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In this paper we introduce the optimal control of a kinetic model describing agents who migrate on a graph and interact within its nodes exchanging a physical quantity. As a prototype model, we consider the spread of an infectious disease on a graph, so that the exchanged quantity is the viral-load. The control, exerted on both the mobility and on the interactions separately, aims at minimising the average macroscopic viral-load. We prove that minimising the average viral-load weighted by the mass in each node is the most effective and convenient strategy. We consider two different interactions: in the first one the infection (gain) and the healing (loss) processes happen within the same interaction, while in the second case the infection and healing result from two different processes. With the appropriate controls, we prove that in the first case it is possible to stop the increase of the disease, but paying a very high cost in terms of control, while in the second case it is possible to eradicate the disease. We test numerically the role of each intervention and the interplay between the mobility and the interaction control strategies in each model.

Highly concentrated patterns have been observed in a spatially heterogeneous, nonlocal, model of BGK type implementing a velocity-jump process. We study both a linear and a nonlinear case and describe the concentration profile. In particular, we analyse a hyperbolic (or high frequency) regime that can be interpreted both as a local (microscopic) or as a nonlocal (macroscopic) rescaling. We consider a Hopf-Cole transform and derive a Hamilton-Jacobi equation. The concentrations are then explained as a consequence of the stationary points of the Hamiltonian that is spatially heterogeneous like the velocity-jump process. After revising the classical hydrodynamic limits for the aggregate quantities and the eikonal equation that can be derived from those with a Hopf-Cole transform, we find that the Hamilton-Jacobi equation is a second order approximation of the eikonal equation in the limit of small diffusivity. For nonlinear turning kernels, the Hopf-Cole transform allows to study the stability of the possible homogeneous configurations and of patterns and the results of a linear stability analysis previously obtained are found and extended to a nonlinear regime. In particular, it is shown that instability (pattern formation) occurs when the Hamiltonian is convex-concave.

In this paper, we derive a kinetic description of swarming particle dynamics in an interacting multi-agent system featuring emerging leaders and followers. Agents are classically characterized by their position and velocity plus a continuous parameter quantifying their degree of leadership. The microscopic processes ruling the change of velocity and degree of leadership are independent, non-conservative and non-local in the physical space, so as to account for long-range interactions. Out of the kinetic description, we obtain then a macroscopic model under a hydrodynamic limit reminiscent of that used to tackle the hydrodynamics of weakly dissipative granular gases, thus relying in particular on a regime of small non-conservative and short-range interactions. Numerical simulations in one- and two-dimensional domains show that the limiting macroscopic model is consistent with the original particle dynamics and furthermore can reproduce classical emerging patterns typically observed in swarms., Comment: 32 pages, 7 figures

We propose and investigate general kinetic models %of Boltzmann type with transition probabilities that can describe the simultaneous change of multiple microscopic states of the interacting agents. These models can be applied to many problems in socio-economic sciences, where individuals may change both their compartment and their characteristic kinetic variable, as for instance kinetic models for epidemics or for international trade with possible transfers of agents. Mathematical properties of our kinetic model are proved, as existence and uniqueness of a solution for the Cauchy problem in suitable Wasserstein spaces. The quasi-invariant asymptotic regime, leading to simpler kinetic Fokker-Planck-type equations, is investigated and commented on in comparison with other existing models. Some numerical tests are performed in order to show time evolution of distribution functions and of meaningful macroscopic fields, even in case of non-constant interaction probabilities.

The viral load is known to be a chief predictor of the risk of transmission of infectious diseases. In this work, we investigate the role of the individuals' viral load in the disease transmission by proposing a new susceptible-infectious-recovered epidemic model for the densities and mean viral loads of each compartment. To this aim, we formally derive the compartmental model from an appropriate microscopic one. Firstly, we consider a multi-agent system in which individuals are identified by the epidemiological compartment to which they belong and by their viral load. Microscopic rules describe both the switch of compartment and the evolution of the viral load. In particular, in the binary interactions between susceptible and infectious individuals, the probability for the susceptible individual to get infected depends on the viral load of the infectious individual. Then, we implement the prescribed microscopic dynamics in appropriate kinetic equations, from which the macroscopic equations for the densities and viral load momentum of the compartments are eventually derived. In the macroscopic model, the rate of disease transmission turns out to be a function of the mean viral load of the infectious population. We analytically and numerically investigate the case that the transmission rate linearly depends on the viral load, which is compared to the classical case of constant transmission rate. A qualitative analysis is performed based on stability and bifurcation theory. Finally, numerical investigations concerning the model reproduction number and the epidemic dynamics are presented., Comment: 18 pages, 4 figures. arXiv admin note: text overlap with arXiv:2106.14480

