论文标题
通过缺氧引起的血管生成的胶质瘤模式的通量限制模型
A flux-limited model for glioma patterning with hypoxia-induced angiogenesis
论文作者
论文摘要
我们在酸度，血管生成和组织各向异性的影响下提出了一个微局部肿瘤环境中神经胶质瘤模式的模型。自下而上的模型扣除最终导致了神经胶质瘤和内皮细胞种群密度的反应扩散税方程的系统，前者在自扩散和出租车方面都限制了通量限制。该模型扩展了最近引入的[34]对神经胶质瘤的形成的描述，目的是研究缺氧诱导的肿瘤血管化对这些组织学模式的建立和维持的影响，这些组织学是高级脑癌的典型特征。进行了人口水平动态的数值模拟，以研究包含这种情况并进一步影响的几种模型场景。
We propose a model for glioma patterns in a microlocal tumor environment under the influence of acidity, angiogenesis, and tissue anisotropy. The bottom-up model deduction eventually leads to a system of reaction-diffusion-taxis equations for glioma and endothelial cell population densities, of which the former infers flux limitation both in the self-diffusion and taxis terms. The model extends a recently introduced [34] description of glioma pseudopalisade formation, with the aim of studying the effect of hypoxia-induced tumor vascularization on the establishment and maintenance of these histological patterns which are typical for high grade brain cancer. Numerical simulations of the population level dynamics are performed to investigate several model scenarios containing this and further effects.
