Updated on 2026/02/27

写真a

 
MIHARA Hiroshi
 
Organization
Medical Development Center Dean Department of Educational Development Associate Professor
Title
Associate Professor
Profile

1996年3月 富山県立高岡高等学校卒業
1996年4月 富山医科薬科大学医学部医学科入学
2002年3月 富山医科薬科大学医学部医学科修了
2007年4月 富山大学大学院生命・臨床医学専攻入学
2011年3月 富山大学大学院生命・臨床医学専攻修了
2002年4月 富山医科薬科大学附属病院 見学生
2002年5月 富山医科薬科大学附属病院 第三内科医員・研修医
2003年4月 同・院内ローテート研修（小児科、第二外科）
2003年10月 厚生連高岡病院麻酔救急治療科研修
2004年4月 富山市民病院 内科
2005年4月 高岡市民病院 胃腸科
2007年4月 富山大学附属病院 第三内科 医員
2008年5月 生理学研究所 岡崎統合バイオサイエンスセンター細胞生理研究部門
2010年10月 富山大学第三内科リサーチアシスタント
2011年4月 富山大学附属病院 第三内科 医員
2012年4月 富山大学附属病院 第三内科 診療助手
2015年7月 富山大学医学部医学教育センター 助教
2016年8月 富山大学医学部医師キャリアパス創造センター（組織改編のため） 助教
2022年9月 札幌医科大学総合診療医学講座　准教授

ORCID ID
0000-0002-8427-2868
External link

Degree

  • 博士（医学） ( 富山大学大学院 )

Research Areas

  • Humanities & Social Sciences / Education

  • Life Science / General internal medicine

  • Life Science / Gastroenterology

Papers

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Books

MISC

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Research Projects

  • Development of a distance learning program to improve the emergency medical skills for non-emergency physicians and verification of the educational outcome

    Grant number：25K13417  2025.4 - 2029.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）

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  • Research for induction or normalization factor for colonic TRPV4 methylation aiming at curing constipation

    Grant number：19K08366  2019.4 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Mihara Hiroshi

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    Grant amount：\4290000 （ Direct Cost: \3300000 、 Indirect Cost：\990000 ）

    TRPV4 ion channel, a receptor for stretching and microinflammation, was highly expressed in the epithelium in constipated patients from the small intestine to the rectum and was associated with decreased stool frequency and duration of disease. When colon epithelial cell lines and bacteria were co-cultured, bacteria was divided into those that transiently decreased, those that remained constant, and those that increased TRPV4 expression. ; K.oxytoca, E.faecalis, and E.coli increased TRPV4 expression; the bacteria themselves did not increase the expression, but culture components did. Butyrate, a short-chain fatty acid, and TNF-α inhibitors suppressed increased expression, and constipation symptoms were associated with the ratio of E.faecalis in the colonic mucosa of constipated patients, suggesting that maintaining butyrate-producing bacteria and suppressing the TNF-α pathway may prevent or treat chronic constipation.

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  • TRP ion channel related to the pathogenic mechanism of small intestinal ulceration induced by NSAIDs use

    Grant number：15K08947  2015.4 - 2019.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Sugiyama Toshiro

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    Grant amount：\4550000 （ Direct Cost: \3500000 、 Indirect Cost：\1050000 ）

    NSAIDs-induced small intestinal ulcerations are rapidly increasing, however the effective prevention has not been established. As the ulcerations are prevented by the use of broad spectrum antibiotics, the intestinal inflammation by intestinal flora or the metabolites should be attributed. However, the molecular mechanism related to increased permeability of small intestinal epithelial cells by NSAIDs use is not elucidated.
    By the permeability experiment with small intestinal epithelial cells, NSAIDs accelerated the permeability via the accumulation of 8, 9 EET, which is the metabolites of membrane arachidonic acids and activated TRPV4. The activated TRPV4 is attributed to the increase of permeability. By this assay system, one candidate drug was selected, which showed the inhibition of TRPV4 activation and inhibited the increased permeability of intestinal epithelial cells induced by NSAIDs. Clinical trials are planning to confirm the preventing effect of the candidate.

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  • Molecular mechanism of luminal pressure reception and ATP release in gastrointestinal epithelium

    Grant number：26870214  2014.4 - 2018.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)

    Mihara Hiroshi, NISHIZONO Hirofumi, SUGIYAMA Toshiro, TOMINAGA Makoto, TABUCHI Yoshiaki, WATANABE Shiro, UCHIDA Kunitoshi, KOIZUMI Schuichi, Boudaka Ammar, YAMAWAKI Hidemoto, SUZUKI Nobuhiro, Muhammad Jibran Sualeh, KOZAWA Toyomi, Fujinami Haruka, ANDO Takayuki, NANJO Sohachi

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    Grant amount：\3380000 （ Direct Cost: \2600000 、 Indirect Cost：\780000 ）

    Approximately 15% of Japanese people have chronic abdominal pain of unknown origin and hypersensitivity to gastrointestinal pressure is one of possible causes. The esophagus senses a tension with mechano-sensitive TRPV4 ion channel and releases bag-like adenosine triphosphate (ATP) using its transporter (VNUT). As a result of the study, TRPV4 and VNUT are present not only in the esophagus but also from the stomach to the rectum, and ATP is released via VNUT by TRPV4 stimulation, including stretch stimuli. Mice lacking TRPV4 have gastric motor abnormality and Helicobacter pylori infection decreases TRPV4 (gene methylation). It has also succeeded in quantifying the TRPV4 stimulating component synthesized in the gastrointestinal tract and so the possibility of quantifying invisible abdominal pain has come out.

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