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Register a new userStochastic dynamics of dengue epidemics
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We use a stochastic Markovian dynamics approach to describe the spreading of vector-transmitted diseases, like dengue, and the threshold of the disease. The coexistence space is composed by two structures representing the human and mosquito populations. The human population follows a susceptible-infected-recovered (SIR) type dynamics and the mosquito population follows a susceptible-infected-susceptible (SIS) type dynamics. The human infection is caused by infected mosquitoes and vice-versa so that the SIS and SIR dynamics are interconnected. We develop a truncation scheme to solve the evolution equations from which we get the threshold of the disease and the reproductive ratio. The threshold of the disease is also obtained by performing numerical simulations. We found that for certain values of the infection rates the spreading of the disease is impossible whatever is the death rate of infected mosquito.
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Cancer cell population dynamics often exhibit remarkably replicable, universal laws despite their underlying heterogeneity. Mechanistic explanations of universal cell population growth remain partly unresolved to this day, whereby population feedback between the microscopic and mesoscopic configurations can lead to macroscopic growth laws. We here present a unification under density-dependent birth events via contact inhibition. We consider five classical tumor growth laws: exponential, generalized logistic, Gompertz, radial growth, and fractal growth, which can be seen as manifestations of a single microscopic model. Our theory is substantiated by agent based simulations and can explain growth curve differences in experimental data from in vitro cancer cell population growth. Thus, our framework offers a possible explanation for the large number of mean-field laws that can adequately capture seemingly unrelated cancer or microbial growth dynamics.
Quantifying the attack ratio of disease is key to epidemiological inference and Public Health planning. For multi-serotype pathogens, however, different levels of serotype-specific immunity make it difficult to assess the population at risk. In this paper we propose a Bayesian method for estimation of the attack ratio of an epidemic and the initial fraction of susceptibles using aggregated incidence data. We derive the probability distribution of the effective reproductive number, R t , and use MCMC to obtain posterior distributions of the parameters of a single-strain SIR transmission model with time-varying force of infection. Our method is showcased in a data set consisting of 18 years of dengue incidence in the city of Rio de Janeiro, Brazil. We demonstrate that it is possible to learn about the initial fraction of susceptibles and the attack ratio even in the absence of serotype specific data. On the other hand, the information provided by this approach is limited, stressing the need for detailed serological surveys to characterise the distribution of serotype-specific immunity in the population.
Stochastic epidemic models on networks are inherently high-dimensional and the resulting exact models are intractable numerically even for modest network sizes. Mean-field models provide an alternative but can only capture average quantities, thus offering little or no information about variability in the outcome of the exact process. In this paper we conjecture and numerically prove that it is possible to construct PDE-limits of the exact stochastic SIS epidemics on regular and ErdH{o}s-Renyi networks. To do this we first approximate the exact stochastic process at population level by a Birth-and-Death process (BD) (with a state space of $O(N)$ rather than $O(2^N)$) whose coefficients are determined numerically from Gillespie simulations of the exact epidemic on explicit networks. We numerically demonstrate that the coefficients of the resulting BD process are density-dependent, a crucial condition for the existence of a PDE limit. Extensive numerical tests for Regular and ErdH{o}s-Renyi networks show excellent agreement between the outcome of simulations and the numerical solution of the Fokker-Planck equations. Apart from a significant reduction in dimensionality, the PDE also provides the means to derive the epidemic outbreak threshold linking network and disease dynamics parameters, albeit in an implicit way. Perhaps more importantly, it enables the formulation and numerical evaluation of likelihoods for epidemic and network inference as illustrated in a worked out example.
We use a stochastic birth-death model for a population of cells to estimate the normal tissue complication probability (NTCP) under a particular radiotherapy protocol. We specifically allow for interaction between cells, via a nonlinear logistic growth model. To capture some of the effects of intrinsic noise in the population we develop several approximations of NTCP, using Kramers-Moyal expansion techniques. These approaches provide an approximation to the first and second moments of a general first-passage time problem in the limit of large, but finite populations. We use this method to study NTCP in a simple model of normal cells and in a model of normal and damaged cells. We also study a combined model of normal tissue cells and tumour cells. Based on existing methods to calculate tumour control probabilities, and our procedure to approximate NTCP, we estimate the probability of complication free tumour control.
We revisit well-established concepts of epidemiology, the Ising-model, and percolation theory. Also, we employ a spin $S$ = 1/2 Ising-like model and a (logistic) Fermi-Dirac-like function to describe the spread of Covid-19. Our analysis reinforces well-established literature results, namely: emph{i}) that the epidemic curves can be described by a Gaussian-type function; emph{ii}) that the temporal evolution of the accumulative number of infections and fatalities follow a logistic function, which has some resemblance with a distorted Fermi-Dirac-like function; emph{iii}) the key role played by the quarantine to block the spread of Covid-19 in terms of an emph{interacting} parameter, which emulates the contact between infected and non-infected people. Furthermore, in the frame of elementary percolation theory, we show that: emph{i}) the percolation probability can be associated with the probability of a person being infected with Covid-19; emph{ii}) the concepts of blocked and non-blocked connections can be associated, respectively, with a person respecting or not the social distancing, impacting thus in the probability of an infected person to infect other people. Increasing the number of infected people leads to an increase in the number of net connections, giving rise thus to a higher probability of new infections (percolation). We demonstrate the importance of social distancing in preventing the spread of Covid-19 in a pedagogical way. Given the impossibility of making a precise forecast of the disease spread, we highlight the importance of taking into account additional factors, such as climate changes and urbanization, in the mathematical description of epidemics. Yet, we make a connection between the standard mathematical models employed in epidemics and well-established concepts in condensed matter Physics, such as the Fermi gas and the Landau Fermi-liquid picture.
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