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:抑制肺修复的内源机理*

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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)是儿童和成年人ICU的发病率和死亡率的重要贡献者。 由于Ashbaugh及其同事描述了ARDS的临床特征,因此Ashbaugh和同事(1)描述了,Ali的病理生理学已经很好地表征,并且主要分子和细胞途径导致中性噬菌体炎症,上皮和胎盘损伤, 对赤藓糖溶解的解除管制凝血并造成了大量定义(2)。 然而,尽管有这些进步,但特别是肺损伤的开始或进展的疗法令人窒息。

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