The Nlrp3 inflammasome promotes myocardial dysfunction in structural cardiomyopathy through interleukin-1β

导出原文传递

翻译打印收藏纠错

作者： Bracey,N.A. ^[1] ; Beck,P.L. ^[2] ; Muruve,D.A. ^[3] ; Hirota,S.A. ^[4] ; Guo,J. ; Jabagi,H. ; WrightJr,J.R. ; Macdonald,J.A. ; Lees-Miller,J.P. ; Roach,D. ; Semeniuk,L.M. ; Duff,H.J.

作者单位： Department of Medicine, University of Calgary, Calgary, AB, Canada ^[1] Department of Medicine, University of Calgary, Calgary, AB, Canada, Libin Cardiovascular Institute ^[2] Libin Cardiovascular Institute, University of Calgary, Calgary, AB, Canada ^[3] Department of Pathology, University of Calgary, Calgary, AB, Canada ^[4]

发布时间 2014-01-21

翻译满意度评价：

准确一般字义偏差语意偏离译文作用小提交

浏览3

Experimental Physiology

2013年98卷2期

462-472页

相似文献

中文期刊
外文期刊
学位论文
会议论文

检索历史清除

The Nlrp3 inflammasome promotes myocardial dysfunction in structural cardiomyopathy through interleukin-1β

Experimental Physiology

相似文献

Experimental Physiology

相关期刊

参考文献：
指定格式：	NoteExpress EndNote RefWorks NoteFirst

检索历史 清除

The Nlrp3 inflammasome promotes myocardial dysfunction in structural cardiomyopathy through interleukin-1β

Experimental Physiology

相似文献

Experimental Physiology

相关期刊

检索历史清除