The Human Subjects Core provides the Burn Trauma Center with clinical, physiologic, pathophysiologic, and outcomes data to promote the analysis and interpretation of the multiple metabolic interactions in patients with a burn-induced immuno-inflammatory hypermetabolic response. It serves as a tool to establish a clinical infrastructure for study design, and accrual and analysis of data from critically ill patients. An advancement from this core is the establishment and dissemination of guidelines, tools, and standard operating procedures (SOPs), which can be accessed and utilized by investigators in the field of burns and trauma. The study of burn-injured patients and healthy volunteers is essential to our understanding of the human response to injury. This activity requires careful oversight and quality control to maintain maximum safety and patient protection and to insure high quality data collection. The Human Subjects Core personnel allow complex human studies to be performed at each of our study locations: the Burn Centers at the MGH and'SHC, the MGH PET Camera Facility, the MGH general surgical units, and the Peoples Liberafion Army Hospital 304 and Beijing China. The core acts most efficiently to prevent duplicate and unnecessary blood drawing and testing. To anticipate maximum coordination of research efforts and close cooperation among investigators, human study information obtained from our studies on the clinical units is effectively coordinated and organized in this core facility, thus providing an efficient mechanism of data management. Establishment of a separate human studies core within the PSO funding mechanism provides an excellent opportunity to consolidate acquisition and management of the human subjects for our Projects 2, and 4. The Human Subjects Core is responsible forthe development and implementation of standard operating procedures (SOPs), recruitment and obtaining consent of subjects, collection and distribution of samples, record-keeping, and coordination with the subprojects. This core allows the human research performed in our Burn Trauma Center to be conducted with remarkable accuracy, sensitivity, and reproducibility.

Public Health Relevance

The Human Subjects Core provides the Burn Trauma Center with clinical, physiologic, pathophysiologic, and outcomes data to promote the analysis and interpretation of the multiple metabolic interactions in patients with a burn-induced immuno-inflammatory hypermetabolic response. It serves as a tool to establish a clinical infrastructure for study design, and accrual and analysis of data from critically ill patients.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Specialized Center (P50)
Project #
2P50GM021700-32A1
Application #
8414943
Study Section
Special Emphasis Panel (ZGM1-SRC-5 (TB))
Project Start
Project End
Budget Start
2013-06-01
Budget End
2014-05-31
Support Year
32
Fiscal Year
2013
Total Cost
$407,520
Indirect Cost
$173,313
Name
Massachusetts General Hospital
Department
Type
DUNS #
073130411
City
Boston
State
MA
Country
United States
Zip Code
02199
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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
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
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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
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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
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
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
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

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