Syphilis is a sexually transmitted infection (STI) caused by the bacterium Treponema pallidum subspecies pallidum (T. pallidum). Syphilis is still a global health concern, as its incidence is rising in high-income countries like the United States and it is still endemic in low-income countries, where it causes significant mortality due to congenital transmission. Our chances at syphilis control would improve if a vaccine against syphilis was available. The past century of research has only yielded experimental vaccines able to produce partial protection, but the use of new techniques could improve this outcome. One possibility would be to use an array of known protective epitopes from other T. pallidum antigens crafted onto a protein carrier to induce a protective immune response. Currently, we are investigating the use of the Tp17 protein of T. pallidum as a scaffolding for a future vaccine. The Tp17 protein has a β-barrel structure with loops around the edges of the barrel. To use this protein as a scaffolding for a vaccine, we will be performing epitope mapping to determine the hierarchy of immunodominant epitopes in Tp17 to find the ideal candidate regions that will be substituted with other epitopes. We are using Enzyme-Linked Immunosorbent Assay (ELISA) to attain these data in combination with human sera to define the reactivity of the different peptides. The results will determine the most immunogenic peptides, thus indicating the ideal areas to be replaced by protective epitopes in a potential vaccine. We anticipate that several of the most reactive peptides will correspond to the protein loops outside of the β-barrel, which should be easily replaceable without affecting Tp17 structure.

In long term data collection, sampling is a key parameter that can dictate the amount of data collected and also influence the available conclusions to be drawn. In the context of passive acoustic monitoring, recording an area’s soundscape at intervals (i.e., subsampling based on duty cycles) can alleviate data management costs, and has been widely investigated in the bird monitoring literature. However, the influence of duty cycle-based subsampling in passive acoustic monitoring of bats has not been thoroughly studied. Here, we discuss the effects of subsampling on ultrasonic recordings collected using AudioMoth recorders in the Union Bay Natural Area in 2022. We recorded continuously over the summer and then computationally applied duty cycles onto our data to generate subsampled data. The subsampled data was then fed into multiple bat call detection algorithms to understand the influence of different subsampling schemes. Our results show that subsampling schemes can impact the trends and activities that can be acoustically observed from echolocating bats. The results also show how the subsampling parameters may be tuned to collect valuable information while keeping data management costs low. We anticipate that this detailed investigation will aid in the design of efficient, long-term bat acoustic monitoring projects.

Colorectal cancer (CRC) is a prevalent and often lethal form of cancer, with complex underlying biology and a wide range of associated risk factors. CRC is a significant global public health challenge, it is the second leading cause of cancer-related deaths in the United States. A growing body of research suggests that activin can stimulate the MAPK pathway which plays a critical role in the development and progression of CRC. In the context of colorectal tumors, innate immune cells such as macrophages, dendritic cells, and natural killer (NK) cells can both promote and suppress tumor progression. Macrophages, for example, can either promote tumor growth by secreting growth factors that stimulate angiogenesis and immune suppression, or they can suppress tumor growth by producing cytokines that activate T cells and other immune cells. In this study, our aim is to examine the relationship between activin and the MAPK signaling pathway in macrophages and to determine the role of macrophages in producing and responding to activin. We will be using RAW264.7 macrophage cell line to study the role of macrophages in cancer and Western blot to detect changes in specific proteins in macrophages stimulated with activin. We predict to see an increase in MAPK activation in activin-stimulated macrophages which will enhance tumor elimination. Our findings will also improve the understanding of the innate immune response to colorectal tumors and how it can be modulated by targeting activin signaling. This research will provide new insights into the complex interplay between the immune system and colorectal tumors and may inform the development of new diagnostic methods and more effective treatments.

Colorectal cancer (CRC) is the third most common cancer globally, and the second leading cause of cancer deaths in the US due to metastasis. The five year mortality rate of Stage IV CRC patients remains around 90%, and most treatments for stage IV CRC are palliative. Activin A, a cytokine that regulates proliferation and apoptosis, is known to induce metastatic phenotypes in CRC cells primarily through the PI3K/ AKT pathway. Glycogen synthase kinase-3 beta (GSK3β) is an enzyme downstream of AKT that regulates energy metabolism and apoptosis. An inactive form, phosphorylated GSK3β (pGSK3β), is unable to inhibit β-catenin activity, which promotes proliferation and epithelial to mesenchymal transition. Very few connections between activin A signaling in colorectal adenocarcinoma cells and GSK3β phosphorylation have been established in scientific literature. Our project aims to study the correlation between activin A signaling and pGSK3β by testing the hypothesis that activin A signaling induces phosphorylation of GSK3β in CRC tumor cells, promoting the attenuation of cell cycle arrest. We will perform Western blot analyses on FET cells treated with a vehicle control, activin A, or TGF-β, a cytokine that is activin-dependent in the context of CRC, to measure the levels of pGSK3β relative to GSK3β. We expect to see the highest levels of pGSK3β relative to GSK3β in FET cells treated with activin A and the lowest relative pGSK3β levels in cells treated with the vehicle control. The findings of this project can contribute to identifying biomarkers useful for risk stratification in metastatic CRC to provide more individualized treatments for patients.