Modelling contagious viral dynamics: a kinetic approach based on mutual utility.

The temporal evolution of a contagious viral disease is modelled as the dynamic progression of different classes of population with individuals interacting pairwise. This interaction follows a binary mechanism typical of kinetic theory, wherein agents aim to improve their condition with respect to a mutual utility target. To this end, we introduce kinetic equations of Boltzmann-type to describe the time evolution of the probability distributions of the multi-agent system. The interactions between agents are defined using principles from price theory, specifically employing Cobb-Douglas utility functions for binary exchange and the Edgeworth box to depict the common exchange area where utility increases for both agents. Several numerical experiments presented in the paper highlight the significance of this mechanism in driving the phenomenon toward endemicity.

Modeling essential hypertension with a closed-loop mathematical model for the entire human circulation.

Arterial hypertension, defined as an increase in systemic arterial pressure, is a major risk factor for the development of diseases affecting the cardiovascular system. Every year, 9.4 million deaths worldwide are caused by complications arising from hypertension. Despite well-established approaches to diagnosis and treatment, fewer than half of all hypertensive patients have adequately controlled blood pressure. In this scenario, computational models of hypertension can be a practical approach for better quantifying the role played by different components of the cardiovascular system in the determination of this condition. In the present work we adopt a global closed-loop multi-scale mathematical model for the entire human circulation to reproduce a hypertensive scenario. In particular, we modify the model to reproduce alterations in the cardiovascular system that are cause and/or consequence of the hypertensive state. The adaptation does not only affect large systemic arteries and the heart but also the microcirculation, the pulmonary circulation and the venous system. Model outputs for the hypertensive scenario are validated through assessment of computational results against current knowledge on the impact of hypertension on the cardiovascular system.

Spatial spread of COVID-19 outbreak in Italy using multiscale kinetic transport equations with uncertainty.

In this paper we introduce a space-dependent multiscale model to describe the spatial spread of an infectious disease under uncertain data with particular interest in simulating the onset of the COVID-19 epidemic in Italy. While virus transmission is ruled by a SEIAR type compartmental model, within our approach the population is given by a sum of commuters moving on a extra-urban scale and non commuters interacting only on the smaller urban scale. A transport dynamics of the commuter population at large spatial scales, based on kinetic equations, is coupled with a diffusion model for non commuters at the urban scale. Thanks to a suitable scaling limit, the kinetic transport model used to describe the dynamics of commuters, within a given urban area coincides with the diffusion equations that characterize the movement of non-commuting individuals. Because of the high uncertainty in the data reported in the early phase of the epidemic, the presence of random inputs in both the initial data and the epidemic parameters is included in the model. A robust numerical method is designed to deal with the presence of multiple scales and the uncertainty quantification process. In our simulations, we considered a realistic geographical domain, describing the Lombardy region, in which the size of the cities, the number of infected individuals, the average number of daily commuters moving from one city to another, and the epidemic aspects are taken into account through a calibration of the model parameters based on the actual available data. The results show that the model is able to describe correctly the main features of the spatial expansion of the first wave of COVID-19 in northern Italy.

Computational hemodynamics in arteries with the one-dimensional augmented fluid-structure interaction system: viscoelastic parameters estimation and comparison with in-vivo data.

Mathematical models are widely recognized as a valuable tool for cardiovascular diagnosis and the study of circulatory diseases, especially to obtain data that require otherwise invasive measurements. To correctly simulate body hemodynamics, the viscoelastic properties of vessels walls are a key aspect to be taken into account as they play an essential role in cardiovascular behavior. The present work aims to apply the augmented fluid-structure interaction system of blood flow to real case studies to assess the validity of the model as a valuable resource to improve cardiovascular diagnostics and the treatment of pathologies. Main contributions of the paper include the evaluation of viscoelastic tube laws, estimation of viscoelastic parameters and comparison of models with literature results and in-vivo experiments. The ability of the model to correctly simulate pulse waveforms in single arterial segments is verified using literature benchmark test cases, designed taking into account a simple elastic behavior of the wall in the upper thoracic aorta and in the common carotid artery. Furthermore, in-vivo pressure waveforms, extracted from tonometric measurements performed on four human common carotid arteries and two common femoral arteries, are compared to numerical solutions. It is highlighted that the viscoelastic damping effect of arterial walls is required to avoid an overestimation of pressure peaks. Finally, an effective procedure to estimate the viscoelastic parameters of the model is herein proposed, which returns hysteresis curves of the common carotid arteries dissipating energy fractions in line with values calculated from literature hysteresis loops in the same vessel.