Publications by authors named "Pierre Magal"

Background: Predicting the endemic/epidemic transition during the temporal evolution of a contagious disease.

Methods: Indicators for detecting the transition endemic/epidemic, with four scalars to be compared, are calculated from the daily reported news cases: coefficient of variation, skewness, kurtosis and entropy. The indicators selected are related to the shape of the empirical distribution of the new cases observed over 14 days.

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In this review, we successively present the methods for phenomenological modeling of the evolution of reported and unreported cases of COVID-19, both in the exponential phase of growth and then in a complete epidemic wave. After the case of an isolated wave, we present the modeling of several successive waves separated by endemic stationary periods. Then, we treat the case of multi-compartmental models without or with age structure.

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This article proposes a new model to describe human intra-city mobility. The goal is to combine the convection-diffusion equation to describe commuting people's movement and the density of individuals at home. We propose a new model extending our previous work with a compartment of office workers.

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The chronological age used in demography describes the linear evolution of the life of a living being. The chronological age cannot give precise information about the exact developmental stage or aging processes an organism has reached. On the contrary, the biological age (or epigenetic age) represents the true evolution of the tissues and organs of the living being.

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Background: The age of infection plays an important role in assessing an individual's daily level of contagiousness, quantified by the daily reproduction number. Then, we derive an autoregressive moving average model from a daily discrete-time epidemic model based on a difference equation involving the age of infection. Novelty: The article's main idea is to use a part of the spectrum associated with this difference equation to describe the data and the model.

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In this work, we develop a mathematical model to describe the local movement of individuals by taking into account their return to home after a period of travel. We provide a suitable functional framework to handle this system and study the large-time behavior of the solutions. We extend our model by incorporating a colonization process and applying the return to home process to an epidemic.

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In this article we study the efficacy of vaccination in epidemiological reconstructions of COVID-19 epidemics from reported cases data. Given an epidemiological model, we developed in previous studies a method that allowed the computation of an instantaneous transmission rate that produced an exact fit of reported cases data of the COVID-19 outbreak. In this article, we improve the method by incorporating vaccination data.

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The COVID-19 outbreak, which started in late December 2019 and rapidly spread around the world, has been accompanied by an unprecedented release of data on reported cases. Our objective is to offer a fresh look at these data by coupling a phenomenological description to the epidemiological dynamics. We use a phenomenological model to describe and regularize the reported cases data.

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With the spread of COVID-19 across the world, a large amount of data on reported cases has become available. We are studying here a potential bias induced by the daily number of tests which may be insufficient or vary over time. Indeed, tests are hard to produce at the early stage of the epidemic and can therefore be a limiting factor in the detection of cases.

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We model the COVID-19 coronavirus epidemic in China. We use early reported case data to predict the cumulative number of reported cases to a final size. The key features of our model are the timing of implementation of major public policies restricting social movement, the identification and isolation of unreported cases, and the impact of asymptomatic infectious cases.

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A SIRU-type epidemic model is employed for the prediction of the COVID-19 epidemy evolution in Brazil, and analyze the influence of public health measures on simulating the control of this infectious disease. The proposed model allows for a time variable functional form of both the transmission rate and the fraction of asymptomatic infectious individuals that become reported symptomatic individuals, to reflect public health interventions, towards the epidemy control. An exponential analytical behavior for the accumulated reported cases evolution is assumed at the onset of the epidemy, for explicitly estimating initial conditions, while a Bayesian inference approach is adopted for the estimation of parameters by employing the direct problem model with the data from the first phase of the epidemy evolution, represented by the time series for the reported cases of infected individuals.

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We investigate the age structured data for the COVID-19 outbreak in Japan. We consider a mathematical model for the epidemic with unreported infectious patient with and without age structure. In particular, we build a new mathematical model and a new computational method to fit the data by using age classes dependent exponential growth at the early stage of the epidemic.

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In this work, we discuss a cell-cell repulsion model based on a hyperbolic Keller-Segel equation with two populations, which aims at describing the cell growth and dispersion in the co-culture experiment from the work of Pasquier et al. (Biol Direct 6(1):5, 2011). We introduce the notion of solution integrated along the characteristics, which allows us to prove the existence and uniqueness of solutions and the segregation property for the two species.

