Continuous-time random walks are generalisations of random walks frequently used to account for the consistent observations that many molecules in living cells undergo anomalous diffusion, i.e. subdiffusion. Here, we describe the subdiffusive continu
ous-time random walk using age-structured partial differential equations with age renewal upon each walker jump, where the age of a walker is the time elapsed since its last jump. In the spatially-homogeneous (zero-dimensional) case, we follow the evolution in time of the age distribution. An approach inspired by relative entropy techniques allows us to obtain quantitative explicit rates for the convergence of the age distribution to a self-similar profile, which corresponds to convergence to a stationnary profile for the rescaled variables. An important difficulty arises from the fact that the equation in self-similar variables is not autonomous and we do not have a specific analyitcal solution. Therefore, in order to quantify the latter convergence, we estimate attraction to a time-dependent pseudo-equilibrium, which in turn converges to the stationnary profile.
We study the dynamics of a one-dimensional non-linear and non-local drift-di usion equation set in the half-line, with the coupling involving the trace value on the boundary. The initial mass M of the density determines the behaviour of the equation:
attraction to self similar pro le, to a steady state of nite time blow up for supercritical mass. Using the logarithmic Sobolev and the HWI inequalities we obtain a rate of convergence for the cases subcritical and critical mass. Moreover, we prove a comparison principle on the equation obtained after space integration. This concentration-comparison principle allows proving blow-up of solutions for large initial data without any monotonicity assumption on the initial data.
We prove global existence in time of solutions to relaxed conservative cross diffusion systems governed by nonlinear operators of the form $u_ito partial_tu_i-Delta(a_i(tilde{u})u_i)$ where the $u_i, i=1,...,I$ represent $I$ density-functions, $tilde
{u}$ is a spatially regularized form of $(u_1,...,u_I)$ and the nonlinearities $a_i$ are merely assumed to be continuous and bounded from below. Existence of global weak solutions is obtained in any space dimension. Solutions are proved to be regular and unique when the $a_i$ are locally Lipschitz continuous.
Molecular circadian clocks, that are found in all nucleated cells of mammals, are known to dictate rhythms of approximately 24 hours (circa diem) to many physiological processes. This includes metabolism (e.g., temperature, hormonal blood levels) and
cell proliferation. It has been observed in tumor-bearing laboratory rodents that a severe disruption of these physiological rhythms results in accelerated tumor growth. The question of accurately representing the control exerted by circadian clocks on healthy and tumour tissue proliferation to explain this phenomenon has given rise to mathematical developments, which we review. The main goal of these previous works was to examine the influence of a periodic control on the cell division cycle in physiologically structured cell populations, comparing the effects of periodic control with no control, and of different periodic controls between them. We state here a general convexity result that may give a theoretical justification to the concept of cancer chronotherapeutics. Our result also leads us to hypothesize that the above mentioned effect of disruption of circadian rhythms on tumor growth enhancement is indirect, that, is this enhancement is likely to result from the weakening of healthy tissue that are at work fighting tumor growth.
This paper investigates the connection between discrete and continuous models describing prion proliferation. The scaling parameters are interpreted on biological grounds and we establish rigorous convergence statements. We also discuss, based on the
asymptotic analysis, relevant boundary conditions that can be used to complete the continuous model.
