The inclusion of cognitive processes, such as perception, learning and memory, are inevitable in mechanistic animal movement modelling. Cognition is the unique feature that distinguishes animal movement from mere particle movement in chemistry or physics. Hence, it is essential to incorporate such knowledge-based processes into animal movement models. Here, we summarize popular deterministic mathematical models derived from first principles that begin to incorporate such influences on movement behaviour mechanisms. Most generally, these models take the form of nonlocal reaction-diffusion-advection equations, where the nonlocality may appear in the spatial domain, the temporal domain, or both. Mathematical rules of thumb are provided to judge the model rationality, to aid in model development or interpretation, and to streamline an understanding of the range of difficulty in possible model conceptions. To emphasize the importance of biological conclusions drawn from these models, we briefly present available mathematical techniques and introduce some existing "measures of success" to compare and contrast the possible predictions and outcomes. Throughout the review, we propose a large number of open problems relevant to this relatively new area, ranging from precise technical mathematical challenges, to more broad conceptual challenges at the cross-section between mathematics and ecology. This review paper is expected to act as a synthesis of existing efforts while also pushing the boundaries of current modelling perspectives to better understand the influence of cognitive movement mechanisms on movement behaviours and space use outcomes.

Consider a branching process whose reproduction law is homogeneous. Sampling a single cell uniformly from the population at a time [Formula: see text] and looking along the sampled cell's ancestral lineage, we find that the reproduction law is heterogeneous-the expected reproductive output of ancestral cells on the lineage from time 0 to time T continuously increases with time. This 'inspection paradox' is due to sampling bias, that cells with a larger number of offspring are more likely to have one of their descendants sampled by virtue of their prolificity. The bias's strength changes with the random population size and/or the sampling time T. Our main result explicitly characterises the evolution of reproduction rates and sizes along the sampled ancestral lineage as a mixture of Poisson processes, which simplifies in special cases. The ancestral bias helps to explain recently observed variation in mutation rates along lineages of the developing human embryo.

In this paper, we discuss the embedding problem for centrosymmetric matrices, which are higher order generalizations of the matrices occurring in strand symmetric models. These models capture the substitution symmetries arising from the double helix structure of the DNA. Deciding whether a transition matrix is embeddable or not enables us to know if the observed substitution probabilities are consistent with a homogeneous continuous time substitution model, such as the Kimura models, the Jukes-Cantor model or the general time-reversible model. On the other hand, the generalization to higher order matrices is motivated by the setting of synthetic biology, which works with different sizes of genetic alphabets.

Theoretical and applied cancer studies that use individual-based models (IBMs) have been limited by the lack of a mathematical formulation that enables rigorous analysis of these models. However, spatial cumulant models (SCMs), which have arisen from theoretical ecology, describe population dynamics generated by a specific family of IBMs, namely spatio-temporal point processes (STPPs). SCMs are spatially resolved population models formulated by a system of differential equations that approximate the dynamics of two STPP-generated summary statistics: first-order spatial cumulants (densities), and second-order spatial cumulants (spatial covariances). We exemplify how SCMs can be used in mathematical oncology by modelling theoretical cancer cell populations comprising interacting growth factor-producing and non-producing cells. To formulate model equations, we use computational tools that enable the generation of STPPs, SCMs and mean-field population models (MFPMs) from user-defined model descriptions (Cornell et al. Nat Commun 10:4716, 2019). To calculate and compare STPP, SCM and MFPM-generated summary statistics, we develop an application-agnostic computational pipeline. Our results demonstrate that SCMs can capture STPP-generated population density dynamics, even when MFPMs fail to do so. From both MFPM and SCM equations, we derive treatment-induced death rates required to achieve non-growing cell populations. When testing these treatment strategies in STPP-generated cell populations, our results demonstrate that SCM-informed strategies outperform MFPM-informed strategies in terms of inhibiting population growths. We thus demonstrate that SCMs provide a new framework in which to study cell-cell interactions, and can be used to describe and perturb STPP-generated cell population dynamics. We, therefore, argue that SCMs can be used to increase IBMs' applicability in cancer research.

