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 PET Camera Facility, and the MGH general surgical units. 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 P50 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 for the 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 i-esearch performed in our Burn Trauma Center to be conducted with remarkable accuracy, sensitivity, and reproducibility.
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.
|Zhao, Gaofeng; Yu, Yong-Ming; Kaneki, Masao et al. (2015) Simvastatin reduces burn injury-induced splenic apoptosis via downregulation of the TNF-?/NF-?B pathway. Ann Surg 261:1006-12|
|Watada, Susumu; Yu, Yong-Ming; Fischman, Alan J et al. (2014) Evaluation of intragastric vs intraperitoneal glucose tolerance tests in the evaluation of insulin resistance in a rodent model of burn injury and glucagon-like polypeptide-1 treatment. J Burn Care Res 35:e66-72|
|Zhao, Gaofeng; Yu, Yong-Ming; Shoup, Timothy M et al. (2014) Membrane potential-dependent uptake of 18F-triphenylphosphonium--a new voltage sensor as an imaging agent for detecting burn-induced apoptosis. J Surg Res 188:473-9|
|Carter, Edward A; Paul, Kasie; Bonab, Ali A et al. (2014) Effect of exercise on burn-induced changes in tissue-specific glucose metabolism. J Burn Care Res 35:470-3|
|Lee, Sangseok; Yang, Hong-Seuk; Sasakawa, Tomoki et al. (2014) Immobilization with atrophy induces de novo expression of neuronal nicotinic *7 acetylcholine receptors in muscle contributing to neurotransmission. Anesthesiology 120:76-85|
|Fu, Glenn K; Xu, Weihong; Wilhelmy, Julie et al. (2014) Molecular indexing enables quantitative targeted RNA sequencing and reveals poor efficiencies in standard library preparations. Proc Natl Acad Sci U S A 111:1891-6|
|Khan, Mohammed A S; Sahani, Nita; Neville, Kevin A et al. (2014) Nonsurgically induced disuse muscle atrophy and neuromuscular dysfunction upregulates alpha7 acetylcholine receptors. Can J Physiol Pharmacol 92:1-8|
|Ueda, Masashi; Iwasaki, Hajime; Wang, Shuxing et al. (2014) Cannabinoid receptor type 1 antagonist, AM251, attenuates mechanical allodynia and thermal hyperalgesia after burn injury. Anesthesiology 121:1311-9|
|Ibrahim, Amir; Fagan, Shawn; Keaney, Tim et al. (2014) A simple cost-saving measure: 2.5% mafenide acetate solution. J Burn Care Res 35:349-53|
|Shank, Erik S; Martyn, Jeevendra A; Donelan, Mathias B et al. (2014) Ultrasound-Guided Regional Anesthesia for Pediatric Burn Reconstructive Surgery: A Prospective Study. J Burn Care Res :|
Showing the most recent 10 out of 77 publications