Modelling the motion of a cell population in the extracellular matrix

The paper aims at describing the motion of cells in fibrous tissues taking into account of the interaction with the network fibers and among cells, of chemotaxis, and of contact guidance from network fibers. Both a kinetic model and its continuum limit are described

Modeling cell movement in anisotropic and heterogeneous network tissues

Cell motion and interaction with the extracellular matrix is studied deriving a kinetic model and considering its diffusive limit. The model takes into account of chemotactic and haptotactic effects, and obtains friction as a result of the interactions between cells and between cells and the fibrous environment. The evolution depends on the fibre distribution, as cells preferentially move along the fibre direction and tend to cleave and remodel the extracellular matrix when their direction of motion is not aligned with the fibre direction. Simulations are performed to describe the behavior of ensemble of cells under the action of a chemotactic field and in presence of heterogeneous and anisotropic fibre networks

A user's guide to PDE models for chemotaxis

Mathematical modelling of chemotaxis (the movement of biological cells or organisms in response to chemical gradients) has developed into a large and diverse discipline, whose aspects include its mechanistic basis, the modelling of specific systems and the mathematical behaviour of the underlying equations. The Keller-Segel model of chemotaxis (Keller and Segel in J Theor Biol 26:399-415, 1970; 30:225- 234, 1971) has provided a cornerstone for much of this work, its success being a consequence of its intuitive simplicity, analytical tractability and capacity to replicate key behaviour of chemotactic populations. One such property, the ability to display "auto-aggregation", has led to its prominence as a mechanism for self-organisation of biological systems. This phenomenon has been shown to lead to finite-time blow-up under certain formulations of the model, and a large body of work has been devoted to determining when blow-up occurs or whether globally existing solutions exist. In this paper, we explore in detail a number of variations of the original Keller-Segel model. We review their formulation from a biological perspective, contrast their patterning properties, summarise key results on their analytical properties and classify their solution form. We conclude with a brief discussion and expand on some of the outstanding issues revealed as a result of this work. © Springer-Verlag 2008

Mathematical modelling of glioma growth: The use of Diffusion Tensor Imaging (DTI) data to predict the anisotropic pathways of cancer invasion

The nonuniform growth of certain forms of cancer can present significant complications for their treatment, a particularly acute problem in gliomas. A number of experimental results have suggested that invasion is facilitated by the directed movement of cells along the aligned neural fibre tracts that form a large component of the white matter. Diffusion tensor imaging (DTI) provides a window for visualising this anisotropy and gaining insight on the potential invasive pathways. In this paper we develop a mesoscopic model for glioma invasion based on the individual migration pathways of invading cells along the fibre tracts. Via scaling we obtain a macroscopic model that allows us to explore the overall growth of a tumour. To connect DTI data to parameters in the macroscopic model we assume that directional guidance along fibre tracts is described by a bimodal von Mises-Fisher distribution (a normal distribution on a unit sphere) and parametrised according to the directionality and degree of anisotropy in the diffusion tensors. We demonstrate the results in a simple model for glioma growth, exploiting both synthetic and genuine DTI datasets to reveal the potentially crucial role of anisotropic structure on invasion. © 2013 Elsevier Ltd

Transport and anisotropic diffusion models for movement in oriented habitats

A common feature of many living organisms is the ability to move and navigate in heterogeneous environments. While models for spatial spread of populations are often based on the diffusion equation, here we aim to advertise the use of transport models; in particular in cases where data from individual tracking are available. Rather than developing a full general theory of transport models, we focus on the specific case of animal movement in oriented habitats. The orientations can be given by magnetic cues, elevation profiles, food sources, or disturbances such as seismic lines or roads. In this case we are able to present and contrast the three most common scaling limits, (i) the parabolic scaling, (ii) the hyperbolic scaling, and (iii) the moment closure method. We clearly state the underlying assumptions and guide the reader to an understanding of which scaling method is used in what kind of situations. One interesting result is that the macroscopic drift velocity is given by the mean direction of the underlying linear features, and the diffusion is given by the variance-covariance matrix of the underlying oriented habitat. We illustrate our findings with specific applications to wolf movement in habitats with seismic lines. © 2013 Springer-Verlag Berlin Heidelberg

Blow-up and pattern formation in hyperbolic models for chemotaxis in 1-D

In this paper we study finite time blow-up of solutions of a hyperbolic model for chemotaxis. Using appropriate scaling this hyperbolic model leads to a parabolic model as studied by Othmer and Stevens (1997) and Levine and Sleeman (1997). In the latter paper, explicit solutions which blow-up in finite time were constructed. Here, we adapt their method to construct a corresponding blow-up solution of the hyperbolic model. This construction enables us to compare the blow-up times of the corresponding models. We find that the hyperbolic blow-up is always later than the parabolic blow-up. Moreover, we show that solutions of the hyperbolic problem become negative near blow-up. We calculate the “zero-turning-rate” time explicitly and we show that this time can be either larger or smaller than the parabolic blow-up time. The blow-up models as discussed here and elsewhere are limiting cases of more realistic models for chemotaxis. At the end of the paper we discuss the relevance to biology and exhibit numerical solutions of more realistic models

Modeling cell movement in anisotropic and heterogeneous network tissues

Cell motion and interaction with the extracellular matrix is studied deriving a kinetic model and considering its diffusive limit. The model takes into account of chemotactic and haptotactic effects, and obtains friction as a result of the interactions between cells and between cells and the fibrous environment. The evolution depends on the fibre distribution, as cells preferentially move along the fibre direction and tend to cleave and remodel the extracellular matrix when their direction of motion is not aligned with the fibre direction. Simulations are performed to describe the behavior of ensemble of cells under the action of a chemotactic field and in presence of heterogeneous and anisotropic fibre networks

Global existence for chemotaxis with finite sampling radius

Migrating cells measure the external environment through receptor-binding of specific chemicals at their outer cell membrane. In this paper this non-local sampling is incorporated into a chemotactic model. The existence of global bounded solutions of the non-local model is proven for bounded and unbounded domains in any space dimension. According to a recent classification of spikes and plateaus, it is shown that steady state solutions cannot be of spike-type. Finally, numerical simulations support the theoretical results, illustrating the ability of the model to give rise to pattern formation. Some biologically relevant extensions of the model are also considered

Convergence of a cancer invasion model to a logistic chemotaxis model

A characteristic feature of tumor invasion is the destruction of the healthy tissue surrounding it. Open space is generated, which invasive tumor cells can move into. One such mechanism is the urokinase plasminogen system (uPS), which is found in many processes of tissue reorganization. Lolas, Chaplain and collaborators have developed a series of mathematical models for the uPS and tumor invasion. These models are based upon degradation of the extracellular material through plasmid plus chemotaxis and haptotaxis. In this paper we consider the uPS invasion models in one-space dimension and we identify a condition under which this cancer invasion model converges to a chemotaxis model with logistic growth. This condition assumes that the density of the extracellular material is not too large. Our result shows that the complicated spatio-temporal patterns, which were observed by Lolas and Chaplain et al. are organized by the chaotic attractor of the logistic chemotaxis system. Our methods are based on energy estimates, where, for convergence, we needed to find lower estimates in Lγ for 0 < γ < 1. This is a new method for these types of PDE. © 2013 World Scientific Publishing Company