Kyushu University Academic Staff Educational and Research Activities Database
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HIROYUKI HAMADA Last modified date:2019.05.08

Assistant Professor / Research group for Systems Bioengineering
Department of Bioscience and Biotechnology
Faculty of Agriculture


Graduate School
Undergraduate School


Homepage
http://www.brs.kyushu-u.ac.jp/~hamada/
This home page shows some my reserch profiles.
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http://www.brs.kyushu-u.ac.jp/~syn-center/system/hamada.html
Synthetic Systems Biology Research Center, Kyushu University .
Academic Degree
Doctor of Eng. in Computer Science
Field of Specialization
Medical Engineering , Computer Science
Outline Activities
My work is research and development for the end stage renal disease treatment.
Peritoneal dialysis is one of the renal replacement therapies for the end stage renal disease patient.
I am developing and describing new type software which suggests the better prescriptions according to each patient clinical condition.
I examined the clinical validation of this software by employing clinical data.
The calculated results of this software showed little discrepancy with clinical data.
Moreover, the software predicted the clinical efficiency of arbitrary prescriptions.
Therefore, this software can contribute to improve of quality of life of the end stage renal disease patients.
Research
Research Interests
  • Mathematical modeling and Sensitivity analysis for Staphylococcus aureus pathogenic expression
    keyword : Systems Biology
    2015.04G1-to-S phase is one of the checkpoints for managing a synchronization of the cell cycle. The functional disorder of this phase provides normal cells with an acquisition of infinite proliferation ability which is the greatest feature of cancer. The fully scheduled dynamic behaviors on the G1-to-S phase progress periodically with sequential activations of a few complexes which bind Cyclin-Dependence-Kinase(2,4) and Cyclin(E,D,A). I am interested in the elucidation of factors contributing to the functional disorder of this phase. We designed a macroscopic mathematical model for the G1-to-S phase and explored numerically the factors that affect the sequential activation of these complexes. According to a system analysis of this model, a disruption of dynamics of p27 protein, one of the dominant factors for RB-E2F cycle, induced a significant change in the dynamic behavior of these complexes. It implied that the interactions between p27 protein and these complexes relate with a functional disorder of the dynamic behavior on G1-to-S phase. Then next, we designed a microscopic mathematical model which involved the detailed interactions of p27 protein such as an activation and inhibition. Furthermore we are going on a sensitivity analysis at steady state of this model in order to elucidate a functional disorder of dynamic behavior on G1-to-S phase. I expect that these approaches can solve a mechanism of both an apoptosis and a symptom of cancer..
  • Mathematical modeling and Sensitivity analysis of beating synchronization
    keyword : Beating synchronization, Mathematical analysis
    2008.04G1-to-S phase is one of the checkpoints for managing a synchronization of the cell cycle. The functional disorder of this phase provides normal cells with an acquisition of infinite proliferation ability which is the greatest feature of cancer. The fully scheduled dynamic behaviors on the G1-to-S phase progress periodically with sequential activations of a few complexes which bind Cyclin-Dependence-Kinase(2,4) and Cyclin(E,D,A). I am interested in the elucidation of factors contributing to the functional disorder of this phase. We designed a macroscopic mathematical model for the G1-to-S phase and explored numerically the factors that affect the sequential activation of these complexes. According to a system analysis of this model, a disruption of dynamics of p27 protein, one of the dominant factors for RB-E2F cycle, induced a significant change in the dynamic behavior of these complexes. It implied that the interactions between p27 protein and these complexes relate with a functional disorder of the dynamic behavior on G1-to-S phase. Then next, we designed a microscopic mathematical model which involved the detailed interactions of p27 protein such as an activation and inhibition. Furthermore we are going on a sensitivity analysis at steady state of this model in order to elucidate a functional disorder of dynamic behavior on G1-to-S phase. I expect that these approaches can solve a mechanism of both an apoptosis and a symptom of cancer..
  • Mathematical modeling and Sensitivity analysis of G1/S phase in the cell cycle including the DNA damage signal transduction pathway
    keyword : Cell Cycle, DNA damage, Apoptosis induction
