A Computational Model of Progressive Multifocal Leukoencephalopathy (Update 2)

As my fourth week of summer research draws to a close, I wanted to provide another update on my progress. I’ve been working on a computational model showing the cellular interactions that allow the reactivation and spread of the JC virus, which is the cause of the opportunistic infection Progressive Multifocal Leukoencephalopathy. For the past two weeks, my primary focus has been on transcription factors and the role they play in viral infection. Specifically, I looked at transforming growth factor beta 1 (TGF-B1), tumor necrosis factor alpha (TNFa), and nuclear factor kappa beta (NFkB). All three of these factors promote viral transcription, furthering the spread of the JC virus throughout the body, and most devastatingly, the brain.

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Field Work: Coring Lakes in Lofoten, Norway

In northern Norway, general trends of sea level lowering throughout the Holocene have been developed, with sea level in this area lowering ~10m over the past 6000 years. However, the details of this lowering are poorly constrained during the late Holocene (the past ~5000 years) (Møller, 1986). For my senior research project, I am studying sediment records from isolation basins (coastal lakes characterized by their past connection to and isolation from the sea due to relative sea level changes) in Lofoten, Norway. Using these sediment cores, I hope to better constrain the rate and magnitude of sea level lowering during the late Holocene in Norway and to understand how these changes may have affected human activity (think: Vikings) in Lofoten.

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