The PET and muPET Facility Core provides the Burn Trauma Center with the capability to apply nuclear imaging techniques to study phenomena at the tissue, cellular, and genetic levels. The facility core supports research that allows us to study a wide range of biological processes in both humans and living laboratory animals. In particular, this technology using either state-of-the-art conventional PET cameras or a muPET camera provides us with the ability to study an animal more than once, allows each animal to serve as its own control, and allows interventional strategies to be followed over time. Furthermore, identical studies can also be conducted non-invasively directly in normal human volunteers and patients. The muPET camera, which enables imaging at resolutions of 1 mm or less in both humans and animals, is mobile and will make imaging skeletal muscle possible in our intensive care patients while they are still acutely ill. Further development of molecular imaging methodologies with high resolution will enable investigators to image gene expression in relevant tissues and skeletal muscle apoptosis to better understand the immuno-inflammatory host response initially in C57BL/6 mice and later in humans. The PET and muPET Facility Core allows complex studies to be performed within the Human Subjects Core and Animal Research Cores at the MGH, Shriners Hospital, and MIT. The facility core provides the Burn Trauma Center investigators with the capability to apply PET technology to test scientific hypotheses without the need to become PET experts themselves. The PET and muPET Facility Core offers several services to the Burn Trauma Center. (1) Design and development of new physiological imaging agents labeled with 18F, 11C, 13N, or 15O. (2) Routine Production and dispensing of existing and new imaging agents for PET study protocols. (3) Design of imaging and data analysis protocols for new agents. (4) Routine execution of existing imaging protocols and data analyses. (5) Development of new instrumentation for specific applications within the Center (e.g. mu PET camera). (6) Development of new technology for real-time molecular imaging of apoptosis and gene expression. Support is requested in this facility for methodology and development that will be very helpful in all four projects.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Specialized Center (P50)
Project #
5P50GM021700-30
Application #
7391264
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
$133,019
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

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