Coarsening to Chaos-Stabilized Fronts

We investigate a model for pattern formation in the presence of Galilean symmetry proposed by Matthews and Cox [Phys.\ Rev.\ E \textbf{62}, R1473 (2000)], which has the form of coupled generalized Burgers and Ginzburg-Landau-type equations. With only the system size $L$ as a parameter, we find distinct "small-$L$" and "large-$L$" regimes exhibiting clear differences in their dynamics and scaling behavior. The long-time statistically stationary state contains a single $L$-dependent front, stabilized globally by spatiotemporally chaotic dynamics localized away from the front. For sufficiently large domains, the transient dynamics include a state consisting of several viscous shock-like structures which coarsens gradually, before collapsing to a single front when one front absorbs the others.Comment: 4 pages, 7 figures; submitte

Models of self-organization in biological development

Bibliography: p. 297-320.In this thesis we thus wish to consider the concept of self-organization as an overall paradigm within which various theoretical approaches to the study of development may be described and evaluated. In the process, an attempt is made to give a fair and reasonably comprehensive overview of leading modelling approaches in developmental biology, with particular reference to self-organization. The work proceeds from a physical or mathematical perspective, but not unduly so - the major mathematical derivations and results are relegated to appendices - and attempts to fill a perceived gap in the extant review literature, in its breadth and attempted impartiality of scope. A characteristic of the present account is its markedly interdisciplinary approach: it seeks to place self-organization models that have been proposed for biological pattern formation and morphogenesis both within the necessary experimentally-derived biological framework, and in the wider physical context of self-organization and the mathematical techniques that may be employed in its study. Hence the thesis begins with appropriate introductory chapters to provide the necessary background, before proceeding to a discussion of the models themselves. It should be noted that the work is structured so as to be read sequentially, from beginning to end; and that the chapters in the main text were designed to be understood essentially independently of the appendices, although frequent references to the latter are given. In view of the vastness of the available information and literature on developmental biology, a working knowledge of embryological principles must be assumed. Consequently, rather than attempting a comprehensive introduction to experimental embryology, chapter 2 presents just a few biological preliminaries, to 'set the scene', outlining some of the major issues that we are dealing with, and sketching an indication of the current status of knowledge and research on development. The chapter is aimed at furnishing the necessary biological, experimental background, in the light of which the rest of the thesis should be read, and which should indeed underpin and motivate any theoretical discussions. We encounter the different hierarchical levels of description in this chapter, as well as some of the model systems whose experimental study has proved most fruitful, some of the concepts of experimental embryology, and a brief reference to some questions that will not be addressed in this work. With chapter 3, we temporarily move away from developmental biology, and consider the wider physical and mathematical concepts related to the study of self-organization. Here we encounter physical and chemical examples of spontaneous structure formation, thermodynamic considerations, and different approaches to the description of complexity. Mathematical approaches to the dynamical study of self-organization are also introduced, with specific reference to reaction-diffusion equations, and we consider some possible chemical and biochemical realizations of self-organizing kinetics. The chapter may be read in conjunction with appendix A, which gives a somewhat more in-depth study of reaction-diffusion equations, their analysis and properties, as an example of the approach to the analysis of self-organizing dynamical systems and mathematically-formulated models. Appendix B contains a more detailed discussion of the Belousov-Zhabotinskii reaction, which provides a vivid chemical paradigm for the concepts of symmetry-breaking and self-organization. Chapter 3 concludes with a brief discussion of a model biological system, the cellular slime mould, which displays rudimentary development and has thus proved amenable to detailed study and modelling. The following two chapters form the core of the thesis, as they contain discussions of the detailed application of theoretical concepts and models, largely based on self-organization, to various developmental situations. We encounter a diversity of models which has arisen largely in the last quarter century, each of which attempts to account for some aspect of biological pattern formation and morphogenesis; an aim of the discussion is to assess the extent of the underlying unity of these models in terms of the self-organization paradigm. In chapter 4 chemical pre-patterns and positional information are considered, without the overt involvement of cells in the patterning. In chapter 5, on the other hand, cellular interactions and activities are explicitly taken into account; this chapter should be read together with appendix C, which contains a brief introduction to the mathematical formulation and analysis of some of the models discussed. The penultimate chapter, 6, considers two other approaches to the study of development; one of these has faded away, while the other is still apparently in the ascendant. The assumptions underlying catastrophe theory, the value of its applications to developmental biology and the reasons for its decline in popularity, are considered. Lastly, discrete approaches, including the recently fashionable cellular automata, are dealt with, and the possible roles of rule-based interactions, such as of the so-called L-systems, and of fractals and chaos are evaluated. Chapter 7 then concludes the thesis with a brief assessment of the value of the self-organization concept to the study of biological development

