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In this paper we study the following nonlinear fractional Hartree (or Choquard-Pekar) equation (−Δ)su+μu=(Iα*F(u))F′(u) inRN, ${\left(-{\Delta}\right)}^{s}u+\mu u=\left({I}_{\alpha }{\ast}F\left(u\right)\right){F}^{\prime }\left(u\right)\quad \text{in} {\mathbb{R}}^{N},$ (*) where μ > 0, s ∈ (0, 1), N ≥ 2, α ∈ (0, N), Iα∼1|x|N−α ${I}_{\alpha }\sim \frac{1}{\vert x{\vert }^{N-\alpha }}$ is the Riesz potential, and F is a general subcritical nonlinearity. The goal is to prove existence of multiple (radially symmetric) solutions u∈Hs(RN) $u\in {H}^{s}\left({\mathbb{R}}^{N}\right)$ , by assuming F odd or even: we consider both the case μ > 0 fixed and the case ∫RNu2=m>0 ${\int }_{{\mathbb{R}}^{N}}{u}^{2}=m{ >}0$ prescribed. Here we also simplify some arguments developed for s = 1 (S. Cingolani, M. Gallo, and K. Tanaka, “Multiple solutions for the nonlinear Choquard equation with even or odd nonlinearities,” Calc. Var. Partial Differ. Equ., vol. 61, no. 68, p. 34, 2022). A key point in the proof is given by the research of suitable multidimensional odd paths, which was done in the local case by Berestycki and Lions (H. Berestycki and P.-L. Lions, “Nonlinear scalar field equations II: existence of infinitely many solutions,” Arch. Ration. Mech. Anal., vol. 82, no. 4, pp. 347–375, 1983); for (*) the nonlocalities play indeed a special role. In particular, some properties of these paths are needed in the asymptotic study (as μ varies) of the mountain pass values of the unconstrained problem, then exploited to describe the geometry of the constrained problem and detect infinitely many normalized solutions for any m > 0. The found solutions satisfy in addition a Pohozaev identity: in this paper we further investigate the validity of this identity for solutions of doubly nonlocal equations under a C 1-regularity.

A proper understanding of the links between varying gene expression levels and complex trait adaptation is still lacking, despite recent advances in sequencing techniques leading to new insights on their importance in some evolutionary processes. This calls for extensions of the continuum-of-alleles framework first introduced by Kimura (1965 Proc. Natl Acad. Sci. USA 54 731–36) that bypass the classical Gaussian approximation. Here, we propose a novel mathematical framework to study the evolutionary dynamics of quantitative alleles for sexually reproducing populations under natural selection and competition through an integro-differential equation. It involves a new reproduction operator which is nonlinear and nonlocal. This reproduction operator is different from the infinitesimal operator used in other studies with sexual reproduction because of different underlying genetic structures. In an asymptotic regime where initially the population has a small phenotypic variance, we analyse the long-term dynamics of the phenotypic distributions according to the methodology of small variance (Diekmann et al 2005 Theor. Popul. Biol. 67 257–71). In particular, we prove that the reproduction operator strains the limit distribution to be a product measure. Under some assumptions on the limit equation, we show that the population remains monomorphic, that is the phenotypic distribution remains concentrated as a moving Dirac mass. Moreover, in the case of a monomorphic distribution, we derive a canonical equation describing the dynamics of the dominant alleles. [ABSTRACT FROM AUTHOR]

We 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. [ABSTRACT FROM AUTHOR]

