| Project/Area Number |
14571359
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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 |
Orthopaedic surgery
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| Research Institution | Chiba University |
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Principal Investigator |
MURATA Atsushi Chiba University, University Hospital, Assistant, 医学部附属病院, 助手 (20344997)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAZAKI Masashi Chiba University, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (50281712)
YOSHINAGA Katsunori Chiba University, University Hospital, Associate Professor, 医学部附属病院, 助教授 (30270870)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Semaphorin 3A / Spinal cord injury / gene expression / セマフォリン / 神経細胞 / in situ hybridization / RT-PCR |
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| Research Abstract |
Semaphorin 3A (Sama3A) is a secreted protein involved in repulsive axon guidance expressed in spinal motoneurons and some kinds of neurons in brain. We demonstrate here the variation of sema3A expression in the spinal cord afar transection injury. Waster mis (8w, male) were subjected to complete spinal cord transection injury. Total RNA was extracted and cryosections of transected spinal cord were prepared For histological brain examination, Water rats were subjected to spinal cord hemisection Total RNA samples from completely transected spinal cords was reverse transcribed and cDNA was amplified using sema3A primers Band densities was analyzed using NIHImage software. Sema3A digoxigenin-labeled cRNA probes wane hybridized sand density decreased and reached a minimum at 24 hours. It than increased gradually to 4/5 the normal control level In the normal control spinal cord, many sema3A-positive motoneurons were present, and at 24 hours the number of sema3A-positive motoneurons decreased. In situ hybridization of brain sections on spinal cord hamisection revealed that the sema3A signal decreased in the contralateral temporal cortex, ipsilateral spinal trigeminal nucleus and caudate putamen neurons
Before and after complete spinal cord transection, sema3A mRNA decreased with the decrease in the member of motoneurons. In addition, brain sections from spinal cord hemisection revealed that the sema3A signal decreased at the temporal cortex and some nuclei
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