I am working in the Kurtis lab with the mission to combat P. falciparum malaria. Malaria continues to be a leading global infectious disease, claiming the lives of over 1,000 children daily. Our research is focused on developing vaccines, small-molecule drugs, and monoclonal antibodies designed with novel targets in mind, such as PIGARP.

I am currently investigating the effects of drugs on chemosensitivity and blood brain barrier permeability for treatment of Diffuse Intrinsic Pontine Glioma(DIPG). DIPG is a highly invasive pediatric brain tumor that affects children with a median age of 6-7 years old. There are currently no therapies that target invasion and a major obstacle for treatment is the blood brain barrier(BBB) which prevents the delivery of effective concentrations of drug into the brain. In the Lawler lab, we are working to provide a potential new therapeutic approach for the treatment of DIPG blocking invasion and enhancing drug delivery across the BBB.

High-aspect-ratio nanoparticles (HARPs) exhibit an extraordinary ability to stimulate activation, proliferation, and death in various cell types. We aim to use this platform to fabricate functionalized poly(caprolactone) (PCL) nanowires to target and influence immune cell activity. In the Desai Lab, my research focuses on evaluating the versatility of this platform in conjunction with novel antibody therapies in an effort to impact the treatment of immune-related morbidities.

Vascular remodeling is a prominent phenotype of Pulmonary Hypertension (PH), a deadly condition with unknown causes and no known treatment. Using in vivo models of pulmonary vascular disease, our lab has identified CHI3L1 and its receptors as major contributors of PH responses. My goal is to study the mechanisms that underlie vascular remodeling in PH and develop nanoparticle-based drug delivery systems against CHI3L1 and its receptors to treat vascular remodeling in PH.

My work focuses on understanding the structure and function of mutations within the hnRNPA2 RNA binding proteins that have been demonstrated to cause the formation of insoluble fibrils associated with a number of neurodegenerative diseases. This work will provide a better understanding of how RNA regulates hnRNPA2 granule assembly, and could also provide the basis for rational design of nucleic acid-based drugs that disrupt disease-causing hnRNPA2 mutants.

My work focuses on investigating how sex differences in gene expression contribute to the onset and progression of neurodegenerative disease. I use single-nucleus RNA-seq datasets from both Drosophila and mouse models of tauopathy, to build and refine customized pipelines to identify sex-specific transcriptional changes across time and genotype.

I am working in Marty Taylor's lab focusing on molecular biology, biochemistry, and cancer biology. My research centers on the mechanistic biology of LINE-1 retrotransposons and how retroelements can be leveraged as a therapeutic tool.