    2003.04G1-to-S phase is one of the checkpoints for managing a synchronization of the cell cycle. The functional disorder of this phase provides normal cells with an acquisition of infinite proliferation ability which is the greatest feature of cancer. The fully scheduled dynamic behaviors on the G1-to-S phase progress periodically with sequential activations of a few complexes which bind Cyclin-Dependence-Kinase(2,4) and Cyclin(E,D,A). I am interested in the elucidation of factors contributing to the functional disorder of this phase. We designed a macroscopic mathematical model for the G1-to-S phase and explored numerically the factors that affect the sequential activation of these complexes. According to a system analysis of this model, a disruption of dynamics of p27 protein, one of the dominant factors for RB-E2F cycle, induced a significant change in the dynamic behavior of these complexes. It implied that the interactions between p27 protein and these complexes relate with a functional disorder of the dynamic behavior on G1-to-S phase. Then next, we designed a microscopic mathematical model which involved the detailed interactions of p27 protein such as an activation and inhibition. Furthermore we are going on a sensitivity analysis at steady state of this model in order to elucidate a functional disorder of dynamic behavior on G1-to-S phase. I expect that these approaches can solve a mechanism of both an apoptosis and a symptom of cancer..
  • Mathematical modeling for spatiotemporal development of leaf primordium
    keyword : Morphogenesis, Development, Mathematical modeling
    2003.06The number of botanical species on the globe is more than 400 thousands. Their leaf shapes are formed based on the cultivation condition such as clime, nutritional state, the mesophyll expanse and the growth of vein. I am interested in the adaptability of the morphogenesis of the leaf shapes. We designed a qualitative mathematical model for the morphogenesis of the leaf shapes represented by the nonlinear simultaneous partial differential equations, taking into consideration a transport phenomenon of the nutrients. According to the numerical simulations and system analysis, kinetic parameters and the boundary conditions in this model affected remarkably the morphogenesis of the leaf shape. An exquisite combination of these factors can qualitatively elucidate the morphogenesis of the mesophyll. And then, we applied the L-system theory to this model in order to induce the variety of growth of the vein. We supposed consciously a transport phenomenon of the morphogens of vein such as the Auxin. Furthermore we are enacting a rule for the growth of vein which is employed in the L-system theory. Since this rule affects critically the morphogenesis of the leaf shapes, we need to explore an exquisite object function based on the detailed relationships between the genotype and the phenotype. I think that this methodology can apply not only to the morphogenesis of the leaf shapes, but also to the mammalian organ’s shapes. Final goal of this study is the inference of the interactions of complex biological networks from the genotype to the phenotype..
  • Research and development of the end stage renal disease treatment
    keyword : Peritoneal dialysis, Hemodialysis, Computer aided diagnosis
    2000.04Title: Research and development of the end stage renal disease treatment Peritoneal dialysis is one of the renal replacement therapies for the end stage renal disease patient. I am developing and describing new type software which suggests the better prescriptions according to each patient clinical condition. I examined the clinical validation of this software by employing clinical data. The calculated results of this software showed little discrepancy with clinical data. Moreover, the software predicted the clinical efficiency of arbitrary prescriptions. Therefore, this software can contribute to improve of quality of life of the end stage renal disease patients..
Academic Activities
Works, Software and Database
1. I developed novel computer-aided diagnosis system for the combining chronic peritoneal dialysis and hemo-dialysis therapy, which suggests some better prescriptions according to each patient clinical condition..
2. I developed novel computer-aided diagnosis system for the combining chronic peritoneal dialysis and hemo-dialysis therapy, which suggests some better prescriptions according to each patient clinical condition..
3. I developed novel computer-aided diagnosis system for chronic peritoneal dialysis therapy, which suggests some better prescriptions according to each patient clinical condition..
Membership in Academic Society
  • Biophysical Society
  • The Society for Biotechnology, Japan
  • Japanese Society for Bioinformatics
  • Japanese Society for Mathematical Biology
  • Japanese Society for Peritoneal Dialysis
  • Japanese Society for Artificial Organs
  • Japanese Society for Dialysis Therapy
Educational
Educational Activities
Undergraduate School : Numerical analysis
Graduated School: Lecture of Systems bioengineering