Two Duke Internal Medicine Residents selected for new NHLBI and NIAID R38 grant funding

Tuesday, January 15, 2019

Two Duke Internal Medicine Residents have been selected for the Duke Stimulating Access to Research in Residency Program (StARR), a new program that is funded by two R38 grants from the National Heart, Lung, and Blood Institute and the National Institute of Allergy and Infectious Diseases.

The awards reflect a collaborative effort among multiple PI investigators and departments, including Scott Palmer, MD, MHS, professor of medicine and immunology; Sallie Permar, MD, PhD, professor of pediatrics, immunology, and molecular genetics and microbiology; and David Harpole, MD, professor of surgery and pathology.

Junior assistant residents Jessica Regan, MD, and Sonali Bracken, MD, PhD, will begin the R38 StARR research training pathway in July 2019.

“Both Jessica and Sonali submitted outstanding applications and show great promise as physician-investigators,” Dr. Palmer said. “I am thrilled we have the R38 StARR research pathway available to support our Duke residents; this novel grant mechanism will give them protected time and mentorship to help launch their academic research careers at this early stage.”

Dr. Regan, with support from mentor Svati Shah, MD, MHS, will investigate the role of Clonal Hematopoiesis of Indeterminate Potential (CHIP) in cardiovascular disease.

“My ultimate research goals are to better understand genetic risk, metabolic pathways and inflammation in cardiovascular disease to improve clinical outcomes for patients. The support provided through this dedicated research track will provide a platform to build upon in my career as an academic clinician investigator,” Regan said. Learn more about Regan’s research.

Dr. Bracken, with support from mentor Donghai Wang, PhD, will investigate the role of the protein geranylgeranylation in the pathogenesis of rheumatoid arthritis, specifically examining the molecular mechanisms by which geranylgeranylation affects T cells that, when imbalanced, cause the chronic, autoimmune disorder. Learn more about Braken’s research.

“I am extremely excited to be among the first to take advantage of this exciting, new opportunity and am overwhelmed by the willingness of the Duke Internal Medicine Residency Program and by the Duke University School of Medicine to support the mission of aspiring physician-scientists like myself,” Bracken said.

The Duke R38 StARR research pathway in the Department of Medicine is a 4-year internal medicine residency that incorporates 18 months of protected time for research for residents who are committed to a career as a physician-investigator in academic medicine.

Residents appointed to the R38 StARR research pathway are given support and mentorship to establish a track record of scholarly activities, including submission of an application for an external individual career development award; participation in scientific meetings; and submission of research manuscripts to peer-reviewed journals.

“We have been fortunate to have the full support of Aimee Zaas, MD, MHS, program director, Duke Internal Medicine Residency and associate professor of medicine (Infectious Diseases), to assist in identifying promising candidates and provide support during residency for their protected research time,” Palmer said.

Maria Price Rapoza, PhD, executive director of the Duke Cardiovascular Research Center, works closely with Palmer to implement the program within the Department of Medicine.

R38 StARR Resident Research

Sonali Bracken, MD, PhD
Junior Assistant Resident
MD, University of Connecticut School of Medicine
PhD, Immunology, University of Connecticut
Mentor: Donghai Wang, PhD, professor of medicine (Rheumatology and Immunology) and Immunology

Bracken's Research

I will be investigating the role of protein geranylgeranylation (a specific type of post-translational protein modification) in the pathogenesis of rheumatoid arthritis.

Rheumatoid arthritis is a chronic, autoimmune disorder that affects over 1 million Americans and 1% of the population worldwide. This disease is predominantly mediated by an imbalance in pro-inflammatory and regulatory T cells, with the latter being dominated by the presence of pathogenic T helper 17 (Th17) lymphocytes in patients with this disorder.

The Wang lab has exciting new data to suggest that inhibiting protein geranylgeranylation can restore the balance and function of regulatory T cells while simultaneously inhibiting the detrimental affects of Th17 cells. 

The aim of my proposal is to elucidate the molecular mechanisms by which protein geranylgeranylation affects this T lymphocyte balance and particularly the stability of regulatory T cells. I will be combining my expertise in basic immunology with cutting-edge technologies in biochemistry and metabolomics in order to answer these questions.

Over the 18-month fellowship period, I hope to establish a mouse model of rheumatoid arthritis in the Wang lab and use this model system to engage in the aforementioned basic and mechanistic studies. I will be testing the efficacy of blocking protein geranylgeranylation by small molecule inhibition in the treatment of rheumatoid arthritis.

Should these studies show promise, my ultimate goal is to target this pathway as an avenue for the treatment of rheumatoid arthritis in human subjects during my years as a clinical fellow. I hope that this dedicated research period will afford me time to learn new techniques and develop the systems that I will need to establish to "jumpstart" the work in which I will engage after I complete my internal medicine residency. 


Jessica Regan, MD
Junior Assistant Resident
MD, Virginia Commonwealth University
Mentor: Svati Shah, MD, professor of medicine (Cardiology) and associate director of clinical translation, Duke Molecular and Physiology Institute

Regan's Research

The focus of my research is examining the role of Clonal Hematopoiesis of Indeterminate Potential (CHIP) in cardiovascular disease. Unlike germline genetic variants that patients are born with, CHIP is the presence of expanded somatic clones in the blood in the absence of other hematologic abnormalities and CHIP mutations have been shown to increase with age. CHIP has been linked to the development of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) and a increased risk of all-cause mortality.

More recent data, that helped inspire the project I will work on as part of the R38 research pathway, has linked CHIP to cardiovascular disease. This association makes CHIP a novel biomarker for cardiovascular disease risk; however, the mechanisms of how this relationship is mediated are not well understood. My goal is to help explain this relationship through looking at intermediate cardiometabolic risk factors and the underlying metabolic pathways that may be dysregulated in CHIP. 

During the course of of the R38 research pathway I will gain experience in complex genetic and statistical analysis and have the opportunity to attend research seminars and hope to ultimately present my research at national conferences.