Living organisms are limited in the range of values of ecological factors they can explore. This defines where animals exist (or could exist) and forms an ecological fingerprint that explains species' distribution at global scales. Species' ecological fingerprints can be represented as a n-dimensional hypervolume - known as Hutchinson's niche hypervolume. This concept has enabled significant progress in our understanding of species' ecological needs and distributions across environmental gradients. Nevertheless, the properties of Hutchinson's n-dimensional hypervolumes can be challenging to calculate and several methods have been proposed to extract meaningful measurements of hypervolumes' properties. One key property of hypervolumes are holes, which provide important information about the ecological occupancy of species. However, to date, current methods rely on volume estimates and set operations to identify holes in hypervolumes. Yet, this approach can be problematic because in high-dimensions, the volume of region enclosing a hole tends to zero. We propose the use of persistence homology (PH) to identify holes in hypervolumes and in ecological datasets more generally. PH allows for the estimates of topological properties in n-dimensional niche hypervolumes independent of the volume estimates of the hypervolume. We demonstrate the application of PH to canonical datasets and to the identification of holes in the hypervolumes of five vertebrate species with diverse niches, highlighting the potential benefits of this approach to gain further insights into animal ecology. Overall, our approach enables the study of a yet unexplored property of Hutchinson's hypervolumes, and thus, have important implications to our understanding of animal ecology.

We explore the relationship between Eulerian and Lagrangian approaches for modeling movement in vector-borne diseases for discrete space. In the Eulerian approach we account for the movement of hosts explicitly through movement rates captured by a graph Laplacian matrix L. In the Lagrangian approach we only account for the proportion of time that individuals spend in foreign patches through a mixing matrix P. We establish a relationship between an Eulerian model and a Lagrangian model for the hosts in terms of the matrices L and P. We say that the two modeling frameworks are consistent if for a given matrix P, the matrix L can be chosen so that the residence times of the matrix P and the matrix L match. We find a sufficient condition for consistency, and examine disease quantities such as the final outbreak size and basic reproduction number in both the consistent and inconsistent cases. In the special case of a two-patch model, we observe how similar values for the basic reproduction number and final outbreak size can occur even in the inconsistent case. However, there are scenarios where the final sizes in both approaches can significantly differ by means of the relationship we propose.

We study a susceptible-exposed-infected-recovered (SEIR) model considered by Aguas et al. (In: Herd immunity thresholds for SARS-CoV-2 estimated from unfolding epidemics, 2021), Gomes et al. (In: J Theor Biol. 540:111063, 2022) where individuals are assumed to differ in their susceptibility or exposure to infection. Under this heterogeneity assumption, epidemic growth is effectively suppressed when the percentage of the population having acquired immunity surpasses a critical level - the herd immunity threshold - that is lower than in homogeneous populations. We derive explicit formulas to calculate herd immunity thresholds and stable configurations, especially when susceptibility or exposure are gamma distributed, and explore extensions of the model.

An intraguild predation model with intraguild predator diffusion is proposed and studied in this work. It is shown that the local system can have four boundary equilibria and at most two interior equilibria. The interior equilibria may exist even when the system is not uniformly persistent. When only intraguild predator diffusion is incorporated into our three-species model, the resulting model is a partially degenerate reaction-diffusion system. For this partially degenerate system, we show that the solution semiflow is bounded dissipative and the positive orbits of bounded sets are bounded. We also demonstrate that intraguild predator diffusion can lead to the occurrence of spatially nonhomogeneous oscillations and spatiotemporal chaos. Further, we show that intraguild predator diffusion can induce transitions between spatially homogeneous oscillations, spatially nonhomogeneous oscillations and chaos.

