| Project/Area Number |
09671440
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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 | Osaka City University Medical School |
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Principal Investigator |
HAKUBA Akira Osaka City University Medical School, Department of Neurosurgery, Professor, 医学部, 教授 (10047011)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Makoto Fukui Medical University, Department of Anatomy (2), Professor, 医学部, 教授 (10222019)
TAKAGI Hiroshi Osaka City University Medical School, First Department of Anatomy, Professor, 医学部, 教授 (30163174)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | spinal cord / corticospinal tract / pyramidal tract / axon / microglia / recovery / blood-brain-barrier / 脊髄損傷 / 橋 / 再生 / 神経再生 |
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| Research Abstract |
The basilar pons plays an important role in the establishment of the corticopontine projection by releasing a diffusible molecule which induces and directs collateral branchings along the carticospinal axon shafts. We have attempted to apply this nature of pons-derived diffusible factor that enhances the sprouting of cortical axons and controls their growth direction to recovery the damaged cortical axons in the spinal cord. Before applying this potential pons-derived factor, we need to identify and clone the responsible pons factor(s). Then, we modified the mRNA differential display to search for genes expressed differentially in the basilar pons during the formation of the corticopontine projection to identify the authentic and/or pans-related molecules.
Results we have obtained so far are as follows :
(1) Three gene fragments which are potentially the pontine-derived molecules have been identified. Full- length cDNA clones of two candidate fragments have been obtained.
(2) In addition to the experiments mentioned above, we tried to utilize the nature of some kind of microglial cells that can enter the brain through the blood-brain-barrier (Sawada et al., ). Since the microglial cells tend to accumulate around the injured site, it is ideal to employ the microglial cells that deliver the neurotrophic factor(s) which enhances the neuron survival/axon repair. We reconfirm the ability of some kind of micraglial cells of entering into the brain. We still in the process of searching for the efficient method of generating, genetically modified microglial cells.
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