Waugh2006 - Diabetic Wound Healing - Macrophage Dynamics

This a model from the article:
Macrophage dynamics in diabetic wound dealing.

Waugh HV, Sherratt JA. Bull Math Biol
2006 Jan;68(1):197-207 16794927
,
Abstract:

Wound healing in diabetes is a complex process, characterised by a chronic
inflammation phase. The exact mechanism by which this occurs is not fully
understood, and whilst several treatments for healing diabetic wounds exist,
very little research has been conducted towards the causes of the extended
inflammation phase. We describe a mathematical model which offers a possible
explanation for diabetic wound healing in terms of the distribution of
macrophage phenotypes being altered in the diabetic patient compared to normal
wound repair. As a consequence of this, we put forward a suggestion for
treatment based on rectifying the macrophage phenotype imbalance.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Waugh HV, Sherratt JA. (2006) - version=1.0

The original CellML model was created by:
Catherine Lloyd

[e-mail]
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..

To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

本模型源自下述论文：
糖尿病伤口处理中的巨噬细胞动力学
Waugh HV, Sherratt JA. 《数学生物学公报》（Bull Math Biol）
2006年1月；68(1):197-207，PubMed ID: 16794927

【摘要】
糖尿病伤口愈合是一类复杂的病理过程，其核心特征为慢性炎症阶段的持续存在。目前学界尚未完全阐明其确切发病机制，尽管现有数种糖尿病伤口愈合治疗方案，但针对延长炎症阶段诱因的相关研究仍十分匮乏。本研究构建了一套数学模型，相较于正常伤口修复过程，糖尿病患者体内巨噬细胞表型分布发生显著改变，该模型可为糖尿病伤口愈合机制提供一种可行的解释。基于此模型结果，我们提出了一种旨在纠正巨噬细胞表型失衡的治疗策略。

本模型取自细胞标记建模语言（CellML）模型库，并被自动转换为系统生物学标记语言（SBML）格式。原始模型信息如下：
Waugh HV, Sherratt JA. (2006) - 版本号=1.0

原始细胞标记建模语言（CellML）模型由Catherine Lloyd创建，联系邮箱：[e-mail]，隶属于奥克兰大学。

本模型源自生物模型数据库（BioModels Database，http://www.ebi.ac.uk/biomodels/），该数据库是一个收录经过注释的已发表模型的资源库。其版权归属于2005-2011年的BioModels.net团队所有。在法律允许的最大范围内，本编码模型的所有版权及相关邻接权利已被捐赠至全球公共领域。更多信息请参阅CC0公共领域贡献协议（CC0 Public Domain Dedication）。

简言之，您可自由以任何合适方式使用本编码模型，包括原样复用、修改后使用、单独部署或嵌入更大的上下文环境中，可进行再分发，无论是否用于商业用途、是否存在使用限制。

若需引用生物模型数据库，请使用以下文献格式：Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) 《生物模型数据库：面向已发表定量动力学模型的增强、整理与注释资源》，BMC Syst Biol., 4:92。