九州大学 研究者情報
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基本情報 研究活動 教育活動 社会活動
嶋吉 隆夫(しまよし たかお) データ更新日:2018.06.11



主な研究テーマ
数値計算アルゴリズムを対象とした形式手法
キーワード:ソフトウェア工学, 記述言語, 数値計算
2010.04.
細胞生理機能モデルの数理解析手法
キーワード:計算生理学, フィジオーム
2009.04.
心循環器系の多階層シミュレーション
キーワード:心臓, 心室, 血管系, 細胞生理学, 電気生理学, 構造力学
2003.04.
研究業績
主要原著論文
1. Takao Shimayoshi, Chae Young Cha, Akira Amano, Quantitative Decomposition of Dynamics of Mathematical Cell Models: Method and Application to Ventricular Myocyte Models, PLOS ONE, 10.1371/journal.pone.0124970, 10, 6, 2015.06.
2. Takeda Y, Shimayoshi T, Holz GG, Noma A, Modeling analysis of inositol 1,4,5-trisphosphate receptor-mediated Ca2+ mobilization under the control of glucagon-like peptide-1 in mouse pancreatic β-cells, American journal of physiology. Cell physiology, 10.1152/ajpcell.00234.2015, 2016.03, Glucagon-like peptide-1 (GLP-1) is an intestinally derived blood glucose-lowering hormone that potentiates glucose-stimulated insulin secretion from pancreatic β-cells. The secretagogue action of GLP-1 is explained, at least in part, by its ability to stimulate cAMP production so that cAMP may facilitate the release of Ca(2+) from inositol trisphosphate receptor (IP3R)-regulated Ca(2+) stores. However, a quantitative model has yet to be provided that explains the molecular mechanisms and dynamic processes linking GLP-1-stimulated cAMP production to Ca(2+) mobilization. Here, we performed simulation studies to investigate how GLP-1 alters the abilities of Ca(2+) and IP3 to act as coagonists at IP3R Ca(2+) release channels. A new dynamic model was constructed based on the Kaftan model, which demonstrates dual steady-state allosteric regulation of the IP3R by Ca(2+) and IP3. Data obtained from β-cells were then analyzed to understand how GLP-1 facilitates IP3R-mediated Ca(2+) mobilization when UV flash photolysis is used to uncage Ca(2+) and IP3 intracellularly. When the dynamic model for IP3R activation was incorporated into a minimal cell model, the Ca(2+) transients and oscillations induced by GLP-1 were successfully reconstructed. Simulation studies indicated that transient and oscillatory responses to GLP-1 were produced by sequential positive and negative feedback regulation due to fast activation and slow inhibition of the IP3R by Ca(2+). The slow rate of Ca(2+)-dependent inhibition was revealed to provide a remarkable contribution to the time course of the decay of cytosolic Ca(2+) transients. It also served to drive and pace Ca(2+) oscillations that are significant when evaluating how GLP-1 stimulates insulin secretion..
3. Hasegawa Y, Takao Shimayoshi, Amano A, Matsuda T, Application of the Kalman Filter for Faster Strong Coupling of Cardiovascular Simulations, IEEE journal of biomedical and health informatics, 10.1109/JBHI.2015.2436212, 20, 4, 1100-1106, 2016.07.
主要総説, 論評, 解説, 書評, 報告書等
主要学会発表等
学会活動
所属学会名
Institute of Electrical and Electronics Engineers
情報処理学会
電子情報通信学会
日本生体医工学会
受賞
生体医工学シンポジウム2016ポスターアワード, 生体医工学シンポジウム2016, 2016.09.
研究資金
科学研究費補助金の採択状況(文部科学省、日本学術振興会)
2014年度~2016年度, 挑戦的萌芽研究, 代表, 反復型数値解法の宣言的記述による形式手法.

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