| Project/Area Number |
17390401
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | The University of Tokushima |
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Principal Investigator |
NAGAHIRO Shinji The University of Tokushima, Institute of Health Biosciences, Professor, 大学院ヘルスバイオサイエンス研究部, 教授 (60145315)
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Koichi The University of Tokushima, Institute of Health Biosciences, Associate Professor, 大学院ヘルスバイオサイエンス研究部, 助教授 (90225938)
MATSUBARA Shunji Tokushima University, Hospital, Assistant Professor, 医学部・歯学部附属病院, 講師 (60294675)
NISHI Kyoko Tokushima University, Hospital, Instructor, 医学部・歯学部附属病院, 助手 (60335817)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥13,500,000 (Direct Cost: ¥13,500,000)
Fiscal Year 2006: ¥5,600,000 (Direct Cost: ¥5,600,000)
Fiscal Year 2005: ¥7,900,000 (Direct Cost: ¥7,900,000)
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| Keywords | cerebral aneurysm / pathogenesis / experimental model / estrogen / hypertension / female |
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| Research Abstract |
Based on epidemiological data indicative of a high incidence of cerebral aneurysm (CA) in postmenopausal women, we established a reproducible CA model in female rats. To identify early ultrastructural morphological changes that lead to the formation of experimental cerebral aneurysm (CA), we induced renal hypertension and right common carotid artery ligation. To further elucidate the role of hormones, we examined the effects of oophorectomy.. The oophorectomy increased the susceptibility of rats to aneurysm formation and the incidence of CA was reduced by hormone replacement therapy, indicating that hormones play a role in the pathogenesis of cerebral aneurysms. (J Neurosurg. 2005 ; 103 : 1046-51) (J Neurosurg. 2005 ; 103 : 1052-7)
To clarify the series of early events that leads to IA formation, the aneurysmal morphological changes on vascular corrosion cast to its parallel pathological changes in cerebral arteries were compared. We proposed that the formation of IAs starts with endothelial injury at the apical intimal pad (stage I), this lead to the formation of inflammatory zone (stage II). Partial tear or defect in the inflammatory zone will follow. Expansion of this defect forms the nidus for IA (stage III). Ours is the first demonstratation of the sequence of ultrastructural morphological and pathological changes that leads to the formation of saccular IAs in vivo. Detailed knowledge regarding these changes is crucial for an understanding of IA pathogenesis, and for introducing new preventive and therapeutic strategies that interrupt this cascade of aneurysmal changes (J Neurosurg. 2007, in press).
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