1,721,020 research outputs found
Uniform estimates for some degenerating quasilinear elliptic equations and a bound on the Harnack constant for linear equations
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Invasion fronts and adaptive dynamics in a model for the growth of cell populations with heterogeneous mobility
Full text linkWe consider a model for the dynamics of growing cell populations with heterogeneous mobility and proliferation rate. The cell phenotypic state is described by a continuous structuring variable and the evolution of the local cell population density function (i.e. the cell phenotypic distribution at each spatial position) is governed by a non-local advection-reaction-diffusion equation. We report on the results of numerical simulations showing that, in the case where the cell mobility is bounded, compactly supported travelling fronts emerge. More mobile phenotypic variants occupy the front edge, whereas more proliferative phenotypic variants are selected at the back of the front. In order to explain such numerical results, we carry out formal asymptotic analysis of the model equation using a Hamilton-Jacobi approach. In summary, we show that the locally dominant phenotypic trait (i.e. the maximum point of the local cell population density function along the phenotypic dimension) satisfies a generalised Burgers' equation with source term, we construct travelling-front solutions of such transport equation and characterise the corresponding minimal speed. Moreover, we show that, when the cell mobility is unbounded, front edge acceleration and formation of stretching fronts may occur. We briefly discuss the implications of our results in the context of glioma growth
On interfaces between cell populations with different mobilities
Full text linkPartial differential equations describing the dynamics of cell population densities from a fluid mechanical perspective can model the growth of avascular tumours. In this framework, we consider a system of equations that describes the interaction between a population of dividing cells and a population of non-dividing cells. The two cell populations are characterised by different mobilities. We present the results of numerical simulations displaying two-dimensional spherical waves with sharp interfaces between dividing and non-dividing cells. Furthermore, we numerically observe how different ratios between the mobilities change the morphology of the interfaces, and lead to the emergence of finger-like patterns of invasion above a threshold. Motivated by these simulations, we study the existence of one-dimensional travelling wave solutions
Wave-like solutions for nonlocal reaction-diffusion equations: A toy model
Full text linkTraveling waves for the nonlocal Fisher Equation can exhibit much more complex behaviour than for the usual Fisher equation. A striking numerical observation is that a traveling wave with minimal speed can connect a dynamically unstable steady state 0 to a Turing unstable steady state 1, see [12]. This is proved in [1, 6] in the case where the speed is far from minimal, where we expect the wave to be monotone. Here we introduce a simplified nonlocal Fisher equation for which we can build simple analytical traveling wave solutions that exhibit various behaviours. These traveling waves, with minimal speed or not, can (i) connect monotonically 0 and 1, (ii) connect these two states non-monotonically, and (iii) connect 0 to a wavetrain around 1. The latter exist in a regime where time dynamics converges to another object observed in [3, 8]: a wave that connects 0 to a pulsating wave around 1. © 2013 EDP Sciences
Modeling the Effects of Space Structure and Combination Therapies on Phenotypic Heterogeneity and Drug Resistance in Solid Tumors
Full text linkHistopathological evidence supports the idea that the emergence of phenotypic heterogeneity and resistance to cytotoxic drugs can be considered as a process of selection in tumor cell populations. In this framework, can we explain intra-tumor heterogeneity in terms of selection driven by the local cell environment? Can we overcome the emergence of resistance and favor the eradication of cancer cells by using combination therapies? Bearing these questions in mind, we develop a model describing cell dynamics inside a tumor spheroid under the effects of cytotoxic and cytostatic drugs. Cancer cells are assumed to be structured as a population by two real variables standing for space position and the expression level of a phenotype of resistance to cytotoxic drugs. The model takes explicitly into account the dynamics of resources and anticancer drugs as well as their interactions with the cell population under treatment. We analyze the effects of space structure and combination therapies on phenotypic heterogeneity and chemotherapeutic resistance. Furthermore, we study the efficacy of combined therapy protocols based on constant infusion and bang–bang delivery of cytotoxic and cytostatic drugs
Kinetic models for epidemic dynamics with social heterogeneity
No full textWe introduce a mathematical description of the impact of the number of daily contacts 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
Populational adaptive evolution, chemotherapeutic resistance and multiple anti-cancer therapies
Full text linkResistance to chemotherapies, particularly to anticancer treatments, is an increasing medical concern. Among the many mechanisms at work in cancers, one of the most important is the selection of tumor cells expressing resistance genes or phenotypes. Motivated by the theory of mutation-selection in adaptive evolution, we propose a model based on a continuous variable that represents the expression level of a resistance gene (or genes, yielding a phenotype) influencing in healthy and tumor cells birth/death rates, effects of chemotherapies (both cytotoxic and cytostatic) and mutations. We extend previous work by demonstrating how qualitatively different actions of chemotherapeutic and cytostatic treatments may induce different levels of resistance. The mathematical interest of our study is in the formalism of constrained Hamilton-Jacobi equations in the framework of viscosity solutions. We derive the long-term temporal dynamics of the fittest traits in the regime of small mutations. In the context of adaptive cancer management, we also analyse whether an optimal drug level is better than the maximal tolerated dose. © EDP Sciences, SMAI, 2013
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