For over 25 years, I have conducted both basic and clinical research exploring the pathophysiology underlying diabetes. My efforts have spanned from epidemiological studies relating to patient outcomes following pancreas transplantation, to clinical trials (islet transplantation, immunotherapy trials, and efforts attempting to promote beta cell regeneration), to animal models using (as appropriate for the question being addressed) non-human primates or mice, to cellular (studying pancreatic beta cells and the islet inflammatory infiltrate underlying T1D), to molecular (gene expression studies, promoter analyses, insulin splice forms). In February 2010, I accepted an offer from the University of Massachusetts to serve as Co-Director of their recently established Diabetes Center of Excellence, and Chief of the Diabetes Division within the Department of Medicine. My current basic research focuses on better understanding of beta cell biology, testing techniques to block the immune mediated beta cell killing underlying T1D, and developing better diabetes care delivery models. My team has developed innovative techniques to sort human pancreatic islet endocrine cell subsets, including from donors with diabetes (T1D and T2D) to determine the transcriptome from those purified cells. We have also rejuvenated diabetes care at UMass, more than tripling clinic volume in 6 years, and developing novel communication tools to better engage patients in their own care.
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Key: MeSH Term KeywordAdolescent Adult Amino Acid Sequence Beta cell Biomarkers CD4-Positive T-Lymphocytes Child, Preschool Dendritic Cells Diabetes Mellitus, Type 1 Epitopes Female Fetus Gene Expression Profiling Glucagon-Secreting Cells Humans Hypoglycemia Islets of Langerhans MafB Transcription Factor Male Mice, Inbred C57BL Mice, Inbred NOD Middle Aged Molecular Sequence Data Peptides Pregnancy Trimester, Second Primates Rats Rodentia Sequence Analysis, RNA Single-Cell Analysis Somatostatin-Secreting Cells