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Armando G. M. Neves

Publications and source records attributed to Armando G. M. Neves.

10 recordsLinked to original sources

Predator-dependent replicator dynamics or a predator-prey model with two prey types and frequency dependence

Braga and Wardil [J. Phys. A: Math. Theor. 55 (2022) 025601] introduced a population model for two prey species that compete among themselves and are preyed upon by a single predator species. They showed the existence of 16 dynamic scenarios and stated sufficient conditions for the stable coexistence of the three species. The model, which can be seen as replicator dynamics with predator-dependent fitnesses for the prey, is based on two pay-off matrices: one for prey reproduction and one for interaction between prey and predators. We argue that the model can also be seen as a Lotka-Volterra-type predator-prey model with a single prey species, logistic limitation for prey, and frequency-dependent reproduction and capture coefficients. Using this alternative viewpoint, we obtain conditions for the existence of equilibria with the three types of individuals. We also prove theorems on the stability or instability of equilibria with only two species and relate the stability change of these equilibria to the appearance or disappearance of equilibria with the three species. When all parameters, except the one that regulates carrying capacities, are fixed, a rich cascade of bifurcations may appear. Solutions range from predator extinction due to insufficient prey to predators coexisting with one or two prey types. Sometimes stable limit cycles involving all species appear.

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On the design and stability of cancer adaptive therapy cycles: deterministic and stochastic models

Adaptive therapy is a promising paradigm for treating cancers, that exploits competitive interactions between drug-sensitive and drug-resistant cells, thereby avoiding or delaying treatment failure due to evolution of drug resistance within the tumor. Previous studies have shown the mathematical possibility of building cyclic schemes of drug administration which restore tumor composition to its exact initial value in deterministic models. However, algorithms for cycle design, the conditions on which such algorithms are certain to work, as well as conditions for cycle stability remain elusive. Here, we state biologically motivated hypotheses that guarantee existence of such cycles in two deterministic classes of mathematical models already considered in the literature: Lotka-Volterra and adjusted replicator dynamics. We stress that not only existence of cyclic schemes, but also stability of such cycles is a relevant feature for applications in real clinical scenarios. We also analyze stochastic versions of the above deterministic models, a necessary step if we want to take into account that real tumors are composed by a finite population of cells subject to randomness, a relevant feature in the context of low tumor burden. We argue that the stability of the deterministic cycles is also relevant for the stochastic version of the models. In fact, Dua, Ma and Newton [Cancers (2021)] and Park and Newton [Phys. Rev. E (2023)] observed breakdown of deterministic cycles in a stochastic model (Moran process) for a tumor. Our findings indicate that the breakdown phenomenon is not due to stochasticity itself, but to the deterministic instability inherent in the cycles of the referenced papers. We then illustrate how stable deterministic cycles avoid for very large times the breakdown of cyclic treatments in stochastic tumor models.

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Asymptotic behavior of mean fixation times in the Moran process with frequency-independent fitnesses

We derive asymptotic formulae in the limit when population size N tends to infinity for mean fixation times (conditional and unconditional) in a population with two types of individuals, A and B, governed by the Moran process. We consider only the case in which the fitness of the two types do not depend on the population frequencies. Our results start with the important cases in which the initial condition is a single individual of any type, but we also consider the initial condition of a fraction x, 0<x<1, of A individuals, where x is kept fixed and the total population size tends to infinity. In the cases covered by Antal and Scheuring (Bull Math Biol 68(8):1923-1944, 2006), i.e. conditional fixation times for a single individual of any type, it will turn out that our formulae are much more accurate than the ones they found. As quoted, our results include other situations not treated by them.

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Predicting the evolution of the COVID-19 epidemic with the A-SIR model: Lombardy, Italy and São Paulo state, Brazil

The presence of a large number of infected individuals with few or no symptoms is an important epidemiological difficulty and the main mathematical feature of COVID-19. The A-SIR model, i.e. a SIR (Susceptible-Infected-Removed) model with a compartment for infected individuals with no symptoms or few symptoms was proposed by Giuseppe Gaeta, arXiv:2003.08720 [q-bio.PE] (2020). In this paper we investigate a slightly generalized version of the same model and propose a scheme for fitting the parameters of the model to real data using the time series only of the deceased individuals. The scheme is applied to the concrete cases of Lombardy, Italy and São Paulo state, Brazil, showing different aspects of the epidemics. For each case we show that we may have good fits to the data up to the present, but with very large differences in the future behavior. The reasons behind such disparate outcomes are the uncertainty on the value of a key parameter, the probability that an infected individual is fully symptomatic, and on the intensity of the social distancing measures adopted. This conclusion enforces the necessity of trying to determine the real number of infected individuals in a population, symptomatic or asymptomatic.

