MITOCHONDRIAL MODULATION OF INTRACELLULAR CA++ SIGNALING

这个奖学金的长期目标是为我提供一个 深入了解线粒体对细胞内Ca2+的影响 信号和数学建模的专业知识， 建立一个独立的研究计划，结合实验和 建模 在未来，我有兴趣进行细胞生物学 和生物物理研究的影响，线粒体疾病， 神经系统 异常的Ca2+信号，尤其是线粒体的开放 过渡孔由Ca2+，自由基和其他调节剂，已被 在病理情况下与神经元和其他细胞死亡有关。 该奖学金的具体研究目的是：1）延长博士。 Keizer致力于将线粒体构建成Ca2+信号模型， 结合线粒体过渡孔和2）解决这些问题 二维和三维空间的系统。 目标是能够 对线粒体功能的影响做出可测试的预测， 正常的Ca2+信号传导和涉及Ca2+的病理过程， 细胞中的线粒体。

The long term objective of this fellowship is to provide me with a thorough knowledge of the effects of mitochondria on intracellular Ca2+ signaling and the expertise in mathematical modeling necessary to establish an independent research program that combines experiment and modeling. In the future I am interested in conducting cell biological and biophysical research on the effects of mitochondrial disorders on the nervous system. Aberrant Ca2+ signaling, and especially the opening of the mitochondrial transition pore by Ca2+, free radicals and other modulators, has been implicated in neuronal and other cell death in pathological situations. The specific research aims of this fellowship are 1) to extend Dr. Keizer s efforts to build mitochondria into Ca2+ signaling models by incorporating the mitochondrial transition pore and 2) to solve these systems in two and three spatial dimensions. The goal is to be able to make testable predictions about the effect of mitochondrial function on both normal Ca2+ signaling and pathological processes involving Ca2+ and mitochondria in cells.