ENDOTHELIAL CELL ACTIVATION AND DECOMPENSATION IN CHF

CHF 中的内皮细胞激活和失代偿

• 批准号: 6594790
• 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/6594790
• 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）： 候选人保罗·C博士科隆博是一名四年级的心脏病学研究员， 完成他在慢性心力衰竭（CHF）和血管生物学方面的培训， 阿尔伯特·爱因斯坦医学院（AECOM）的指导下，博士。 蒂埃里·H Le Jemtel和J. Anthony Ware博士。科隆博医生目前 由NIH机构培训补助金（T32）支持。科隆博博士将加入 7月在AECOM医学系担任讲师 2001.科隆博博士最感兴趣的是开发新的方法， 以研究为导向，利用他的基础科学背景。的 AECOM的心血管部门及其高效的 心力衰竭和血管生物学的研究人员提供了一个特殊的 支持科隆博博士的环境吗的职业目标。 博士科隆博开发了一种研究血管内皮的新方法。 在400-900个内皮细胞中通过免疫荧光定量蛋白表达。 用插入浅静脉的导丝收集细胞（EC）。他 初步数据表明，从失代偿到 CHF中的代偿状态与EC激活的减少相关， 氧化应激 该应用程序包括两个项目。第一个将调查 假设EC活化和氧化应激先于并促成 CHF患者的临床失代偿。科隆博医生将 因CHF失代偿而住院的研究依从性患者，并非由于合并症 事件他将监测EC激活和氧化应激的标志物， 血浆细胞因子，血流介导的扩张，肾和心脏功能， 失代偿，在返回到补偿状态之后，连续地直到 第二次失代偿 第二个项目将测试EC激活减少的假设， 而体育锻炼引起的氧化应激有助于降低 CHF失代偿的风险。发生第二次发作的患者 第一个方案中的失代偿患者将在代偿后随机分配至 日常活动或训练。内皮细胞活化和氧化 应激、血浆细胞因子、血流介导的舒张、肾和心功能 将连续评估六个月或直到下一集 代偿失调