=400-402}}
* ''Look, here &lt;u&gt;comes&lt;/u&gt; '''your boyfriend'''!''
* ''Little &lt;u&gt;does&lt;/u&gt; '''he''' realize how much he means to us.'' 
* ''The new policy is beneficial to the environment, as &lt;u&gt;are&lt;/u&gt; '''the prior regulations'''.'' 

=== Complement–Verb agreement ===
When the subject is far from the verb, the verb is sometimes matched to the complement.{{sfn|Swan|2016|p=205}}
* '''''The main problem with the new policy''', along with several unexpected complications, &lt;u&gt;are/is&lt;/u&gt; '''the unclear rules and guidelines'''.''

This often occurs when the subject is a relative clause introduced by ''what'', especially if the complement is long.{{sfn|Swan|2016|p=206}}&lt;ref name=&quot;:25&quot; /&gt;{{sfn|Hewings|2023|p=80}}
* ''What we need to consider &lt;u&gt;is&lt;/u&gt; '''the potential consequence''' of this decision.''

If the complement is plural, the verb can be plural (more formal) or singular.{{sfn|Hewings|2023|p=80}}
* ''What we need to consider &lt;u&gt;are&lt;/u&gt; '''the potential consequences''' of this decision.'' (more formally)
* ''What we need to consider &lt;u&gt;is&lt;/u&gt; '''the potential consequences''' of this decision.''

=== Parentheses ===
Parentheses can always be removed, so they don't affect the agreement.&lt;ref name=&quot;grammarbook&quot; /&gt;&lt;ref&gt;{{cite web |title=How to use parenthesis: brackets, dashes and commas |url=https://www.bbc.co.uk/bitesize/articles/zhpt7yc |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref&gt;{{cite web |title=Parentheses vs. Brackets: Definitions and Examples |date=16 November 2022 |url=https://www.grammarly.com/blog/punctuation-capitalization/parentheses-and-brackets |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Einsohn|p=348}}{{sfn|Eastwood|1994|p=192}}
* '''''Our laptop computer''' (and its accessories) &lt;u&gt;comes&lt;/u&gt; with a two-year warranty.''

=== Complex nouns ===
When a noun is complex, i.e., it contains a preposition, prepositional phrase, adverb, adverbial phrase (e.g., ''with'', ''in addition to'', ''along with'', ''as well (as)'', ''together with'', ''besides'', or ''not''), or a relative clause, the verb usually agrees with the head noun or pronoun.&lt;ref name=&quot;grammarbook&quot; /&gt;&lt;ref name=&quot;:25&quot; /&gt;{{sfn|Hewings|2023|p=80}}{{sfn|Swan|2016|p=206}}&lt;ref&gt;{{cite web |url=https://owl.purdue.edu/owl/general_writing/grammar/subject_verb_agreement.html |title=Making Subjects and Verbs Agree |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* '''''The engine''' of the car &lt;u&gt;needs&lt;/u&gt; to be repaired.''
* '''''The man''' who lives next door &lt;u&gt;is&lt;/u&gt; very outgoing.''
* '''''The computer''' as well as the printer &lt;u&gt;is&lt;/u&gt; malfunctioning.''
* '''''The teachers''' in my school &lt;u&gt;are&lt;/u&gt; notoriously unprepared for classes.''

==== Quantifying expressions ====
However, with quantifying expressions (phrases expressing parts), percentages, and fractions, the verb agrees with the noun or pronoun following ''of''.{{sfn|Swan|2016|p=204}}&lt;ref name=&quot;grammarbook&quot; /&gt;&lt;ref name=&quot;:25&quot; /&gt;&lt;ref&gt;{{cite web |title=fraction |url=https://www.oxfordlearnersdictionaries.com/definition/english/fraction |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Hewings|2023|p=84}}
* ''Half of '''the team members''' &lt;u&gt;are&lt;/u&gt; working remotely today.''
* ''Less than 2% of '''water''' in the world &lt;u&gt;is&lt;/u&gt; drinkable.''
* ''Only a handful of '''students''' &lt;u&gt;were&lt;/u&gt; on time for the class.''

== Pronoun-Antecedent agreement ==
=== Number agreement ===
A singular pronoun is used for a singular noun.{{sfn|ELT|COBUILD|2017|p=106}}
* '''''The computer''' is on the desk, and &lt;u&gt;it&lt;/u&gt; is not working properly.''

A plural pronoun is used for a plural noun.{{sfn|ELT|COBUILD|2017|p=106}}
* '''''The computers''' are on the desk, and &lt;u&gt;they&lt;/u&gt; are not working properly.''

=== Gender agreement ===
Pronouns are also matched for gender. ''He'' or ''she'' and ''who'' are normally used for people.{{sfn|Swan|2016|p=513}}{{sfn|ELT|COBUILD|2017|p=106}}
* '''''My uncle''' is a doctor. &lt;u&gt;He&lt;/u&gt; works in the city hospital.''

When referring back to indefinite pronouns such as ''somebody'', ''someone'', ''anybody'', ''anyone'', ''no one'', ''nobody'', ''everybody'', and ''everyone'', the phrase ''he or she'' is used.&lt;ref name=&quot;MW-they&quot;&gt;{{cite web |title=they |url=https://www.merriam-webster.com/dictionary/they |access-date=26 April 2026}}&lt;/ref&gt;&lt;ref name=&quot;Oxford-they&quot;&gt;{{cite web |title=they |url=https://www.oxfordlearnersdictionaries.com/definition/english/they |access-date=26 April 2026}}&lt;/ref&gt;{{sfn|Swan|2016|p=264}}
* ''If '''someone''' wants to join, &lt;u&gt;he or she&lt;/u&gt; must register online.''

Nowadays, it is also generally considered correct to use the word ''they''.&lt;ref name=&quot;MW-they&quot; /&gt;&lt;ref name=&quot;Oxford-they&quot; /&gt;{{sfn|Swan|2016|p=264}}
* ''If '''someone''' wants to join, &lt;u&gt;they&lt;/u&gt; must register online.''

''It'' and ''which'' are normally used for things or animals.{{sfn|Swan|2016|p=513}}
* ''I saw '''a cat'''. &lt;u&gt;It&lt;/u&gt; was sleeping on the sofa.''

When animals are thought of as having personality, intelligence, or feelings, ''he'' or ''she'' may sometimes be used; this is common with pets.{{sfn|Swan|2016|p=513}}
* ''This is '''Bella''', a friendly golden retriever. &lt;u&gt;She&lt;/u&gt; enjoys playing fetch with her owner.''

In such cases, ''who'' is used instead of ''which''.{{sfn|Swan|2016|p=513}}
* ''Meet '''Luna''', a playful cat &lt;u&gt;who&lt;/u&gt; loves to chase toys.''

Sometimes ''she'' is used for cars and motorcycles as well as countries, though ''it'' is more common in modern usage.{{sfn|Swan|2016|p=513}}&lt;ref name=&quot;she-cambridge&quot;&gt;{{cite web |title=she |url=https://dictionary.cambridge.org/dictionary/english/she}}&lt;/ref&gt;&lt;ref name=&quot;she-longman&quot;&gt;{{cite web |title=she |url=https://www.ldoceonline.com/dictionary/she}}&lt;/ref&gt;
* ''I love '''my car'''. &lt;u&gt;It/She&lt;/u&gt; never lets me down.''
* '''''Italy''' is famous for &lt;u&gt;its/her&lt;/u&gt; cuisine.''

Sailors often refer to ships and boats as ''she'', but it's less common than it used to be.{{sfn|Swan|2016|p=513}}&lt;ref name=&quot;she-cambridge&quot; /&gt;&lt;ref name=&quot;she-longman&quot; /&gt;
* ''This is '''my ship'''. &lt;u&gt;She&lt;/u&gt;'s got a long history of cruising.''

== Determiner–Noun agreement ==
Some determiners are used only with certain kinds of nouns. For example, ''this'' and ''that'' change to ''these'' and ''those'' when the following noun is plural.{{sfn|Swan|2016}}
* &lt;u&gt;this&lt;/u&gt; '''cat''' — &lt;u&gt;these&lt;/u&gt; '''cats'''
* &lt;u&gt;that&lt;/u&gt; '''cat''' — &lt;u&gt;those&lt;/u&gt; '''cats'''

The table below shows which determiners and determiner phrases combine with which kinds of nouns:

{| class=&quot;wikitable&quot;
!Determiner
!Countable singular nouns (e.g. notebook, week)
!Uncountable nouns (e.g. luggage, music)
!Countable plural nouns (e.g. notebooks, weeks)
|-
|a / an / each{{sfn|Hewings|2023|p=82}}{{sfn|Swan|2016|p=239}}&lt;ref name=&quot;:39&quot;&gt;{{cite web |title=each |url=https://www.oxfordlearnersdictionaries.com/definition/english/each |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref&gt;{{cite web |title=each |url=https://www.ldoceonline.com/dictionary/each |access-date=5 April 2026 |language=en}}&lt;/ref&gt; / many a/an&lt;ref&gt;{{cite web |title=many |url=https://www.oxfordlearnersdictionaries.com/definition/english/many |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref&gt;{{cite web |title=many a/an |url=https://www.merriam-webster.com/dictionary/many%20a%2Fan |access-date=5 April 2026 |language=en}}&lt;/ref&gt; / one / either{{sfn|Swan|2016|p=242}}&lt;ref name=&quot;:29&quot;&gt;{{cite web |title=either |url=https://www.ldoceonline.com/dictionary/either |access-date=5 April 2026 |language=en}}&lt;/ref&gt; / neither{{sfn|Swan|2016|p=243}}&lt;ref name=&quot;:30&quot;&gt;{{cite web |title=neither |url=https://www.ldoceonline.com/dictionary/neither |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
|{{yes}}
|{{no}}
|{{no}}
|-
|many / quite a few / a good few / a good many / not a few / a number of / few / fewer&lt;ref name=&quot;:23&quot;&gt;{{cite web |url=https://www.ldoceonline.com/dictionary/less |title=less |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref name=&quot;:24&quot;&gt;{{cite web |url=https://dictionary.cambridge.org/grammar/british-grammar/less-or-fewer |title=Less or fewer? |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref name=&quot;:42&quot;&gt;{{cite web |url=https://www.britannica.com/dictionary/less |title=less |access-date=5 April 2026 |language=en}}&lt;/ref&gt; / fewest / a few / several&lt;ref&gt;{{cite web |url=https://www.oxfordlearnersdictionaries.com/grammar/online-grammar/quantifiers-both-several-most-and-all |title=both, several, most, all |access-date=5 April 2026 |language=en}}&lt;/ref&gt; / these / those / zero, two, three, etc. / umpteen
|{{no}}
|{{no}}
|{{yes}}
|-
|much / little / a little
|{{no}}
|{{yes}}
|{{no}}
|-
|this / that
|{{yes}}
|{{yes}}
|{{no}}
|-
|quantity of&lt;ref&gt;{{cite web |url=https://dictionary.cambridge.org/grammar/british-grammar/amount-of-number-of-or-quantity-of |title=Amount of, number of or quantity of? |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Carter|McCarthy|2006|p=361}} / enough / a lot of / lots of
|{{no}}
|{{yes}}
|{{yes}}
|-
|amount of&lt;ref&gt;{{cite web |url=https://www.oxfordlearnersdictionaries.com/definition/english/amount_1 |title=amount |access-date=5 April 2026 |language=en}}&lt;/ref&gt; / a good deal of&lt;ref name=&quot;:26&quot;&gt;{{cite web |url=https://www.ldoceonline.com/dictionary/a-great-good-deal |title=a great/good deal |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Carter|McCarthy|2006|p=348}}{{sfn|Swan|2016|p=257}} / a great deal of&lt;ref name=&quot;:26&quot; /&gt;{{sfn|Carter|McCarthy|2006|p=361}}{{sfn|Swan|2016|p=257}} / less&lt;ref name=&quot;:23&quot; /&gt;&lt;ref name=&quot;:24&quot; /&gt;&lt;ref&gt;{{cite web |url=https://www.oxfordlearnersdictionaries.com/definition/english/less_1 |title=less |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref name=&quot;:42&quot; /&gt; / least
|{{no}}
|{{yes}}
|style=&quot;text-align:center;&quot;|Questionable
|-
|all&lt;ref&gt;{{cite web |url=https://www.oxfordlearnersdictionaries.com/definition/english/all_1 |title=all |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Swan|2016|p=235}} / some / any
|{{yes}}
|{{yes}}
|{{yes}}
|}

=== Every ===
''Every'' is followed by a singular noun.{{sfn|Swan|2016|p=237}}{{sfn|Hewings|2023|p=82}}&lt;ref name=&quot;:43&quot;&gt;{{cite web |title=every |url=https://dictionary.cambridge.org/grammar/british-grammar/every |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* '''''Every''' &lt;u&gt;episode&lt;/u&gt; of the series &lt;u&gt;presents&lt;/u&gt; a new story.''

''Every'' is used with a plural noun when it refers to intervals.{{sfn|Swan|2016|p=238}}&lt;ref name=&quot;:43&quot; /&gt;
* ''A train leaves the station &lt;u&gt;every&lt;/u&gt; '''three hours'''.''

=== No ===
The word ''no'' is followed by a singular noun when referring to the absence of even a single item.{{sfn|Hewings|2023|p=92}}&lt;ref name=&quot;:47&quot;&gt;{{cite web |url=https://www.bbc.co.uk/worldservice/learningenglish/grammar/learnit/learnitv354.shtml |title=no = not / not any |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* ''He has '''no''' &lt;u&gt;passport&lt;/u&gt;.''
The word ''no'' is followed by a plural noun when referring to the absence of multiple items.{{sfn|Hewings|2023|p=92}}&lt;ref name=&quot;:47&quot; /&gt;
* ''He has '''no''' &lt;u&gt;socks&lt;/u&gt;.''
Often both are possible though it's more formal to use a singular noun.{{sfn|Hewings|2023|p=98}}&lt;ref name=&quot;:47&quot; /&gt;
* '''''No''' &lt;u&gt;dog&lt;/u&gt; allowed!'' (more formally)
* '''''No''' &lt;u&gt;dogs&lt;/u&gt; allowed!''

=== Kind(s)/Sort(s)/Type(s) of ===
After ''kind/sort/type of'', a singular noun is usually used.&lt;ref&gt;{{cite web |title=kinds / types / sorts / varieties (of music) |url=https://www.bbc.co.uk/worldservice/learningenglish/grammar/learnit/learnitv310.shtml |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Swan|2016|p=684–685}}{{sfn|Uk|2019|p=281,282,485,539}}&lt;ref name=&quot;:36&quot;&gt;{{cite web |title=kind |url=https://www.oxfordlearnersdictionaries.com/definition/english/kind_1 |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref&gt;{{cite web |title=kind |url=https://ahdictionary.com/word/search.html?q=kind |website=The American Heritage Dictionary of the English Language |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* ''What &lt;u&gt;sort of&lt;/u&gt; '''book''' do you usually read?''

It's also possible to use ''kind/sort/type of'' with a plural noun.{{sfn|Swan|2016|p=684–685}}&lt;ref name=&quot;:36&quot; /&gt;
* ''What &lt;u&gt;sort of&lt;/u&gt; '''books''' do you usually read?''

The phrases ''kinds/sorts/types of'' can also be used with either a singular or a plural noun.{{sfn|Uk|2019|p=281,282,485,539}}&lt;ref name=&quot;:36&quot; /&gt;
* ''We studied &lt;u&gt;many sorts of&lt;/u&gt; '''political system(s)'''.''

Certain structures with ''this'', ''that'', ''these'', and ''those'' occur, but they are considered incorrect.{{sfn|Swan|2016|p=684–685}}{{sfn|Uk|2019|p=281,282,485,539}}&lt;ref name=&quot;:36&quot; /&gt;
* ''&lt;u&gt;This kind of&lt;/u&gt; '''problems''' is difficult.'' (this/that + kind/sort/type of + plural noun)
* ''&lt;u&gt;These kind of&lt;/u&gt; '''problems''' is difficult.'' (these/those + kind/sort/type of + plural noun)
* ''&lt;u&gt;These kinds of&lt;/u&gt; '''problem''' are difficult.'' (these/those + kinds/sorts/types of + singular noun)

In formal style, a plural verb followed by ''of this/that kind/sort/type'' is also possible.{{sfn|Swan|2016|p=684–685}}{{sfn|Uk|2019|p=281,282,485,539}}
* '''''Problems''' &lt;u&gt;of this kind&lt;/u&gt; are difficult.''

=== Dozen, hundred, thousand, million, and billion ===
The words ''dozen'', ''hundred'', ''thousand'', ''million'', and ''billion'' are used without the -s ending when they follow a number.{{sfn|Swan|2016|p=505}}&lt;ref&gt;{{cite web |last1=hundred |title=Definition of 'hundred'; Collins English Dictionary |url=https://www.collinsdictionary.com/dictionary/english/hundred |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref&gt;{{cite web |title=hundred |url=https://www.oxfordlearnersdictionaries.com/definition/english/hundred |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|ELT|COBUILD|2017|p=302}}{{sfn|Uk|2019|p=727}}
* ''The population of South Korea grew to almost &lt;u&gt;52&lt;/u&gt; '''million''' and then began to decline.''
* ''I have &lt;u&gt;two&lt;/u&gt; '''hundred''' dollars on me.''

=== Fractions ===
Fractions between 1 and 2 are used with plural nouns.{{sfn|Swan|2016|p=207}}
* ''The meeting lasted around &lt;u&gt;1.25&lt;/u&gt; '''hours'''.''

== Notional agreement ==
'''Notional agreement''' (also called '''notional concord''' or '''synesis''') is a type of agreement that stems from the meaning. It is more commonly used in British English than in American English.&lt;ref&gt;{{cite web |title=On Notional Agreement, the Majority Speak |url=https://www.merriam-webster.com/grammar/notional-agreement-subject-verb-principle-proximity}}&lt;/ref&gt;

=== And ===
Expressions joined by ''and'' generally take a plural verb.{{sfn|ELT|COBUILD|2017|p=799}}&lt;ref name=&quot;grammarbook&quot; /&gt;{{sfn|Swan|2016|p=206}}{{sfn|Hewings|2023|p=82}}
* '''''A cat and a dog''' &lt;u&gt;are&lt;/u&gt; playing in the garden.''

If the nouns, however, suggest one idea or refer to the same thing or person, the verb is singular.{{sfn|ELT|COBUILD|2017|p=799}}&lt;ref name=&quot;grammarbook&quot; /&gt;{{sfn|Swan|2016|p=206}}{{sfn|Hewings|2023|p=82}}
* '''''The new bed and breakfast''' &lt;u&gt;opens&lt;/u&gt; this week.''
* '''''The singer and songwriter''' &lt;u&gt;is&lt;/u&gt; performing tonight.''

When expressions joined by ''and'' follow ''each'' or ''every'', the verb is singular.{{sfn|ELT|COBUILD|2017|p=799}}{{sfn|Hewings|2023|p=82}}
* '''''Each teacher and student''' &lt;u&gt;has&lt;/u&gt; completed the survey.''

The verb is also singular when uncountable nouns joined by ''and'' follow ''all''.{{sfn|ELT|COBUILD|2017|p=799}}
* '''''All the information and advice''' &lt;u&gt;is&lt;/u&gt; available on our website.''

=== Amounts and quantities ===
Expressions of distance, sums of money, periods of time, etc., regarded as one unit, take singular determiners, verbs, and pronouns.{{sfn|Swan|2016|p=204}}&lt;ref name=&quot;grammarbook&quot; /&gt;{{sfn|Murphy|2019|p=158}}&lt;ref name=&quot;:37&quot;&gt;{{cite web |url=https://www.bbc.co.uk/learningenglish/course/towards-advanced/unit-21/tab/grammar |title=Subject–Verb Agreement 2 |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Hewings|2023|p=84}}
* '''''Five minutes''' &lt;u&gt;is&lt;/u&gt; all I need.''
* '''''Fifty dollars''' &lt;u&gt;is&lt;/u&gt; a fair price.''
* '''''Two liters''' of water &lt;u&gt;is&lt;/u&gt; required for the experiment.''
However, when these expressions are deemed separate individual units, they are plural.&lt;ref name=&quot;grammarbook&quot; /&gt;&lt;ref name=&quot;:37&quot; /&gt;
* '''''A few dollars''' &lt;u&gt;were&lt;/u&gt; missing from the victim's wallet.''

=== Calculations ===
When speaking calculations, both singular and plural verbs are possible depending on the phrasing.&lt;ref name=&quot;:37&quot; /&gt;{{sfn|Swan|2016|p=507}}
* '''''Three and three''' &lt;u&gt;is/are&lt;/u&gt; six.''
* '''''Three plus three''' &lt;u&gt;is&lt;/u&gt; six.''

=== Groups ===
==== American English ====
In American English, collective nouns (i.e. nouns expressing groups singular in form such as ''committee'', ''team'', ''Sony'' and ''The United Nations''){{sfn|Swan|2016|p=205}}{{sfn|Carter|McCarthy|2006|p=351}}{{sfn|Hewings|2023|p=80}} generally take singular verbs{{sfn|Murphy|2019|p=301}}&lt;ref&gt;{{cite web |title=family |url=https://www.britannica.com/dictionary/family |access-date=5 April 2026}}&lt;/ref&gt; and either singular or plural pronouns.{{sfn|Swan|2016|p=203}}
* '''''The committee''' &lt;u&gt;was&lt;/u&gt; arguing among &lt;u&gt;itself/themselves&lt;/u&gt; during the session.''
* '''''My family''' &lt;u&gt;is&lt;/u&gt; all coming over for Thanksgiving.''
* '''''The United Nations''' &lt;u&gt;is&lt;/u&gt; holding a conference next month. &lt;u&gt;It/They&lt;/u&gt; &lt;u&gt;has/have&lt;/u&gt; invited delegates from all over the world to attend.''

==== British English ====
In British English, collective nouns may take either singular or plural verb and pronouns forms.{{sfn|Swan|2016|p=203}}{{sfn|Murphy|2019|p=301}}

Singular forms are used when the emphasis is on the group as a whole.{{sfn|Swan|2016|p=203}}{{sfn|Hewings|2023|p=80}}
* '''''The committee''' &lt;u&gt;has&lt;/u&gt; postponed &lt;u&gt;its&lt;/u&gt; meeting until next week.''

In these cases ''which'' is also used as the relative pronoun.{{sfn|Swan|2016|p=203}}
* '''''The band''', &lt;u&gt;which&lt;/u&gt; was formed in the 1980s, gained international fame.''

Plural forms are used when the emphasis is on the individual members.{{sfn|Swan|2016|p=203}}{{sfn|Hewings|2023|p=80}}
* '''''The committee''' &lt;u&gt;were&lt;/u&gt; arguing among &lt;u&gt;themselves&lt;/u&gt; during the session.''

In those cases ''who'' is often used as the relative pronoun.{{sfn|Swan|2016|p=203}}
* '''''The band''', &lt;u&gt;who&lt;/u&gt; have been performing together for decades, released a new album.''

=== Indefinite pronouns ===
As subjects, ''another'', ''anybody'', ''anyone'', ''anything'', ''each'', ''either'', ''every'', ''everybody'', ''everyone'', ''everything'', ''less'', ''little'', ''much'', ''neither'', ''no one'', ''nobody'', ''nothing'', ''one'', ''somebody'', ''someone'', and ''something'' take singular verbs.{{sfn|Murphy|2019|p=170, 180}}
* '''''Everybody''' &lt;u&gt;is&lt;/u&gt; a genius.''

The pronouns ''both'', ''few'', ''fewer'', ''many'', ''others'', and ''several'' take plural verbs.
* '''''Few''' &lt;u&gt;know&lt;/u&gt; the full story.''

The pronouns ''all'', ''any'', ''enough'', ''more'', ''most'', ''none'', ''some'', and ''such'' take a singular verb when they refer to an uncountable noun or a plural verb when they refer to a plural noun.&lt;ref&gt;{{cite web |url=https://dictionary.cambridge.org/grammar/british-grammar/no-none-and-none-of |title=No, none and none of |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref name=&quot;grammarbook&quot; /&gt;
* ''I found '''the equipment''' in the garage, but it turned out that '''none''' &lt;u&gt;is&lt;/u&gt; useful.''
* ''I found '''the tools''' in the garage, but it turned out that '''none''' &lt;u&gt;are&lt;/u&gt; useful.''

=== &quot;the number of&quot; vs &quot;a number of&quot; and &quot;the total&quot; vs &quot;a total of&quot; ===
The literal phrase ''the number of'' takes a singular verb, whereas the fixed phrase ''a number of'' is treated as plural.&lt;ref&gt;{{cite web |url=https://www.ldoceonline.com/dictionary/number |title=number |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref&gt;{{cite web |last=Straus |first=Jane |url=https://www.grammarbook.com/blog/numbers/the-number-vs-a-number |title=The Number vs. A Number |date=9 December 2010 |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref&gt;{{cite web |url=https://www.noslangues-ourlanguages.gc.ca/en/writing-tips-plus/verb-agreement-with-number |title=Verb agreement with &quot;number&quot; |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* '''''The number of''' cars on the roads &lt;u&gt;has&lt;/u&gt; decreased.''
* '''''A number of''' people &lt;u&gt;have&lt;/u&gt; complained about the noise.''

The same is true for ''the total'' and ''a total of''.&lt;ref&gt;{{Citation |editor-last=Iverson |editor-first=Cheryl |title=AMA Manual of Style |edition=10th |publisher=[[Oxford University Press]] |location=Oxford, Oxfordshire |year=2007 |isbn=978-0-19-517633-9 |url=https://archive.org/details/amamanualofstyle0000unse |section=7.8.11 Number |url-access=registration }}&lt;/ref&gt;
* '''''The total''' &lt;u&gt;was&lt;/u&gt; growing.''
* '''''A total of''' 28 volunteers &lt;u&gt;have&lt;/u&gt; submitted applications.''

== Special cases ==
=== Titles and names ===
Titles and names plural in form and referring to a single thing  (e.g. countries, movies, restaurants, and quotations) take singular verbs.{{sfn|Hewings|2023|p=80}}{{sfn|Eastwood|1994|p=192}}{{sfn|Swan|2016|p=205}}
* '''''The Netherlands''' &lt;u&gt;is&lt;/u&gt; famous for &lt;u&gt;its&lt;/u&gt; fields of tulips.''
* '' '''''The Avengers''''' &lt;u&gt;has&lt;/u&gt; been a huge box-office success.''
* '''''The New York Times''' &lt;u&gt;is&lt;/u&gt; an American newspaper.''
* '''''&quot;Sales figures&quot;''' &lt;u&gt;is&lt;/u&gt; the phrase used in the report title.''

==== the United States ====
Usually ''the United States'' is used with a singular verb just like other countries. However, it's possible to use it with a plural noun though it's not common.&lt;ref&gt;{{cite web |title=fraction |url=https://www.oxfordlearnersdictionaries.com/definition/english/the-united-states-of-america |access-date=10 July 2026 |language=en}}&lt;/ref&gt;
* '''''The United States''' &lt;u&gt;is&lt;/u&gt; (or rarely: &lt;u&gt;are&lt;/u&gt;) the country with the largest number of English native speakers.''

=== What/Who questions ===
In questions, ''what'' and ''who'' are followed by a singular verb when they are used as subject.{{sfn|Swan|2016|p=207}}{{sfn|Hewings|2023|p=52}}
* '''''Who''' &lt;u&gt;lives&lt;/u&gt; in that house?''

However, when they are used as complements (this happens often after linking verbs), they are followed by either a plural or singular verb.{{sfn|Swan|2016|p=207}}{{sfn|Hewings|2023|p=52}}
* '''''Who''' &lt;u&gt;is&lt;/u&gt; the person living in that house?''
* '''''Who''' &lt;u&gt;are&lt;/u&gt; the people living in that house?''

Both versions are also possible in echo questions if the subject is plural or consists of at least two nouns with &quot;and&quot;.{{sfn|Hewings|2023|p=52}}
* '''''John and Mary''' are coming tomorrow. – &lt;u&gt;Who are&lt;/u&gt; coming tomorrow?''
* '''''John and Mary''' are coming tomorrow. – &lt;u&gt;Who's&lt;/u&gt; coming tomorrow?''

=== A pair of ===
After ''a pair of,'' both singular and plural verbs can be used.&lt;ref&gt;{{cite web |title=pair |url=https://www.oxfordlearnersdictionaries.com/definition/english/pair_1 |access-date=5 April 2026}}&lt;/ref&gt;
* '''''A pair of glasses''' &lt;u&gt;is/are&lt;/u&gt; on the bench.''

=== Clauses ===
Singular verbs are used with clauses used as subjects.{{sfn|Hewings|2023|p=80}}{{sfn|Eastwood|1994|p=193}}
* '''''What she said''' &lt;u&gt;was&lt;/u&gt; suspicious.''
* '''''For all of us to get enough sleep''' &lt;u&gt;is&lt;/u&gt; crucial.''
* '''''To err''' &lt;u&gt;is&lt;/u&gt; human.''
* '''''Where they went''' &lt;u&gt;remains&lt;/u&gt; unknown.''

==== Everyone, everybody, and each ====
When pronouns refer back to ''everyone'', ''everybody'', and ''each'' they may be singular (more formal) or plural (less formal).{{sfn|Swan|2016|p=238}}&lt;ref name=&quot;:39&quot; /&gt;
* '''''Everyone''' is responsible for &lt;u&gt;his or her&lt;/u&gt; actions.''
* '''''Everyone''' is responsible for &lt;u&gt;their&lt;/u&gt; actions.''

==== Each ====
When ''each'' refers to the subject and is in mid-position, plural nouns, pronouns, and verbs are used.{{sfn|Swan|2016|p=240}}&lt;ref name=&quot;:39&quot; /&gt;
* ''&lt;u&gt;The students&lt;/u&gt; '''each''' &lt;u&gt;have&lt;/u&gt; &lt;u&gt;their&lt;/u&gt; own locker.''

=== More than one ===
The expression ''more than one'' uses a singular noun and verb.{{sfn|Swan|2016|p=204}}
* '''''More than one''' &lt;u&gt;factor&lt;/u&gt; &lt;u&gt;contributes&lt;/u&gt; to climate change.''

=== Here's, there's, and where's ===
In informal style, ''here's, there's, and where's'' are often used with plural nouns (instead of ''here are, there are, where are''); sometimes this is considered incorrect.{{sfn|Swan|2016|p=207}}&lt;ref name=&quot;grammarbook&quot; /&gt;{{sfn|Hewings|2023|p=82}}
* ''&lt;u&gt;Where are&lt;/u&gt; (or questionable: &lt;u&gt;Where's&lt;/u&gt;) '''my keys'''?''

=== Any of, none of, either of, and neither of ===
After ''any of''{{sfn|Swan|2016|p=246}}{{sfn|Hewings|2023|p=82}}, ''none of''{{sfn|Swan|2016|p=249}}{{sfn|Murphy|2019|p=172}}{{sfn|Hewings|2023|p=82}}, ''either of''{{sfn|Swan|2016|p=242}}&lt;ref&gt;{{cite web |url=https://www.oxfordlearnersdictionaries.com/definition/english/either_1 |title=either |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref name=&quot;:29&quot; /&gt;{{sfn|Hewings|2023|p=82}}&lt;ref&gt;{{cite web |url=https://www.britannica.com/dictionary/either |title=either |access-date=5 April 2026 |language=en}}&lt;/ref&gt;, and ''neither of''{{sfn|Swan|2016|p=243}}{{sfn|Murphy|2019|p=178}}&lt;ref&gt;{{cite web |url=https://www.oxfordlearnersdictionaries.com/definition/english/neither_1 |title=neither |access-date=5 April 2026 |language=en}}&lt;/ref&gt;&lt;ref name=&quot;:30&quot; /&gt;{{sfn|Hewings|2023|p=82}}&lt;ref&gt;{{cite web |url=https://www.britannica.com/dictionary/neither |title=neither |access-date=5 April 2026 |language=en}}&lt;/ref&gt;, English uses a plural personal pronoun or a plural determiner and noun and optionally a singular verb in formal style or a plural verb in informal style.
* '''''Any of''' &lt;u&gt;the students&lt;/u&gt; &lt;u&gt;is/are&lt;/u&gt; allowed to retake the test.''
* '''''None of''' &lt;u&gt;the students&lt;/u&gt; &lt;u&gt;is/are&lt;/u&gt; ready for the exam.''
* '''''Either of''' &lt;u&gt;them&lt;/u&gt; &lt;u&gt;is/are&lt;/u&gt; welcome to join us.''
* '''''Neither of''' &lt;u&gt;them&lt;/u&gt; &lt;u&gt;is/are&lt;/u&gt; ready yet.''

=== Each of ===
''Each of'' is normally followed by a plural personal pronoun or a plural determiner and noun and a singular verb{{sfn|Swan|2016|p=239-240}}. However in informal style a plural verb is sometimes used.{{sfn|Hewings|2023|p=82}}&lt;ref&gt;{{cite web |url=https://dictionary.cambridge.org/grammar/british-grammar/each |title=Each |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* '''''Each of''' &lt;u&gt;the books&lt;/u&gt; &lt;u&gt;has&lt;/u&gt; (or informally: &lt;u&gt;have&lt;/u&gt;) a different cover design.''

=== Expressions with &quot;in&quot; and &quot;out of&quot; ===
After number followed by ''in'' or ''out of'', English uses a number with a plural noun and either a singular or plural verb.{{sfn|Swan|2016|p=503}}
* ''Almost '''nine in ten students''' &lt;u&gt;hate(s)&lt;/u&gt; math.''
* ''Over '''six out of ten young men''' &lt;u&gt;feel(s)&lt;/u&gt; lonely regularly.''

=== Every one of ===
''Every one of'' is followed by a plural personal pronoun or a plural determiner and noun and a singular verb.{{sfn|Swan|2016|p=237}}
* '''''Every one of''' &lt;u&gt;her arguments&lt;/u&gt; &lt;u&gt;is&lt;/u&gt; wrong.''

=== One of ===
The expression ''one of'' is usually followed by a plural noun.{{sfn|Swan|2016|p=204}}
* ''&lt;u&gt;One of&lt;/u&gt; '''the apples''' is rotten.''

Sometimes ''one of'' is used with a singular noun referring to a group.{{sfn|Swan|2016|p=661}}
* ''Why don't you invite &lt;u&gt;one of&lt;/u&gt; '''the team''' for lunch?''

The verb after the noun is singular.{{sfn|Swan|2016|p=204}}
* '''''One of my co-workers''' &lt;u&gt;is&lt;/u&gt; from Seoul.''

After ''one of'' in the relative clauses, both plural and singular verbs are used; the plural form is generally considered correct.{{sfn|Swan|2016|p=205}}
* ''He's '''one of the professors''' who &lt;u&gt;teach&lt;/u&gt; quantum physics.''

=== The ===
The phrase consisting of ''the'' and an adjective is plural when referring to well-known groups of people in a particular physical or social condition.{{sfn|Swan|2016|p=279}}{{sfn|ELT|COBUILD|2017|p=65}}{{sfn|Murphy|2019|p=152}}&lt;ref name=&quot;:40&quot;&gt;{{cite web |title=Subject-Verb Agreement 1 |url=https://www.bbc.co.uk/learningenglish/course/towards-advanced/unit-20/tab/grammar |access-date=5 April 2026 |language=en}}&lt;/ref&gt;
* ''Do '''the disabled''' &lt;u&gt;have&lt;/u&gt; special facilities?''

In certain fixed, formal expressions, the phrase consisting of ''the'' and an adjective may be singular.{{sfn|Swan|2016|p=279}}
* '''''The deceased''' &lt;u&gt;has&lt;/u&gt; not yet been formally identified.''

The phrase consisting of ''the'' and an adjective is singular when it refers to general abstract ideas.{{sfn|Swan|2016|p=280}}
* '''''The unknown''' &lt;u&gt;is&lt;/u&gt; often scarier than the known.''

The phrase consisting of ''the'' and an adjective is plural when referring to people from a specific country.{{sfn|Swan|2016|p=279}}{{sfn|Murphy|2019|p=152}}&lt;ref name=&quot;:40&quot; /&gt;
* '''''The Japanese''' &lt;u&gt;value&lt;/u&gt; punctuality highly.''

