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  • articleNo Access

    A MATHEMATICAL MODEL FOR PHYTOPLANKTON

    This paper introduces a model of growth and dispersion of the marine phytoplankton, focusing on the effects of the currents (3D) and vertical mixing. Our method consists of describing these effects as the product of the horizontal current, which is solved along the characteristic lines, and the coupled action of vertical current and vertical diffusion, restricted on each characteristic line of the horizontal current. We show that the trivial steady state loses its stability and a nontrivial (non-constant in space) steady state is created.

  • articleNo Access

    EQUILIBRIUM OF TWO POPULATIONS SUBJECT TO CHEMOTAXIS

    We consider a system of four partial differential equations modelling the dynamics of two populations interacting via chemical agents. Classes of nontrivial equilibrium solutions are studied and a rescaled total biomass is shown to play the role of a bifurcation parameter.

  • articleNo Access

    MATHEMATICAL ANALYSIS AND CHALLENGES ARISING FROM MODELS OF TUMOR GROWTH

    In the last four decades, various cancer models have been developed in which the evolution of the densities of cells (abnormal, normal, or dead) and the concentrations of biochemical species are described in terms of differential equations. In this paper, we deal with tumor models in which the tumor occupies a well-defined region in space; the boundary of this region is held together by the forces of cell-to-cell adhesion. We shall refer to such tumors as "solid" tumors, although they may sometimes consist of fluid-like tissue, such as in the case of brain tumors (e.g. gliomas) and breast tumors. The most common class of solid tumors is carcinoma: a cancer originating from epithelial cells, that is, from the closely packed cells which align the internal cavities of the body.

    Models of solid tumors must take spatial effects into account, and are therefore described in terms of partial differential equations (PDEs). They also need to take into account the fact that the tumor region is changing in time; in fact, the tumor region, say Ω(t), and its boundary Γ(t), are unknown in advance. Thus one needs to determine both the unknown "free boundary" Γ(t) together with the solution of the PDEs in Ω(t). These types of problems are called free boundary problems. The models described in this paper are free boundary problems, and our primary interest is the spatial/geometric features of the free boundary. Some of the basic questions we shall address are: What is the shape of the free boundary? How does the free boundary behave as t → ∞? Does the tumor volume increase or shrink as t → ∞? Under what conditions does the tumor eventually become dormant? Finally, we shall explore the dependence of the free boundary on some biological parameters, and this will give rise to interesting bifurcation phenomena.

    The structure of the paper is as follows. In Secs. 1 and 2 we consider models in which all the cells are of one type, they are all proliferating cells. The tissue is modeled either as a porous medium (in Sec. 1) or as a fluid medium (in Sec. 2). The models are extended in Secs. 3 and 4 to include three types of cells: proliferating, quiescent, and dead. Finally, in Sec. 5 we outline a general multiphase model that includes gene mutations.

  • articleNo Access

    PATTERN FORMATION IN A RING NETWORK WITH DELAY

    We consider a ring network of three identical neurons with delayed feedback. Regarding the coupling coefficients as bifurcation parameters, we obtain codimension one bifurcation (including a Fold bifurcation and Hopf bifurcation) and codimension two bifurcations (including Fold–Fold bifurcations, Fold–Hopf bifurcations and Hopf–Hopf bifurcations). We also give concrete formulas for the normal form coefficients derived via the center manifold reduction that provide detailed information about the bifurcation and stability of various bifurcated solutions. In particular, we obtain stable or unstable equilibria, periodic solutions, and quasi-periodic solutions.

  • articleNo Access

    Predator–prey model with diffusion and indirect prey-taxis

    We analyze predator–prey models in which the movement of predator searching for prey is the superposition of random dispersal and taxis directed toward the gradient of concentration of some chemical released by prey (e.g. pheromone), Model II, or released from damaged or injured prey due to predation (e.g. blood), Model I. The logistic O.D.E. describing the dynamics of prey population is coupled to a fully parabolic chemotaxis system describing the dispersion of chemoattractant and predator’s behavior. Global-in-time solutions are proved in any space dimension and stability of homogeneous steady states is shown by linearization for a range of parameters. For space dimension N2 the basin of attraction of such a steady state is characterized by means of nonlinear analysis under some structural assumptions. In contrast to Model II, Model I possesses spatially inhomogeneous steady states at least in the case N=1.