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Exact fixation probabilities for the Birth-Death and Death-Birth frequency-dependent Moran processes on the star graph

Broom and Rychtář [Proc. R. Soc. A (2008) 464, 2609--2627] found an exact solution for the fixation probabilities of the Moran process for a structured population, in which the interaction structure among individuals is given by the so-called star graph, i.e. one central vertex and $n$ leaves, the leaves connecting only to the center. We generalize on their solution by allowing individuals' fitnesses to depend on the population frequency, and also by allowing a possible change in the order of reproduction and death draws. In their cited paper, Broom and Rychtář considered the birth-death (BD) process, in which at each time step an individual is first drawn for reproduction and then an individual is selected for death. In the death-birth (DB) process, the order of the draws is reversed. It may be seen that the order of the draws makes a big difference in the fixation probabilities. Our solution method applies to both the BD and the DB cases. As expected, the exact formulae for the fixation probabilities are complicated. We will also illustrate them with some examples and provide results on the asymptotic behavior of the fixation probabilities when the number $n$ of leaves in the graph tends to infinity.

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Fixation probabilities for the Moran process with three or more strategies: general and coupling results

We study fixation probabilities for the Moran stochastic process for the evolution of a population with three or more types of individuals and frequency-dependent fitnesses. Contrarily to the case of populations with two types of individuals, in which fixation probabilities may be calculated by an exact formula, here we must solve a large system of linear equations. We first show that this system always has a unique solution. Other results are upper and lower bounds for the fixation probabilities obtained by coupling the Moran process with three strategies with birth-death processes with only two strategies. We also apply our bounds to the problem of evolution of cooperation in a population with three types of individuals already studied in a deterministic setting by Núñez Rodríguez and Neves (J. Math. Biol. (2016) 73:1665--1690). We argue that cooperators will be fixated in the population with probability arbitrarily close to 1 for a large region of initial conditions and large enough population sizes.

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Fixation probabilities for the Moran process in evolutionary games with two strategies: graph shapes and large population asymptotics

This paper is based on the complete classification of evolutionary scenarios for the Moran process with two strategies given by Taylor et al. (B. Math. Biol. 66(6): 1621--1644, 2004). Their classification is based on whether each strategy is a Nash equilibrium and whether the fixation probability for a single individual of each strategy is larger or smaller than its value for neutral evolution. We improve on this analysis by showing that each evolutionary scenario is characterized by a definite graph shape for the fixation probability function. A second class of results deals with the behavior of the fixation probability when the population size tends to infinity. We develop asymptotic formulae that approximate the fixation probability in this limit and conclude that some of the evolutionary scenarios cannot exist when the population size is large.

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Evolution of cooperation in a particular case of the infinitely repeated Prisoner's Dilemma with three strategies

We will study a population of individuals playing the infinitely repeated Prisoner's Dilemma under replicator dynamics. The population consists of three kinds of individuals using the following reactive strategies: ALLD (individuals which always defect), ATFT (almost tit-for-tat: individuals which almost always repeat the opponent's last move) and G (generous individuals, which always cooperate when the opponent cooperated in the last move and have a positive probability $q$ of cooperating when they are defected). Our aim is studying in a mathematically rigorous fashion the dynamics of a simplified version for the computer experiment in [Nowak, Sigmund, Nature, 355, pp. 250--53, 1992] involving 100 reactive strategies. We will see that as the generosity degree of the G individuals varies, equilibria (rest points) of the dynamics appear or disappear, and the dynamics changes accordingly. Not only we will prove that the results of the experiment are true in our simplified version, but we will have complete control on the existence or non-existence of the equilbria for the dynamics for all possible values of the parameters, given that ATFT individuals are close enough to TFT. For most values of the parameters the dynamics will be completely determined.

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Extremely rare interbreeding events can explain Neanderthal DNA in modern humans

Considering the recent experimental discovery of Green et al that present day non-Africans have 1 to 4% of their nuclear DNA of Neanderthal origin, we propose here a model which is able to quantify the interbreeding events between Africans and Neanderthals at the time they coexisted in the Middle East. The model consists of a solvable system of deterministic ordinary differential equations containing as a stochastic ingredient a realization of the neutral Wright-Fisher drift process. By simulating the stochastic part of the model we are able to apply it to the interbreeding of African and Neanderthal subpopulations and estimate the only parameter of the model, which is the number of individuals per generation exchanged between subpopulations. Our results indicate that the amount of Neanderthal DNA in non-Africans can be explained with maximum probability by the exchange of a single pair of individuals between the subpopulations at each 77 generations, but larger exchange frequencies are also allowed with sizeable probability. The results are compatible with a total interbreeding population of order 10,000 individuals and with all living humans being descendents of Africans both for mitochondrial DNA and Y chromosome.

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Interbreeding conditions for explaining Neandertal DNA in living humans: the nonneutral case

We consider here an extension of a previous work by Neves and Serva, still unpublished, which estimates the amount of interbreeding between anatomically modern Africans and Neandertals necessary for explaining the experimental fact that 1 to 4% of the DNA in non-African living humans is of Neandertal origin. In that work we considered that Africans and Neandertals had the same fitness (neutral hypothesis) and Neandertal extinction was thus an event of fortune. In this work we consider that Africans had larger fitnesses. We show results for four values for the fitness difference: 1%, 5%, 10% and 20% and compare them with the corresponding neutral results. Some technical differences with respect to the neutral case appear. We conclude that even with 1% fitness difference Neandertals extinction comes up in too small a time, so the neutral model looks more suitable for explaining the known data on occupation of some caves in Israel for a very long time, alternately by Africans and Neandertals.

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