=== (Either) or, (neither) nor, not only (but) also ===
The verb should agree with the expression in these structures closest to it ('''the rule of proximity'''). Other forms of agreement occur, but they are not considered correct.{{sfn|Swan|2016|p=206}}{{sfn|ELT|COBUILD|2017|p=799}}&lt;ref name=&quot;grammarbook&quot; /&gt;&lt;ref name=&quot;:25&quot;&gt;{{cite web |url=https://www.bbc.co.uk/learningenglish/course/towards-advanced/unit-22/tab/grammar |title=Subject–Verb Agreement 3 |access-date=5 April 2026 |language=en}}&lt;/ref&gt;{{sfn|Hewings|2023|p=82}}
* ''Either my teacher or '''I''' &lt;u&gt;am&lt;/u&gt; wrong.''
* ''&lt;u&gt;Are&lt;/u&gt; neither '''the employees''' nor the manager aware of the change?''

== References ==
{{reflist}}

== Bibliography ==
=== Books ===
* {{cite book |last=Swan |first=Michael |title=Practical English Usage |edition=4th |year=2016 |publisher=Oxford University Press |location=Oxford |isbn=978-0-19-420243-5}}
* {{cite book |last=Hewings |first=Martin |title=Advanced Grammar in Use: Book with Answers and eBook and Online Test |edition=4th |year=2023 |publisher=Cambridge University Press &amp; Assessment |location=Oxford |isbn=9781108920216}}
* {{cite book |last=Murphy |first=Raymond |title=English Grammar in Use |edition=5th |year=2019 |publisher=Cambridge University Press}}
* {{cite book |last=Eastwood |first=John |title=Oxford Guide to English Grammar |publisher=Oxford University Press |year=1994}}
* {{cite book |last1=Carter |first1=Ronald |last2=McCarthy |first2=Michael |title=Cambridge Grammar of English: A Comprehensive Guide |year=2006}}
* {{cite book |last1=ELT |first1=Collins |last2=COBUILD |first2=Collins |title=Collins COBUILD Grammar - COBUILD English Grammar |publisher=Collins Cobuild |date=2017-03-23 |isbn=978-0-00-813581-2}}
* {{cite book |last=Uk |first=Collins |title=Collins COBUILD Grammar - English Usage: B1-C2 |date=2019 |isbn=978-0-00-835640-8 |publisher=HarperCollins Publishers Limited |edition=Fourth}}
* {{cite book |last=Einsohn |first=Amy  |title=The Copyeditor's Handbook: A Guide for Book Publishing and Corporate Communications |edition=Fourth}}

{{BookCat}}</text>
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    <title>Taiwan history/The Political Movements of Chiang Wei-shui and Lin Hsien-tang</title>
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      <text bytes="925" sha1="5fywbs8qja9pja8drslu7dggivrja7c" xml:space="preserve">Chiang Wei-shui and Lin Hsien-tang were the foremost pioneers of Taiwan’s non-violent political and cultural movements during the Japanese colonial era. Together, they founded the Taiwanese Cultural Association in 1921 to awaken Taiwanese national consciousness, subsequently championing separate political, economic, and democratic reforms.
==Taiwanese Parliament Petition Movement==
[[File:1924 臺灣議會請願團在東京 Taiwanese Petition Group for Democratically-Elected Assembly in Tokyo 1.jpg|thumb|The Petition Movement in Tokyo]]
Lin led a decade-long, organized effort beginning in 1921 to petition the Imperial Diet in Tokyo for the establishment of a popularly elected, self-governing assembly in Taiwan.

==Taiwanese Cultural Association==
Co-founded with Lin in 1921, Chiang used it to combat what he termed &quot;cultural malnutrition&quot; through public lectures, night schools, and film screenings.

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This wikibook, '''Five Rules for Meaningful Living''', is based on the teachings of three scholars on overcoming inner suffering and living a meaningful life.

Viktor Frankl was a Holocaust survivor. Carl Jung was a famous psychologist. And Alan Watts is a Zenz philosopher. Despite these three men coming from very different backgrounds, their insights converged on the understanding that many of our greatest struggles in life arise not only from life's external hardships, but also from the psychological patterns through which we respond to them. All three argued that we can suffer and fare poorly due to the invisible psychological traps we refuse to confront, and that sustainable growth and meaning depends on confronting the fears, assumptions, and habits that shape our experience.

Much of their shared wisdom can be refined to 5 fundamental rules which are;

# Release micromanagement of outcomes
# Embrace a more flexible identity
# Face avoided realities
# Have responsibility for self instead of waiting for motivation or perfect conditions
# Step into discomfort for growth

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances, making it a sustainable path to psychological freedom, flexibility, and personal growth.

'''How to use this book?'''
To help readers both understand and later master these rules, this book is divided into 2 sections which is to be read in order.

The first section, '''Core Principles''', is about being aware of your own patterns and seeing if this book is suited to you. It will be a brief introduction to help you understand what the teachings are.

The second section, '''Application''' is dedicated to practical application where actionable exercises are provided, as well as strategies for overcoming common barriers like fear and perfectionism in modern routines.

==1. Introduction==
Viktor Frankl was a Holocaust survivor. Carl Jung was a famous psychologist. And Alan Watts is a Zenz philosopher. Despite these three men coming from very different backgrounds, their insights converged on the understanding that many of our greatest struggles in life arise not only from life's external hardships, but also from the psychological patterns through which we respond to them. All three argued that we can suffer and fare poorly due to the invisible psychological traps we refuse to confront, and that sustainable growth and meaning depends on confronting the fears, assumptions, and habits that shape our experience.

==2. Core Principles==
The five rules, based on the insights of Frankl, Jung, and Watts, do not promise constant happiness but instead provide practical path for cultivating courage, purpose, responsibility, acceptance, adaptability, and psychological resilience. They are;

'''1. Seek meaning over happiness'''

'''2. Taking action on situations that you avoid or put off and do it even if feeling less than perfect to reduce long-term anxiety'''

'''3. Have responsibility for self instead of waiting for motivation or perfect conditions.'''

'''4.  Develop strong internal locus of control where you accept limits of control  - and let go of micromanaging outcomes by setting intentions then accepting the results.'''

'''5. Cultivate a fluid identity and regularly questioning rigid self-views on what you can and can't do.'''

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances,  providing a practical framework for psychological freedom, flexibility, and personal growth.

==3. Application==

==4. Further reading==
This chapter provides references for readers who wish to further study related ideas and the philosophical and psychological works that influenced the ''Five Rules for Meaningful Living''.

It include selected works that introduces key concepts from Viktor Frankl, Carl Jung, and Alan Watts as well as related ideas from other thinkers.

=== Viktor Frankl ===
* [[wikipedia:Man's Search for Meaning|''Man's Search for Meaning'']]

=== Carl Jung ===
* [[wikipedia:Man and His Symbols|''Man and His Symbols'']]

=== Alan Watts ===
* [https://books.google.com.au/books?id=tKy_sIIr4RcC ''The Book: On the Taboo Against Knowing Who You Are'']
=== Marcus Aurelius ===
* [[wikipedia:Meditations|''Meditations'']]

=== M. Scott Peck ===
* [[wikipedia:M. Scott Peck#The Road Less Traveled|''The Road Less Traveled'']]

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This wikibook, '''Five Rules for Meaningful Living''', is based on the teachings of three scholars on overcoming inner suffering and living a meaningful life.

Viktor Frankl was a Holocaust survivor. Carl Jung was a famous psychologist. And Alan Watts is a Zenz philosopher. Despite these three men coming from very different backgrounds, their insights converged on the understanding that many of our greatest struggles in life arise not only from life's external hardships, but also from the psychological patterns through which we respond to them. All three argued that we can suffer and fare poorly due to the invisible psychological traps we refuse to confront, and that sustainable growth and meaning depends on confronting the fears, assumptions, and habits that shape our experience.

Much of their shared wisdom can be refined to 5 fundamental rules which are;

# Release micromanagement of outcomes
# Embrace a more flexible identity
# Face avoided realities
# Have responsibility for self instead of waiting for motivation or perfect conditions
# Step into discomfort for growth

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances, making it a sustainable path to psychological freedom, flexibility, and personal growth.

'''How to use this book?'''
To help readers both understand and later master these rules, this book is divided into 2 sections which is to be read in order.

The first section, '''Core Principles''', is about being aware of your own patterns and seeing if this book is suited to you. It will be a brief introduction to help you understand what the teachings are.

The second section, '''Application''' is dedicated to practical application where actionable exercises are provided, as well as strategies for overcoming common barriers like fear and perfectionism in modern routines.

==2. Core Principles==
The five rules, based on the insights of Frankl, Jung, and Watts, do not promise constant happiness but instead provide practical path for cultivating courage, purpose, responsibility, acceptance, adaptability, and psychological resilience. They are;

'''1. Seek meaning over happiness'''

'''2. Taking action on situations that you avoid or put off and do it even if feeling less than perfect to reduce long-term anxiety'''

'''3. Have responsibility for self instead of waiting for motivation or perfect conditions.'''

'''4.  Develop strong internal locus of control where you accept limits of control  - and let go of micromanaging outcomes by setting intentions then accepting the results.'''

'''5. Cultivate a fluid identity and regularly questioning rigid self-views on what you can and can't do.'''

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances,  providing a practical framework for psychological freedom, flexibility, and personal growth.

==3. Application==

==4. Further reading==
This chapter provides references for readers who wish to further study related ideas and the philosophical and psychological works that influenced the ''Five Rules for Meaningful Living''.

It include selected works that introduces key concepts from Viktor Frankl, Carl Jung, and Alan Watts as well as related ideas from other thinkers.

=== Viktor Frankl ===
* [[wikipedia:Man's Search for Meaning|''Man's Search for Meaning'']]

=== Carl Jung ===
* [[wikipedia:Man and His Symbols|''Man and His Symbols'']]

=== Alan Watts ===
* [https://books.google.com.au/books?id=tKy_sIIr4RcC ''The Book: On the Taboo Against Knowing Who You Are'']
=== Marcus Aurelius ===
* [[wikipedia:Meditations|''Meditations'']]

=== M. Scott Peck ===
* [[wikipedia:M. Scott Peck#The Road Less Traveled|''The Road Less Traveled'']]

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This wikibook, '''Five Rules for Meaningful Living''', is based on the teachings of three scholars on overcoming inner suffering and living a meaningful life.

Viktor Frankl was a Holocaust survivor. Carl Jung was a famous psychologist. And Alan Watts is a Zenz philosopher. Despite these three men coming from very different backgrounds, their insights converged on the understanding that many of our greatest struggles in life arise not only from life's external hardships, but also from the psychological patterns through which we respond to them. All three argued that we can suffer and fare poorly due to the invisible psychological traps we refuse to confront, and that sustainable growth and meaning depends on confronting the fears, assumptions, and habits that shape our experience.

Much of their shared wisdom can be refined to 5 fundamental rules which are;

# Release micromanagement of outcomes
# Embrace a more flexible identity
# Face avoided realities
# Have responsibility for self instead of waiting for motivation or perfect conditions
# Step into discomfort for growth

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances, making it a sustainable path to psychological freedom, flexibility, and personal growth.

'''How to use this book?'''
To help readers both understand and later master these rules, this book is divided into 2 sections which is to be read in order.

The first section, '''Core Principles''', is about being aware of your own patterns and seeing if this book is suited to you. It will be a brief introduction to help you understand what the teachings are.

The second section, '''Application''' is dedicated to practical application where actionable exercises are provided, as well as strategies for overcoming common barriers like fear and perfectionism in modern routines.

==Core Principles==
The five rules, based on the insights of Frankl, Jung, and Watts, do not promise constant happiness but instead provide practical path for cultivating courage, purpose, responsibility, acceptance, adaptability, and psychological resilience. They are;

'''1. Seek meaning over happiness'''

'''2. Taking action on situations that you avoid or put off and do it even if feeling less than perfect to reduce long-term anxiety'''

'''3. Have responsibility for self instead of waiting for motivation or perfect conditions.'''

'''4.  Develop strong internal locus of control where you accept limits of control  - and let go of micromanaging outcomes by setting intentions then accepting the results.'''

'''5. Cultivate a fluid identity and regularly questioning rigid self-views on what you can and can't do.'''

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances,  providing a practical framework for psychological freedom, flexibility, and personal growth.

==3. Application==

==4. Further reading==
This chapter provides references for readers who wish to further study related ideas and the philosophical and psychological works that influenced the ''Five Rules for Meaningful Living''.

It include selected works that introduces key concepts from Viktor Frankl, Carl Jung, and Alan Watts as well as related ideas from other thinkers.

=== Viktor Frankl ===
* [[wikipedia:Man's Search for Meaning|''Man's Search for Meaning'']]

=== Carl Jung ===
* [[wikipedia:Man and His Symbols|''Man and His Symbols'']]

=== Alan Watts ===
* [https://books.google.com.au/books?id=tKy_sIIr4RcC ''The Book: On the Taboo Against Knowing Who You Are'']
=== Marcus Aurelius ===
* [[wikipedia:Meditations|''Meditations'']]

=== M. Scott Peck ===
* [[wikipedia:M. Scott Peck#The Road Less Traveled|''The Road Less Traveled'']]

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This wikibook, '''Five Rules for Meaningful Living''', is based on the teachings of three scholars on overcoming inner suffering and living a meaningful life.

Viktor Frankl was a Holocaust survivor. Carl Jung was a famous psychologist. And Alan Watts is a Zenz philosopher. Despite these three men coming from very different backgrounds, their insights converged on the understanding that many of our greatest struggles in life arise not only from life's external hardships, but also from the psychological patterns through which we respond to them. All three argued that we can suffer and fare poorly due to the invisible psychological traps we refuse to confront, and that sustainable growth and meaning depends on confronting the fears, assumptions, and habits that shape our experience.

Much of their shared wisdom can be refined to 5 fundamental rules which are;

# Release micromanagement of outcomes
# Embrace a more flexible identity
# Face avoided realities
# Have responsibility for self instead of waiting for motivation or perfect conditions
# Step into discomfort for growth

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances, making it a sustainable path to psychological freedom, flexibility, and personal growth.

'''How to use this book?'''
To help readers both understand and later master these rules, this book is divided into 2 sections which is to be read in order.

The first section, '''Core Principles''', is about being aware of your own patterns and seeing if this book is suited to you. It will be a brief introduction to help you understand what the teachings are.

The second section, '''Application''' is dedicated to practical application where actionable exercises are provided, as well as strategies for overcoming common barriers like fear and perfectionism in modern routines.

==Core Principles==
The five rules, based on the insights of Frankl, Jung, and Watts, do not promise constant happiness but instead provide practical path for cultivating courage, purpose, responsibility, acceptance, adaptability, and psychological resilience. They are;

# Seek meaning over happiness
# Taking action on situations that you avoid or put off and do it even if feeling less than perfect to reduce long-term anxiety
# Have responsibility for self instead of waiting for motivation or perfect conditions.
# Develop strong internal locus of control where you accept limits of control  - and let go of micromanaging outcomes by setting intentions then accepting the results.
# Cultivate a fluid identity and regularly questioning rigid self-views on what you can and can't do.

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances,  providing a practical framework for psychological freedom, flexibility, and personal growth.

==3. Application==

==4. Further reading==
This chapter provides references for readers who wish to further study related ideas and the philosophical and psychological works that influenced the ''Five Rules for Meaningful Living''.

It include selected works that introduces key concepts from Viktor Frankl, Carl Jung, and Alan Watts as well as related ideas from other thinkers.

=== Viktor Frankl ===
* [[wikipedia:Man's Search for Meaning|''Man's Search for Meaning'']]

=== Carl Jung ===
* [[wikipedia:Man and His Symbols|''Man and His Symbols'']]

=== Alan Watts ===
* [https://books.google.com.au/books?id=tKy_sIIr4RcC ''The Book: On the Taboo Against Knowing Who You Are'']
=== Marcus Aurelius ===
* [[wikipedia:Meditations|''Meditations'']]

=== M. Scott Peck ===
* [[wikipedia:M. Scott Peck#The Road Less Traveled|''The Road Less Traveled'']]

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This wikibook, '''Five Rules for Meaningful Living''', is based on the teachings of three scholars on overcoming inner suffering and living a meaningful life.

Viktor Frankl was a Holocaust survivor. Carl Jung was a famous psychologist. And Alan Watts is a Zenz philosopher. Despite these three men coming from very different backgrounds, their insights converged on the understanding that many of our greatest struggles in life arise not only from life's external hardships, but also from the psychological patterns through which we respond to them. All three argued that we can suffer and fare poorly due to the invisible psychological traps we refuse to confront, and that sustainable growth and meaning depends on confronting the fears, assumptions, and habits that shape our experience.

Much of their shared wisdom can be refined to 5 fundamental rules which are;

# Release micromanagement of outcomes
# Embrace a more flexible identity
# Face avoided realities
# Have responsibility for self instead of waiting for motivation or perfect conditions
# Step into discomfort for growth

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances, making it a sustainable path to psychological freedom, flexibility, and personal growth.

'''How to use this book?'''
To help readers both understand and later master these rules, this book is divided into 2 sections which is to be read in order.

The first section, '''Core Principles''', is about being aware of your own patterns and seeing if this book is suited to you. It will be a brief introduction to help you understand what the teachings are.

The second section, '''Application''' is dedicated to practical application where actionable exercises are provided, as well as strategies for overcoming common barriers like fear and perfectionism in modern routines.

==Core Principles==
The five rules, based on the insights of Frankl, Jung, and Watts, do not promise constant happiness but instead provide practical path for cultivating courage, purpose, responsibility, acceptance, adaptability, and psychological resilience. They are;

# Seek meaning over happiness
# Taking action on situations that you avoid or put off and do it even if feeling less than perfect to reduce long-term anxiety
# Have responsibility for self instead of waiting for motivation or perfect conditions.
# Develop strong internal locus of control where you accept limits of control  - and let go of micromanaging outcomes by setting intentions then accepting the results.
# Cultivate a fluid identity and regularly questioning rigid self-views on what you can and can't do.

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances,  providing a practical framework for psychological freedom, flexibility, and personal growth.

==Application==

==4. Further reading==
This chapter provides references for readers who wish to further study related ideas and the philosophical and psychological works that influenced the ''Five Rules for Meaningful Living''.

It include selected works that introduces key concepts from Viktor Frankl, Carl Jung, and Alan Watts as well as related ideas from other thinkers.

=== Viktor Frankl ===
* [[wikipedia:Man's Search for Meaning|''Man's Search for Meaning'']]

=== Carl Jung ===
* [[wikipedia:Man and His Symbols|''Man and His Symbols'']]

=== Alan Watts ===
* [https://books.google.com.au/books?id=tKy_sIIr4RcC ''The Book: On the Taboo Against Knowing Who You Are'']
=== Marcus Aurelius ===
* [[wikipedia:Meditations|''Meditations'']]

=== M. Scott Peck ===
* [[wikipedia:M. Scott Peck#The Road Less Traveled|''The Road Less Traveled'']]

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This wikibook, '''Five Rules for Meaningful Living''', is based on the teachings of three scholars on overcoming inner suffering and living a meaningful life.

Viktor Frankl was a Holocaust survivor. Carl Jung was a famous psychologist. And Alan Watts is a Zenz philosopher. Despite these three men coming from very different backgrounds, their insights converged on the understanding that many of our greatest struggles in life arise not only from life's external hardships, but also from the psychological patterns through which we respond to them. All three argued that we can suffer and fare poorly due to the invisible psychological traps we refuse to confront, and that sustainable growth and meaning depends on confronting the fears, assumptions, and habits that shape our experience.

Much of their shared wisdom can be refined to 5 fundamental rules which are;

# Release micromanagement of outcomes
# Embrace a more flexible identity
# Face avoided realities
# Have responsibility for self instead of waiting for motivation or perfect conditions
# Step into discomfort for growth

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances, making it a sustainable path to psychological freedom, flexibility, and personal growth.

'''How to use this book?'''
To help readers both understand and later master these rules, this book is divided into 2 sections which is to be read in order.

The first section, '''Core Principles''', is about being aware of your own patterns and seeing if this book is suited to you. It will be a brief introduction to help you understand what the teachings are.

The second section, '''Application''' is dedicated to practical application where actionable exercises are provided, as well as strategies for overcoming common barriers like fear and perfectionism in modern routines.

==Core Principles==
The five rules, based on the insights of Frankl, Jung, and Watts, do not promise constant happiness but instead provide practical path for cultivating courage, purpose, responsibility, acceptance, adaptability, and psychological resilience. They are;

# Seek meaning over happiness
# Taking action on situations that you avoid or put off and do it even if feeling less than perfect to reduce long-term anxiety
# Have responsibility for self instead of waiting for motivation or perfect conditions.
# Develop strong internal locus of control where you accept limits of control  - and let go of micromanaging outcomes by setting intentions then accepting the results.
# Cultivate a fluid identity and regularly questioning rigid self-views on what you can and can't do.

Together these 5 principles aim to develop qualities that are relatively stable and less dependent on external circumstances,  providing a practical framework for psychological freedom, flexibility, and personal growth.

==Application==

==Further reading==
This chapter provides references for readers who wish to further study related ideas and the philosophical and psychological works that influenced the ''Five Rules for Meaningful Living''.

It include selected works that introduces key concepts from Viktor Frankl, Carl Jung, and Alan Watts as well as related ideas from other thinkers.

=== Viktor Frankl ===
* [[wikipedia:Man's Search for Meaning|''Man's Search for Meaning'']]

=== Carl Jung ===
* [[wikipedia:Man and His Symbols|''Man and His Symbols'']]

=== Alan Watts ===
* [https://books.google.com.au/books?id=tKy_sIIr4RcC ''The Book: On the Taboo Against Knowing Who You Are'']
=== Marcus Aurelius ===
* [[wikipedia:Meditations|''Meditations'']]

=== M. Scott Peck ===
* [[wikipedia:M. Scott Peck#The Road Less Traveled|''The Road Less Traveled'']]

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    <title>Hereditary Multiple Exostoses</title>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Do advocate for yourself. 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.'' 

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.'' 

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

=== Case studies ===
'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.'' 

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.'' 

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

=== Case studies ===
'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.'' 

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

=== Case studies ===
'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.'' 

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

=== Case studies ===
'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

=== Case studies ===
'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Ahn, YS., Kim, S., Kim, WJ. et al. Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses. BMC Musculoskelet Disord 22, 153 (2021). &lt;nowiki&gt;https://doi.org/10.1186/s12891-021-04021-1&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Ahn |first=Yeong-Seub |last2=Kim |first2=Sungmin |last3=Kim |first3=Woo-Jong |last4=Lim |first4=Jun-Hyuk |last5=Jung |first5=Sung-Taek |date=2021-02-06 |title=Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses |url=https://doi.org/10.1186/s12891-021-04021-1 |journal=BMC Musculoskeletal Disorders |language=en |volume=22 |issue=1 |pages=153 |doi=10.1186/s12891-021-04021-1 |issn=1471-2474 |pmc=7868013 |pmid=33549073}}&lt;/ref&gt; ''Between 2001 and 2019, total 51 patients (102 hips) were evaluated in this study. Patients with MHE were classified to femoro-acetabular impingement (FAI) symptom group, ischio-femoral impingement (IFI) symptom group and non-impingement symptom group by comparing the symptoms, clinical signs and imaging studies.'' 

'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Anel-Quimpo, Joselynna, Mark Anthony Santiago Sandoval, Frances Lina Lantion-Ang, 2011. Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses. BMJ Journals. &lt;nowiki&gt;https://casereports.bmj.com/content/2011/bcr.12.2010.3651&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Anel-Quimpo |first=Joselynna |last2=Sandoval |first2=Mark Anthony Santiago |last3=Lantion-Ang |first3=Frances Lina |date=2011-05-17 |title=Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses |url=https://casereports.bmj.com/content/2011/bcr.12.2010.3651 |journal=BMJ Case Reports |language=en |volume=2011 |pages=bcr1220103651 |doi=10.1136/bcr.12.2010.3651 |issn=1757-790X}}&lt;/ref&gt; ''The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Caino, Silvia, Marisa Angelica Cubilla, Romina Alba, María Gabriela Obregón, Virginia Fano, Abel Gómez, Lorena Zecchini, Pablo Lapunzina, Miriam Aza-Carmona, Karen E. Heath, and et al. 2022. &quot;Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients&quot; Genes 13, no. 11: 2063.''' '''&lt;nowiki&gt;https://doi.org/10.3390/genes13112063&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Caino |first=Silvia |last2=Cubilla |first2=Marisa Angelica |last3=Alba |first3=Romina |last4=Obregón |first4=María Gabriela |last5=Fano |first5=Virginia |last6=Gómez |first6=Abel |last7=Zecchini |first7=Lorena |last8=Lapunzina |first8=Pablo |last9=Aza-Carmona |first9=Miriam |last10=Heath |first10=Karen E. |last11=Asteggiano |first11=Carla Gabriela |date=2022-11-07 |title=Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients |url=https://www.mdpi.com/2073-4425/13/11/2063 |journal=Genes |language=en |volume=13 |issue=11 |pages=2063 |doi=10.3390/genes13112063 |issn=2073-4425 |pmc=9690389 |pmid=36360300}}&lt;/ref&gt; ''Multiple Osteochondromatosis (MO, MIM 133700 &amp; 133701), an autosomal dominant O-glycosylation disorder (EXT1/EXT2-CDG), can be associated with a reduction in skeletal growth, bony deformity, restricted joint motion, shortened stature and pathogenic variants in two tumor suppressor genes, EXT1 and EXT2. In this work, we report a cross-sectional study including 35 index patients and 20 affected family members. Clinical phenotyping of all 55 affected cases was obtained, but genetic studies were performed only in 35 indexes.'' 

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Ahn, YS., Kim, S., Kim, WJ. et al. Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses. BMC Musculoskelet Disord 22, 153 (2021). &lt;nowiki&gt;https://doi.org/10.1186/s12891-021-04021-1&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Ahn |first=Yeong-Seub |last2=Kim |first2=Sungmin |last3=Kim |first3=Woo-Jong |last4=Lim |first4=Jun-Hyuk |last5=Jung |first5=Sung-Taek |date=2021-02-06 |title=Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses |url=https://doi.org/10.1186/s12891-021-04021-1 |journal=BMC Musculoskeletal Disorders |language=en |volume=22 |issue=1 |pages=153 |doi=10.1186/s12891-021-04021-1 |issn=1471-2474 |pmc=7868013 |pmid=33549073}}&lt;/ref&gt; ''Between 2001 and 2019, total 51 patients (102 hips) were evaluated in this study. Patients with MHE were classified to femoro-acetabular impingement (FAI) symptom group, ischio-femoral impingement (IFI) symptom group and non-impingement symptom group by comparing the symptoms, clinical signs and imaging studies.'' 

'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Anel-Quimpo, Joselynna, Mark Anthony Santiago Sandoval, Frances Lina Lantion-Ang, 2011. Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses. BMJ Journals. &lt;nowiki&gt;https://casereports.bmj.com/content/2011/bcr.12.2010.3651&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Anel-Quimpo |first=Joselynna |last2=Sandoval |first2=Mark Anthony Santiago |last3=Lantion-Ang |first3=Frances Lina |date=2011-05-17 |title=Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses |url=https://casereports.bmj.com/content/2011/bcr.12.2010.3651 |journal=BMJ Case Reports |language=en |volume=2011 |pages=bcr1220103651 |doi=10.1136/bcr.12.2010.3651 |issn=1757-790X}}&lt;/ref&gt; ''The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Caino, Silvia, Marisa Angelica Cubilla, Romina Alba, María Gabriela Obregón, Virginia Fano, Abel Gómez, Lorena Zecchini, Pablo Lapunzina, Miriam Aza-Carmona, Karen E. Heath, and et al. 2022. &quot;Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients&quot; Genes 13, no. 11: 2063.''' '''&lt;nowiki&gt;https://doi.org/10.3390/genes13112063&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Caino |first=Silvia |last2=Cubilla |first2=Marisa Angelica |last3=Alba |first3=Romina |last4=Obregón |first4=María Gabriela |last5=Fano |first5=Virginia |last6=Gómez |first6=Abel |last7=Zecchini |first7=Lorena |last8=Lapunzina |first8=Pablo |last9=Aza-Carmona |first9=Miriam |last10=Heath |first10=Karen E. |last11=Asteggiano |first11=Carla Gabriela |date=2022-11-07 |title=Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients |url=https://www.mdpi.com/2073-4425/13/11/2063 |journal=Genes |language=en |volume=13 |issue=11 |pages=2063 |doi=10.3390/genes13112063 |issn=2073-4425 |pmc=9690389 |pmid=36360300}}&lt;/ref&gt; ''Multiple Osteochondromatosis (MO, MIM 133700 &amp; 133701), an autosomal dominant O-glycosylation disorder (EXT1/EXT2-CDG), can be associated with a reduction in skeletal growth, bony deformity, restricted joint motion, shortened stature and pathogenic variants in two tumor suppressor genes, EXT1 and EXT2. In this work, we report a cross-sectional study including 35 index patients and 20 affected family members. Clinical phenotyping of all 55 affected cases was obtained, but genetic studies were performed only in 35 indexes.''

'''Hariri O, Al Laham O, Ibrahim Basha Z, Ghannam E, Ghannam M, Mohammad A. Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review. Int J Surg Case Rep. 2024 Apr 12;118:109633. doi: 10.1016/j.ijscr.2024.109633. Epub ahead of print. PMID: 38626641; PMCID: PMC11035074.'''&lt;ref&gt;{{Cite journal |last=Hariri |first=Omar |last2=Al Laham |first2=Omar |last3=Ibrahim Basha |first3=Zein |last4=Ghannam |first4=Eman |last5=Ghannam |first5=Mohammad |last6=Mohammad |first6=Ammar |date=2024-05 |title=Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review |url=https://journals.lww.com/10.1016/j.ijscr.2024.109633 |journal=International Journal of Surgery Case Reports |language=en |volume=118 |issue=C |doi=10.1016/j.ijscr.2024.109633 |issn=2210-2612 |pmc=11035074 |pmid=38626641}}&lt;/ref&gt; ''We present the case of a 37-year-old Middle Eastern male with Multiple Hereditary Exostoses who experienced sudden-onset left lower limb pain persisting for a month prior to admission. It was associated with coldness and paresthesia of the ipsilateral lower limb. The presurgical radiological workup uncovered a popliteal pseudoaneurysm subsequent to Multiple Hereditary Exostoses.''

'''Kambouris, M., Fadda A, Al-Arraj, Y, et al., 2016. Putative Relation Between Autism Spectrum Disease &amp; Hereditary Multiple Exostosis Investigated by Whole Genome Sequencing &amp; Comparative Genome Analyses in a Family with ASD and HME with EXT-1 Mutations''' ''A family with two male children affected with ASD and HME as well as an unaffected female child, was studied to identify the Genetic basis of ASD in the family and the possible relation between ASD &amp; HME. The HME unaffected parent [mother] contributed heterozygous variants in the Heparan Sulfate biosynthesis pathway that in synergy with the EXT-1 mutation could be the genetic causes of ASD in the family.''

'''Kim, Min Jeong, Yunjin Lee, Sang Ook Nam, Young Mi Kim, 2021. An 8q24.11q24.13 Microdeletion Encompassing EXT1 in a Boy with Autistic Spectrum Disorder, Intellectual Disability, and Multiple Hereditary Exostoses. Annals of Child Neurology. Letter to the Editor, 11/9/2021.''' ''Here, we describe the case of a boy with a microdeletion (8q24.11q24.13 [118,625,768-124,169,620]×1), who presented with autism, intellectual disability, and MHE. the parents signed informed consent and approved the anonymous use of clinical and molecular data for the present diagnostic study'''''.'''

'''Küçükesmen, Çiḡdem DDS, PhD, Buḡra Özen, DDS, PhD,b and Mustafa Akçam, DDS, PhDc, 1997. Multiple Hereditary Osteochondromatosis: A Case Report. Eur J Dent. 2007 Jul; 1(3): 183–187.&lt;nowiki&gt;https://www.ncbi.nlm.nih&lt;/nowiki&gt;.''' ''Common carious lesions owing to vomiting are not widespread in children. In this case, we aimed to report an 11-years-old male patient with common carious lesions due to repeated vomitings, chewing and eating difficulty and retarded growth with Multiple Hereditary Osteochondromatosis (MHO).''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Ahn, YS., Kim, S., Kim, WJ. et al. Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses. BMC Musculoskelet Disord 22, 153 (2021). &lt;nowiki&gt;https://doi.org/10.1186/s12891-021-04021-1&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Ahn |first=Yeong-Seub |last2=Kim |first2=Sungmin |last3=Kim |first3=Woo-Jong |last4=Lim |first4=Jun-Hyuk |last5=Jung |first5=Sung-Taek |date=2021-02-06 |title=Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses |url=https://doi.org/10.1186/s12891-021-04021-1 |journal=BMC Musculoskeletal Disorders |language=en |volume=22 |issue=1 |pages=153 |doi=10.1186/s12891-021-04021-1 |issn=1471-2474 |pmc=7868013 |pmid=33549073}}&lt;/ref&gt; ''Between 2001 and 2019, total 51 patients (102 hips) were evaluated in this study. Patients with MHE were classified to femoro-acetabular impingement (FAI) symptom group, ischio-femoral impingement (IFI) symptom group and non-impingement symptom group by comparing the symptoms, clinical signs and imaging studies.'' 

'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Anel-Quimpo, Joselynna, Mark Anthony Santiago Sandoval, Frances Lina Lantion-Ang, 2011. Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses. BMJ Journals. &lt;nowiki&gt;https://casereports.bmj.com/content/2011/bcr.12.2010.3651&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Anel-Quimpo |first=Joselynna |last2=Sandoval |first2=Mark Anthony Santiago |last3=Lantion-Ang |first3=Frances Lina |date=2011-05-17 |title=Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses |url=https://casereports.bmj.com/content/2011/bcr.12.2010.3651 |journal=BMJ Case Reports |language=en |volume=2011 |pages=bcr1220103651 |doi=10.1136/bcr.12.2010.3651 |issn=1757-790X}}&lt;/ref&gt; ''The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Caino, Silvia, Marisa Angelica Cubilla, Romina Alba, María Gabriela Obregón, Virginia Fano, Abel Gómez, Lorena Zecchini, Pablo Lapunzina, Miriam Aza-Carmona, Karen E. Heath, and et al. 2022. &quot;Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients&quot; Genes 13, no. 11: 2063.''' '''&lt;nowiki&gt;https://doi.org/10.3390/genes13112063&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Caino |first=Silvia |last2=Cubilla |first2=Marisa Angelica |last3=Alba |first3=Romina |last4=Obregón |first4=María Gabriela |last5=Fano |first5=Virginia |last6=Gómez |first6=Abel |last7=Zecchini |first7=Lorena |last8=Lapunzina |first8=Pablo |last9=Aza-Carmona |first9=Miriam |last10=Heath |first10=Karen E. |last11=Asteggiano |first11=Carla Gabriela |date=2022-11-07 |title=Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients |url=https://www.mdpi.com/2073-4425/13/11/2063 |journal=Genes |language=en |volume=13 |issue=11 |pages=2063 |doi=10.3390/genes13112063 |issn=2073-4425 |pmc=9690389 |pmid=36360300}}&lt;/ref&gt; ''Multiple Osteochondromatosis (MO, MIM 133700 &amp; 133701), an autosomal dominant O-glycosylation disorder (EXT1/EXT2-CDG), can be associated with a reduction in skeletal growth, bony deformity, restricted joint motion, shortened stature and pathogenic variants in two tumor suppressor genes, EXT1 and EXT2. In this work, we report a cross-sectional study including 35 index patients and 20 affected family members. Clinical phenotyping of all 55 affected cases was obtained, but genetic studies were performed only in 35 indexes.''

'''Hariri O, Al Laham O, Ibrahim Basha Z, Ghannam E, Ghannam M, Mohammad A. Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review. Int J Surg Case Rep. 2024 Apr 12;118:109633. doi: 10.1016/j.ijscr.2024.109633. Epub ahead of print. PMID: 38626641; PMCID: PMC11035074.'''&lt;ref&gt;{{Cite journal |last=Hariri |first=Omar |last2=Al Laham |first2=Omar |last3=Ibrahim Basha |first3=Zein |last4=Ghannam |first4=Eman |last5=Ghannam |first5=Mohammad |last6=Mohammad |first6=Ammar |date=2024-05 |title=Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review |url=https://journals.lww.com/10.1016/j.ijscr.2024.109633 |journal=International Journal of Surgery Case Reports |language=en |volume=118 |issue=C |doi=10.1016/j.ijscr.2024.109633 |issn=2210-2612 |pmc=11035074 |pmid=38626641}}&lt;/ref&gt; ''We present the case of a 37-year-old Middle Eastern male with Multiple Hereditary Exostoses who experienced sudden-onset left lower limb pain persisting for a month prior to admission. It was associated with coldness and paresthesia of the ipsilateral lower limb. The presurgical radiological workup uncovered a popliteal pseudoaneurysm subsequent to Multiple Hereditary Exostoses.''

