Analysis of the mechanism for efficient rehabilitation using cell signaling mutant cells
Project/Area Number |
23650341
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Rehabilitation science/Welfare engineering
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Research Institution | Kibi International University |
Principal Investigator |
KANO Yoshio 吉備国際大学, 保健医療福祉学部, 教授 (70116200)
|
Co-Investigator(Kenkyū-buntansha) |
KAWAMURA Kenji 吉備国際大学, 保健医療福祉学部, 教授 (40278974)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | p38MAPK / JNK / Akt / PI3K / ERK / Aging / Anti aging / Aiging / Anti aiging / Fibroblast / Mouse / p38MAPK USA / JNK USA / Akt USA / P13K USA / ERK USA / Aging USA / Anti aging USA |
Research Abstract |
In this study, we carried out experiments using cell signaling mutant cells to improve nerve regeneration and efficiency of rehabilitation with the aims of elucidating the mechanism of rehabilitation at the molecular level and establishing a method for recovery of paralysis due to cerebral infarction. In the experiments, we used three newly developed cell signaling mutant cell lines and found that (1) rehabilitation stimulus by, for example, thermotherapy, promotes nerve regeneration by acting p38 kinase in the cell signaling pathway, (2) acetylcholine, which acts to improve hemiplegia caused by cerebral infarction, activates EFK enzyme in the same signaling pathway, and (3) Akt enzyme functions for long-term survival of neurons.
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Report
(4 results)
Research Products
(20 results)