A compartment model for an in-host liquid nanoparticle delivered mRNA vaccine is presented. Through non-dimensionalisation, five timescales are identified that dictate the lifetime of the vaccine in-host: decay of interferon gamma, antibody priming, autocatalytic growth, antibody peak and decay, and interleukin cessation. Through asymptotic analysis we are able to obtain semi-analytical solutions in each of the time regimes which allows us to predict maximal concentrations and better understand parameter dependence in the model. We compare our model to 22 data sets for the BNT162b2 and mRNA-1273 mRNA vaccines demonstrating good agreement. Using our analysis, we estimate the values for each of the five timescales in each data set and predict maximal concentrations of plasma B-cells, antibody, and interleukin. Through our comparison, we do not observe any discernible differences between vaccine candidates and sex. However, we do identify an age dependence, specifically that vaccine activation takes longer and that peak antibody occurs sooner in patients aged 55 and greater.

Acquired immunity to a dengue virus serotype (whether by infection or the only licensed dengue vaccine) can produce antibody-dependent enhancement (ADE) in later infections with another dengue serotype, resulting in higher viral loads and more severe symptoms such as dengue hemorrhagic fever, unless the person already has immunity to multiple dengue serotypes. Screening to confirm dengue seropositivity is therefore recommended before vaccination. Recent studies suggest that the closely-related Zika virus may also interact with dengue through ADE. This study uses a mathematical model to evaluate the likely impact of imperfect screening and dengue vaccination on the spread of both viruses in a population where only one dengue serotype circulates, although the vaccine may take against any or all of the four recognized serotypes. Analysis focuses on the reproductive numbers of the viruses. Results indicate that vaccination increases the spread of Zika through induced ADE, while its impact on the spread of dengue depends on screening specificity and serotype-specific vaccine efficacies, as well as the intensity of ADE. Numerical analysis identifies the roles played by age-in and catch-up vaccination as well as screening characteristics and prior dengue exposure.

A characteristic of ecosystems is the existence of manifold of independencies which are highly complex. Various mathematical models have made considerable contributions in gaining a better understanding of the predator-prey interactions. The main components of any predator-prey models are, firstly, how the different population classes grow and secondly, how the prey and predator interacts. In this paper, the two populations' growth rates obey the logistic law and the carrying capacity of the predator depends on the available number of prey are considered. Our aim is to clarify the relationship between models and Holling types functional and numerical responses in order to gain insights into predator interferences and to answer an important question how competition is carried out. We consider a predator-prey model and a two-predator one-prey model to explain the idea. The novel approach is explained for the mechanism measurement of predator interference through depending on numerical response. Our approach gives good correspondence between an important real data and computer simulations.

We formulate a general age-of-infection epidemic model with two pathways: the symptomatic infections and the asymptomatic infections. We then calculate the basic reproduction number [Formula: see text] and establish the final size relation. It is shown that the ratio of accumulated counts of symptomatic patients and asymptomatic patients is determined by the symptomatic ratio f which is defined as the probability of eventually becoming symptomatic after being infected. We also formulate and study a general age-of-infection model with disease deaths and with two infection pathways. The final size relation is investigated, and the upper and lower bounds for final epidemic size are given. Several numerical simulations are performed to verify the analytical results.

We incorporate the disease state and testing state into the formulation of a COVID-19 epidemic model. For this model, the basic reproduction number is identified and its dependence on model parameters related to the testing process and isolation efficacy is discussed. The relations between the basic reproduction number, the final epidemic and peak sizes, and the model parameters are further explored numerically. We find that fast test reporting does not always benefit the control of the COVID-19 epidemic if good quarantine while awaiting test results is implemented. Moreover, the final epidemic and peak sizes do not always increase along with the basic reproduction number. Under some circumstances, lowering the basic reproduction number increases the final epidemic and peak sizes. Our findings suggest that properly implementing isolation for individuals who are waiting for their testing results would lower the basic reproduction number as well as the final epidemic and peak sizes.

