We develop and analyse a discrete model of cell motility in one dimension which incorporates the effects of volume filling and cell-to-cell adhesion. The formal continuum limit of the model is a nonlinear diffusion equation with a diffusivity which can become negative if the adhesion coefficient is sufficiently large. This appears to be related to the presence of spatial oscillations and the development of plateaus (pattern formation) in numerical solutions of the discrete model. A combination of stability analysis of the discrete equations and steady-state analysis of the limiting PDE (and a higher-order correction thereof) can be used to shed light on these and other qualitative predictions of the model.

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The bacterial cell to cell signalling system known as quorum sensing (QS) is essential for the regulation of virulence in many pathogens and offers a specific biochemical target for novel antibacterial therapies. Expanding on earlier work, in which consideration was given to the primary QS system (lasR system) in a homogeneous population of the common human pathogen Pseudomonas aeruginosa, we build a simple spatial model of an early-stage P. aeruginosa biofilm subject to treatment with topically applied anti-QS drugs (of two specific kinds) and conventional antibiotics. In the case of a slowly growing biofilm we show that both kinds of anti-quorum sensing drug are effective in reducing the level of the relevant signal molecule (3-oxo-C12-homoserine lactone; henceforth AHL), in each case obtaining an explicit bound on the steady-state AHL profile in terms of a prescribed surface drug concentration. Using numerical methods, we are also able to reproduce the hysteretic phenomena exhibited by the homogeneous model, in particular showing that for each kind of anti-QS drug there is a parameter regime in which a catastrophic collapse occurs in the steady-state AHL concentration as the surface drug concentration passes some critical value; an alternative way of interpreting this result is to say that, for a prescribed surface drug concentration, there is a critical biofilm depth such that treatment is successful until this depth is reached, but fails thereafter. In the thick-biofilm limit we show that the critical concentration of each drug increases exponentially with the biofilm thickness (or, conversely, that the critical depth increases logarithmically with surface drug concentration); this is dramatically different to the behaviour observed in the corresponding homogeneous model, where the critical concentrations grow linearly with bacterial carrying capacity, and thus highlights the relative difficulty of treating a large, spatially-structured population with diffusing antibacterials.

Consideration is given to a non-convex variational model for a shear experiment in the framework of single-crystal linearised plasticity with infinite cross-hardening. The rectangular shear sample is clamped at each end, and is subjected to a prescribed horizontal or diagonal shear, modelled by an appropriate hard Dirichlet condition. We ask: how much energy is required to impose such a shear, and how does it depend on the aspect ratio? Assuming that just two slip systems are active, we show that there is a critical aspect ratio, above which the energy is strictly positive, and below which it is zero. Furthermore, in the respective regimes determined by the aspect ratio, we prove energy scaling bounds, expressed in terms of the amount of prescribed shear.

We consider the variational formulation of both geometrically linear and geometrically nonlinear elasto-plasticity subject to a class of hard singleslip conditions. Such side conditions typically render the associated boundary-value problems non-convex. We show that, for a large class of non-smooth plastic distortions, a given single-slip condition (specification of Burgers vectors) can be relaxed by introducing a microstructure through a two-stage process of mollification and lamination. The relaxed model can be thought of as an aid to simulating macroscopic plastic behaviour without the need to resolve arbitrarily fine spatial scales.

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We consider a family of multi-phase Stefan problems for a certain 1-d model of cell-to-cell adhesion and diffusion, which takes the form of a nonlinear forward-backward parabolic equation. In each material phase the cell density stays either high or low, and phases are connected by jumps across an 'unstable' interval. We develop an existence theory for such problems which allows for the annihilation of phases and the subsequent continuation of solutions. Stability results for the long-time behaviour of solutions are also obtained, and, where necessary, the analysis is complemented by numerical simulations. *