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Nicolas has a B.S. in Biology from Case Western Reserve University. When he’s not in the lab, you can find Nicolas at the campus pottery studio, tending to his succulents, or out with friends.
- Genome-wide cell type-specific and sex-specific transcriptional dysregulation in the islet of Langerhans underlies islet dysfunction in Down syndrome-related diabetes
- The RNA-binding protein CPEB1 marks healthy adult β cells in mice but is dispensable for β cell identity and function
- Kidney deletions of Cyp27b1 fail to reduce serum 1,25(OH)<sub>2</sub>D<sub>3</sub>
- TIFAB modulates metabolic pathways in KMT2A::MLLT3-induced AML through HNF4A
The risk of developing type 2 diabetes (T2D) has increased five percent yearly over the past decade, yet young adults with Down syndrome have a ten-fold higher probability. Although elevated BMI at younger ages may contribute to this increased risk for T2D, the trisomy of Dyrk1a and Rcan1 on chromosome 21, previously shown to decrease beta cell proliferation when overexpressed, represents a novel genetic explanation. We hypothesize that genetically stunted beta cell proliferation during metabolic stress increases the risk of T2D for individuals with Down syndrome. Utilizing the Ts65Dn mouse model of Down syndrome, I aim to distinguish the rate of pancreatic islet proliferation during metabolic stress and determine why it differs from wild-type mice.