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脓毒性休克的病理生理学。

The pathophysiology of septic shock.

机构信息

Division of Critical Care Medicine, Department of Internal Medicine, Cooper University Hospital, Camden, NJ, USA.

出版信息

Crit Care Clin. 2009 Oct;25(4):677-702, vii. doi: 10.1016/j.ccc.2009.08.002.

DOI:10.1016/j.ccc.2009.08.002
PMID:19892247
Abstract

There is a profound cellular dysfunction in sepsis, that clinically manifests as a continuum from simple, uncomplicated sepsis to severe sepsis, and finally to septic shock. Septic shock remains a significant challenge for clinicians. Recent advances in cellular and molecular biology have significantly improved our understanding of its pathogenetic mechanisms. These improvements will translate to better care and improved outcomes for these patients.

摘要

脓毒症存在深刻的细胞功能障碍,临床上表现为从简单、非复杂性脓毒症到严重脓毒症,最终到感染性休克的连续过程。感染性休克仍然是临床医生面临的重大挑战。细胞和分子生物学的最新进展极大地提高了我们对其发病机制的理解。这些进展将转化为这些患者更好的护理和改善的结果。

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The pathophysiology of septic shock.脓毒性休克的病理生理学。
Crit Care Clin. 2009 Oct;25(4):677-702, vii. doi: 10.1016/j.ccc.2009.08.002.
2
The pathophysiology of septic shock.脓毒性休克的病理生理学
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[Septic shock].[脓毒性休克]
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Toll-like receptor pathway signaling is differently regulated in neutrophils and peripheral mononuclear cells of patients with sepsis, severe sepsis, and septic shock.在脓毒症、严重脓毒症和脓毒性休克患者的中性粒细胞和外周血单核细胞中,Toll样受体途径信号传导受到不同的调节。
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Recent advances in the pathobiology of septicemia and septic shock.败血症和脓毒性休克病理生物学的最新进展
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Molecular mechanisms involved in the pathogenesis of septic shock.脓毒性休克发病机制中涉及的分子机制。
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Toll-like receptor pathway signaling is differently regulated in neutrophils and peripheral mononuclear cells of patients with sepsis, severe sepsis, and septic shock.在脓毒症、严重脓毒症和脓毒性休克患者的中性粒细胞和外周单核细胞中,Toll样受体途径信号传导受到不同的调节。
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Molecular biology of inflammation and sepsis: a primer.炎症与脓毒症的分子生物学:入门指南
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MIF regulates innate immune responses through modulation of Toll-like receptor 4.巨噬细胞迁移抑制因子通过调节Toll样受体4来调控先天性免疫反应。
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Critical advances in septicemia and septic shock.败血症和脓毒性休克的重大进展。
Crit Care. 2000;4(5):290-6. doi: 10.1186/cc711. Epub 2000 Sep 7.

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