The program trains physician-scientists and post-doctoral PhD scientists in aspects of the pathophysiological processes that occur after traumatic injury and critical illness. Over the past 4 years we have successfully recruited to fill our positions and have addressed a key concern that was raised in our previous competitive renewal regarding diversity in our program. We have paid particular attention to identifying and recruiting strong under-represented minority candidates. Our previous competitive renewal also focused upon the """"""""key initiatives"""""""", defined by the leaders at the National Institutes of Health and termed the """"""""NIH Roadmap"""""""". This had direct bearing on the structure and direction of this training program. Briefly, the key initiatives or themes are: (1) New Pathways to Discovery, (2) Research Teams of the Future and (3) Reengineering the Clinical Research Enterprise. We propose to continue to educate trainees in established molecular biology techniques and will expand their training to include cutting edge research and analysis (i.e. biomedical computing) techniques. Through collaborations with basic scientists and integration with the available research education programs at the University of Washington, we will expose trainees to broad-based research teams and programs. Trainee education and experience will continue to include concepts of translational research, whereby basic observations will be evaluated as potential diagnostic and therapeutic benefit for critically ill patients. In summary, we aim to prepare a diverse group of interested scientists for academic careers as independent investigators and educators. Through a multidisciplinary and collaborative effort, trainees learn how to identify important research questions, how to design, conduct and analyze experiments that will address these questions and how to translate their findings into clinically relevant interventions.

Public Health Relevance

Trauma remains an important public health problem. Injuries are responsible for a high proportion of deaths in people of all ages and medical care for injury victims is costly. Our training program has successfully educated surgeons, physicians and post-doctoral students in aspects of the applied biology of injury and inflammation. Graduates from our program have demonstrated a commitment to understanding the biology of injury and to the care of critically ill injury victims.

National Institute of Health (NIH)
National Institute of General Medical Sciences (NIGMS)
Institutional National Research Service Award (T32)
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Special Emphasis Panel (ZGM1-BRT-5 (PD))
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Somers, Scott D
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University of Washington
Schools of Medicine
United States
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Shubin, Nicholas J; Pham, Tam N; Staudenmayer, Kristan Lea et al. (2018) A Potential Mechanism for Immune Suppression by Beta-Adrenergic Receptor Stimulation following Traumatic Injury. J Innate Immun 10:202-214
(2018) The Priming Effect of C5a on Monocytes is Predominantly Mediated by the p38 MAPK Pathway. Shock 50:127
Parent, Brodie A; Seaton, Max; Djukovic, Danijel et al. (2017) Parenteral and enteral nutrition in surgical critical care: Plasma metabolomics demonstrates divergent effects on nitrogen, fatty-acid, ribonucleotide, and oxidative metabolism. J Trauma Acute Care Surg 82:704-713
Seaton, Max E; Parent, Brodie A; Sood, Ravi F et al. (2017) Melanocortin-1 Receptor Polymorphisms and the Risk of Complicated Sepsis After Trauma: A Candidate Gene Association Study. Shock 47:79-85
Parent, Brodie A; Mandell, Samuel P; Maier, Ronald V et al. (2016) Safety of minimizing preoperative starvation in critically ill and intubated trauma patients. J Trauma Acute Care Surg 80:957-63
Plevin, Rebecca E; Knoll, Megan; McKay, Meghan et al. (2016) The Role of Lipopolysaccharide Structure in Monocyte Activation and Cytokine Secretion. Shock 45:22-7
Sood, Ravi F; Gibran, Nicole S; Arnoldo, Brett D et al. (2016) Early leukocyte gene expression associated with age, burn size, and inhalation injury in severely burned adults. J Trauma Acute Care Surg 80:250-7
Sood, Ravi F; Arbabi, Saman; Honari, Shari et al. (2016) Missense Variant in MAPK Inactivator PTPN5 Is Associated with Decreased Severity of Post-Burn Hypertrophic Scarring. PLoS One 11:e0149206
Thompson, Callie M; Sood, Ravi F; Honari, Shari et al. (2015) What score on the Vancouver Scar Scale constitutes a hypertrophic scar? Results from a survey of North American burn-care providers. Burns 41:1442-8
Sood, Ravi F; Hocking, Anne M; Muffley, Lara A et al. (2015) Genome-wide Association Study of Postburn Scarring Identifies a Novel Protective Variant. Ann Surg 262:563-9

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