Shreya Singh (URCAD)

Research Overview:

My capstone project examines physician burnout through a qualitative case study of Jillian Horton’s memoir, We Are All Perfectly Fine. In this project, I analyze Horton’s first-person reflections on burnout and compare her lived experience to the existing body of burnout literature in psychology and public health. I also interpret her experiences through the lens of Daniel M. Haybron’s Emotional State Theory of Happiness to explore how well this philosophical framework captures the subjective experience of burnout. By placing these perspectives in dialogue, my project evaluates the strengths and limitations of both empirical and philosophical approaches, ultimately investigating whether Haybron’s theory can offer unique insight into the nature of physician burnout.

Research Mentor: Fernando Vonhoff, Biological Sciences

Research Overview:

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by challenges in social interactions, communication, and atypical behaviors, with symptoms typically emerging in early childhood. Affecting about 1 in 100 children worldwide, ASD presents a wide range of abilities and needs. Synaptic elimination, or pruning, shapes neural circuitry by removing incorrect synaptic connections. Disruptions are linked to ASD. Over 100 genes are associated with ASD development. This project investigated the role of USP8, an autism associated gene, in synaptic regulation in Drosophila melanogaster larvae. Loss- and gain-of-function manipulations were compared with controls. Microscopy revealed increased ectopic synapses at the neuromuscular junctions (NMJ), possibly indicating that both reduced and elevated USP8 activity disrupt synaptic development and synaptic pruning. Further analysis of cIVda sensory neuron projections in the central nervous system (CNS) showed increased axonal projection volume for both loss- and gain-of-function genotypes, but imaging revealed distinct morphological differences. Behavioral assays showed altered nociceptive responses across groups. These results point to a dose-dependent requirement for USP8 in synaptic development and provide insight into how dysregulated synaptic pruning may contribute to ASD.