In mathematical biology, there is a great deal of interest in producing continuum models by scaling discrete agent-based models governed by local stochastic rules. We discuss a particular example of this approach: a model for the proliferation of neural crest cells that can help us understand the development of Hirschprung's disease, a potentially-fatal condition in which the enteric nervous system of a new-born child does not extend all the way through the intestine and colon. Our starting point is a discrete-state, continuous-time Markov chain model proposed by Hywood et al. (2013a) for the location of the neural crest cells that make up the enteric nervous system. Hywood et al. (2013a) scaled their model to derive an approximate second order partial differential equation describing how the limiting expected number of neural crest cells evolve in space and time. In contrast, we exploit the relationship between the above-mentioned Markov chain model and the well-known Yule-Furry process to derive the exact form of the scaled version of the process. Furthermore, we provide expressions for other features of the domain agent occupancy process, such as the variance of the marginal occupancy at a particular site, the distribution of the number of agents that are yet to reach a given site and a stochastic description of the process itself.

We present a quasi-steady state mechanistic derivation of the Monod bioreaction equation based upon a conceptual model involving aqueous phase diffusive transport of substrate towards a spherical microbe; transport of the substrate across its surface membrane; and reaction depleting the substrate within the microbe. The resulting Monod coefficients [Formula: see text] and [Formula: see text] are dependent upon substrate-species pairs and the mass transfer properties of the system. Two substrate transport scenarios are investigated: (1) a constant rate model that is a function of a constant flux across the surface of the microbe; and (2) a linear rate model that is the product of a constant transport velocity and the concentration of substrate in contact with the surface of the microbe. The model is verified and parameterized using benzene, toluene, and phenol depletion and biomass growth data obtained from Reardon et al. (Biotechnol Bioeng: 385-400, 2000). Calibration results indicate a normalized surface to bulk concentration ratio of nearly unity in all simulations for benzene, toluene, and phenol when paired with P. putida F1, implying that the process is not aqueous phase diffusion limited.

Various vaccines have been approved for use to combat COVID-19 that offer imperfect immunity and could furthermore wane over time. We analyze the effect of vaccination in an SLIARS model with demography by adding a compartment for vaccinated individuals and considering disease-induced death, imperfect and waning vaccination protection as well as waning infections-acquired immunity. When analyzed as systems of ordinary differential equations, the model is proven to admit a backward bifurcation. A continuous time Markov chain (CTMC) version of the model is simulated numerically and compared to the results of branching process approximations. While the CTMC model detects the presence of the backward bifurcation, the branching process approximation does not. The special case of an SVIRS model is shown to have the same properties.

Human health and physiology is strongly influenced by interactions between human cells and intestinal microbiota in the gut. In mammals, the host-microbiota crosstalk is mainly mediated by regulations at the intestinal crypt level: the epithelial cell turnover in crypts is directly influenced by metabolites produced by the microbiota. Conversely, enterocytes maintain hypoxia in the gut, favorable to anaerobic bacteria which dominate the gut microbiota. We constructed an individual-based model of epithelial cells interacting with the microbiota-derived chemicals diffusing in the crypt lumen. This model is formalized as a piecewise deterministic Markov process (PDMP). It accounts for local interactions due to cell contact (among which are mechanical interactions), for cell proliferation, differentiation and extrusion which are regulated spatially or by chemicals concentrations. It also includes chemicals diffusing and reacting with cells. A deterministic approximated model is also introduced for a large population of small cells, expressed as a system of porous media type equations. Both models are extensively studied through numerical exploration. Their biological relevance is thoroughly assessed by recovering bio-markers of an healthy crypt, such as cell population distribution along the crypt or population turn-over rates. Simulation results from the deterministic model are compared to the PMDP model and we take advantage of its lower computational cost to perform a sensitivity analysis by Morris method. We finally use the crypt model to explore butyrate supplementation to enhance recovery after infections by enteric pathogens.

The effective degree SIR model describes the dynamics of diseases with lifetime acquired immunity on a static random contact network. It is typically modeled as a system of ordinary differential equations describing the probability distribution of the infection status of neighbors of a susceptible node. Such a construct may not be used to study networks with an infinite degree distribution, such as an infinite scale-free network. We propose a new generating function approach to rewrite the effective degree SIR model as a nonlinear transport type partial differential equation. We show the existence and uniqueness of the solutions the are biologically relevant. In addition we show how this model may be reduced to the Volz model with the assumption that the infection statuses of the neighbors of an susceptible node are initially independent to each other. This paper paves the way to study the stability of the disease-free steady state and the disease threshold of the infinite dimensional effective degree SIR models.