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EXERCISE AND POLYPOSIS IN THE APCMIN/+ MOUSE

EXERCISE AND POLYPOSIS IN THE APCMIN/+ MOUSE
APCMIN/小鼠的运动和息肉病
批准号:
7610470
负责人:
James A Carson
金额:
$12.09万
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:
2007-08-01 至 2008-05-31

项目摘要

项目成果

James A Carson的其他基金

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中文摘要
翻译
这个子项目是许多利用 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。 博士卡森的项目研究了运动减少癌症易感ApcMin/+小鼠息肉形成的机制。 评估了影响的机制。 此外,该项目还研究了恶病质的过程,即,肌肉和脂肪损失,在老化ApcMin/+小鼠。 促进恶病质的细胞和分子因子,如炎性细胞因子(白细胞介素-6)和信号分子,正在被检查作为恶病质的介质。
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. Dr. Carson's project examines the mechanisms by which exercise reduces polyp formation in the cancer-predisposed ApcMin/+ mouse. Mechanisms of the effects are assessed. In addition, the project examines the cachexic process, i.e., muscle and fat loss, in aging ApcMin/+ mice. Cellular and molecular factors promoting cachexia, such as inflammatory cytokines (interleukin-6) and signaling molecules, are being examined as mediators of cachexia.
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会议论文
Muscle GPRC6A regulation of protein turnover with overload and disuse recovery
Muscle GPRC6A regulation of protein turnover with overload and disuse recovery
(PQ 12) The Regulation of Physical Function and Skeletal Muscle Metabolic Signaling After Cessation of 5-Fluorouracil Treatment
Cachexia in ApcMin/+ mice: The role of IL-6
海外基金