We use global sensitivity analysis (specifically, Partial Rank Correlation Coefficients) to explore the roles of ecological and epidemiological processes in shaping the temporal dynamics of a parameterized SIR-type model of two host species and an environmentally transmitted pathogen. We compute the sensitivities of disease prevalence in each host species to model parameters. Sensitivity rankings are calculated, interpreted biologically, and contrasted for cases where the pathogen is introduced into a disease-free community and cases where a second host species is introduced into an endemic single-host community. In some cases the magnitudes and dynamics of the sensitivities can be predicted only by knowing the host species' characteristics (i.e., their competitive abilities and disease competence) whereas in other cases they can be predicted by factors independent of the species' characteristics (specifically, intraspecific versus interspecific processes or a species' roles of invader versus resident). For example, when a pathogen is initially introduced into a disease-free community, disease prevalence in both hosts is more sensitive to the burst size of the first host than the second host. In comparison, disease prevalence in each host is more sensitive to its own infection rate than the infection rate of the other host species. In total, this study illustrates that global sensitivity analysis can provide useful insight into how ecological and epidemiological processes shape disease dynamics and how those effects vary across time and system conditions. Our results show that sensitivity analysis can provide quantification and direction when exploring biological hypotheses.

In this paper, we first formulate a system of ODEs-PDE to model diseases with latency-age and differential infectivity. Then, based on the ways how latent individuals leave the latent stage, one ODE and two DDE models are derived. We only focus on the global stability of the models. All the models have some similarities in the existence of equilibria. Each model has a threshold dynamics for global stability, which is completely characterized by the basic reproduction number. The approach is the Lyapunov direct method. We propose an idea on constructing Lyapunov functionals for the two DDE and the original ODEs-PDE models. During verifying the negative (semi-)definiteness of derivatives of the Lyapunov functionals along solutions, a novel positive definite function and a new inequality are used. The idea here is also helpful in applying the Lyapunov direct method to prove the global stability of some epidemic models with age structure or delays.

We analyse a generalisation of the stochastic gene expression model studied recently in Fromion et al. (SIAM J Appl Math 73:195-211, 2013) and Robert (Probab Surv 16:277-332, 2019) that keeps track of the production of both mRNA and protein molecules, using techniques from the theory of point processes, as well as ideas from the theory of matrix-analytic methods. Here, both the activity of a gene and the creation of mRNA are modelled with an arbitrary Markovian Arrival Process governed by finitely many phases, and each mRNA molecule during its lifetime gives rise to protein molecules in accordance with a Poisson process. This modification is important, as Markovian Arrival Processes can be used to approximate many types of point processes on the nonnegative real line, meaning this framework allows us to further relax our assumptions on the overall process of transcription.

This paper proposes and analyzes an immune-structured population model of tilapia subject to Tilapia Lake Virus (TiLV) disease. The model incorporates within-host dynamics, used to describe the interaction between the pathogen, the immune system and the waning of immunity. Individuals infected with a low dose acquire a low immunity level and those infected with a high dose acquire a high level of immunity. Since individuals' immune status plays an important role in the spread of infectious diseases at the population level, the within-host dynamics are connected to the between-host dynamics in the population. We define an explicit formula for the reproductive number [Formula: see text] and show that the disease-free equilibrium is locally asymptotically stable when [Formula: see text], while it is unstable when [Formula: see text]. Furthermore, we prove that an endemic equilibrium exists. We also study the influence of the initial distribution of host resistance on the spread of the disease, and find that hosts' initial resistance plays a crucial role in the disease dynamics. This suggests that the genetic selection aiming to improve hosts' initial resistance to TiLV could help fight the disease. The results also point out the crucial role played by the inoculum size. We find that the higher the initial inoculum size, the faster the dynamics of infection. Moreover, if the initial inoculum size is below a certain threshold, it may not result in an outbreak at the between-host level. Finally, the model shows that there is a strong negative correlation between heterogeneity and the probability of pathogen invasion.

