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Register a new userA Mathematical Framework Exhibiting the Emergence of Dynamic Expansion of Task Repertoire in emph{Pheidole dentata}
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The division of labor (DOL) and task allocation among groups of ants living in a colony is thought to be highly efficient, and key to the robust survival of a colony. A great deal of experimental and theoretical work has been done toward gaining a clear understanding of the evolution of, and underlying mechanisms of these phenomena. Much of this research has utilized mathematical modeling. Here we continue this tradition by developing a mathematical model for a particular aspect of task allocation, known as age-related repertoire expansion, that has been observed in the minor workers of the ant species emph{Pheidole dentata}. In fact, we present a relatively broad mathematical modeling framework based on the dynamics of the frequency with which members of specific age groups carry out distinct tasks. We apply our modeling approach to a specific task allocation scenario, and compare our theoretical results with experimental data. It is observed that the model predicts perceived behavior, and provides a possible explanation for the aforementioned experimental results.
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Some bacteria and archaea possess an immune system, based on the CRISPR-Cas mechanism, that confers adaptive immunity against phage. In such species, individual bacteria maintain a cassette of viral DNA elements called spacers as a memory of past infections. The typical cassette contains a few dozen spacers. Given that bacteria can have very large genomes, and since having more spacers should confer a better memory, it is puzzling that so little genetic space would be devoted by bacteria to their adaptive immune system. Here, we identify a fundamental trade-off between the size of the bacterial immune repertoire and effectiveness of response to a given threat, and show how this tradeoff imposes a limit on the optimal size of the CRISPR cassette.
This paper describes a mathematical model for the spread of a virus through an isolated population of a given size. The model uses three, color-coded components, called molecules (red for infected and still contagious; green for infected, but no longer contagious; and blue for uninfected). In retrospect, the model turns out to be a digital analogue for the well-known SIR model of Kermac and McKendrick (1927). In our RGB model, the number of accumulated infections goes through three phases, beginning at a very low level, then changing to a transition ramp of rapid growth, and ending in a plateau of final values. Consequently, the differential change or growth rate begins at 0, rises to a peak corresponding to the maximum slope of the transition ramp, and then falls back to 0. The properties of these time variations, including the slope, duration, and height of the transition ramp, and the width and height of the infection rate, depend on a single parameter - the time that a red molecule is contagious divided by the average time between collisions of the molecules. Various temporal milestones, including the starting time of the transition ramp, the time that the accumulating number of infections obtains its maximum slope, and the location of the peak of the infection rate depend on the size of the population in addition to the contagious lifetime ratio. Explicit formulas for these quantities are derived and summarized. Finally, Appendix E has been added to describe the effect of vaccinations.
The question as to why most higher organisms reproduce sexually has remained open despite extensive research, and has been called the queen of problems in evolutionary biology. Theories dating back to Weismann have suggested that the key must lie in the creation of increased variability in offspring, causing enhanced response to selection. Rigorously quantifying the effects of assorted mechanisms which might lead to such increased variability, and establishing that these beneficial effects outweigh the immediate costs of sexual reproduction has, however, proved problematic. Here we introduce an approach which does not focus on particular mechanisms influencing factors such as the fixation of beneficial mutants or the ability of populations to deal with deleterious mutations, but rather tracks the entire distribution of a population of genotypes as it moves across vast fitness landscapes. In this setting simulations now show sex robustly outperforming asex across a broad spectrum of finite or infinite population models. Concentrating on the additive infinite populations model, we are able to give a rigorous mathematical proof establishing that sexual reproduction acts as a more efficient optimiser of mean fitness, thereby solving the problem for this model. Some of the key features of this analysis carry through to the finite populations case.
Disease transmission is studied through disciplines like epidemiology, applied mathematics, and statistics. Mathematical simulation models for transmission have implications in solving public and personal health challenges. The SIR model uses a compartmental approach including dynamic and nonlinear behavior of transmission through three factors: susceptible, infected, and removed (recovered and deceased) individuals. Using the Lambert W Function, we propose a framework to study solutions of the SIR model. This demonstrates the applications of COVID-19 transmission data to model the spread of a real-world disease. Different models of disease including the SIR, SIRm and SEIR model are compared with respect to their ability to predict disease spread. Physical distancing impacts and personal protection equipment use will be discussed in relevance to the COVID-19 spread.
Probabilistic modeling is fundamental to the statistical analysis of complex data. In addition to forming a coherent description of the data-generating process, probabilistic models enable parameter inference about given data sets. This procedure is well-developed in the Bayesian perspective, in which one infers probability distributions describing to what extent various possible parameters agree with the data. In this paper we motivate and review probabilistic modeling for adaptive immune receptor repertoire data then describe progress and prospects for future work, from germline haplotyping to adaptive immune system deployment across tissues. The relevant quantities in immune sequence analysis include not only continuous parameters such as gene use frequency, but also discrete objects such as B cell clusters and lineages. Throughout this review, we unravel the many opportunities for probabilistic modeling in adaptive immune receptor analysis, including settings for which the Bayesian approach holds substantial promise (especially if one is optimistic about new computational methods). From our perspective the greatest prospects for progress in probabilistic modeling for repertoires concern ancestral sequence estimation for B cell receptor lineages, including uncertainty from germline genotype, rearrangement, and lineage development.
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