| Project/Area Number |
07671550
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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 | Kansai Medical University |
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Principal Investigator |
YAMANOUCHI Yasuo Kansai Medical University, Faculty of medicine, Associate professor, 医学部, 助教授 (00121997)
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| Co-Investigator(Kenkyū-buntansha) |
YASUDA Takasumi Kansai Medical University, Faculty of medicine, Assistant, 医学部, 助手 (60230223)
INAGAKI Takayuki Kansai Medical University, Faculty of medicine, Assistant professor (lecturer), 医学部, 講師 (10213109)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Chiari malformation / spinal dysraphism / pathogenesis / experimental study / Myelomenigocele / Mouse model / Exo-utero culture / Myelomeningocele / mouse model / mouse medel / ヒト |
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| Research Abstract |
Previous results have shown that in the splotch-delayed mouse (Pax3^<Sp-d>) embryo, a strain in which the homozygote develops an open neural tube defect, a small posterior fossa develops and the deformity of this region appears similar to that in the Chiari-II abnormality in humans. In addition, in mouse embryos with open neural tube defects induced with vitamin A, a Chiari-II-like posterior fossa deformity develops. Similarly, in rodent fetuses treated with trypan blue, salicylate, or ethylenethiourea, a Chiari-II-like posterior fossa deformity forms in association with an open neural tube defect.
The continuous positive pressure of the cerebrospinal fluid (CSF) in early stages of embryogenesis is mandatory for normal development of the nervous system. We have hypothesized that intracranial abnormalities may result in part from the leakage of CSF through the opening at the caudal spinal cord during critical periods of rapid enlargement of brain.
Mouse embryos were exposed and surgically treated at gestation day 12 to produce spina bifida aperta, and operated embryos were cultured exo utero in the peritoneal cavity of the pregnant dam. Embryos were harvested at gestation day 14 and 16. Open neural tube defects resulted in 13 out of 25 embryos surviving surgery on gestation day 14. Histological examination revealed that the sizes of ventricles in both the supra-and infra-tentorial compartments were greatly reduced in embryos with spina bifida aperta compared with control embryos. This result supports the hypothesis that leakage of cerebrospinal fluid through the opening of the caudal spine may be a major cause of brain abnormalities patients with myelomeningocele. The problem is that it is difficult to let survive operated-embryos longer than two days in exo utero, so far.
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