| Project/Area Number |
09670450
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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 |
Legal medicine
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| Research Institution | Iwate Medical University |
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Principal Investigator |
AOKI Yasuhiro School of Medicine, Iwate Medical University, Professor, 医学部, 教授 (90202481)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAYAMA Yumi School of Medicine, Iwate Medical University, Research Associate, 医学部, 助手 (10295967)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1999: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | brain injury / axonal injury / immunohistochemistry / animal experiment / cell culture / ultramicrostructure / 免疫組織化学 / fluid percussion モデル / 三叉神経節 / fluid percussionモデル |
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| Research Abstract |
To investigate mechanical effect of repeated minor impact to the pathobiology of the brain, 2 experimental head injury models were designed. In vivo, adult rats were injured utilizing weight-drop device consisting of brass weight(450g) falling through a acrylic guide tube(1m). After 3 insults at an interval of 24 hours, the brain were perfused with 4% Paraformaldehyde in phosphate buffer solution and removed. Histopathological and immunohistochemical studies disclosed neuronal injury in the cerebral cortex, and brain edema in the corpus callosum. Despite the lack of diffuse axonal changes, this model would be suitable for studying neuronal, changes associated with minor head trauma. In vitro model of axonal injury using cultured cells was designed to introduce traumatic alterations on neuronal processes and to identify mechanisms responsible for the formation of focal swellings by observation with phase-contrast and transmission electron microscopes. The culture dishes were oscillated
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one-dimensionally and horizontally 1, 2 or 3 times; repeating at intervals of an hour, 5 seconds a time; on a heat controlled shaker. The amplitude and frequency of the oscillation was 40 mm and 1 Hz, respectively. The injured processes showed two forms: the terminal increase in diameter of the processes and beading depending on injured portions. The microscopic finding suggests that the stress would destroy a cytoskeletal network, and then cause the spherical deformation of the processes. Ultramicroscopically, the beads contained compactly and sparsely misaligned cytoskeletons and prominently gathered densecore vesicles. The cytoskeletal reconstruction within the regenerated growth cones was also noted in the terminal swellings and beads. The destruction of these linkers would be responsible to initiate the cytoskeletal destruction. The initiating point of the cytoskeletal alterations, however, must be confirmed using three dimensional imaging of samples without soluble proteins and immunohistochemical study. Less
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