'''Kambouris, M., Fadda A, Al-Arraj, Y, et al., 2016. Putative Relation Between Autism Spectrum Disease &amp; Hereditary Multiple Exostosis Investigated by Whole Genome Sequencing &amp; Comparative Genome Analyses in a Family with ASD and HME with EXT-1 Mutations''' ''A family with two male children affected with ASD and HME as well as an unaffected female child, was studied to identify the Genetic basis of ASD in the family and the possible relation between ASD &amp; HME. The HME unaffected parent [mother] contributed heterozygous variants in the Heparan Sulfate biosynthesis pathway that in synergy with the EXT-1 mutation could be the genetic causes of ASD in the family.''

'''Kim, Min Jeong, Yunjin Lee, Sang Ook Nam, Young Mi Kim, 2021. An 8q24.11q24.13 Microdeletion Encompassing EXT1 in a Boy with Autistic Spectrum Disorder, Intellectual Disability, and Multiple Hereditary Exostoses. Annals of Child Neurology. Letter to the Editor, 11/9/2021.''' ''Here, we describe the case of a boy with a microdeletion (8q24.11q24.13 [118,625,768-124,169,620]×1), who presented with autism, intellectual disability, and MHE. the parents signed informed consent and approved the anonymous use of clinical and molecular data for the present diagnostic study'''''.'''

'''Küçükesmen, Çiḡdem DDS, PhD, Buḡra Özen, DDS, PhD,b and Mustafa Akçam, DDS, PhDc, 1997. Multiple Hereditary Osteochondromatosis: A Case Report. Eur J Dent. 2007 Jul; 1(3): 183–187.&lt;nowiki&gt;https://www.ncbi.nlm.nih&lt;/nowiki&gt;.''' ''Common carious lesions owing to vomiting are not widespread in children. In this case, we aimed to report an 11-years-old male patient with common carious lesions due to repeated vomitings, chewing and eating difficulty and retarded growth with Multiple Hereditary Osteochondromatosis (MHO).''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Malagón, V., 2001.  Development of Hip Dysplasia in Hereditary Multiple Exostosis. Journal of Pediatric Orthopaedics, 21(2): 205-211.  &lt;nowiki&gt;https://journals.lww.com/pedorthopaedics/Abstract/2001/03000/Development_of_Hip_Dysplasia_in_Hereditary.14.aspx&lt;/nowiki&gt;''.'''''&lt;ref&gt;{{Cite web |title=Development of Hip Dysplasia in Hereditary... : Journal of Pediatric Orthopaedics |url=https://www.ovid.com/jnls/pedorthopaedics/fulltext/01241398-200103000-00014~development-of-hip-dysplasia-in-hereditary-multiple |access-date=2026-07-16 |website=Ovid |language=en}}&lt;/ref&gt; ''In approximately 25% of patients with hereditary multiple exostosis, there is an abnormal osteochondral formation localized in the femoral proximal metaphysis. Although this entity is rather frequent and quite severe, it is rarely found in the medical literature. The author describes six private cases, taken from a total of 24,000 patients (0.25/1000) as examples of this entity, and provides a review of the literature.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

'''Puiu1, Maria , Iulia Simina-Jurca, Simona Dumitriu, Smaranda Arghirescu,  Adela Chirita-Emandi,  2012. . Multiple Hereditary Exostoses - Clinical Features and Management.''' ''We report two cases of skeletally immature patients who presented with multiple exostoses, bone deformation without bone pain; and growth and pubertal retardation. The cases need adequate counseling, long-term follow-up, and measures to improve the quality of life of patients with multiple hereditary exostoses.''

'''Stitzman Wengrowicz, M.L., J  Pretell-Mazzini,  J.P. Dormans, R.S. Davidson, 2011.. Regression of a Sessile Osteochondroma: A Case Study and Review of the Literature.''' ''&lt;nowiki&gt;https://www.researchgate.net/publication/267426996_Regression_of_a_Sessile_Osteochondroma_A_Case_Study_and_Review_of_the_Literature&lt;/nowiki&gt; . The most common benign bone tumor is osteochondroma.  Its natural history is poorly understood as a consequence of its benign symptomatology in most cases. It typically grows in childhood and growth during adulthood can be a sign of malignant  degeneration. We present  a case of  spontaneous regression of  a solitary osteochondroma.  A review of the  current  literature which  reveals 21  other cases of  spontaneous regression  of solitary  osteochondromas is also discussed. We believe that the possibility of regression of solitary osteochondromas should be taken into account when considering surgical excision.''

'''Viala P, Vanel D, Larbi A, Cyteval C, Laredo JD. Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. Skeletal Radiol. 2012;41:1637–40. [PubMed] &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/22865159/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Viala |first=Pierre |last2=Vanel |first2=Daniel |last3=Larbi |first3=Ahmed |last4=Cyteval |first4=Catherine |last5=Laredo |first5=Jean-Denis |date=2012-12 |title=Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses |url=https://pubmed.ncbi.nlm.nih.gov/22865159 |journal=Skeletal Radiology |volume=41 |issue=12 |pages=1637–1640 |doi=10.1007/s00256-012-1488-0 |issn=1432-2161 |pmid=22865159}}&lt;/ref&gt; ''We report a case of bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. The association of exostoses and femoral metaphyseal widening resulted in the narrowing of the ischiofemoral spaces.''

'''Wang YZ, Park KW, Oh CS, Ahn YS, Kang QL, Jung ST, Song HR. Developmental pattern of the hip in patients with hereditary multiple exostoses. BMC Musculoskelet Disord. 2015;16:54'''''.'' '''https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Wang |first=Ya-Zhou |last2=Park |first2=Kwang-Won |last3=Oh |first3=Chang-Seon |last4=Ahn |first4=Yeong-Seub |last5=Kang |first5=Qing-Lin |last6=Jung |first6=Sung-Taek |last7=Song |first7=Hae-Ryong |date=2015-03-15 |title=Developmental pattern of the hip in patients with hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/ |journal=BMC musculoskeletal disorders |volume=16 |pages=54 |doi=10.1186/s12891-015-0514-5 |issn=1471-2474 |pmc=4429362 |pmid=25888017}}&lt;/ref&gt; '''C'''''oxa valga is a common clinical feature of hereditary multiple exostoses (HME). The current study aimed to determine the unique developmental pattern of the hip in patients with HME and evaluate the factors that influence its progression.''

'''Wiater JM, Farley FA. Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature. Am J Orthop (Belle Mead NJ). 1999 Jul;28(7):412-6. PMID: 10426440.'''&lt;ref&gt;{{Cite journal |last=Wiater |first=J. M. |last2=Farley |first2=F. A. |date=1999-07 |title=Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature |url=https://pubmed.ncbi.nlm.nih.gov/10426440 |journal=American Journal of Orthopedics |volume=28 |issue=7 |pages=412–416 |issn=1078-4519 |pmid=10426440}}&lt;/ref&gt; ''A male 17-year-old with multiple hereditary exostoses presented with a mass in the distal left thigh several days after lifting weights. An arteriogram showed a popliteal artery pseudoaneurysm adjacent to a femoral osteochondroma. The osteochondroma was excised and the artery was repaired with a saphenous vein interposition graft. A review of the literature identified 23 similar reports. The average age of the patients was 21.3 years. Seventy-eight percent were men and half of the patients had multiple hereditary exostoses. Ten patients were initially misdiagnosed. The clinician should consider the diagnosis of pseudoaneurysm in a young patient with an osteochondroma and a mass about the knee.''

'''Zaijun L, Xinhai Y, Zhipeng W, Wending H, Quan H, Zhenhua Z, Dapeng F, Jisheng Z, Wei Z, Jianru X. 2013. Outcome and prognosis of myelopathy and radiculopathy from osteochondroma in the mobile spine: a report on 14 patients. J Spinal Disord Tech 26:194–199.''' ''Fourteen symptomatic spinal osteochondroma (OC)  cases, including 2 hereditary multiple exostoses, were treated surgically from 2001 to 2010.'' 

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt; 

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== How to advocate for your child with HME in schools ==
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Ahn, YS., Kim, S., Kim, WJ. et al. Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses. BMC Musculoskelet Disord 22, 153 (2021). &lt;nowiki&gt;https://doi.org/10.1186/s12891-021-04021-1&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Ahn |first=Yeong-Seub |last2=Kim |first2=Sungmin |last3=Kim |first3=Woo-Jong |last4=Lim |first4=Jun-Hyuk |last5=Jung |first5=Sung-Taek |date=2021-02-06 |title=Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses |url=https://doi.org/10.1186/s12891-021-04021-1 |journal=BMC Musculoskeletal Disorders |language=en |volume=22 |issue=1 |pages=153 |doi=10.1186/s12891-021-04021-1 |issn=1471-2474 |pmc=7868013 |pmid=33549073}}&lt;/ref&gt; ''Between 2001 and 2019, total 51 patients (102 hips) were evaluated in this study. Patients with MHE were classified to femoro-acetabular impingement (FAI) symptom group, ischio-femoral impingement (IFI) symptom group and non-impingement symptom group by comparing the symptoms, clinical signs and imaging studies.'' 

'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Anel-Quimpo, Joselynna, Mark Anthony Santiago Sandoval, Frances Lina Lantion-Ang, 2011. Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses. BMJ Journals. &lt;nowiki&gt;https://casereports.bmj.com/content/2011/bcr.12.2010.3651&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Anel-Quimpo |first=Joselynna |last2=Sandoval |first2=Mark Anthony Santiago |last3=Lantion-Ang |first3=Frances Lina |date=2011-05-17 |title=Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses |url=https://casereports.bmj.com/content/2011/bcr.12.2010.3651 |journal=BMJ Case Reports |language=en |volume=2011 |pages=bcr1220103651 |doi=10.1136/bcr.12.2010.3651 |issn=1757-790X}}&lt;/ref&gt; ''The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Caino, Silvia, Marisa Angelica Cubilla, Romina Alba, María Gabriela Obregón, Virginia Fano, Abel Gómez, Lorena Zecchini, Pablo Lapunzina, Miriam Aza-Carmona, Karen E. Heath, and et al. 2022. &quot;Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients&quot; Genes 13, no. 11: 2063.''' '''&lt;nowiki&gt;https://doi.org/10.3390/genes13112063&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Caino |first=Silvia |last2=Cubilla |first2=Marisa Angelica |last3=Alba |first3=Romina |last4=Obregón |first4=María Gabriela |last5=Fano |first5=Virginia |last6=Gómez |first6=Abel |last7=Zecchini |first7=Lorena |last8=Lapunzina |first8=Pablo |last9=Aza-Carmona |first9=Miriam |last10=Heath |first10=Karen E. |last11=Asteggiano |first11=Carla Gabriela |date=2022-11-07 |title=Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients |url=https://www.mdpi.com/2073-4425/13/11/2063 |journal=Genes |language=en |volume=13 |issue=11 |pages=2063 |doi=10.3390/genes13112063 |issn=2073-4425 |pmc=9690389 |pmid=36360300}}&lt;/ref&gt; ''Multiple Osteochondromatosis (MO, MIM 133700 &amp; 133701), an autosomal dominant O-glycosylation disorder (EXT1/EXT2-CDG), can be associated with a reduction in skeletal growth, bony deformity, restricted joint motion, shortened stature and pathogenic variants in two tumor suppressor genes, EXT1 and EXT2. In this work, we report a cross-sectional study including 35 index patients and 20 affected family members. Clinical phenotyping of all 55 affected cases was obtained, but genetic studies were performed only in 35 indexes.''

'''Hariri O, Al Laham O, Ibrahim Basha Z, Ghannam E, Ghannam M, Mohammad A. Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review. Int J Surg Case Rep. 2024 Apr 12;118:109633. doi: 10.1016/j.ijscr.2024.109633. Epub ahead of print. PMID: 38626641; PMCID: PMC11035074.'''&lt;ref&gt;{{Cite journal |last=Hariri |first=Omar |last2=Al Laham |first2=Omar |last3=Ibrahim Basha |first3=Zein |last4=Ghannam |first4=Eman |last5=Ghannam |first5=Mohammad |last6=Mohammad |first6=Ammar |date=2024-05 |title=Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review |url=https://journals.lww.com/10.1016/j.ijscr.2024.109633 |journal=International Journal of Surgery Case Reports |language=en |volume=118 |issue=C |doi=10.1016/j.ijscr.2024.109633 |issn=2210-2612 |pmc=11035074 |pmid=38626641}}&lt;/ref&gt; ''We present the case of a 37-year-old Middle Eastern male with Multiple Hereditary Exostoses who experienced sudden-onset left lower limb pain persisting for a month prior to admission. It was associated with coldness and paresthesia of the ipsilateral lower limb. The presurgical radiological workup uncovered a popliteal pseudoaneurysm subsequent to Multiple Hereditary Exostoses.''

'''Kambouris, M., Fadda A, Al-Arraj, Y, et al., 2016. Putative Relation Between Autism Spectrum Disease &amp; Hereditary Multiple Exostosis Investigated by Whole Genome Sequencing &amp; Comparative Genome Analyses in a Family with ASD and HME with EXT-1 Mutations''' ''A family with two male children affected with ASD and HME as well as an unaffected female child, was studied to identify the Genetic basis of ASD in the family and the possible relation between ASD &amp; HME. The HME unaffected parent [mother] contributed heterozygous variants in the Heparan Sulfate biosynthesis pathway that in synergy with the EXT-1 mutation could be the genetic causes of ASD in the family.''

'''Kim, Min Jeong, Yunjin Lee, Sang Ook Nam, Young Mi Kim, 2021. An 8q24.11q24.13 Microdeletion Encompassing EXT1 in a Boy with Autistic Spectrum Disorder, Intellectual Disability, and Multiple Hereditary Exostoses. Annals of Child Neurology. Letter to the Editor, 11/9/2021.''' ''Here, we describe the case of a boy with a microdeletion (8q24.11q24.13 [118,625,768-124,169,620]×1), who presented with autism, intellectual disability, and MHE. the parents signed informed consent and approved the anonymous use of clinical and molecular data for the present diagnostic study'''''.'''

'''Küçükesmen, Çiḡdem DDS, PhD, Buḡra Özen, DDS, PhD,b and Mustafa Akçam, DDS, PhDc, 1997. Multiple Hereditary Osteochondromatosis: A Case Report. Eur J Dent. 2007 Jul; 1(3): 183–187.&lt;nowiki&gt;https://www.ncbi.nlm.nih&lt;/nowiki&gt;.''' ''Common carious lesions owing to vomiting are not widespread in children. In this case, we aimed to report an 11-years-old male patient with common carious lesions due to repeated vomitings, chewing and eating difficulty and retarded growth with Multiple Hereditary Osteochondromatosis (MHO).''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Malagón, V., 2001.  Development of Hip Dysplasia in Hereditary Multiple Exostosis. Journal of Pediatric Orthopaedics, 21(2): 205-211.  &lt;nowiki&gt;https://journals.lww.com/pedorthopaedics/Abstract/2001/03000/Development_of_Hip_Dysplasia_in_Hereditary.14.aspx&lt;/nowiki&gt;''.'''''&lt;ref&gt;{{Cite web |title=Development of Hip Dysplasia in Hereditary... : Journal of Pediatric Orthopaedics |url=https://www.ovid.com/jnls/pedorthopaedics/fulltext/01241398-200103000-00014~development-of-hip-dysplasia-in-hereditary-multiple |access-date=2026-07-16 |website=Ovid |language=en}}&lt;/ref&gt; ''In approximately 25% of patients with hereditary multiple exostosis, there is an abnormal osteochondral formation localized in the femoral proximal metaphysis. Although this entity is rather frequent and quite severe, it is rarely found in the medical literature. The author describes six private cases, taken from a total of 24,000 patients (0.25/1000) as examples of this entity, and provides a review of the literature.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

'''Puiu1, Maria , Iulia Simina-Jurca, Simona Dumitriu, Smaranda Arghirescu,  Adela Chirita-Emandi,  2012. . Multiple Hereditary Exostoses - Clinical Features and Management.''' ''We report two cases of skeletally immature patients who presented with multiple exostoses, bone deformation without bone pain; and growth and pubertal retardation. The cases need adequate counseling, long-term follow-up, and measures to improve the quality of life of patients with multiple hereditary exostoses.''

'''Stitzman Wengrowicz, M.L., J  Pretell-Mazzini,  J.P. Dormans, R.S. Davidson, 2011.. Regression of a Sessile Osteochondroma: A Case Study and Review of the Literature.''' ''&lt;nowiki&gt;https://www.researchgate.net/publication/267426996_Regression_of_a_Sessile_Osteochondroma_A_Case_Study_and_Review_of_the_Literature&lt;/nowiki&gt; . The most common benign bone tumor is osteochondroma.  Its natural history is poorly understood as a consequence of its benign symptomatology in most cases. It typically grows in childhood and growth during adulthood can be a sign of malignant  degeneration. We present  a case of  spontaneous regression of  a solitary osteochondroma.  A review of the  current  literature which  reveals 21  other cases of  spontaneous regression  of solitary  osteochondromas is also discussed. We believe that the possibility of regression of solitary osteochondromas should be taken into account when considering surgical excision.''

'''Viala P, Vanel D, Larbi A, Cyteval C, Laredo JD. Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. Skeletal Radiol. 2012;41:1637–40. [PubMed] &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/22865159/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Viala |first=Pierre |last2=Vanel |first2=Daniel |last3=Larbi |first3=Ahmed |last4=Cyteval |first4=Catherine |last5=Laredo |first5=Jean-Denis |date=2012-12 |title=Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses |url=https://pubmed.ncbi.nlm.nih.gov/22865159 |journal=Skeletal Radiology |volume=41 |issue=12 |pages=1637–1640 |doi=10.1007/s00256-012-1488-0 |issn=1432-2161 |pmid=22865159}}&lt;/ref&gt; ''We report a case of bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. The association of exostoses and femoral metaphyseal widening resulted in the narrowing of the ischiofemoral spaces.''

'''Wang YZ, Park KW, Oh CS, Ahn YS, Kang QL, Jung ST, Song HR. Developmental pattern of the hip in patients with hereditary multiple exostoses. BMC Musculoskelet Disord. 2015;16:54'''''.'' '''https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Wang |first=Ya-Zhou |last2=Park |first2=Kwang-Won |last3=Oh |first3=Chang-Seon |last4=Ahn |first4=Yeong-Seub |last5=Kang |first5=Qing-Lin |last6=Jung |first6=Sung-Taek |last7=Song |first7=Hae-Ryong |date=2015-03-15 |title=Developmental pattern of the hip in patients with hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/ |journal=BMC musculoskeletal disorders |volume=16 |pages=54 |doi=10.1186/s12891-015-0514-5 |issn=1471-2474 |pmc=4429362 |pmid=25888017}}&lt;/ref&gt; '''C'''''oxa valga is a common clinical feature of hereditary multiple exostoses (HME). The current study aimed to determine the unique developmental pattern of the hip in patients with HME and evaluate the factors that influence its progression.''

'''Wiater JM, Farley FA. Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature. Am J Orthop (Belle Mead NJ). 1999 Jul;28(7):412-6. PMID: 10426440.'''&lt;ref&gt;{{Cite journal |last=Wiater |first=J. M. |last2=Farley |first2=F. A. |date=1999-07 |title=Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature |url=https://pubmed.ncbi.nlm.nih.gov/10426440 |journal=American Journal of Orthopedics |volume=28 |issue=7 |pages=412–416 |issn=1078-4519 |pmid=10426440}}&lt;/ref&gt; ''A male 17-year-old with multiple hereditary exostoses presented with a mass in the distal left thigh several days after lifting weights. An arteriogram showed a popliteal artery pseudoaneurysm adjacent to a femoral osteochondroma. The osteochondroma was excised and the artery was repaired with a saphenous vein interposition graft. A review of the literature identified 23 similar reports. The average age of the patients was 21.3 years. Seventy-eight percent were men and half of the patients had multiple hereditary exostoses. Ten patients were initially misdiagnosed. The clinician should consider the diagnosis of pseudoaneurysm in a young patient with an osteochondroma and a mass about the knee.''

'''Zaijun L, Xinhai Y, Zhipeng W, Wending H, Quan H, Zhenhua Z, Dapeng F, Jisheng Z, Wei Z, Jianru X. 2013. Outcome and prognosis of myelopathy and radiculopathy from osteochondroma in the mobile spine: a report on 14 patients. J Spinal Disord Tech 26:194–199.''' ''Fourteen symptomatic spinal osteochondroma (OC)  cases, including 2 hereditary multiple exostoses, were treated surgically from 2001 to 2010.'' 

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt;

= Spanish Translation =


Problemas de deficiencia de proteoglicano de sulfato de heparán (HSPG). La MHE es el resultado de una mutación en los genes EXT1 y EXT2. Los pacientes con MHE tienen una biosíntesis de HSPG defectuosa: sus cuerpos no producen HSPG (cf Cueller et al. 2013 y Jones et al. 2014). Los HSPG son parte de cada superficie celular y regulan los procesos biológicos (cf Zak et al. 2002, Meneghetti et al. 2015). Desempeñan un papel vital en la adhesión, migración, crecimiento y comunicación celular (Vicente et al. 2018). Whitlock e Iozzo (2005) han identificado varias enfermedades relacionadas con la ausencia de HSPG (es decir, si un proceso corporal requiere HSPG y no hay suficiente HSPG para completar esa función, entonces podrían ocurrir estos problemas). Los pacientes con MHE han reportado síntomas como:

* Baja masa ósea (Nozawa et al. 2018 y Matsumoto et al. 2020)
* Deficiencias neurológicas: Trastorno del espectro autista (Li et al, 2002, Fumitoshi et al. 2012, Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); y problemas cognitivos (Farhan et al. 2015)
* Demencia frontotemporal (Narvid et al. 2009) y TDAH (Mooney et al. 2016), función cerebral (Condomitti y Wit 2018). Vea también el vídeo de ratones MHE en &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Enfermedades oculares (Park y Shukla, 2013)
* Defectos dentales (Kucukesmen et al. 2007 y Wiweger et al. 2012)
* Prediabetes (Heibert 2021)Diabetes y dificultad para controlar la glucosa (Matsuzawa 2021)
* Reacciones medicamentosas inusuales (muchos medicamentos actúan sobre el dominio de unión del heparán [Boer y Gaillard 2007]) 
* Fatiga severa y continua (Berg et al. 1999)
* Problemas gástricos graves, incluidas úlceras no causadas por H. pylori (Ascencio et al. 1993 y Chmiela et al. 1995), cáncer gástrico (Weihua et al. 2002) y síndrome de vómitos cíclicos (Kucukesmen et al. 2007 y Theoharides et al. 1999)
* Cálculos renales y otros problemas (véase Van den Born et al. 1993 y Farhan et al. 2015)
* Vértigo e hiperacusia (Lundberg et al., 2014) y migrañas
* Problemas pulmonares (Nackerts et al. 1997 y Haeger et al. 2016)
* Anemia (Poli et al. 2017), coágulos sanguíneos y coagulación (Stringer y Gallagher 1997 y Ho et al. 1997), pseudoaneurismas (Wiater y Farley 1996 y Harari et al. 2024)
* Problemas menstruales y de embarazo extremadamente dolorosos (Alphin et al. 1988, Yin et al. 2018)
* Inflamación (Parroquia 2005); cicatrización lenta de heridas (Zhongjun et al. 2004); cicatrices y queloides (Hosalkar et al. 2007, y problemas del tejido conectivo (Forsberg y Kjellen, 2001 y Otsuka et al. 2020).
* Funciones hepáticas (Arnold et al. 2020 y Dituri et al. 2022)
* Funciones del colesterol y los lípidos (Kolsett y Salmverta 1999) y Síntesis de vitamina D (Cooper 2021)  '''Problemas de crecimiento óseo.''' En la MHE, la falta de HSPG hace que los pacientes desarrollen exostosis, que son tumores benignos en múltiples ubicaciones en todo el cuerpo (Brown 2008, Thompson 2011 y Mansouri et al. 2017). La gravedad (número y tamaño de los tumores y otras complicaciones) de la MHE varía de un paciente a otro. Las exostosis en sí mismas pueden causar numerosos problemas, incluidos: irritación de tendones y músculos que produce dolor y pérdida de movimiento, deformidad esquelética, baja estatura, discrepancia en la longitud de las extremidades, subluxaciones y deformidad angular. Los problemas directamente asociados con estas exostosis incluyen:

* Dolor crónico y problemas con la calidad de vida (Goud et al. 2012)
* Inflamación, respuestas inmunitarias (Callaghan et al. 2018 y Collins y Troeberg 2019)
* Formación de bursa y bursitis resultante, así como artritis de aparición temprana.
* Problemas respiratorios y pulmonares al estar sobre costillas que sobresalen hacia la cavidad torácica (Mazza et al. 2017)
* Irritación de un nervio cercano (dolor, debilidad, entumecimiento, hormigueo)
* Aneurisma de vasos sanguíneos por exostosis que presionan los vasos sanguíneos u otros problemas vasculares (Albokhari et al. 2023)
* Problemas de compresión de la médula espinal: incontinencia, daño nerv'''Résumé de la MEM pour les médecins et les écoles'''

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== Children's Corner ==

=== Teach your child to live with MHE ===
You just got a diagnosis for your child and you are terrified for their life.  Yeah, MHE sucks. And it is a life-long, untreatable disease. Sure you can have surgery, sure, physical therapy helps. But the underlying condition will be there every day for the rest of your life. So. How can you prepare your child to live successfully with MHE?

=== How to advocate for your child with HME in schools ===
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Ahn, YS., Kim, S., Kim, WJ. et al. Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses. BMC Musculoskelet Disord 22, 153 (2021). &lt;nowiki&gt;https://doi.org/10.1186/s12891-021-04021-1&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Ahn |first=Yeong-Seub |last2=Kim |first2=Sungmin |last3=Kim |first3=Woo-Jong |last4=Lim |first4=Jun-Hyuk |last5=Jung |first5=Sung-Taek |date=2021-02-06 |title=Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses |url=https://doi.org/10.1186/s12891-021-04021-1 |journal=BMC Musculoskeletal Disorders |language=en |volume=22 |issue=1 |pages=153 |doi=10.1186/s12891-021-04021-1 |issn=1471-2474 |pmc=7868013 |pmid=33549073}}&lt;/ref&gt; ''Between 2001 and 2019, total 51 patients (102 hips) were evaluated in this study. Patients with MHE were classified to femoro-acetabular impingement (FAI) symptom group, ischio-femoral impingement (IFI) symptom group and non-impingement symptom group by comparing the symptoms, clinical signs and imaging studies.'' 

'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Anel-Quimpo, Joselynna, Mark Anthony Santiago Sandoval, Frances Lina Lantion-Ang, 2011. Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses. BMJ Journals. &lt;nowiki&gt;https://casereports.bmj.com/content/2011/bcr.12.2010.3651&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Anel-Quimpo |first=Joselynna |last2=Sandoval |first2=Mark Anthony Santiago |last3=Lantion-Ang |first3=Frances Lina |date=2011-05-17 |title=Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses |url=https://casereports.bmj.com/content/2011/bcr.12.2010.3651 |journal=BMJ Case Reports |language=en |volume=2011 |pages=bcr1220103651 |doi=10.1136/bcr.12.2010.3651 |issn=1757-790X}}&lt;/ref&gt; ''The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Caino, Silvia, Marisa Angelica Cubilla, Romina Alba, María Gabriela Obregón, Virginia Fano, Abel Gómez, Lorena Zecchini, Pablo Lapunzina, Miriam Aza-Carmona, Karen E. Heath, and et al. 2022. &quot;Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients&quot; Genes 13, no. 11: 2063.''' '''&lt;nowiki&gt;https://doi.org/10.3390/genes13112063&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Caino |first=Silvia |last2=Cubilla |first2=Marisa Angelica |last3=Alba |first3=Romina |last4=Obregón |first4=María Gabriela |last5=Fano |first5=Virginia |last6=Gómez |first6=Abel |last7=Zecchini |first7=Lorena |last8=Lapunzina |first8=Pablo |last9=Aza-Carmona |first9=Miriam |last10=Heath |first10=Karen E. |last11=Asteggiano |first11=Carla Gabriela |date=2022-11-07 |title=Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients |url=https://www.mdpi.com/2073-4425/13/11/2063 |journal=Genes |language=en |volume=13 |issue=11 |pages=2063 |doi=10.3390/genes13112063 |issn=2073-4425 |pmc=9690389 |pmid=36360300}}&lt;/ref&gt; ''Multiple Osteochondromatosis (MO, MIM 133700 &amp; 133701), an autosomal dominant O-glycosylation disorder (EXT1/EXT2-CDG), can be associated with a reduction in skeletal growth, bony deformity, restricted joint motion, shortened stature and pathogenic variants in two tumor suppressor genes, EXT1 and EXT2. In this work, we report a cross-sectional study including 35 index patients and 20 affected family members. Clinical phenotyping of all 55 affected cases was obtained, but genetic studies were performed only in 35 indexes.''

'''Hariri O, Al Laham O, Ibrahim Basha Z, Ghannam E, Ghannam M, Mohammad A. Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review. Int J Surg Case Rep. 2024 Apr 12;118:109633. doi: 10.1016/j.ijscr.2024.109633. Epub ahead of print. PMID: 38626641; PMCID: PMC11035074.'''&lt;ref&gt;{{Cite journal |last=Hariri |first=Omar |last2=Al Laham |first2=Omar |last3=Ibrahim Basha |first3=Zein |last4=Ghannam |first4=Eman |last5=Ghannam |first5=Mohammad |last6=Mohammad |first6=Ammar |date=2024-05 |title=Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review |url=https://journals.lww.com/10.1016/j.ijscr.2024.109633 |journal=International Journal of Surgery Case Reports |language=en |volume=118 |issue=C |doi=10.1016/j.ijscr.2024.109633 |issn=2210-2612 |pmc=11035074 |pmid=38626641}}&lt;/ref&gt; ''We present the case of a 37-year-old Middle Eastern male with Multiple Hereditary Exostoses who experienced sudden-onset left lower limb pain persisting for a month prior to admission. It was associated with coldness and paresthesia of the ipsilateral lower limb. The presurgical radiological workup uncovered a popliteal pseudoaneurysm subsequent to Multiple Hereditary Exostoses.''

'''Kambouris, M., Fadda A, Al-Arraj, Y, et al., 2016. Putative Relation Between Autism Spectrum Disease &amp; Hereditary Multiple Exostosis Investigated by Whole Genome Sequencing &amp; Comparative Genome Analyses in a Family with ASD and HME with EXT-1 Mutations''' ''A family with two male children affected with ASD and HME as well as an unaffected female child, was studied to identify the Genetic basis of ASD in the family and the possible relation between ASD &amp; HME. The HME unaffected parent [mother] contributed heterozygous variants in the Heparan Sulfate biosynthesis pathway that in synergy with the EXT-1 mutation could be the genetic causes of ASD in the family.''

'''Kim, Min Jeong, Yunjin Lee, Sang Ook Nam, Young Mi Kim, 2021. An 8q24.11q24.13 Microdeletion Encompassing EXT1 in a Boy with Autistic Spectrum Disorder, Intellectual Disability, and Multiple Hereditary Exostoses. Annals of Child Neurology. Letter to the Editor, 11/9/2021.''' ''Here, we describe the case of a boy with a microdeletion (8q24.11q24.13 [118,625,768-124,169,620]×1), who presented with autism, intellectual disability, and MHE. the parents signed informed consent and approved the anonymous use of clinical and molecular data for the present diagnostic study'''''.'''

'''Küçükesmen, Çiḡdem DDS, PhD, Buḡra Özen, DDS, PhD,b and Mustafa Akçam, DDS, PhDc, 1997. Multiple Hereditary Osteochondromatosis: A Case Report. Eur J Dent. 2007 Jul; 1(3): 183–187.&lt;nowiki&gt;https://www.ncbi.nlm.nih&lt;/nowiki&gt;.''' ''Common carious lesions owing to vomiting are not widespread in children. In this case, we aimed to report an 11-years-old male patient with common carious lesions due to repeated vomitings, chewing and eating difficulty and retarded growth with Multiple Hereditary Osteochondromatosis (MHO).''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Malagón, V., 2001.  Development of Hip Dysplasia in Hereditary Multiple Exostosis. Journal of Pediatric Orthopaedics, 21(2): 205-211.  &lt;nowiki&gt;https://journals.lww.com/pedorthopaedics/Abstract/2001/03000/Development_of_Hip_Dysplasia_in_Hereditary.14.aspx&lt;/nowiki&gt;''.'''''&lt;ref&gt;{{Cite web |title=Development of Hip Dysplasia in Hereditary... : Journal of Pediatric Orthopaedics |url=https://www.ovid.com/jnls/pedorthopaedics/fulltext/01241398-200103000-00014~development-of-hip-dysplasia-in-hereditary-multiple |access-date=2026-07-16 |website=Ovid |language=en}}&lt;/ref&gt; ''In approximately 25% of patients with hereditary multiple exostosis, there is an abnormal osteochondral formation localized in the femoral proximal metaphysis. Although this entity is rather frequent and quite severe, it is rarely found in the medical literature. The author describes six private cases, taken from a total of 24,000 patients (0.25/1000) as examples of this entity, and provides a review of the literature.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

'''Puiu1, Maria , Iulia Simina-Jurca, Simona Dumitriu, Smaranda Arghirescu,  Adela Chirita-Emandi,  2012. . Multiple Hereditary Exostoses - Clinical Features and Management.''' ''We report two cases of skeletally immature patients who presented with multiple exostoses, bone deformation without bone pain; and growth and pubertal retardation. The cases need adequate counseling, long-term follow-up, and measures to improve the quality of life of patients with multiple hereditary exostoses.''

'''Stitzman Wengrowicz, M.L., J  Pretell-Mazzini,  J.P. Dormans, R.S. Davidson, 2011.. Regression of a Sessile Osteochondroma: A Case Study and Review of the Literature.''' ''&lt;nowiki&gt;https://www.researchgate.net/publication/267426996_Regression_of_a_Sessile_Osteochondroma_A_Case_Study_and_Review_of_the_Literature&lt;/nowiki&gt; . The most common benign bone tumor is osteochondroma.  Its natural history is poorly understood as a consequence of its benign symptomatology in most cases. It typically grows in childhood and growth during adulthood can be a sign of malignant  degeneration. We present  a case of  spontaneous regression of  a solitary osteochondroma.  A review of the  current  literature which  reveals 21  other cases of  spontaneous regression  of solitary  osteochondromas is also discussed. We believe that the possibility of regression of solitary osteochondromas should be taken into account when considering surgical excision.''

'''Viala P, Vanel D, Larbi A, Cyteval C, Laredo JD. Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. Skeletal Radiol. 2012;41:1637–40. [PubMed] &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/22865159/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Viala |first=Pierre |last2=Vanel |first2=Daniel |last3=Larbi |first3=Ahmed |last4=Cyteval |first4=Catherine |last5=Laredo |first5=Jean-Denis |date=2012-12 |title=Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses |url=https://pubmed.ncbi.nlm.nih.gov/22865159 |journal=Skeletal Radiology |volume=41 |issue=12 |pages=1637–1640 |doi=10.1007/s00256-012-1488-0 |issn=1432-2161 |pmid=22865159}}&lt;/ref&gt; ''We report a case of bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. The association of exostoses and femoral metaphyseal widening resulted in the narrowing of the ischiofemoral spaces.''

'''Wang YZ, Park KW, Oh CS, Ahn YS, Kang QL, Jung ST, Song HR. Developmental pattern of the hip in patients with hereditary multiple exostoses. BMC Musculoskelet Disord. 2015;16:54'''''.'' '''https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Wang |first=Ya-Zhou |last2=Park |first2=Kwang-Won |last3=Oh |first3=Chang-Seon |last4=Ahn |first4=Yeong-Seub |last5=Kang |first5=Qing-Lin |last6=Jung |first6=Sung-Taek |last7=Song |first7=Hae-Ryong |date=2015-03-15 |title=Developmental pattern of the hip in patients with hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/ |journal=BMC musculoskeletal disorders |volume=16 |pages=54 |doi=10.1186/s12891-015-0514-5 |issn=1471-2474 |pmc=4429362 |pmid=25888017}}&lt;/ref&gt; '''C'''''oxa valga is a common clinical feature of hereditary multiple exostoses (HME). The current study aimed to determine the unique developmental pattern of the hip in patients with HME and evaluate the factors that influence its progression.''

