Hybrid and multiscale modelling.
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Biomedical subjects
Publications and source records attributed to Luigi Preziosi.
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In vertebrates, networks of capillary vessels supply tissues with nutrients. Capillary patterns are closely mimicked by endothelial cells cultured on basement membrane proteins that allow single randomly dispersed cells to self-organize into vascular networks. Here we provide a model including chemoattraction as the fundamental mechanism for cell-to-cell communication in order to identify key parameters in the complexity of the formation of vascular patterns. By flanking biological experiments, theoretical insights and numerical simulations, we provide strong evidence that endothelial cell number and the range of activity of a chemoattractant factor regulate vascular network formation and size. We propose a mechanism linking the scale of formed endothelial structures to the range of cell-to-cell interaction mediated by the release of chemoattractants.
In this paper the theory of mixtures is used to develop a two-phase model of an avascular tumour, which comprises a solid, cellular, phase and a liquid phase. Mass and momentum balances which are used to derive the governing equations are supplemented by constitutive laws that distinguish the two phases and enable the stresses within the tumour to be calculated. Novel features of the model include the dependence of the cell proliferation rate on the cellular stress and the incorporation of mass exchange between the two phases. A combination of numerical and analytical techniques is used to investigate the sensitivity of equilibrium tumour configurations to changes in the model parameters. Variation of parameters such as the maximum cell proliferation rate and the rate of natural cell death yield results which are consistent with analyses performed on simpler tumour growth models and indicate that the two-phase formulation is a natural extension of the earlier models. New predictions relate to the impact of mechanical effects on the tumour's equilibrium size which decreases under increasing stress and/or external loading. In particular, as a parameter which measures the reduction in cell proliferation due to cell stress is increased a critical value is reached, above which the tumour is eliminated.