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Starting from a general equation for organism (or cell system) growth and attributing additional cell death rate (besides the natural rate) to therapy, we derive an equation for cell response to {alpha} radiation. Different from previous models that are based on statistical theory, the present model connects the consequence of radiation with the growth process of a biosystem and each variable or parameter has meaning regarding the cell evolving process. We apply this equation to model the dose response for {alpha}-particle radiation. It interprets the results of both high and low linear energy transfer (LET) radiations. When LET is high, the additional death rate is a constant, which implies that the localized cells are damaged immediately and the additional death rate is proportional to the number of cells present. While at low LET, the additional death rate includes a constant term and a linear term of radiation dose, implying that the damage to some cell nuclei has a time accumulating effect. This model indicates that the oxygen-enhancement ratio (OER) decreases while LET increases consistently.
This paper focuses on the analytic modelling of responses of cells in the body to ionizing radiation. The related mechanisms are consecutively taken into account and discussed. A model of the dose- and time-dependent adaptive response is considered,
A quantitative description of the flagellar dynamics in the procyclic T. brucei is presented in terms of stationary oscillations and traveling waves. By using digital video microscopy to quantify the kinematics of trypanosome flagellar waveforms. A t
To maintain bone mass during bone remodelling, coupling is required between bone resorption and bone formation. This coordination is achieved by a network of autocrine and paracrine signalling molecules between cells of the osteoclast lineage and cel
Genetically identical cells under the same environmental conditions can show strong variations in protein copy numbers due to inherently stochastic events in individual cells. We here develop a theoretical framework to address how variations in enzym
Cell migration in morphogenesis and cancer metastasis typically involves interplay between different cell types. We construct and study a minimal, one-dimensional model comprised of two different motile cells with each cell represented as an active e