Dr. George Ford
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Contact Information
Department of Physiology and Biophysics Virginia Commonwealth University P.O. Box 980551 Richmond, Virginia 23298-0551 Tel: 804-828-9501 Fax: 804-828-7382 email: ford@vcu.edu |
George D. Ford received his B.S. in Physics (1961) from West Virginia University, his M.S. in Physics (1964) from Iowa University, and his Ph.D. in Pharmacology (1967) from West Virginia University. Following postdoctoral training in Biophysics at the University of Rochester with Dr. D.A. Goldstein, Dr. Ford joined the department in 1970. He is the Departmental Director of Graduate Programs, and Assistant Dean of Medicine for Sponsored Programs Research.
Teaching/Administration
As the Assistant Dean for Sponsored Programs, I review all requests for extramural funding by or involving all faculty in the School of Medicine. Reviews are primarily focused on insuring compliance with all policies and regulations imposed by the School, University and regulatory agencies. But I also assist in finding funding sources and developing proposals.
I am also the Executive Secretary for the A. D. Williams Committee, a local foundation that provides a wide variety of support for scholarship and research by the faculty of all schools on the MC campus.
In addition I currently teach cardiovascular and respiratory physiology to a wide variety of students including graduate, medical, dental, pharmacy and biomedical engineering students. I have had extensive experience directing numerous professional courses. I have also co-developed several computer-assisted instructional programs for use in laboratory teaching programs.
Research
My research focused on the role of excitation-contraction (E-C) coupling mechanisms in regulating tension development by arterial smooth muscle and how such agents such as reactive oxygen metabolites and Mg2+ influence this muscle's tension development through their effects on these coupling mechanisms. Vascular smooth muscle, like cardiac muscle, is a functional syncytium and therefore apparently devoid of motor units. Unlike cardiac muscle, vascular smooth muscle does not exhibit a singular length-tension relationship. This means its tension development must be regulated by factors which influence the E-C coupling sequence. Recently two lines of study have suggested that a class of chemicals known as free radicals may exert a major influence on the E-C coupling mechanisms of vascular smooth muscle. The first line was prompted by the discovery of the synergistic relationship between the endothelial cells of the blood vessel lining and the underlying smooth muscle. The signal producing this synergistic action has since been identified, at least peripherally, as the free radical species nitric oxide or simply NO. The second line was the demonstration that certain species of reactive oxygen intermediates, including free radical species such as the superoxide anion and the hydroxyl radical, are causal factors in several pathophysiological states triggered by deterioration of vascular function, e.g. inflammation and circulatory shock.
The most recent studies of my laboratory established the susceptibility of the Ca2+ dynamics of subcellular fractions of arterial smooth muscle, such as the sarcoplasmic reticulum and actomyosin, to reactive oxygen intermediates generated by the enzyme xanthine oxidase and its substrates xanthine and hypoxanthine. Other studies used the intracellular superoxide generator, nitrazepam, to verify the contractile activity of arterial smooth muscle is affected in a manner predicted by the effects observed on the subcellular fractions.
The last project I worked on was the development of a new technique for the measurement of superoxide production at both the cellular and tissue level using photon counting and a recently discovered chemiluminescent indicator. This technique allows highly selective detection of superoxide production in the sub-picomolar range. It also allows detection of both extracellular and intracellular production.
My contributions to the research mission now though are largely confined to administrative activities.
Selected Publications
Suzuki, Y. and Ford, G.D., Superoxide stimulates IP3-induced Ca2+ release from vascular smooth muscle sarcoplasmic reticulum. Amer. J. Physiol. 262:H114-116, 1992. PubMed
Suzuki, Yuichiro J. and Ford, George D., Mathematical Model Supporting the Superoxide Theory of Oxygen Toxicity. Free Radic. Bio. Med. 16:63-72, 1994.
Suzuki, Yuichiro J. and Ford, George D., Redox Regulation of Signal Transduction in Cardiac and Smooth Muscle. J. Mol. Cell. Cardiol. 31:345-353, 1999.
Ford, G. D., Descaire, L., Feher, J. J., Jafir, A., and Ridgway, E. B. A Dynamic Chemiluminescent Technique to Measure Intracellular Superoxide Production. FASEB J. 15: A1132 (2001).
Vaughan, J.E., Walsh, S. W., and Ford, G. D. Thromboxane mediates neutrophil superoxide production in pregnancy. Am J Obstet Gynecol. 195(5):1415-20 (2006). PubMed