We propose a non-local model for contact guidance and steric hindrance depending on a single external cue, namely the extracellular matrix, that affects in a twofold way the polarization and speed of motion of the cells. We start from a microscopic description of the stochastic processes underlying the cell re-orientation mechanism related to the change of cell speed and direction. Then, we formally derive the corresponding kinetic model that implements exactly the prescribed microscopic dynamics and, from it, it is possible to deduce the macroscopic limit in the appropriate regime. Moreover, we test our model in several scenarios. In particular, we numerically investigate the minimal microscopic mechanisms that are necessary to reproduce cell dynamics by comparing the outcomes of our model with some experimental results related to breast cancer cell migration. This allows us to validate the proposed modeling approach and, also, to highlight its capability of predicting the qualitative cell behaviors in diverse heterogeneous microenvironments.

In this paper, we propose a Boltzmann-type kinetic description of opinion formation on social networks, which takes into account a general connectivity distribution of the individuals. We consider opinion exchange processes inspired by the Sznajd model and related simplifications but we do not assume that individuals interact on a regular lattice. Instead, we describe the structure of the social network statistically, assuming that the number of contacts of a given individual determines the probability that their opinion reaches and influences the opinion of another individual. From the kinetic description of the system, we study the evolution of the mean opinion, whence we find precise analytical conditions under which a \textit{polarisation switch} of the opinions, i.e. a change of sign between the initial and the asymptotic mean opinions, occurs. In particular, we show that a non-zero correlation between the initial opinions and the connectivity of the individuals is necessary to observe polarisation switch. Finally, we validate our analytical results through Monte Carlo simulations of the stochastic opinion exchange processes on the social network., Comment: 16 pages, 2 figures

Experiments show that when a monolayer of cells cultured on an elastic substrate is subject to a cyclic stretch, cells tend to re-orient either perpendicularly or at an oblique angle with respect to the main direction of the stretch. Due to stochastic effects, however, the distribution of angles achieved by the cells is broader and, experimentally, histrograms over the interval [0, 90] are reported. Here we will determine the evolution and the stationary state of probability density functions describing the statistical distribution of the orientations of the cells using Fokker-Planck equations derived from microscopic rules for the evolution of the orientation of the cell. As a first attempt, we shall use a stochastic differential equation related to a very general elastic energy and we will show that the results of the time integration and of the stationary state of the related forward Fokker-Planck equation compare very well with experimental results obtained by different researchers. Then, in order to model more accurately the microscopic process of cell re-orientation, we consider discrete in time random processes that allow to recover Fokker- Planck equations through the well known technique of quasi-invariant limit. In particular, we shall introduce a non-local rule related to the evaluation of the state of stress experienced by the cell extending its protrusions, and a model of re-orientation as a result of an optimal control internally activated by the cell. Also in the latter case the results match very well with experiments.

Mathematical models are formal and simplified representations of the knowledge related to a phenomenon. In classical epidemic models, a neglected aspect is the heterogeneity of disease transmission and progression linked to the viral load of each infectious individual. Here, we attempt to investigate the interplay between the evolution of individuals' viral load and the epidemic dynamics from a theoretical point of view. In the framework of multi-agent systems, we propose a particle stochastic model describing the infection transmission through interactions among agents and the individual physiological course of the disease. Agents have a double microscopic state: a discrete label, that denotes the epidemiological compartment to which they belong and switches in consequence of a Markovian process, and a microscopic trait, representing a normalized measure of their viral load, that changes in consequence of binary interactions or interactions with a background. Specifically, we consider Susceptible--Infected--Removed--like dynamics where infectious individuals may be isolated from the general population and the isolation rate may depend on the viral load sensitivity and frequency of tests. We derive kinetic evolution equations for the distribution functions of the viral load of the individuals in each compartment, whence, via suitable upscaling procedures, we obtain a macroscopic model for the densities and viral load momentum. We perform then a qualitative analysis of the ensuing macroscopic model, and we present numerical tests in the case of both constant and viral load-dependent isolation control. Also, the matching between the aggregate trends obtained from the macroscopic descriptions and the original particle dynamics simulated by a Monte Carlo approach is investigated., Comment: 20 pages, 5 figures

