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急性肺部感染和败血症的遗传风险。

Genetic risk of acute pulmonary infections and sepsis.

作者信息

Waterer Grant W, Bruns Anke H W

机构信息

School of Medicine and Pharmacology, University of Western Australia, Level 4 MRF Building, Royal Perth Hospital, GPO Box X2213, Perth 6847, Australia.

出版信息

Expert Rev Respir Med. 2010 Apr;4(2):229-38. doi: 10.1586/ers.10.13.

Abstract

The focus of this review is the genetic influence on pneumonia and sepsis. A large number of polymorphisms in a diverse collection of genes have been identified as potential candidates to explain the genetic variability in susceptibility to acute pulmonary infection and its adverse outcomes. Unfortunately, apart from polymorphisms in mannose-binding lectin, CD14 and the IgG2 receptor, there is little consensus on which polymorphisms are truly important. As well as discussing some of the major published findings, this review will focus on the reasons for failure to make more progress. We will also address the issues for future research, particularly the need to address the limitations of past studies, including the grouping of patients with different pathogens, as the relationship between genotype and phenotype may be highly pathogen dependent. Finally, our approach to reporting genetic studies needs to change to minimize the number of publications of spurious findings.

摘要

本综述的重点是基因对肺炎和败血症的影响。在各种各样的基因中,大量的多态性已被确定为解释急性肺部感染易感性及其不良后果中基因变异性的潜在候选因素。遗憾的是,除了甘露糖结合凝集素、CD14和IgG2受体的多态性外,对于哪些多态性真正重要几乎没有共识。除了讨论一些已发表的主要研究结果外,本综述还将关注未能取得更大进展的原因。我们还将探讨未来研究的问题,特别是需要解决以往研究的局限性,包括对不同病原体患者的分组,因为基因型和表型之间的关系可能高度依赖病原体。最后,我们报告基因研究的方式需要改变,以尽量减少虚假研究结果的发表数量。

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