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Ouchi, Noriyuki
Hoken Butsuri, 40(2), p.166 - 169, 2005/06
Development of the new mathematical model of the carcinogenesis in a low dose in mind is reported. The new model which describes from cell canceration to the tumorigenesis in consideration of the physical dynamics of a cell level was built. In a cell group level, it has both intra-cellular dynamics, such as mutation, cell division, and cell death, and physical dynamics such as, adhesion between cells, modification, and movement, and a model can investigate with time that tumor is formed.
Hattori, Yuya; Yokoya, Akinari; Watanabe, Ritsuko
no journal, ,
no abstracts in English
Ouchi, Noriyuki
no journal, ,
Radiation sensitivity via cell survival shows cyclic radiation response, i.e. minimal when cells are irradiated in the early post-mitotic (G1) and the pre-mitotic (G2) phases of the cell cycle, and maximal in the mitotic (M) phase and late G1 or early synthesis (S) phases. Origin of the cell-cycle dependent radiation sensitivity is supposed to be a consequence of some intra-cellular dynamics, e.g. regulation mechanism of cell-cycle checkpoint, repair ability of DNA damage and higher order structure of chromosomes, no explicit theoretical explanation exists on this cyclic response yet. Here, cell-cycle dependent radiation sensitivity is studied from the viewpoints of dynamical aspects of chromosome in association with its cell-cycle dependent structural changes. For this purpose, dynamical model of chromosome is mathematically constructed based on the elastic nature of chromosomes and its radiation effects are simulated by introducing DNA double strand break (DSB) to the model.
Hattori, Yuya; Yokoya, Akinari; Watanabe, Ritsuko
no journal, ,
no abstracts in English
Hattori, Yuya; Yokoya, Akinari; Watanabe, Ritsuko
no journal, ,
no abstracts in English
Hattori, Yuya; Yokoya, Akinari; Watanabe, Ritsuko
no journal, ,
When only a limited number of cells in a population are hit by radiation, non-irradiated cells might receive from the irradiated cells intercellular signals that induce biological effects known as "bystander effects". To understand the responses of each cell in the inhomogeneous population, we have developed a mathematical model of intercellular signaling and individual cellular responses, particularly focusing on cell cycle progression, cell cycle arrest, and cell death. In our model, the cellular population was described by grids. Each grid represented each cell. We assumed that absorbed dose was given in each grid (cell). The intercellular-signals emitted from the cells were assumed to be transferred through culture medium and gap junctions, and their concentrations in each grid were calculated based on a diffusion equation. We assumed that individual cell have targets which are necessary to progress the cell cycle. Both irradiation and the intercellular signals were assumed to inactivate "targets" in the cell. The number of inactivated targets decides cellular state, cell cycle progression, cell cycle arrest or cell death. The cell cycle was described as a virtual clock with cyclic stages (G1, S, G2, M phases) and several check-points. In the condition of normal cell-cycle progression and proliferation, our model successfully reproduced growth curves of experimental data previously reported for non-irradiated cellular population. When we irradiated one cell in the center of cellular population, some of non-irradiated cells caused inactivation of the targets by the intercellular signals, resulting in cell cycle arrest and cell death. Based on the simulation and analysis of the temporal and spatial dynamics of intercellular signaling, inactivated targets, cell cycle arrest and cell death, we will discuss the mechanism of radiation-induced responses in inhomogeneous cellular populations.
