课题基金 / 基金详情

DEFINING STRATEGIES FOR IMPROVING ENDOTHELIAL/FIBRINOLYTIC DYFUNCTION IN OBESITY

DEFINING STRATEGIES FOR IMPROVING ENDOTHELIAL/FIBRINOLYTIC DYFUNCTION IN OBESITY
制定改善肥胖症内皮/纤溶功能障碍的策略
批准号:
7731488
负责人:
Douglas E Vaughan
金额:
$0.05万
依托单位:
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:
2006-12-01 至 2007-09-16

项目摘要

项目成果

Douglas E Vaughan的其他基金

相关文献

中文摘要
翻译
这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者(PI)可能从另一个NIH来源获得了主要资金, 因此可以在其他CRISP条目中表示。所列机构为 研究中心,而研究中心不一定是研究者所在的机构。 中心假设是,血管性派-1过量促进血管内血栓形成的发展。我们将测试放射细胞分泌的因子具有自分泌、旁分泌和内分泌效应,这些效应通过增强派-1的产生或损害内皮t-PA的释放对纤溶系统产生有害影响。
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. The central hypothesis is that vacular PAI-1 excess promotes the development of intravascular thrombosis. We will test that secreted factors from adiocytes have autocrine, paracrine, and endocrine effects that have deleterious effect on the fibrinolytic system, either by enhancing PAI-1 production or impairing endothelial t-PA release.
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会议论文
Evolutionary Advantage of Heterozygous PAI-1 Deficiency in Humans
Spontaneous cardiac fibrosis in PAI-1-deficient mice and men: A rare mutation informs a common molecular pathophysiology
Spontaneous cardiac fibrosis in PAI-1-deficient mice and men: A rare mutation informs a common molecular pathophysiology
Cardiovascular Regenerative Medicine