Gerald S. Davis, M.D.

Professor of Medicine
Pulmonary Disease & Critical Care Medicine;

Room C-325 Given Building
University of Vermont, College of Medicine
149 Beaumont Avenue
Burlington, VT 05405

Voice: (802) 656-2182
Fax:(802) 656-3854

E-mail:gerald.davis@uvm.edu

• B.S. (1966) Biology; Yale University, New Haven, CT.
• M.D. (1970) Medicine; College of Medicine, University of Virginia, Charlottesville, VA.
• Internship (1970-71) Internal Medicine; University of Vermont / Medical Center Hospital of Vermont, Burlington, VT.
• Residency (1971-72) Internal Medicine; University of Vermont / Medical Center Hospital of Vermont, Burlington, VT.
• Fellowship (1972-75) Pulmonary Disease; University of Vermont / Medical Center Hospital of Vermont, Burlington, VT.
• Research Associate and Clinical Instructor (1974-1975), Dept. Medicine, University of VT, Burlington, VT.
• Assistant Professor (1975-1979), Dept. Medicine, University of Vermont, Burlington, VT.
• Associate Professor (1979-1983), Dept. Medicine, University of Vermont, Burlington, VT.
• Director (1979-2000), Pulmonary Disease and Critical Care Medicine Unit, Dept Medicine, University of Vermont, Burlington, VT.
• Professor (1983- ), Dept. Medicine, University of Vermont, Burlington, VT.

My research interests focus on mechanisms of pulmonary fibrosis and on the management of asthma, involving both basic laboratory and clinical science.

• Occupational and environmental lung diseases
• Silicosis
• Mechanisms of pulmonary fibrosis caused by silica
• Idiopathic pulmonary fibrosis
• Sarcoidosis
• Clinical management of asthma

• Review: occupational and environmental lung disease.
   
   
• Lymphocytes, lymphokines, and silicosis.
   
   
• Rapid early onset lymphocyte cell death in mice resistant, but not susceptible to Leishmania major infection.
   
   
• Interferon-gamma production by specific lung lymphocyte phenotypes in silicosis in mice.
   
   
• Quantitative image analysis of lung connective tissue in murine silicosis.
   
   
• gamma delta+ T cells regulate major histocompatibility complex class II(IA and IE)-dependent susceptibility to coxsackievirus B3-induced autoimmune myocarditis.