James A. Thomas, M.D. is an Associate Professor in the Departments of Pediatrics and Molecular Biology at the University of Texas Southwestern Medical Center. He is also the clinical Chief of Critical Care Services, Children’s Medical Center, Dallas, Texas.
Dr. Thomas graduated from Princeton University in 1981, magna cum laude with an A.B. in Romance Languages and Literature/Latin American Fiction. He obtained his M.D. in 1989 from Stanford University where he received a Research Honors Award for Distinguished Research in Pediatrics. He completed his pediatrics residency at the Children’s Hospital of Los Angeles, receiving the Victor E. Stork Award for "excellent work at the hospital and for promise of future abilities in the care of children"; and the Frances Nunnally Winzer Scholarship for "the resident who has shown unusual potential for growth and professional development"; In 1992, Dr. Thomas came to Dallas for fellowship and research training in pediatric critical care under the auspices of the NIH-funded Pediatric Scientist Development Program. In 1995, the critical care physicians, nurses and respiratory therapists awarded him the Jaws Award for Outstanding Fellow. He joined the Pediatrics faculty in the same year, was later appointed to the Molecular Biology Department. In 2003, was promoted to Associate Professor with tenure.
Dr. Thomas is a Diplomat of the Sub-Board Pediatric Critical Care Medicine, American Board of Pediatrics. He is a Fellow of the American Academy of Pediatrics, and is affiliated with the American Association for the Advancement of Science, the Society of Critical Care Medicine, the Shock Society, and the International Endotoxin Society. He was recently elected to the Society for Pediatric Research. He serves as an ad-hoc reviewer for six different medical journals and sits on a NICHD scientific review panel.
Dr. Thomas research interests focus on the role of the innate immune system in the host response to infection and injury, in particular the impact of the TLR/IL-1 intracellular signaling pathway on the inflammatory response to infection, myocardial dysfunction, and autoimmune disease.