'''Wiater JM, Farley FA. Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature. Am J Orthop (Belle Mead NJ). 1999 Jul;28(7):412-6. PMID: 10426440.'''&lt;ref&gt;{{Cite journal |last=Wiater |first=J. M. |last2=Farley |first2=F. A. |date=1999-07 |title=Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature |url=https://pubmed.ncbi.nlm.nih.gov/10426440 |journal=American Journal of Orthopedics |volume=28 |issue=7 |pages=412–416 |issn=1078-4519 |pmid=10426440}}&lt;/ref&gt; ''A male 17-year-old with multiple hereditary exostoses presented with a mass in the distal left thigh several days after lifting weights. An arteriogram showed a popliteal artery pseudoaneurysm adjacent to a femoral osteochondroma. The osteochondroma was excised and the artery was repaired with a saphenous vein interposition graft. A review of the literature identified 23 similar reports. The average age of the patients was 21.3 years. Seventy-eight percent were men and half of the patients had multiple hereditary exostoses. Ten patients were initially misdiagnosed. The clinician should consider the diagnosis of pseudoaneurysm in a young patient with an osteochondroma and a mass about the knee.''

'''Zaijun L, Xinhai Y, Zhipeng W, Wending H, Quan H, Zhenhua Z, Dapeng F, Jisheng Z, Wei Z, Jianru X. 2013. Outcome and prognosis of myelopathy and radiculopathy from osteochondroma in the mobile spine: a report on 14 patients. J Spinal Disord Tech 26:194–199.''' ''Fourteen symptomatic spinal osteochondroma (OC)  cases, including 2 hereditary multiple exostoses, were treated surgically from 2001 to 2010.'' 

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt;

= Spanish Translation =


Problemas de deficiencia de proteoglicano de sulfato de heparán (HSPG). La MHE es el resultado de una mutación en los genes EXT1 y EXT2. Los pacientes con MHE tienen una biosíntesis de HSPG defectuosa: sus cuerpos no producen HSPG (cf Cueller et al. 2013 y Jones et al. 2014). Los HSPG son parte de cada superficie celular y regulan los procesos biológicos (cf Zak et al. 2002, Meneghetti et al. 2015). Desempeñan un papel vital en la adhesión, migración, crecimiento y comunicación celular (Vicente et al. 2018). Whitlock e Iozzo (2005) han identificado varias enfermedades relacionadas con la ausencia de HSPG (es decir, si un proceso corporal requiere HSPG y no hay suficiente HSPG para completar esa función, entonces podrían ocurrir estos problemas). Los pacientes con MHE han reportado síntomas como:

* Baja masa ósea (Nozawa et al. 2018 y Matsumoto et al. 2020)
* Deficiencias neurológicas: Trastorno del espectro autista (Li et al, 2002, Fumitoshi et al. 2012, Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); y problemas cognitivos (Farhan et al. 2015)
* Demencia frontotemporal (Narvid et al. 2009) y TDAH (Mooney et al. 2016), función cerebral (Condomitti y Wit 2018). Vea también el vídeo de ratones MHE en &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Enfermedades oculares (Park y Shukla, 2013)
* Defectos dentales (Kucukesmen et al. 2007 y Wiweger et al. 2012)
* Prediabetes (Heibert 2021)Diabetes y dificultad para controlar la glucosa (Matsuzawa 2021)
* Reacciones medicamentosas inusuales (muchos medicamentos actúan sobre el dominio de unión del heparán [Boer y Gaillard 2007]) 
* Fatiga severa y continua (Berg et al. 1999)
* Problemas gástricos graves, incluidas úlceras no causadas por H. pylori (Ascencio et al. 1993 y Chmiela et al. 1995), cáncer gástrico (Weihua et al. 2002) y síndrome de vómitos cíclicos (Kucukesmen et al. 2007 y Theoharides et al. 1999)
* Cálculos renales y otros problemas (véase Van den Born et al. 1993 y Farhan et al. 2015)
* Vértigo e hiperacusia (Lundberg et al., 2014) y migrañas
* Problemas pulmonares (Nackerts et al. 1997 y Haeger et al. 2016)
* Anemia (Poli et al. 2017), coágulos sanguíneos y coagulación (Stringer y Gallagher 1997 y Ho et al. 1997), pseudoaneurismas (Wiater y Farley 1996 y Harari et al. 2024)
* Problemas menstruales y de embarazo extremadamente dolorosos (Alphin et al. 1988, Yin et al. 2018)
* Inflamación (Parroquia 2005); cicatrización lenta de heridas (Zhongjun et al. 2004); cicatrices y queloides (Hosalkar et al. 2007, y problemas del tejido conectivo (Forsberg y Kjellen, 2001 y Otsuka et al. 2020).
* Funciones hepáticas (Arnold et al. 2020 y Dituri et al. 2022)
* Funciones del colesterol y los lípidos (Kolsett y Salmverta 1999) y Síntesis de vitamina D (Cooper 2021)  '''Problemas de crecimiento óseo.''' En la MHE, la falta de HSPG hace que los pacientes desarrollen exostosis, que son tumores benignos en múltiples ubicaciones en todo el cuerpo (Brown 2008, Thompson 2011 y Mansouri et al. 2017). La gravedad (número y tamaño de los tumores y otras complicaciones) de la MHE varía de un paciente a otro. Las exostosis en sí mismas pueden causar numerosos problemas, incluidos: irritación de tendones y músculos que produce dolor y pérdida de movimiento, deformidad esquelética, baja estatura, discrepancia en la longitud de las extremidades, subluxaciones y deformidad angular. Los problemas directamente asociados con estas exostosis incluyen:

* Dolor crónico y problemas con la calidad de vida (Goud et al. 2012)
* Inflamación, respuestas inmunitarias (Callaghan et al. 2018 y Collins y Troeberg 2019)
* Formación de bursa y bursitis resultante, así como artritis de aparición temprana.
* Problemas respiratorios y pulmonares al estar sobre costillas que sobresalen hacia la cavidad torácica (Mazza et al. 2017)
* Irritación de un nervio cercano (dolor, debilidad, entumecimiento, hormigueo)
* Aneurisma de vasos sanguíneos por exostosis que presionan los vasos sanguíneos u otros problemas vasculares (Albokhari et al. 2023)
* Problemas de compresión de la médula espinal: incontinencia, daño nerv'''Résumé de la MEM pour les médecins et les écoles'''

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== Children's Corner ==

=== Teach your child to live with MHE ===
You just got a diagnosis for your child and you are terrified for their life.  Yeah, MHE sucks. And it is a life-long, untreatable disease. Sure you can have surgery, sure, physical therapy helps. But the underlying condition will be there every day for the rest of your life. So. How can you prepare your child to live successfully with MHE?

* '''Believe their pain.''' MHE can have some strange symptoms. Even the bones can subluxate (go in and out) within seconds, so the kid who could not walk two minutes ago is running now. Believe your child. Do not let the doctors gaslight you or your child into pretending that nothing is wrong. 
* '''Let your child master their pain.''' 

=== Advocate for your child with HME in schools ===
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Ahn, YS., Kim, S., Kim, WJ. et al. Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses. BMC Musculoskelet Disord 22, 153 (2021). &lt;nowiki&gt;https://doi.org/10.1186/s12891-021-04021-1&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Ahn |first=Yeong-Seub |last2=Kim |first2=Sungmin |last3=Kim |first3=Woo-Jong |last4=Lim |first4=Jun-Hyuk |last5=Jung |first5=Sung-Taek |date=2021-02-06 |title=Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses |url=https://doi.org/10.1186/s12891-021-04021-1 |journal=BMC Musculoskeletal Disorders |language=en |volume=22 |issue=1 |pages=153 |doi=10.1186/s12891-021-04021-1 |issn=1471-2474 |pmc=7868013 |pmid=33549073}}&lt;/ref&gt; ''Between 2001 and 2019, total 51 patients (102 hips) were evaluated in this study. Patients with MHE were classified to femoro-acetabular impingement (FAI) symptom group, ischio-femoral impingement (IFI) symptom group and non-impingement symptom group by comparing the symptoms, clinical signs and imaging studies.'' 

'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Anel-Quimpo, Joselynna, Mark Anthony Santiago Sandoval, Frances Lina Lantion-Ang, 2011. Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses. BMJ Journals. &lt;nowiki&gt;https://casereports.bmj.com/content/2011/bcr.12.2010.3651&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Anel-Quimpo |first=Joselynna |last2=Sandoval |first2=Mark Anthony Santiago |last3=Lantion-Ang |first3=Frances Lina |date=2011-05-17 |title=Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses |url=https://casereports.bmj.com/content/2011/bcr.12.2010.3651 |journal=BMJ Case Reports |language=en |volume=2011 |pages=bcr1220103651 |doi=10.1136/bcr.12.2010.3651 |issn=1757-790X}}&lt;/ref&gt; ''The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Caino, Silvia, Marisa Angelica Cubilla, Romina Alba, María Gabriela Obregón, Virginia Fano, Abel Gómez, Lorena Zecchini, Pablo Lapunzina, Miriam Aza-Carmona, Karen E. Heath, and et al. 2022. &quot;Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients&quot; Genes 13, no. 11: 2063.''' '''&lt;nowiki&gt;https://doi.org/10.3390/genes13112063&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Caino |first=Silvia |last2=Cubilla |first2=Marisa Angelica |last3=Alba |first3=Romina |last4=Obregón |first4=María Gabriela |last5=Fano |first5=Virginia |last6=Gómez |first6=Abel |last7=Zecchini |first7=Lorena |last8=Lapunzina |first8=Pablo |last9=Aza-Carmona |first9=Miriam |last10=Heath |first10=Karen E. |last11=Asteggiano |first11=Carla Gabriela |date=2022-11-07 |title=Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients |url=https://www.mdpi.com/2073-4425/13/11/2063 |journal=Genes |language=en |volume=13 |issue=11 |pages=2063 |doi=10.3390/genes13112063 |issn=2073-4425 |pmc=9690389 |pmid=36360300}}&lt;/ref&gt; ''Multiple Osteochondromatosis (MO, MIM 133700 &amp; 133701), an autosomal dominant O-glycosylation disorder (EXT1/EXT2-CDG), can be associated with a reduction in skeletal growth, bony deformity, restricted joint motion, shortened stature and pathogenic variants in two tumor suppressor genes, EXT1 and EXT2. In this work, we report a cross-sectional study including 35 index patients and 20 affected family members. Clinical phenotyping of all 55 affected cases was obtained, but genetic studies were performed only in 35 indexes.''

'''Hariri O, Al Laham O, Ibrahim Basha Z, Ghannam E, Ghannam M, Mohammad A. Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review. Int J Surg Case Rep. 2024 Apr 12;118:109633. doi: 10.1016/j.ijscr.2024.109633. Epub ahead of print. PMID: 38626641; PMCID: PMC11035074.'''&lt;ref&gt;{{Cite journal |last=Hariri |first=Omar |last2=Al Laham |first2=Omar |last3=Ibrahim Basha |first3=Zein |last4=Ghannam |first4=Eman |last5=Ghannam |first5=Mohammad |last6=Mohammad |first6=Ammar |date=2024-05 |title=Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review |url=https://journals.lww.com/10.1016/j.ijscr.2024.109633 |journal=International Journal of Surgery Case Reports |language=en |volume=118 |issue=C |doi=10.1016/j.ijscr.2024.109633 |issn=2210-2612 |pmc=11035074 |pmid=38626641}}&lt;/ref&gt; ''We present the case of a 37-year-old Middle Eastern male with Multiple Hereditary Exostoses who experienced sudden-onset left lower limb pain persisting for a month prior to admission. It was associated with coldness and paresthesia of the ipsilateral lower limb. The presurgical radiological workup uncovered a popliteal pseudoaneurysm subsequent to Multiple Hereditary Exostoses.''

'''Kambouris, M., Fadda A, Al-Arraj, Y, et al., 2016. Putative Relation Between Autism Spectrum Disease &amp; Hereditary Multiple Exostosis Investigated by Whole Genome Sequencing &amp; Comparative Genome Analyses in a Family with ASD and HME with EXT-1 Mutations''' ''A family with two male children affected with ASD and HME as well as an unaffected female child, was studied to identify the Genetic basis of ASD in the family and the possible relation between ASD &amp; HME. The HME unaffected parent [mother] contributed heterozygous variants in the Heparan Sulfate biosynthesis pathway that in synergy with the EXT-1 mutation could be the genetic causes of ASD in the family.''

'''Kim, Min Jeong, Yunjin Lee, Sang Ook Nam, Young Mi Kim, 2021. An 8q24.11q24.13 Microdeletion Encompassing EXT1 in a Boy with Autistic Spectrum Disorder, Intellectual Disability, and Multiple Hereditary Exostoses. Annals of Child Neurology. Letter to the Editor, 11/9/2021.''' ''Here, we describe the case of a boy with a microdeletion (8q24.11q24.13 [118,625,768-124,169,620]×1), who presented with autism, intellectual disability, and MHE. the parents signed informed consent and approved the anonymous use of clinical and molecular data for the present diagnostic study'''''.'''

'''Küçükesmen, Çiḡdem DDS, PhD, Buḡra Özen, DDS, PhD,b and Mustafa Akçam, DDS, PhDc, 1997. Multiple Hereditary Osteochondromatosis: A Case Report. Eur J Dent. 2007 Jul; 1(3): 183–187.&lt;nowiki&gt;https://www.ncbi.nlm.nih&lt;/nowiki&gt;.''' ''Common carious lesions owing to vomiting are not widespread in children. In this case, we aimed to report an 11-years-old male patient with common carious lesions due to repeated vomitings, chewing and eating difficulty and retarded growth with Multiple Hereditary Osteochondromatosis (MHO).''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Malagón, V., 2001.  Development of Hip Dysplasia in Hereditary Multiple Exostosis. Journal of Pediatric Orthopaedics, 21(2): 205-211.  &lt;nowiki&gt;https://journals.lww.com/pedorthopaedics/Abstract/2001/03000/Development_of_Hip_Dysplasia_in_Hereditary.14.aspx&lt;/nowiki&gt;''.'''''&lt;ref&gt;{{Cite web |title=Development of Hip Dysplasia in Hereditary... : Journal of Pediatric Orthopaedics |url=https://www.ovid.com/jnls/pedorthopaedics/fulltext/01241398-200103000-00014~development-of-hip-dysplasia-in-hereditary-multiple |access-date=2026-07-16 |website=Ovid |language=en}}&lt;/ref&gt; ''In approximately 25% of patients with hereditary multiple exostosis, there is an abnormal osteochondral formation localized in the femoral proximal metaphysis. Although this entity is rather frequent and quite severe, it is rarely found in the medical literature. The author describes six private cases, taken from a total of 24,000 patients (0.25/1000) as examples of this entity, and provides a review of the literature.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

'''Puiu1, Maria , Iulia Simina-Jurca, Simona Dumitriu, Smaranda Arghirescu,  Adela Chirita-Emandi,  2012. . Multiple Hereditary Exostoses - Clinical Features and Management.''' ''We report two cases of skeletally immature patients who presented with multiple exostoses, bone deformation without bone pain; and growth and pubertal retardation. The cases need adequate counseling, long-term follow-up, and measures to improve the quality of life of patients with multiple hereditary exostoses.''

'''Stitzman Wengrowicz, M.L., J  Pretell-Mazzini,  J.P. Dormans, R.S. Davidson, 2011.. Regression of a Sessile Osteochondroma: A Case Study and Review of the Literature.''' ''&lt;nowiki&gt;https://www.researchgate.net/publication/267426996_Regression_of_a_Sessile_Osteochondroma_A_Case_Study_and_Review_of_the_Literature&lt;/nowiki&gt; . The most common benign bone tumor is osteochondroma.  Its natural history is poorly understood as a consequence of its benign symptomatology in most cases. It typically grows in childhood and growth during adulthood can be a sign of malignant  degeneration. We present  a case of  spontaneous regression of  a solitary osteochondroma.  A review of the  current  literature which  reveals 21  other cases of  spontaneous regression  of solitary  osteochondromas is also discussed. We believe that the possibility of regression of solitary osteochondromas should be taken into account when considering surgical excision.''

'''Viala P, Vanel D, Larbi A, Cyteval C, Laredo JD. Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. Skeletal Radiol. 2012;41:1637–40. [PubMed] &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/22865159/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Viala |first=Pierre |last2=Vanel |first2=Daniel |last3=Larbi |first3=Ahmed |last4=Cyteval |first4=Catherine |last5=Laredo |first5=Jean-Denis |date=2012-12 |title=Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses |url=https://pubmed.ncbi.nlm.nih.gov/22865159 |journal=Skeletal Radiology |volume=41 |issue=12 |pages=1637–1640 |doi=10.1007/s00256-012-1488-0 |issn=1432-2161 |pmid=22865159}}&lt;/ref&gt; ''We report a case of bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. The association of exostoses and femoral metaphyseal widening resulted in the narrowing of the ischiofemoral spaces.''

'''Wang YZ, Park KW, Oh CS, Ahn YS, Kang QL, Jung ST, Song HR. Developmental pattern of the hip in patients with hereditary multiple exostoses. BMC Musculoskelet Disord. 2015;16:54'''''.'' '''https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Wang |first=Ya-Zhou |last2=Park |first2=Kwang-Won |last3=Oh |first3=Chang-Seon |last4=Ahn |first4=Yeong-Seub |last5=Kang |first5=Qing-Lin |last6=Jung |first6=Sung-Taek |last7=Song |first7=Hae-Ryong |date=2015-03-15 |title=Developmental pattern of the hip in patients with hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/ |journal=BMC musculoskeletal disorders |volume=16 |pages=54 |doi=10.1186/s12891-015-0514-5 |issn=1471-2474 |pmc=4429362 |pmid=25888017}}&lt;/ref&gt; '''C'''''oxa valga is a common clinical feature of hereditary multiple exostoses (HME). The current study aimed to determine the unique developmental pattern of the hip in patients with HME and evaluate the factors that influence its progression.''

'''Wiater JM, Farley FA. Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature. Am J Orthop (Belle Mead NJ). 1999 Jul;28(7):412-6. PMID: 10426440.'''&lt;ref&gt;{{Cite journal |last=Wiater |first=J. M. |last2=Farley |first2=F. A. |date=1999-07 |title=Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature |url=https://pubmed.ncbi.nlm.nih.gov/10426440 |journal=American Journal of Orthopedics |volume=28 |issue=7 |pages=412–416 |issn=1078-4519 |pmid=10426440}}&lt;/ref&gt; ''A male 17-year-old with multiple hereditary exostoses presented with a mass in the distal left thigh several days after lifting weights. An arteriogram showed a popliteal artery pseudoaneurysm adjacent to a femoral osteochondroma. The osteochondroma was excised and the artery was repaired with a saphenous vein interposition graft. A review of the literature identified 23 similar reports. The average age of the patients was 21.3 years. Seventy-eight percent were men and half of the patients had multiple hereditary exostoses. Ten patients were initially misdiagnosed. The clinician should consider the diagnosis of pseudoaneurysm in a young patient with an osteochondroma and a mass about the knee.''

'''Zaijun L, Xinhai Y, Zhipeng W, Wending H, Quan H, Zhenhua Z, Dapeng F, Jisheng Z, Wei Z, Jianru X. 2013. Outcome and prognosis of myelopathy and radiculopathy from osteochondroma in the mobile spine: a report on 14 patients. J Spinal Disord Tech 26:194–199.''' ''Fourteen symptomatic spinal osteochondroma (OC)  cases, including 2 hereditary multiple exostoses, were treated surgically from 2001 to 2010.'' 

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt;

= Spanish Translation =


Problemas de deficiencia de proteoglicano de sulfato de heparán (HSPG). La MHE es el resultado de una mutación en los genes EXT1 y EXT2. Los pacientes con MHE tienen una biosíntesis de HSPG defectuosa: sus cuerpos no producen HSPG (cf Cueller et al. 2013 y Jones et al. 2014). Los HSPG son parte de cada superficie celular y regulan los procesos biológicos (cf Zak et al. 2002, Meneghetti et al. 2015). Desempeñan un papel vital en la adhesión, migración, crecimiento y comunicación celular (Vicente et al. 2018). Whitlock e Iozzo (2005) han identificado varias enfermedades relacionadas con la ausencia de HSPG (es decir, si un proceso corporal requiere HSPG y no hay suficiente HSPG para completar esa función, entonces podrían ocurrir estos problemas). Los pacientes con MHE han reportado síntomas como:

* Baja masa ósea (Nozawa et al. 2018 y Matsumoto et al. 2020)
* Deficiencias neurológicas: Trastorno del espectro autista (Li et al, 2002, Fumitoshi et al. 2012, Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); y problemas cognitivos (Farhan et al. 2015)
* Demencia frontotemporal (Narvid et al. 2009) y TDAH (Mooney et al. 2016), función cerebral (Condomitti y Wit 2018). Vea también el vídeo de ratones MHE en &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Enfermedades oculares (Park y Shukla, 2013)
* Defectos dentales (Kucukesmen et al. 2007 y Wiweger et al. 2012)
* Prediabetes (Heibert 2021)Diabetes y dificultad para controlar la glucosa (Matsuzawa 2021)
* Reacciones medicamentosas inusuales (muchos medicamentos actúan sobre el dominio de unión del heparán [Boer y Gaillard 2007]) 
* Fatiga severa y continua (Berg et al. 1999)
* Problemas gástricos graves, incluidas úlceras no causadas por H. pylori (Ascencio et al. 1993 y Chmiela et al. 1995), cáncer gástrico (Weihua et al. 2002) y síndrome de vómitos cíclicos (Kucukesmen et al. 2007 y Theoharides et al. 1999)
* Cálculos renales y otros problemas (véase Van den Born et al. 1993 y Farhan et al. 2015)
* Vértigo e hiperacusia (Lundberg et al., 2014) y migrañas
* Problemas pulmonares (Nackerts et al. 1997 y Haeger et al. 2016)
* Anemia (Poli et al. 2017), coágulos sanguíneos y coagulación (Stringer y Gallagher 1997 y Ho et al. 1997), pseudoaneurismas (Wiater y Farley 1996 y Harari et al. 2024)
* Problemas menstruales y de embarazo extremadamente dolorosos (Alphin et al. 1988, Yin et al. 2018)
* Inflamación (Parroquia 2005); cicatrización lenta de heridas (Zhongjun et al. 2004); cicatrices y queloides (Hosalkar et al. 2007, y problemas del tejido conectivo (Forsberg y Kjellen, 2001 y Otsuka et al. 2020).
* Funciones hepáticas (Arnold et al. 2020 y Dituri et al. 2022)
* Funciones del colesterol y los lípidos (Kolsett y Salmverta 1999) y Síntesis de vitamina D (Cooper 2021)  '''Problemas de crecimiento óseo.''' En la MHE, la falta de HSPG hace que los pacientes desarrollen exostosis, que son tumores benignos en múltiples ubicaciones en todo el cuerpo (Brown 2008, Thompson 2011 y Mansouri et al. 2017). La gravedad (número y tamaño de los tumores y otras complicaciones) de la MHE varía de un paciente a otro. Las exostosis en sí mismas pueden causar numerosos problemas, incluidos: irritación de tendones y músculos que produce dolor y pérdida de movimiento, deformidad esquelética, baja estatura, discrepancia en la longitud de las extremidades, subluxaciones y deformidad angular. Los problemas directamente asociados con estas exostosis incluyen:

* Dolor crónico y problemas con la calidad de vida (Goud et al. 2012)
* Inflamación, respuestas inmunitarias (Callaghan et al. 2018 y Collins y Troeberg 2019)
* Formación de bursa y bursitis resultante, así como artritis de aparición temprana.
* Problemas respiratorios y pulmonares al estar sobre costillas que sobresalen hacia la cavidad torácica (Mazza et al. 2017)
* Irritación de un nervio cercano (dolor, debilidad, entumecimiento, hormigueo)
* Aneurisma de vasos sanguíneos por exostosis que presionan los vasos sanguíneos u otros problemas vasculares (Albokhari et al. 2023)
* Problemas de compresión de la médula espinal: incontinencia, daño nerv'''Résumé de la MEM pour les médecins et les écoles'''

== References ==</text>
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[[W: Hereditary Multiple Exostoses|Hereditary Multiple Exostoses]] is a rare disease. It is also referred to as Multiple Hereditary Exostoses, hereditary multiple osteochondromas, and Multiple Osteochondromedas.

== Bone Issues ==
The first sign of HME is usually multiple bone tumors. See the online Multiple Osteochondromas Mutation Database  for an overview of the reported variants.&lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123 |issn=1098-1004}}&lt;/ref&gt;  In MHE, the lack of HSPG causes patients to develop exostoses, which are benign tumors in multiple locations throughout the body (Brown 2008, Thompson 2011, and Mansouri et al. 2017). The severity (number and size of tumors and other complications) for MHE varies from patient to patient. Exostoses themselves can cause numerous problems including: irritation of tendons and muscles resulting in pain and loss of motion, skeletal deformity, short stature, limb length discrepancy, subluxations, and angular deformity, with a chance for chondrosarcoma (Fei et al. 2018). Problems directly associated with these exostoses include:

* Chronic pain and issues with quality of life (Goud et al. 2012, Bathen et al. 2019, Tremorsini 2025)
* Inflammation, immune responses (Callaghan et al. 2018, Collins and Troeberg 2019)  
* Bursa formation (Rueda et al. 2025) and resulting bursitis as well as early onset arthritis 
* Breathing and lung issues when on ribs protruding into the thoracic cavity (Mazza et al. 2017)
*  Irritation of a nearby nerve (pain, weakness, numbness, tingling) 
*  Blood vessel aneurysm from exostoses pressing on blood vessels or other vascular problems (Albokhari et al. 2023)
* Spinal cord compression issues: incontinence, nerve damage and nerve problems associated with spinal tumors (Bari et al. 2012, Burki et al. 2011, Zaijun et al. 2013, Montgomery et al. 2019, and Monroig-Rivera et al. 2025)

== List of associated issues ==
'''Heparan Sulfate ProteoGlycan (HSPG) Deficiency Issues.''' MHE results from a mutation in the EXT1 and EXT2 genes.  MHE patients have defective HSPG biosynthesis--their bodies do not produce HSPG ('''cf''' Cueller et al. 2013, Jones et al,. 2014, and Pacifici et al. 2019&lt;ref name=&quot;:7&quot;&gt;{{Cite journal |last=Pacifici |first=Maurizio |date=2018-10 |title=The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC6015767/ |journal=Matrix Biology: Journal of the International Society for Matrix Biology |volume=71-72 |pages=28–39 |doi=10.1016/j.matbio.2017.12.011 |issn=1569-1802 |pmc=6015767 |pmid=29277722}}&lt;/ref&gt;).  HSPGs are part of every cell surface and regulate biological processes ( '''cf''' Zak et al. 2002, Meneghetti et al. 2015). HSPGs  play a vital role in cell adhesion, migration, growth, and communication (Bishop et al. 20017, Kempf et al 2017, Vicente et al. 2018). Whitlock and Iozzo (2005) have identified '''various diseases related to HSPG's absence''' (i.e., i'''f a body process requires HSPG and there is not enough HSPG to complete that function, then these issues could occur).  MHErs reported symptoms such as:'''

* Severe and continuing fatigue (Berg et al. 1999, Bathen 2019) 
* Neurological deficiencies: Autism Spectrum Disorder (Fumitoshi et al. 2012,  Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); cognitive issues (Farhan et al. 2015); tremors (Aldunate et al. 2004)
* Vertigo and hyperacusis (Lundberg et al., 2014) and migraines
* Low bone mass (Nozawa et al. 2018 and Matsumoto et al. 2020) 
* Severe gastric issues  (Huang et al. 2018, Rueda et al. 2025) , including non ''H. Pylori'' ulcers (Ascencio et al. 1993 and Chmiela et al. 1995), gastric cancer (Weihua et al. 2002) and Cyclic Vomiting Syndrome (Kucukesmen et al. 2007)
* Fronto-temporal dementia (Narvid et al. 2009) and ADHD (Mooney et al. 2016), brain function (Condomitti and Wit 2018). Also see video of MHE mice at &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Eyesight/ocular diseases (Park and Shukla, 2013)
* Dental defects (Kucukesmen et al. 2007 and Wiweger et al. 2012)
* Prediabetes  (Heibert 2021)Diabetes and glucose difficulty (Matsuzawa 2021)
* Unusual drug reactions (many drugs act on heparan-binding domain [Boer and Gaillard 2007])
* Kidney stones and other problems (See Van den Born et al. 1993 and Farhan et al. 2015)
* Lung issues (Nackerts et al. 1997 and Haeger et al. 2016)
* Anemia (Poli et al. 2017), blood clots and coagulation (Stringer and Gallagher 1997 and Ho et al. 1997), psuedoaneurysms (Wiater and Farley 1996 and Harari et al. 2024)
* Extremely painful menstruation and pregnancy issues (Alphin et al. 1988, Yin et al. 2018)
* Inflammation (Parish 2005); slow wound healing (Zhongjun et al. 2004); scarring and keloids  (Hosalkar et al. 2007)
* Connective tissue issues (Forsberg and Kjellen, 2001 and Otsuka et al. 2020).
* Liver functions (Arnold et al. 2020 and Dituri et al. 2022)
* Cholesterol and lipid functions (Kolsett and Salmverta 1999)
* Deficient Vitamin D synthesis (Cooper 2021)

== Children's Corner ==

=== Teach your child to live with MHE ===
You just got a diagnosis for your child and you are terrified for their life.  Yeah, MHE sucks. And it is a life-long, untreatable disease. Sure you can have surgery, sure, physical therapy helps. But the underlying condition will be there every day for the rest of your life. So. How can you prepare your child to live successfully with MHE?

* '''Believe their pain.''' MHE can have some strange symptoms. Even the bones can subluxate (go in and out) within seconds, so the kid who could not walk two minutes ago is running now. Believe your child. Do not let the doctors gaslight you or your child into pretending that nothing is wrong.
* '''Let your child master their pain.''' Give your child as much control and autonomy as possible. Provide a &quot;pain corner&quot; with comfy pillows, their favorite toys, quiet activities, warmies or coolies. Let your child go to that pain area whenever they feel the need--when they are tired or in pain. This lets them regulate their own pain and functions. 
* '''Teach your child to brainstorm and plan around problems.''' Pain and limited mobility may limit certain options, but life still goes on. So when your child can not do something, brainstorm with them. Use your imaginations. You can not climb these steps. Ok, how can you get into the room? Can you slide on your butt? Should we get a giraffe from next door to help out? (Throw in silly suggestions because that expands their imagination and puts a bit of humor into the situation.) 

=== Advocate for your child with HME in schools ===
It is vital to advocate for your child so that they can work well in schools. Here are some suggested ways to ask for accommodations for this complex disease. Note that not every child will need all of these accommodations. 

My child has MHE, which involves bony bumps on their bones that can vary in size, location, and number as well as some neurological and other physical symptoms.Accommodations are needed for my child’s symptoms, which include:

*  '''Limited mobility.&lt;ref name=&quot;:1&quot;&gt;{{Cite journal |last=Amajjar |first=Ihsane |last2=Vergauwen |first2=Kuni |last3=Willigenburg |first3=Nienke W. |last4=Huijnen |first4=Ivan P. J. |last5=Smeets |first5=Rob J. E. M. |last6=Ham |first6=S. John |date=2025-05-30 |title=Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study |url=https://www.nature.com/articles/s41598-025-02812-3 |journal=Scientific Reports |language=en |volume=15 |issue=1 |pages=18990 |doi=10.1038/s41598-025-02812-3 |issn=2045-2322}}&lt;/ref&gt;''' Allow my child to participate in sports and in activities to the best of their abilities. When starting something new, allow my child to go last and ask my child privately if they can perform that action. If not, quietly allow them to pursue a different prearranged activity. Note that mobility changes daily and sometimes hourly, depending on the bone growth stages, whether muscle has moved over a bone growth,  or other complications.
*  '''Neurological symptoms'''. My child has Asperger-like and ADHD symptoms,&lt;ref name=&quot;:4&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://www.pnas.org/doi/abs/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109}}&lt;/ref&gt;&lt;ref name=&quot;:5&quot;&gt;{{Cite journal |last=Irie |first=Fumitoshi |last2=Badie-Mahdavi |first2=Hedieh |last3=Yamaguchi |first3=Yu |date=2012-03-27 |title=Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate |url=https://pnas.org/doi/full/10.1073/pnas.1117881109 |journal=Proceedings of the National Academy of Sciences |language=en |volume=109 |issue=13 |pages=5052–5056 |doi=10.1073/pnas.1117881109 |issn=0027-8424 |pmc=3323986 |pmid=22411800}}&lt;/ref&gt;&lt;ref name=&quot;:8&quot;&gt;{{Cite journal |last=Pérez |first=Christine |last2=Sawmiller |first2=Darrell |last3=Tan |first3=Jun |date=2016-04-18 |title=The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation |url=https://doi.org/10.1186/s13064-016-0066-x |journal=Neural Development |language=en |volume=11 |issue=1 |pages=11 |doi=10.1186/s13064-016-0066-x |issn=1749-8104 |pmc=4836088 |pmid=27089953}}&lt;/ref&gt; so please engage all measures for children on the spectrum as well as ADHD. Bone tumors on the spine can also create neurological issues.&lt;ref name=&quot;:2&quot;&gt;{{Cite web |url=https://www.semanticscholar.org/paper/Hereditary-multiple-exostoses-causing-cord-Bari-Alam/4687ea7d1225f1ecf4ecf4742a794f84576dce6d/figure/0 |access-date=2026-07-15 |website=www.semanticscholar.org}}&lt;/ref&gt; Please understand that bright lights or sound may cause pain or other issues. Please report any behavioral issues so that we can determine if MHE may be underlying these problems and we can address the issues with reasonable accommodations and an Individual Education Plan.
*  '''Frequent pain and fatigue&lt;ref name=&quot;:0&quot;&gt;{{Cite journal |last=Mitchell |first=Christina M. |last2=Beals |first2=Janette |last3=Whitesell |first3=Nancy Rumbaugh |last4=Voices of Indian Teens team |last5=Pathways of Choice team |date=2008-09 |title=Alcohol use among American Indian high school youths from adolescence and young adulthood: a latent Markov model |url=https://pubmed.ncbi.nlm.nih.gov/18781241 |journal=Journal of Studies on Alcohol and Drugs |volume=69 |issue=5 |pages=666–675 |issn=1937-1888 |pmc=2575396 |pmid=18781241}}&lt;/ref&gt;'''. If my child is in pain or is tired, allow them to rest in preplanned area with preplanned quiet activities (reading, watching an educational video, etc.). This area should be equipped with a heating pad and medication should be dispensed as agreed upon by me and the school.  
* '''Writing difficulties'''.&lt;ref name=&quot;:1&quot; /&gt; My child may have extra bones on their wrists or hands, making writing painful. Please allow my child to use a computer.  Typing may be slow and please allow other software such as Dragon Naturally Speaking or Otter AI.
*  '''Coordination difficulties'''. My child may have neurological difficulties and problems coordinating eyesight. Please allow more time for tests if needed. Administer tests that require filling in bubbles in an alternative method.
* '''Incontinence/Vomiting'''. Please allow my child free access to the restroom without requiring a pass for sudden issues. Keep a spare set of clothing at the school in case of accidents.
* '''Hall passes.'''  Give my child access to the nurse and bathroom as they determine that they need to go. My child may have bathroom urgencies or need to get pain medication quickly. My child may also have a limb that has &quot;gone out&quot; or stopped working for a few seconds to a few days and will need to attend to that medical urgency. 

=== Advocation Laws and Directives ===
In U.S. cite Section 504 of the Rehabilitation Act.


= How to Respond to Doctors =
There are suggested treatment protocols for MHE (see Rueda et al., 2025). However, MHE is a rare disease, and you will probably be the first patient that a medical practitioner has ever seen with this disease.  Try to be patient with the doctors and get doctors who work with you as a partner--you having lived with MHE do know a lot about your body! Ill-informed or too-busy doctors often rely on research that is outdated or inaccurate. Here are some common misconceptions that a doctor might tell you and how to respond. Before you go to the doctor, write out your questions. Take someone with you to take notes. Advocate for yourself! 

