首页> 外文期刊>Thrombosis Research: An International Journal on Vascular Obstruction, Hemorrhage and Hemostasis >Role of 4G/5G promoter polymorphism of Plasminogen Activator Inhibitor-1 (PAI-1) gene in outcome of sepsis.
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Role of 4G/5G promoter polymorphism of Plasminogen Activator Inhibitor-1 (PAI-1) gene in outcome of sepsis.

机译:纤溶酶原激活物抑制剂1(PAI-1)基因的4G / 5G启动子多态性在败血症结果中的作用。

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摘要

Serious infections trigger a systemic inflammatory response which results in sepsis. Severe sepsis is sepsis complicated by organ dysfunction and when sepsis results in hypotension despite adequate fluid resuscitation, it is called septic shock having a poor prognosis [1 ]. Even though significant advances, both in supportive care and in understanding its molecular bases, sepsis is the most common cause of death among patients in an intensive care unit (ICU) [2]. The innate immune system acts releasing cytokines and mediators that stimulate the adaptive immune responses although these are injurious to various tissues and organs [3]. It is possible that the persistence of high concentration of certain proinflammatory cytokines or the incapacity of raising certain cytokines at a specific moment might perpetuate the inflammatory response resulting in sepsis or septic shock [1-3].
机译:严重感染会引起全身性炎症反应,从而导致败血症。严重的脓毒症是由器官功能障碍引起的脓毒症,尽管尽管有足够的液体复苏,但脓毒症仍导致低血压,故称为败血症性休克,预后较差[1]。即使在支持治疗和了解其分子基础方面取得了重大进展,败血症仍是重症监护病房(ICU)患者最常见的死亡原因[2]。虽然这些先天免疫系统对各种组织和器官有害,但它们会释放细胞因子和介质,从而刺激适应性免疫反应[3]。高浓度的某些促炎细胞因子的持久性或在特定时刻不能升高某些细胞因子的能力可能会使炎症反应永久化,导致败血症或败血性休克[1-3]。

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