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Institution

Shriners Hospitals for Children - Galveston

HealthcareGalveston, Texas, United States
About: Shriners Hospitals for Children - Galveston is a healthcare organization based out in Galveston, Texas, United States. It is known for research contribution in the topics: Burn injury & Lean body mass. The organization has 249 authors who have published 420 publications receiving 15311 citations.


Papers
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Journal ArticleDOI
01 Jun 2015-Burns
TL;DR: Overall the groups were comparable in their reports of disability and quality of life, and inhalation injury did not affect long-termquality of life.

23 citations

Journal ArticleDOI
TL;DR: There is increasing research on pain management modalities, but available studies are inadequate to create a true standard of care and it is called for more burn specific research into modalities for burn pain control as well as research on multimodal pain control.
Abstract: The ABA pain guidelines were developed 14 years ago and have not been revised despite evolution in the practice of burn care. A sub-committee of the American Burn Association's Committee on the Organization and Delivery of Burn Care was created to revise the adult pain guidelines. A MEDLINE search of English-language publications from 1968 to 2018 was conducted using the keywords "burn pain," "treatment," and "assessment." Selected references were also used from the greater pain literature. Studies were graded by two members of the committee using Oxford Centre for Evidence-based Medicine-Levels of Evidence. We then met as a group to determine expert consensus on a variety of topics related to treating pain in burn patients. Finally, we assessed gaps in the current knowledge and determined research questions that would aid in providing better recommendations for optimal pain management of the burn patient. The literature search produced 189 papers, 95 were found to be relevant to the assessment and treatment of burn pain. From the greater pain literature 151 references were included, totaling 246 papers being analyzed. Following this literature review, a meeting to establish expert consensus was held and 20 guidelines established in the areas of pain assessment, opioid medications, nonopioid medications, regional anesthesia, and nonpharmacologic treatments. There is increasing research on pain management modalities, but available studies are inadequate to create a true standard of care. We call for more burn specific research into modalities for burn pain control as well as research on multimodal pain control.

23 citations

Journal ArticleDOI
TL;DR: It is suggested that the deleterious effect of burn injury on skeletal muscle AA metabolism persists for up to 1 year post burn and nutritional and pharmacological strategies aimed at attenuating muscle protein breakdown post burn may be a more efficacious approach to maintaining muscle mass in severely burned patients.
Abstract: BACKGROUND Burn injury results in increased skeletal muscle protein turnover, where the magnitude of protein breakdown outweighs synthesis, resulting in muscle wasting. The effect of increased amino acid (AA) provision on skeletal muscle fractional synthesis rate (FSR) in severely burned patients during their convalescence after discharge from hospital is not known. Subsequently, the purpose of this study was to determine skeletal muscle FSR in response to AA infusion in severely burned pediatric patients at discharge from hospital and at 6 and 12 months after injury. METHODS Stable isotope infusion studies were performed in the fasted state and during intravenous AA infusion. Skeletal muscle biopsies were obtained and isotope enrichment was determined to calculate skeletal muscle FSR. Patients were studied at discharge from hospital (n = 11) and at 6 (n = 15) and 12 months (n = 14) after injury. RESULTS The cohorts of patients studied at each time point after injury were not different with regard to age, body mass, or burn size. AA infusion failed to stimulate FSR above basal values at discharge from hospital (mean [SEM]: 0.27% [0.04%] vs. 0.26% [0.06%] per hour), 6 months after injury (0.20% [0.04%] vs. 0.22% [0.03%] per hour), and 12 months after injury (0.16% [0.03%] vs. 0.15% [0.03%] per hour). Daily FSR was numerically lower at 6 months after burn (5.13% [0.78%] per day) and significantly (p < 0.05) lower at 12 months after burn (3.67% [0.65%] per day) relative to discharge group (6.32% [1.02%] per day). DISCUSSION The findings of the current study suggest that the deleterious effect of burn injury on skeletal muscle AA metabolism persists for up to 1 year post burn. In light of these findings, nutritional and pharmacological strategies aimed at attenuating muscle protein breakdown post burn may be a more efficacious approach to maintaining muscle mass in severely burned patients. LEVEL OF EVIDENCE Prognostic study, level II.

23 citations

Journal ArticleDOI
TL;DR: Pulmonary sepsis in mice may be beneficially influenced by specific pharmacological nN OS inhibition at an earlier time point and iNOS inhibition at a later time points post-injury, according to the time changes of the expression and activation of NOS isoforms.

23 citations

Journal ArticleDOI
TL;DR: Results indicate that sepsis stemming from P. aeruginosa burn‐wound infection is accelerated by burn‐induced Gr‐1+CD11b+ cells with abilities to suppress antimicrobial peptide production by epidermal keratinocytes.
Abstract: Using a mouse model of thermal injury, we studied why antimicrobial peptides are not produced at the burn-site tissues and how this defect contributes to the increased susceptibility to Pseudomonas aeruginosa burn-wound infection. Logarithmic growth of P. aeruginosa was demonstrated locally (at the burn site) and systemically (in circulation) in thermally injured mice exposed to 10(2) CFU/mouse of the pathogen beneath the burn wound. However, neither systemic nor local growth of the pathogen was observed in sham burn mice when they were infected intradermally with 10(6) CFU/mouse P. aeruginosa. Murine beta-defensins (MBDs) were detected in the skin homogenates of sham burn mice. However, the amounts of MBDs were reduced greatly in the same tissue homogenates from thermally injured mice. Gr-1(+)CD11b(+) cells, with an ability to suppress antimicrobial peptide production by skin keratinocytes, were isolated from tissues surrounding the burn areas, and these cells were not obtained from skin tissues of sham burn mice. After intradermal inoculation of Gr-1(+)CD11b(+) cells, which were isolated from burn-site tissues, the production of antimicrobial peptides around the cell-inoculation site of sham burn mice decreased. Also, like thermally injured mice, these mice were shown to be susceptible to P. aeruginosa intradermal infection. These results indicate that sepsis stemming from P. aeruginosa burn-wound infection is accelerated by burn-induced Gr-1(+)CD11b(+) cells with abilities to suppress antimicrobial peptide production by epidermal keratinocytes.

22 citations


Authors

Showing all 250 results

NameH-indexPapersCitations
Robert R. Wolfe12456654000
Csaba Szabó12395861791
David N. Herndon108122754888
Steven E. Wolf7441921329
Blake B. Rasmussen6515218951
Marc G. Jeschke6417413903
Daniel L. Traber6262914801
Nicole S. Gibran6027314304
Donald S. Prough5850811644
David L. Chinkes5615111871
Labros S. Sidossis5322411636
Robert E. Barrow511307114
Ashok K. Chopra491997568
James A. Carson491577554
Celeste C. Finnerty4817210647
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20221
20215
202026
201928
201822
201746