Office of Undergraduate Research

Permanent URI for this communityhttp://hdl.handle.net/1903/20157

Emphasizing equitable and inclusive access to research opportunities, the University of Maryland's Office of Undergraduate Research (OUR) empowers undergraduates and faculty to engage and succeed in inquiry, creative activity, and scholarship. This collection includes materials shared by undergraduate researchers during OUR events. It also encompasses materials from Undergraduate Research Day 2020, Undergraduate Research Day 2021, and Undergraduate Research Day 2022, which were organized by the Maryland Center for Undergraduate Research.

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    Novel Computational Methods for the Comparison of Leishmania Genomes and Transcriptomes
    (2024-04) Klimes, Daniel; Belew, Trey; El-Sayed, Najib
    Leishmania is a genus of protozoan parasites and the causative agent of Leishmaniasis. Twenty-one infectious species have been identified, with many previously being investigated by DNA and RNA-sequencing. However, significant genetic variation has prevented the comparison of this data across Leishmania species. Gene orthology grouping fails to compare over 70% of Leishmania genes’ expression across multiple species because of this variation. Here, we describe a novel method to reliably compare the genomes and transcriptomes of multiple Leishmania. This method produces a hybrid genome from the genetic sequence of any Leishmania species, while containing the rich sequence annotations of the L. major reference genome. In a demonstrative analysis, our approach allowed the comparison of 87% of genes in L. major against 5 other Leishmania species. Significant genetic variation was found to prevent comparison of many virulence-implicated genes, including surface antigens (e.g. amastins), cysteine proteases, and HSP-83. Within genes that could be compared, parasite transcriptomes segregated primarily by developmental stage (promastigote and amastigote). Transcriptomes secondarily separated by species. Genes upregulated in infection across all Leishmania were identified and included surface amastins, methyltransferases, and an apoptosis inhibition factor. Downregulated genes showed significantly greater sequence conservation than upregulated genes and comprised paraflagellar, flagellar, and HSP-70 proteins among others. The transcriptome differences between the clinical manifestations of leishmaniasis were additionally characterized. Taken together, these results provide much needed insight into the shared Leishmania pathway of infection and survival.
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    The Role of Lipid Metabolism in B Cell Immune Functions
    (2020) Beher, Richa; Song, Wenxia
    Evidence indicates that lipid accumulation due to obesity triggers a low-grade, chronic inflammation, which is correlated with the occurrence of Type 2 diabetes (T2D). Recent studies provide evidence for the essential role that B cells play in obesity-induced inflammation and the development of insulin resistance. In visceral adipose tissue (VAT), B cells generate self-reactive antibodies (autoantibodies), which increase their pathogenicity. They also activate the production of cytokines by T cells through antigen presentation. Lastly, B cells themselves increase the production of inflammatory cytokines while decreasing the production of the anti-inflammatory cytokine IL-10. We hypothesize that neutral lipid accumulation exclusively in B cells will cause them to infiltrate VAT, trigger autoantibody production, and develop an autoimmune pathology. Preliminary research has led to the generation of a B cell-specific CGI-58 knockout (BKO) mice model in order to induce neutral lipid accumulation in B cells. It was found that increased accumulation of triglycerides in CGI-58 BKO mice significantly increased the levels of spontaneous activation in B cells, shown by the increases in the number of germinal center B cells, the surface expression levels of B cell activation markers, and the number of infiltrated lymphocytes in VAT, compared to Flox controls. The goal of this project is to determine the mechanism by which B cell lipid metabolism regulates B cell activation and pathogenicity in obesity-associated insulin resistance.