碳水化合物发酵与结直肠癌的联合常微分方程模型
A Combined ODE Model of Carbohydrate Fermentation and Colorectal Cancer
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中文总结 AI 辅助
本研究构建并分析了一个描述丁酸盐、结直肠癌细胞和宿主细胞相互作用的常微分方程模型，预测丁酸盐由纤维摄入驱动且可抑制肿瘤，并发现高噪声强度下癌症几乎必然消除。
中文摘要 AI 辅助
我们构建并分析了一个非线性常微分方程组，该方程组描述了由纤维发酵肠道微生物群产生的丁酸盐、结直肠癌细胞和宿主细胞群体之间的关键代谢和免疫相互作用。该模型既被独立研究，也与一个已有的碳水化合物发酵模型联合研究。通过敏感性分析探索了参数空间。我们进行了模拟实验，以说明由丁酸盐可用性驱动的不同动力学行为的出现。我们的模型预测，丁酸盐的产生由纤维摄入驱动，并在微生物失调的情况下进一步得到益生菌的支持。模型还表明，丁酸盐可能有助于抑制肿瘤生长。我们还证明，通过添加足够高强度的噪声，在无限时间内癌症消除几乎必然发生，并且该噪声强度阈值随丁酸盐浓度的增加而降低。
英文摘要
We formulate and analyze a system of non-linear ordinary differential equations that describe key metabolic and immunological interactions between butyrate produced by fiber-fermenting gut microbiota, colorectal cancer cells and host cell populations. The model is studied both independently and in conjunction with a pre-existing carbohydrate fermentation model. The parameter space is explored through sensitivity analyses. Simulation experiments are conducted to illustrate the emergence of varying dynamical behaviour driven by butyrate availability. Our model predicts that butyrate production is driven by fiber consumption and further supported by probiotics in the case of microbial dysbiosis. It also suggests that butyrate may help in suppressing tumour growth. We also show that by adding noise with sufficiently high intensity, cancer elimination occurs almost surely in infinite time and that this threshold level of noise intensity decreases with increasing butyrate concentrations.