When studying the dynamics of trait distribution of populations in a heterogeneous environment, classical models from quantitative genetics choose to look at its system of moments, specifically the first two ones. Additionally, in order to close the resulting system of equations, they often assume the local trait distributions are Gaussian [see for instance Ronce and Kirkpatrick (Evolution 55(8):1520–1531, 2001. )]. The aim of this paper is to introduce a mathematical framework that follows the whole trait distribution (without prior assumption) to study evolutionary dynamics of sexually reproducing populations. Specifically, it focuses on complex traits, whose inheritance can be encoded by the infinitesimal model of segregation (Fisher in Trans R Soc Edinb 52(2):399–433, 1919. ). We show that it allows us to derive a regime in which our model gives the same dynamics as when assuming Gaussian local trait distributions. To support that, we compare the stationary problems of the system of moments derived from our model with the one given in Ronce and Kirkpatrick (Evolution 55(8):1520–1531, 2001. ) and show that they are equivalent under this regime and do not need to be otherwise. Moreover, under this regime of equivalence, we show that a separation bewteen ecological and evolutionary time scales arises. A fast relaxation toward monomorphism allows us to reduce the complexity of the system of moments, using a slow-fast analysis. This reduction leads us to complete, still in this regime, the analytical description of the bistable asymmetrical equilibria numerically found in Ronce and Kirkpatrick (Evolution 55(8):1520–1531, 2001. ). More globally, we provide explicit modelling hypotheses that allow for such local adaptation patterns to occur. [ABSTRACT FROM AUTHOR]

We present an SI epidemic model whereby a continuous structuring variable captures variability in proliferative potential and resistance to infection among susceptible individuals. The occurrence of heritable, spontaneous changes in these phenotypic characteristics and the presence of a fitness trade-off between resistance to infection and proliferative potential are explicitly incorporated into the model. The model comprises an ordinary differential equation for the number of infected individuals that is coupled with a partial integrodifferential equation for the population density function of susceptible individuals through an integral term. The expression for the basic reproduction number R 0 is derived, the disease-free equilibrium and endemic equilibrium of the model are characterised and a threshold theorem involving R 0 is proved. Analytical results are integrated with the results of numerical simulations of a calibrated version of the model based on the results of artificial selection experiments in a host-parasite system. The results of our mathematical study disentangle the impact of different evolutionary parameters on the spread of infectious diseases and the consequent phenotypic adaption of susceptible individuals. In particular, these results provide a theoretical basis for the observation that infectious diseases exerting stronger selective pressures on susceptible individuals and being characterised by higher infection rates are more likely to spread. Moreover, our results indicate that heritable, spontaneous phenotypic changes in proliferative potential and resistance to infection can either promote or prevent the spread of infectious diseases depending on the strength of selection acting on susceptible individuals prior to infection. Finally, we demonstrate that, when an endemic equilibrium is established, higher levels of resistance to infection and lower degrees of phenotypic heterogeneity among susceptible individuals are to be expected in the presence of infections which are characterised by lower rates of death and exert stronger selective pressures. [ABSTRACT FROM AUTHOR]

A rigorous limit procedure is presented which links nonlocal models involving adhesion or nonlocal chemotaxis to their local counterparts featuring haptotaxis and classical chemotaxis, respectively. It relies on a novel reformulation of the involved nonlocalities in terms of integral operators applied directly to the gradients of signal-dependent quantities. The proposed approach handles both model types in a unified way and extends the previous mathematical framework to settings that allow for general solution-dependent coefficient functions. The previous forms of nonlocal operators are compared with the new ones introduced in this paper and the advantages of the latter are highlighted by concrete examples. Numerical simulations in 1D provide an illustration of some of the theoretical findings. [ABSTRACT FROM AUTHOR]

The objective is to prove the asynchronous exponential growth of the growth-fragmentation equation in large weighted L 1 spaces and under general assumptions on the coefficients. The key argument is the creation of moments for the solutions to the Cauchy problem, resulting from the unboundedness of the total fragmentation rate. It allows us to prove the quasi-compactness of the associated (rescaled) semigroup, which in turn provides the exponential convergence toward the projector on the Perron eigenfunction. [ABSTRACT FROM AUTHOR]