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We develop a mathematical model to provide epidemic predictions for the COVID-19 epidemic in Wuhan, China. We use reported case data up to 31 January 2020 from the Chinese Center for Disease Control and Prevention and the Wuhan Municipal Health Commission to parameterize the model. From the parameterized model, we identify the number of unreported cases.

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Article Synopsis
  • P-glycoprotein (P-gp) is a protein commonly overexpressed in cancer cells that contributes to their resistance to multiple chemotherapy drugs.
  • A mathematical model was developed to analyze both direct protein transfer between cells and indirect transfer from cells to the surrounding liquid.
  • The study found that including the indirect transfer in simulations improved the alignment of mathematical predictions with experimental results, highlighting its impact, which is often overlooked in experiments.
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A model of an epidemic outbreak incorporating multiple subgroups of susceptible and infected individuals is investigated. The asymptotic behavior of the model is analyzed and it is proved that the infected classes all converge to 0. A computational algorithm is developed for the cumulative final size of infected individuals over the course of the epidemic.

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A SIR epidemic model is analyzed with respect to identification of its parameters, based upon reported case data from public health sources. The objective of the analysis is to understand the relation of unreported cases to reported cases. In many epidemic diseases the ratio of unreported to reported cases is very high, and of major importance in implementing measures for controlling the epidemic.

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In this article we build a mathematical model for forest growth and we compare this model with a computer forest simulator named SORTIE. The main ingredient taken into account in both models is the competition for light between trees. The parameters of the mathematical model are estimated by using SORTIE model, when the parameter values of SORTIE model correspond to the ones previously evaluated for the Great Mountain Forest in USA.

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This special issue is dedicated to the 70th birthday of Glenn F. Webb. The topics of the 12 articles appearing in this special issue include evolutionary dynamics of population growth, spatio-temporal dynamics in reaction-diffusion biological models, transmission dynamics of infectious diseases, modeling of antibiotic-resistant bacteria in hospitals, analysis of Prion models, age-structured models in ecology and epidemiology, modeling of immune response to infections, modeling of cancer growth, etc.

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A differential equations model is developed for the 2014 Ebola epidemics in Sierra Leone and Liberia. The model describes the dynamic interactions of the susceptible and infected populations of these countries. The model incorporates the principle features of contact tracing, namely, the number of contacts per identified infectious case, the likelihood that a traced contact is infectious, and the efficiency of the contact tracing process.

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The classical susceptible-infectious-recovered (SIR) model, originated from the seminal papers of Ross [51] and Ross and Hudson [52,53] in 1916-1917 and the fundamental contributions of Kermack and McKendrick [36-38] in 1927-1932, describes the transmission of infectious diseases between susceptible and infective individuals and provides the basic framework for almost all later epidemic models, including stochastic epidemic models using Monte Carlo simulations or individual-based models (IBM). In this paper, by defining the rules of contacts between susceptible and infective individuals, the rules of transmission of diseases through these contacts, and the time of transmission during contacts, we provide detailed comparisons between the classical deterministic SIR model and the IBM stochastic simulations of the model. More specifically, for the purpose of numerical and stochastic simulations we distinguish two types of transmission processes: that initiated by susceptible individuals and that driven by infective individuals.

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In this article we analyze a mathematical model presented in [11]. The model consists of two scalar ordinary differential equations, which describe the interaction between bacteria and amoebae. We first give the sufficient conditions for the uniform persistence of the model, then we prove that the model can undergo Hopf bifurcation and Bogdanov-Takens bifurcation for some parameter values, respectively.

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Multi-drug resistance (MDR) is a phenomenon by which tumor cells exhibit resistance to a variety of chemically unrelated chemotherapeutic drugs. The classical form of multidrug resistance is connected to overexpression of membrane P-glycoprotein (P-gp), which acts as an energy dependent drug efflux pump. P-glycoprotein expression is known to be controlled by genetic and epigenetic mechanisms.

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Background: Cancer is a proliferation disease affecting a genetically unstable cell population, in which molecular alterations can be somatically inherited by genetic, epigenetic or extragenetic transmission processes, leading to a cooperation of neoplastic cells within tumoural tissue. The efflux protein P-glycoprotein (P-gp) is overexpressed in many cancer cells and has known capacity to confer multidrug resistance to cytotoxic therapies. Recently, cell-to-cell P-gp transfers have been shown.

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