1.'''I have never seen an MHE patient. Surely this is just a bone condition!''' The condition involves much more than bone growths. MHErs do not biosynthesize heparan sulfate proteoglycans (HSPG), in much the same way that diabetics do not biosynthesize insulin (see Cueller et al. 2013 and Jones et al. 2014). Those HSPGs play a vital role in pretty much every single cell and every system in a human body (Bishop et al. 2017). Therefore, since I do not have sufficient levels of HSPG, I can have many different problems. Let's rule out anything comorbid (in other words, any other disease I might have at the same time). IF we can not find something to explain the cause of my symptoms of {REPEAT YOUR SYMPTOMS HERE} then we can blame the MHE and treat the symptoms.

'''2. You do not feel pain. It is just stress.'''  Bone does not have nerves, therefore there is no pain.  Even if that were true (which it is not--see Nencini and Ivanusic 2016&lt;ref name=&quot;:6&quot;&gt;{{Cite journal |last=Nencini |first=Sara |last2=Ivanusic |first2=Jason J. |date=2016-04-26 |title=The Physiology of Bone Pain. How Much Do We Really Know? |url=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157/full |journal=Frontiers in Physiology |language=English |volume=7 |doi=10.3389/fphys.2016.00157 |issn=1664-042X |pmc=4844598 |pmid=27199772}}&lt;/ref&gt; for example ), then you wouldn't mind putting a stone in your shoe, right? Because the stone would not feel any pain. Oh, you wouldn't like that because it might hurt? Really? Ok. So I have an extra bone (LIKE A STONE) where there should only be muscle, nerve, and ligaments (LIKE A FOOT). For MHE-specific pain studies, see Darilek et al. 2005.

3. '''Your MHE did not cause x symptom.'''  I had one MHE patient (or read a case study) and they did not have x symptom, so therefore you do not have x symptom (or x symptom is unrelated). MHE is a rare and complex disease. Sometimes medical professionals will resort to explanations of hypochondria or Munchausens to explain away something that they do not understand. MHE is different for each patient, as there are different genetic mutations (EXT1, EXT2, EXT3 genes all play a role, as well as your other genetic profiles). There is not enough research to determine whether your symptoms are or are not caused by MHE. It is best to work with a doctor who will look for causes and accept that your MHE is not the same as anyone else's--including your own family members. Also, look at the list below for similar case studies on HME.  

'''4. No one else has had that reaction to that drug. You are lying or mistaken.''' No. HSPG plays a role in nearly every body function and is assumed to be present. My body does not produce HSPG. Therefore my drug interactions may well differ!&lt;ref name=&quot;:3&quot;&gt;{{Cite journal |last=Boer |first=A. G. de |last2=Gaillard |first2=P. J. |date=2007-02-10 |title=Drug Targeting to the Brain |url=https://www.annualreviews.org/content/journals/10.1146/annurev.pharmtox.47.120505.105237 |journal=Annual Review of Pharmacology and Toxicology |language=en |volume=47 |issue=Volume 47, 2007 |pages=323–355 |doi=10.1146/annurev.pharmtox.47.120505.105237 |issn=0362-1642}}&lt;/ref&gt;  

5. '''The bones do not grow past puberty. If they have, then it is cancer.''' While studies have assumed this, it is not true. This has not been well researched, because it is difficult to have full xrays and to monitor over a lifetime, which would be required for absolute proof. But while there is a slight chance of chondrosarcoma, other MHE patients have reported bone growth past puberty. See the pictures of the 92- year old woman's skeleton with MHE. Bones grew back over her surgeries at age 70 and 80. If bones do not grow back, how do you explain the growths on her implants?

=== Questions to ask doctors if you are not being taken seriously ===
'''Scripts to Use When You Feel Dismissed'''

'''• This is affecting my daily life. I can not function well with this problem.''' Show pictures. Keep a diary of your pain and what you are not able to do. For example: When the tumor on my rib prevents me from raising my arm, I can not dress myself or brush my hair. When the fatigue is so bad, I can not go to class. When the pain is over a 5 (slamming your hand in a car door) continually, then I can not think well.

'''• Yes, the test results you got were normal, but I have problems.''' However, there are no tests for Heparan Sulfate Proteoglycans, which may play a role. Therefore, we need to look deeper. I still have these issues. Explain again that you have MHE and do not biosynthesize HSPG, which plays a role in every cell. Look for common problems--because of course you can still have those! But do not let the doctor gaslight you into thinking it is all in your head. If nothing else, look in Google Scholar with HSPG and your symptom. 

'''• I’m still concerned. Can we talk about next steps?'''  What can we do, and how long should we wait to see if that step works? Ask again about your specific symptom. There may be a medication to try, or physical therapy. Note what you have tried--keep a record!

'''Scripts for When Symptoms Are Minimized'''

'''• This may seem mild to you, but this is really affecting my life.''' Again, be specific. Use the analogy of a rock in your shoe or anything else that makes sense to you.

'''• I'm a zebra. I have a rare complex disease. What can we do?''' Again remind them that MHE is a complex systemic disease and the extra bones are only one symptom of a wider range of problems stemming from not biosynthesizing  HSPG. 

• '''While this may seem mild, I think it is part of an overall pattern. This symptom is persistent and worsening, which is why I’m concerned.''' (Keep a diary. Keep images over time). 

'''Scripts for Redirecting the Conversation'''

'''• I know my body is complex. But here is my main issue now--let's focus on that'''. Before your appointment, write out and send a list of your main symptoms. This is a complex disease and you will not get to everything.

• '''Can we  go back to what I mentioned earlier?''' I know that everything is connected, but I am most concerned about ... so I can live my life. Keep that list. Have someone else in the room taking notes on that list of symptoms. 

'''• Please send me a copy of my medical chart.''' I want to be sure my concern is documented in my chart. Always ask for a copy of your medical records, including doctors' notes.

'''Scripts for Asking for Clarification'''

• “Can you explain why you don’t think further evaluation is needed?” (MHE is a life long condition.)

• “What would be a red flag that should prompt me to follow up?” (Ask about red flags for chondrosarcoma)

• “If this doesn’t improve, what’s the next step?” (Get referrals.)

= Research and medical studies =
Italics after a citation is a sentence directly from that work that summarizes the main points for HME patients and their doctors. Please go to the actual study cited. 

== HME Specific studies ==
'''Amajjar I, Vergauwen K, Willigenburg NW, Huijnen IPJ, Smeets RJEM, Ham SJ, 2025, Scientific report. Physical activity level and health-related quality of life in adults with multiple osteochondromas: a Dutch cross-sectional study. 2045-2322, 2025 May 30, Vol. 15, Issue 1'''&lt;ref name=&quot;:1&quot; /&gt; ''Multiple Osteochondromas (MO) can significantly impact physical functioning,..These results underscore the need for targeted interventions focusing on pain management, psychological factors, and lifestyle changes to improve both PAL and HRQOL in MO patients.''

'''Bathen T, Fredwall S, Steen U, 2019. Fatigue and pain in children and adults with multiple osteochondromas in Norway, a cross-sectional study. International journal of orthopaedic and trauma nursing [Int J Orthop Trauma Nurs] 2019 Aug; Vol. 34, pp. 28-35. Date of Electronic Publication: 2019 Feb 10.  ISSN: 18781241''' &lt;ref name=&quot;:0&quot; /&gt; ''Background: Multiple Osteochondromas (MO) is a rare skeletal disorder frequently needing orthopaedic surgery. High prevalence of pain has been reported, however fatigue has not previously been investigated.'' ''Results: Children with MO reported significantly higher fatigue than healthy children. Adults reported significantly higher fatigue than the general Norwegian population. Six of 11 children and 20 of 21 adults reported pain. Severe fatigue was more prevalent in persons with high age, high pain intensity and many pain locations; however none of these differences were significant.''

'''Burki, Vincent, Alexander So, Bérengère Aubry-Rozier, 2011. Cervical myelopathy in hereditary multiple exostoses, Joint Bone Spine, Volume 78, Issue 4, &lt;nowiki&gt;https://doi.org/10.1016/j.jbspin.2011.02.021&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Burki |first=Vincent |last2=So |first2=Alexander |last3=Aubry-Rozier |first3=Bérengère |date=2011-07 |title=Cervical myelopathy in hereditary multiple exostoses |url=https://linkinghub.elsevier.com/retrieve/pii/S1297319X11000558 |journal=Joint Bone Spine |language=en |volume=78 |issue=4 |pages=412–414 |doi=10.1016/j.jbspin.2011.02.021}}&lt;/ref&gt;'''.''' ''Spinal cord compression due to cervical exostoses is a rare but recognized complication of hereditary multiple exostosis (HME), an autosomal dominant disorder. This disease, also called multiple osteochondromatosis, is characterised by osteocartilaginous exostoses, typically involving the juxtaepiphyseal regions of long bones. Complications such as transformation to sarcoma (1 to 5%) or neurological compression (of the spinal cord, 1 to 9%) can arise during the course of the disease.''

'''Bukowska-Olech Ewelina, Trzebiatowska Wiktoria, Czech Wiktor, Drzymała Olga, Frąk Piotr, Klarowski Franciszek, Kłusek Piotr, Szwajkowska Anna, Jamsheer Aleksander, Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies. &lt;nowiki&gt;https://www.frontiersin.org/article/10.3389/fgene.2021.759129&lt;/nowiki&gt; '''&lt;ref&gt;{{Cite journal |last=Bukowska-Olech |first=Ewelina |last2=Trzebiatowska |first2=Wiktoria |last3=Czech |first3=Wiktor |last4=Drzymała |first4=Olga |last5=Frąk |first5=Piotr |last6=Klarowski |first6=Franciszek |last7=Kłusek |first7=Piotr |last8=Szwajkowska |first8=Anna |last9=Jamsheer |first9=Aleksander |date=2021-12-10 |title=Hereditary Multiple Exostoses—A Review of the Molecular Background, Diagnostics, and Potential Therapeutic Strategies |url=https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2021.759129/full |journal=Frontiers in Genetics |language=English |volume=12 |doi=10.3389/fgene.2021.759129 |issn=1664-8021 |pmc=8704583 |pmid=34956317}}&lt;/ref&gt; ''' '''''Hereditary multiple exostoses (HMEs) syndrome, also known as multiple osteochondromas, represents a rare and severe human skeletal disorder. The disease may severely affect the quality of patients’ life due to motion impairments, skeletal deformations, chronic pain, or growth retardation and possibility of malignant transformation of exostoses.''

'''Darilek, Sandra MS*; Wicklund, Catherine MS†; Novy, Diane PhD‡; Scott, Allison MD§; Gambello, Michael MD, PhD*; Johnston, Dennis PhD¶; Hecht, Jacqueline PhD*. Hereditary Multiple Exostosis and Pain. Journal of Pediatric Orthopaedics 25(3):p 369-376, May 2005. | DOI: 10.1097/01.bpo.0000150813.18673.''' ''This study was undertaken to characterize pain in individuals with hereditary multiple exostosis (HME).  Eighty-four percent of participants reported having pain, indicating that pain is a real problem in HME.''

'''Fei, Li,  Clara Ngoh, Daniel E. Porter, Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model, Journal of Bone Oncology, Volume 13, 2018, Pages 114-122, ISSN 2212-1374, &lt;nowiki&gt;https://doi.org/10.1016/j.jbo.2018.09.011&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Fei |first=Li |last2=Ngoh |first2=Clara |last3=Porter |first3=Daniel E. |date=2018-11-01 |title=Chondrosarcoma transformation in hereditary multiple exostoses: A systematic review and clinical and cost-effectiveness of a proposed screening model |url=https://www.sciencedirect.com/science/article/pii/S2212137418300903 |journal=Journal of Bone Oncology |volume=13 |pages=114–122 |doi=10.1016/j.jbo.2018.09.011 |issn=2212-1374 |pmc=6303411 |pmid=30591865}}&lt;/ref&gt;''  The most serious complication of hereditary multiple exostoses (HME) is chondrosarcoma transformation. Three HME screening strategies were then developed and compared using cost per life-year gained and incremental cost-effectiveness ratio (ICER).''

'''Goud, A. L., de Lange, J., Scholtes, V. A. B., Bulstra, S. K., &amp; Ham, S. J. (2012). Pain, Physical and Social Functioning, and Quality of Life in Individuals with Multiple Hereditary Exostoses in the Netherlands. Journal of Bone and Joint Surgery-American Volume, 94A(11), 1013-1020. &lt;nowiki&gt;https://doi.org/10.2106/JBJS.K.00406&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |title=Pain, Physical and Social Functioning, and... : Journal of Bone and Joint Surgery |url=https://www.ovid.com/jnls/jbjsjournal/fulltext/10.2106/jbjs.k.00406~pain-physical-and-social-functioning-and-quality-of-life-in |access-date=2026-07-16 |website=Ovid |language=en |doi=10.2106/JBJS.K.00406}}&lt;/ref&gt; ''Our study confirms that multiple hereditary exostoses is a chronic disease causing a profound impact on quality of life. The results suggest that pain is not the only problem associated with multiple hereditary exostoses, as it has an extensive influence on daily activities, as well as on social and psychological well-being, causing significant disability.''

'''Hosalkar, Harish MD, MBMS (Ortho), FCPS (Ortho), DNB (Ortho)*; Greenberg, Jared MD†; Gaugler, Rebecca L. BS‡; Garg, Sumeet MD§; Dormans, John P. MD∥, 2007. Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses Journal of Pediatric Orthopaedics: May 2007 - Volume 27 - Issue 3 - p 333-337 doi: 10.1097/BPO.0b013e3180326732'''&lt;ref&gt;{{Cite journal |last=Hosalkar |first=Harish |last2=Greenberg |first2=Jared |last3=Gaugler |first3=Rebecca L. |last4=Garg |first4=Sumeet |last5=Dormans |first5=John P. |date=2007-05 |title=Abnormal Scarring With Keloid Formation After Osteochondroma Excision in Children With Multiple Hereditary Exostoses |url=https://journals.lww.com/01241398-200704000-00017 |journal=Journal of Pediatric Orthopaedics |language=en |volume=27 |issue=3 |pages=333–337 |doi=10.1097/BPO.0b013e3180326732 |issn=0271-6798}}&lt;/ref&gt;  ''Although this study has limited numbers, the results demonstrate a statistically significant correlation between keloid formation and MHE. The risk for abnormal scarring and keloid formation should be discussed with all patients before surgery.''

'''Matsumoto, K., Ogawa, H., Nozawa, S. et al. An analysis of osteoporosis in patients with hereditary multiple exostoses. Osteoporos Int 31, 2355–2361 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s00198-020-05533-7&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Matsumoto |first=K. |last2=Ogawa |first2=H. |last3=Nozawa |first3=S. |last4=Akiyama |first4=H. |date=2020-12-01 |title=An analysis of osteoporosis in patients with hereditary multiple exostoses |url=https://doi.org/10.1007/s00198-020-05533-7 |journal=Osteoporosis International |language=en |volume=31 |issue=12 |pages=2355–2361 |doi=10.1007/s00198-020-05533-7 |issn=1433-2965}}&lt;/ref&gt; ''We analyzed osteoporosis in 20 HME patients. Our results indicate HME patients have low bone mass. They do not have abnormal bone metabolism.''

'''Monroig-Rivera, Carlos MD1; Bockhorn, Lauren MD1,2; Thornberg, David BS1; Santillan, Brenda BS1,2; Rathjen, Karl E. MD1,2,a. Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses. JBJS Open Access 10(1):e24.00072, January-March 2025. | DOI: 10.2106/JBJS.OA.24.00072.''' &lt;ref&gt;{{Cite journal |last=Monroig-Rivera |first=Carlos |last2=Bockhorn |first2=Lauren |last3=Thornberg |first3=David |last4=Santillan |first4=Brenda |last5=Rathjen |first5=Karl E. |date=2025-01 |title=Prevalence of Osteochondromas in the Spine in Patients with Multiple Hereditary Exostoses |url=https://journals.lww.com/10.2106/JBJS.OA.24.00072 |journal=JBJS Open Access |language=en |volume=10 |issue=1 |doi=10.2106/JBJS.OA.24.00072 |issn=2472-7245}}&lt;/ref&gt;''Although nearly half of the patients had spinal osteochondromas, neural impingement was rare (4%). Neither age, gender, nor the presence of rib and pelvic osteochondromas were associated with spinal involvement, osteochondromas in the canal, or neural impingement. This information can be used to guide clinical decision-making regarding the use of MRI scans for patient screening'''''.'''

'''Phan, A. Q., Pacifici, M., &amp; Esko, J. D. (2017). Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference. Connective Tissue Research, 59(1), 85–98. &lt;nowiki&gt;https://doi.org/10.1080/03008207.2017.1394295&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite web |url=https://www.tandfonline.com/action/cookieAbsent |access-date=2026-07-16 |website=www.tandfonline.com |doi=10.1080/03008207.2017.1394295 |pmc=7604901 |pmid=29099240}}&lt;/ref&gt;''  MHE, also known as hereditary multiple exostoses (HME) or multiple osteochondromas (MO), is characterized by cartilage-capped outgrowths called osteochondromas that develop adjacent to the growth plates of skeletal elements in young patients. These benign tumors can affect growth plate function, leading to skeletal growth retardation, or deformations, and can encroach on nerves, tendons, muscles, and other surrounding tissues and cause motion impairment, chronic pain, and early onset osteoarthritis. In about 2–5% of patients, the osteochondromas can become malignant and life threatening.''

'''Rueda-de-Eusebio, A., Gomez-Pena, S., Moreno-Casado, M.J. et al. Hereditary multiple exostoses: an educational review. Insights Imaging 16, 46 (2025). &lt;nowiki&gt;https://doi.org/10.1186/s13244-025-01899-6&lt;/nowiki&gt;''' ''  This review summarises current knowledge on the clinical presentation, pathogenesis, imaging characteristics, complications, and treatment of HME.''

'''Stiever, JR., and J.P. Dormans (2005). Manifestations of hereditary multiple exostoses. Journal of the American Academy of Orthopaedic Surgeons, 13: 110-120'''''.'' '''&lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/15850368/&lt;/nowiki&gt;''' ''Hereditary multiple exostosis is an autosomal dominant disorder manifested by the presence of multiple osteochondromas. Linkage analysis has implicated mutations in the EXT gene family, resulting in an error in the regulation of normal chondrocyte proliferation and maturation that leads to abnormal bone growth. Although exostoses are benign lesions, they are often associated with characteristic progressive skeletal deformities and may cause clinical symptoms. Patients with hereditary multiple exostosis have a slight risk of sarcomatous transformation of the cartilaginous portion of the exostosis.''

'''Tremosini, M., Morri, M., Forni, C., Pedrini, E., Mordenti, M., Gnoli, M., Di Cecco, A., Moroni, A., &amp; Sangiorgi, L. (2025). Pain in patients with multiple inherited osteochondromas: Incidence and potential prognostic factors. Journal of Bone Oncology, 52, 100672.''' ''Purpose: the purpose of this study was to describe the baseline characteristics, presenting phenotype and treatment interventions for patients diagnosed with multiple osteochondromas who presented with severe pain'' ''symptoms. .Conclusion: from the early stages of multiple osteochondromas diagnosis, pain symptoms must be carefully assessed. An increase in age is associated with a worsening of pain; IOR classification of the multiple osteo-chondromas phenotype does not currently allow an association between the various classes and pain. A re-evaluation of the classification in this light could be an important new element for clinical practice.''

'''Van der Woude HJ, Flipsen M, Welsink C, Van der Zwan AL, Ham SJ, 2025. Is total-body MRI useful as a screening tool to rule out malignant progression in patients with multiple osteochondromas? Results in a single-center cohort of 319 adult patients. By''''':''  '''Skeletal radiology, 1432-2161, 2024 Jan, Vol. 53, Issue 1.'''''To evaluate the results of total-body (TB) MRI used as a screening tool for assessment or exclusion of malignant transformation in patients with hereditary multiple osteochondromas (HMO). Conclusion: TB-MRI can identify malignant transformation of osteochondromas in HMO patients. All peripheral chondrosarcomas occurred in flat bones (ribs, scapula, pelvis) in our study. TB-MRI might assist in triage between higher risk patients with a high burden of OC, including the location of OC in main flat bones vs lower risk patients without OC of the flat bones.''

'''Wiweger, Malgorzata I. Wiweger, Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, and Pancras C. W. Hogendoorn, 2012. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. PLOS 1. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;'''''.'' ''Here we analyse dental defects present in ext2−/− fish. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth. Our findings from zebrafish model were validated in a dental survey that was conducted with assistance of the MHE Research Foundation. The presence of the malformed and/or displaced teeth with abnormal enamel was declared by half of the respondents indicating that MO might indeed be also associated with dental problems.''

'''Wiweger, M.I., Zhe Zhao, Richard J. P. van Merkesteyn, Henry H. Roehl, Pancras C. W. Hogendoorn. HSPG-Deficient Zebrafish Uncovers Dental Aspect of Multiple Osteochondromas. Published: January 11, 2012. &lt;nowiki&gt;https://doi.org/10.1371/journal.pone.0029734&lt;/nowiki&gt;''' ''Multiple Osteochondromas (MO; previously known as multiple hereditary exostosis) is an autosomal dominant genetic condition that is characterized by the formation of cartilaginous bone tumours (osteochondromas) at multiple sites in the skeleton, secondary bursa formation and impingement of nerves, tendons and vessels, bone curving, and short stature. MO is also known to be associated with arthritis, general pain, scarring and occasional malignant transformation of osteochondroma into secondary peripheral chondrosarcoma. MO patients present additional complaints but the relevance of those in relation to the syndromal background needs validation. Histological analysis reveals that ext2−/− fish have very severe defects associated with the formation and the morphology of teeth.''

'''Yamaguchi, Yu. Research on rare bone disorder reveals new insights into autism. &lt;nowiki&gt;https://www.eurekalert.org/news-releases/857331&lt;/nowiki&gt; March 2012,''' ''Sanford-Burnham researchers discover the molecular basis of autistic symptoms in children with a rare bone disorder -- findings that also provide new insights for the general autistic population.Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) used a mouse model of MHE to investigate cognitive function. They found that mice with a genetic defect that models human MHE show symptoms that meet the three defining characteristics of autism: social impairment, language deficits, and repetitive behavior.''

''Yu Yamaguchi, M.D., Ph.D. - YouTube''

== Genetic studies (EXT genes) ==
As HME is associated with genetic issues on the EXT genes, here is a list of genetic studies:

'''Benoist-Lasselina, Catherine Emmanuel de Margerieb, Linda Gibbsa, Sarah Cormierc, Caroline Silvec, Gisèle Nicolasd, Martine LeMerrera, Jean-Francois Mallete, Arno­­­­ld Munnicha, Jacky Bonaventurea, Louise Zylberbergb, Laurence Legeai-Malleta,  2006.  ''Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients''. Bone, Volume 39, Issue 1, July 2006, Pages 17–26'''.&lt;ref&gt;{{Cite journal |last=Benoist-Lasselin |first=Catherine |last2=de Margerie |first2=Emmanuel |last3=Gibbs |first3=Linda |last4=Cormier |first4=Sarah |last5=Silve |first5=Caroline |last6=Nicolas |first6=Gisèle |last7=LeMerrer |first7=Martine |last8=Mallet |first8=Jean-Francois |last9=Munnich |first9=Arnold |last10=Bonaventure |first10=Jacky |last11=Zylberberg |first11=Louise |last12=Legeai-Mallet |first12=Laurence |date=2006-07 |title=Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients |url=http://www.thebonejournal.com/article/S8756-3282(05)00540-5/fulltext |journal=Bone |volume=39 |issue=1 |pages=17–26 |doi=10.1016/j.bone.2005.12.003 |issn=8756-3282}}&lt;/ref&gt; . ''Multiple hereditary exostoses (MHE) is an autosomal dominant skeletal disorder caused by mutations in one of the two EXT genes and characterized by multiple osteochondromas that generally arise near the ends of growing long bones.''

'''Busse-Wicher, Marta; Wicher, Krzysztof B.; Kusche-Gullberg, Marion (2014). &quot;The extostosin family: Proteins with many functions&quot;. Matrix Biology. Elsevier BV. 35: 25–33. doi:10.1016/j.matbio.2013.10.001. hdl:1956/10590. ISSN 0945-053X.''' ''Mutations in either EXT1 or EXT2 cause hereditary multiple osteochondromas (HMO), an autosomal dominant disorder characterized by bone deformities and cartilage-capped bony outgrowths, called exostoses or osteochondromas, at the ends of the long bones (reviewed in (Jennes et al., 2009)). HMO is one of the most common inherited skeletal disorders with an estimated incidence of 1–2 per 100 000 live births.''

'''Cuellar, A., Reddi, A.H. Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates. International Orthopaedics (SICOT) 37, 1591–1596 (2013). &lt;nowiki&gt;https://doi.org/10.1007/s00264-013-1906-5&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Cuellar |first=Araceli |last2=Reddi |first2=A. Hari |date=2013-08-01 |title=Cell biology of osteochondromas: Bone morphogenic protein signalling and heparan sulphates |url=https://doi.org/10.1007/s00264-013-1906-5 |journal=International Orthopaedics |language=en |volume=37 |issue=8 |pages=1591–1596 |doi=10.1007/s00264-013-1906-5 |issn=1432-5195 |pmc=3728397 |pmid=23771188}}&lt;/ref&gt; ''While factors for severity remain unknown, mutations in exostosin 1 and exostosin 2 genes, encoding glycosyltransferases involved in the biosynthesis of ubiquitously expressed heparan sulphate (HS) chains, are associated with MHE.''

'''Nozawa S, Inubushi T, Irie F, et al. Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass. JCI Insight. 2018;3(3):e89624. Published 2018 Feb 8. doi:10.1172/jci.insight.89624.'''&lt;ref&gt;{{Cite journal |last=Nozawa |first=Satoshi |last2=Inubushi |first2=Toshihiro |last3=Irie |first3=Fumitoshi |last4=Takigami |first4=Iori |last5=Matsumoto |first5=Kazu |last6=Shimizu |first6=Katsuji |last7=Akiyama |first7=Haruhiko |last8=Yamaguchi |first8=Yu |date=2018-02-08 |title=Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass |url=https://insight.jci.org/articles/view/89624 |journal=JCI Insight |language=en |volume=3 |issue=3 |doi=10.1172/jci.insight.89624 |issn=2379-3708 |pmc=5821205 |pmid=29415886}}&lt;/ref&gt; ''To determine the role of HS in bone homeostasis, we conditionally ablated Ext1, which encodes an essential glycosyltransferase for HS biosynthesis, in osteoblasts. Resultant conditional mutant mice developed severe osteopenia. Surprisingly, this phenotype is not due to impairment in bone formation but to enhancement of bone resorption. We also show that bone mineral density is reduced in patients with multiple hereditary exostoses, a genetic bone disorder caused by heterozygous mutations of Ext1, suggesting that the mechanism revealed in this study may be relevant to low bone mass conditions in humans.''

'''Pacifici M. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses. Matrix Biol. 2018 Oct;71-72:28-39. doi: 10.1016/j.matbio.2017.12.011. Epub 2017 Dec 24. PMID: 29277722; PMCID: PMC6015767'''''.''&lt;ref name=&quot;:7&quot; /&gt; ''Heparan sulfate (HS) is an essential component of cell surface and matrix proteoglycans (HS-PGs) that include syndecans and perlecan. Because of their unique structural features, the HS chains are able to specifically interact with signaling proteins–including bone morphogenetic proteins (BMPs)-via their HS-binding domain, regulating protein availability, distribution and action on target cells. Hereditary Multiple Exostoses (HME) is a rare pediatric disorder linked to germline heterozygous loss-of-function mutations in EXT1 or EXT2 that encode Golgi-resident glycosyltransferases responsible for HS synthesis, resulting in a systemic HS deficiency. HME is characterized by cartilaginous/bony tumors-called osteochondromas or exostoses- that form within perichondrium in long bones, ribs and other elements. This review examines most recent studies in HME, framing them in the context of classic studies. New findings show that the spectrum of EXT mutations is larger than previously realized and the clinical complications of HME extend beyond the skeleton.''

'''Sefcik R, Earl D. Hereditary Multiple Osteochondromas. 2000 Aug 3 [Updated 2026 Jan 29]. In: Adam MP, Bick S, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from: &lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/books/NBK1235&lt;/nowiki&gt;.''' ''Each child of an individual with HMO has a 50% chance of inheriting an HMO-causing pathogenic variant.''

'''Zak, B.M., B.E. Crawford, and J.D. Esko, 2002. Hereditary multiple exostoses and heparan sulfate polymerization Biochimica et Biophysica Acta (BBA) Volume 1573, Issue 3, 19 December 2002, Pages 346–355 &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0304416502004026&lt;/nowiki&gt;''' ''Hereditary multiple exostoses (HME, OMIM 133700, 133701) results from mutations in EXT1 and EXT2, genes encoding the copolymerase responsible for heparan sulfate (HS) biosynthesis. Here, we provide an overview of HME, the EXT family of proteins, and possible models for the relationship of altered HS biosynthesis to the ectopic bone growth characteristic of the disease.''

== HSPG-Related studies ==
While HME is a rare disease and rarely studied, the connection between HME and HSPG is noted. Therefore, this list of research articles covers HME, HSPG, and the genetic issues associated with the EXT1, EXT2, and EXT3 genes.

'''Aldunate, Rebecca, Juan Carlos Casar, Enrique Brandan, Nibaldo C. Inestrosa, 2004. Structural and functional organization of synaptic acetylcholinesterase, Brain Research Reviews, Volume 47, Issues 1–3,''' &lt;ref&gt;{{Cite journal |last=Aldunate |first=Rebeca |last2=Casar |first2=Juan Carlos |last3=Brandan |first3=Enrique |last4=Inestrosa |first4=Nibaldo C. |date=2004-12 |title=Structural and functional organization of synaptic acetylcholinesterase |url=https://linkinghub.elsevier.com/retrieve/pii/S0165017304001092 |journal=Brain Research Reviews |language=en |volume=47 |issue=1-3 |pages=96–104 |doi=10.1016/j.brainresrev.2004.07.019}}&lt;/ref&gt; ''&quot;The presence of two heparin-binding domains in ColQ that interact with heparan sulfate proteoglycans (HSPGs) at the synaptic basal lamina; and second, a knockout mouse for perlecan, a HSPG concentrated in nerve–muscle contact, in which absence of asymmetric AChE at the NMJ is observed.&quot;''

'''Aplin, J.D., Charlton, A.K. &amp; Ayad, S.  1988. An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy. Cell Tissue Res. 253: 231. &lt;nowiki&gt;https://doi.org/10.1007/BF00221758&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Aplin |first=J. D. |last2=Charlton |first2=A. K. |last3=Ayad |first3=S. |date=1988-07-01 |title=An immunohistochemical study of human endometrial extracellular matrix during the menstrual cycle and first trimester of pregnancy |url=https://doi.org/10.1007/BF00221758 |journal=Cell and Tissue Research |language=en |volume=253 |issue=1 |pages=231–240 |doi=10.1007/BF00221758 |issn=1432-0878}}&lt;/ref&gt; ''Changes in the organisation and composition of extracellular matrix in human endometrium during the menstrual cycle and early pregnancy have been assessed by immunofluorescence.'' 

'''Arnold, K. Y-E. Liao, and J. Liu, 2020. ''Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage. Biomedicines 2020, 8(11), 503;''''' &lt;ref&gt;{{Cite journal |last=Arnold |first=Katelyn |last2=Liao |first2=Yi-En |last3=Liu |first3=Jian |date=2020-11-16 |title=Potential Use of Anti-Inflammatory Synthetic Heparan Sulfate to Attenuate Liver Damage |url=https://www.mdpi.com/2227-9059/8/11/503 |journal=Biomedicines |language=en |volume=8 |issue=11 |pages=503 |doi=10.3390/biomedicines8110503 |issn=2227-9059}}&lt;/ref&gt; ''Heparan sulfate (HS) is an essential glycan for liver function.''

'''Ascencio, F. L. Å. Fransson and T. WadstrÖum, 1993. ''Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminoglycan heparan sulphate'' J Med Microbiol April 1993 vol. 38 no. 4 240-244''' &lt;ref&gt;{{Cite web |last=F |first=Ascencio |last2=A |first2=Fransson, L. |last3=T |first3=Wadstrom |date=1993-04-01 |title=Affinity of the gastric pathogen Helicobacter pylori for the N-sulphated glycosaminogly… |url=https://www.sgmjournals.org/jmm/content/38/4/240 |access-date=2026-07-15 |website=SGM Journals |language=en}}&lt;/ref&gt;'''.''' ''Binding of 125I-heparan sulphate was a common property of Helicobacter pylori strains isolated from patients with gastroduodenal ulcer diseases.''

'''Berg et al., 1999. Chronic fatigue syndrome and/or Fibromyalgia as a variation of Antiphospholipid antibody syndrome: an explanatory model and approach to laboratory  diagnosis'''&lt;ref&gt;{{Cite journal |last=Berg |first=D. |last2=Berg |first2=L. H. |last3=Couvaras |first3=J. |last4=Harrison |first4=H. |date=1999-10 |title=Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis |url=https://pubmed.ncbi.nlm.nih.gov/10695770 |journal=Blood Coagulation &amp; Fibrinolysis: An International Journal in Haemostasis and Thrombosis |volume=10 |issue=7 |pages=435–438 |doi=10.1097/00001721-199910000-00006 |issn=0957-5235 |pmid=10695770}}&lt;/ref&gt; Not in this paper, but the logic is that low levels of HSPG are found in patients with chronic fatigue, and there is probably a correlation with MHE fatigue and low levels of HSPG.

'''Bishop, J., Schuksz, M. &amp; Esko, J. Heparan sulphate proteoglycans fine-tune mammalian physiology. Nature 446, 1030–1037 (2007). &lt;nowiki&gt;https://doi.org/10.1038/nature05817&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Bishop |first=Joseph R. |last2=Schuksz |first2=Manuela |last3=Esko |first3=Jeffrey D. |date=2007-04 |title=Heparan sulphate proteoglycans fine-tune mammalian physiology |url=https://www.nature.com/articles/nature05817 |journal=Nature |language=en |volume=446 |issue=7139 |pages=1030–1037 |doi=10.1038/nature05817 |issn=1476-4687}}&lt;/ref&gt; ''Heparan sulphate proteoglycans reside on the plasma membrane of all animal cells studied so far and are a major component of extracellular matrices. . A recurrent theme is the electrostatic interaction of the heparan sulphate chains with protein ligands, which affects metabolism, transport, information transfer, support and regulation in all organ systems.'' 

'''Boer and Gaillard, 2007. Drug Targeting to the Brain. Annual Review of Pharmacology and Toxicology. Volume 47, 2007. Pp 323-355'''&lt;ref name=&quot;:3&quot; /&gt;'''.'''''… For many diseases of the brain, such as Alzheimer's disease, Parkinson's disease, stroke, depression, schizophrenia, epilepsia and migraine headache, the drugs on the market … enter the cell following binding to heparan sulfate proteoglycan (HSPG) receptors …''

'''Brown, Anissa Joy. Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation University of Delaware, ProQuest Dissertations Publishing, 2008. 3324491.'''&lt;ref&gt;{{Cite web |title=Function of heparan sulfate proteoglycans (HSPGs) and heparanase (HPSE) in endochondral bone formation. by Brown, Anissa Joy (9781243986054) {{!}} Browns Books |url=https://www.brownsbfs.co.uk/Product/Brown-Anissa-Joy/Function-of-heparan-sulfate-proteoglycans-HSPGs-and-hepar/9781243986054 |access-date=2026-07-15 |website=www.brownsbfs.co.uk}}&lt;/ref&gt; ''Endochondral bone formation is a tightly regulated process involving coordination among cell-cell, cell-matrix and growth factor signaling that eventually results in the production of mineralized bone from a cartilage template. Chondrogenic and osteogenic differentiation occur in sequence during this process, and the temporospatial patterning clearly requires the activities of heparan sulfate proteoglycans (HSPGs), heparin binding growth factors (HBGFs) and their receptors.''

'''O'Callaghan P, Zhang X, Li JP. 2018. Heparan Sulfate Proteoglycans as Relays of Neuroinflammation. J Histochem Cytochem. 2018 Apr;66(4):305-319. doi: 10.1369/0022155417742147. Epub 2018 Jan 1. PMID: 29290138; PMCID: PMC5958378'''&lt;ref&gt;{{Cite journal |last=O'Callaghan |first=Paul |last2=Zhang |first2=Xiao |last3=Li |first3=Jin-Ping |date=2018-04 |title=Heparan Sulfate Proteoglycans as Relays of Neuroinflammation |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC5958378/ |journal=The Journal of Histochemistry and Cytochemistry: Official Journal of the Histochemistry Society |volume=66 |issue=4 |pages=305–319 |doi=10.1369/0022155417742147 |issn=1551-5044 |pmc=5958378 |pmid=29290138}}&lt;/ref&gt;'''.''' ''.'' ''We summarize some of the contrasting roles that HS and heparanase have been assigned in diseases associated with chronic inflammatory states, including Alzheimer's disease (AD).'' 

