ENDOTHELIAL CELL ACTIVATION AND DECOMPENSATION IN CHF

CHF 中的内皮细胞激活和失代偿

• 批准号: 6888157
• 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/6888157
• 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·科伦坡博士是心脏病学四年级研究员，他是 完成慢性心力衰竭(CHF)和血管生物学方面的训练 阿尔伯特·爱因斯坦医学院(Albert Einstein College of Medicine，AECOM)在他的指导下成立。 蒂埃里·H·勒杰姆特尔和J·安东尼·威尔博士。科伦坡医生目前 由国立卫生研究院机构培训补助金(T32)支持。科伦坡博士将加入 AECOM医学系7月担任讲师 2001年。科伦坡博士最感兴趣的是开发治疗患者的新方法 以研究为导向，利用他的基础科学背景。这个 AECOM心血管事业部及其高生产率团队 心力衰竭和血管生物学的研究人员提供了一个特殊的 支持科伦坡博士的环境？S的职业目标。 科伦坡博士开发了一种研究血管内皮细胞的新方法。 免疫荧光法测定400-900血管内皮细胞的蛋白表达 S用导丝插入浅静脉采集细胞(EC)。他的 初步数据表明，从失代偿到失代偿的转变 充血性心力衰竭的代偿状态与EC激活减少和 氧化应激。 这个应用程序由两个项目组成。第一个将调查 假设EC激活和氧化应激先于并促成 充血性心力衰竭患者的临床失代偿。科伦坡博士将前瞻性地 符合研究要求的患者因CHF失代偿而住院，而不是由于共病 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、肾和心功能 失代偿，在恢复到补偿状态后，并连续进行，直到 失代偿第二集。 第二个项目将检验这一假设，即EC激活的减少 而体育锻炼引起的氧化应激有助于降低 充血性心力衰竭失代偿的风险。经历第二次肺炎发作的患者 一旦补偿，第一个方案中的失代偿将被随机化，以 例行活动或训练。内皮细胞的激活和氧化 应激、血浆细胞因子、血流介导的扩张、肾和心功能 将连续评估六个月或最多到下一集 失代偿。