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IDENTIFICATION OF GENETIC, BIOCHEMICAL AND HORMONAL FACTORS CONTRIBUTING TO L

IDENTIFICATION OF GENETIC, BIOCHEMICAL AND HORMONAL FACTORS CONTRIBUTING TO L
鉴定导致 L 的遗传、生化和激素因素
批准号:
7377723
负责人:
MIA CHUNG
金额:
$7.35万
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-04-01 至 2007-03-31

项目摘要

项目成果

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中文摘要
翻译
该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者(PI)可能从另一个NIH来源获得主要资金,因此可以在其他CRISP条目中表示。所列机构为中心,不一定是研究者所在机构。翻译后摘要:孤立性心房颤动或原发性心房颤动是一种心律失常的特点是不与心脏病。孤立性心房颤动的病因仍然不明确。遗传、生化或激素因素可能导致房颤的发展或持续存在。本研究提案的目的是制定一项研究计划,收集500例孤立性房颤受试者的血液和数据,并在两年期间建立基因库登记。我们还将使用来自克利夫兰诊所GeneBank Repository的500名正常对照的血液样本。主要目的是确定孤立性心房颤动发病机制的分子和蛋白质组学机制。这可能会建立一个新的机制,遗传,生化或体液因素可能有助于心律失常,从而导致新的治疗目标。该登记处和血库将用于未来的研究。血液可用于绘制和鉴定遗传性人类心房颤动的基因,以及鉴定这种心律失常发病机制的新的遗传、生化和体液机制。这些研究可能会提高我们对孤立性房颤的认识和理解,并可能建立一个新的机制,遗传,生化和体液因素可能有助于这种心律失常。疾病基因的鉴定可以改善预防房颤进展为更持久疾病的策略,并预防或逆转心房结构建模。疾病基因的表征可能为人类疾病的分子机制和致病过程提供额外的一般性见解,并可能为未来的研究指明新的方向。 沿着采集本试验入组受试者的血液样本,我们将采集一般病史、人口统计学数据、心电图数据、超声心动图数据和实验室数据用于登记研究。
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Abstract: Lone Atrial Fibillation or primary atrial fibrillation is an arrhythmia characterized by not being associated with heart disease. The etiology of lone atrial fibrillation remains poorly defined. Genetic, biochemical or hormonal factors may contribute to the development or perpetuation of atrial fibrillation. The purpose of this research proposal is to deliniate a research plan to collect blood and data from 500 subjects with lone atrial fibrillation and establish a gene bank registry over a two-year period. We will additionally use blood samples from 500 normal conrtrols taken from the GeneBank Repository at the Cleveland Clinic. The primary aim is to identify the molecular and proteomic mechanisms underlying the pathogenesis of lone atrial fibrillation. This may establish a novel mechanism by which genetic, biochemical or humoral factors might contribute to arrhythmias and thereby lead to targets for new therapies. This registry and bank of blood will be used for future research. The blood may be used to map and identify genes responsible for inherited human atrial fibrillation, as well as to identify new genetic, biochemical and humoral mechanisms underlying the pathogenesis of this arrhythmia. These studies are likely to improve our knowledge and understanding of lone atrial fibrillation and may establish a novel mechanism by which genetic, biochemical and humoral factors might contribute to this arrhythmia. Identification of disease genes could improve strategies that prevent the progression of atrial fibrillation to more persistent disease and prevent or reverse atrial structural modeling. Characterization of disease genes can potentially provide additional general insight into molecular mechanisms and pathogenic processes of human diseases and may point to new directions for future research. Along with the blood sample collected for subjects enrolled in this trial, we will collect general medical history, demographic data, electrocardiographic data, echocardiographic data and laboratory data for the registry.
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IDENTIFICATION OF GENETIC, BIOCHEMICAL AND HORMONAL FACTORS CONTRIBUTING TO L
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