The catalytic reaction system (CRS) formalism by Hordijk and Steel is a versatile method to model autocatalytic biochemical reaction networks. It is particularly suited, and has been widely used, to study self-sustainment and self-generation properties. Its distinguishing feature is the explicit assignment of a catalytic function to chemicals that are part of the system. In this work, it is shown that the subsequent and simultaneous catalytic functions give rise to an algebraic structure of a semigroup with the additional compatible operation of idempotent addition and a partial order. The aim of this article is to demonstrate that such semigroup models are a natural setup to describe and analyze self-sustaining CRS. The basic algebraic properties of the models are established and the notion of the function of any set of chemicals on the whole CRS is made precise. This leads to a natural discrete dynamical system on the power set of chemicals, which is obtained by iteratively considering the self-action on a set of chemicals by its own function. The fixed points of this dynamical system are proven to correspond to self-sustaining sets of chemicals, which are functionally closed. Finally, as the main application, a theorem on the maximal self-sustaining set and a structure theorem on the set of functionally closed self-sustaining sets of chemicals are proven.

A discrete epidemic model with vaccination and limited medical resources is proposed to understand its underlying dynamics. The model induces a nonsmooth two dimensional map that exhibits a surprising array of dynamical behavior including the phenomena of the forward-backward bifurcation and period doubling route to chaos with feasible parameters in an invariant region. We demonstrate, among other things, that the model generates the above described phenomena as the transmission rate or the basic reproduction number of the disease gradually increases provided that the immunization rate is low, the vaccine failure rate is high and the medical resources are limited. Finally, the numerical simulations are provided to illustrate our main results.

The ability of a chemical reaction network to generate itself by catalyzed reactions from constantly present environmental food sources is considered a fundamental property in origin-of-life research. Based on Kaufmann's autocatalytic sets, Hordijk and Steel have constructed the versatile formalism of catalytic reaction systems (CRS) to model and to analyze such self-generating networks, which they named reflexively autocatalytic and food-generated. Recently, it was established that the subsequent and simultaenous catalytic functions of the chemicals of a CRS give rise to an algebraic structure, termed a semigroup model. The semigroup model allows to naturally consider the function of any subset of chemicals on the whole CRS. This gives rise to a generative dynamics by iteratively applying the function of a subset to the externally supplied food set. The fixed point of this dynamics yields the maximal self-generating set of chemicals. Moreover, the set of all functionally closed self-generating sets of chemicals is discussed and a structure theorem for this set is proven. It is also shown that a CRS which contains self-generating sets of chemicals cannot have a nilpotent semigroup model and thus a useful link to the combinatorial theory of finite semigroups is established. The main technical tool introduced and utilized in this work is the representation of the semigroup elements as decorated rooted trees, allowing to translate the generation of chemicals from a given set of resources into the semigroup language.