'''Chmiela, M. et al. 1995. The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages. &lt;nowiki&gt;http://onlinelibrary.wiley.com/doi/10.1111/j.1699-0463.1995.tb01133.x/full&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Chmiela |first=M. |last2=Paziak-Domanska |first2=B. |last3=Rudnicka |first3=W. |last4=WadstrÖM |first4=T. |date=1995 |title=The role of heparan sulphate-binding activity of Helicobacter pylori bacteria in their adhesion to murine macrophages |url=https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1699-0463.1995.tb01133.x |journal=APMIS |language=en |volume=103 |issue=1-6 |pages=469–474 |doi=10.1111/j.1699-0463.1995.tb01133.x |issn=1600-0463}}&lt;/ref&gt; ''The role of heparan sulphate (HS)-binding activity of Helicobacter pylori microbes in their adhesion to and ingestion by inflammatory peritoneal macrophages.'' 

'''Collins LE, Troeberg L. 2019. Heparan sulfate as a regulator of inflammation and immunity. J Leukoc Biol. 2019 Jan;105(1):81-92. doi: 10.1002/JLB.3RU0618-246R. Epub 2018 Oct 30. PMID: 30376187.'''&lt;ref&gt;{{Cite journal |last=Collins |first=Laura E |last2=Troeberg |first2=Linda |date=2018-12-27 |title=Heparan sulfate as a regulator of inflammation and immunity |url=https://academic.oup.com/jleukbio/article/105/1/81/6935486 |journal=Journal of Leukocyte Biology |language=en |volume=105 |issue=1 |pages=81–92 |doi=10.1002/JLB.3RU0618-246R |issn=1938-3673}}&lt;/ref&gt; ''In this review, we discuss the multiple roles for HS in regulating immune responses, and the evidence for inflammation-associated changes to HS structure.Keywords: chemokines; cytokines; heparan sulfate; inflammation; leukocyte.''

'''Condomitti, G., &amp; de Wit, J. (2018). Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity. Frontiers in molecular neuroscience, 11, 14. &lt;nowiki&gt;https://doi.org/10.3389/fnmol.2018.00014&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Condomitti |first=Giuseppe |last2=de Wit |first2=Joris |date=2018-01-26 |title=Heparan Sulfate Proteoglycans as Emerging Players in Synaptic Specificity |url=https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2018.00014/full |journal=Frontiers in Molecular Neuroscience |language=English |volume=11 |doi=10.3389/fnmol.2018.00014 |issn=1662-5099 |pmc=5790772 |pmid=29434536}}&lt;/ref&gt; ''The heparan sulfate proteoglycan (HSPG) family of cell-surface proteins is emerging as a key regulator of connectivity. HSPGs are expressed throughout brain development and play important roles in axon guidance, synapse development and synapse function.''

'''Cooper, Isabella D.; Brookler, Kenneth H.; Crofts, Catherine A. P. (2021-09-06). &quot;Rethinking  Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas&quot; Biomedicines 9, no. 9: 1165.'''&lt;ref&gt;{{Cite journal |last=Cooper |first=Isabella D. |last2=Brookler |first2=Kenneth H. |last3=Crofts |first3=Catherine A. P. |date=2021-09-06 |title=Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas |url=https://www.mdpi.com/2227-9059/9/9/1165 |journal=Biomedicines |language=en |volume=9 |issue=9 |pages=1165 |doi=10.3390/biomedicines9091165 |issn=2227-9059}}&lt;/ref&gt; ''&lt;nowiki&gt;https://doi.org/10.3390/biomedicines9091165&lt;/nowiki&gt;  Hyperinsulinaemia negatively impacts HSPG function and availability, via impairment of vitamin D regulation. Vitamin D regulates sulfate synthesis, required for heparan sulphate ['''145'''].''

'''Dituri F, Gigante G, Scialpi R, Mancarella S, Fabregat I, Giannelli G. Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma. Cancers. 2022; 14(8):1902. &lt;nowiki&gt;https://doi.org/10.3390/cancers14081902&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Dituri |first=Francesco |last2=Gigante |first2=Gianluigi |last3=Scialpi |first3=Rosanna |last4=Mancarella |first4=Serena |last5=Fabregat |first5=Isabel |last6=Giannelli |first6=Gianluigi |date=2022-04-09 |title=Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma |url=https://www.mdpi.com/2072-6694/14/8/1902 |journal=Cancers |language=en |volume=14 |issue=8 |pages=1902 |doi=10.3390/cancers14081902 |issn=2072-6694 |pmc=9024587 |pmid=35454809}}&lt;/ref&gt; ''Proteoglycans are a class of highly glycosylated proteins expressed in virtually all tissues, which are localized within membranes, but more often in the pericellular space and extracellular matrix (ECM), and are involved in tissue homeostasis and remodeling of the stromal microenvironment during physiological and pathological processes, such as tissue regeneration, angiogenesis, and cancer.''

'''Farhan, S.M.K. , Wang J, Robinson JF, et al., 2015. Old gene, new phenotype: mutations in heparan sulfate synthesis enzyme, EXT2 leads to seizure and developmental disorder, no exostoses. Journal of Medical Genetics 2015;52:666-675. ''' ''Many genes are involved in modulating heparan sulfate synthesis, and when these genes are mutated, they can give rise to early-onset developmental disorders affecting multiple body systems.'' 

'''Forsberg E. and L. Kjellen, 2001. Heparan sulfate: lessons from knockout mice. Journal of Clinical Investigation. &lt;nowiki&gt;https://www.jci.org/articles/view/13561&lt;/nowiki&gt;.''' &lt;ref&gt;{{Cite journal |last=Forsberg |first=Erik |last2=Kjellén |first2=Lena |date=2001-07-15 |title=Heparan sulfate: lessons from knockout mice |url=https://www.jci.org/articles/view/13561 |journal=The Journal of Clinical Investigation |language=en |volume=108 |issue=2 |pages=175–180 |doi=10.1172/JCI13561 |issn=0021-9738 |pmid=11457868}}&lt;/ref&gt; ''Kidney'' ''agenesis, “broken heart,” abnormal mast cells, somatic overgrowth, lung dysfunction, and chondrodysplasia are some phenotypes of mice where different genes important for heparan sulfate (HS) expression have been knocked out.The authors speculate that, during inflammation or wounding when fibronectin is degraded, syndecan-4 may be important for focal adhesion formation and actin fiber organization, which in turn contribute to cell migration.'' 

'''Fumitoshi Irie, Hedieh Badie-Mahdavi, and Yu Yamaguchi, 2012. ''Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate''. PNAS 2012 109 (13) 5052-5056;  March 27, 2012 vol. 109 no. 13'''&lt;ref name=&quot;:4&quot; /&gt; '''&lt;nowiki&gt;http://www.pnas.org/content/109/13/5052.short&lt;/nowiki&gt;''' ''Heparan sulfate regulates diverse cell-surface signaling events, and its roles in the development of the nervous system recently have been increasingly uncovered by studies using genetic models carrying mutations of genes encoding enzymes for its synthesis. Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypes characteristic for autism.''

'''Ge, Xiao Na, Bastan, Idil, Ha, Sung Gil, Greenberg, Yana G., Esko, Jeffrey D., Rao, Savita P., Sriramarao, P., 2018. Regulation of eosinophil recruitment and allergic airway inflammation by heparan sulfate proteoglycan (HSPG) modifying enzymes. Experimental Lung Research, 01902148, Mar2018, Vol. 44, Issue''' ''Our study demonstrates that allergen exposure reduces expression of Hs2st; loss of uronyl 2-O-sulfation in endothelial and leukocyte HSPG amplifies recruitment of eosinophils likely due to a compromised vascular endothelium resulting in persistent inflammation whereas loss of N-sulfation limits eosinophilia and attenuates inflammation underscoring the importance of site-specific sulfation in HSPG to their role in AAI.''

'''Haeger SM, Yang Y, Schmidt EP. Heparan Sulfate in the Developing, Healthy, and Injured Lung. Am J Respir Cell Mol Biol. 2016;55(1):5-11. doi:10.1165/rcmb.2016-0043TR''' '''''&lt;nowiki&gt;https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4942210/&lt;/nowiki&gt;'''''&lt;ref&gt;{{Cite journal |last=Haeger |first=Sarah M. |last2=Yang |first2=Yimu |last3=Schmidt |first3=Eric P. |date=2016-07 |title=Heparan Sulfate in the Developing, Healthy, and Injured Lung |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4942210/ |journal=American Journal of Respiratory Cell and Molecular Biology |volume=55 |issue=1 |pages=5–11 |doi=10.1165/rcmb.2016-0043TR |issn=1535-4989 |pmc=4942210 |pmid=26982577}}&lt;/ref&gt; ''This Translational Review highlightsthe importance of athe glycosaminoglycan heparan sulfate (HS) on lung health and disease.''

'''Hiebert, Linda M. 2021. Heparan Sulfate Proteoglycans in Diabetes. DOI: 10.1055/s-0041-1724118. Thieme E-''' '''Journals - Seminars in Thrombosis and Hemostasis / Abstract (thieme-connect.com).''' &lt;ref&gt;{{Cite journal |last=Hiebert |first=Linda M. |date=2021-04 |title=Heparan Sulfate Proteoglycans in Diabetes |url=http://www.thieme-connect.de/DOI/DOI?10.1055/s-0041-1724118 |journal=Seminars in Thrombosis and Hemostasis |language=en |volume=47 |issue=03 |pages=261–273 |doi=10.1055/s-0041-1724118 |issn=0094-6176}}&lt;/ref&gt; ''Understanding the role of HSPGs and how they are modified by diabetes may lead to new treatments as well as preventative measures to reduce the morbidity and mortality associated with this complex condition.''

'''Ho, G., G Broze, A. Schwartz, 1997. Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes. CELL BIOLOGY AND METABOLISM| VOLUME 272, ISSUE 27, P16838-16844, JULY 1997.&lt;nowiki&gt;https://www.jbc.org/article/S0021-9258(18)39299-8/fulltext&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Ho |first=Guyu |last2=Broze |first2=George J. |last3=Schwartz |first3=Alan L. |date=1997-07-04 |title=Role of Heparan Sulfate Proteoglycans in the Uptake and Degradation of Tissue Factor Pathway Inhibitor-Coagulation Factor Xa Complexes * |url=https://www.jbc.org/article/S0021-9258(18)39299-8/abstract |journal=Journal of Biological Chemistry |language=English |volume=272 |issue=27 |pages=16838–16844 |doi=10.1074/jbc.272.27.16838 |issn=0021-9258}}&lt;/ref&gt;''These results suggest that heparan sulfate proteoglycans (HSPGs) are required for the uptake and degradation of 125I-TFPI·fXa complexes.'' 

'''Huang M, He H, Belenkaya T, Lin X. Multiple roles of epithelial heparan sulfate in stomach morphogenesis. J Cell Sci. 2018 May 29;131(10):jcs210781. doi: 10.1242/jcs.210781. PMID: 29700203; PMCID: PMC6031332.''' &lt;ref&gt;{{Cite journal |last=Huang |first=Meina |last2=He |first2=Hua |last3=Belenkaya |first3=Tatyana |last4=Lin |first4=Xinhua |date=2018-05-15 |title=Multiple roles of epithelial heparan sulfate in stomach morphogenesis |url=https://journals.biologists.com/jcs/article/131/10/jcs210781/56866/Multiple-roles-of-epithelial-heparan-sulfate-in |journal=Journal of Cell Science |language=en |volume=131 |issue=10 |doi=10.1242/jcs.210781 |issn=1477-9137 |pmc=6031332 |pmid=29700203}}&lt;/ref&gt; ''In the posterior stomach, HS depletion disrupts glandular stomach patterning and cytodifferentiation via attenuation of Fgf signaling activity.'' 

'''Irie, F.,  H. Badie-Mahdavi, Y. Yamaguchi, 2012. Autism-like socio-communicative deficits and stereotypies in mice lacking heparan sulfate Proc. Natl. Acad. Sci. U. S. A., 109 (2012), pp. 5052-5056. &lt;nowiki&gt;https://www.pnas.org/doi/pdf/10.1073/pnas.1117881109&lt;/nowiki&gt;.''' &lt;ref name=&quot;:5&quot; /&gt;''Our results demonstrate that heparan sulfate is critical for normal functioning of glutamatergic synapses and that its deficiency mediates socio-communicative deficits and stereotypies characteristic for autism.''

'''Jennes I, Pedrini E, Zuntini M, Mordenti M, Balkassmi S, Asteggiano CG, Casey B, Bakker B, Sangiorgi L, Wuyts W. Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb). Hum Mutat. 2009 Dec;30 (12):1620-7. doi: 10.1002/humu.21123. PMID: 19810120.''' &lt;ref&gt;{{Cite journal |last=Jennes |first=Ivy |last2=Pedrini |first2=Elena |last3=Zuntini |first3=Monia |last4=Mordenti |first4=Marina |last5=Balkassmi |first5=Sahila |last6=Asteggiano |first6=Carla G. |last7=Casey |first7=Brett |last8=Bakker |first8=Bert |last9=Sangiorgi |first9=Luca |last10=Wuyts |first10=Wim |date=2009-12 |title=Multiple osteochondromas: mutation update and description of the multiple osteochondromas mutation database (MOdb) |url=https://onlinelibrary.wiley.com/doi/10.1002/humu.21123 |journal=Human Mutation |language=en |volume=30 |issue=12 |pages=1620–1627 |doi=10.1002/humu.21123}}&lt;/ref&gt;''MO is genetically heterogeneous, and is associated with mutations in Exostosin-1 (EXT1) or Exostosin-2 (EXT2), both tumor-suppressor genes of the EXT gene family. All members of this multigene family encode glycosyltransferases involved in the adhesion and/or polymerization of heparin sulfate (HS) chains at HS proteoglycans (HSPGs).'' 

'''Jones, K. B., Pacifici, M., &amp; Hilton, M. J. (2014). Multiple hereditary exostoses (MHE): elucidating the pathogenesis of a rare skeletal disorder through interdisciplinary research. Connective Tissue Research, 55(2), 80–88. &lt;nowiki&gt;https://doi.org/10.3109/03008207.2013.867957&lt;/nowiki&gt;.''' ''MHE is largely caused by autosomal dominant mutations in EXT1 or EXT2, genes encoding Golgi-associated glycosyltransferases responsible for heparan sulfate (HS) synthesis. HS chains are key constituents of cell surface- and extracellular matrix-associated proteoglycans, which are known regulators of skeletal development. MHE affected individuals are HS-deficient, can display skeletal growth retardation and deformities, and consistently develop benign, cartilage-capped bony outgrowths (termed exostoses or osteochondromas) near the growth plates of many skeletal elements. Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes.''

'''Kemp, Annissa et al. 2017. Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction, Developmental Cell, Volume 43, Issue 1, 24 - 34.e5 &lt;nowiki&gt;https://www.cell.com/developmental-cell/fulltext/S1534-5807(17)30674-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Kempf |first=Anissa |last2=Boda |first2=Enrica |last3=Kwok |first3=Jessica C. F. |last4=Fritz |first4=Rafael |last5=Grande |first5=Valentina |last6=Kaelin |first6=Andrea M. |last7=Ristic |first7=Zorica |last8=Schmandke |first8=Andre |last9=Schmandke |first9=Antonio |last10=Tews |first10=Bjoern |last11=Fawcett |first11=James W. |last12=Pertz |first12=Olivier |last13=Buffo |first13=Annalisa |last14=Schwab |first14=Martin E. |date=2017-10-09 |title=Control of Cell Shape, Neurite Outgrowth, and Migration by a Nogo-A/HSPG Interaction |url=https://www.cell.com/developmental-cell/abstract/S1534-5807(17)30674-3 |journal=Developmental Cell |language=English |volume=43 |issue=1 |pages=24–34.e5 |doi=10.1016/j.devcel.2017.08.014 |issn=1534-5807 |pmid=28943240}}&lt;/ref&gt; ''Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migration-related processes. Here, we show that the transmembrane protein, Nogo-A, inhibits neurite outgrowth and cell spreading in neurons and Nogo-A-responsive cell lines via HSPGs. Finally, we show in explant cultures ex vivo that Nogo-A-?20 promotes the migration of neuroblasts via HSPGs but not S1PR2.''

'''Kolset, S., Salmivirta, M. Cell surface heparan sulfate proteoglycans and lipoprotein metabolism. CMLS, Cell. Mol. Life Sci. 56, 857–870 (1999). &lt;nowiki&gt;https://doi.org/10.1007/s000180050031&lt;/nowiki&gt;''' [https://link.springer.com/article/10.1007/s000180050031. https://link.springer.com/article/10.1007/s000180050031.]  ''Heparan sulfate has been further implicated in presentation and stabilization of lipoprotein lipase and hepatic lipase on cell surfaces and in the transport of lipoprotein lipase from extravascular cells to the luminal surface of the endothelia. In atherosclerosis, heparan sulfate is intimately involved in several events important to the pathophysiology of the disease.''

'''Laabs, T.; Carulli, D.; Geller, H.M.; Fawcett, J.W. Chondroitin sulfate proteoglycans in neural development and regeneration. Curr. Opin. Neurobiol. 2005, 15, 116–120. [Google Scholar] [CrossRef] [PubMed]'''&lt;ref&gt;{{Cite journal |last=Carulli |first=Daniela |last2=Laabs |first2=Tracy |last3=Geller |first3=Herbert M. |last4=Fawcett |first4=James W. |date=2005-02 |title=Chondroitin sulfate proteoglycans in neural development and regeneration |url=https://pubmed.ncbi.nlm.nih.gov/15721753 |journal=Current Opinion in Neurobiology |volume=15 |issue=1 |pages=116–120 |doi=10.1016/j.conb.2005.01.014 |issn=0959-4388 |pmid=15721753}}&lt;/ref&gt; ''Proteoglycans are of two main types, chondroitin sulfate (CSPGs) and heparin sulfate (HSPGs). The CSPGs act mainly as barrier-forming molecules, whereas the HSPGs stabilise the interactions of receptors and ligands.'' 

'''Lundberg, Y.W., Y. Xu, K.D. Theissen, and K.L. Framer, 2014. Mechanisms of otoconia and otolith development. Developmental Dynamics, 9/24/2014.''' &lt;ref&gt;{{Cite journal |last=Lundberg |first=Yunxia Wang |last2=Xu |first2=Yinfang |last3=Thiessen |first3=Kevin D. |last4=Kramer |first4=Kenneth L. |date=2015 |title=Mechanisms of otoconia and otolith development |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/dvdy.24195 |journal=Developmental Dynamics |language=en |volume=244 |issue=3 |pages=239–253 |doi=10.1002/dvdy.24195 |issn=1097-0177 |pmc=4482761 |pmid=25255879}}&lt;/ref&gt;  ''Deletion of different HSPGs and CSPGs causes calcification deficiencies  which exemplifies their critical role in bone and teeth formation.''

'''Mansouri, R., Jouan, Y., Hay, E. et al. Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells. Cell Death Dis 8, e2902 (2017). &lt;nowiki&gt;https://doi.org/10.1038/cddis.2017.287&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Mansouri |first=Rafik |last2=Jouan |first2=Yohann |last3=Hay |first3=Eric |last4=Blin-Wakkach |first4=Claudine |last5=Frain |first5=Monique |last6=Ostertag |first6=Agnès |last7=Le Henaff |first7=Carole |last8=Marty |first8=Caroline |last9=Geoffroy |first9=Valérie |last10=Marie |first10=Pierre J. |last11=Cohen-Solal |first11=Martine |last12=Modrowski |first12=Dominique |date=2017-06 |title=Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells |url=https://www.nature.com/articles/cddis2017287 |journal=Cell Death &amp; Disease |language=en |volume=8 |issue=6 |pages=e2902–e2902 |doi=10.1038/cddis.2017.287 |issn=2041-4889 |pmc=5520938 |pmid=28661485}}&lt;/ref&gt;  ''Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented.'' 

'''Matsuzawa, T. et al., 2021. Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis. Journal of Biological Chemistry.'''&lt;ref&gt;{{Cite journal |last=Matsuzawa |first=Takuro |last2=Morita |first2=Masanobu |last3=Shimane |first3=Ai |last4=Otsuka |first4=Rina |last5=Mei |first5=Yu |last6=Irie |first6=Fumitoshi |last7=Yamaguchi |first7=Yu |last8=Yanai |first8=Kazuhiko |last9=Yoshikawa |first9=Takeo |date=2021-09 |title=Heparan sulfate promotes differentiation of white adipocytes to maintain insulin sensitivity and glucose homeostasis |url=https://pubmed.ncbi.nlm.nih.gov/34310946 |journal=The Journal of Biological Chemistry |volume=297 |issue=3 |pages=101006 |doi=10.1016/j.jbc.2021.101006 |issn=1083-351X |pmc=8379462 |pmid=34310946}}&lt;/ref&gt; ''We observed that Ext1Δ/WT mice showed glucose intolerance because of insulin resistance. Our results demonstrate that HS plays a crucial role in the differentiation of white adipocytes through BMP4–FGF1 signaling pathways, thereby contributing to insulin sensitivity and glucose homeostasis.''

'''Meneghetti, Maria C. Z.; Hughes, Ashley J.; Rudd, Timothy R.; Nader, Helena B.; Powell, Andrew K.; Yates, Edwin A.; Lima, Marcelo A. (2015-09-06). &quot;Heparan sulfate and heparin interactions with proteins&quot;. Journal of the Royal Society, Interface. 12 (110): 0589. doi:10.1098/rsif.2015.0589. ISSN 1742-5662. PMC 4614469. &lt;nowiki&gt;PMID 26289657&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Echits |first=S. V. |last2=Pichko |first2=V. B. |last3=Tikhomirova |first3=A. S. |last4=Letunova |first4=E. V. |date=1975 |title=[Preparation and properties of beta-galactosidase linked covalently with KM-cellulose] |url=https://pubmed.ncbi.nlm.nih.gov/1742 |journal=Prikladnaia Biokhimiia I Mikrobiologiia |volume=11 |issue=6 |pages=848–851 |issn=0555-1099 |pmid=1742}}&lt;/ref&gt;''. Heparan sulfate (HS) polysaccharides are ubiquitous components of the cell surface and extracellular matrix of all multicellular animals, whereas heparin is present within mast cells and can be viewed as a more sulfated, tissue-specific, HS variant. HS and heparin regulate biological processes through interactions with a large repertoire of proteins. Owing to these interactions and diverse effects observed during in vitro, ex vivo and in vivo experiments, manifold biological/pharmacological activities have been attributed to them'''''.'''

'''Mooney et al. 2016.Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach. American Journal of Medical Genetics. Volume 171, Sept 2016. &lt;nowiki&gt;https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446&lt;/nowiki&gt;''' &lt;ref&gt;{{Cite journal |last=Mooney |first=Michael A. |last2=McWeeney |first2=Shannon K. |last3=Faraone |first3=Stephen V. |last4=Hinney |first4=Anke |last5=Hebebrand |first5=Johannes |last6=Consortium |first6=Image2 |last7=Group |first7=German ADHD GWAS |last8=Nigg |first8=Joel T. |last9=Wilmot |first9=Beth |date=2016 |title=Pathway analysis in attention deficit hyperactivity disorder: An ensemble approach |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.b.32446 |journal=American Journal of Medical Genetics Part B: Neuropsychiatric Genetics |language=en |volume=171 |issue=6 |pages=815–826 |doi=10.1002/ajmg.b.32446 |issn=1552-485X |pmc=4983253 |pmid=27004716}}&lt;/ref&gt; ''These results support previous hypotheses about the role of regulation of neurotransmitter release, neurite outgrowth and axon guidance in contributing to the ADHD phenotype and suggest the value of cross-method convergence in evaluating pathway analysis results.''

'''Nackaerts, K. et al. 1997. Heparan Sulfate Proteoglycan Expression In Human Lung-Cancer Cells. Int. J. Cancer (Pred. Oncol.): 74, 335–345 (1997) r 1997 Wiley-Liss, Inc. &lt;nowiki&gt;https://www.researchgate.net/profile/Maurits_Demedts/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells/links/5600565108aeafc8ac8c7374.pdf&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Nackaerts |first=Kris |last2=Verbeken |first2=Erik |last3=Deneffe |first3=Georges |last4=Vanderschueren |first4=Bernadette |last5=Demedts |first5=Maurits |last6=David |first6=Guido |date=1997-07-01 |title=Heparan sulfate proteoglycan expression in human lung-cancer cells |url=https://www.researchgate.net/publication/13997415_Heparan_sulfate_proteoglycan_expression_in_human_lung-cancer_cells |journal=International journal of cancer. Journal international du cancer |volume=74 |pages=335–45 |doi=10.1002/(SICI)1097-0215(19970620)74:33.3.CO;2-4}}&lt;/ref&gt; ''Heparan sulfate (HS) functions as a co-factor in several signal-transduction systems that affect cellular growth, differentiation, adhesion and motility. HS, therefore, may also play a role in the malignant transformation of cells, tumor growth, cell invasiveness and the formation of tumor metastases. Our results suggest that poorly differentiated lung tumors have markedly altered patterns of HSPG expression, which may contribute to their invasive phenotype. Int. J. Cancer 74:335– 345, 1997.''

'''Nencini Sara , Ivanusic Jason J. The Physiology of Bone Pain. How Much Do We Really Know? Frontiers in Physiology. Volume 7 - 2016.''' '''&lt;nowiki&gt;https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2016.00157&lt;/nowiki&gt;. DOI=10.3389/fphys.2016.00157. ISSN=1664-042X'''&lt;ref name=&quot;:6&quot; /&gt; ''Pain is associated with most bony pathologies. Clinical and experimental observations suggest that bone pain can be derived from noxious stimulation of the periosteum or bone marrow Whilst these provide some clues as to the way information about bone pain is centrally coded, they need to be expanded to further our understanding of other central territories involved.''

'''Otsu, K.; Kato, S.; Ohtake, K.; Akamatsu, N. Alteration of rat liver proteoglycans during regeneration. Arch. Biochem. Biophys. 1992, 294, 544–549. Alteration of rat liver proteoglycans during regeneration - PubMed (nih.gov)'''''. Heparan sulfates (HS) are probably the major GAGs present on the surface of hepatocytes under normal conditions. Nevertheless, HSPGs expression increases during liver regeneration. Using [35S] sulfuric acid incorporation, Otsu et al. showed that, in the hepatic regeneration phase after hepatectomy, the synthesis of heparin sulfate proteoglycans, and to a lesser extent, of chondroitin/dermatan sulfate proteoglycans, increases up to 3–5 days and is temporally shifted compared to the stage of maximum mitosis that occurs 1–2 days following the surgical procedure [94].'' 

'''Otsuka, T., Phan, A.Q., Laurencin, C.T. et al. Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration. Regen. Eng. Transl. Med. 6, 7–17 (2020). &lt;nowiki&gt;https://doi.org/10.1007/s40883-019-00140-3&lt;/nowiki&gt; &lt;nowiki&gt;https://link.springer.com/article/10.1007/s40883-019-00140-3&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Otsuka |first=T. |last2=Phan |first2=A. Q. |last3=Laurencin |first3=C. T. |last4=Esko |first4=J. D. |last5=Bryant |first5=S. V. |last6=Gardiner |first6=D. M. |date=2020-03 |title=Identification of Heparan-Sulfate Rich Cells in the Loose Connective Tissues of the Axolotl (Ambystoma mexicanum) with the Potential to Mediate Growth Factor Signaling during Regeneration |url=http://link.springer.com/10.1007/s40883-019-00140-3 |journal=Regenerative Engineering and Translational Medicine |language=en |volume=6 |issue=1 |pages=7–17 |doi=10.1007/s40883-019-00140-3 |issn=2364-4133 |pmc=7971174 |pmid=33748405}}&lt;/ref&gt; ''. We hypothesized that there are cells in the axolotl that synthesize specific HSPGs that control growth factor signaling in time and space. Given their high level of HSPG expression, their stellate morphology, and their distribution throughout the loose connective tissues, we refer to these as the positional information GRID (Groups that are Regenerative, Interspersed and Dendritic) cells.''

'''Parish, C., 2005. Heparan sulfate and inflammation. Nature Immunology 6(9):861-2 ·  October. &lt;nowiki&gt;https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Parish |first=Christopher |date=2005-10-01 |title=Heparan sulfate and inflammation |url=https://www.researchgate.net/publication/7645220_Heparan_sulfate_and_inflammation |journal=Nature immunology |volume=6 |pages=861–2 |doi=10.1038/ni0905-861}}&lt;/ref&gt; ''Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.''

'''Park, P.J, and D. Shukla. Role of heparan sulfate in ocular diseases, Experimental Eye Research, Volume 110, 2013, Pages 1-9, ISSN 0014-4835, &lt;nowiki&gt;https://doi.org/10.1016/j.exer.2013.01.015&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Park |first=Paul J. |last2=Shukla |first2=Deepak |date=2013-05-01 |title=Role of heparan sulfate in ocular diseases |url=https://www.sciencedirect.com/science/article/pii/S0014483513000274 |journal=Experimental Eye Research |volume=110 |pages=1–9 |doi=10.1016/j.exer.2013.01.015 |issn=0014-4835 |pmc=3638857 |pmid=23410824}}&lt;/ref&gt; ''Abstract: Heparan sulfate (HS), a ubiquitous and structurally diverse cell surface polysaccharide and extracellular matrix component, is a factor common to several major eye pathologies. Its multitude of functions and variable distribution among the different ocular tissues makes it an important contributor to a variety of disease states. Although HS facilitates the pathogenesis of many disorders, its role in each varies. Unique functions of HS have been particularly noted in viral and bacterial keratitis and age-related macular degeneration.'' 

'''Pérez, C., Sawmiller, D. &amp; Tan, J. The role of heparan sulfate deficiency in autistic phenotype: potential involvement of Slit/Robo/srGAPs-mediated dendritic spine formation. Neural Dev 11, 11 (2016). &lt;nowiki&gt;https://doi.org/10.1186/s13064-016-0066-x&lt;/nowiki&gt;''' &lt;ref name=&quot;:8&quot; /&gt; ''Autism Spectrum Disorders (ASD) are the second most common developmental cause of disability in the United States. The brains of ASD patients have marked structural abnormalities, in the form of increased dendritic spines and decreased long distance connections. These structural differences may be due to deficiencies in Heparin Sulfate (HS), a proteoglycan involved in a variety of neurodevelopmental processes. Through interference with this pathway, HS deficiency can lead to excess spine formation.''

'''Poli, Maura, Michela Asperti, Paola Ruzzenenti, Annamaria Naggi, and Paolo Arosio. 2017. &quot;Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia&quot; Molecules 22, no. 4: 598. &lt;nowiki&gt;https://doi.org/10.3390/molecules22040598&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Poli |first=Maura |last2=Asperti |first2=Michela |last3=Ruzzenenti |first3=Paola |last4=Naggi |first4=Annamaria |last5=Arosio |first5=Paolo |date=2017-04-08 |title=Non-Anticoagulant Heparins Are Hepcidin Antagonists for the Treatment of Anemia |url=https://www.mdpi.com/1420-3049/22/4/598 |journal=Molecules |language=en |volume=22 |issue=4 |pages=598 |doi=10.3390/molecules22040598 |issn=1420-3049 |pmc=6154463 |pmid=28397746}}&lt;/ref&gt; ''This review summarizes recent findings on the anti-hepcidin activity of heparins and their possible use for the treatment of anemia caused by hepcidin excess, including the anemia of chronic diseases.''

'''Russel A.L. and M.F.McCarty, 2000 Glucosamine for migraine prophylaxis?  Medical Hypotheses. Volume 55, Issue 3, September 2000, Pages 195-198. &lt;nowiki&gt;http://www.sciencedirect.com/science/article/pii/S0306987799910125&lt;/nowiki&gt;''' ''We postulate that supplemental glucosamine can boost mast cell heparin synthesis – perhaps correcting a functional heparin deficiency – thereby preventing or ameliorating the neurogenic inflammation that mediates pain in vascular headache. Whether or not this idea has validity, a controlled study of glucosamine for migraine prophylaxis appears to be warranted.''

'''Stringer, S.E. and Gallagher. 1997. Molecules in focus. Heparan sulphate. The International Journal of Biochemistry &amp; Cell Biology, Volume 29, Issue 5, 1997.''' ''Heparan sulphates, the N-sulphated polysaccharides components of proteoglycans, are common constituents of cell surfaces and the extracellular matrix. The diverse functions of heparan sulphate, which range from the control of blood coagulation to the regulation of cell growth and adhesion, depend on the capacity of the chains to activate protein ligands, such as antithrombin III and members of the fibroblast growth factor family. These properties are currently being exploited in the development of synthetic heparan sulphates as anticoagulants and promoters of wound healing. Conversely organic mimics of growth factor activating saccharides could possibly be designed to suppress tumour growth and prevent restenosis after coronary vessel angioplasty.''

'''Theoharides TC et al.  1999. Stress-induced rat intestinal mast cell intragranular activation and inhibitory effect of sulfated proteoglycans.  Digestive Diseases and Sciences [1999, 44 (8 Suppl):87S-93S]. Pages 709-714. &lt;nowiki&gt;http://europepmc.org/abstract/med/10490045&lt;/nowiki&gt;''' ''Cyclic vomiting syndrome is characterized by sudden episodes of vomiting and abdominal pain. It occurs primarily in children, is exacerbated by stress, and is often considered a migraine equivalent. Migraines have been linked to mast cells, which are often found close to neurons where they are activated by neuropeptides. We investigated the ultrastructural appearance of rat ileal brush border and mast cells following acute stress by immobilization.These results suggest the possible usefulness of chondroitin sulfate in conditions such as cyclic vomiting syndrome.''

'''Thompson, W.R. 2011. Perlecan modulates the function of the osteocyte lacuno-canalicular system. University of Delaware, ProQuest Dissertations Publishing, 2011. 3443246.''' ''In this study, along with my colleagues, I examined osteocyte lacunocanalicular morphology in mice deficient in the large heparan sulfate proteoglycan (HSPG) PLN in this tissue. . . Ultrastructural measurements using electron micrograph images of PLN deficient mice demonstrate a significant decrease in osteocyte canalicular pericellular area, resulting from a reduction in the total canalicular area, when compared to controls. Additionally, PLN deficient mice show significantly diminished canalicular density and a significant reduction in the number of transverse tethering elements per canaliculus.''

'''van den Born J, van den Heuvel LP, Bakker MA, Veerkamp JH, Assmann KJ, Weening JJ, Berden JH., 1993. ''Distribution of GBM heparan sulfate proteoglycan core protein and side chains in human glomerular diseases.'' Kidney Int. 1993 Feb;43(2):454-63. &lt;nowiki&gt;http://www.ncbi.nlm.nih.gov/pubmed/8441243&lt;/nowiki&gt;'''  ''Using monoclonal antibodies (mAbs) recognizing either the core protein or the heparan sulfate (HS) side chain of human GBM heparan sulfate proteoglycan (HSPG), we investigated their glomerular distribution on cryostat sections of human kidney tissues. In conclusion, major alterations were observed in the glomerular distribution of HS and HSPG-core in various human glomerulopathies. The mAbs can be useful to further delineate the significance of HSPG and HS for glomerular diseases.''

'''Vicente, Carolina Meloni, da Silva, Daiana Aparecida, Sartorio, Priscila Veronica, Silva, Tiago Donizetti, Saad, Sarhan Sydney, Nader, Helena Bonciani, Forones, Nora Manoukian, Toma, Leny, Heparan Sulfate Proteoglycans in Human Colorectal Cancer, Analytical Cellular Pathology, 2018, 8389595, 10 pages, 2018.''' &lt;nowiki&gt;https://doi.org/10.1155/2018/8389595&lt;/nowiki&gt;'''  &lt;nowiki&gt;https://www.hindawi.com/journals/acp/2018/8389595/&lt;/nowiki&gt;''' ''Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. Heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.''

'''Vlodavestky, I. et al. 2007. Heparanase: Structure, Biological Functions, and Inhibition by Heparin-Derived Mimetics of Heparan Sulfate. Current Pharmaceutical Design, Volume 13, Number 20, July 2007, pp. 2057-2073(17). &lt;nowiki&gt;http://www.ingentaconnect.com/content/ben/cpd/2007/00000013/00000020/art00004&lt;/nowiki&gt;''' ''Heparanase is an endoglycosidase which cleaves heparan sulfate (HS) and hence participates in degradation and remodeling of the extracellular matrix (ECM). Heparanase is preferentially expressed in human tumors and its over-expression in tumor cells confers an invasive phenotype in experimental animals. These observations and the unexpected identification of a single functional heparanase, suggest that the enzyme is a promising target for anti-cancer and anti-inflammatory drug development.''

