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This paper proposes a further development of the mathematical theory of swarms to behavioral dynamics of social and economic systems, with an application to the modeling of price series in a market. The complexity features of the system are properly described by modeling the asymmetric interactions between buyers and sellers, specifically considering the so-called cherry picking phenomenon, by which not only prices but also qualities are considered when buying a good. Finally, numerical simulations are performed to depict the predictive ability of the model and to show interesting emerging behaviors, as the coordination of buyers and their division in endogenous clusters.

This paper proposes a model of the dynamics of credit contagion through non-performing loans on financial networks. Credit risk contagion is modeled in the context of the classical SIS (Susceptibles-Infected-Susceptibles) epidemic processes on networks but with a fundamental novelty. In fact, we assume the presence of two different classes of infected agents, and then we differentiate the dynamics of assets subject to idiosyncratic risk from those affected by systemic risk by adopting a SIIS (Susceptible-Infected1-Infected2-Susceptible) model. In the recent literature in this field, the effect of systemic credit risk on the performance of the financial network is a hot topic. We perform numerical simulations intended to explore the roles played by two different network structures on the long-term behavior of assets affected by systemic risk in order to analyze the effect of the topology of the underlying network structure on the spreading of systemic risk on the structure. Random graphs, i.e., the Erdös−Rényi model, are considered “benchmark” network structures while core-periphery structures are often indicated in the literature as idealized structures, although they are able to capture interesting, specific features of real-world financial networks. Moreover, as a matter of comparison, we also perform numerical experiments on small-world networks.

Abstract As the COVID-19 pandemic progressed, research on mathematical modeling became imperative and very influential to understand the epidemiological dynamics of disease spreading. The momentary reproduction ratio r(t) of an epidemic is used as a public health guiding tool to evaluate the course of the epidemic, with the evolution of r(t) being the reasoning behind tightening and relaxing control measures over time. Here we investigate critical fluctuations around the epidemiological threshold, resembling new waves, even when the community disease transmission rate $$\beta$$ β is not significantly changing. Without loss of generality, we use simple models that can be treated analytically and results are applied to more complex models describing COVID-19 epidemics. Our analysis shows that, rather than the supercritical regime (infectivity larger than a critical value, $$\beta > \beta _c$$ β > β c ) leading to new exponential growth of infection, the subcritical regime (infectivity smaller than a critical value, $$\beta < \beta _c$$ β < β c ) with small import is able to explain the dynamic behaviour of COVID-19 spreading after a lockdown lifting, with $$r(t) \approx 1$$ r ( t ) ≈ 1 hovering around its threshold value.

Dengue fever is a viral mosquito-borne infection and a major international public health concern. With 2.5 billion people at risk of acquiring the infection around the world, disease severity is influenced by the immunological status of the individual, seronegative or seropositive, prior to natural infection. Caused by four antigenically related but distinct serotypes, DENV-1 to DENV-4, infection by one serotype confers life-long immunity to that serotype and a period of temporary cross-immunity (TCI) to other serotypes. The clinical response on exposure to a second serotype is complex with the so-called antibody-dependent enhancement (ADE) process, a disease augmentation phenomenon when pre-existing antibodies to previous dengue infection do not neutralize but rather enhance the new infection, used to explain the etiology of severe disease. In this paper, we present a minimalistic mathematical model framework developed to describe qualitatively the dengue immunological response mediated by antibodies. Three models are analyzed and compared: (i) primary dengue infection, (ii) secondary dengue infection with the same (homologous) dengue virus and (iii) secondary dengue infection with a different (heterologous) dengue virus. We explore the features of viral replication, antibody production and infection clearance over time. The model is developed based on body cells and free virus interactions resulting in infected cells activating antibody production. Our mathematical results are qualitatively similar to the ones described in the empiric immunology literature, providing insights into the immunopathogenesis of severe disease. Results presented here are of use for future research directions to evaluate the impact of dengue vaccines.

This paper deals with the modeling of wealth distribution considering a society with non-constant population and non-conservative wealth trades. The modeling approach is based on the kinetic theory of active particles, where individuals are distinguished by a scalar variable (the activity) which expresses their social state. A qualitative analysis of the model focusing on asymptotic behaviors and measurement of inequality through the Gini coefficient is presented. Finally, some specific case-studies are proposed in order to carry out numerical experiments to validate our model, characterize societies and investigate emerging behaviors.