Overcompensation of transient and permanent death rate increases in age-structured models with cannibalistic interactions.

There has been renewed interest in understanding the mathematical structure of ecological population models that lead to overcompensation, the process by which a population recovers to a higher level after suffering a permanent increase in predation or harvesting. Here, we apply a recently formulated kinetic population theory to formally construct an age-structured single-species population model that includes a cannibalistic interaction in which older individuals prey on younger ones. Depending on the age-dependent structure of this interaction, our model can exhibit transient or steady-state overcompensation of an increased death rate as well as oscillations of the total population, both phenomena that have been observed in ecological systems.

How Naive T-Cell Clone Counts Are Shaped By Heterogeneous Thymic Output and Homeostatic Proliferation.

The specificity of T cells is that each T cell has only one T cell receptor (TCR). A T cell clone represents a collection of T cells with the same TCR sequence. Thus, the number of different T cell clones in an organism reflects the number of different T cell receptors (TCRs) that arise from recombination of the V(D)J gene segments during T cell development in the thymus.

Spatial Resolved Surface Ozone with Urban and Rural Differentiation during 1990-2019: A Space-Time Bayesian Neural Network Downscaler.

Long-term exposure to ambient ozone (O) can lead to a series of chronic diseases and associated premature deaths, and thus population-level environmental health studies hanker after the high-resolution surface O concentration database. In response to this demand, we innovatively construct a space-time Bayesian neural network parametric regressor to fuse TOAR historical observations, CMIP6 multimodel simulation ensemble, population distributions, land cover properties, and emission inventories altogether and downscale to 10 km × 10 km spatial resolution with high methodological reliability ( = 0.89-0.

Why case fatality ratios can be misleading: individual- and population-based mortality estimates and factors influencing them.

Different ways of calculating mortality during epidemics have yielded very different results, particularly during the current COVID-19 pandemic. For example, the 'CFR' has been interchangeably called the case fatality ratio, case fatality rate, and case fatality risk, often without standard mathematical definitions. The most commonly used CFR is the case fatality ratio, typically constructed using the estimated number of deaths to date divided by the estimated total number of confirmed infected cases to date.

Why estimating population-based case fatality rates during epidemics may be misleading.

Different ways of calculating mortality ratios during epidemics can yield widely different results, particularly during the COVID-19 pandemic. We formulate both a survival probability model and an associated infection duration-dependent SIR model to define individual- and population-based estimates of dynamic mortality ratios. The key parameters that affect the dynamics of the different mortality estimates are the incubation period and the length of time individuals were infected before confirmation of infection.

PDE MODELS OF ADDER MECHANISMS IN CELLULAR PROLIFERATION.

Cell division is a process that involves many biochemical steps and complex biophysical mechanisms. To simplify the understanding of what triggers cell division, three basic models that subsume more microscopic cellular processes associated with cell division have been proposed. Cells can divide based on the time elapsed since their birth, their size, and/or the volume added since their birth-the timer, sizer, and adder models, respectively.