Abstract

The object of this research proposal is the improvement of the care of burned patients. We believe that the most rational way to achieve this end is to focus our research efforts along critical problem areas in the treatment of burned patients. The overall approach is a coordinated multidisciplinary effort involving clinicians and basic scientists carrying out clinical studies correlated with multidisciplinary-based laboratory investigations, each examining the same traumatized subject extending from in vivo studies to organ perfusion, organ culture, and cellular investigations. The areas that have been identified for investigation are: 1) gastrointestinal function after thermal injury, 2) effect of burn injury on substrate metabolism, 3) burn injury extension, 4) burn injury - protein, amino acid and energy metabolism, 5) molecular pathology of healing and burn scar, and 6) burn trauma cellular endocrine response.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Specialized Center (P50)
Project #
3P50GM021700-11S1
Application #
3106020
Study Section
(SRC)
Project Start
1977-12-01
Project End
1987-11-30
Budget Start
1985-12-01
Budget End
1987-11-30
Support Year
11
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199

  Publications

Tao, Rongya; Wang, Caixia; Stöhr, Oliver et al. (2018) Inactivating hepatic follistatin alleviates hyperglycemia. Nat Med 24:1058-1069
Nakazawa, Harumasa; Chang, Kyungho; Shinozaki, Shohei et al. (2017) iNOS as a Driver of Inflammation and Apoptosis in Mouse Skeletal Muscle after Burn Injury: Possible Involvement of Sirt1 S-Nitrosylation-Mediated Acetylation of p65 NF-?B and p53. PLoS One 12:e0170391
Frydman, Galit H; Marini, Robert P; Bakthavatchalu, Vasudevan et al. (2017) Local and Systemic Changes Associated with Long-term, Percutaneous, Static Implantation of Titanium Alloys in Rhesus Macaques (Macaca mulatta). Comp Med 67:165-175
Khan, Mohammed A S; Khan, Mohammed F; Kashiwagi, Shizuka et al. (2017) An ALPHA7 Nicotinic Acetylcholine Receptor Agonist (GTS-21) Promotes C2C12 Myonuclear Accretion in Association with Release of Interleukin-6 (IL-6) and Improves Survival in Burned Mice. Shock 48:227-235
Li, Peng; Tompkins, Ronald G; Xiao, Wenzhong et al. (2017) KERIS: kaleidoscope of gene responses to inflammation between species. Nucleic Acids Res 45:D908-D914
Kashiwagi, Shizuka; Khan, Mohammed A S; Yasuhara, Shingo et al. (2017) Prevention of Burn-Induced Inflammatory Responses and Muscle Wasting by GTS-21, a Specific Agonist for ?7 Nicotinic Acetylcholine Receptors. Shock 47:61-69
Agarwal, Shailesh; Loder, Shawn; Brownley, Cameron et al. (2016) Inhibition of Hif1? prevents both trauma-induced and genetic heterotopic ossification. Proc Natl Acad Sci U S A 113:E338-47
Shank, Erik S; Martyn, Jeevendra A; Donelan, Mathias B et al. (2016) Ultrasound-Guided Regional Anesthesia for Pediatric Burn Reconstructive Surgery: A Prospective Study. J Burn Care Res 37:e213-7
Copps, Kyle D; Hançer, Nancy J; Qiu, Wei et al. (2016) Serine 302 Phosphorylation of Mouse Insulin Receptor Substrate 1 (IRS1) Is Dispensable for Normal Insulin Signaling and Feedback Regulation by Hepatic S6 Kinase. J Biol Chem 291:8602-17
Law, Nathan C; White, Morris F; Hunzicker-Dunn, Mary E (2016) G protein-coupled receptors (GPCRs) That Signal via Protein Kinase A (PKA) Cross-talk at Insulin Receptor Substrate 1 (IRS1) to Activate the phosphatidylinositol 3-kinase (PI3K)/AKT Pathway. J Biol Chem 291:27160-27169

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