MD Candidate UCSF School of Medicine | 2026
A.B. Cornell University | 2018

Tell us about your career goals?
My goal is to become an orthopedic surgeon-scientist and combine clinical questions with basic science solutions. Beyond research, I hope to help mentor the next generation of doctors. Mentorship played a huge role in shaping my path, and I want to provide that same support and opportunity to others.

Who are your academic/scientific mentors?
Two of my primary mentors are Dr. Brian Feeley and Dr. Sigurd Berven. When I first came to UCSF, I started working with Dr. Berven on clinical research. He taught me how to identify problems that genuinely interested me, how to approach them scientifically, and how to find meaningful answers. Later, during a clinical elective, I met Dr. Feeley and learned about the basic science work happening in his lab. I had always wanted to be involved in basic science, and he gave me space to explore ideas and develop as a scientist. Watching how both of them translate research into better patient care shaped my vision of the kind of physician I hope to become. And of course, I’ve been fortunate to have many other mentors along the way who have helped me grow.

Tell us more about why you decided to participate in the 3-minute original research pitch this year?
I first learned about the competition through the ORS newsletter and thought it would be a great opportunity to share our work in a different format while learning what others were working on in the field. I also wanted to hear how others interpreted the work we were doing and the questions it raised for them, which could help us consider directions we had not explored yet.

Tell us about how the notion of exploring the endogenous antimicrobial properties of FAP came about?
We know that fibroadipogenic progenitors (FAPs) play a role in fracture healing, so we began asking what happens in the setting of infected fractures, which have much higher rates of nonunion. During early pilot experiments, we had a surprising observation that the FAPs appeared to be killing bacteria. This activity was only seen in FAPs from younger patients and was absent in older patients. Although this antibacterial behavior has been described in other mesenchymal cell populations, what makes FAPs unique is their location and that they should almost always play some role at the fracture site making this more biologically and clinically relevant.

What are the clinical implications of your 3MT results?
There are two major implications. One, it emphasizes the importance of preserving muscle near a fracture site after trauma. Muscle may act not only as a physical barrier, but also as an immunologic barrier that helps reduce infection risk. Two, if we can identify what FAPs secrete to kill bacteria, we may be able to use these factors or induce their production to treat or prevent infection. This is especially important as antibiotic resistance is on the rise and could serve as a complementary strategy along with traditional therapies.