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Hugh O’Brodovich, MD FRCP(C) is the Arline and Pete Harman Professor of Pediatrics (Emeritus) at the Stanford School of Medicine. He was the chair of the Department of Pediatrics at Stanford University School of Medicine and the Adalyn Jay Physician in Chief at Lucile Packard Children's Hospital from January 2008 through June 2016. Prior to his arrival at Stanford University he was the Chair of Paediatrics at the University of Toronto and the Paediatrician in Chief at the Hospital for Sick Children (SickKids) during which time he was the inaugural President of the Pediatric Chairs of Canada. In 2010 he became the inaugural Director of the Stanford Child Health Research Institute. His laboratory conducted research on how the lung’s airspaces become fluid filled (mechanisms of pulmonary edema), how airspace fluid is cleared under both physiologic (fetal lung liquid at birth) and pathophysiologic (pulmonary edema) conditions and population-based studies to discover genetic influences on the development of bronchopulmonary dysplasia and the long term outcomes of neonatal lung disease. Dr. O'Brodovich has been the Chair of the Pediatric Pulmonology Sub-Board of the American Board of Pediatrics, an Associate Editor of the American Review of Respiratory Disease, Editor of Pediatric Research, member of the editorial board of the American Journal of Physiology and President of the Fleischner Society. He served on the Council of the American Pediatric Society from 2011 to 2016. He has published 177 peer reviewed manuscripts, 23 book chapters, 1 book and was elected as a Fellow of both the Canadian Academy of Health Sciences and the American Association for the Advancement of Science. Currently, he is the Chair of the Board of Directors for Headwaters Health Care Centre.
I am interested in the mechanisms resulting in, and new therapies to prevent and treat, the respiratory distress syndrome (RDS) and its sequelae, bronchopulmonary dysplasia (BPD). Previous research focused on how the lung's airspaces become fluid filled (mechanisms of pulmonary edema) and how airspace fluid is cleared under both physiologic (fetal lung liquid at birth) and pathophysiologic (pulmonary edema) conditions. Since the rate limiting step in airspace fluid clearance is the active transport of Na+ by distal lung epithelium, our studies investigated the effect of lung maturity, mediators and hormones on the pre and post-translational regulation of the epithelial Na+ channel (ENaC). More recent research focused on:- perinatal risk factors that are associated with long term clinical outcomes of infants and children with BPD.- identifying the genetic factors that explain the heritability of BPD, currently estimated to explain 50-80% of the risk for BPD. Population based studies have used both Genome Wide Association Studies (GWAS) and exome sequencing to identify genetic risk factors for this significant long term pulmonary disorder.