Mentor: Dr. Dr. Todd Brusko
College of Medicine
"I was inspired to be a physician after meeting my own pediatrician at as a child and when I came to the University of Florida, I hoped to be involved in medical research affecting pediatric populations. Research has provided me with a new outlook on the science and technology behind the practice of medicine, and the ongoing advancements of these techniques."
Microbiology and Cell Science
- Type 1 Diabetes
- Bright Futures - 2012
- Howard Hughs Medical Institute (HHMI) Science For Life Award - 2014
- Pediatric Science Day 1st Place Student Presentation - 2015
- University Scholars Program 2015-2016
- Mobile Outreach Clinic
- Child Life Program
- Boys & Girls Club of Alachua County
Hobbies and Interests
- Foreign Languages
Multivariate Analysis of Immunophenotyping Studies in UFDI Patients
The University of Florida Diabetes Institute (UFDI) has pooled clinical and research data into a database that contains Type 1 diabetes (T1D) -associated autoantibody detection, T1D-associated single nucleotide polymorphisms (SNP) typing, C-peptide concentration, blood glucose levels, complete blood count (CBC), and flow cytometry analysis of immune cell subsets. The overarching objective of this analysis is to develop strategies for more personalized medicine which included therapies for T1D that are more patient-specific than those that exist currently. The information in the database was analyzed to assist in the comprehension of the relationships between Type 1 diabetics’ SNP-type and concentration of lymphocytes. Unsurprisingly, most of these genes are associated with T cell signaling and proliferation. Previous studies have conflicting claims over concentrations of lymphocyte subsets in patients with T1D. These results are the first indication that substitution mutations in nucleotide sequence within these genes can affect concentrations of lymphocytes in peripheral blood samples. The next step will be to analyze the flow cytometry data and to determine which subpopulations are being favorably skewed toward susceptibility and to determine if those populations play a role in causing the autoimmune destruction of the insulin-producing beta-cells in the pancreas.