缺血性卒中凝血系统微量元素的临床研究

L. L. Klimenko, A. Deev, I. S. Baskakov, M. N. Budanova, A. Zabirova, M. S. Uzhenceva, A. N. Mazilina, M. S. Savostina, O. Senko, A. Kuznecova
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引用次数: 0

摘要

缺血性脑组织发病机制的基础是血液系统疾病。众所周知,二价离子影响纤维蛋白的形成和结构。与此相关的事实是,在临床表现出现之前,宏观和微量元素平衡的变化可以作为大脑神经营养紊乱的标志。金属配体稳态失衡是缺血性脑卒中发病的不利背景。在多因子凝血系统中,特定的蛋白质——蛋白质C和蛋白质d二聚体——占据着关键的位置。许多宏观和微量元素是体内平衡和血栓形成的介质:元素体内平衡的破坏是缺血过程的分子基础。在临床环境中进行的一项研究中,蛋白质C和d二聚体以及宏量元素和微量元素的复合物的组合动力学显示出高度确定性。利用Spearman相关分析,揭示了缺血性损伤患者体内蛋白C、d -二聚体浓度与宏量元素和微量元素之间的可靠相关性。最后对结果进行数学处理,通过多元回归分析,得出凝血系统成分蛋白C与参与缺血性卒中发病核心机制的宏微量元素复合物浓度之间的可靠关系:R = 0.95938848, R2 = 0.92042626。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
TRACE ELEMENTS IN THE BLOOD COAGULATION SYSTEM IN ISCHEMIC STROKE: A CLINICAL STUDY
The basis of the mechanism of ischemic brain tissue are hematological disorders. It is known that divalent ions influence the formation and structure of fibrin. In connection with this fact, a change in macro- and microelement balance serves as a marker of neurotrophic disturbances in the brain long before their clinical manifestations. The imbalance of metal-ligand homeostasis is an unfavorable background for the debut of ischemic stroke. In a multifactorial coagulation system, specific proteins - Protein C and D-dimers - occupy a key place. Many macro- and microelements are mediators of homeostasis and thrombosis: violations of elemental homeostasis are the molecular basis of the ischemic process. In a study conducted in a clinical setting, the combined dynamics of protein C and D-dimers and a complex of macro- and microelements are shown with a high degree of certainty. Using Spearman correlation analysis, reliable correlations were revealed between the concentrations of protein C, D-dimers and macro- and microelements in patients diagnosed with ischemic insult. In the final part of the mathematical processing of the results, multiple regression analysis was used, with the help of which a reliable relationship between protein C, a component of the blood coagulation system, and the concentration of a complex of macro- and microelements contributing to the central mechanism of etiopathogenesis of ischemic stroke is shown: R = 0.95938848, R2 = 0.92042626.
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