Diabetes and Related Metabolic Diseases
糖尿病及相关代谢疾病
基本信息
- 批准号:9429380
- 负责人:
- 金额:$ 1.12万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-02-11 至 2017-06-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION (provided by applicant):
This competitive renewal application represents the merger of two successful diabetes research training programs at Washington University, DK007120 (based in the Department of Medicine) and KD007296 (based in the Department of Pathology & Immunology), into a single program entitled Diabetes and Related Metabolic Diseases (DK007120). For more than 35 years, these two T32 programs have trained a large number of biomedical scientists who have generated important insights into diabetes. To continue training outstanding scientists and physicians capable of developing novel approaches to address the striking increase in diabetes and its complications, we have integrated these two longstanding programs into one. The goal of this merged program is to provide mentoring expertise spanning model systems to outcomes research within a nurturing, structured environment that will produce independent diabetes scientists likely to change the landscape of research in diabetes and its complications. The program is directed by two PIs with complementary skill sets, one in immunology, the other in metabolism, to facilitate training opportunities in the emerging field of immunometabolism. The merged program represents the only NIH-supported mechanism for postdoctoral training in diabetes research at Washington University. The program is continually evolving in response to our ongoing assessment of its effectiveness, the needs of our trainees, and the dynamic nature of diabetes research. It is multidisciplinary and team-oriented. We propose to continue to train MD, MD PhD, and PhD scientists for 2-3 years through a structured program that leverages numerous strengths that include but are not limited to: • An exceptional pool of 29 mentors focused on diabetes. These scientists are pursuing research in basic mechanisms, proof of principle T1 translation, T2/T3 translation to patients and practice, and T3/T4 translatio to practice and populations. This group includes two members of the National Academy of Sciences and one member of the Institute of Medicine, each having mentored trainees during this most recent funding period, and several new members representing a broad spectrum of career stage and diversity. • A core curriculum in diabetes science required of all trainees to ensure that individuals with different backgrounds establish a standard knowledge base. • Training with a clinical context for PhD scientists as well as those with clinical degrees in order
to inform translational efforts. • Clearly defined metrics of success that are monitored by a personalized Career Development Committee for each trainee. • A series of mechanisms to assess quality and effectiveness of the program as well as established procedures to take action in response to the results of these assessment tools. • A dynamically integrated short-term research training program operated in close collaboration with our NIDDK Diabetes Research Center. • Well-established mechanisms for enhancing diversity. Our trainees are productive, having published more than 250 papers that have been cited more than 8000 times in the past 10 years. They are successful in terms of obtaining grant support for their research that includes (in the past 10 years) two R01s, several R01 equivalents (in the EU), three K01s, two K12s, two KL2s, one K99/R00, several pilot and feasibility awards, awards from the American Diabetes Association and the American Heart Association, and others. They are successful in terms of achieving productive scientific careers since our trainees enter academics (in the past 10 years) at a rate ~50-100% greater (depending on degree) than the biomedical workforce based on data cited by NIH. Our integration of two programs has achieved synergies leading to improvements in the mentor pool, enhancements in recruitment and mentoring strategies, and expanded efforts to increase diversity that collectively perpetuate a culture of multidisciplinary training with a very high likelihood of exerting a sustained and powerful influence on diabetes research.
