Regulation of Prostacyclin in Pulmonary Hypertension
Regulation of Prostacyclin in Pulmonary Hypertension
批准号:
7106518
负责人:
SERGE PATRICK NANASINKAM
金额:
$13.15万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2004
资助国家:
美国
项目状态:
已结题
起止时间:
2004-08-15 至 2009-07-31
关键词:
biological modelsbiological signal transductioncardiovascular pharmacologyclinical researchenzyme linked immunosorbent assaygene expressiongenetic polymorphismgenetic promoter elementgenetic regulationgenetic susceptibilitygenetic transcriptiongenetically modified animalshemodynamicshuman subjecthypoxialaboratory mousemodel design /developmentmuscle cellsoxidoreductaseplatelet derived growth factorprostacyclinspulmonary hypertensionregenerationvascular endothelial growth factorsvascular smooth muscle
中文摘要
描述(由申请人提供):
候选人:候选人,帕特里克纳纳-辛卡姆,医学博士,是科罗拉多大学健康科学中心肺科学和重症监护医学部的讲师。 他目前由美国国立卫生研究院少数民族补充补助金的父母补助金NIH E PATHO支持。PROJ IV 5P01 HL 066254 - 03S1,"重度肺动脉高压中的前列环素合酶和前列环素受体。Nana-Sinkam博士以前曾研究过转基因小鼠疾病模型,并对类花生酸途径及其在疾病易感性中的作用以及鉴定具有临床应用的产品产生了特别的兴趣。 他的短期目标是继续发展专业和研究技能,最终成为一名独立调查员。 从长远来看,Nana-Sinkam博士希望在类花生酸生物学方面建立一个成功的、独立资助的实验室。 这个建议指导临床科学家奖将为他提供支持,以发展这些技能。
职业发展:Nana-Sinkam博士的职业发展将包括:1)开发新的研究技能,如转基因动物模型的开发,研究设计和学术中心所需的专业技能,2)正式的教育活动,包括分子生物学技术和赠款写作课程,和3)参与对发展专业技能至关重要的行政活动,如在医学院的招生和奖学金委员会任职,少数民族事务委员会。
环境:Nana-Sinkam博士目前处于有利于优秀研究的环境中。 他的赞助商Mark Geraci博士和共同赞助商Norbert Voelkel博士和Raphael Nemenoff博士都是杰出的、由校外资助的独立研究人员,在研究方面有着良好的记录。
调研:Nana-Sinkam博士的总体目标是试图阐明前列环素预防血管重塑和调节肺动脉高压的机制。 假设1)前列环素合酶过表达的条件性转基因鼠模型的开发可以帮助确定基因表达和重塑之间的时间关系,2)参与肺动脉高压中前列环素抑制的基因转录的关键调节因子可以通过基因转录调节模型来鉴定,和3)前列环素合成酶基因多态性存在于确定的人群中,并对基因功能和随后的疾病易感性具有潜在影响。
英文摘要
DESCRIPTION (provided by applicant):
Candidate: The candidate, Patrick Nana-Sinkam, M.D., is an Instructor in the Division of Pulmonary Sciences and Critical Care Medicine at the University of Colorado Health Sciences Center. He is currently supported by an NIH minority supplement grant to the parent grant NIH E PATHO. PROJ IV 5P01 HL066254-03S1, "Prostacyclin Synthase and Prostacyclin Receptor in Severe Pulmonary Hypertension." Dr. Nana-Sinkam has previously worked on transgenic murine models of disease and has developed a particular interest in the eicosanoid pathway and its role in disease susceptibility as well as identifying products with clinical application. His short-term goal is to continue to develop both the professional and research skills to eventually become an independent investigator. Long term, Dr. Nana-Sinkam hopes to develop a successful, independently funded laboratory in eicosanoid biology. This proposed Mentored Clinical Scientist Award would provide him with the support to develop these skills.
Career Development: Dr. Nana-Sinkam's career development will include: 1) developing new research skills such as the development of transgenic animal models, research design and professional skills necessary in an academic center, 2) formal educational activities including courses in molecular biology techniques and grant writing, and 3) involvement in administrative activities essential to developing professional skills such as serving on the School of Medicine's Admission and Scholarship Committees and Ethnic Minority Affairs Committee.
Environment: Dr. Nana-Sinkam is currently in an environment that is conducive to excellent research. His sponsor, Dr. Mark Geraci, and co-sponsors, Drs. Norbert Voelkel and Raphael Nemenoff, are outstanding, extramurally funded, independent investigators with established records in research.
Research: Dr. Nana-Sinkam's general goals will be to attempt to elucidate the mechanisms by which prostacyclin prevent vascular remodeling and are regulated in pulmonary hypertension. The hypotheses will be that 1) the development of a conditional transgenic murine model for overexpression of prostacyclin synthase can assist in defining the temporal relationship between gene expression and remodeling, 2) key regulators of gene transcription involved in suppression of prostacyclin in pulmonary hypertension can be identified by a model for gene transcriptional regulation, and 3) prostacyclin synthease gene polymorphisms exist in defined human populations and have a potential impact on gene function and subsequent susceptibility to disease.
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