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ENDOTHELIAL CELL ACTIVATION AND DECOMPENSATION IN CHF

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
依托单位国家:
美国
项目类别:
财政年份:
2002
资助国家:
美国
项目状态:
已结题
起止时间:
2002-08-15 至 2007-05-31

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中文摘要
翻译
描述(由申请人提供): 候选人 Paolo C. Colombo 博士是一名四年级心脏病学研究员, 在完成慢性心力衰竭 (CHF) 和血管生物学方面的培训 在阿尔伯特·爱因斯坦医学院 (AECOM) 博士的指导下 Thierry H. Le Jemtel 和 J. Anthony Ware 博士。科伦坡博士目前 得到 NIH 机构培训补助金 (T32) 的支持。科伦坡博士将加入 7月在AECOM医学系担任讲师 2001. Colombo 博士最感兴趣的是开发治疗患者的新方法 利用他的基础科学背景进行定向研究。的 AECOM 心血管部门及其高产团队 心力衰竭和血管生物学的研究人员提供了一个特殊的 支持科伦坡博士职业目标的环境。 科伦坡博士开发了一种研究血管内皮的新方法。 通过免疫荧光对 400-900 内皮细胞中的蛋白质表达进行定量 用插入浅静脉的导丝收集细胞(EC)。他的 初步数据表明,从失代偿期到失代偿期的转变 CHF 的代偿状态与 EC 激活的减少有关 氧化应激。 该应用程序由两个项目组成。首先将调查 假设 EC 激活和氧化应激先于并促成 CHF 患者的临床失代偿。科伦坡博士未来将 符合研究要求的患者因 CHF 失代偿而住院,但并非由于共病 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、肾脏和心脏功能 失代偿,返回补偿状态后依次进行,直到 第二次失代偿发作。 第二个项目将检验 EC 激活减少的假设 体能训练引起的氧化应激有助于降低 CHF 失代偿的风险。经历过第二次发作的患者 第一个方案中的失代偿将被随机化,一旦补偿, 日常活动或训练。内皮细胞活化和氧化 应激、血浆细胞因子、血流介导的扩张、肾功能和心脏功能 将连续评估六个月或直到下一集 失代偿。
英文摘要
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.
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Cardiac Lipotoxicity and Ceramide Metabolism in Heart Failure
Endothelial Oxidative Stress and Inflammation:Mechanisms and Human Studies
Endothelial Oxidative Stress and Inflammation:Mechanisms and Human Studies
Endothelial Oxidative Stress and Inflammation:Mechanisms and Human Studies
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