Closeout Bridging Administrative Supplement to R01AG049611

R01AG049611 的清仓桥接管理补充

基本信息

批准号：
10281452
负责人：
Elena Volpi
金额：
$ 35.59万
依托单位：
UNIVERSITY OF TEXAS MED BR GALVESTON
依托单位国家：
美国
项目类别：
财政年份：
2016
资助国家：
美国
起止时间：
2016-08-15 至 2023-05-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10281452
关键词：
Acceleration Acute Administrative Supplement Adverse event Aging Amino Acid Transporter Amino Acids Anabolism Award Bed rest Budgets COVID-19 pandemic Chronic Clinical Clinical Research Complex Data Development Direct Costs Elderly Equilibrium Event Exercise FRAP1 gene Fire - disasters Floods Funding Grant Health Hospitalization Hospitals Housing Human Resources Hurricane Inpatients Intervention Knowledge Life Mission Muscle Proteins Muscular Atrophy Non-Insulin-Dependent Diabetes Mellitus Parents Patient Care Physical Function Protein Biosynthesis Public Health Reporting Research Research Activity Research Project Grants Research Subjects Resistance Sampling Signal Transduction Skeletal Muscle Societies Stimulus Suspensions Transportation United States National Institutes of Health Wages Work base care costs cost dietary disability disability burden experimental study extracellular improved innovation laboratory experiment parent grant prevent recruit resistance exercise sarcopenia

项目摘要

PROJECT SUMMARY This administrative supplement for closeout bridge funding is requested to complete the research activities of the parent R01 grant after the end of the grant period. The parent award has suffered three major delays due to catastrophic events we have suffered over the past four years, which have slowed down subject recruitment and completion of the planned aims: 1) a hospital fire in 2017 which produced a 3 month delay; 2) flooding from Hurricane Harvey in 2017, which resulted in another major delay in grant-related activities due to destruction brought by the flood to personnel and research subjects' housing and transportation and dramatically reduced recruitment pace well into the Winter 2017-2018; 3) the COVID-19 Pandemic 2020, which caused another 5-month delay. Overall, these three devastating events add up to an approximately 1-year delay in parent grant study activities. During the three events we were able to save budget for supplies and patient care costs, but we were unable to save personnel costs. This closeout bridging administrative supplement will allow us to complete the planned studies during the no-cost extension year of the parent grant with no change to its scope. The parent grant objective is to examine the basic mechanisms that underlie accelerated sarcopenia in older adults and identify potential targets for interventions. The central hypothesis, based on our preliminary data, is that a global and fundamental mechanism of acute or chronic acceleration of sarcopenia is a reduction in skeletal muscle amino acid transport, which decreases muscle protein anabolism, and can be reversed by activation of the mammalian/mechanistic Target of Rapamycin Complex 1 (mTORC1) signaling with a non- amino acid stimulus such as exercise. The aims are: 1) Determine the effect of T2DM on the sensitivity of skeletal muscle amino acid transport to dietary amino acids. 2) Determine the effect of short- term bed rest inactivity on the sensitivity of skeletal muscle amino acid transport to dietary amino acids. 3) Determine the effect of resistance exercise on the sensitivity of amino acid transport to dietary amino acids in acute and chronic accelerated sarcopenia induced by inactivity and T2DM.

项目概要要求此收尾过桥资金行政补充以完成以下研究活动：资助期结束后的母 R01 资助。家长奖因以下原因遭受了三次重大延误：过去四年来我们遭受了灾难性事件，这些事件减缓了受试者的招募以及计划目标的完成情况： 1) 2017 年发生医院火灾，导致延迟了 3 个月； 2) 水浸 2017 年哈维飓风导致赠款相关活动再次出现重大延误，原因是洪水对人员和科研人员的住房、交通造成破坏直到 2017-2018 年冬季，招聘速度才大幅降低； 3) 2020 年 COVID-19 大流行，又造成了5个月的延误。总体而言，这三起毁灭性事件加起来大约持续了 1 年家长资助研究活动的延迟。在这三场活动中，我们节省了用品和病人的护理费用，但我们无法节省人员费用。此收尾桥接行政补助金将使我们能够在父母补助金的免费延期年内完成计划的研究其范围没有改变。家长资助的目标是检查其背后的基本机制加速老年人的肌肉减少症并确定潜在的干预目标。中心假设，根据我们的初步数据，这是急性或慢性加速的全球性基本机制肌肉减少症是骨骼肌氨基酸运输的减少，从而降低肌肉蛋白质的合成代谢，并且可以通过激活哺乳动物/雷帕霉素靶标复合物 1 (mTORC1) 来逆转通过非氨基酸刺激（例如运动）发出信号。目的是： 1) 确定 T2DM 对骨骼肌氨基酸转运对膳食氨基酸的敏感性。 2）确定短路的影响长期卧床不活动对骨骼肌氨基酸转运对膳食氨基酸的敏感性的影响。 3）确定抗阻运动对氨基酸转运对膳食氨基酸敏感性的影响缺乏活动和 T2DM 诱发的急性和慢性加速性肌肉减少症。