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Elucidation of the inhibitory mechanism of histamine H2 receptor antagonist against posterior longitudinal ligament ossification

Research Project

Project/Area Number 15K10389
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Orthopaedic surgery
Research InstitutionThe University of Tokyo

Principal Investigator

Yamamoto Kenichi  東京大学, 大学院工学系研究科(工学部), 特任研究員 (90583162)

Co-Investigator(Kenkyū-buntansha) 鄭 雄一  東京大学, 大学院工学系研究科(工学部), 教授 (30345053)
Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords後縦靭帯骨化症 / ヒスタミンH2受容体拮抗薬 / ヒスタミンH2ブロッカー / TTWマウス / ヒスタミンH2受容体拮抗薬 / tip toe mouse / 石灰沈着性腱炎 / 異所性骨化 / 後縦靱帯骨化症
Outline of Final Research Achievements

We investigated the prophylactic and therapeutic effects of H2 receptor antagonists on posterior longitudinal ligament ossification ophthalmopathy, clarified the point of action, and investigated the involvement of histamine in mineralization. We used tip toe mouse (TTWmouse) which is a model mouse of OPLL. Famotidine administration group showed a tendency to suppress ectopic ossification. Analysis of the pathology of OPLL in complex mutant mice born by mating of histamine H2 receptor knockout mice with TTW mice revealed a shrinkage tendency of OPLL at μCT but no obvious change in tissue sections was seen.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report

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Published: 2015-04-16   Modified: 2019-03-29  

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