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PICTURE WILL GO HERE |
Dr. John A. Watts, Jr.
Director
Emergency Medicine Preclinical Research
Carolinas
Medical Center
Tel.:704-355-2528
jwatts@carolinas.org
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Research Interests
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Cor pulmonale:
We currently study the pathologic effects of lung dysfunction on the
right side of the heart, a process that is termed cor pulmonale.
Clinical research indicates that some 40% of patients recovering from
pulmonary embolism have measurable dysfunction in the right ventricle of
their heart and about 12% have limited mobility as a result of this
dysfunction, however the mechanisms responsible for this damage are
poorly understood. Our studies examine the mechanisms of right
ventricular stress, cellular damage and inflammation in models of
experimental pulmonary embolism.
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Lung injury:
Additional studies examine the contribution of excessive inflammation to
lung injury and vascular remodeling following pulmonary embolism.
Professional Experience
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Carolinas Medical Center, Department of Emergency Medicine
Associate Director, Emergency Medicine Research, 1994-1995
Director, Emergency Medicine Preclinical Research 1996-present
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University of North Carolina at Charlotte, Department of
Biology
Assistant Professor 1979-1985
Associate Professor 1985-1990
Professor 1990-1994
Adjunct Professor & Program Faculty Interdisciplinary Ph.D. 1994-present
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University of North Carolina, Chapel Hill, Department of
Emergency Medicine
Adjunct Research Assistant Professor, 1994-1996
Adjunct Research Associate Professor, 1996-2003
Adjunct Research Professor, 2003 - present
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Pennsylvania State University
M.S. Hershey Medical Center, Physiology Dept., Post-Doctoral Fellow
1977- 1979
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University of Maryland
Graduate Teaching Assistant, 1971-1975, 1977
Research Assistant 1976
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Children's School for Science
Woods Hole, Massachusetts, Instructor, summer, 1971
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Drew University - Undergraduate Teaching Assistant, 1969
Education
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B.A. Drew University 1971, Zoology
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Ph.D University of Maryland 1977, Zoology
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Non-accredited: Experimental Invertebrate Zoology
Program
Marine Biological Laboratory, Woods Hole, Mass, Summer, 1970
Rose Memorial Scholarship - Drew University
Selected Recent Publications
1. Watts,
J.A., J. Zagorski, M.A. Gellar, B.G. Stevinson, J.A. Kline. Cardiac
inflammation contributes to right ventricular dysfunction following
experimental pulmonary embolism in rats. J. Mol. Cell. Cardiol.
2006;41:296-307.
2. Watts, J.A., J.A. Kline, L.R. Thornton, R.M. Grattan, S.S. Brar.
Metabolic dysfunction and depletion of mitochondria in hearts of septic
rats. J. Mol. Cell. Cardiol. 2004;36(1):141-150.
3. Watts, J.A., J.A. Kline. Bench-to-Bedside: The role of mitochondrial
medicine in the pathogenesis and treatment of cellular injury. Acad.
Emerg. Med. 2003:10(9)885-897.
4. Zagorski, J., J. Debelak, M. Gellar, J.A. Watts, J.A. Kline.
Chemokines accumulate in the lungs of rats with severe pulmonary
embolism induced by polystyrene microspheres. J. Immunol.
2003;171:5529-5536.
5. Jones, A.E., J.A. Watts, J.P. Debelak, L.R. Thronton, J.D. Younger,
J.A. Kline. Inhibition of prostaglandin synthesis during polystyrene
microsphere-induced pulmonary embolism in the rat. Am. J. Physiol. Lung
Cell. Mol. Physiol. 2003;284(6):L1072-L1081.
6. Roshon, M.J., J.A. Kline, L.R. Thornton, J.A. Watts. Cardiac UCP2
expression and myocardial oxidative metabolism during acute septic shock
in the rat. SHOCK 2003;19(6):570-576.
7. Courtney, D.M., J.A. Watts, J.A. Kline. End tidal CO2 is reduced
during hypotension and cardiac arrest in a rat model of massive
pulmonary embolism. Resuscitation 2002;53(1);83-91.
8. Glimer, B., J. Kilkenny, C. Tomaszewski, J.A. Watts. Hyperbaric
oxygen does not prevent delayed neurological sequelae after carbon
monoxide poisoning. Acad. Emerg. Med. 2002;9(1):1-8.
9. Watts, J.A., R.M. Grattan II, B.S. Whitlow, J.A. Kline. Activation of
Poly(ADP-ribose) Polymerase in Severe Hemorrhagic Shock and
Resuscitation. Amer. J. Physiol. Gasterointest. Liver Physiol.
2001;281:G498-G506.
10. D. Matthew Sullivan, J.A. Watts, J.A. Kline. Biventricular
dysfunction after acute pulmonary embolism in the rat. J. App. Physiol.
2001;90:1648-1656.
11. Custalow, C.B., J.A. Kline, L. Thornton, P. O’Malley, R.W. Barbee,
R.M. Grattan, G.D. Lopaschuk, J.A. Watts. Substrate dependent recovery
of cardiac function following hemorrhage and retransfusion in the
isolated working rat heart. SHOCK 2001;15(3):231-238.
12. Thourani, V.H., S.S. Brar, T.P. Kennedy, L.R. Thornton, J.A. Watts,
R.S. Ronson, Z.Q. Zhao, A.L. Sturrock, J.R. Hoidal, J.Vinten-Johansen.
Nonanticoagulant heparin with low activity against complement inhibits
nuclear factor- activation and reduces myocardial reperfusion injury.
Am. J. Physiol. Heart Circ. Physiol. 2000;48:H2084-H2093.
13. J.A. Kline, L.R. Thornton, G.D. Lopaschuk, R.W. Barbee, J.A. Watts.
Lactate improves cardiac efficiency after hemorrhagic shock. SHOCK
2000;14:215-221.
14. Barbee, R.W., J.A. Kline, J.A. Watts. Depletion of lactate by
dichloroacetate reduces cardiac efficiency after hemorrhagic shock.
SHOCK 2000;14:208-214.
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