Structured model conserving biomass for the size-spectrum evolution in aquatic ecosystems.

Mathematical modelling of the evolution of the size-spectrum dynamics in aquatic ecosystems was discovered to be a powerful tool to have a deeper insight into impacts of human- and environmental driven changes on the marine ecosystem. In this article we propose to investigate such dynamics by formulating and investigating a suitable model. The underlying process for these dynamics is given by predation events, causing both growth and death of individuals, while keeping the total biomass within the ecosystem constant. The main governing equation investigated is deterministic and non-local of quadratic type, coming from binary interactions. Predation is assumed to strongly depend on the ratio between a predator and its prey, which is distributed around a preferred feeding preference value. Existence of solutions is shown in dependence of the choice of the feeding preference function as well as the choice of the search exponent, a constant influencing the average volume in water an individual has to search until it finds prey. The equation admits a trivial steady state representing a died out ecosystem, as well as-depending on the parameter-regime-steady states with gaps in the size spectrum, giving evidence to the well known cascade effect. The question of stability of these equilibria is considered, showing convergence to the trivial steady state in a certain range of parameters. These analytical observations are underlined by numerical simulations, with additionally exhibiting convergence to the non-trivial equilibrium for specific ranges of parameters.

Kinetic models for epidemic dynamics with social heterogeneity.

We introduce a mathematical description of the impact of the number of daily contacts in the spread of infectious diseases by integrating an epidemiological dynamics with a kinetic modeling of population-based contacts. The kinetic description leads to study the evolution over time of Boltzmann-type equations describing the number densities of social contacts of susceptible, infected and recovered individuals, whose proportions are driven by a classical SIR-type compartmental model in epidemiology. Explicit calculations show that the spread of the disease is closely related to moments of the contact distribution. Furthermore, the kinetic model allows to clarify how a selective control can be assumed to achieve a minimal lockdown strategy by only reducing individuals undergoing a very large number of daily contacts. We conduct numerical simulations which confirm the ability of the model to describe different phenomena characteristic of the rapid spread of an epidemic. Motivated by the COVID-19 pandemic, a last part is dedicated to fit numerical solutions of the proposed model with infection data coming from different European countries.

Directional persistence of chemotactic bacteria in a traveling concentration wave.

Chemotactic bacteria are known to collectively migrate towards sources of attractants. In confined convectionless geometries, concentration "waves" of swimming Escherichia coli can form and propagate through a self-organized process involving hundreds of thousands of these microorganisms. These waves are observed in particular in microcapillaries or microchannels; they result from the interaction between individual chemotactic bacteria and the macroscopic chemical gradients dynamically generated by the migrating population. By studying individual trajectories within the propagating wave, we show that, not only the mean run length is longer in the direction of propagation, but also that the directional persistence is larger compared to the opposite direction. This modulation of the reorientations significantly improves the efficiency of the collective migration. Moreover, these two quantities are spatially modulated along the concentration profile. We recover quantitatively these microscopic and macroscopic observations with a dedicated kinetic model.

Prion dynamics with size dependency-strain phenomena.

Models for the polymerization process involved in prion self-replication are well-established and studied [H. Engler, J. Pruss, and G.F. Webb, Analysis of a model for the dynamics of prions II, J. Math. Anal. Appl. 324 (2006), pp. 98-117; M.L. Greer, L. Pujo-Menjouet, and G.F. Webb, A mathematical analysis of the dynamics of prion proliferation, J. Theoret. Biol. 242 (2006), pp. 598-606; J. Pruss, L. Pujo-Menjouet, G.F. Webb, and R. Zacher, Analysis of a model for the dynamics of prions, Discrete Cont. Dyn. Sys. Ser. B 6(1) (2006), pp. 215-225] in the case where the dynamics coefficients do not depend on the size of polymers. However, several experimental studies indicate that the structure and size of the prion aggregates are determinant for their pathological effect. This motivated the analysis in Calvez et al. [Size distribution dependence of prion aggregates infectivity, Math Biosci. 217 (2009), pp. 88-99] where the authors take into account size-dependent replicative properties of prion aggregates. We first improve a result concerning the dynamics of prion aggregates when a pathological state exists (high production of the normal protein). Then we study the strain phenomena and more specifically we wonder what specific replicative properties are determinant in strain propagation. We propose to interpret it also as a dynamical property of size repartitions.