Cooperative SIR dynamics as a model for spontaneous blood clot initiation

Philip Greulich
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Abstract

Blood clotting is an important physiological process to suppress bleeding upon injury, but when it occurs inadvertently, it can cause thrombosis, which can lead to life threatening conditions. Hence, understanding the microscopic mechanistic factors for inadvertent, spontaneous blood clotting, in absence of a vessel breach, can help in predicting and adverting such conditions. Here, we present a minimal model -- reminiscent of the SIR model -- for the initiating stage of spontaneous blood clotting, the collective activation of blood platelets. This model predicts that in the presence of very small initial activation signals, macroscopic activation of the platelet population requires a sufficient degree of heterogeneity of platelet sensitivity. To propagate the activation signal and achieve collective activation of the bulk platelet population, it requires the presence of, possibly only few, hyper-sensitive platelets, but also a sufficient proportion of platelets with intermediate, yet higher-than-average sensitivity. A comparison with experimental results demonstrates a qualitative agreement for high platelet signalling activity.
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作为自发血凝块形成模型的合作 SIR 动力学
凝血是抑制受伤后出血的重要生理过程,但如果不慎凝血,则可能导致血栓形成,从而危及生命。因此,在没有血管破裂的情况下,了解不经意间自发凝血的微观机制因素有助于预测和预防此类情况的发生。在此,我们提出了自发性血液凝结的初始阶段--血小板的集体激活--的最小模型(类似于 SIR 模型)。该模型预测,在初始激活信号很小的情况下,血小板群的宏观激活需要血小板敏感性有足够的异质性。要传播活化信号并实现大量血小板群的集体活化,可能需要有少数超敏感血小板,但也需要有足够比例的具有中等或高于平均敏感度的血小板。与实验结果的比较表明,两者在高血小板信号活性的定性上是一致的。
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