Sam Hawgood, MB, BS
Dean, School of Medicine
Vice Chancellor, Medical Affairs
505 Parnassus Ave, Moffitt Hospital M696
University of California, San Francisco, Box 0110
San Francisco, CA. 94143 – 0110
Phone: (415) 476-9181
- 1970-1975, University of Queensland, Brisbane, Australia, M.B., B.S.,
- 1978-1980, Royal Children’s Hospital, Brisbane, Pediatrics Residency
University of California San Francisco, San Francisco, CA Neonatal Fellowship, 1982-84
- Monash University, Melbourne, Australia, Neonatal Fellowship, 1981
- Royal Australasian College of Pediatrics 1982
• University of California San Francisco, Department of Pediatrics, Assistant Professor, 1996-99
• University of California San Francisco, Department of Pediatrics, Associate Professor, 1999-2004
• University of California San Francisco, cardiovascular Research Institute, San Francisco, CA, Postdoctoral Fellow (Laboratory of John Clements), 1982-84
- Lung development and biology
Dr. Sam Hawgood is currently the W.H. and Marie Wattis Distinguished Chair of Pediatrics, Chair of the Department of Pediatrics, and Interim Dean of the School of Medicine at the University of California San Francisco (UCSF). He has concurrent appointments as Physician-in-Chief of UCSF Children’s Hospital, Associate Director of the Cardiovascular Research Institute, and President of the UCSF Medical Group. Hawgood graduated with First Class Honors from the University of Queensland in Australia in 1975. After graduation, he trained in Australia in pediatrics with a sub-speciality interest in neonatology.
Hawgood moved to UCSF in 1982 as a research fellow with Lasker Awardee, Dr. John Clements, the scientist that discovered pulmonary surfactant in the late 1950’s. He started his own laboratory, focused on the proteins associated with surfactant, in 1984. A multi-disciplinary Program Project Grant from the National Heart, Lung and Blood Institute has continuously supported his work since then. Hawgood has maintained an active presence in clinical medicine, serving as Division Chief of Neonatology at UCSF from 1994 to 2006. Hawgood served on the Council of the Society for Pediatric Research for seven years between 1992 and 2000 and was President of the Society in 1999. He chaired the Program Committee for the Pediatric Academic Societies from 1998-2000 and in 2005 received the Distinguished Service Award from the Society for Pediatric Research. He is currently a Trustee and Secretary-Treasurer of the International Pediatric Research Society. Hawgood has served on study sections for the NIH and is currently a member of the Program Project Parent Committee of the National Heart, Lung, and Blood Institute.
Sam Hawgood's research activity is focused on the biology of the pulmonary alveolus with a particular emphasis on the structure and function of the pulmonary surfactant apoproteins. The human lung is made up of some 500 million alveoli each with a diameter of 200 microns and a septal wall thickness of only 5-8 microns. The large surface area provided by this foam-like architecture is ideal for rapid respiratory gas exchange but necessitates some unique biological answers to the threat to structural stability posed by the problem of high surface tension and the constant exposure to environmental pollutants, allergens and microbes. Pulmonary surfactant, a lipoprotein secretion of the alveolar epithelial type II cell, stabilizes alveolar structure by reducing the retractile surface forces that would otherwise act to collapse the lung at end expiration. The surfactant apoproteins also act as components of the pulmonary innate defense system protecting the lung from inflammation and infection.
We now know that the surfactant proteins have important roles in the activity of surfactant, particularly the ability to rapidly spread phospholipids at the alveolar surface. The proteins also regulate surfactant turnover and metabolism in the alveolus and play a part in non-antibody mediated response to infection and inflammation in the alveolus. The biology of these proteins is complex and they apparently function as interacting hetero-oligomers to mediate their multiple effects on surfactant biology. At least two of the surfactant proteins, SP-B and SP-C, are present in exogenous surfactants approved for clinical use and fatal human disease has been linked to inherited mutations in both these proteins. This clear link to human disease provides a strong rationale to obtain a detailed understanding of their structure and function.