Dominance, sharing, and assessment in an iterated Hawk-Dove game.

Animals use a wide variety of strategies to reduce or avoid aggression in conflicts over resources. These strategies range from sharing resources without outward signs of conflict to the development of dominance hierarchies, in which initial fighting is followed by the submission of subordinates. Although models have been developed to analyse specific strategies for resolving conflicts over resources, little work has focused on trying to understand why particular strategies are more likely to arise in certain situations. In this paper, we use a model based on an iterated Hawk-Dove game to analyse how resource holding potentials (RHPs) and other factors affect whether sharing, dominance relationships, or other behaviours are evolutionarily stable. We find through extensive numerical simulations that sharing is stable only when the cost of fighting is low and the animals in a contest have similar RHPs, whereas dominance relationships are stable in most other situations. We also explore what happens when animals are unable to assess each other's RHPs without fighting, and we compare a range of strategies for contestants using simulations. We find (1) that the most successful strategies involve a limited period of assessment followed by a stable relationship in which fights are avoided and (2) that the duration of assessment depends both on the costliness of fighting and on the difference between the animals' RHPs. Along with our direct work on modelling and simulations, we develop extensive software to facilitate further testing. It is available at https://bitbucket.org/CameronLHall/dominancesharingassessmentmatlab/.

A fibrocontractive mechanochemical model of dermal wound closure incorporating realistic growth factor kinetics.

Fibroblasts and their activated phenotype, myofibroblasts, are the primary cell types involved in the contraction associated with dermal wound healing. Recent experimental evidence indicates that the transformation from fibroblasts to myofibroblasts involves two distinct processes: The cells are stimulated to change phenotype by the combined actions of transforming growth factor ß (TGFß) and mechanical tension. This observation indicates a need for a detailed exploration of the effect of the strong interactions between the mechanical changes and growth factors in dermal wound healing. We review the experimental findings in detail and develop a model of dermal wound healing that incorporates these phenomena. Our model includes the interactions between TGFß and collagenase, providing a more biologically realistic form for the growth factor kinetics than those included in previous mechanochemical descriptions. A comparison is made between the model predictions and experimental data on human dermal wound healing and all the essential features are well matched.

A two-compartment mechanochemical model of the roles of transforming growth factor ß and tissue tension in dermal wound healing.

The repair of dermal tissue is a complex process of interconnected phenomena, where cellular, chemical and mechanical aspects all play a role, both in an autocrine and in a paracrine fashion. Recent experimental results have shown that transforming growth factor -ß (TGFß) and tissue mechanics play roles in regulating cell proliferation, differentiation and the production of extracellular materials. We have developed a 1D mathematical model that considers the interaction between the cellular, chemical and mechanical phenomena, allowing the combination of TGFß and tissue stress to inform the activation of fibroblasts to myofibroblasts. Additionally, our model incorporates the observed feature of residual stress by considering the changing zero-stress state in the formulation for effective strain. Using this model, we predict that the continued presence of TGFß in dermal wounds will produce contractures due to the persistence of myofibroblasts; in contrast, early elimination of TGFß significantly reduces the myofibroblast numbers resulting in an increase in wound size. Similar results were obtained by varying the rate at which fibroblasts differentiate to myofibroblasts and by changing the myofibroblast apoptotic rate. Taken together, the implication is that elevated levels of myofibroblasts is the key factor behind wounds healing with excessive contraction, suggesting that clinical strategies which aim to reduce the myofibroblast density may reduce the appearance of contractures.

Role of modularity in self-organization dynamics in biological networks.

Interconnected ensembles of biological entities are perhaps some of the most complex systems that modern science has encountered so far. In particular, scientists have concentrated on understanding how the complexity of the interacting structure between different neurons, proteins, or species influences the functioning of their respective systems. It is well established that many biological networks are constructed in a highly hierarchical way with two main properties: short average paths that join two apparently distant nodes (neuronal, species, or protein patches) and a high proportion of nodes in modular aggregations. Although several hypotheses have been proposed so far, still little is known about the relation of the modules with the dynamical activity in such biological systems. Here we show that network modularity is a key ingredient for the formation of self-organizing patterns of functional activity, independently of the topological peculiarities of the structure of the modules. In particular, we propose a self-organizing mechanism which explains the formation of macroscopic spatial patterns, which are homogeneous within modules. This may explain how spontaneous order in biological networks follows their modular structural organization. We test our results on real-world networks to confirm the important role of modularity in creating macroscale patterns.

A model for one-dimensional morphoelasticity and its application to fibroblast-populated collagen lattices.

The mechanical behaviour of solid biological tissues has long been described using models based on classical continuum mechanics. However, the classical continuum theories of elasticity and viscoelasticity cannot easily capture the continual remodelling and associated structural changes in biological tissues. Furthermore, models drawn from plasticity theory are difficult to apply and interpret in this context, where there is no equivalent of a yield stress or flow rule. In this work, we describe a novel one-dimensional mathematical model of tissue remodelling based on the multiplicative decomposition of the deformation gradient. We express the mechanical effects of remodelling as an evolution equation for the effective strain, a measure of the difference between the current state and a hypothetical mechanically relaxed state of the tissue. This morphoelastic model combines the simplicity and interpretability of classical viscoelastic models with the versatility of plasticity theory. A novel feature of our model is that while most models describe growth as a continuous quantity, here we begin with discrete cells and develop a continuum representation of lattice remodelling based on an appropriate limit of the behaviour of discrete cells. To demonstrate the utility of our approach, we use this framework to capture qualitative aspects of the continual remodelling observed in fibroblast-populated collagen lattices, in particular its contraction and its subsequent sudden re-expansion when remodelling is interrupted.

The magneto-elastica: from self-buckling to self-assembly.

Spherical neodymium-iron-boron magnets are permanent magnets that can be assembled into a variety of structures owing to their high magnetic strength. A one-dimensional chain of these magnets responds to mechanical loadings in a manner reminiscent of an elastic rod. We investigate the macroscopic mechanical properties of assemblies of ferromagnetic spheres by considering chains, rings and chiral cylinders of magnets. Based on energy estimates and simple experiments, we introduce an effective magnetic bending stiffness for a chain of magnets and show that, used in conjunction with classic results for elastic rods, it provides excellent estimates for the buckling and vibration dynamics of magnetic chains. We then use this estimate to understand the dynamic self-assembly of a cylinder from an initially straight chain of magnets.

Intracellular flow in optic nerve axons: a mechanism for cell death in glaucoma.

PURPOSE: In glaucoma, elevated intraocular pressure causes a progressive loss of retinal ganglion cells and results in optic neuropathy. The authors propose a potential mechanism for cell death, whereby elevated intraocular pressure causes fluid to permeate axonal membranes, creating a passive intracellular fluid flow within the axons. It is hypothesized that this intracellular flow locally depletes the adenosine triphosphate (ATP) concentration, disrupting axonal transport and leading to cell death. METHODS: A mathematical model was developed that takes into account the biomechanical principles underpinning the proposed hypothesis, and was solved to determine the implications of the mechanism. RESULTS: The model suggests that the raised intraocular pressures present in glaucoma are adequate to produce significant intracellular fluid flow. In the periphery of the optic nerve head, this flow may be sufficient to disrupt the diffusion of ATP and hence interrupt active axonal transport. CONCLUSIONS: The mathematical model demonstrates that it is physically plausible that a passive intracellular fluid flow could significantly contribute to the pathophysiology of the retinal ganglion cell axon in glaucoma.