首页> 外文期刊>Pediatric critical care medicine: a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies >Impaired Mobilization of Endothelial Progenitor Cells in Acute Lung Injury/Acute Respiratory Distress Syndrome: Inhibition of an Endogenous Mechanism of Lung Repair*
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Impaired Mobilization of Endothelial Progenitor Cells in Acute Lung Injury/Acute Respiratory Distress Syndrome: Inhibition of an Endogenous Mechanism of Lung Repair*

机译:急性肺损伤/急性呼吸窘迫综合征中内皮祖细胞的动员受损:抑制肺修复的内源性机制*

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摘要

Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) are important contributors to morbidity and mortality in the ICU for both children and adults. Over the four^lecades since the clinical features of ARDS were described by Ashbaugh and colleagues (1), the pathophysiology of ALI has been well characterized, and the major molecular and cellular pathways that lead to the neutrophilic alveolar inflammation, epithelial and endofhelial damage, deregulated coagulation, and instigation of nbroproliferation have been largely defined (2). However, despite these advances, therapies to specifically block the initiation or progression of lung injury have been woefully disappointing.
机译:急性肺损伤和急性呼吸窘迫综合征(ALI / ARDS)是儿童和成人ICU发病率和死亡率的重要因素。自Ashbaugh及其同事(1)描述ARDS的临床特征以来的四个世纪以来,ALI的病理生理学已得到很好的表征,导致中性粒细胞肺炎,上皮和血管内皮损伤的主要分子和细胞途径,失调的凝血和促成核细胞增殖已被广泛定义(2)。然而,尽管取得了这些进展,但是特异性地阻断肺损伤的发生或发展的疗法却令人失望。

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