This paper studies the periodic trajectories of a novel age-structured prey–predator system with Michaelis–Menten functional response including delays and asymmetric diffusion. To begin with, the system is turned into an abstract non-densely defined Cauchy problem, and a time-lag effect in their interaction is investigated. Next, we acquire that this system appears a periodic orbit near the positive steady state by employing the method of integrated semigroup and the Hopf bifurcation theory for semilinear equations with non-dense domain, which is also the main result of this article. Finally, in order to illustrate our theoretical analysis more vividly, we make some numerical simulations and give some discussions.

We study a mathematical model proposed in the literature with the aim of describing the interactions between tumor cells and the immune system, when a periodic treatment of immunotherapy is applied. Combining some techniques from non-linear analysis (degree theory, lower and upper solutions, and theory of free-homeomorphisms in the plane), we give a detailed global analysis of the model. We also observe that for certain therapies, the maximum level of aggressiveness of a cancer, for which the treatment works (or does not work), can be computed explicitly. We discuss some strategies for designing therapies. The mathematical analysis is completed with numerical results and conclusions.

We derive and numerically implement various asymptotic approximations for the lowest or principal eigenvalue of the Laplacian with a periodic arrangement of localised traps of small \mathcal{O}(\varepsilon ) $$\mathcal{O}(\varepsilon )$$ spatial extent that are centred at the lattice points of an arbitrary Bravais lattice in {\mathbb{R}^2} $${\mathbb{R}^2}$$ . The expansion of this principal eigenvalue proceeds in powers of \nu \equiv - 1/\log (\varepsilon {d_c}) $$\nu \equiv - 1/\log (\varepsilon {d_c})$$ , where dc is the logarithmic capacitance of the trap set. An explicit three-term approximation for this principal eigenvalue is derived using strong localised perturbation theory, with the coefficients in this series evaluated numerically by using an explicit formula for the source-neutral periodic Green’s function and its regular part. Moreover, a transcendental equation for an improved approximation to the principal eigenvalue, which effectively sums all the logarithmic terms in powers of v, is derived in terms of the regular part of the periodic Helmholtz Green’s function. By using an Ewald summation technique to first obtain a rapidly converging infinite series representation for this regular part, a simple Newton iteration scheme on the transcendental equation is implemented to numerically evaluate the improved ‘log-summed’ approximation to the principal eigenvalue. From a numerical computation of the PDE eigenvalue problem defined on the fundamental Wigner–Seitz (WS) cell for the lattice, it is shown that the three-term asymptotic approximation for the principal eigenvalue agrees well with the numerical result only for a rather small trap radius. In contrast, the log-summed asymptotic result provides a very close approximation to the principal eigenvalue even when the trap radius is only moderately small. For a circular trap, the first few transcendental correction terms that further improves the log-summed approximation for the principal eigenvalue are derived. Finally, it is shown numerically that, amongst all Bravais lattices with a fixed area of the primitive cell, the principal eigenvalue is maximised for a regular hexagonal arrangement of traps.

Based on the fact that the incubation periods of epidemic disease in asymptomatically infected and infected individuals are inevitable and different, we propose a diffusive susceptible, asymptomatically infected, symptomatically infected and vaccinated (SAIV) epidemic model with delays in this paper. To see whether epidemic disease can propagate spatially with a constant speed, we focus on the travelling wave solution for this model. When the basic reproduction number of the corresponding spatial-homogenous delayed differential system is greater than one and the wave speed is greater than or equal to the critical speed, we prove that this model admits nontrivial positive travelling wave solutions. Our theoretical results are of benefit to the prevention and control of epidemic.

This paper is concerned with the asymptotic propagations for a nonlocal dispersal population model with shifting habitats. In particular, we verify that the invading speed of the species is determined by the speed c of the shifting habitat edge and the behaviours near infinity of the species’ growth rate which is nondecreasing along the positive spatial direction. In the case where the species declines near the negative infinity, we conclude that extinction occurs if c > c*(∞), while c < c*(∞), spreading happens with a leftward speed min{−c, c*(∞)} and a rightward speed c*(∞), where c*(∞) is the minimum KPP travelling wave speed associated with the species’ growth rate at the positive infinity. The same scenario will play out for the case where the species’ growth rate is zero at negative infinity. In the case where the species still grows near negative infinity, we show that the species always survives ‘by moving’ with the rightward spreading speed being either c*(∞) or c*(−∞) and the leftward spreading speed being one of c*(∞), c*(−∞) and −c, where c*(−∞) is the minimum KPP travelling wave speed corresponding to the growth rate at the negative infinity. Finally, we give some numeric simulations and discussions to present and explain the theoretical results. Our results indicate that there may exists a solution like a two-layer wave with the propagation speeds analytically determined for such type of nonlocal dispersal equations.

Cells and organisms follow aligned structures in their environment, a process that can generate persistent migration paths. Kinetic transport equations are a popular modelling tool for describing biological movements at the mesoscopic level, yet their formulations usually assume a constant turning rate. Here we relax this simplification, extending to include a turning rate that varies according to the anisotropy of a heterogeneous environment. We extend known methods of parabolic and hyperbolic scaling and apply the results to cell movement on micropatterned domains. We show that inclusion of orientation dependence in the turning rate can lead to persistence of motion in an otherwise fully symmetric environment and generate enhanced diffusion in structured domains.

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.