| Project/Area Number |
09470319
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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 |
Orthopaedic surgery
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
IBARAKI Kunio University of the Ryukyus, School of Medicine, Professor, 医学部, 教授 (00107187)
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| Co-Investigator(Kenkyū-buntansha) |
OWAN Ichiro University of the Ryukyus, School of Medicine, Assistant Professor, 医学部, 助手 (80295310)
YOSHIKAWA Tomoaki University of the Ryukyus, School of Medicine, Instructor, 医学部・附属病院, 講師 (10264491)
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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 |
¥12,100,000 (Direct Cost: ¥12,100,000)
Fiscal Year 1999: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥7,900,000 (Direct Cost: ¥7,900,000)
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| Keywords | mechanotransduction / senescence accelerated mouse / osteoblast / bone formation |
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| Research Abstract |
Bone function is modulated by mechanical forces. The mechanism by which mechanical strain induces bone formation remains unclear. SAM-P/6 is a novel murine model of senile osteoporosis which is characterized by low peak bone mass. In contrast, SAM-R/1 is a strain with high peak bone mass. To study the effects of mechanical strain on bone metabolism and identify a novel gone which is involved in mechanotransduction, the bone formation response to mechanical strain is compared between SAM-P/6 and SAM-R/1.
Mechanical loading increased the expression of several factors such as COX-2, c-fos, and osteopontin mRNA much higher in SAM-R/1 than SAM-P/6 derived osteoblasts. However, a novel gene which is upregulated by mechanical loading in SAM-R/1 but not in SAM-P/6 could not be identified so far, and still under investigation.
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