2015

Dr. Herazo-Maya is an instructor in medicine in the Section of Pulmonary and Critical Care at Yale University. He obtained his MD degree at the University of Cartagena School of Medicine in Colombia. In 2008, he became a post-doctoral research fellow at the University of Pittsburgh, Simmons Center for Interstitial Lung Disease, under the mentorship of Dr. Naftali Kaminski, where he worked in the area of functional genomics, molecular biology, and bioinformatics. He completed his internal medicine residency at the University of Pittsburgh and Pulmonary and Critical Care Medicine Fellowship at Pittsburgh and Yale.

Dr. Herazo-Maya’s research focus is the identification of molecular profiles associated with increased mortality in idiopathic pulmonary fibrosis (IPF) using high-throughput “omic” technologies and precision medicine approaches. His ultimate goal is to identify new therapeutic targets for IPF that can improve patient survival. His previous research demonstrated a 52-gene signature that predicted survival in IPF and tied these gene expression changes with shifts in immune cell subpopulations. Most recently, he has developed an interest in studying microRNAs in serum as potential diagnostic and prognostic biomarkers in IPF and their mechanistic role in disease severity and progression.

Dr. Kropski is an assistant professor of medicine in the Division of Allergy, Pulmonary and Critical Care Medicine at Vanderbilt University in Nashville, Tennessee. He obtained his undergraduate degree from Davidson College and completed his medical education, internal medicine residency, and pulmonary/critical care fellowship at Vanderbilt. Dr. Kropski’s research interest focuses on determining the molecular mechanisms that mediate the early pathogenesis of pulmonary fibrosis, with an emphasis on the role of genetic factors that influence alveolar epithelial injury and repair. As a fellow working under Dr. Timothy Blackwell, Dr. Kropski identified mutations in DKC1 and RTEL1 as the basis for disease in some families with pulmonary fibrosis. His independent work now utilizes cell and animal-based models to determine the mechanisms through which these and other genetic risk factors for pulmonary fibrosis contribute to the development of disease. His ultimate goal is to use genetic and genomic profiling to develop rational and specific therapies for patients with pulmonary fibrosis.