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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
TL;DR: The absence of any up‐regulation of MMP‐1 and M MP‐3 in hypertrophic scar fibroblasts, in response to IL‐6, suggests that suppression of matrix metalloproteinases may play a role in the excessive accumulation of collagen formed in hypertrophied scars.
Abstract: The structural rearrangement of collagen fibres in hypertrophic scar causes abnormal contracture, low tensile strength, and raised scars, which cause functional impairment and disfigurement. It is hypothesized that changes in the genes of cytokines, extracellular matrix proteins, and proteins regulating programmed cell death are related to hypertrophic scar formation. To test this hypothesis, fibroblasts were cultured from hypertrophic scars and their response to interleukin-6 (IL-6) stimulation was studied by defining their gene expression profiles. Affymetrix gene chip analysis was used to identify up- or down-regulation in the 12 625 genes present in the affymetrix array. RT-PCR and ELISA assays were used to validate microarray expression profiles further. Comparison of gene profiles showed an increase of 12 genes in hypertrophic scar fibroblasts compared with normal skin fibroblasts, while the expression of 14 genes decreased. Thirty-three genes were affected by IL-6 treatment in the hypertrophic scar fibroblasts, while 57 genes were affected in normal skin fibroblasts. Messenger RNA to beta-actin ratios for matrix metalloproteinase-1 (MMP-1) and MMP-3 were increased with IL-6 in normal skin fibroblasts from 2.43 +/- 0.06 to 5.50 +/- 0.45 and from 0.75 +/- 0.09 to 1.98 +/- 0.01, respectively. No change in these matrix metalloproteinases could be shown with IL-6 stimulation in hypertrophic scar fibroblasts. Secreted protein levels of pro-MMP-1 and MMP-3 were elevated in the supernatants from normal skin fibroblasts from 2.00 +/- 0.09 and 1.72 +/- 0.10 ng/ml to 4.60 +/- 0.12 and 3.41 +/- 0.20 ng/ml, respectively, after treatment with IL-6 (p < 0.05). No changes were observed in hypertrophic scar fibroblasts treated with IL-6. Values are means +/- SEM. The absence of any up-regulation of MMP-1 and MMP-3 in hypertrophic scar fibroblasts, in response to IL-6, suggests that suppression of matrix metalloproteinases may play a role in the excessive accumulation of collagen formed in hypertrophic scars. While the pathogenesis of abnormal hypertrophic scars remains poorly understood, the use of gene expression arrays may prove helpful in identifying the mechanisms responsible for this type of abnormal scar formation and in formulating an effective therapeutic protocol.

73 citations

Journal ArticleDOI
TL;DR: A multidisciplinary group of advanced burn care professionals have compiled, critiqued, and summarized the current evidence of practice in nursing, nutrition, and rehabilitation as it pertains to the prevention of pressure sores after burn injuries.
Abstract: Pressure ulcers represent a complex clinical problem, with a reported incidence of 2.7% to 29.5% in hospitalized patients and an etiology that is multifactorial. The prevention of pressure sores in the burn patient population is clearly an area of practice in need of guidelines for care. A multidisciplinary group of advanced burn care professionals have compiled, critiqued, and summarized herein the current evidence of practice in nursing, nutrition, and rehabilitation as it pertains to the prevention of pressure sores after burn injuries. A broad overview of risk factors and assessment scales is described, and current intervention practices and recommendations for care are provided based, whenever possible, on research findings. In addition, research questions are generated in an attempt to move the specialty of burns toward the formal investigation of pressure sores with the ultimate goal being the development of evidence-based practice guidelines.

