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Register a new userAnalytical models for well-mixed populations of cooperators and defectors under limiting resources
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In the study of the evolution of cooperation, resource limitations are usually assumed just to provide a finite population size. Recently, however, agent-based models have pointed out that resource limitation may modify the original structure of the interactions and allow for the survival of unconditional cooperators in well-mixed populations. Here, we present analytical simplifi
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Recently the A/H1N1-2009 virus pandemic appeared in Mexico and in other nations. We present a study of this pandemic in the Mexican case using the SIR model to describe epidemics. This model is one of the simplest models but it has been a successful description of some epidemics of closed populations. We consider the data for the Mexican case and use the SIR model to make some predictions. Then, we generalize the SIR model in order to describe the spatial dynamics of the disease. We make a study of the spatial and temporal spread of the infected population with model parameters that are consistent with temporal SIR model parameters obtained by fitting to the Mexican case.
The two most fundamental processes describing change in biology, development and evolu-tion, occur over drastically different timescales, difficult to reconcile within a unified framework. Development involves temporal sequences of cell states controlled by hierarchies of regulatory structures. It occurs over the lifetime of a single individual, and is associated to the gene expression level change of a given genotype. Evolution, by contrast entails genotypic change through the acquisition/loss of genes and changes in the network topology of interactions among genes. It involves the emergence of new, environmentally selected phenotypes over the lifetimes of many individuals. Here we present a model of regulatory network evolution that accounts for both timescales. We extend the framework of Boolean models of gene regulatory networks (GRN)-currently only applicable to describing development to include evolutionary processes. As opposed to one-to-one maps to specific attractors, we identify the phenotypes of the cells as the relevant macrostates of the GRN. A phenotype may now correspond to multiple attractors, and its formal definition no longer requires a fixed size for the genotype. This opens the possibility for a quantitative study of the phenotypic change of a genotype, which is itself changing over evolutionary timescales. We show how the realization of specific phenotypes can be controlled by gene duplication events (used here as an archetypal evolutionary event able to change the genotype), and how successive events of gene duplication lead to new regulatory structures via selection. At the same time, we show that our generalized framework does not inhibit network controllability and the possibility for network control theory to describe epigenetic signaling during development.
Recently, a first step was made by the authors towards a systematic investigation of the effect of reaction-step-size noise - uncertainty in the step size of the reaction - on the dynamics of stochastic populations. This was done by investigating the effect of bursty influx on the switching dynamics of stochastic populations. Here we extend this formalism to account for bursty reproduction processes, and improve the accuracy of the formalism to include subleading-order corrections. Bursty reproduction appears in various contexts, where notable examples include bursty viral production from infected cells, and reproduction of mammals involving varying number of offspring. The main question we quantitatively address is how bursty reproduction affects the overall fate of the population. We consider two complementary scenarios: population extinction and population survival; in the former a population gets extinct after maintaining a long-lived metastable state, whereas in the latter a population proliferates despite undergoing a deterministic drift towards extinction. In both models reproduction occurs in bursts, sampled from an arbitrary distribution. In the extinction problem, we show that bursty reproduction broadens the quasi-stationary distribution of population sizes in the metastable state, which results in an exponential decrease of the mean time to extinction. In the survival problem, bursty reproduction yields an exponential increase in survival probability of the population. Close to the bifurcation limit our analytical results simplify considerably and are shown to depend solely on the mean and variance of the burst-size distribution. Our formalism is demonstrated on several realistic distributions which all compare well with numerical Monte-Carlo simulations.
We analyse the dynamics of fishing vessels with different home ports in an area where these vessels, in choosing where to fish, are influenced by their own experience in the past and by their current observation of the locations of other vessels in the fleet. Empirical data from the boats near Ancona and Pescara shows stylized statistical properties that are reminiscent of Kirman and Follmers ant recruitment model, although with two ant colonies represented by the two ports. From the point of view of a fisherman, the two fishing areas are not equally attractive, and he tends to prefer the one closer to where he is based. This piece of evidence led us to extend the original ants model to a situation with two asymmetric zones and finite resources. We show that, in the mean-field regime, our model exhibits the same properties as the empirical data. We obtain a phase diagram that separates high and low herding regimes, but also fish population extinction. Our analysis has interesting policy implications for the ecology of fishing areas. It also suggests that herding behaviour here, just as in financial markets, will lead to significant fluctuations in the amount of fish landed, as the boat concentration on one area at a given point in time will diminish the overall catch, such loss not being compensated by the reproduction of fish in the other area. In other terms, individually rational behaviour will not lead to collectively optimal results.
Epidemic spreading has been studied for a long time and most of them are focused on the growing aspect of a single epidemic outbreak. Recently, we extended the study to the case of recurrent epidemics (Sci. Rep. {bf 5}, 16010 (2015)) but limited only to a single network. We here report from the real data of coupled regions or cities that the recurrent epidemics in two coupled networks are closely related to each other and can show either synchronized outbreak phase where outbreaks occur simultaneously in both networks or mixed outbreak phase where outbreaks occur in one network but do not in another one. To reveal the underlying mechanism, we present a two-layered network model of coupled recurrent epidemics to reproduce the synchronized and mixed outbreak phases. We show that the synchronized outbreak phase is preferred to be triggered in two coupled networks with the same average degree while the mixed outbreak phase is preferred for the case with different average degrees. Further, we show that the coupling between the two layers is preferred to suppress the mixed outbreak phase but enhance the synchronized outbreak phase. A theoretical analysis based on microscopic Markov-chain approach is presented to explain the numerical results. This finding opens a new window for studying the recurrent epidemics in multi-layered networks.
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