Graphene quantum dots (GQDs) are a frontier of research in the interdisciplinary world of biology and medicine. They have been hallmarked for their remarkable applications, from cellular imaging to drug delivery. Due to their unique physicochemical and optical properties, there is a strong desire to bring them to clinical application. However, prior to any therapeutic and bioimaging studies comprehensive analysis of GQDs cytotoxicity has to be done in vitro. In our research, we assess the biocompatibility of a variety GQDs synthesized from different carbon-based precursors in non-cancerous cells through cell viability assay. Our results show that GQDs prepared from chitosan and glucosamine demonstrate 80% cell availability at 1.2 and 2.2 mg/mL concentrations, respectively, making them the most promising candidates for further therapeutic applications among over 15 GQD candidates tested.

The SARS-CoV-2 virus, which induced a global pandemic in 2020, is a serious pathogen that can cause acute respiratory distress in infected individuals. In order to garner a greater understanding of the SARS-CoV-2 virus and attenuate its effects, researchers have aimed to estimate key viral kinetic parameters. In this study, data from a previously published challenge study on the impacts of SARS-CoV-2 on young adults, including viral load, upsit score, and symptom score, was used to calibrate a system of ordinary differential equations, generating pathogenic parameters. In addition, Pearson covariance values and the Lyapunov exponents were calculated for each participant from the challenge study. For a majority of participants, the Lyapunov exponents were positive and finite, indicating chaotic behavior in vector space. Similarly, for most participants, there was a weak positive correlation between upsit/symptom scores and viral load. Future research will consist of implementing a newer system of ordinary differential equations that may be a better fit for the data

The SARS-CoV-2 pandemic initially made landfall in the United States in early 2020, and at that point in the pandemic, few developed treatments left the initial prevention of the disease largely up to preventative measures like mask mandates, quarantines for infected individuals, and social distancing policies. As a result, we must understand how preventative measures affect the transmission of infectious diseases to prepare us to fight the future spread of similar diseases. To accomplish this, we used a SEIR model with a variable transmission rate and fit SARS-CoV-2 case data to it. Principally, we used four models for the change in transmission rate: instant, linear, exponential, and logistic. Then using these models for the decay of transmission rate, we obtained SSR and parameter values that allowed us to compare models for each state. After comparing models between the four states we fit, there was no evident best-fit model for the decay in transmission. These results may suggest that regional differences like behavior, socioeconomic status, and exact preventative measures enforced could be responsible for the disparity in how the transmission rate decayed.

The most common immunological models for analyzing viral infections assume even spatial distribution between virus particles and healthy target cells. However, throughout an infection, the spatial distribution of virus and cells changes. Initially, virus and infected cells are localized so that a target cell in an area with lower virus presence will be less likely to be infected than a cell close to a location of viral production. A density-dependent rate has the potential to improve models that treat cellular infection probability as constant. A Beddington-DeAngelis model was used to understand how density dependent parameters could impact the severity of an influenza infection. Parameter values were varied to understand implications of density constraints. For low density dependence, a steeper increase in number of virus and greater viral peak was predicted. Higher density dependence predicted a longer time to viral load maximum and a greater infection duration. Initial localization of infected cells likely slows the progression of infection. The model demonstrates that accounting for density dependence when analyzing influenza infection severity can result in an altered expectation for viral progression. A density-dependent infection rate may provide a more complete view of the interaction between infected and healthy cells.

Mathematical models of cancer cells can be used by researchers to study the use of oncolytic viruses to treat tumors. With these models, we are able to help predict the viral characteristics needed in order for a virus to effectively kill a tumor. Our approach uses non-cancerous cells in addition to the tumor to determine when the virus will spread to non-cancerous cells. However, there are several models used to describe cancer growth, including the exponential, Mendelsohn, logistic, linear, surface, Gompertz, and Bertalanffy. We study how the choice of a particular model affects the predicted outcome of treatment.