Classical models of morphogenesis by Murray and Meinhardt and of epidemics by Ross andMcKendrick can be revisited in order to consider the colocalizations favoring interaction between morphogens and cells or between pathogens and hosts. The classical epidemic models suppose, for example, that the populations in interaction have a constant size and are spatially fixed during the epidemic waves, but the presently observed pandemics show that the long duration of their spread during months or years imposes to take into account the pathogens, hosts and vectors migration in epidemics, as well as the morphogens and cells diffusion in morphogenesis. That leads naturally to study the occurrence of complex spatio-temporal behaviors in dynamics of population sizes and also to consider preferential zones of interaction, i.e. the zero-diffusion sets, for respectively building anatomic frontiers and confining contagion domains. Three examples of application will be presented, the first proposing a model of Black Death spread in Europe (1348-1350), and the last ones related to two morphogenetic processes, feather morphogenesis in chicken and gastrulation in Drosophila.
Morphogenesis is a general concept in biology including all the processes which generate tissue shapes and cellular organizations in a living organism. Many hybrid formalizations (i.e., with both discrete and continuous parts) have been proposed for modelling morphogenesis in embryonic or adult animals, like gastrulation. We propose first to study the ventral furrow invagination as the initial step of gastrulation, early stage of embryogenesis. We focus on the study of the connection between the apical constriction of the ventral cells and the initiation of the invagination. For that, we have created a 3D biomechanical model of the embryo of the Drosophila melanogaster based on the finite element method. Each cell is modelled by an elastic hexahedron contour and is firmly attached to its neighbouring cells. A uniform initial distribution of elastic and contractile forces is applied to cells along the model. Numerical simulations show that invagination starts at ventral curved extremities of the embryo and then propagates to the ventral medial layer. Then, this observation already made in some experiments can be attributed uniquely to the specific shape of the embryo and we provide mechanical evidence to support it. Results of the simulations of the "pill-shaped" geometry of the Drosophila melanogaster embryo are compared with those of a spherical geometry corresponding to the Xenopus lævis embryo. Eventually, we propose to study the influence of cell proliferation on the end of the process of invagination represented by the closure of the ventral furrow.
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