The burden of sexually transmitted infections (STIs) poses a challenge due to its large negative impact on sexual and reproductive health worldwide. Besides simple prevention measures and available treatment efforts, prophylactic vaccination is a powerful tool for controlling some viral STIs and their associated diseases. Here, we investigate how prophylactic vaccines are best distributed to prevent and control STIs. We consider sex-specific differences in susceptibility to infection, as well as disease severity outcomes. Different vaccination strategies are compared assuming distinct budget constraints that mimic a scarce vaccine stockpile. Vaccination strategies are obtained as solutions to an optimal control problem subject to a two-sex Kermack-McKendrick-type model, where the control variables are the daily vaccination rates for females and males. One important aspect of our approach relies on conceptualizing a limited but specific vaccine stockpile via an isoperimetric constraint. We solve the optimal control problem via Pontryagin's Maximum Principle and obtain a numerical approximation for the solution using a modified version of the forward-backward sweep method that handles the isoperimetric budget constraint in our formulation. The results suggest that for a limited vaccine supply ([Formula: see text]-[Formula: see text] vaccination coverage), one-sex vaccination, prioritizing females, appears to be more beneficial than the inclusion of both sexes into the vaccination program. Whereas, if the vaccine supply is relatively large (enough to reach at least [Formula: see text] coverage), vaccinating both sexes, with a slightly higher rate for females, is optimal and provides an effective and faster approach to reducing the prevalence of the infection.

The transmission dynamics of HIV are closely tied to the duration and overlap of sexual partnerships. We develop an autonomous population model that can account for the possibilities of an infection from either a casual sexual partner or a long-term partner who was either infected at the start of the partnership or has been newly infected since the onset of the partnership. The impact of the long-term partnerships on the rate of infection is captured by calculating the expected values of the rate of infection from these extended contacts. The model includes three stages of infectiousness: acute, chronic, and virally suppressed. We calculate HIV incidence and the fraction of new infections attributed to casual contacts and long-term partnerships allowing for variability in condom usage, the effect of achieving and maintaining viral suppression, and early intervention by beginning HAART during the acute phase of infection. We present our results using data on MSM HIV transmission from the CDC in the U.S. While the acute stage is the most infectious, the majority of the new infections will be transmitted by long-term partners in the chronic stage when condom use is infrequent as is common in long-term relationships. Time series analysis of the solution, as well as parameter sensitivity analysis, are used to determine effective intervention strategies.

In this paper, we study a stochastic parabolic problem that emerges in the modeling and control of an electrically actuated MEMS (micro-electro-mechanical system) device. The dynamics under consideration are driven by an one dimensional fractional Brownian motion with Hurst index [Formula: see text]. We derive conditions under which the resulting SPDE has a global in time solution, and we provide analytic estimates for certain statistics of interest, such as quenching times and the corresponding quenching probabilities. Our results demonstrate the non-trivial impact of the fractional noise on the dynamics of the system. Given the significance of MEMS devices in biomedical applications, such as drug delivery and diagnostics, our results provide valuable insights into the reliability of these devices in the presence of positively correlated noise.

In this paper we consider a non-local bistable reaction-diffusion equation which is a simplified version of the wave-pinning model of cell polarization. In the small diffusion limit, a typical solution u(x, t) of this model approaches one of the stable states of the bistable nonlinearity in different parts of the spatial domain [Formula: see text], separated by an interface moving at a normal velocity regulated by the integral [Formula: see text]. In what is often referred to as wave-pinning, feedback between mass-conservation and bistablity causes the interface to slow and approach a fixed limit. In the limit of a small diffusivity [Formula: see text], we prove that for any [Formula: see text] the interface can be estimated within [Formula: see text] of the location as predicted using formal asymptotics. We also discuss the sharpness of our result by comparing the formal asymptotic results with numerical simulations.

A nonlinear partial differential equation containing a nonlocal advection term and a diffusion term is analyzed to study wound closure outcomes in wound healing experiments. There is an extensive literature of similar models for wound healing experiments. In this paper we study the character of wound closure in these experiments in terms of the sensing radius of cells and the force of cell-cell adhesion. We prove a bifurcation result which differentiates uniform closure of the wound from nonuniform closure of the wound, based on a critical value [Formula: see text] of the force of cell-cell adhesion parameter [Formula: see text]. For [Formula: see text] the steady state solution [Formula: see text] of the model is stable and the wound closes uniformly. For [Formula: see text] the steady state solution [Formula: see text] of the model is unstable and the wound closes nonuniformly. We provide numerical simulations of the model to illustrate our results.