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Information entropy-based fitting of the disease trajectory of brain ischemia-induced vascular cognitive impairment

机译:基于信息熵的脑缺血诱发的血管性认知障碍疾病轨迹的拟合

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The present study investigated the disease trajectory of vascular cognitive impairment using the entropy of information in a neural network mathematical simulation based on the free radical and excitatory amino acids theories. Glutamate, malondialdehyde, and inducible nitric oxide synthase content was significantly elevated, but acetylcholine, catalase, superoxide dismutase, glutathione peroxidase and constitutive nitric oxide synthase content was significantly decreased in our vascular cognitive impairment model. The fitting curves for each factor were obtained using Matlab software. Nineteen, 30 and 49 days post ischemia were the main output time frames of the influence of these seven factors. Our results demonstrated that vascular cognitive impairment involves multiple factors. These factors include excitatory amino acid toxicity and nitric oxide toxicity. These toxicities disrupt the dynamic equilibrium of the production and removal of oxygen free radicals after cerebral ischemia, reducing the ability to clear oxygen free radicals and worsening brain injury. Abbreviations: VCI, vascular cognitive impairment; iNOS, inducible nitric oxide synthase; cNOS, constitutive nitric oxide synthase
机译:本研究利用信息熵在基于自由基和兴奋性氨基酸理论的神经网络数学模拟中研究了血管性认知障碍的疾病轨迹。在我们的血管性认知障碍模型中,谷氨酸,丙二醛和诱导型一氧化氮合酶含量显着升高,但乙酰胆碱,过氧化氢酶,超氧化物歧化酶,谷胱甘肽过氧化物酶和组成型一氧化氮合酶含量显着降低。使用Matlab软件获得每个因子的拟合曲线。缺血后第19、30和49天是这七个因素影响的主要输出时间范围。我们的结果表明,血管性认知障碍涉及多个因素。这些因素包括兴奋性氨基酸毒性和一氧化氮毒性。这些毒性破坏了脑缺血后氧自由基产生和清除的动态平衡,降低了清除氧自由基的能力,并加剧了脑损伤。缩写:VCI,血管性认知障碍; iNOS,诱导型一氧化氮合酶; cNOS,组成型一氧化氮合酶

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