Elizabeth K. Tam, M.D., Ph.D.

University of Hawai’i at Manoa

John A. Burns School of Medicine

651 Ilalo Street, BSB 222-C

Honolulu, HI 96813 USA

Tel:     808-692-1502
Fax:    808-

Email :  tameliza@hawaii.edu

Pubmed Link 




Dr. Tam is a minority investigator whose research focuses on gene-environment interactions in the pathogenesis of asthma and other chronic inflammatory diseases of the lung. Chronic respiratory disease is now the 4th leading cause of death in the US and is projected to rise to the second leading cause of death by 2010. Many of the insights gained in other populations may not fully apply to our people in Hawaii, either because of different frequencies of genetic variations associated with respiratory disease, local environmental factors, or our cultural and behavioral diversity. It is our long-range goal to extend research into interactions between gene, environment, and culture that may be particular to respiratory disease in Hawaii. Inflammatory respiratory conditions are complex traits, defined by genetic susceptibility conferred by multiple genes and environmental exposures. Variations in the structure, transcription, or interaction of several genes may predispose to: 1) an exaggerated and persistent inflammatory response to inhaled irritants or allergens, 2) exaggerated bronchoconstriction, or 3) persistent fibrosis even after the environmental insult has ended. In terms of environment, Hawaii poses some unique geological, meteorological, and botanical aspects not commonly described elsewhere, but shares with the nation and the world several indoor allergens and the pervasiveness of environmental tobacco smoke, now considered causal in the pathogenesis of asthma, not merely a trigger.

The team has developed research tools that span cellular and molecular biology, clinical phenotype characterization, genotype-phenotype association studies to community-participatory environmental health research. Under Dr. Claude Jourdan-Le Saux's direction, the team studies the role of caveolin in allergic asthma-induced airway remodeling. A model based on sensitized caveolin-deficient or wild type mice provides the foundation to understand gene expression and regulation, protein elaboration, structure, and functional changes that result from Th2 stimulation. The team also examines the association between clinical traits of inflammatory airway disease and variations in several candidate genes, including glutathione S-transferase M1, interleukins, and the beta2-adrenergic receptor. These genes respectively represent pathways that metabolize environmental toxins, modulate inflammation, or change airway smooth muscle tone and reactivity.


Gries, D.M. Tam, E.K. Blaisdell J.M., Iwamoto, L.M., Fujiwara, N., Uyehara, C.F.T., Nakamura, K.T.  The relative effects of inhaled nitric oxide and hyperoxia on pulmonary dysfunction in newborn guinea pigs, AFP: Regulatory, Integrative and Comparative Physiology.  in press

Balaraman, V., Meister, J., Ku, T.L., Sood, S.L., Tam, E., Killeen, J., etal. (1998) Lavage administration of dilute surfactants after acute lung injury in neonatal piglets.  Am. J. Respir. Crit. Care Med. 158(1):12-7.

Tam, E.K. (1997) Implications of genetic research for medical practice and education.  Hawaii Med. J. 56(6):140-1.

Raymond, W.W., Tam, E.K., Blount, J.L. Caughey, G.H. (1995) Purification and characterization of dog mast cell protease-3, an oligomeric relative of tryptases.  J. Biol. Chem. 270:13164-13170.

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