Kyushu University Academic Staff Educational and Research Activities Database
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Takao Shimayoshi Last modified date:2018.07.06





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. Yuki Hasegawa, Takao Shimayoshi, Akira Amano, Tetsuya Matsuda, 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, In this paper, we propose a method for reducing the computational cost of strong coupling for multiscale cardiovascular simulation models. In such a model, individual model modules of myocardial cell, left ventricular structural dynamics, and circulatory hemodynamics are coupled. The strong coupling method enables stable and accurate calculation, but requires iterative calculations which are computationally expensive. The iterative calculations can be reduced, if accurate initial approximations are made available by predictors. The proposed method uses the Kalman filter to estimate accurate predictions by filtering out noise included in past values. The performance of the proposed method was assessed with an application to a previously published multiscale cardiovascular model. The proposed method reduced the number of iterations by 90% and 62% compared with no prediction and Lagrange extrapolation, respectively. Even when the parameters were varied and number of elements of the left ventricular finite-element model increased, the number of iterations required by the proposed method was significantly lower than that without prediction. These results indicate the robustness, scalability, and validity of the proposed method..
2. Yukari Takeda, Takao Shimayoshi, George G. Holz, Akinori Noma, 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, 310, 5, C337-C347, 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 Ca2+from inositol trisphosphate receptor (IP3R)-regulated Ca2+ 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 Ca2+ mobilization. Here, we performed simulation studies to investigate how GLP-1 alters the abilities of Ca2+ and IP3 to act as coagonists at IP3R Ca2+ release channels. A new dynamic model was constructed based on the Kaftan model, which demonstrates dual steady-state allosteric regulation of the IP3R by Ca2+ and IP3. Data obtained from β-cells were then analyzed to understand how GLP-1 facilitates IP3R-mediated Ca2+ mobilization when UV flash photolysis is used to uncage Ca2+ and IP3 intracellularly. When the dynamic model for IP3R activation was incorporated into a minimal cell model, the Ca2+ 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 Ca2+. The slow rate of Ca2+ -dependent inhibition was revealed to provide a remarkable contribution to the time course of the decay of cytosolic Ca2+ transients. It also served to drive and pace Ca2+ oscillations that are significant when evaluating how GLP-1 stimulates insulin secretion..
3. 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.
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