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A Multiscale Computational Framework to Understand Vascular Adaptation.
Journal of Computational Science ( IF 3.1 ) Pub Date : 2015-02-16 , DOI: 10.1016/j.jocs.2015.02.002
Marc Garbey 1 , Mahbubur Rahman 2 , Scott A Berceli 3
Affiliation  

The failure rate for vascular interventions (vein bypass grafting, arterial angioplasty/stenting) remains unacceptably high. Over the past two decades, researchers have applied a wide variety of approaches to investigate the primary failure mechanisms, neointimal hyperplasia and aberrant remodeling of the wall, in an effort to identify novel therapeutic strategies. Despite incremental progress, specific cause/effect linkages among the primary drivers of the pathology, (hemodynamic factors, inflammatory biochemical mediators, cellular effectors) and vascular occlusive phenotype remain lacking. We propose a multiscale computational framework of vascular adaptation to develop a bridge between theory and experimental observation and to provide a method for the systematic testing of relevant clinical hypotheses. Cornerstone to our model is a feedback mechanism between environmental conditions and dynamic tissue plasticity described at the cellular level with an agent based model. Our implementation (i) is modular, (ii) starts from basic mechano-biology principle at the cell level and (iii) facilitates the agile development of the model.



中文翻译:


了解血管适应的多尺度计算框架。



血管介入治疗(静脉旁路移植术、动脉血管成形术/支架置入术)的失败率仍然高得令人无法接受。在过去的二十年中,研究人员应用了多种方法来研究主要失效机制、新内膜增生和壁的异常重塑,以期找出新的治疗策略。尽管取得了渐进的进展,但病理的主要驱动因素(血流动力学因素、炎症生化介质、细胞效应物)和血管闭塞表型之间的具体因果联系仍然缺乏。我们提出了血管适应的多尺度计算框架,以建立理论和实验观察之间的桥梁,并为相关临床假设的系统测试提供方法。我们模型的基石是环境条件和动态组织可塑性之间的反馈机制,通过基于代理的模型在细胞水平上进行描述。我们的实现(i)是模块化的,(ii)从细胞水平的基本机械生物学原理开始,(iii)促进模型的敏捷开发。

更新日期:2015-02-16
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