'''Weihua T. et al. 2002. Heparanase: A Key Enzyme in Invasion and Metastasis of Gastric Carcinoma.Mod Pathol 2002;15(6):593–59. &lt;nowiki&gt;http://www.nature.com/modpathol/journal/v15/n6/abs/3880571a.html&lt;/nowiki&gt;''' ''Previous reports have shown that the biochemical activity of heparanase is significantly correlated with the invasion and metastasis of malignant cells in vitro.'' ''It was concluded that heparanase might play an important role in the development of invasion and metastasis of the gastric cancer. It was indicated that patients with heparanase-positive gastric carcinoma would have a greater chance of metastasis with a poor prognosis.''

'''Whitelock John M. and Renato V. Iozzo, 2005. H''eparan Sulfate:  A Complex Polymer Charged with Biological Activity''. Chem. Rev., 2005, 105 (7), pp 2745–2764. &lt;nowiki&gt;http://pubs.acs.org/doi/pdf/10.1021/cr0102&lt;/nowiki&gt;''' ''  “HS is a complex and highly active biopolymer…” one section is on heparan sulfate therapies,''

'''Yan Yin, Adam Wang, Li Feng, Yu Wang, Hong Zhang, Ivy Zhang, Brent M Bany, Liang Ma, Heparan Sulfate Proteoglycan Sulfation Regulates Uterine Differentiation and Signaling During Embryo Implantation, Endocrinology, Volume 159, Issue 6, June 2018, Pages 2459–2472, &lt;nowiki&gt;https://doi.org/10.1210/en.2018-00105&lt;/nowiki&gt;'''  ''One important modulator of these signaling pathways is the cell surface and extracellular matrix macromolecules, heparan sulfate proteoglycans (HSPGs). HSPGs play crucial roles in signal transduction by regulating morphogen transport and ligand binding. In this study, we examine the role of HSPG sulfation in regulating uterine receptivity…''

'''Zhongjun Zhou et al. 2004.  Impaired Angiogenesis, Delayed Wound Healing and Retarded Tumor Growth in Perlecan Heparan Sulfate-Deficient Mice. DOI: 10.1158/0008-5472.CAN-04-0810 Published July 2004. &lt;nowiki&gt;http://cancerres.aacrjournals.org/content/64/14/4699&lt;/nowiki&gt;.''' ''Perlecan, a modular proteoglycan carrying primary heparan sulfate (HS) side chains, is a major component of blood vessel basement membranes.Perlecan HS-deficient (Hspg2Δ3/Δ3) mice survived embryonic development and were apparently healthy as adults. However, mutant mice exhibited significantly delayed wound healing, retarded FGF-2-induced tumor growth, and defective angiogenesis.''

'''Zhu W, Li J, Liang G. How does cellular heparan sulfate function in viral pathogenicity? Biomed Environ Sci. 2011 Feb;24(1):81-7. doi: 10.3967/0895-3988.2011.01.011. PMID: 2144084'''4. ''Heparan sulfate (HS) is ubiquitously expressed on the surfaces and in the extracellular matrix of virtually all cell types, making it an ideal receptor for viral infection. Understanding how heparan sulfate functions during virus infection in vivo may prove critical for elucidating the molecular mechanism of viral pathogenesis, and may contribute to the development of therapeutics targeting HS''.

=== Case studies ===
'''Ahn, YS., Kim, S., Kim, WJ. et al. Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses. BMC Musculoskelet Disord 22, 153 (2021). &lt;nowiki&gt;https://doi.org/10.1186/s12891-021-04021-1&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Ahn |first=Yeong-Seub |last2=Kim |first2=Sungmin |last3=Kim |first3=Woo-Jong |last4=Lim |first4=Jun-Hyuk |last5=Jung |first5=Sung-Taek |date=2021-02-06 |title=Characteristics of hip impingement syndrome in patients with multiple hereditary exostoses |url=https://doi.org/10.1186/s12891-021-04021-1 |journal=BMC Musculoskeletal Disorders |language=en |volume=22 |issue=1 |pages=153 |doi=10.1186/s12891-021-04021-1 |issn=1471-2474 |pmc=7868013 |pmid=33549073}}&lt;/ref&gt; ''Between 2001 and 2019, total 51 patients (102 hips) were evaluated in this study. Patients with MHE were classified to femoro-acetabular impingement (FAI) symptom group, ischio-femoral impingement (IFI) symptom group and non-impingement symptom group by comparing the symptoms, clinical signs and imaging studies.'' 

'''Albokhari, Daniah, Christopher R. Bailey, Francis Hwang, Clifford R. Weiss, Jonathan Forsberg, Nara Sobreira.  2023. Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands.  American Journal of Medical Genetics.''' '' ''&lt;ref&gt;{{Cite journal |last=Albokhari |first=Daniah |last2=Bailey |first2=Christopher R. |last3=Hwang |first3=Francis |last4=Weiss |first4=Clifford R. |last5=Forsberg |first5=Jonathan |last6=Sobreira |first6=Nara |date=2023 |title=Venous malformation may be a feature of EXT1-related hereditary multiple exostoses: A report of two unrelated probands |url=https://onlinelibrary.wiley.com/doi/abs/10.1002/ajmg.a.63158 |journal=American Journal of Medical Genetics Part A |language=en |volume=191 |issue=6 |pages=1570–1575 |doi=10.1002/ajmg.a.63158 |issn=1552-4833}}&lt;/ref&gt; ''Report two unrelated probands that presented with a clinical and molecular diagnosis of HME with venous malformation, a clinical feature not previously reported in individuals with HME.''

'''Anel-Quimpo, Joselynna, Mark Anthony Santiago Sandoval, Frances Lina Lantion-Ang, 2011. Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses. BMJ Journals. &lt;nowiki&gt;https://casereports.bmj.com/content/2011/bcr.12.2010.3651&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Anel-Quimpo |first=Joselynna |last2=Sandoval |first2=Mark Anthony Santiago |last3=Lantion-Ang |first3=Frances Lina |date=2011-05-17 |title=Hypercalcaemia from genitourinary tuberculosis in a female with multiple exostoses |url=https://casereports.bmj.com/content/2011/bcr.12.2010.3651 |journal=BMJ Case Reports |language=en |volume=2011 |pages=bcr1220103651 |doi=10.1136/bcr.12.2010.3651 |issn=1757-790X}}&lt;/ref&gt; ''The authors present a puzzling case of nephrolithiasis, hypercalcaemia, amenorrhoea, short stature and gross skeletal deformities in a 30-year-old female. Multiple pituitary hormone deficiency and metabolic bone disease were initially considered but were eventually excluded. The final diagnosis is genitourinary tuberculosis (TB) which caused the hypercalcaemia, nephrolithiasis and amenorrhoea, and also found to have the syndrome of multiple exostoses which explained the gross skeletal deformities and the short stature. After treatment with anti-TB therapy, there was resolution of hypercalcaemia and return of regular menstruation. The short stature and gross skeletal deformities remain as part of the congenital syndrome.''

'''Bari MS, Jahangir Alam MM, Chowdhury FR, Dhar PB, Begum A. 2012. Hereditary multiple exostoses causing cord compression. J Coll Physicians Surg Pak 22:797–799.'''&lt;ref name=&quot;:2&quot; /&gt;''' ''' ''Neurological presentations are rare and usually happened due to direct compression of a peripheral nerve or nerve root or less often the spinal cord. This case is possibly the first case of HME described from Bangladesh, presented with dorsal cord compression. Decompression was done and the complaints of myelopathy were improved.''

'''Caino, Silvia, Marisa Angelica Cubilla, Romina Alba, María Gabriela Obregón, Virginia Fano, Abel Gómez, Lorena Zecchini, Pablo Lapunzina, Miriam Aza-Carmona, Karen E. Heath, and et al. 2022. &quot;Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients&quot; Genes 13, no. 11: 2063.''' '''&lt;nowiki&gt;https://doi.org/10.3390/genes13112063&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Caino |first=Silvia |last2=Cubilla |first2=Marisa Angelica |last3=Alba |first3=Romina |last4=Obregón |first4=María Gabriela |last5=Fano |first5=Virginia |last6=Gómez |first6=Abel |last7=Zecchini |first7=Lorena |last8=Lapunzina |first8=Pablo |last9=Aza-Carmona |first9=Miriam |last10=Heath |first10=Karen E. |last11=Asteggiano |first11=Carla Gabriela |date=2022-11-07 |title=Clinical and Genetic Analysis of Multiple Osteochondromas in a Cohort of Argentine Patients |url=https://www.mdpi.com/2073-4425/13/11/2063 |journal=Genes |language=en |volume=13 |issue=11 |pages=2063 |doi=10.3390/genes13112063 |issn=2073-4425 |pmc=9690389 |pmid=36360300}}&lt;/ref&gt; ''Multiple Osteochondromatosis (MO, MIM 133700 &amp; 133701), an autosomal dominant O-glycosylation disorder (EXT1/EXT2-CDG), can be associated with a reduction in skeletal growth, bony deformity, restricted joint motion, shortened stature and pathogenic variants in two tumor suppressor genes, EXT1 and EXT2. In this work, we report a cross-sectional study including 35 index patients and 20 affected family members. Clinical phenotyping of all 55 affected cases was obtained, but genetic studies were performed only in 35 indexes.''

'''Hariri O, Al Laham O, Ibrahim Basha Z, Ghannam E, Ghannam M, Mohammad A. Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review. Int J Surg Case Rep. 2024 Apr 12;118:109633. doi: 10.1016/j.ijscr.2024.109633. Epub ahead of print. PMID: 38626641; PMCID: PMC11035074.'''&lt;ref&gt;{{Cite journal |last=Hariri |first=Omar |last2=Al Laham |first2=Omar |last3=Ibrahim Basha |first3=Zein |last4=Ghannam |first4=Eman |last5=Ghannam |first5=Mohammad |last6=Mohammad |first6=Ammar |date=2024-05 |title=Multiple Hereditary Exostoses instigating a popliteal pseudoaneurysm in a young Middle Eastern male: A case report and literature review |url=https://journals.lww.com/10.1016/j.ijscr.2024.109633 |journal=International Journal of Surgery Case Reports |language=en |volume=118 |issue=C |doi=10.1016/j.ijscr.2024.109633 |issn=2210-2612 |pmc=11035074 |pmid=38626641}}&lt;/ref&gt; ''We present the case of a 37-year-old Middle Eastern male with Multiple Hereditary Exostoses who experienced sudden-onset left lower limb pain persisting for a month prior to admission. It was associated with coldness and paresthesia of the ipsilateral lower limb. The presurgical radiological workup uncovered a popliteal pseudoaneurysm subsequent to Multiple Hereditary Exostoses.''

'''Kambouris, M., Fadda A, Al-Arraj, Y, et al., 2016. Putative Relation Between Autism Spectrum Disease &amp; Hereditary Multiple Exostosis Investigated by Whole Genome Sequencing &amp; Comparative Genome Analyses in a Family with ASD and HME with EXT-1 Mutations''' ''A family with two male children affected with ASD and HME as well as an unaffected female child, was studied to identify the Genetic basis of ASD in the family and the possible relation between ASD &amp; HME. The HME unaffected parent [mother] contributed heterozygous variants in the Heparan Sulfate biosynthesis pathway that in synergy with the EXT-1 mutation could be the genetic causes of ASD in the family.''

'''Kim, Min Jeong, Yunjin Lee, Sang Ook Nam, Young Mi Kim, 2021. An 8q24.11q24.13 Microdeletion Encompassing EXT1 in a Boy with Autistic Spectrum Disorder, Intellectual Disability, and Multiple Hereditary Exostoses. Annals of Child Neurology. Letter to the Editor, 11/9/2021.''' ''Here, we describe the case of a boy with a microdeletion (8q24.11q24.13 [118,625,768-124,169,620]×1), who presented with autism, intellectual disability, and MHE. the parents signed informed consent and approved the anonymous use of clinical and molecular data for the present diagnostic study'''''.'''

'''Küçükesmen, Çiḡdem DDS, PhD, Buḡra Özen, DDS, PhD,b and Mustafa Akçam, DDS, PhDc, 1997. Multiple Hereditary Osteochondromatosis: A Case Report. Eur J Dent. 2007 Jul; 1(3): 183–187.&lt;nowiki&gt;https://www.ncbi.nlm.nih&lt;/nowiki&gt;.''' ''Common carious lesions owing to vomiting are not widespread in children. In this case, we aimed to report an 11-years-old male patient with common carious lesions due to repeated vomitings, chewing and eating difficulty and retarded growth with Multiple Hereditary Osteochondromatosis (MHO).''

'''Li H, Yamagata T, Mori M, Momoi MY. 2002.Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1. J Hum Genet 2002;47:262-5. &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/12032595/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Li |first=Hung |last2=Yamagata |first2=Takanori |last3=Mori |first3=Masato |last4=Momoi |first4=Mariko Y. |date=2002 |title=Association of autism in two patients with hereditary multiple exostoses caused by novel deletion mutations of EXT1 |url=https://pubmed.ncbi.nlm.nih.gov/12032595 |journal=Journal of Human Genetics |volume=47 |issue=5 |pages=262–265 |doi=10.1007/s100380200036 |issn=1434-5161 |pmid=12032595}}&lt;/ref&gt;''  Two boys from separate families presented with hereditary multiple exostoses (EXT) and autism associated with mental retardation.'' 

'''Malagón, V., 2001.  Development of Hip Dysplasia in Hereditary Multiple Exostosis. Journal of Pediatric Orthopaedics, 21(2): 205-211.  &lt;nowiki&gt;https://journals.lww.com/pedorthopaedics/Abstract/2001/03000/Development_of_Hip_Dysplasia_in_Hereditary.14.aspx&lt;/nowiki&gt;''.'''''&lt;ref&gt;{{Cite web |title=Development of Hip Dysplasia in Hereditary... : Journal of Pediatric Orthopaedics |url=https://www.ovid.com/jnls/pedorthopaedics/fulltext/01241398-200103000-00014~development-of-hip-dysplasia-in-hereditary-multiple |access-date=2026-07-16 |website=Ovid |language=en}}&lt;/ref&gt; ''In approximately 25% of patients with hereditary multiple exostosis, there is an abnormal osteochondral formation localized in the femoral proximal metaphysis. Although this entity is rather frequent and quite severe, it is rarely found in the medical literature. The author describes six private cases, taken from a total of 24,000 patients (0.25/1000) as examples of this entity, and provides a review of the literature.'' 

'''Mazza, D., Fabbri, M., Calderaro, C., Iorio, C., Labianca, L., Poggi, C., Turturro, F., Montanaro, A., &amp; Ferretti, A. (2017). Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature. World journal of orthopedics, 8(5), 436–440. https://doi.org/10.5312/wjo.v8.i5.436&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Mazza |first=Daniele |last2=Fabbri |first2=Mattia |last3=Calderaro |first3=Cosma |last4=Iorio |first4=Carlo |last5=Labianca |first5=Luca |last6=Poggi |first6=Camilla |last7=Turturro |first7=Francesco |last8=Montanaro |first8=Antonello |last9=Ferretti |first9=Andrea |date=2017 |title=Chest pain caused by multiple exostoses of the ribs: A case report and a review of literature |url=http://www.wjgnet.com/2218-5836/full/v8/i5/436.htm |journal=World Journal of Orthopedics |language=en |volume=8 |issue=5 |pages=436 |doi=10.5312/wjo.v8.i5.436 |issn=2218-5836 |pmc=5434351 |pmid=28567348}}&lt;/ref&gt; ''An exceptional case of multiple internal exostoses of the ribs in a young patient affected by multiple hereditary exostoses (MHE) coming to our observation for chest pain as the only symptom of an intra-thoracic localization. The computed tomography (CT) scan revealed the presence of three exostoses located on the left third, fourth and sixth ribs, all protruding into the thoracic cavity, directly in contact with visceral pleura. Moreover, the apex of the one located on the sixth rib revealed to be only 12 mm away from pericardium.'' 

'''Montgomery BK, Cahan EM, Frick S. Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey- PubMed''' '''. Cureus. 2019 Dec 23;11(12):e6452. doi: 10.7759/cureus.6452. PMID: 32010535; PMCID: PMC6975245'''''.''&lt;ref&gt;{{Cite journal |last=Montgomery |first=Blake K |last2=Cahan |first2=Eli M |last3=Frick |first3=Steve |date=2019-12-23 |title=Spinal Screening MRI Trends in Patients with Multiple Hereditary Exostoses: National Survey |url=https://www.cureus.com/articles/23789-spinal-screening-mri-trends-in-patients-with-multiple-hereditary-exostoses-national-survey |journal=Cureus |language=en |doi=10.7759/cureus.6452 |issn=2168-8184 |pmc=6975245 |pmid=32010535}}&lt;/ref&gt;  ''Background Multiple hereditary exostoses (MHE) is a rare disease characterized by multiple osteochondromas. Osteochondromas growing into the spinal canal can produce devastating consequences, including permanent neurologic deficits and even death.  This study presents a case of an intracanal osteochondroma at C1 identified by routine screening and a survey describing current practices of MHE experts.''

'''Narvid, J., M. L. Gorno-Tempini, A. Slavotinek, S. J. DeArmond, Y. H. Cha, B. L. Miller &amp; K. Rankin, 2009. Of brain and bone: The unusual case of Dr. A. Neurocase Vol. 15, Iss. 3, 2009.''' '''&lt;nowiki&gt;http://www.tandfonline.com/doi/full/10.1080/13554790802632967&lt;/nowiki&gt;'''&lt;ref&gt;{{Cite journal |last=Narvid |first=J. |last2=Gorno-Tempini |first2=M. L. |last3=Slavotinek |first3=A. |last4=DeArmond |first4=S. J. |last5=Cha |first5=Y. H. |last6=Miller |first6=B. L. |last7=Rankin |first7=K. |date=2009-06-01 |title=Of brain and bone: The unusual case of Dr. A |url=https://doi.org/10.1080/13554790802632967 |journal=Neurocase |volume=15 |issue=3 |pages=190–205 |doi=10.1080/13554790802632967 |issn=1355-4794 |pmc=2997763 |pmid=20183548}}&lt;/ref&gt;''. Frontotemporal dementia (FTD) is a clinical syndrome characterized by progressive decline in social conduct and a focal pattern of frontal and temporal lobe damage. Its biological basis is still poorly understood but the focality of the brain degeneration provides a powerful model to study the cognitive and anatomical basis of social cognition. Here, we present Dr. A, a patient with a rare hereditary bone disease (hereditary multiple exostoses) and FTD (pathologically characterized as Pick's disease),  This case provides new evidence regarding the neural basis of social cognition and suggests a possible genetic link between bone disease and FTD.''

'''Puiu1, Maria , Iulia Simina-Jurca, Simona Dumitriu, Smaranda Arghirescu,  Adela Chirita-Emandi,  2012. . Multiple Hereditary Exostoses - Clinical Features and Management.''' ''We report two cases of skeletally immature patients who presented with multiple exostoses, bone deformation without bone pain; and growth and pubertal retardation. The cases need adequate counseling, long-term follow-up, and measures to improve the quality of life of patients with multiple hereditary exostoses.''

'''Stitzman Wengrowicz, M.L., J  Pretell-Mazzini,  J.P. Dormans, R.S. Davidson, 2011.. Regression of a Sessile Osteochondroma: A Case Study and Review of the Literature.''' ''&lt;nowiki&gt;https://www.researchgate.net/publication/267426996_Regression_of_a_Sessile_Osteochondroma_A_Case_Study_and_Review_of_the_Literature&lt;/nowiki&gt; . The most common benign bone tumor is osteochondroma.  Its natural history is poorly understood as a consequence of its benign symptomatology in most cases. It typically grows in childhood and growth during adulthood can be a sign of malignant  degeneration. We present  a case of  spontaneous regression of  a solitary osteochondroma.  A review of the  current  literature which  reveals 21  other cases of  spontaneous regression  of solitary  osteochondromas is also discussed. We believe that the possibility of regression of solitary osteochondromas should be taken into account when considering surgical excision.''

'''Viala P, Vanel D, Larbi A, Cyteval C, Laredo JD. Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. Skeletal Radiol. 2012;41:1637–40. [PubMed] &lt;nowiki&gt;https://pubmed.ncbi.nlm.nih.gov/22865159/&lt;/nowiki&gt;.'''&lt;ref&gt;{{Cite journal |last=Viala |first=Pierre |last2=Vanel |first2=Daniel |last3=Larbi |first3=Ahmed |last4=Cyteval |first4=Catherine |last5=Laredo |first5=Jean-Denis |date=2012-12 |title=Bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses |url=https://pubmed.ncbi.nlm.nih.gov/22865159 |journal=Skeletal Radiology |volume=41 |issue=12 |pages=1637–1640 |doi=10.1007/s00256-012-1488-0 |issn=1432-2161 |pmid=22865159}}&lt;/ref&gt; ''We report a case of bilateral ischiofemoral impingement in a patient with hereditary multiple exostoses. The association of exostoses and femoral metaphyseal widening resulted in the narrowing of the ischiofemoral spaces.''

'''Wang YZ, Park KW, Oh CS, Ahn YS, Kang QL, Jung ST, Song HR. Developmental pattern of the hip in patients with hereditary multiple exostoses. BMC Musculoskelet Disord. 2015;16:54'''''.'' '''https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/&lt;nowiki/&gt;.'''&lt;ref&gt;{{Cite journal |last=Wang |first=Ya-Zhou |last2=Park |first2=Kwang-Won |last3=Oh |first3=Chang-Seon |last4=Ahn |first4=Yeong-Seub |last5=Kang |first5=Qing-Lin |last6=Jung |first6=Sung-Taek |last7=Song |first7=Hae-Ryong |date=2015-03-15 |title=Developmental pattern of the hip in patients with hereditary multiple exostoses |url=https://pmc.ncbi.nlm.nih.gov/articles/PMC4429362/ |journal=BMC musculoskeletal disorders |volume=16 |pages=54 |doi=10.1186/s12891-015-0514-5 |issn=1471-2474 |pmc=4429362 |pmid=25888017}}&lt;/ref&gt; '''C'''''oxa valga is a common clinical feature of hereditary multiple exostoses (HME). The current study aimed to determine the unique developmental pattern of the hip in patients with HME and evaluate the factors that influence its progression.''

'''Wiater JM, Farley FA. Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature. Am J Orthop (Belle Mead NJ). 1999 Jul;28(7):412-6. PMID: 10426440.'''&lt;ref&gt;{{Cite journal |last=Wiater |first=J. M. |last2=Farley |first2=F. A. |date=1999-07 |title=Popliteal pseudoaneurysm caused by an adjacent osteochondroma: a case report and review of the literature |url=https://pubmed.ncbi.nlm.nih.gov/10426440 |journal=American Journal of Orthopedics |volume=28 |issue=7 |pages=412–416 |issn=1078-4519 |pmid=10426440}}&lt;/ref&gt; ''A male 17-year-old with multiple hereditary exostoses presented with a mass in the distal left thigh several days after lifting weights. An arteriogram showed a popliteal artery pseudoaneurysm adjacent to a femoral osteochondroma. The osteochondroma was excised and the artery was repaired with a saphenous vein interposition graft. A review of the literature identified 23 similar reports. The average age of the patients was 21.3 years. Seventy-eight percent were men and half of the patients had multiple hereditary exostoses. Ten patients were initially misdiagnosed. The clinician should consider the diagnosis of pseudoaneurysm in a young patient with an osteochondroma and a mass about the knee.''

'''Zaijun L, Xinhai Y, Zhipeng W, Wending H, Quan H, Zhenhua Z, Dapeng F, Jisheng Z, Wei Z, Jianru X. 2013. Outcome and prognosis of myelopathy and radiculopathy from osteochondroma in the mobile spine: a report on 14 patients. J Spinal Disord Tech 26:194–199.''' ''Fourteen symptomatic spinal osteochondroma (OC)  cases, including 2 hereditary multiple exostoses, were treated surgically from 2001 to 2010.'' 

== People and books with HME: ==
[[w:Deena_Larsen|Deena Larsen]] wrote about her mother at http://www.deenalarsen.net/firs

Irv Rosenfeld wrote about his experiences with medical marijuana from the U.S. government in My Medicine.&lt;ref&gt;{{Cite web |title=MY MEDICINE |url=https://www.goodreads.com/book/show/22078567-my-medicine |access-date=2026-07-15 |website=Goodreads |language=en}}&lt;/ref&gt;

= Spanish Translation =


Problemas de deficiencia de proteoglicano de sulfato de heparán (HSPG). La MHE es el resultado de una mutación en los genes EXT1 y EXT2. Los pacientes con MHE tienen una biosíntesis de HSPG defectuosa: sus cuerpos no producen HSPG (cf Cueller et al. 2013 y Jones et al. 2014). Los HSPG son parte de cada superficie celular y regulan los procesos biológicos (cf Zak et al. 2002, Meneghetti et al. 2015). Desempeñan un papel vital en la adhesión, migración, crecimiento y comunicación celular (Vicente et al. 2018). Whitlock e Iozzo (2005) han identificado varias enfermedades relacionadas con la ausencia de HSPG (es decir, si un proceso corporal requiere HSPG y no hay suficiente HSPG para completar esa función, entonces podrían ocurrir estos problemas). Los pacientes con MHE han reportado síntomas como:

* Baja masa ósea (Nozawa et al. 2018 y Matsumoto et al. 2020)
* Deficiencias neurológicas: Trastorno del espectro autista (Li et al, 2002, Fumitoshi et al. 2012, Irie et al, 2012, Yamaguchi 2012, Perez et al. 2015, Kambouris et al. 2016, Kim et al 2022); y problemas cognitivos (Farhan et al. 2015)
* Demencia frontotemporal (Narvid et al. 2009) y TDAH (Mooney et al. 2016), función cerebral (Condomitti y Wit 2018). Vea también el vídeo de ratones MHE en &lt;nowiki&gt;https://www.youtube.com/watch?v=6-EXRt_YL6A&lt;/nowiki&gt;.
* Enfermedades oculares (Park y Shukla, 2013)
* Defectos dentales (Kucukesmen et al. 2007 y Wiweger et al. 2012)
* Prediabetes (Heibert 2021)Diabetes y dificultad para controlar la glucosa (Matsuzawa 2021)
* Reacciones medicamentosas inusuales (muchos medicamentos actúan sobre el dominio de unión del heparán [Boer y Gaillard 2007]) 
* Fatiga severa y continua (Berg et al. 1999)
* Problemas gástricos graves, incluidas úlceras no causadas por H. pylori (Ascencio et al. 1993 y Chmiela et al. 1995), cáncer gástrico (Weihua et al. 2002) y síndrome de vómitos cíclicos (Kucukesmen et al. 2007 y Theoharides et al. 1999)
* Cálculos renales y otros problemas (véase Van den Born et al. 1993 y Farhan et al. 2015)
* Vértigo e hiperacusia (Lundberg et al., 2014) y migrañas
* Problemas pulmonares (Nackerts et al. 1997 y Haeger et al. 2016)
* Anemia (Poli et al. 2017), coágulos sanguíneos y coagulación (Stringer y Gallagher 1997 y Ho et al. 1997), pseudoaneurismas (Wiater y Farley 1996 y Harari et al. 2024)
* Problemas menstruales y de embarazo extremadamente dolorosos (Alphin et al. 1988, Yin et al. 2018)
* Inflamación (Parroquia 2005); cicatrización lenta de heridas (Zhongjun et al. 2004); cicatrices y queloides (Hosalkar et al. 2007, y problemas del tejido conectivo (Forsberg y Kjellen, 2001 y Otsuka et al. 2020).
* Funciones hepáticas (Arnold et al. 2020 y Dituri et al. 2022)
* Funciones del colesterol y los lípidos (Kolsett y Salmverta 1999) y Síntesis de vitamina D (Cooper 2021)  '''Problemas de crecimiento óseo.''' En la MHE, la falta de HSPG hace que los pacientes desarrollen exostosis, que son tumores benignos en múltiples ubicaciones en todo el cuerpo (Brown 2008, Thompson 2011 y Mansouri et al. 2017). La gravedad (número y tamaño de los tumores y otras complicaciones) de la MHE varía de un paciente a otro. Las exostosis en sí mismas pueden causar numerosos problemas, incluidos: irritación de tendones y músculos que produce dolor y pérdida de movimiento, deformidad esquelética, baja estatura, discrepancia en la longitud de las extremidades, subluxaciones y deformidad angular. Los problemas directamente asociados con estas exostosis incluyen:

* Dolor crónico y problemas con la calidad de vida (Goud et al. 2012)
* Inflamación, respuestas inmunitarias (Callaghan et al. 2018 y Collins y Troeberg 2019)
* Formación de bursa y bursitis resultante, así como artritis de aparición temprana.
* Problemas respiratorios y pulmonares al estar sobre costillas que sobresalen hacia la cavidad torácica (Mazza et al. 2017)
* Irritación de un nervio cercano (dolor, debilidad, entumecimiento, hormigueo)
* Aneurisma de vasos sanguíneos por exostosis que presionan los vasos sanguíneos u otros problemas vasculares (Albokhari et al. 2023)
* Problemas de compresión de la médula espinal: incontinencia, daño nerv'''Résumé de la MEM pour les médecins et les écoles'''

== References ==</text>
      <sha1>2azevmycls58y1h7ytklx2ywxm91efo</sha1>
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  <page>
    <title>Taiwan history/Taiwan in World War II</title>
    <ns>0</ns>
    <id>484819</id>
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      <timestamp>2026-07-16T12:09:19Z</timestamp>
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        <username>MathXplore</username>
        <id>3097823</id>
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      <text bytes="1183" sha1="cj38r083uyz3so2swdyou7enrjk0orw" xml:space="preserve">After Japan started invading China, Southeast Asia and the America, Taiwan, as a colony of Japan, automatically entered the war.
==Affect==
===Military===
[[File:Takasago Volunteer Corps.JPG|thumb|Taiwan Indigenous Volunteer Troops]]
More than 200,000 Taiwanese men served in the Imperial Japanese Army and Navy. Around 2,000 Taiwanese women were forced into sexual slavery by the Japanese military system. Taiwan's strategic location along the resource logistics route to Southeast Asia and the Japanese home islands made it a key operational hub. Japan used Taiwanese airfields to launch strikes on the Philippines, Malaysia, and Indonesia. Starting in late 1943, American began bombing Taiwan until the end of the war.
===Culture===
The Japanese colonial government banned Chinese-language sections in newspapers and prohibited the use of local dialects. Most of the political movement was forced to end.Japan pressured Taiwanese families to abandon their Chinese surnames and adopt Japanese ones.Literature, theater, and music were strictly censored and repurposed to serve the war effort. Pop music and traditional opera were replaced by patriotic military marches.

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      <text bytes="1644" sha1="2mrp9w92t0hlrsaiiejcdq9muywoywa" xml:space="preserve">(currently under reflexion)

== A space-time reference frame without massive particles ==

Let us consider a one-dimensional space.

Let A and B be two photon trains moving in opposite directions. We assume that the photons within a given train are evenly spaced, like the crests of a periodic wave.

Let A(i) be the i-th photon of train A and B(i) be the i-th photon of train B. We assume that A moves from left to right and that its photons are numbered in the direction opposite to the motion; B moves from right to left, and its photons are also numbered in the direction opposite to the motion.

The encounter between A(i) and B(i) constitutes an event e(i) in space-time. All events e(i) lie along the same time-like trajectory. The interval between e(i) and e(i+1) is constant and can serve as a unit of time measurement.

More generally, the encounter between A(i+j) and B(i-j) constitutes an event e(i,j) in spacetime. For a given j, all events e(i,j) lie on the same timelike trajectory T(j). All trajectories T(j) are parallel to one another, in the sense that they never intersect. They can therefore be identified as the trajectories of objects at rest relative to each other. The interval between e(i,j) and e(i,j+1) depends on neither i nor j; it is spacelike and can serve as a unit of distance measurement.

The events e(i,j) can therefore be regarded as a space-time reference frame, as they allow for the measurement of distances and durations.

In three-dimensional space, six photon trains traveling in opposite directions along three spatial axes are required to establish a space-time reference frame.

(...)

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      <comment>/* A space-time reference frame without massive particles */</comment>
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      <text bytes="2384" sha1="bctie6uhc6vrm5ex4ut9mglp9ar8kse" xml:space="preserve">(currently under reflexion)

== A space-time reference frame without massive particles ==

Let us consider a one-dimensional space.

Let A and B be two photon trains moving in opposite directions. We assume that the photons within a given train are evenly spaced, like the crests of a periodic wave.

Let A(i) be the i-th photon of train A and B(i) be the i-th photon of train B. We assume that A moves from left to right and that its photons are numbered in the direction opposite to the motion; B moves from right to left, and its photons are also numbered in the direction opposite to the motion.

The encounter between A(i) and B(i) constitutes an event e(i) in space-time. All events e(i) lie along the same time-like trajectory. The interval between e(i) and e(i+1) is constant and can serve as a unit of time measurement.

More generally, the encounter between A(i+j) and B(i-j) constitutes an event e(i,j) in spacetime. For a given j, all events e(i,j) lie on the same timelike trajectory T(j). All trajectories T(j) are parallel to one another, in the sense that they never intersect. They can therefore be identified as the trajectories of objects at rest relative to each other. The interval between e(i,j) and e(i,j+1) depends on neither i nor j; it is spacelike and can serve as a unit of distance measurement.

The events e(i,j) can therefore be regarded as a space-time reference frame, as they allow for the measurement of distances and durations.

In three-dimensional space, six photon trains traveling in opposite directions along three spatial axes are required to establish a space-time reference frame.

Consider two monochromatic plane waves that do not travel in exactly the same direction. There always exists a reference frame—indeed, an infinite number of them—in which these two monochromatic plane waves travel in opposite directions and have the same wavelength. In such a frame, the superposition of the two plane waves forms a standing wave. A standing wave simultaneously defines a unit of time (its period) and a unit of length (its wavelength). Two monochromatic plane waves traveling in different directions always define reference frames in which their superposition is stationary. Six monochromatic plane waves traveling in suitably chosen directions define a unique rest frame: the frame in which they are all stationary.

(...)

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      <comment>/* A space-time reference frame without massive particles */</comment>
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      <text bytes="2762" sha1="94vjcn4ekr5cqiklbkjhchxiftiqvfa" xml:space="preserve">(currently under reflexion)

== A space-time reference frame without massive particles ==

Let us consider a one-dimensional space.

Let A and B be two photon trains moving in opposite directions. We assume that the photons within a given train are evenly spaced, like the crests of a periodic wave.

Let A(i) be the i-th photon of train A and B(i) be the i-th photon of train B. We assume that A moves from left to right and that its photons are numbered in the direction opposite to the motion; B moves from right to left, and its photons are also numbered in the direction opposite to the motion.

The encounter between A(i) and B(i) constitutes an event e(i) in space-time. All events e(i) lie along the same time-like trajectory. The interval between e(i) and e(i+1) is constant and can serve as a unit of time measurement.

More generally, the encounter between A(i+j) and B(i-j) constitutes an event e(i,j) in spacetime. For a given j, all events e(i,j) lie on the same timelike trajectory T(j). All trajectories T(j) are parallel to one another, in the sense that they never intersect. They can therefore be identified as the trajectories of objects at rest relative to each other. The interval between e(i,j) and e(i,j+1) depends on neither i nor j; it is spacelike and can serve as a unit of distance measurement.

The events e(i,j) can therefore be regarded as a space-time reference frame, as they allow for the measurement of distances and durations.

In three-dimensional space, six photon trains traveling in opposite directions along three spatial axes are required to establish a space-time reference frame.

Consider two monochromatic plane waves that do not travel in exactly the same direction. There always exists a reference frame—indeed, an infinite number of them—in which these two monochromatic plane waves travel in opposite directions and have the same wavelength. In such a frame, the superposition of the two plane waves forms a standing wave. A standing wave simultaneously defines a unit of time (its period) and a unit of length (its wavelength). Two monochromatic plane waves traveling in different directions always define reference frames in which their superposition is stationary. Six monochromatic plane waves traveling in suitably chosen directions define a unique rest frame: the frame in which they are all stationary.

Conclusion: restless particles, such as photons, which always travel at the speed of light, suffice to determine the geometry of spacetime. They define rest frames from which all geometric relations can be determined. Massive particles are not necessary to determine the geometry of spacetime. Restless particles therefore appear to be more fundamental than massive particles.