A new continuous spatially-distributed model of solid tumor growth and progression is presented. The model explicitly accounts for mutations/epimutations of tumor cells which take place upon their division. The tumor grows in normal tissue and its progression is driven only by competition between populations of malignant cells for limited nutrient supply. Two reasons for the motion of tumor cells in space are taken into consideration, i.e., their intrinsic motility and convective fluxes, which arise due to proliferation of tumor cells. The model is applied to investigation of solid tumor progression under phenotypic alterations that inversely affect cell proliferation rate and cell motility by increasing the value of one of the parameters at the expense of another.It is demonstrated that the crucial feature that gives evolutionary advantage to a cell population is the speed of its intergrowth into surrounding normal tissue. Of note, increase in tumor intergrowth speed in not always associated with increase in motility of tumor cells. Depending on the parameters of functions, that describe phenotypic alterations, tumor cellular composition may evolve towards: (1) maximization of cell proliferation rate, (2) maximization of cell motility, (3) non-extremum values of cell proliferation rate and motility. Scenarios are found, where after initial tendency for maximization of cell proliferation rate, the direction of tumor progression sharply switches to maximization of cell motility, which is accompanied by decrease in total speed of tumor growth. [ABSTRACT FROM AUTHOR]

This work is devoted to the study of an integro-differential system of equations modelling the genetic adaptation of a pathogen by taking into account both mutation and selection processes. First, we study the asymptotic behaviour of the system and prove that it eventually converges to a stationary state. Next, we more closely investigate the behaviour of the system in the presence of multiple EAs. Under suitable assumptions and based on a small mutation variance asymptotic, we describe the existence of a long transient regime during which the pathogen population remains far from its asymptotic behaviour and highly concentrated around some phenotypic value that is different from the one described by its asymptotic behaviour. In that setting, the time needed for the system to reach its large time configuration is very long and multiple evolutionary attractors may act as a barrier of evolution that can be very long to bypass. [ABSTRACT FROM AUTHOR]

Recent progress in genetic techniques has shed light on the complex co-evolution of malignant cell clones in leukemias. However, several aspects of clonal selection still remain unclear. In this paper, we present a multi-compartmental continuously structured population model of selection dynamics in acute leukemias, which consists of a system of coupled integro-differential equations. Our model can be analysed in a more efficient way than classical models formulated in terms of ordinary differential equations. Exploiting the analytical tractability of this model, we investigate how clonal selection is shaped by the self-renewal fraction and the proliferation rate of leukemic cells at different maturation stages. We integrate analytical results with numerical solutions of a calibrated version of the model based on real patient data. In summary, our mathematical results formalise the biological notion that clonal selection is driven by the self-renewal fraction of leukemic stem cells and the clones that possess the highest value of this parameter are ultimately selected. Moreover, we demonstrate that the self-renewal fraction and the proliferation rate of non-stem cells do not have a substantial impact on clonal selection. Taken together, our results indicate that interclonal variability in the self-renewal fraction of leukemic stem cells provides the necessary substrate for clonal selection to act upon. [ABSTRACT FROM AUTHOR]

Tumours consist of heterogeneous populations of cells. The sub-populations can have different features, including cell motility, proliferation and metastatic potential. The interactions between clonal sub-populations are complex, from stable coexistence to dominant behaviours. The cell-cell interactions, i.e. attraction, repulsion and alignment, processes critical in cancer invasion and metastasis, can be influenced by the mutation of cancer cells. In this study, we develop a mathematical model describing cancer cell invasion and movement for two polarised cancer cell populations with different levels of mutation. We consider a system of non-local hyperbolic equations that incorporate cell-cell interactions in the speed and the turning behaviour of cancer cells, and take a formal parabolic limit to transform this model into a non-local parabolic model. We then investigate the possibility of aggregations to form, and perform numerical simulations for both hyperbolic and parabolic models, comparing the patterns obtained for these models. [ABSTRACT FROM AUTHOR]

