| Project/Area Number |
24700459
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biomedical engineering/Biological material science
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| Research Institution | Tokyo Metropolitan University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 頭部外傷 / びまん性軸索損傷 / アミロイド前駆体タンパク質 / 脳神経細胞 / 細胞引張実験 / 衝撃ひずみ / 免疫蛍光染色 / 微細加工 / 軸索損傷 / 軸索伸長方向制御 / 神経活動電位 / β-アミロイド前駆体タンパク質 |
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| Research Abstract |
Traumatic brain injury caused by traffic accidents, blow, falls and contact sports, is an important public health problem throughout societies because of a contribution of disability and death. While diffuse axonal injury (DAI) is one of the most serious traumatic brain injuries, DAI is caused by sudden inertial loading to the head associated with rapid deformation of brain tissue, resulting in the stretching of neural axons. In this study, the cultured rat brain neuronal cells were stretched, the beta-amyloid precursor protein (beta-APP) that is conveyed by axonal transport accumulates where axonal transport is disrupted, was stained and observed using fluorescence microscopy.
The results show that the threshold of interruption of axonal transport is strains of 15-22% at strain rates of 21-27/s and the accumulation of beta-APP is a quantitative marker for traumatic axonal injury at a cellular level.
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