SCOR IN ISCHEMIC HEART DISEASE IN BLACKS

这个专门的缺血性心脏研究中心(SCOR)的目标是 黑人疾病是为了阐明过度的病理生理学基础 非裔美国人缺血性心脏病的发病率和死亡率 糖尿病患者，并制定有效的对策 来解决这个问题。SCOR将由8个研究单位组成 和3个核心单元。调查范围将从基础研究到 旨在影响医学的临床研究的疾病机制 在短期内练习。研究单位I，“冠脉血流与心肌 在患有NIDDM的黑人中的供需关系“将测试 黑人糖尿病患者冠状动脉反应性异常的假说 是可逆的，至少部分是通过增加胰岛素的干预来实现的 敏感性和改善与以下相关的代谢紊乱 NIDDM。研究单位二，“风险分层的基因分型”，将 检测血管紧张素转换酶基因对缺血性脑血管病临床表现的重要性 共享等位基因在黑人心脏病中的新应用 在大家庭中进行分析。研究单元III，“对人的反射控制 NIDDM的外周循环“，将定义胰岛素的机制 阻力调节骨骼肌反射的神经源性控制 血液循环，导致黑人高血压和左心室肥厚。研究 第四单元，“热休克蛋白70对缺血心肌的保护”将阐明 热休克蛋白70在脑缺血中的细胞保护作用机制 心。研究单元V，“糖尿病患者中的αB-晶状体蛋白/小分子热休克蛋白 心脏“，将检验小型热休克蛋白单独行动的假设，和/或 与HSP70协同，延缓HSP70的发生和发展 缺血心肌内不可逆性损伤。研究六组， “糖尿病心肌病发病机制中的高脂血症”，Will 检测升高的游离脂肪酸在加重缺血性疾病中的作用 糖尿病心脏的损伤。研究单元七，“基因改造 肥胖/胰岛素抵抗中的脂蛋白代谢“，将评估 纠正葡萄糖清除异常和脂肪异常的可行性 肝脏基因转移在II型动物模型中的酸氧化 糖尿病。研究单元八，“脂蛋白的基因修饰” 肥胖/胰岛素抵抗中的代谢“，将使用体细胞基因 改变动物模型中胆固醇代谢的方法转移到 纠正与糖尿病相关的致动脉粥样硬化性脂蛋白。 行政、生物技术和组织病理学的核心单位将 支持和扩大研究单位的活动。研究 在这项SCOR内进行的研究旨在改善对缺血性疾病的医学治疗 心脏病，并促进国家心脏的总体使命， 肺和血液研究所在减少人类痛苦和死亡中的作用 可归因于心血管疾病。

The goal of this Specialized Center of Research (SCOR) for Ischemic Heart Disease in Blacks is to elucidate the pathophysiological basis for excess morbidity and mortality from ischemic heart disease in African-American persons with diabetes mellitus, and to develop effective countermeasures to address this problem. The SCOR will be comprised of 8 research units and 3 core units. Investigations will range from fundamental studies of disease mechanisms to clinical research designed to influence medical practice in the near term. Research unit I, "Coronary flow and myocardial supply/demand relationships in blacks with NIDDM", will test the hypothesis that abnormalities in coronary reactivity in black diabetics are reversible, at least in part, by interventions that increase insulin sensitivity and ameliorate the metabolic perturbations associated with NIDDM. Research unit II, "Genotyping for risk stratification", will examine the importance of the ACE gene for manifestations of ischemic heart disease in blacks using a novel application of shared allele analysis in large families. Research unit III, "Reflex control of the peripheral circulation in NIDDM", will define mechanisms by which insulin resistance modulates the reflex neurogenic control of the skeletal muscle circulation and contributes to hypertension and LVH in blacks. Research unit IV, "Protection of the ischemic myocardium by hsp70" will elucidate mechanisms of the cytoprotective function of hsp70 within the ischemic heart. Research unit V, "alpha B-crystallin/small HSP in the diabetic heart", will test the hypothesis that small hsps act alone, and/or synergistically with hsp70, to delay the onset and progression of irreversible injury within the ischemic myocardium. Research unit VI, "Hyperlipacidemia in the pathogenesis of diabetic cardiomyopathy", will examine the role of elevated free fatty acids in exacerbating ischemic injury in the diabetic heart. Research unit VII, "Genetic modification of lipoprotein metabolism in obesity/insulin resistance", will assess the feasibility of correcting abnormalities in glucose clearance and fatty acid oxidation by hepatic gene transfer in an animal model of type II diabetes. Research unit VIII, "Genetic modification of lipoprotein metabolism in obesity/insulin resistance", will employ somatic cell gene transfer methods to modify cholesterol metabolism in animal models to correct the atherogenic lipoprotein profile associated with diabetes. Core units for Administration, Biotechnology, and Histopathology will support and expand the activities of the research units. Research conducted within this SCOR seeks to improve medical therapy of ischemic heart disease, and to promote the overall mission of the National Heart, Lung and Blood Institute in reducing human suffering and death attributable to cardiovascular disorders.