md/phd candidate · rna biologist · computational pathology
I’m a physician-scientist in training at The Ohio State University, finishing my MD in the NIH-funded Medical Scientist Training Program. My PhD in Biomedical Engineering asked how a single chemical mark on messenger RNA, m6A, shapes the way the heart responds to stress and how the heart uses it to signal to the rest of the body. That work was supported by an NIH F30 fellowship and led to first-author papers in Circulation, JCI Insight, and RNA.
These days I’m focused on pathology and on how machine learning is changing it: I’m training clinically in pathology and have annotated whole-slide images for computational pathology research. I trained in the U.S., in Italy as a Fulbright Scholar, and in Germany. I’m also active in biotech entrepreneurship through Nucleate.
Long-form, illustrated guides to the fields I work in. Written for curious scientists, clinicians, and engineers.
A field guide · RNA biology
Seventy years of RNA in seven parts, from the discovery of the messenger to splicing, microRNAs, the m⁶A epitranscriptome, my own work on RNA methylation in the heart, RNA drugs, and what machine learning can and can't yet do with RNA.
A field guide · RNA therapeutics & biotech
The business side of RNA medicines: the modalities, why chemistry and delivery became moats, how Ionis, Alnylam, and Moderna were built, pricing, dealmaking, what goes wrong, and how I'd evaluate an RNA startup.
A field guide · AI in pathology
From Virchow's microscope to gigapixel slides, CAMELYON16, weakly supervised learning, self-supervised foundation models, and vision–language copilots, plus an honest look at what keeps AI from the sign-out desk.
My PhD asked how one chemical mark on messenger RNA, m6A, shapes the way the heart responds to stress, and how the heart uses it to signal to the rest of the body.
1 Circulation · 2024 first author
Nanopore direct RNA sequencing mapped METTL3-dependent m6A sites in adult cardiomyocytes. Whether the mark fell in the coding sequence or the 3′ UTR tracked with differences in protein output, and it pointed to targets in mitochondrial metabolism.
read the paper →2 JCI Insight · 2025 first author
On a Western diet, deleting METTL3 in cardiomyocytes protected mice from the diet's harmful effects, while raising it worsened weight gain, adiposity, and glucose intolerance. Cardiac m6A stabilizes FGF1 mRNA, a heart-to-fat signal.
read the paper →3 RNA · 2025 first author
Mice lacking YTHDF3 in cardiomyocytes showed less pathological remodeling after pressure overload. YTHDF3 controls stress-induced protein synthesis and cardiomyocyte size, which makes it a candidate cardioprotective target.
read the paper →MD (expected 2027) · Medical Scientist Training Program, NIH/NIGMS
PhD, Biomedical Engineering (2025) · Dissertation: At the Heart of the Epitranscriptome: METTL3, m6A, and the YTHDF Proteins in Cardiac Disease · Advisor: Federica Accornero, PhD
Credential of Readiness (CORe) with Honors (2025) · Business Analytics, Economics for Managers, Financial Accounting
BS, Biomedical Engineering, summa cum laude (2018) · Engineering Honors Academy · Aresty Research Scholar
Fulbright Scholar, Molecular Medicine Laboratory (2018–2019)
DAAD RISE Scholar, Cardiovascular Research (2017)
American Heart Association Undergraduate Fellow, Rosenzweig Lab (2016)