| William B. Weglicki, Ph.D. |
Professor,
Department of Physiology and Experimental Medicine, School
of Medicine
George Washington University
Washington, DC 20052
Email: wweg@gwu.edu
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| William B. Weglicki is the interim Chair of the Department
of Physiology and Experimental Medicine. Although by most standards,
this is a small basic science department, members of its faculty
with active research programs have distinguished themselves
through nationally and internationally recognized research endeavors,
Its faculty members have been funded in diverse areas of research
in the biomedical and biophysical sciences, and have a strong
record of publication. The vitality of the current departmental
research program comes from the fact that the faculty have in
many instances, obtained finding from sources that are both
traditional (Department of Agriculture, Department of Defense,
American Heart Association, Institutional and continuous NIH
funding for more than 20 years) and non-traditional (Kingdom
of Saudi Arabia, and private sector corporations) in nature.
In addition, they have a long history of developing scientific
collaborations with researchers from other institutions as well
as from other GWU-MC and GWU departments. Major examples are
collaborations with GWU-MC faculty from the Departments of Medicine/Cardiology,
Anesthesiology, Surgery, Neurosurgery, Pathology, Immunology,
Biochemistry and Molecular Biology, and Anatomy and Cell Biology.
Past and current areas of departmental research strength include
studies to evaluate: the mechanisms of inflammatory / oxidative
stress injury to cardiovascular tissue and cells, the mechanisms
of myocardial reperfusion injury using in vitro models, free
radical detection (nitric oxide, superoxide anion, hydroxyl
and lipid radicals) and quantification in vivo and in vitro
using EPR spectroscopy, antioxidant modulation of the lipid
peroxidation pathway with cardiovascular drugs, membrane and
cellular pathobiology, in vivo and in vitro cardiovascular pathobiology
resulting from changes in nutritional feeding patterns (dietary
magnesium deficiency), in vivo and in vitro pathobiology resulting
from excessive trace metal exposure (iron), the mechanism of
sepsis (LIPS)-induced inflammation in vivo, the pathobiology
associated with AZT therapy and the murine AIDS model (MAIDS)
and collaborative studies of the pathobiology of ‘ferritin
knockout’ and thalassemia murine models. |
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