A nonlocal dispersal SIR epidemic model with nonlinear incidence rate is introduced. It is shown that the existence and non-existence of nontrivial and nonnegative traveling wave solutions of this model are fully determined by the threshold values, that is, the basic reproduction number R 0 and the minimal wave speed c ∗ . For R 0 > 1 and c ≥ c ∗ , the existence theorem is obtained by the method of auxiliary system, Schauder’s fixed point theorem and three limiting arguments. For R 0 > 1 and 0 < c < c ∗ , the non-existence theorem is derived by applying the two-sided Laplace transform and making full use of the structure of the model. For R 0 = 1 with c > 0 and R 0 < 1 with c > 0 , the non-existence theorems are also established. [ABSTRACT FROM AUTHOR]

Cellular adhesion provides one of the fundamental forms of biological interaction between cells and their surroundings, yet the continuum modelling of cellular adhesion has remained mathematically challenging. In 2006, Armstrong et al. proposed a mathematical model in the form of an integro-partial differential equation. Although successful in applications, a derivation from an underlying stochastic random walk has remained elusive. In this work we develop a framework by which non-local models can be derived from a space-jump process. We show how the notions of motility and a cell polarization vector can be naturally included. With this derivation we are able to include microscopic biological properties into the model. We show that particular choices yield the original Armstrong model, while others lead to more general models, including a doubly non-local adhesion model and non-local chemotaxis models. Finally, we use random walk simulations to confirm that the corresponding continuum model represents the mean field behaviour of the stochastic random walk. [ABSTRACT FROM AUTHOR]

In this work, we analyze a one-dimensional steady-state Poisson-Nernst-Planck type model for ionic flow through a membrane channel including ionic interactions modeled from the Density Functional Theory in a simple setting: Two oppositely charged ion species are involved with electroneutrality boundary conditions and with zero permanent charge, and only the hard sphere component of the excess (beyond the ideal) electrochemical potential is included. The model can be viewed as a singularly perturbed integro-differential system with a parameter resulting from a dimensionless scaling of the problem as the singular parameter. Our analysis is a combination of geometric singular perturbation theory and functional analysis. The existence of a solution of the model problem for small ion sizes is established and, treating the sizes as small parameters, we also derive an approximation of the I-V (current-voltage) relation. For this relatively simple situation, it is found that the ion size effect on the I-V relation can go either way-enhance or reduce the current. More precisely, there is a critical potential value V so that, if V > V, then the ion size enhances the current; if V < V, it reduces the current. There is another critical potential value V so that, if V > V, the current is increasing with respect to λ = r/ r where r and r are, respectively, the radii of the positively and negatively charged ions; if V < V, the current is decreasing in λ. To our knowledge, the existence of these two critical values for the potential was not previously identified. [ABSTRACT FROM AUTHOR]

We study the Cauchy problem on the real line for the nonlocal Fisher-KPP equation in one spatial dimension, \begin{equation*} u_t = D u_{xx} + u(1-\phi *u), \end{equation*} where $\phi *u$ is a spatial convolution with the top hat kernel, $\phi (y) \equiv H\left (\frac{1}{4}-y^2\right )$ . After observing that the problem is globally well-posed, we demonstrate that positive, spatially periodic solutions bifurcate from the spatially uniform steady state solution $u=1$ as the diffusivity, $D$ , decreases through $\Delta _1 \approx 0.00297$ (the exact value is determined in Section 3). We explicitly construct these spatially periodic solutions as uniformly valid asymptotic approximations for $D \ll 1$ , over one wavelength, via the method of matched asymptotic expansions. These consist, at leading order, of regularly spaced, compactly supported regions with width of $O(1)$ where $u=O(1)$ , separated by regions where $u$ is exponentially small at leading order as $D \to 0^+$ . From numerical solutions, we find that for $D \geq \Delta _1$ , permanent form travelling waves, with minimum wavespeed, $2 \sqrt{D}$ , are generated, whilst for $0 \lt D \lt \Delta _1$ , the wavefronts generated separate the regions where $u=0$ from a region where a steady periodic solution is created via a distinct periodic shedding mechanism acting immediately to the rear of the advancing front, with this mechanism becoming more pronounced with decreasing $D$ . The structure of these transitional travelling wave forms is examined in some detail.