The Mass and NMR Spectroscopy Facility Core provides the Burn Trauma Center with the capability to apply mass spectroscopy and nuclear magnetic resonance (NMR) spectroscopy techniques to study phenomena at the tissue, cellular, and genetic levels. The Mass Spectroscopy Facility supports research that allows our investigators to apply tracer techniques for the following applications in our research: amino acid metabolism, glucose metabolism, lipid metabolism, nitrate/nitric oxide, protein turnover, protein phosphorylation, and substrate kinetics/oxidaticn. The Mass Spectroscopy Facility offers several services to the Burn Trauma Center. (1) Provides timely and accurate determinations of stable isotope enrichments of tracers and their derivatives in bodily fluids, tissues, and expired air. (2) Assists in the development of new methods for isotope analyses of compounds in blood, tissues, and urine as required to meet the needs of our investigators. (3) Provides quality control for all analysis conducted in support of the research studies that involve the use of stable nuclides as tracers. The NMR Spectroscopy Facility supports research to develop methodologies that will permit our investigators to assess key metabolites in the TCA Cycle in tissue extracts and using magnetic angle spinning, in the whole tissue. In addition, the investigators will be able to assess mitochondrial energy coupling in vivo, as expressed by the ratio of ATP synthesis to TCA cycle, using C13/P31 NMR. Finally, the investigators will be able to assess the mitochondrial 2-oxogulterate-malate carrier especially since there is no transport of NADH across the mitochondrial membrane and reducing equivalents produced in the cytosol from glycolysis are carried into the mitochondria as malate. The NMR Spectroscopy Facility offers several services to the Burn Trauma Center. (1) Noninvasive assessment of gluconeogenesis and TCA cycle flux in humans. (2) NMR of tissue extracts using existing and new techniques. (3) Development of new technologies using high resolution magnetic angle spinning to perform NMR measurements in small, intact, unprocessed tissues. (4) In vivo NMR spectroscopy and MR imaging microscopy (MRI) of murine models of burn injury. These facilities enable research in all 4 projects and funds to support these activities directly are included in each project. Support is requested for personnel and supplies for methodology and technology development.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Specialized Center (P50)
Project #
5P50GM021700-30
Application #
7391265
Study Section
Special Emphasis Panel (ZGM1)
Project Start
Project End
Budget Start
2007-04-01
Budget End
2008-03-31
Support Year
30
Fiscal Year
2007
Total Cost
$146,743
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
073130411
City
Boston
State
MA
Country
United States
Zip Code
02199
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
Ueki, Ryusuke; Liu, Li; Kashiwagi, Shizuka et al. (2016) Role of Elevated Fibrinogen in Burn-Induced Mitochondrial Dysfunction: Protective Effects of Glycyrrhizin. Shock 46:382-9
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

Showing the most recent 10 out of 110 publications