In this paper, we propose a Boltzmann-type kinetic model of the spreading of an infectious disease on a network. The latter describes the connections among countries, cities or districts depending on the spatial scale of interest. The disease transmission is represented in terms of the viral load of the individuals and is mediated by social contacts among them, taking into account their displacements across the nodes of the network. We formally derive the hydrodynamic equations for the density and the mean viral load of the individuals on the network and we analyse the large-time trends of these quantities with special emphasis on the cases of blow-up or eradication of the infection. By means of numerical tests, we also investigate the impact of confinement measures, such as quarantine or localised lockdown, on the diffusion of the disease on the network., Comment: 24 pages, 7 figures

Cells and organisms follow aligned structures in their environment, a process that can generate persistent migration paths. Kinetic transport equations are a popular modelling tool for describing biological movements at the mesoscopic level, yet their formulations usually assume a constant turning rate. Here we relax this simplification, extending to include a turning rate that varies according to the anisotropy of a heterogeneous environment. We extend known methods of parabolic and hyperbolic scaling and apply the results to cell movement on micro-patterned domains. We show that inclusion of orientation dependence in the turning rate can lead to persistence of motion in an otherwise fully symmetric environment, and generate enhanced diffusion in structured domains.

In this paper, we propose a Boltzmann-type kinetic description of mass-varying interacting multi-agent systems. Our agents are characterised by a microscopic state, which changes due to their mutual interactions, and by a label, which identifies a group to which they belong. Besides interacting within and across the groups, the agents may change label according to a state-dependent Markov-type jump process. We derive general kinetic equations for the joint interaction/label switch processes in each group. For prototypical birth/death dynamics, we characterise the transient and equilibrium kinetic distributions of the groups via a Fokker-Planck asymptotic analysis. Then we introduce and analyse a simple model for the contagion of infectious diseases, which takes advantage of the joint interaction/label switch processes to describe quarantine measures., Comment: 26 pages, 6 figures

The aim of the article is to study the stability of a non-local kinetic model proposed by Loy and Preziosi (2019a). We split the population in two subgroups and perform a linear stability analysis. We show that pattern formation results from modulation of one non-dimensional parameter that depends on the tumbling frequency, the sensing radius, the mean speed in a given direction, the uniform configuration density and the tactic response to the cell density. Numerical simulations show that our linear stability analysis predicts quite precisely the ranges of parameters determining instability and pattern formation. We also extend the stability analysis in the case of different mean speeds in different directions. In this case, for parameter values leading to instability travelling wave patterns develop.

Migrating cells choose their preferential direction of motion in response to different signals and stimuli sensed by spanning their external environment. However, the presence of dense fibrous regions, lack of proper substrate, and cell overcrowding may hamper cells from moving in certain directions or even from sensing beyond regions that practically act like physical barriers. We extend the non-local kinetic model proposed by Loy and Preziosi (2019) to include situations in which the sensing radius is not constant, but depends on position, sensing direction and time as cells' behavior might be determined on the basis of information collected before reaching physically limiting configurations. We analyze how the actual possible sensing of the environment influences the dynamics by recovering the appropriate macroscopic limits and by integrating numerically the kinetic transport equation.

Cells move by run and tumble, a kind of dynamics in which the cell alternates runs over straight lines and re-orientations. This erratic motion may be influenced by external factors, like chemicals, nutrients, the extra-cellular matrix, in the sense that the cell measures the external field and elaborates the signal eventually adapting its dynamics. We propose a kinetic transport equation implementing a velocity-jump process in which the transition probability takes into account a double bias, which acts, respectively, on the choice of the direction of motion and of the speed. The double bias depends on two different non-local sensing cues coming from the external environment. We analyze how the size of the cell and the way of sensing the environment with respect to the variation of the external fields affect the cell population dynamics by recovering an appropriate macroscopic limit and directly integrating the kinetic transport equation. A comparison between the solutions of the transport equation and of the proper macroscopic limit is also performed.

Multi-agent systems can be successfully described by kinetic models, which allow one to explore the large scale aggregate trends resulting from elementary microscopic interactions. The latter may be formalised as collision-like rules, in the spirit of the classical kinetic approach in gas dynamics, but also as Markov jump processes, which assume that every agent is stimulated by the other agents to change state according to a certain transition probability distribution. In this paper we establish a parallelism between these two descriptions, whereby we show how the understanding of the kinetic jump process models may be improved taking advantage of techniques typical of the collisional approach., Comment: 25 pages, 5 figures