Research Interests

• 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.

• ·Lung injury: Additional studies examine the contribution of excessive inflammation to lung injury and vascular remodeling following pulmonary embolism.

Professional Experience

• Carolinas Medical Center, Department of Emergency Medicine

• Associate Director, Emergency Medicine Research, 1994-1995

• Director, Emergency Medicine Preclinical Research 1996-present

• 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

• 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

• Pennsylvania State University

• M.S. Hershey Medical Center, Physiology Dept., Post-Doctoral Fellow 1977- 1979

• University of Maryland

• Graduate Teaching Assistant, 1971-1975, 1977

• Research Assistant 1976

• Children's School for Science

• Woods Hole, Massachusetts, Instructor, summer, 1971

• Drew University - Undergraduate Teaching Assistant, 1969

Education

• B.A.  Drew University 1971, Zoology

• Ph.D  University of Maryland 1977, Zoology

• 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.