Kyushu University Academic Staff Educational and Research Activities Database
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Takao Shimayoshi Last modified date:2018.04.18





E-Mail
Homepage
http://ri2t.kyushu-u.ac.jp/~simayosi/
Academic Degree
Ph.D. (Informatics)
Field of Specialization
Software Engineering, Computational Physiology
Research
Research Interests
  • Formal method for numerical algorithms
    keyword : Software engineering, description language, numerical computation
    2010.04.
  • Methods for mathematical analysis of cell-physiology models
    keyword : Computational Physiology, Physiome
    2009.04.
  • Multi-scale Simulation of Cardiovascular System
    keyword : Heart, Ventricle, Vascular system, Cell physiology, Electrophysiology, Structural mechanics
    2003.04.
Academic Activities
Papers
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.
Membership in Academic Society
  • Institute of Electrical and Electronics Engineers
  • Information Processing Society of Japan
  • Institute of Electronics, Information and Communication Engineers
  • Japanese Society for Medical and Biological Engineering