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Register a new userFractal and Small-World Networks Formed by Self-Organized Critical Dynamics
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We propose a dynamical model in which a network structure evolves in a self-organized critical (SOC) manner and explain a possible origin of the emergence of fractal and small-world networks. Our model combines a network growth and its decay by failures of nodes. The decay mechanism reflects the instability of large functional networks against cascading overload failures. It is demonstrated that the dynamical system surely exhibits SOC characteristics, such as power-law forms of the avalanche size distribution, the cluster size distribution, and the distribution of the time interval between intermittent avalanches. During the network evolution, fractal networks are spontaneously generated when networks experience critical cascades of failures that lead to a percolation transition. In contrast, networks far from criticality have small-world structures. We also observe the crossover behavior from fractal to small-world structure in the network evolution.
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In this paper, a simple dynamical model in which fractal networks are formed by self-organized critical (SOC) dynamics is proposed; the proposed model consists of growth and collapse processes. It has been shown that SOC dynamics are realized by the combined processes in the model. Thus, the distributions of the cluster size and collapse size follow a power-law function in the stationary state. Moreover, through SOC dynamics, the networks become fractal in nature. The criticality of SOC dynamics is the same as the universality class of mean-field theory. The model explains the possibility that the fractal nature in complex networks emerges by SOC dynamics in a manner similar to the case with fractal objects embedded in a Euclidean space.
Self-organized bistability (SOB) is the counterpart of self-organized criticality (SOC), for systems tuning themselves to the edge of bistability of a discontinuous phase transition, rather than to the critical point of a continuous one. The equations defining the mathematical theory of SOB turn out to bear strong resemblance to a (Landau-Ginzburg) theory recently proposed to analyze the dynamics of the cerebral cortex. This theory describes the neuronal activity of coupled mesoscopic patches of cortex, homeostatically regulated by short-term synaptic plasticity. The theory for cortex dynamics entails, however, some significant differences with respect to SOB, including the lack of a (bulk) conservation law, the absence of a perfect separation of timescales and, the fact that in the former, but not in the second, there is a parameter that controls the overall system state (in blatant contrast with the very idea of self-organization). Here, we scrutinize --by employing a combination of analytical and computational tools-- the analogies and differences between both theories and explore whether in some limit SOB can play an important role to explain the emergence of scale-invariant neuronal avalanches observed empirically in the cortex. We conclude that, actually, in the limit of infinitely slow synaptic-dynamics, the two theories become identical, but the timescales required for the self-organization mechanism to be effective do not seem to be biologically plausible. We discuss the key differences between self-organization mechanisms with/without conservation and with/without infinitely separated timescales. In particular, we introduce the concept of self-organized collective oscillations and scrutinize the implications of our findings in neuroscience, shedding new light into the problems of scale invariance and oscillations in cortical dynamics.
We explore simple models aimed at the study of social contagion, in which contagion proceeds through two stages. When coupled with demographic turnover, we show that two-stage contagion leads to nonlinear phenomena which are not present in the basic `classical models of mathematical epidemiology. These include: bistability, critical transitions, endogenous oscillations, and excitability, suggesting that contagion models with stages could account for some aspects of the complex dynamics encountered in social life. These phenomena, and the bifurcations involved, are studied by a combination of analytical and numerical means.
Productive societies feature high levels of cooperation and strong connections between individuals. Public Goods Games (PGGs) are frequently used to study the development of social connections and cooperative behavior in model societies. In such games, contributions to the public good are made only by cooperators, while all players, including defectors, can reap public goods benefits. Classic results of game theory show that mutual defection, as opposed to cooperation, is the Nash Equilibrium of PGGs in well-mixed populations, where each player interacts with all others. In this paper, we explore the coevolutionary dynamics of a low information public goods game on a network without spatial constraints in which players adapt to their environment in order to increase individual payoffs. Players adapt by changing their strategies, either to cooperate or to defect, and by altering their social connections. We find that even if players do not know other players strategies and connectivity, cooperation can arise and persist despite large short-term fluctuations.
We introduce a mathematical description of the impact of sociality 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.
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