Microextensive Chaos of a Spatially Extended System

By analyzing chaotic states of the one-dimensional Kuramoto-Sivashinsky equation for system sizes L in the range 79 <= L <= 93, we show that the Lyapunov fractal dimension D scales microextensively, increasing linearly with L even for increments Delta{L} that are small compared to the average cell size of 9 and to various correlation lengths. This suggests that a spatially homogeneous chaotic system does not have to increase its size by some characteristic amount to increase its dynamical complexity, nor is the increase in dimension related to the increase in the number of linearly unstable modes.Comment: 5 pages including 4 figures. Submitted to PR

OPTIMAL PARAMETER-DEPENDENT BOUNDS FOR KURAMOTO-SIVASHINSKY-TYPE EQUATIONS

Abstract. We derive a priori estimates on the absorbing ball in L 2 for the stabilized and destabilized Kuramoto-Sivashinsky (KS) equations, and for a sixth-order analog, the Nikolaevskiy equation, and in each case obtain bounds whose parameter dependence is demonstrably optimal. This is done by extending a Lyapunov function construction developed by Bronski and Gambill (Nonlinearity 19, 2023-2039) to take into account the dependence on both large and small parameters in the system. In the case of the destabilized KS equation, the rigorous bound lim sup t→∞ u ≤ KαL 3/2 is sharp in both the large parameter α and the system size L. We also apply our methods to improve previous estimates on a nonlocal variant of the KS equation

Changing Risk Behaviours and the HIV Epidemic: A Mathematical Analysis in the Context of Treatment as Prevention

Background Expanding access to highly active antiretroviral therapy (HAART) has become an important approach to HIV prevention in recent years. Previous studies suggest that concomitant changes in risk behaviours may either help or hinder programs that use a Treatment as Prevention strategy. Analysis We consider HIV-related risk behaviour as a social contagion in a deterministic compartmental model, which treats risk behaviour and HIV infection as linked processes, where acquiring risk behaviour is a prerequisite for contracting HIV. The equilibrium behaviour of the model is analysed to determine epidemic outcomes under conditions of expanding HAART coverage along with risk behaviours that change with HAART coverage. We determined the potential impact of changes in risk behaviour on the outcomes of Treatment as Prevention strategies. Model results show that HIV incidence and prevalence decline only above threshold levels of HAART coverage, which depends strongly on risk behaviour parameter values. Expanding HAART coverage with simultaneous reduction in risk behaviour act synergistically to accelerate the drop in HIV incidence and prevalence. Above the thresholds, additional HAART coverage is always sufficient to reverse the impact of HAART optimism on incidence and prevalence. Applying the model to an HIV epidemic in Vancouver, Canada, showed no evidence of HAART optimism in that setting. Conclusions Our results suggest that Treatment as Prevention has significant potential for controlling the HIV epidemic once HAART coverage reaches a threshold. Furthermore, expanding HAART coverage combined with interventions targeting risk behaviours amplify the preventive impact, potentially driving the HIV epidemic to elimination

Equilibrium stability regions with fixed risk behaviour propagation rate.

<p>The red curve, which represents the equilibrium HAART coverage needed for extinction of the HIV epidemic as given by <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062321#pone.0062321.e148" target="_blank">equation (20</a>), separates the HIV-endemic and HIV-free regions. For less than approximately , the HIV epidemic is not sustained. For greater than approximately , the epidemic cannot be eliminated by HAART in the chronic HIV phase alone. The risk behaviour propagation rate is fixed at .</p

Equilibrium stability regions with fixed untreated chronic phase infectivity.

<p>The untreated chronic phase infectivity is fixed at (a) and (b) Regions represent values of the risk behaviour initiation rate and equilibrium HAART coverage for which both HIV and risk behaviour are endemic, only risk behaviour is endemic, and neither HIV nor risk behaviour are endemic. The red curve separates the HIV-endemic and HIV-free regions. The blue line separates risk behaviour-endemic and risk behaviour-free regions.</p