CD39 AND PLATELET REACTIVITY IN ARTERIAL AND VENOUS THROMBOSIS
CD39 AND PLATELET REACTIVITY IN ARTERIAL AND VENOUS THROMBOSIS
批准号:
7604159
负责人:
JORGE R KIZER
金额:
$0.02万
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-04-01 至 2007-09-16
关键词:
AcuteAddressAtherosclerosisBloodBlood PlateletsComputer Retrieval of Information on Scientific Projects DatabaseCross-Sectional StudiesFundingGrantHumanInstitutionPathogenesisPatientsPhasePlatelet ActivationProtein IsoformsRNA SplicingResearchResearch PersonnelResourcesRoleSourceTestingTherapeuticThromboembolismThrombosisUnited States National Institutes of HealthVariantVenousVenous Thrombosisacute coronary syndromenovel therapeutics
中文摘要
这个子项目是众多研究子项目之一
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.
We propose a cross-sectional study of younger patients with acute coronary syndromes (ACS) or spontaneous venous thromboembolism (VTE) and healthy controls to address 4 specific aims: 1) Investigate whether reduced CD39 activity, and increased expression of CD39 splice variant 1.5, are associated with ACS in patients with premature atherosclerosis, both in the acute and convalescent phases; 2) Evaluate relationship between CD39 activity, CD39 isoform expression, and spontaneous VTE, both in the acute and convalescent phases; 3) Determine whether, and to what degree, increased platelet reactivity is associated with spontaneous VTE, and to compare its extent to that in ACS; 4) Assess the role of blood-borne TF in premature arterial and venous thrombosis.
The significance of this study is that it addresses potentially central molecules in human thromboregulation and thrombogenesis. A role for CD39 deficiency in human thrombosis would spur additional study into determinants of this reduced activity, and provide a strong rationale for testing soluble CD39 for therapeutic application. Novel therapeutic options could be opened by determining the role of blood-borne TF in the pathogenesis of premature arterial and venous thrombosis. Last, by demonstrating whether, and to what extent, platelet activation is involved in VTE, the study could re-focus research appropriately, with clear therapeutic implications.
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