描述(由申请人提供):
这一竞争性更新申请代表了华盛顿大学两个成功的糖尿病研究培训项目 DK007120(位于医学系)和 KD007296(位于病理学和免疫学系)的合并,成为一个名为“糖尿病和相关代谢疾病”的单一项目(DK007120) 超过 35 年以来,这两个 T32 项目培养了大量对糖尿病产生重要见解的生物医学科学家。杰出的科学家和医生能够开发新的方法来解决糖尿病及其并发症的显着增加,我们将这两个长期项目整合为一个项目,这一合并项目的目标是提供涵盖模型系统到结果研究的指导专业知识。一个结构化的环境,将培养独立的糖尿病科学家,可能会改变糖尿病及其并发症的研究格局。该项目由两名具有互补技能的 PI 指导,一名负责免疫学,另一名负责代谢,以促进新兴领域的培训机会。免疫代谢领域。合并后的项目是华盛顿大学唯一由 NIH 支持的糖尿病研究博士后培训机制。该项目根据我们对其有效性、学员需求以及糖尿病研究的动态性质的持续评估而不断发展。是多学科和以团队为导向的。我们建议通过一个结构化的计划继续培训医学博士、医学博士和博士科学家,该计划利用了众多优势,包括但不限于: • 由 29 名导师组成的优秀人才库。这些科学家正在研究糖尿病。基础机制研究、原理证明 T1 翻译、T2/T3 翻译到患者和实践、T3/T4 翻译到实践和人群 该小组包括两名美国科学院院士和一名医学研究所成员。每个人都在最近的资助期间指导了学员,并且几位新成员代表了广泛的职业阶段和多样性。 • 所有学员都需要糖尿病科学的核心课程,以确保具有不同背景的个人建立标准的知识库。博士生临床背景培训科学家以及具有临床学位的人
为转化工作提供信息 • 明确定义的成功指标,由每个学员的个性化职业发展委员会进行监控 • 评估计划质量和有效性的一系列机制以及针对结果采取行动的既定程序。 • 与我们的 NIDDK 糖尿病研究中心密切合作开展的动态综合短期研究培训计划。 • 我们的学员富有成效,已发表了 250 多篇论文。多于在过去 10 年中,他们成功获得了 8000 次研究资助,其中包括(在过去 10 年中)两个 R01、多个 R01 等效项(在欧盟)、三个 K01、两个 K12、两个 KL2、自从我们成立以来,他们在取得富有成效的科学事业方面取得了成功。根据 NIH 引用的数据,受训人员进入学术界(过去 10 年)的比率(取决于学位)比生物医学人员高出 50-100%。我们对两个项目的整合实现了协同效应,从而改善了导师库。 ,加强招募和指导策略,并加大力度增加多样性,共同延续多学科培训文化,极有可能对糖尿病研究产生持续而强大的影响。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Clay F. Semenkovich其他文献
Utilisation de chloroquine en vue de traiter un syndrome metabolique
代谢综合征中氯喹的利用
- DOI:
- 发表时间:
2006 - 期刊:
- 影响因子:0
- 作者:
Michael B. Kastan;Clay F. Semenkovich;Jochen Schneider - 通讯作者:
Jochen Schneider
Inhibition of fatty acid synthase plays a protective role in vascular smooth muscle cell proliferation and neointimal formation.
抑制脂肪酸合酶在血管平滑肌细胞增殖和新内膜形成中发挥保护作用。
- DOI:
- 发表时间:
2016 - 期刊:
- 影响因子:0
- 作者:
Naomi Oshima;Hiroki Matsui;Hiroaki Sunaga;Tatsuya Iso;Clay F. Semenkovich;Tomoyuki Yokoyama;Masahiko Kurabayashi. - 通讯作者:
Masahiko Kurabayashi.
Inhibition of fatty acid synthase suppresses vascular smooth muscle cell proliferation and neointimal formation: potential therapeutic target in atherosclerosis
抑制脂肪酸合酶可抑制血管平滑肌细胞增殖和新内膜形成:动脉粥样硬化的潜在治疗靶点
- DOI:
- 发表时间:
2018 - 期刊:
- 影响因子:0
- 作者:
Hiroki Matsui;Hiroaki Sunaga;Naomi Ohshima;Tatsuya Iso;Clay F. Semenkovich;Tomoyuki Yokoyama;Masahiko Kurabayashi - 通讯作者:
Masahiko Kurabayashi
Genetic deletion of fatty acid synthase in vascular smooth muscle cell suppresses injury-induced neointima formation in mice
血管平滑肌细胞脂肪酸合酶的基因缺失抑制小鼠损伤诱导的新内膜形成
- DOI:
- 发表时间:
2017 - 期刊:
- 影响因子:0
- 作者:
Naomi Oshima;Hiroki Matsui;Hiroaki Sunaga;Tatsuya Iso;Clay F. Semenkovich;Masahiko Kurabayashi;Tomoyuki Yokoyama - 通讯作者:
Tomoyuki Yokoyama
Clay F. Semenkovich的其他文献
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{{ truncateString('Clay F. Semenkovich', 18)}}的其他基金
GLUCOCORTICOID RECEPTOR POST-TRANSLATIONAL MODIFICATIONS IN INSULIN RESISTANCE
胰岛素抵抗中的糖皮质激素受体翻译后修饰
- 批准号:
9980364 - 财政年份:2016
- 资助金额:
$ 1.12万 - 项目类别:
MODULATING PHYSIOLOGIC EFFECTS OF PHOSPHOLIPID METABOLISM IN OBESITY AND DIABETES
调节磷脂代谢对肥胖和糖尿病的生理影响
- 批准号:
8885119 - 财政年份:2015
- 资助金额:
$ 1.12万 - 项目类别:
MODULATING PHYSIOLOGIC EFFECTS OF PHOSPHOLIPID METABOLISM IN OBESITY AND DIABETES
调节磷脂代谢对肥胖和糖尿病的生理影响
- 批准号:
9221327 - 财政年份:2015
- 资助金额:
$ 1.12万 - 项目类别:
MACROPHAGE FATTY-ACID SYNTHASE DEFICIENCY DECREASES DIET-INDUCED ATHEROSCLEROSIS
巨噬细胞脂肪酸合酶缺乏可减少饮食引起的动脉粥样硬化
- 批准号:
8361454 - 财政年份:2011
- 资助金额:
$ 1.12万 - 项目类别:
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