No Arabic abstract
Reaction-diffusion models have been used over decades to study biological systems. In this context, evolution equations for probability distribution functions and the associated stochastic differential equations have nowadays become indispensable tools. In population dynamics, say, such approaches are utilized to study many systems, e.g., colonies of microorganisms or ecological systems. While the majority of studies focus on the case of a static domain, the time-dependent case is also important, as it allows one to deal with situations where the domain growth takes place over time scales that are relevant for the computation of reaction rates and of the associated reactant distributions. Such situations are indeed frequently encountered in the field of developmental biology, notably in connection with pattern formation, embryo growth or morphogen gradient formation. In this chapter, we review some recent advances in the study of pure diffusion processes in growing domains. These results are subsequently taken as a starting point to study the kinetics of a simple reaction-diffusion process, i.e., the encounter-controlled annihilation reaction. The outcome of the present work is expected to pave the way for the study of more complex reaction-diffusion systems of possible relevance in various fields of research.
Reaction-diffusion equations are widely used as the governing evolution equations for modeling many physical, chemical, and biological processes. Here we derive reaction-diffusion equations to model transport with reactions on a one-dimensional domain that is evolving. The model equations, which have been derived from generalized continuous time random walks, can incorporate complexities such as subdiffusive transport and inhomogeneous domain stretching and shrinking. A method for constructing analytic expressions for short time moments of the position of the particles is developed and moments calculated from this approach are shown to compare favourably with results from random walk simulations and numerical integration of the reaction transport equation. The results show the important role played by the initial condition. In particular, it strongly affects the time dependence of the moments in the short time regime by introducing additional drift and diffusion terms. We also discuss how our reaction transport equation could be applied to study the spreading of a population on an evolving interface.
The cell cytoskeleton is a striking example of active medium driven out-of-equilibrium by ATP hydrolysis. Such activity has been shown recently to have a spectacular impact on the mechanical and rheological properties of the cellular medium, as well as on its transport properties : a generic tracer particle freely diffuses as in a standard equilibrium medium, but also intermittently binds with random interaction times to motor proteins, which perform active ballistic excursions along cytoskeletal filaments. Here, we propose for the first time an analytical model of transport limited reactions in active media, and show quantitatively how active transport can enhance reactivity for large enough tracers like vesicles. We derive analytically the average interaction time with motor proteins which optimizes the reaction rate, and reveal remarkable universal features of the optimal configuration. We discuss why active transport may be beneficial in various biological examples: cell cytoskeleton, membranes and lamellipodia, and tubular structures like axons.
We generalize the reaction-diffusion model A + B -> 0 in order to study the impact of an excess of A (or B) at the reaction front. We provide an exact solution of the model, which shows that linear response breaks down: the average displacement of the reaction front grows as the square-root of the imbalance. We argue that this model provides a highly simplified but generic framework to understand the square-root impact of large orders in financial markets.
Diffusion at solid-liquid interfaces is crucial in many technological and biophysical processes. Although its behavior seems deceivingly simple, recent studies showing passive superdiffusive transport suggest diffusion on surfaces may hide rich complexities. In particular, bulk-mediated diffusion occurs when molecules are transiently released from the surface to perform three-dimensional excursions into the liquid bulk. This phenomenon bears the dichotomy where a molecule always return to the surface but the mean jump length is infinite. Such behavior is associated with a breakdown of the central limit theorem and weak ergodicity breaking. Here, we use single-particle tracking to study the statistics of bulk-mediated diffusion on a supported lipid bilayer. We find that the time-averaged mean square displacement (MSD) of individual trajectories, the archetypal measure in diffusion processes, does not converge to the ensemble MSD but it remains a random variable, even in the long observation-time limit. The distribution of time averages is shown to agree with a L{e}vy flight model. Our results also unravel intriguing anomalies in the statistics of displacements. The time averaged MSD is shown to depend on experimental time and investigations of fractional moments show a scaling $langle |r(t)|^qrangle sim t^{q u(q)}$ with non-linear exponents, i.e. $ u(q) eqtextrm{const}$. This type of behavior is termed strong anomalous diffusion and is rare among experimental observations.
We study diffusion-controlled single-species annihilation with sparse initial conditions. In this random process, particles undergo Brownian motion, and when two particles meet, both disappear. We focus on sparse initial conditions where particles occupy a subspace of dimension $delta$ that is embedded in a larger space of dimension $d$. We find that the co-dimension $Delta=d-delta$ governs the behavior. All particles disappear when the co-dimension is sufficiently small, $Deltaleq 2$; otherwise, a finite fraction of particles indefinitely survive. We establish the asymptotic behavior of the probability $S(t)$ that a test particle survives until time $t$. When the subspace is a line, $delta=1$, we find inverse logarithmic decay, $Ssim (ln t)^{-1}$, in three dimensions, and a modified power-law decay, $Ssim (ln t),t^{-1/2}$, in two dimensions. In general, the survival probability decays algebraically when $Delta <2$, and there is an inverse logarithmic decay at the critical co-dimension $Delta=2$.