changes in the monocytic subsets cd14dimcd16+ and cd14++cd16? in chronic systolic heart failure patients单核细胞的变化子集cd14dimcd16 +和cd14 + + cd16 在慢性收缩性心力衰竭患者.pdfVIP

changes in the monocytic subsets cd14dimcd16+ and cd14++cd16? in chronic systolic heart failure patients单核细胞的变化子集cd14dimcd16 +和cd14 + + cd16 在慢性收缩性心力衰竭患者.pdf

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changesinthemonocyticsubsetscd14dimcd16andcd14cd16?inchronicsystolicheartfailurepatients单核细胞的变化子集cd14dimcd16和cd14cd16在慢性收缩性心力衰竭患者

Hindawi Publishing Corporation Mediators of Inflammation Volume 2012, Article ID 616384, 9 pages doi:10.1155/2012/616384 Research Article Changes in the Monocytic Subsets CD14dimCD16+ and CD14++CD16− in Chronic Systolic Heart Failure Patients Offer Amir,1 Ilia Spivak,1, 2 Idit Lavi,3 and Michal Amit Rahat2 1 Heart Failure Center, Division of Cardiology, Lady Davis Carmel Medical Center and the Ruth and Bruce Rappaport Faculty of Medicine, Technion – Israel Institute of Technology, 34362 Haifa, Israel 2 Immunology Research Unit, Lady Davis Carmel Medical Center and the Ruth and Bruce Rappaport Faculty of Medicine, Technion – Israel Institute of Technology, 34362 Haifa, Israel 3 Department of Community Medicine and Epidemiology, Lady Davis Carmel Medical Center and the Ruth and Bruce Rappaport Faculty of Medicine, Technion – Israel Institute of Technology, 34362 Haifa, Israel Correspondence should be addressed to Michal Amit Rahat, rahat miki@.il Received 22 August 2012; Revised 11 October 2012; Accepted 25 October 2012 Academic Editor: Chiou-Feng Lin Copyright © 2012 Offer Amir et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Different monocytic subsets are important in inflammation and tissue remodelling, but although heart failure (HF) is associated with local and systemic inflammation, their roles in HF are yet unknown. We recruited 59 chronic systolic HF patients (aged 58 ±13 years, 45 males and 14 females) and 29 age-matched controls with no pervious heart disease. Compared to the controls, we found no change in the distribution of the CD14+ CD16+ monocytic subset, whereas the classical CD14++ CD1

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