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Mathematical modeling has become a mainstream approach in scientific research when it is not feasible to design adequate experimentation. Agent based modeling provides rapid assessments of possible scenarios, especially in epidemiological studies where the goal is to carry out quick and effective preventive steps when an infection breaks out. In this paper, the relationships between infectiousness, chance of recovery, duration of a micro-parasitic disease, and the population dynamics of the host via parameter sweeps in a simple model system were analyzed. A disease with a very low infection rate is unable to spread in the population, unless the population density is high and the duration of the sickness is long. In cases of low recovery rates the number of sick and immune individuals showed a maximum value at 30% infectiousness. As the size of the population decreases, the population density decreases, and therefore, the transmission rate decreases as well. This effect leads to a new equilibrium population size, where the number of births and deaths will be balanced, and a large proportion of the population has acquired immunity. Based on these simulation models, the dynamic properties of populations contribute to the resilience of illness due to infections from micro-parasitic diseases.
The purpose of this study was to determine the extent of microbial contamination and antimicrobial resistance throughout a typical urban university environment. Determining the numbers of antibiotic resistant bacteria may provide insight into the continued development of antimicrobial resistance, and may lead to changes in university inhabitants' hygiene behaviors. In this study, samples of microorganisms were obtained from 35 surfaces at Pace University-NYC on three separate days. Samples were grown on plates of tryptic soy agar (TSA) and replicated onto control-plates, and plates containing either 100 µg/mL ampicillin, 1.0 µg/mL ciprofloxacin, or 1.0 µg/mL triclosan. The presence of bacterial growth on the drug containing plates after 24 hours indicated antimicrobial resistance. The restroom floors, toilet seats, computers, and cafeteria displayed the highest number of bacterial growth, 171, 301, 87, 143 colony forming units (CFUs) respectively. These sites also contained microorganisms displaying antimicrobial resistance to two or more of the antimicrobial agents. Resistance to triclosan, ciprofloxacin, and ampicillin were observed in 100% (±0), 97% (±0.16), and 68% (±0.47) of sample sites respectively. Finally, an additional study of hygiene behavior of 100 university inhabitants was conducted to observe a possible mechanism in the high level of distribution of drug resistant microorganisms throughout the university. The results of this study have shown that while 88% (±0.32) of inhabitants wash their hands, the time spent washing on average was 4.87 (±3.97) seconds - well below the 20 seconds recommended to sufficiently remove microorganisms from the hands.
The mind-body connection is well-established and evidence is mounting for a connection between stress, decreased immune function and tumor development. The studies described herein investigated the effects of the glucocorticoid hormone, corticosterone (CORT), on the function of tumor-antigen specific CD8 T cells. K11 cells are a clonal CD8 T cell line specific for epitope I of the Simian Virus 40 large tumor antigen (Tag) protein. Tag is a known oncoprotein that induces transformation of cells in vitro and tumor formation in susceptible animals. Control of Tag-induced tumors in vivo is mediated largely by CD8 T cells specific for Tag. Treatment of K11 cells with physiologically relevant levels of CORT decreased their expansion during co-culture with Tag-expressing target cells. IFN-γ production by the K11 cells was also markedly decreased. In contrast, the ability of K11 cells to lyse Tag-expressing target cells was unaffected by CORT treatment. Ultimately, these studies will enhance our understanding of the mechanism(s) whereby stress hormones alter a tumor-specific immune response in vivo.