Nonlocal calculus is often overlooked in the mathematics curriculum. In this paper we present an interesting new class of nonlocal problems that arise from modelling the growth and division of cells, especially cancer cells, as they progress through the cell cycle. The cellular biomass is assumed to be unstructured in size or position, and its evolution governed by a time-dependent system of ordinary differential equations with multiple time delays. The system is linear and taken to be autonomous. As a result, it is possible to reduce its solution to that of a nonlinear matrix eigenvalue problem. This method is illustrated by considering case studies, including a model of the cell cycle developed recently by Simms, Bean and Koeber. The paper concludes by explaining how asymptotic expressions for the distribution of cells across the compartments can be determined and used to assess the impact of different chemotherapeutic agents.

We review the work of the present authors to employ variational calculus to formulate continuous models for the connections between various carbon nanostructures. In formulating such a variational principle, there is some evidence that carbon nanotubes deform as in perfect elasticity, and rather like the elastica, and therefore we seek to minimize the elastic energy. The calculus of variations is utilized to minimize the curvature subject to a length constraint, to obtain an Euler–Lagrange equation, which determines the connection between two carbon nanostructures. Moreover, a numerical solution is proposed to determine the geometric parameters for the connected structures. Throughout this review, we assume that the defects on the nanostructures are axially symmetric and that the into-the-plane curvature is small in comparison to that in the two-dimensional plane, so that the problems can be considered in the two-dimensional plane. Since the curvature can be both positive and negative, depending on the gap between the two nanostructures, two distinct cases are examined, which are subsequently shown to smoothly connect to each other.

In 1991, McNabb introduced the concept of mean action time (MAT) as a finite measure of the time required for a diffusive process to effectively reach steady state. Although this concept was initially adopted by others within the Australian and New Zealand applied mathematics community, it appears to have had little use outside this region until very recently, when in 2010 Berezhkovskii and co-workers [A. M. Berezhkovskii, C. Sample and S. Y. Shvartsman, “How long does it take to establish a morphogen gradient?” Biophys. J. 99 (2010) L59–L61] rediscovered the concept of MAT in their study of morphogen gradient formation. All previous work in this area has been limited to studying single-species differential equations, such as the linear advection–diffusion–reaction equation. Here we generalize the concept of MAT by showing how the theory can be applied to coupled linear processes. We begin by studying coupled ordinary differential equations and extend our approach to coupled partial differential equations. Our new results have broad applications, for example the analysis of models describing coupled chemical decay and cell differentiation processes.

We study the value of European security derivatives in the Black–Scholes model when the underlying asset $\xi $ is approximated by random walks ${\xi }^{(n)} $. We obtain an explicit error formula, up to a term of order $ \mathcal{O} ({n}^{- 3/ 2} )$, which is valid for general approximating schemes and general payoff functions. We show how this error formula can be used to find random walks ${\xi }^{(n)} $ for which option values converge at a speed of $ \mathcal{O} ({n}^{- 3/ 2} )$.

Random networks were first used to model epidemic dynamics in the 1950s, but in the last decade it has been realized that scale-free networks more accurately represent the network structure of many real-world situations. Here we give an analytical and a Monte Carlo method for approximating the basic reproduction number ${R}_{0} $ of an infectious agent on a network. We investigate how final epidemic size depends on ${R}_{0} $ and on network density in random networks and in scale-free networks with a Pareto exponent of 3. Our results show that: (i) an epidemic on a random network has the same average final size as an epidemic in a well-mixed population with the same value of ${R}_{0} $; (ii) an epidemic on a scale-free network has a larger average final size than in an equivalent well-mixed population if ${R}_{0} \lt 1$, and a smaller average final size than in a well-mixed population if ${R}_{0} \gt 1$; (iii) an epidemic on a scale-free network spreads more rapidly than an epidemic on a random network or in a well-mixed population.

We analyse the steady-state operation of a continuous flow bioreactor in which the biochemical reaction is governed by noncompetitive substrate inhibition (Andrews kinetics). A generalized reactor model is used in which the well-stirred bioreactor and the idealized membrane bioreactor are special cases. As generic properties of systems subject to substrate inhibition have been obtained by other authors, we discuss reaction engineering features specific to Andrews kinetics.

Patchy or divided populations can be important to infectious disease transmission. We first show that Lloyd’s mean crowding index, an index of patchiness from ecology, appears as a term in simple deterministic epidemic models of the SIR type. Using these models, we demonstrate that the rate of movement between patches is crucial for epidemic dynamics. In particular, there is a relationship between epidemic final size and epidemic duration in patchy habitats: controlling inter-patch movement will reduce epidemic duration, but also final size. This suggests that a strategy of quarantining infected areas during the initial phases of a virulent epidemic might reduce epidemic duration, but leave the population vulnerable to future epidemics by inhibiting the development of herd immunity.

We propose a modified projected Polak–Ribière–Polyak (PRP) conjugate gradient method, where a modified conjugacy condition and a method which generates sufficient descent directions are incorporated into the construction of a suitable conjugacy parameter. It is shown that the proposed method is a modification of the PRP method and generates sufficient descent directions at each iteration. With an Armijo-type line search, the theory of global convergence is established under two weak assumptions. Numerical experiments are employed to test the efficiency of the algorithm in solving some benchmark test problems available in the literature. The numerical results obtained indicate that the algorithm outperforms an existing similar algorithm in requiring fewer function evaluations and fewer iterations to find optimal solutions with the same tolerance.