72 citations

Journal ArticleDOI
TL;DR: It is shown that NK but not CD1-restricted NKT cells contribute to acute CLP-induced inflammation, which provides new insights into the mechanisms used by NK cells to facilitate acute inflammation during septic shock.
Abstract: Evidence suggests that NK and NKT cells contribute to inflammation and mortality during septic shock caused by cecal ligation and puncture (CLP). However, the specific contributions of these cell types to the pathogenesis of CLP-induced septic shock have not been fully defined. The goal of the present study was to determine the mechanisms by which NK and NKT cells mediate the host response to CLP. Control, NK cell-deficient, and NKT cell-deficient mice underwent CLP. Survival, cytokine production, and bacterial clearance were measured. NK cell trafficking and interaction with myeloid cells was also studied. Results show that mice treated with anti-asialoGM1 (NK cell deficient) or anti-NK1.1 (NK/NKT cell deficient) show less systemic inflammation and have improved survival compared with IgG-treated controls. CD1 knockout mice (NKT cell deficient) did not demonstrate decreased cytokine production or improved survival compared with wild type mice. Trafficking studies show migration of NK cells from blood and spleen into the inflamed peritoneal cavity where they appear to facilitate the activation of peritoneal macrophages (F4-80 + GR-1 − ) and F4-80 + Gr-1 + myeloid cells. These findings indicate that NK but not CD1-restricted NKT cells contribute to acute CLP-induced inflammation. NK cells appear to mediate their proinflammatory functions during septic shock, in part, by migration into the peritoneal cavity and amplification of the proinflammatory activities of specific myeloid cell populations. These findings provide new insights into the mechanisms used by NK cells to facilitate acute inflammation during septic shock.

70 citations

Journal ArticleDOI
TL;DR: In conclusion, incremental starvation produces progressive small bowel atrophy, and the mechanism involves both decreased gut epithelial cell proliferation and increased apoptosis.
Abstract: Starvation induces gut mucosal atrophy, but the effects of progressive dietary restriction are not defined. The study's purpose was to determine the effects of incremental starvation on gut epithelial cell turnover. After food intake of mice was determined, they were divided into five groups: control (ad libitum fed), 75% normal intake, 50% intake, 25% intake, and fasted. Mice were killed after 48 hours, and the proximal small bowel were assessed for weight and protein content. Histologic specimens were examined for villus morphology, apoptosis, and proliferation. After 48 hr of diet restriction, bowel weight decreased in the 50% intake, 25% intake, and fasted groups. Villus density also decreased in the fasted group. Proliferation progressively decreased in the diet-restricted groups. Apoptosis increased in the fasted group, primarily in the villus tip. In conclusion, incremental starvation produces progressive small bowel atrophy. The mechanism involves both decreased gut epithelial cell proliferation and increased apoptosis.

70 citations

Journal ArticleDOI
TL;DR: In this article, the authors examined the incidence and severity of postburn contractures in a large, multicenter, pediatric burn population and determined associated risk factors for the development of contractures.
Abstract: Joint contractures are a major cause of morbidity and functional deficit. The incidence of postburn contractures and their associated risk factors in the pediatric population has not yet been reported. This study examines the incidence and severity of contractures in a large, multicenter, pediatric burn population. Associated risk factors for the development of contractures are determined. Data from the National Institute on Disability and Rehabilitation Research Burn Model System database, for pediatric (younger than 18 years) burn survivors from 1994 to 2003, were analyzed. Demographic and medical data were collected on each subject. The primary outcome measures included the presence of contractures, number of contractures per patient, and severity of contractures at each of nine locations (shoulder, elbow, hip, knee, ankle, wrist, neck, lumbar, and thoracic) at time of hospital discharge. Regression analysis was performed to determine predictors of the presence, severity, and numbers of contractures, with P < .05 used for statistical significance. Of the 1031 study patients, 237 (23%) developed at least 1 contracture at hospital discharge. Among those with at least one contracture, the mean was three (3.3) contractures per person. The shoulder was the most frequently contracted joint (27.9%), followed by the elbow (17.6%), wrist (14.2%), knee (13.3%), and ankle (11.9%). Most contractures were mild (38.5%) or moderate (36.3%) in severity. The statistically significant predictors of contracture development were age and intensive care unit (ICU) length of stay. The statistically significant predictors of severity of contracture were age, ICU length of stay, presence of amputation, and black race. Predictors of the number of contractures included total age, length of stay, length of ICU stay, presence of amputation, TBSA burned, and TBSA grafted. This is the first study to report the epidemiology of postburn contractures in the pediatric population. Approximately one quarter of children with a major burn injury developed a contracture at hospital discharge, and this could potentially increase as the child grows. Contractures develop despite early therapeutic interventions such as positioning and splinting; therefore, it is essential that we identify novel and more effective prevention strategies.

67 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