Start Date  August 30, 2013

I started to work in the biology research lab at Mount St. Mary's University during my sophomore year. I aided Dr. Christine McCauslin with her research concerning the neuroinflammatory pathway in the central nervous system mediated by the protein High Mobility Group Box 1 (HMGB-1) as a response to infection, sterile injury, and neurodegenerative diseases, including Amyloid Lateral Sclerosis, Alzheimer's disease, and Parkinson's Disease. There has been evidence that has shown that the transcription factor CCAAT/enhancer binding protein β (C/EBP β) plays a critical role in glial cell activation and in the progression of the inflammatory response. The expression of this transcription factor increases when the glial cells are activated during an inflammatory response. HMGB-1, which is functionally important in regulating transcription processes, is rapidly released from necrotic cells into its surroundings and causes the activation of glial cells. It is known that C/EBP proteins are involved in promoting expression of pro-inflammatory gene products and are upregulated in activated glial cells after being exposed to HMGB-1. Thus, this led to the hypothesis that C/EBP β could be a downstream effector to HMGB-1 exposure. My work focused on observing the activation of the transcription factor C/EBP β after the cells were treated with HMGB-1. I performed many different time course treatments to observe the expression of C/EBP β in C6 cells related to the amount of time the cells were exposed to HMGB-1. I wanted to determine whether the expression of C/EBP β would increase when they were exposed. Through western blotting analysis, I was able to see that the expression of the transcription factor did in fact increase with a longer exposure to HMGB-1. After these initial results, I was able to repeat the experiment using primary mixed glial cell cultures derived from two-day old mice brains. These new cells, more similar to glial cells in the human brain, are more sensitive than the C6 cells. While working with these new cells, I was able to learn new skills in troubleshooting and method optimization. With the primary cells, I also worked on cell staining and characterization in order to show with certainty that we were working with the cells we needed. I plan to expand my research by exploring the role of C/EBP δ in the neuroinflammatory response. Dr. McCauslin and I believe that it plays an important role in cell regeneration and healing.


I started to work in the chemistry research lab at Mount St. Mary's University during my senior year. In Dr. Christopher Bradley's lab, I was assigned a couple of different experiments. The first one consisted of adding indenyl groups to both nitrogens of piperazine. This data will help us further analyze bonding relationships of bulky groups on a six-membered ring. We hope to expand this to binding three indenes on a six-membered ring using nitrogens, as well as different halogen atoms. The second experiment I was tasked with was synthesizing a large and bulky ligand, which a colleague will then use to attempt to bind three cobalt atoms together with these ligands attached to each cobalt. I reacted indene with an aryl iodide with a palladium catalyst. After NMR and IR analysis, we will be able to observe if we successfully bound two indenes to the benzene ring of aryl iodide. We hope that these bulky will allow three cobalt atoms to form a cyclic cobalt complex.