This paper is concerned with the initial boundary value problem of a class of nonlinear wave equations and reaction–diffusion equations with several nonlinear source terms of different signs. For the initial boundary value problem of the nonlinear wave equations, we derive a blow up result for certain initial data with arbitrary positive initial energy. For the initial boundary value problem of the nonlinear reaction–diffusion equations, we discuss some probabilities of the existence and nonexistence of global solutions and give some sufficient conditions for the global and nonglobal existence of solutions at high initial energy level by employing the comparison principle and variational methods.

We consider a bilinear optimal control problem for a von Kármán plate equation. The control is a function of the spatial variables and acts as a multiplier of the velocity term. We first state the existence of solutions for the von Kármán equation and then derive optimality conditions for a given objective functional. Finally, we show the uniqueness of the optimal control.

We consider a hybrid model, created by coupling a continuum and an agent-based model of infectious disease. The framework of the hybrid model provides a mechanism to study the spread of infection at both the individual and population levels. This approach captures the stochastic spatial heterogeneity at the individual level, which is directly related to deterministic population level properties. This facilitates the study of spatial aspects of the epidemic process. A spatial analysis, involving counting the number of infectious agents in equally sized bins, reveals when the spatial domain is nonhomogeneous.

The Kohlrausch functions $\exp (- {t}^{\beta } )$, with $\beta \in (0, 1)$, which are important in a wide range of physical, chemical and biological applications, correspond to specific realizations of completely monotone functions. In this paper, using nonuniform grids and midpoint estimates, constructive procedures are formulated and analysed for the Kohlrausch functions. Sharper estimates are discussed to improve the approximation results. Numerical results and representative approximations are presented to illustrate the effectiveness of the proposed method.

Endemic infectious diseases constantly circulate in human populations, with prevalence fluctuating about a (theoretical and unobserved) time-independent equilibrium. For diseases for which acquired immunity is not lifelong, the classic susceptible–infectious–recovered–susceptible (SIRS) model provides a framework within which to consider temporal trends in the observed epidemiology. However, in some cases (notably pertussis), sustained multiannual fluctuations are observed, whereas the SIRS model is characterized by damped oscillatory dynamics for all biologically meaningful choices of model parameters. We show that a model that allows for “boosting” of immunity may naturally give rise to undamped oscillatory behaviour for biologically realistic parameter choices. The life expectancy of the population is critical in determining the characteristic dynamics of the system. For life expectancies up to approximately $50$ years, we find that, even with boosting, damped oscillatory dynamics persist. For increasing life expectancy, the system may sustain oscillatory dynamics, or even exhibit bistable behaviour, in which both stable point attractor and limit cycle dynamics may coexist. Our results suggest that rising life expectancy may induce changes in the characteristic dynamics of infections for which immunity is not lifelong, with potential implications for disease control strategies.

Steady water infiltration in homogeneous soils is governed by the Richards equation. This equation can be studied more conveniently by transforming to a type of Helmholtz equation. In this study, a dual-reciprocity boundary element method (DRBEM) is employed to solve the Helmholtz equation numerically. Using the solutions obtained, numerical values of the suction potential are then computed. The proposed method is tested on problems involving infiltration from different types of periodic channels in a homogeneous soil. Moreover, the method is also examined using infiltration from periodic trapezoidal channels in three different types of homogeneous soil.

A second-order in time finite-difference scheme using a modified predictor–corrector method is proposed for the numerical solution of the generalized Burgers–Fisher equation. The method introduced, which, in contrast to the classical predictor–corrector method is direct and uses updated values for the evaluation of the components of the unknown vector, is also analysed for stability. Its efficiency is tested for a single-kink wave by comparing experimental results with others selected from the available literature. Moreover, comparisons with the classical method and relevant analogous modified methods are given. Finally, the behaviour and physical meaning of the two-kink wave arising from the collision of two single-kink waves are examined.

Increased frequency and severity of stressors associated with climate change are drastically altering ecosystems. Caribbean coral reefs differ markedly from just 30 years ago, with much restructuring attributable to infectious disease outbreaks. Using a classic epidemiological approach, we demonstrate how density-dependent demographic rates serve as a mechanism for intrinsic coral resilience to population perturbations arising from disturbances such as disease. We explore the impact of allowing infection status to influence demographic rates and ascertain outbreak thresholds that are corroborated by epizootic patterns observed in the field. We discuss how our threshold calculations may provide metrics of coral epizootic early warning systems. Integrating our infection model with equations describing the interspecific competition for space between coral and macroalgae, we provide new mechanistic understanding of the influence that coral life history dynamism and infectious disease have on the changing face of these threatened ecosystems.

A nation-wide vaccination campaign began in New Zealand in 2004 with the aim of stopping the epidemic of meningococcal B disease. Approximately 80% of those under 20 years of age when the campaign was launched were vaccinated with three doses of a tailor-made vaccine. We propose a framework for a mathematical model based on the susceptible–carrier–infectious–removed (SCIR) structure. We show how the model could be used to calculate the predicted yearly incidence of infection in the absence of vaccination, and compare this to the effect that vaccination had on the course of the epidemic. Our model shows that vaccination led to a considerable decrease in the incidence of infection compared to what would have been seen otherwise. We then use our model to explore the potential effect of alternative vaccination schemes, and show that the one that was implemented was the best of all the possibilities we consider.