Travelling waves in a model of species migration

A model of species migration is presented which takes the form of a reaction-diffusion system. We consider special limits of this model in which we demonstrate the existence of travelling wave solutions. These solutions can be used to describe the migration of cells, bacteria, and some organisms. © 2000 Elsevier Science Ltd. All rights reserved

Diffusion-driven instabilities and emerging spatial patterns in patchy landscapes

Spatial variation in population densities across a landscape is a feature of many ecological systems, from self-organised patterns on mussel beds to spatially restricted insect outbreaks. It occurs as a result of environmental variation in abiotic factors and/or biotic factors structuring the spatial distribution of populations. However the ways in which abiotic and biotic factors interact to determine the existence and nature of spatial patterns in population density remain poorly understood. Here we present a new approach to studying this question by analysing a predator–prey patch-model in a heterogenous landscape. We use analytical and numerical methods originally developed for studying nearest- neighbour (juxtacrine) signalling in epithelia to explore whether and under which conditions patterns emerge. We find that abiotic and biotic factors interact to promote pattern formation. In fact, we find a rich and highly complex array of coexisting stable patterns, located within an enormous number of unstable patterns. Our simulation results indicate that many of the stable patterns have appreciable basins of attraction, making them significant in applications. We are able to identify mechanisms for these patterns based on the classical ideas of long-range inhibition and short-range activation, whereby landscape heterogeneity can modulate the spatial scales at which these processes operate to structure the populations

A non-linear degenerate equation for direct aggregation and traveling wave dynamics

The gregarious behavior of individuals of populations is an important factor in avoiding predators or for reproduction. Here, by using a random biased walk approach, we build a model which, after a transformation, takes the general form [u_{t}=[D(u)u_{x}]_{x}+g(u)] . The model involves a density-dependent non-linear diffusion coefficient [D] whose sign changes as the population density [u] increases. For negative values of [D] aggregation occurs, while dispersion occurs for positive values of [D] . We deal with a family of degenerate negative diffusion equations with logistic-like growth rate [g] . We study the one-dimensional traveling wave dynamics for these equations and illustrate our results with a couple of examples. A discussion of the ill-posedness of the partial differential equation problem is included

Mathematical models of avascular cancer

This review will outline a number of illustrative mathematical models describing the growth of avascular tumours. The aim of the review is to provide a relatively comprehensive list of existing models in this area and discuss several representative models in greater detail. In the latter part of the review, some possible future avenues of mathematical modelling of avascular tumour development are outlined together with a list of key questions

Travelling wave solutions in a negative nonlinear diffusion-reaction model

We use a geometric approach to prove the existence of smooth travelling wave solutions of a nonlinear diffusion-reaction equation with logistic kinetics and a convex nonlinear diffusivity function which changes sign twice in our domain of interest. We determine the minimum wave speed, c*, and investigate its relation to the spectral stability of the travelling wave solutions.Comment: 23 pages, 10 figure

A mathematical model for the capillary endothelial cell-extracellular matrix interactions in wound-healing angiogenesis

Angiogenesis, the process by which new blood capillaries grow into a tissue from surrounding parent vessels, is a key event in dermal wound healing, malignant-tumour growth, and other pathologic conditions. In wound healing, new capillaries deliver vital metabolites such as amino acids and oxygen to the cells in the wound which are involved in a complex sequence of repair processes. The key cellular constituents of these new capillaries are endothelial cells: their interactions with soluble biochemical and insoluble extracellular matrix (ECM) proteins have been well documented recently, although the biological mechanisms underlying wound-healing angiogenesis are incompletely understood. Considerable recent research, including some continuum mathematical models, have focused on the interactions between endothelial cells and soluble regulators (such as growth factors). In this work, a similar modelling framework is used to investigate the roles of the insoluble ECM substrate, of which collagen is the predominant macromolecular protein. Our model consists of a partial differential equation for the endothelial-cell density (as a function of position and time) coupled to an ordinary differential equation for the ECM density. The ECM is assumed to regulate cell movement (both random and directed) and proliferation, whereas the cells synthesize and degrade the ECM. Analysis and numerical solutions of these equations highlights the roles of these processes in wound-healing angiogenesis. A nonstandard approximation analysis yields insight into the travel ling-wave structure of the system. The model is extended to two spatial dimensions (parallel and perpendicular to the plane of the skin), for which numerical simulations are presented. The model predicts that ECM-mediated random motility and cell proliferation are key processes which drive angiogenesis and that the details of the functional dependence of these processes on the ECM density, together with the rate of ECM remodelling, determine the qualitative nature of the angiogenic response. These predictions are experimentally testable, and they may lead towards a greater understanding of the biological mechanisms involved in wound-healing angiogenesis

Travelling waves in a nonlinear degenerate diffusion model for bacterial pattern formation

We study a reaction diffusion model recently proposed in [5] to describe the spatiotemporal evolution of the bacterium Bacillus subtilis on agar plates containing nutrient. An interesting mathematical feature of the model, which is a coupled pair of partial differential equations, is that the bacterial density satisfies a degenerate nonlinear diffusion equation. It was shown numerically that this model can exhibit quasi-one-dimensional constant speed travelling wave solutions. We present an analytic study of the existence and uniqueness problem for constant speed travelling wave solutions. We find that such solutions exist only for speeds greater than some threshold speed giving minimum speed waves which have a sharp profile. For speeds greater than this minimum speed the waves are smooth. We also characterise the dependence of the wave profile on the decay of the front of the initial perturbation in bacterial density. An investigation of the partial differential equation problem establishes,via a global existence and uniqueness argument, that these waves are the only long time solutions supported by the problem. Numerical solutions of the partial differential equation problem are presented and they confirm the results of the analysis

Cellular pattern formation during Dictyostelium aggregation

The development of multicellularity in the life cycle of Dictyostelium discoideum provides a paradigm model system for biological pattern formation. Previously, mathematical models have shown how a collective pattern of cell communication by waves of the messenger molecule cyclic adenosine 3′5′-monophosphate (cAMP) arises from excitable local cAMP kinetics and cAMP diffusion. Here we derive a model of the actual cell aggregation process by considering the chemotactic cell response to cAMP and its interplay with the cAMP dynamics. Cell density, which previously has been treated as a spatially homogeneous parameter, is a crucial variable of the aggregation model. We find that the coupled dynamics of cell chemotaxis and cAMP reaction-diffusion lead to the break-up of the initially uniform cell layer and to the formation of the striking cell stream morphology which characterizes the aggregation process in situ. By a combination of stability analysis and two-dimensional simulations of the model equations, we show cell streaming to be the consequence of the growth of a small-amplitude pattern in cell density forced by the large-amplitude cAMP waves, thus representing a novel scenario of spatial patterning in a cell chemotaxis system. The instability mechanism is further analysed by means of an analytic caricature of the model, and the condition for chemotaxis-driven instability is found to be very similar to the one obtained for the standard (non-oscillatory) Keller-Segel system. The growing cell stream pattern feeds back into the cAMP dynamics, which can explain in some detail experimental observations on the time evolution of the cAMP wave pattern, and suggests the characterization of the Dictyostelium aggregation field as a self-organized excitable medium