| Project/Area Number |
14571346
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Kinki University |
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Principal Investigator |
KATAOKA Kazuo Kinki University, School of Medicine, Associate Professor, 医学部, 助教授 (10221178)
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| Co-Investigator(Kenkyū-buntansha) |
TANEDA Mamoru Kinki University, School of Medicine, Professor, 医学部, 教授 (10236713)
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| Project Period (FY) |
2002 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | brain injury / brain edema / thrombin / protease / aquaporin / 受容体 / 細胞反応 / グリオーマ |
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| Research Abstract |
Brain injury and brain tumor causes brain edema. Brain edema is a pathological water accumulation in injured brain tissues. Prevention of the brain edema leads to the brain protection. A protease THROMBIN and a water channel protein AQUAPORIN may contribute the pathophysiology of the brain edema. aquaporin. Thrombin has both extracellular proteolysis and cell mediated functions thorough the protease-activated receptor 2.
We analyzed the roles of protease-activated receptor 2 and aquaporin on the brain edema using in vivo model of brain injury and in vitro model of cell cultures. Using real-time RT-PCR, we quantitatively evaluated mRNAs of protease-activated receptor 2 and aquaporin.
We could not find the definitive roles of protease-activated receptor 2 on the brain edema. On the other hand, we found a clear role of aquaporin on the brain edema. Osmolarity of injured brain tissues increased after ischemia or contusion. Our study suggests that an increase of osmolarity in injured brain tissues triggers overexpression of aquaporin in astrocytes. Hypothermia inhibits this overexpression of cultured astrocytic aquaporin after the hyper osmolar stimulation.
According to the osmotic gradient, water molecules easily move to the injured tissues through the water channels aquaporin that are excessively expressed. Hypothermia inhibits this overexpression of astrocytic aquaporin. This inhibition may be benefit for the injured brain to prevent the brain edema.
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