Researchers

SHIMADA Takahiro

SHIMADA Takahiro
Associate Professor/Deputy General Manager
Faculty Kindai University Nara Hospital
Researchmap https://researchmap.jp/shimada

Education and Career

Education

  • 1987/04 - 1993/03 , Kindai University, Faculty of Medicine,
  • 1995/04 - 1999/03 , Kindai University FACULTY OF MEDICINE. GRADUATE SCHOOL OF MEDICAL SCIENCES, Faculty of Medicine,

Academic & Professional Experience

  • Apr. 2018 - Today , Kindai University Nara Hospital Kindai University Associate Professor
  • Jan. 2018 - Mar. 2018 , Kindai University Nara Hospital Kindai University lecturer
  • Apr. 2016 - Dec. 2017 , Kindai University Faculty of Medicine lecturer
  • Apr. 2014 - Mar. 2016 , Kishiwada city hospital hematology Director
  • Oct. 2011 - Mar. 2016 , Kindai University Faculty of Medicine lecturer
  • Jan. 2009 - Oct. 2011 , Kindai University Department of Hematology, Faculty of Medicine lecturer
  • May. 2006 - Dec. 2008 , Cedars-Sinai Medical Center Immunobiology Research Institute post doctoral fellow

Research Activities

Research Areas

  • Life sciences , Hematology and oncology

Research Interests

Waldenstrom Macroglobulinemia, MYD88 L256P, multiple myeloma, inflammasome, PIG-A変異細胞, 発作性夜間血色素尿症

Published Papers

  1. 〈Originals〉Efficacy and safety of lenalidomide prednisolone combination treatment for Japanese elderly multiple myeloma patients
    Hanamoto Hitoshi; Fujii Aki; Yamada Kaori; Fujimoto Ko; Fujiwara Ryosuke; Shimada Takahiro
    The Kindai University Medical Association  46  (2)  , 23-28, Dec. 2021  , Refereed
  2. 〈Originals〉Efficacy and safety of Clarithromycin, Lenalidomide and Dexamethasone (BiRd) therapy for Japanese relapsed or refractory multiple myeloma
    Hanamoto Hitoshi; Fujii Aki; Yamada Kaori; Fujimoto Ko; Fujiwara Ryosuke; Shimada Takahiro
    The Kindai;University Medical Association  46  (1)  , 9-15, Jun. 2021  , Refereed
  3. 〈Originals〉Morbidity and mortality associated with development of hypogammaglobulinemia after Rituximab
    Hanamoto Hitoshi; Yamada Kaori; Fujii Aki; Fujimoto Ko; Fujiwara Ryosuke; Shimada Takahiro
    The Kindai;University Medical Association  46  (1)  , 17-21, Jun. 2021  , Refereed

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Conference Activities & Talks

  1. 当院における同種造血幹細胞移植時のダプトマイシンの有用性と安全性 , 芹澤 憲太郎; 森田 泰慶; 江本 正克; 大山 泰世; 福井 彩乃; 井上 宏昭; 川内 超矢; 金井 良高; 平瀨 主税; 田中 宏和; 嶋田 高広; 宮武 淳一; 辰巳 陽一; 芦田 隆司; 松村 到 , 第36回日本造血細胞移植学会総会 , Mar. 2014
  2. 当院における同種造血幹細胞移植時のダプトマイシンの有用性と安全性 , 芹澤憲太郎; 森田泰慶; 江本正克; 大山泰世; 福井彩乃; 井上宏昭; 川内超矢; 金井良高; 平瀬主税; 田中宏和; 嶋田高広; 宮武淳一; 辰巳陽一; 芦田隆司; 松村到 , 日本造血細胞移植学会総会プログラム・抄録集 , 14, Feb. 2014
  3. Efficacy of early intervention of deferasirox in patients with transfusional iron overload , 芦田 隆司; 丸瀬ちほ; 福島靖幸; 川野亜美; 山田枝里佳; 井手大輔; 菅野知恵美; 加藤祐子; 椿本祐子; 伊藤志保; 峯 佳子; 藤田往子; 金光 靖; 森嶋祥之; 森田 泰慶; 田中 宏和; 嶋田 高広; 宮武 淳一; 辰巳 陽一; 松村 到 , 第75回日本血液学会学術集会 , 2014

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MISC

  1. 難治性血栓症を伴うI型クリオグロブリン血症を合併したリンパ形質細胞性リンパ腫の1例 , 國田 裕貴; 口分田 貴裕; 波江野 高大; 森田 泰慶; 嶋田 高広; 田中 宏和; 辰巳 陽一; 芦田 隆司; 松村 到 , 臨床血液 , 59 , 2 , 239 , 240 , Feb. 2018
  2. 複数の免疫異常を合併した脾辺縁帯リンパ腫の1例 , 三宅 義昭; 口分田 貴裕; 波江野 高大; 森田 泰慶; 嶋田 高広; 田中 宏和; 辰巳 陽一; 芦田 隆司; 松村 到 , 臨床血液 , 59 , 2 , 240 , 240 , Feb. 2018
  3. 〈Originals〉Trib1 and Trib2 inhibit granulocytic differentiation by suppressing Akt pathway , Kanai Yoshitaka; Shimada Takahiro; Taniguchi Yasuhiro; Rai Shinya; Hirase Chikara; Hanamoto Hitoshi; Morita Yasuyoshi; Tanaka Hirokazu; Tatsumi Yoichi; Ashida Takashi; Matsumura Itaru , ACTA MEDICA KINKI UNIVERSITY = The Kinki University Medical Association , 39 , 1 , 29 , 37 , 1, Jun. 2014
    Summary:[Abstract] Background :Overexpression of Tribbles homolog 1 (Tribl) and Tribbles homolog 2 (Trib2) in hematopoietic stem/progenitor cells evokes acute myeloid leukemia (AML) in murine transplantation models. Degradation of CCAAT-enhancer-binding-protein α (C/EBPα) plays a crucial role in Trib1 or Trib2-induced AML. However, because C/EBPα knockout mice do not develop AML, it is likely that Trib1 and Trib2 influence other signaling pathways besides C/EBPα. Elevated Akt phosphorylation is considered to contribute to the development of AML. In contrast, two groups recently reported that reduced Akt activity is involved in the pathogenesis of leukemia. We performed this study to reveal the role of Akt signaling in Trib family-induced AML.Methods : G-CSF-induced granulocytic differentiation of 32D cells was assessed morphologically and phenotypically. G-CSF-induced signaling wasassessed by Westernblotting. Results : Overexpression of Trib1 or Trib2 inhibited GCSF-induced granulocytic differentiation of 32D cells, which was accompanied by reduced Akt phosphorylation. Also, an Akt inhibitor API-2 blocked G-CSF-induced granulocytic differentiation independently of C/EBPα degradation. Furthermore, retroviral C/EBPα restoration did not completely abolish the differentiation block caused by Trib1 and Trib2. Conclusion :Trib1 and Trib2 block granulocytic differentiation, at least partially, by suppressing Akt phosphorylation.

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Awards & Honors

  1. 1999, 日本リンパ網内系学会学会, 第39回日本リンパ網内系学会学会奨励賞

Research Grants & Projects

  1. Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Analysis of leukemogenic transgenic mice generated by tetraploid embryonic complementation method using Tet-off system. , Kinki University
  2. Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Roles of leukemogenic oncogenes in the regulation of metabolism, growth, and differentiation of hematopoietic stem cells , Osaka University
  3. 日本学術振興会, 科学研究費助成事業, 再生不良性貧血におけるテロメラーゼ活性の測定とテロメラーゼ構成要素の異常の検索 , 近畿大学

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