ENDOTHELIAL CELL ACTIVATION AND DECOMPENSATION IN CHF

CHF 中的内皮细胞激活和失代偿

• 批准号: 7061751
• 负责人: PAOLO C COLOMBO
• 金额: $ 12.94万
• 依托单位: COLUMBIA UNIVERSITY HEALTH SCIENCES
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-08-15 至 2007-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7061751
• 关键词: cell proliferation; cellular pathology; clinical research; congestive heart failure; cytokine; heart function; human middle age (35-64); human old age (65+); human subject; oxidative stress; pathologic process; patient oriented research; vascular endothelium

DESCRIPTION (provided by applicant): The candidate, Dr. Paolo C. Colombo, a fourth year cardiology fellow, is completing his training in chronic heart failure (CHF) and vascular biology at the Albert Einstein College of Medicine (AECOM) under the guidance of Dr. Thierry H. Le Jemtel and Dr. J. Anthony Ware. Dr. Colombo is currently supported by an NIH Institutional Training Grant (T32). Dr. Colombo will join the Faculty of the Department of Medicine at AECOM as an instructor in July 2001. Dr. Colombo is most interested in developing new approaches to patient oriented research, taking advantage of his basic science background. The Cardiovascular Division at AECOM with its group of highly productive investigators in heart failure and vascular biology offers an exceptional environment to support Dr. Colombo?s career goals. Dr. Colombo developed a new approach to study the vascular endothelium. Protein expression is quantified by immunofluorescence in 400-900 endothelial cells (EC)s collected with a guide wire inserted in a superficial vein. His preliminary data indicate that transition from a decompensated to a compensated state in CHF is associated with a reduction in EC activation and oxidative stress. This application consists of two projects. The first will investigate the hypothesis that EC activation and oxidative stress, precede and contribute to clinical decompensation in patients with CHF. Dr. Colombo will prospectively study compliant patients hospitalized for CHF decompensation not due to co-morbid events. He will monitor markers of EC activation and oxidative stress, plasma cytokines, flow-mediated dilation, renal and cardiac function during decompensation, after return to a compensated state and serially until a second episode of decompensation. The second project will test the hypothesis that a reduction in EC activation and oxidative stress induced by physical training contributes to lowering the risk of CHF decompensation. Patients who experienced a second episode of decompensation in the first protocol will be randomized, once compensated, to routine activity or training. Endothelial cell activation and oxidative stress, plasma cytokines, flow-mediated dilation, renal and cardiac function will be assessed serially for six months or up to the next episode of decompensation.

描述（由申请人提供）：