(...)

{{BookCat}}</text>
      <sha1>94vjcn4ekr5cqiklbkjhchxiftiqvfa</sha1>
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    <revision>
      <id>4654757</id>
      <parentid>4654683</parentid>
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      <text bytes="2695" sha1="eewst9fpp5afk001lm5ckvsko411wd5" xml:space="preserve">(currently under reflexion)

== A space-time reference frame without massive particles ==

Let us consider a one-dimensional space.

Let A and B be two photon trains moving in opposite directions. We assume that the photons within a given train are evenly spaced, like the crests of a periodic wave.

Let A(i) be the i-th photon of train A and B(i) be the i-th photon of train B. We assume that the photons of A and B are numbered in the direction opposite to their motion: A(i+1) follows A(i), and B(i+1) follows B(i).

The encounter between A(i) and B(i) constitutes an event e(i) in space-time. All events e(i) lie along the same time-like trajectory. The interval between e(i) and e(i+1) is constant and can serve as a unit of time measurement.

More generally, the encounter between A(i-j) and B(i+j) constitutes an event e(i,j) in spacetime. For a given j, all events e(i,j) lie on the same timelike trajectory T(j). All trajectories T(j) are parallel to one another, in the sense that they never intersect. They can therefore be identified as the trajectories of objects at rest relative to each other. The interval between e(i,j) and e(i,j+1) depends on neither i nor j; it is spacelike and can serve as a unit of distance measurement.

The events e(i,j) can therefore be regarded as a space-time reference frame, as they allow for the measurement of distances and durations.

In three-dimensional space, six photon trains traveling in opposite directions along three spatial axes are required to establish a space-time reference frame.

Consider two monochromatic plane waves that do not travel in exactly the same direction. There always exists a reference frame—indeed, an infinite number of them—in which these two monochromatic plane waves travel in opposite directions and have the same wavelength. In such a frame, the superposition of the two plane waves forms a standing wave. A standing wave simultaneously defines a unit of time (its period) and a unit of length (its wavelength). Two monochromatic plane waves traveling in different directions always define reference frames in which their superposition is stationary. Six monochromatic plane waves traveling in suitably chosen directions determine a unique rest frame: the frame in which their superposition is stationary.

Conclusion: restless particles, which always travel at the speed of light, such as photons, suffice to determine the geometry of spacetime. They define rest frames from which all geometric relations can be determined. Massive particles are not necessary to determine the geometry of spacetime. Restless particles therefore appear to be more fundamental than massive particles.

(...)

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  <page>
    <title>Chinese (Mandarin)/Lesson 16</title>
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=16.Basic Chinese History (第十六课：基本中国历史/第十六課：基本中國歷史)=
{| width=&quot;80%&quot;
! Traditional Characters
! Simplified Characters
|-
|
唐堯虞舜夏商周， &lt;br /&gt;
春秋戰國亂悠悠。&lt;br /&gt;
秦漢三國西東晉，&lt;br /&gt;
南朝北朝是對頭。&lt;br /&gt;
隋唐五代又十國，&lt;br /&gt;
宋元明清帝王休。&lt;br /&gt;
|
唐尧虞舜夏商周， &lt;br /&gt;
春秋战国乱悠悠。 &lt;br /&gt;
秦汉三国西东晋，&lt;br /&gt;
南朝北朝是对头。 &lt;br /&gt;
隋唐五代又十国，&lt;br /&gt;
宋元明清帝王休。 &lt;br /&gt;
|-
! Pīnyīn
! English
|-
|
Táng yáo yúshùnxià shāng zhōu, &lt;br/&gt;
chūnqiū zhànguó luàn yōuyōu. &lt;Br/&gt;
qínhàn sānguó xī dōngjìn,&lt;br/&gt;
náncháo běicháo shì duìtóu. &lt;Br/&gt;
suítáng wǔdài yòu shí guó,&lt;br/&gt;
sòngyuánmíng qīng dìwáng xiū. &lt;Br/&gt;
|
Yao, Shun, Xia, Shang, Zhou,&lt;br /&gt;
Spring and Autumn, Warring States, chaos in full blow.&lt;br /&gt;
Qin, Han, Three Kingdoms, West and East Jin,&lt;br /&gt;
Southern and Northern Dynasties, rivalries begin.&lt;br /&gt;
Sui, Tang, Five Dynasties and Ten Kingdoms wide,&lt;br/&gt;
Song, Yuan, Ming, Qing, the emperors died. &lt;br/&gt;
|}


=== Vocabulary &amp; Cultural Notes ===
* '''乱悠悠/亂悠悠''' (luàn yōu yōu): A descriptive phrase meaning chaotic, messy, or long-lasting turmoil. 
* '''是对头/是對頭''' (shì duìtóu): An idiom meaning to be adversaries, rivals, or opposing forces.
* '''帝王休''' (dìwáng xiū): Literally translates to &quot;emperors cease/stop,&quot; marking the historical transition from imperial rule to a republic following the 1911 Xinhai Revolution.

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        <id>3609960</id>
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=16.Basic Chinese History (第十六课：基本中国历史/第十六課：基本中國歷史)=
{| width=&quot;80%&quot;
! Traditional Characters
! Simplified Characters
|-
|
唐堯虞舜夏商周， &lt;br /&gt;
春秋戰國亂悠悠。&lt;br /&gt;
秦漢三國西東晉，&lt;br /&gt;
南朝北朝是對頭。&lt;br /&gt;
隋唐五代又十國，&lt;br /&gt;
宋元明清帝王休。&lt;br /&gt;
|
唐尧虞舜夏商周， &lt;br /&gt;
春秋战国乱悠悠。 &lt;br /&gt;
秦汉三国西东晋，&lt;br /&gt;
南朝北朝是对头。 &lt;br /&gt;
隋唐五代又十国，&lt;br /&gt;
宋元明清帝王休。 &lt;br /&gt;
|-
! Pīnyīn
! English
|-
|
Táng yáo yúshùnxià shāng zhōu, &lt;br/&gt;
chūnqiū zhànguó luàn yōuyōu. &lt;Br/&gt;
qínhàn sānguó xī dōngjìn,&lt;br/&gt;
náncháo běicháo shì duìtóu. &lt;Br/&gt;
suítáng wǔdài yòu shí guó,&lt;br/&gt;
sòngyuánmíng qīng dìwáng xiū. &lt;Br/&gt;
|
Yao, Shun, Xia, Shang, Zhou,&lt;br /&gt;
Spring and Autumn, Warring States, chaos in full blow.&lt;br /&gt;
Qin, Han, Three Kingdoms, West and East Jin,&lt;br /&gt;
Southern and Northern Dynasties, rivalries begin.&lt;br /&gt;
Sui, Tang, Five Dynasties and Ten Kingdoms wide,&lt;br/&gt;
Song, Yuan, Ming, Qing, the emperors died. &lt;br/&gt;
|}
==Explaination==
Tang Yao and Yu Shun are two of the most revered legendary sage-kings of ancient China. The Xia, Shang, and Zhou were the first dynasties in ancient China. During the Spring and Autumn and Warring States periods, China broke into many small states that attacked one another. The Qin and Han dynasties successfully unified China. After the Han dynasty fell, China broke into three major states until the Jin unified them all. China later split again into the Northern and Southern dynasties. After the Sui and Tang unified China, the country broke into the Five Dynasties in the north and the Ten Kingdoms in the south. Following multiple subsequent dynasties, the 1911 Xinhai Revolution took place, and China became a republic.
== Vocabulary &amp; Cultural Notes ==
* '''乱悠悠/亂悠悠''' (luàn yōu yōu): A descriptive phrase meaning chaotic, messy, or long-lasting turmoil. 
* '''是对头/是對頭''' (shì duìtóu): An idiom meaning to be adversaries, rivals, or opposing forces.
* '''帝王休''' (dìwáng xiū): Literally translates to &quot;emperors cease/stop,&quot; marking the historical transition from imperial rule to a republic following the 1911 Xinhai Revolution.
==Related Books==
*[[History of China]]
*[[Chinese History]]

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      <comment>/* Neutral density (ND) */  [[[w:en:User:Alexis Jazz/Factotum|Factotum]]]</comment>
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[[File:Neutral density filter demonstration.jpg|thumb|A [[w:Neutral-density filter|neutral-density (ND)]] filter]]
Lens filters can be installed in front of your [[Photography Equipment/Lenses|lens]]. This page will discuss their form factors, describe some popular types, how they work and what to look for when buying.

==Form factors==

===Round screw-on filters===
This is the most common type. They have a screw thread that fits into a groove on your lens. You screw them on, simple as that. The filter typically contains a groove of the same size to allow the stacking of multiple lens filters. Their size is measured in millimeters, you have to make sure that the filter you buy matches the groove on your lens. On your lens you will often find an indication like &quot;∅ 58mm&quot;, this means you need a 58mm filter.

Larger filters can be fitted on smaller lenses with an adapter. The reverse (a smaller filter on a larger lens) is possible but not advised as it will likely result in [[w:vignetting|vignetting]]. It may work on a zoom lens however, as you may be able to zoom past the vignetting. Many cameras also crop the image when shooting video which may remove some vignetting.

If you have multiple lenses with similarly (but not identical) sized lens threads, like a 58mm and a 52mm, you should buy 58mm filters and a 52mm to 58mm adapter. This works for any size, but an 82mm filter on a 37mm lens may be awkward to use.

===Round magnetic filters===
Some filters can be snapped on the lens using magnets. They use a magnetic adapter ring that is screwed onto the lens. Unlike screw-on filters, magnetic filters are not standardized. Magnetic filters and adapter rings from various manufacturers may or may not be interoperable.

===Rectangular slide-in filters===
These are mostly used in professional productions for color filters and fixed neutral density filters as they can be swapped quickly with little risk of accidentally putting fingerprints on them.

==Material==
The very cheapest lens filters could be made of plastic. Do not buy these, buy glass. Not all glass is created equal, but the glass substrate is generally not the limiting factor for image quality.

==Coatings==
Lens filters may have various coatings. The type and quality of coating will vary between manufacturers. If you pay less than 10 USD/EUR per filter, you are almost certainly buying uncoated filters. You can use these, but they may induce [[w:lens flare|lens flare]] and other unwanted reflections. This being said, if you are taking a photo of a car in the sun even a scratched, uncoated CPL filter you found in a garage sale for $3 will vastly improve the final image over no filter at all.

The next step is a &quot;multi coated&quot; filter, often indicated by the initialism &quot;MC&quot; on the side of the filter. These are much better generally and start from 15 USD/EUR.

Finally there are filters with &quot;multiple resistive coatings&quot;, often indicated with the initialism &quot;MRC&quot; on the side of the filter. While uncoated and multi coated filters are sometimes advertised as &quot;anti scratch&quot;, this merely means those filters protect your ''lens'' from being scratched. A filter with MRC has some resistance to getting scratched itself and is easier to clean. This improves their longevity. They tend to cost a bit more, generally starting from roughly 25 USD/EUR.

Some minor scratches or dust or generally not visible in your photos unless you use an extremely small aperture, like f/22.

==Utilitarian filters==

===UV/protectors===
While technically different, these are identical in practice. You don't need a UV filter, it will not improve image quality. It will, however, protect your (potentially expensive) lens from fingerprints, sand, dirt, scratches, etc. Think of it like a screen protector on a smartphone.

===Circular polarization (CPL)===
Similar to [[w:polarized sunglasses|polarized sunglasses]], this is a single sheet of polarized glass. It can be rotated inside of the frame to remove polarized light. This can often remove reflections from windows, cars and water, allowing you to see through them. They may also darken the image on LCD and OLED displays.

A CPL filter will reduce how much light hits your sensor overall, this is normal.

===Neutral density (ND)===
[[File:Long exposure night shot of Sutton pace.jpg|thumb|Long exposure shot resulting in long streaks of headlights]]
[[File:Long exposure done at 5 in the morning (Unsplash).jpg|thumb|Long exposure shot of the sea, making the water appear like mist]]
Often described as &quot;sunglasses for your camera&quot;. In photography they are useful in two cases: if your scene is extremely bright and you are using a lens with a large aperture you might end maxing out your ISO and shutter speed values while still having an overexposed image. This is uncommon, but when it happens an ND-filter is the only solution. More commonly it is used for long-exposure photography, resulting in extreme [[w:motion blur|motion blur]].

In videography, an exposure time of half the length of the frame display time (e.g. 1/48 of a second for 24 frames per second) is commonly used to make a video more pleasant to watch with some motion blur. If your ISO is already maxed out and you'd rather not decrease the aperture you're out of options and need an ND-filter to get the exposure under control.

=====Fixed ND=====
This is the simplest ND filter. It makes the whole image darker and isn't customizable. This generally results in the highest quality, but is the least convenient. A generally useful set would consist of an 8ND (3 stops), 64ND (6 stops)  and 1000ND (9 stops) filter. 3 stops is often used for outdoor videography, 6 stops for outdoor videography on a very sunny day and 9 stops is useful for long-exposure photography.

=====Gradient ND (GND)=====
The same as a fixed ND, but with a gradient in darkness from end to end. Often used to darken the bright sky while allowing more light from the bottom half to reach the lens.

=====Variable ND (VND)=====
This filter consists of two sheets of polarized glass. One of the sheets is fixed while the other can be rotated with a dial. How much light passes through depends on how well the polarization of the two piece of glass aligns.

This filter will result in a color shift, how strong this shift will be varies strongly between various brands and models. When designed poorly it may also result in a &quot;cross&quot; effect where the image is darkened unevenly. Do not buy a VND that promises a range of 1-9 stops, the last three stops will likely be unacceptable.

You can get the effect of a VND by using two CPL filters if you mount one in the wrong direction (possible using a male-male lens adapter). This isn't recommended.

If you don't need to use a lens hood, you should frankly not buy a VND, buy a VND plus CPL instead. That's essentially the same product with an extra dial to control the rotation of both sheets of glass. A VND can be used as a CPL even, by rotating the whole filter within the groove of your lens. This creates a risk of the filter rattling around or even falling out, a problem that is solved by getting a VND plus CPL.

=====VND plus CPL=====
It's the same as a VND, but allows to rotation of both sheets of glass independently. They do have one downside: they generally don't fit when using a lens hood.

===Diopter===
Moves the focus closer. Can be useful for macro photography with a non-macro lens. Will create considerable distortion, though. Stackable.

===Clear sky (FLD)===
Fluorescent filter, often sold as a &quot;clear sky&quot; filter for night photography to counter [[w:light pollution|light pollution]]. May have been useful at one point in time, but has no effect on modern street lighting. Do not buy.

==Artistic filters==
Filters that are used exclusively for artistic purposes. Unless indicated otherwise they can be stacked for a stronger or extra effect.
===Black mist===
Softens light sources. Makes images look less harsh/clinical while maintaining detail in other areas. Comes in different strengths which aren't really standardized. 1/8 is usually a mild effect, 1/4 is &quot;standard&quot;, 1/2 is strong. 1/8 or 1/4 is usually sufficient. Some photographers leave one on their lens permanently.

===White mist===
While similar in name, not quite the same effect as black mist. They create a foggy white dream-like haze.

===Kaleidoscope===
Creates a [[w:kaleidoscope|kaleidoscope]] effect. Could be used to create a &quot;dizzy&quot; effect.

===Blue streak===
Causes blue streaks of light in one direction to radiate from light sources. May create a &quot;futuristic&quot; vibe.

===Starburst===
Causes streaks of light to radiate from light sources, making them look like stars.

===Color filter===
As it says on the tin: it just filters colors, so your image looks blue/yellow/green/etc. May be used for artistic purposes, but the effect is easily and more flexibly achieved in post. Stacking the same color will have little effect.

==Where to buy==

===Used===

===Specialized camera shops===

===Western marketplaces===

===Chinese marketplaces===

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      <contributor>
        <username>Alexis Jazz</username>
        <id>470964</id>
      </contributor>
      <comment>/* VND plus CPL */  [[[w:en:User:Alexis Jazz/Factotum|Factotum]]]</comment>
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[[File:Neutral density filter demonstration.jpg|thumb|A [[w:Neutral-density filter|neutral-density (ND)]] filter]]
Lens filters can be installed in front of your [[Photography Equipment/Lenses|lens]]. This page will discuss their form factors, describe some popular types, how they work and what to look for when buying.

==Form factors==

===Round screw-on filters===
This is the most common type. They have a screw thread that fits into a groove on your lens. You screw them on, simple as that. The filter typically contains a groove of the same size to allow the stacking of multiple lens filters. Their size is measured in millimeters, you have to make sure that the filter you buy matches the groove on your lens. On your lens you will often find an indication like &quot;∅ 58mm&quot;, this means you need a 58mm filter.

Larger filters can be fitted on smaller lenses with an adapter. The reverse (a smaller filter on a larger lens) is possible but not advised as it will likely result in [[w:vignetting|vignetting]]. It may work on a zoom lens however, as you may be able to zoom past the vignetting. Many cameras also crop the image when shooting video which may remove some vignetting.

If you have multiple lenses with similarly (but not identical) sized lens threads, like a 58mm and a 52mm, you should buy 58mm filters and a 52mm to 58mm adapter. This works for any size, but an 82mm filter on a 37mm lens may be awkward to use.

===Round magnetic filters===
Some filters can be snapped on the lens using magnets. They use a magnetic adapter ring that is screwed onto the lens. Unlike screw-on filters, magnetic filters are not standardized. Magnetic filters and adapter rings from various manufacturers may or may not be interoperable.

===Rectangular slide-in filters===
These are mostly used in professional productions for color filters and fixed neutral density filters as they can be swapped quickly with little risk of accidentally putting fingerprints on them.

==Material==
The very cheapest lens filters could be made of plastic. Do not buy these, buy glass. Not all glass is created equal, but the glass substrate is generally not the limiting factor for image quality.

==Coatings==
Lens filters may have various coatings. The type and quality of coating will vary between manufacturers. If you pay less than 10 USD/EUR per filter, you are almost certainly buying uncoated filters. You can use these, but they may induce [[w:lens flare|lens flare]] and other unwanted reflections. This being said, if you are taking a photo of a car in the sun even a scratched, uncoated CPL filter you found in a garage sale for $3 will vastly improve the final image over no filter at all.

The next step is a &quot;multi coated&quot; filter, often indicated by the initialism &quot;MC&quot; on the side of the filter. These are much better generally and start from 15 USD/EUR.

Finally there are filters with &quot;multiple resistive coatings&quot;, often indicated with the initialism &quot;MRC&quot; on the side of the filter. While uncoated and multi coated filters are sometimes advertised as &quot;anti scratch&quot;, this merely means those filters protect your ''lens'' from being scratched. A filter with MRC has some resistance to getting scratched itself and is easier to clean. This improves their longevity. They tend to cost a bit more, generally starting from roughly 25 USD/EUR.

Some minor scratches or dust or generally not visible in your photos unless you use an extremely small aperture, like f/22.

==Utilitarian filters==

===UV/protectors===
While technically different, these are identical in practice. You don't need a UV filter, it will not improve image quality. It will, however, protect your (potentially expensive) lens from fingerprints, sand, dirt, scratches, etc. Think of it like a screen protector on a smartphone.

===Circular polarization (CPL)===
Similar to [[w:polarized sunglasses|polarized sunglasses]], this is a single sheet of polarized glass. It can be rotated inside of the frame to remove polarized light. This can often remove reflections from windows, cars and water, allowing you to see through them. They may also darken the image on LCD and OLED displays.

A CPL filter will reduce how much light hits your sensor overall, this is normal.

===Neutral density (ND)===
[[File:Long exposure night shot of Sutton pace.jpg|thumb|Long exposure shot resulting in long streaks of headlights]]
[[File:Long exposure done at 5 in the morning (Unsplash).jpg|thumb|Long exposure shot of the sea, making the water appear like mist]]
Often described as &quot;sunglasses for your camera&quot;. In photography they are useful in two cases: if your scene is extremely bright and you are using a lens with a large aperture you might end maxing out your ISO and shutter speed values while still having an overexposed image. This is uncommon, but when it happens an ND-filter is the only solution. More commonly it is used for long-exposure photography, resulting in extreme [[w:motion blur|motion blur]].

In videography, an exposure time of half the length of the frame display time (e.g. 1/48 of a second for 24 frames per second) is commonly used to make a video more pleasant to watch with some motion blur. If your ISO is already maxed out and you'd rather not decrease the aperture you're out of options and need an ND-filter to get the exposure under control.

=====Fixed ND=====
This is the simplest ND filter. It makes the whole image darker and isn't customizable. This generally results in the highest quality, but is the least convenient. A generally useful set would consist of an 8ND (3 stops), 64ND (6 stops)  and 1000ND (9 stops) filter. 3 stops is often used for outdoor videography, 6 stops for outdoor videography on a very sunny day and 9 stops is useful for long-exposure photography.

=====Gradient ND (GND)=====
The same as a fixed ND, but with a gradient in darkness from end to end. Often used to darken the bright sky while allowing more light from the bottom half to reach the lens.

=====Variable ND (VND)=====
This filter consists of two sheets of polarized glass. One of the sheets is fixed while the other can be rotated with a dial. How much light passes through depends on how well the polarization of the two piece of glass aligns.

This filter will result in a color shift, how strong this shift will be varies strongly between various brands and models. When designed poorly it may also result in a &quot;cross&quot; effect where the image is darkened unevenly. Do not buy a VND that promises a range of 1-9 stops, the last three stops will likely be unacceptable.

You can get the effect of a VND by using two CPL filters if you mount one in the wrong direction (possible using a male-male lens adapter). This isn't recommended.

If you don't need to use a lens hood, you should frankly not buy a VND, buy a VND plus CPL instead. That's essentially the same product with an extra dial to control the rotation of both sheets of glass. A VND can be used as a CPL even, by rotating the whole filter within the groove of your lens. This creates a risk of the filter rattling around or even falling out, a problem that is solved by getting a VND plus CPL.

=====VND plus CPL=====
It's the same as a VND, but allows rotation of both sheets of glass independently. They do have one downside: they generally don't fit when using a lens hood.

===Diopter===
Moves the focus closer. Can be useful for macro photography with a non-macro lens. Will create considerable distortion, though. Stackable.

===Clear sky (FLD)===
Fluorescent filter, often sold as a &quot;clear sky&quot; filter for night photography to counter [[w:light pollution|light pollution]]. May have been useful at one point in time, but has no effect on modern street lighting. Do not buy.

==Artistic filters==
Filters that are used exclusively for artistic purposes. Unless indicated otherwise they can be stacked for a stronger or extra effect.
===Black mist===
Softens light sources. Makes images look less harsh/clinical while maintaining detail in other areas. Comes in different strengths which aren't really standardized. 1/8 is usually a mild effect, 1/4 is &quot;standard&quot;, 1/2 is strong. 1/8 or 1/4 is usually sufficient. Some photographers leave one on their lens permanently.

===White mist===
While similar in name, not quite the same effect as black mist. They create a foggy white dream-like haze.

===Kaleidoscope===
Creates a [[w:kaleidoscope|kaleidoscope]] effect. Could be used to create a &quot;dizzy&quot; effect.

===Blue streak===
Causes blue streaks of light in one direction to radiate from light sources. May create a &quot;futuristic&quot; vibe.

===Starburst===
Causes streaks of light to radiate from light sources, making them look like stars.

===Color filter===
As it says on the tin: it just filters colors, so your image looks blue/yellow/green/etc. May be used for artistic purposes, but the effect is easily and more flexibly achieved in post. Stacking the same color will have little effect.

==Where to buy==

===Used===

===Specialized camera shops===

===Western marketplaces===

===Chinese marketplaces===

{{BookCat}}</text>
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      <id>4654686</id>
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        <username>Alexis Jazz</username>
        <id>470964</id>
      </contributor>
      <comment>/* Diopter */  [[[w:en:User:Alexis Jazz/Factotum|Factotum]]]</comment>
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[[File:Neutral density filter demonstration.jpg|thumb|A [[w:Neutral-density filter|neutral-density (ND)]] filter]]
Lens filters can be installed in front of your [[Photography Equipment/Lenses|lens]]. This page will discuss their form factors, describe some popular types, how they work and what to look for when buying.

==Form factors==

===Round screw-on filters===
This is the most common type. They have a screw thread that fits into a groove on your lens. You screw them on, simple as that. The filter typically contains a groove of the same size to allow the stacking of multiple lens filters. Their size is measured in millimeters, you have to make sure that the filter you buy matches the groove on your lens. On your lens you will often find an indication like &quot;∅ 58mm&quot;, this means you need a 58mm filter.

Larger filters can be fitted on smaller lenses with an adapter. The reverse (a smaller filter on a larger lens) is possible but not advised as it will likely result in [[w:vignetting|vignetting]]. It may work on a zoom lens however, as you may be able to zoom past the vignetting. Many cameras also crop the image when shooting video which may remove some vignetting.

If you have multiple lenses with similarly (but not identical) sized lens threads, like a 58mm and a 52mm, you should buy 58mm filters and a 52mm to 58mm adapter. This works for any size, but an 82mm filter on a 37mm lens may be awkward to use.

===Round magnetic filters===
Some filters can be snapped on the lens using magnets. They use a magnetic adapter ring that is screwed onto the lens. Unlike screw-on filters, magnetic filters are not standardized. Magnetic filters and adapter rings from various manufacturers may or may not be interoperable.

===Rectangular slide-in filters===
These are mostly used in professional productions for color filters and fixed neutral density filters as they can be swapped quickly with little risk of accidentally putting fingerprints on them.

==Material==
The very cheapest lens filters could be made of plastic. Do not buy these, buy glass. Not all glass is created equal, but the glass substrate is generally not the limiting factor for image quality.

==Coatings==
Lens filters may have various coatings. The type and quality of coating will vary between manufacturers. If you pay less than 10 USD/EUR per filter, you are almost certainly buying uncoated filters. You can use these, but they may induce [[w:lens flare|lens flare]] and other unwanted reflections. This being said, if you are taking a photo of a car in the sun even a scratched, uncoated CPL filter you found in a garage sale for $3 will vastly improve the final image over no filter at all.

The next step is a &quot;multi coated&quot; filter, often indicated by the initialism &quot;MC&quot; on the side of the filter. These are much better generally and start from 15 USD/EUR.

Finally there are filters with &quot;multiple resistive coatings&quot;, often indicated with the initialism &quot;MRC&quot; on the side of the filter. While uncoated and multi coated filters are sometimes advertised as &quot;anti scratch&quot;, this merely means those filters protect your ''lens'' from being scratched. A filter with MRC has some resistance to getting scratched itself and is easier to clean. This improves their longevity. They tend to cost a bit more, generally starting from roughly 25 USD/EUR.

Some minor scratches or dust or generally not visible in your photos unless you use an extremely small aperture, like f/22.

==Utilitarian filters==

===UV/protectors===
While technically different, these are identical in practice. You don't need a UV filter, it will not improve image quality. It will, however, protect your (potentially expensive) lens from fingerprints, sand, dirt, scratches, etc. Think of it like a screen protector on a smartphone.

===Circular polarization (CPL)===
Similar to [[w:polarized sunglasses|polarized sunglasses]], this is a single sheet of polarized glass. It can be rotated inside of the frame to remove polarized light. This can often remove reflections from windows, cars and water, allowing you to see through them. They may also darken the image on LCD and OLED displays.

A CPL filter will reduce how much light hits your sensor overall, this is normal.

===Neutral density (ND)===
[[File:Long exposure night shot of Sutton pace.jpg|thumb|Long exposure shot resulting in long streaks of headlights]]
[[File:Long exposure done at 5 in the morning (Unsplash).jpg|thumb|Long exposure shot of the sea, making the water appear like mist]]
Often described as &quot;sunglasses for your camera&quot;. In photography they are useful in two cases: if your scene is extremely bright and you are using a lens with a large aperture you might end maxing out your ISO and shutter speed values while still having an overexposed image. This is uncommon, but when it happens an ND-filter is the only solution. More commonly it is used for long-exposure photography, resulting in extreme [[w:motion blur|motion blur]].

In videography, an exposure time of half the length of the frame display time (e.g. 1/48 of a second for 24 frames per second) is commonly used to make a video more pleasant to watch with some motion blur. If your ISO is already maxed out and you'd rather not decrease the aperture you're out of options and need an ND-filter to get the exposure under control.

=====Fixed ND=====
This is the simplest ND filter. It makes the whole image darker and isn't customizable. This generally results in the highest quality, but is the least convenient. A generally useful set would consist of an 8ND (3 stops), 64ND (6 stops)  and 1000ND (9 stops) filter. 3 stops is often used for outdoor videography, 6 stops for outdoor videography on a very sunny day and 9 stops is useful for long-exposure photography.

=====Gradient ND (GND)=====
The same as a fixed ND, but with a gradient in darkness from end to end. Often used to darken the bright sky while allowing more light from the bottom half to reach the lens.

=====Variable ND (VND)=====
This filter consists of two sheets of polarized glass. One of the sheets is fixed while the other can be rotated with a dial. How much light passes through depends on how well the polarization of the two piece of glass aligns.

This filter will result in a color shift, how strong this shift will be varies strongly between various brands and models. When designed poorly it may also result in a &quot;cross&quot; effect where the image is darkened unevenly. Do not buy a VND that promises a range of 1-9 stops, the last three stops will likely be unacceptable.

You can get the effect of a VND by using two CPL filters if you mount one in the wrong direction (possible using a male-male lens adapter). This isn't recommended.

If you don't need to use a lens hood, you should frankly not buy a VND, buy a VND plus CPL instead. That's essentially the same product with an extra dial to control the rotation of both sheets of glass. A VND can be used as a CPL even, by rotating the whole filter within the groove of your lens. This creates a risk of the filter rattling around or even falling out, a problem that is solved by getting a VND plus CPL.

=====VND plus CPL=====
It's the same as a VND, but allows rotation of both sheets of glass independently. They do have one downside: they generally don't fit when using a lens hood.

===Diopter / Close-up===
Moves the focus closer. Can be useful for macro photography with a non-macro lens. Will create considerable distortion, though. Stackable.

===Clear sky (FLD)===
Fluorescent filter, often sold as a &quot;clear sky&quot; filter for night photography to counter [[w:light pollution|light pollution]]. May have been useful at one point in time, but has no effect on modern street lighting. Do not buy.

==Artistic filters==
Filters that are used exclusively for artistic purposes. Unless indicated otherwise they can be stacked for a stronger or extra effect.
===Black mist===
Softens light sources. Makes images look less harsh/clinical while maintaining detail in other areas. Comes in different strengths which aren't really standardized. 1/8 is usually a mild effect, 1/4 is &quot;standard&quot;, 1/2 is strong. 1/8 or 1/4 is usually sufficient. Some photographers leave one on their lens permanently.

===White mist===
While similar in name, not quite the same effect as black mist. They create a foggy white dream-like haze.

===Kaleidoscope===
Creates a [[w:kaleidoscope|kaleidoscope]] effect. Could be used to create a &quot;dizzy&quot; effect.

===Blue streak===
Causes blue streaks of light in one direction to radiate from light sources. May create a &quot;futuristic&quot; vibe.

===Starburst===
Causes streaks of light to radiate from light sources, making them look like stars.

===Color filter===
As it says on the tin: it just filters colors, so your image looks blue/yellow/green/etc. May be used for artistic purposes, but the effect is easily and more flexibly achieved in post. Stacking the same color will have little effect.

==Where to buy==

===Used===

===Specialized camera shops===

===Western marketplaces===

===Chinese marketplaces===

{{BookCat}}</text>
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  </page>
  <page>
    <title>User:Manusheikh/sandbox</title>
    <ns>2</ns>
    <id>484823</id>
    <revision>
      <id>4654690</id>
      <timestamp>2026-07-16T15:12:11Z</timestamp>
      <contributor>
        <username>Manusheikh</username>
        <id>3614801</id>
      </contributor>
      <comment>Added a new page about downloading Instagram audio in MP3 format.</comment>
      <origin>4654690</origin>
      <model>wikitext</model>
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      <text bytes="58" sha1="51xyo7qq4gghd8ipfs9zrbyb0n1zvvt" xml:space="preserve">'''''How to Download Instagram Audio in MP3 for Free?'''''</text>
      <sha1>51xyo7qq4gghd8ipfs9zrbyb0n1zvvt</sha1>
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  </page>
  <page>
    <title>Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. e5/3...Bf5/4. Nc3/4...e6/5. g4</title>
    <ns>0</ns>
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        <id>7490</id>
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      <comment>start</comment>
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      <text bytes="577" sha1="iusfldjg3gnnruv1m0jwvplhv4mrt6n" xml:space="preserve">{{Chess Opening Theory/Position|=
|Van der Wiel Attack|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |  |pd|pd|pd|=
   |  |  |pd|  |pd|  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |pl|  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|  |pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
}}

=6. g4 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=
6... Bg6 is the only feasible response for Black here.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=6... Bg6
|eval1=
}}

{{Wikipedia|Caro–Kann Defence}}
{{ChessMid}}
{{ChessFooter}}</text>
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      <text bytes="609" sha1="sr8t7hq5962ht0dekscr0tlgfmwktjk" xml:space="preserve">{{Chess Opening Theory/Position|=
|Van der Wiel Attack|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |  |pd|pd|pd|=
   |  |  |pd|  |pd|  |  |  |=
   |  |  |  |pd|pl|bd|  |  |=
   |  |  |  |pl|  |  |  |  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|pl|pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
}}

=5... Bg6 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=
6. Ne2 is the usual response, planning to continue to harass White's bishop with Nf4.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=6. Ne2
|eval1=
}}

{{Wikipedia|Caro–Kann Defence}}
{{ChessMid}}
{{ChessFooter}}</text>
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|Van der Wiel Attack|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |  |pd|pd|pd|=
   |  |  |pd|  |pd|  |bd|  |=
   |  |  |  |pd|pl|  |  |  |=
   |  |  |  |pl|  |  |pl|  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |  |pl|  |pl|=
   |rl|  |bl|ql|kl|bl|nl|rl|=
}}

=5... Bg6 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=
6. Ne2 is the usual response, planning to continue to harass White's bishop with Nf4.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=6. Ne2
|eval1=
}}

{{Wikipedia|Caro–Kann Defence}}
{{ChessMid}}
{{ChessFooter}}</text>
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|Van der Wiel Attack|
   |rd|nd|  |qd|kd|bd|nd|rd|=
   |pd|pd|  |  |  |pd|pd|pd|=
   |  |  |pd|  |pd|  |bd|  |=
   |  |  |  |pd|pl|  |  |  |=
   |  |  |  |pl|  |  |pl|  |=
   |  |  |nl|  |  |  |  |  |=
   |pl|pl|pl|  |nl|pl|  |pl|=
   |rl|  |bl|ql|kl|bl|  |rl|=
}}

=6. Ne2 · Caro-Kann Defence - Advance Variation, Van Der Wiel Attack=
White threatens Nf4 and h4, so Black must react. Black usually counters in the centre with 6... c5.

==Theory table==
{{ChessTable}}
{{Chess/theory table
|name1=
|line1=6... c5
|eval1=
}}

{{Wikipedia|Caro–Kann Defence}}
{{ChessMid}}
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      <comment>Created page with &quot;This chapter you will learn: *Basic Chinese sentences and grammar #[[Mandarin Chinese/Sentences/Hello|你好。 我是...]] #[[Mandarin Chinese/Sentences/How are you|你好吗？]] #[[Mandarin Chinese/Sentences/He is a student|他是学生。]] #[[Mandarin Chinese/Sentences/What is her name|她的名字是什么？]] #[[Mandarin Chinese/Sentences/I am 42|我四十二岁。]] #[[Mandarin Chinese/Sentences/And you|你呢？]]&quot;</comment>
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*Basic Chinese sentences and grammar
#[[Mandarin Chinese/Sentences/Hello|你好。 我是...]]
#[[Mandarin Chinese/Sentences/How are you|你好吗？]]
#[[Mandarin Chinese/Sentences/He is a student|他是学生。]]
#[[Mandarin Chinese/Sentences/What is her name|她的名字是什么？]]
#[[Mandarin Chinese/Sentences/I am 42|我四十二岁。]]
#[[Mandarin Chinese/Sentences/And you|你呢？]]</text>
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      <text bytes="1201" sha1="pk819n7w4ve9tjbjl6cfyvk0c6r4uuo" xml:space="preserve">{{talk archive}}

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:{{done|Sandbox deleted}} —[[User:Kittycataclysm|Kittycataclysm]] ([[User talk:Kittycataclysm|discuss]] • [[Special:Contributions/Kittycataclysm|contribs]]) 01:26, 3 July 2026 (UTC)
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