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A Computational Model of Micro-vascular Growth

机译:微血管生长的计算模型

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In order to supply a growing tissue with oxygen and nutrients and to remove its metabolic wastes, blood vessels penetrating the tissue are formed. Multiple mechanisms are involved in this process ranging over many orders of magnitude: chemical signaling on the bio-molecular level (10~(-9)m), genetic program on the protein level (10~(-7)m), microscopic mechanical cell interactions (10~(-5)m) and external forces and stresses reaching macroscopic scales ( > 10~(-3)m). Better physiological understanding of this phenomenon could result in many useful medical applications, for example in gene therapy or cancer treatment. We present a simulation framework to study mechanical aspects of the micro-vascular growth using techniques from computational geometry, solid mechanics, computational fluid dynamics and data visualization. Vasculogenesis is modeled as traction driven remodeling of an initially uniform tissue in absence of blood flow. Angiogenesis, the subsequent formation and maturation of blood vessels, is handled as a flow driven remodeling of a porous structure resulting from the preceding stage. The mechanical model of tissue response to the traction forces successfully predicts spontaneous formation of primitive capillary networks. Furthermore, we demonstrate that a shear-stress controlled remodeling of such structures can lead to flow fingering effects observed in real cellular media.
机译:为了用氧气和营养提供越来越多的组织并去除其代谢废物,形成穿透组织的血管。在该过程中涉及多种机制范围范围在许多数量级:生物分子水平上的化学信号传导(10〜(-9)m),蛋白质水平的遗传程序(10〜(-7)m),微观机械细胞相互作用(10〜(-5)m)和外力和应力达到宏观鳞片(> 10〜(-3)m)。更好地理解这种现象可能导致许多有用的医学应用,例如在基因治疗或癌症治疗中。我们提出了一种模拟框架,用于使用计算几何形状,固体力学,计算流体动力学和数据可视化的技术研究微血管生长的机械方面。在没有血流的情况下,血管生成被建模为初始均匀组织的牵引驱动的重塑。血管生成,随后的血管形成和成熟,作为由前一级引起的多孔结构的流动驱动的重塑。对牵引力的组织反应的机械模型成功地预测了原始毛细管网络的自发性形成。此外,我们证明这种结构的剪切应力控制重塑可以导致在真实细胞介质中观察到的流动指令效果。

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