Phi Kappa Phi Student Research and Fine Arts Conference

Permanent URI for this communityhttps://hdl.handle.net/10675.2/624598

The annual Phi Kappa Phi Student Research and Fine Arts Conference is an opportunity for all students at Augusta University, regardless of disciplines, to showcase their scholarly and artistic endeavors. Participating students were competitively selected from abstracts of their proposed conference projects. The proposed project may have been presented elsewhere or be expected to be presented elsewhere, and it must endorsed by a full-time Augusta University faculty member. The conference is open to all undergraduate students. Students and faculty sponsors are not required to be members of Phi Kappa Phi. All presentations are assessed by faculty judges, with awards given to the top presenters in each session.

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Browsing Phi Kappa Phi Student Research and Fine Arts Conference by Author "Bradford, Jennifer"

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    CHARACTERIZATION OF NF-¿B DEFICIENT BONE-MARROW MACROPHAGES
    (2/12/2018) Pepper, Anthony; Fischer, Jeffrey; Augusta University; Department of Biological Sciences; Bradford, Jennifer; Department of Biological Sciences
    The aim of this study was tocharacterize bone-marrow derived macrophages (BMDMs) that lack canonical nuclear factor-kappaB (NF-?B) signaling. The macrophages for the study were obtained by harvesting the bone-marrow fromp65LysMCre (KO) mice and LysMCrecontrolmice.To determine NF-?B deletion efficiency, p65 (a transcription factor in the canonical pathway) protein levels were evaluated by fluorescent microscopyin bothKOand control BMDMs that had been stimulated withlipopolysaccharide(LPS).The induction ofiNOSwasmonitoredin KO and control BMDMswhenactivated by NF-?B stimulatorsIFN-?andLPS.The regulation of iNOSwas assessedby comparing macrophages that had been treated withLPS, IFN-?, or both to a control treatment under fluorescent microscopy. In addition to staining, a nitric oxide assay was employed to help determine the extent of iNOS activity.The macrophages were also visualized under light microcopyby comparing macrophagesthat were stimulated with LPS andIFN-?tounstimulated cellsusing fluorescence microscopy.Currently,a caspase assay is in progress to help further evaluate the effects of p65 losswithin macrophages.
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    Effect of NF-κB Deletion on Bone Marrow Macrophage Respiratory Burst Ability
    (1/31/2020) Soni, Karan; Bradford, Jennifer; Augusta University; Biological Sciences; Bradford, Jennifer
    The nuclear factor-kappaB (NF-κB) signaling pathway is very important in normal immune system function and is also often aberrantly regulated in many different types of cancers. As many cancers are characterized by elevated numbers of infiltrating monocytes/macrophages, we have developed an animal model that lacks canonical NF-κB signaling in bone-marrow derived macrophages (BMDMs). As BMDMs can infiltrate solid cancers, the aim of this particular study was to assess the functionality of phagocyte oxidase ability in NF-κB deficient BMDMs. A respiratory burst assay involves stimulating the phagocyte oxidase enzyme in macrophages to release reactive oxygen species (ROS) so that they can degrade and combat invading pathogens as well as cancer cells. Based on our recent experiments that showed BMDMs lacking p65 had poor phagocytosis ability and low nitrite production, we hypothesize that BMDMs lacking NF-κB signaling will have a decreased respiratory burst response compared to control BMDMs.
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    Isolation and Culture of Microglia
    (2/12/2018) Doughty, Deanna; Venugopal, Natasha; Augusta University; Department of Biological Sciences; Bradford, Jennifer; Department of Biological Sciences
    Glioblastoma (GBM) is the most aggressive and common adult brain tumor subtype, with the majority of patients surviving less than one year. The GBM microenvironment is composed of tumor cells as well as non-cancerous cells, such as microglia, a component of the immune system in the brain. To better understand the role of microglia in GBM, we have optimized in vitroculture conditions for primary microglia. Growing microglia in culture is challenging, but this technique is needed for planned future experiments. Microglia were isolated from mouse neuronal tissue by magnetic bead antibody cell separation using the cellular marker CX3CR1. Isolated microglia were then cultured in various culture conditions, and cellular morphology by light microscopy was used to determine cell health, viability, and activation status. It was determined that the primary microglia grow best in neurobasal media in wells coated with poly-D lysine. Future studies aim to isolate a larger number of cells to allow forco-culture of the inactivated microglia with GBM cells. These results will allow us to better understand the role that microglia play in GBM progression.
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    Production of a NF-¿B Deficient Microglial Animal Model
    (2/12/2018) Goodall, Michael; Soni, Karan; Augusta University; Department of Biological Sciences; Bradford, Jennifer; Department of Biological Sciences
    Our goal is to determine how the nuclear factor-kappaB (NF-?B) signaling pathway is used in the communication between microglia and the progression of glioblastoma (GBM) cancer cells. The NF-?B signaling pathway is very important in normal immune system function and has been implicated in various types of cancers, including, GBM. GBM is the most common type of adult brain cancer, has altered NF-?B signaling, and is also characterized by a large population of microglia, the immune cell of the central nervous system. Based on our recent studies, we hypothesize that deleting the major transcription factor (p65) of the canonical NF-?B pathway in microglia would slow the progression of GBM. To test this hypothesis, we have developed a p65fl/fl/CX3CR1CreERtransgenic animal, which should lack microglial p65 after exposure to tamoxifen. We currently have heterozygous animals and will soon begin characterizing them to determine p65 deletion efficiency.
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    THE ROLE OF CXCL10 AND NF-KB SIGNALING IN MACROPHAGE INFLUENCE ON BREAST CANCER INVASION
    (2/13/2019) Mikulsky, Emilee; Augusta University; Department of Biological Sciences; Bradford, Jennifer
    Breast cancer is the second most deadly cancer with more than 260,000 people being diagnosed, and over 40,900 dying from it annually in the United States. This project focuses on triple negative breast cancer (TNBC), which is very aggressive due to the lack of hormone receptors. TNBC is characterized by an expansive stromal compartment that contains a large percentage of immune system macrophages, which correlates with poor patient prognosis. The Bradford lab has identified that the chemokine CXCL10 was found to be decreased at the mRNA and protein levels in TNBC cells when co-cultured with macrophages. The loss of CXCL10 might result in less destruction of tumors. To better understand the decrease in CXCL10, a cell invasion assay investigating invasion ability of the MDA-MB231 TNBC cell line was completed using macrophage conditioned media, with and without recombinant CXCL10, or a CXCL10 neutralizing antibody. We also investigated whether the NF-kappaB signaling pathway was involved by using primary bone marrow-derived macrophages from a NF-kappaB knockout mouse. The cell invasion assay showed that altering CXCL10 and NF-kappaB signaling in macrophages and/or the MDA-MB231 cells leads to differences in invasion ability.