Shriners Hospitals for Children - Galveston

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.

Alternative splinting methods for the prevention and correction of burn scar torticollis.

Abstract: Significant neck burns may lead to deforming lateral flexion and rotation contractures. A two-device splinting regimen has been designed to prevent such contractures. In the acute phase, the Dynamic Antitorticollis Strap is applied while the patient is in bed to gently rotate the head and neck toward the neutral position. This dynamic strap includes a Velfoam headband attached to Thera-Band secured to the patient's bed. The antitorticollis neck splint is used in the rehabilitation phase and can be serially adjusted to correct lateral flexion contractures of the neck. Thermoplastic material is cut from a modified neck splint pattern and draped over the temporaloccipital region and anterior/posterior shoulder ipsilateral to the contracture and the anterior and contralateral aspect of the neck. The combined use of these devices during the scar maturation phase provides therapists with alternatives in preventing burn scar torticollis.

Effects of metformin on burn-induced hepatic endoplasmic reticulum stress in male rats.

Abstract: Severe burn injury causes hepatic dysfunction that results in major metabolic derangements including insulin resistance and hyperglycemia and is associated with hepatic endoplasmic reticulum (ER) stress. We have recently shown that insulin reduces ER stress and improves liver function and morphology; however, it is not clear whether these changes are directly insulin mediated or are due to glucose alterations. Metformin is an antidiabetic agent that decreases hyperglycemia by different pathways than insulin; therefore, we asked whether metformin affects postburn ER stress and hepatic metabolism. The aim of the present study is to determine the effects of metformin on postburn hepatic ER stress and metabolic markers. Male rats were randomized to sham, burn injury and burn injury plus metformin and were sacrificed at various time points. Outcomes measured were hepatic damage, function, metabolism and ER stress. Burn-induced decrease in albumin mRNA and increase in alanine transaminase (p < 0.01 versus sham) were not normalized by metformin treatment. In addition, ER stress markers were similarly increased in burn injury with or without metformin compared with sham (p < 0.05). We also found that gluconeogenesis and fatty acid metabolism gene expressions were upregulated with or without metformin compared with sham (p < 0.05). Our results indicate that, whereas thermal injury results in hepatic ER stress, metformin does not ameliorate postburn stress responses by correcting hepatic ER stress.

Moderate-intensity aerobic exercise improves skeletal muscle quality in older adults.

Abstract: Sarcopenia, age-associated involuntary loss of muscle and strength, can progress to clinically relevant functional decline. Resistance exercise attenuates muscle and strength loss but may not be feasible for some older adults. Aerobic exercise training (AET) improves cardiopulmonary health; however, effects on protein turnover, muscle mass, and strength are less clear. We aimed to determine whether AET improves basal myofibrillar protein synthesis (MPS) and capillarization, promoting hypertrophy and strength. We hypothesized that AET improves strength with increased MPS and capillarization. Older adults were randomized to non-exercise (NON; n = 11, 71.4 ± 4.18 years) or exercise (EX; n = 12, 73.7 ± 4.05 years). EX completed 24 weeks of AET (walking 3×/week, 45 minutes, 70% heart rate reserve); NON remained sedentary. A stable isotope tracer was infused. MPS and capillarization were analyzed from vastus lateralis muscle biopsies. Strength was measured via isokinetic dynamometry. Lean mass was determined with dual-energy X-ray absorptiometry. Basal MPS increased in EX (+50.7%, P = 0.01) along with capillary density (+66.4%, P = 0.03), peak oxygen consumption (+15.8%, P = 0.01), quadriceps strength (+15.1%, P = 0.01), and muscle quality (peak torque divided by leg lean mass, +15.5%, P = 0.01). Lean mass did not change (P > 0.05). AET increases muscle protein turnover and capillarization in older adults, improving muscle quality.

CD4+ T-cell depletion is not associated with alterations in survival, bacterial clearance, and inflammation after cecal ligation and puncture.

Abstract: Our recent studies indicate that mice depleted of T cells that bear the alphabeta T-cell receptor (alphabeta T cells) show less inflammation, less physiological dysfunction, and improved survival after cecal ligation and puncture (CLP) compared with control mice. Classic CD4(+) and CD8(+) T cells comprise most of the alphabeta T-cell population. We previously showed that CD8(+) T cells, in conjunction with natural killer (NK) cells, participate in CLP-induced inflammation. However, the contribution of CD4(+) T cells to the early inflammatory response caused by CLP is largely undefined. In the present study, we evaluated CLP-induced mortality, bacterial clearance, and inflammation in mice that were depleted of CD4(+) T cells. Compared with control mice, CD4 knockout mice and wild-type mice treated with anti-CD4 did not show significant differences in survival, cytokine production, and systemic bacterial counts. The combined depletion of CD4(+) T and NK cells resulted in improved survival and decreased cytokine production compared with mice possessing a full lymphocyte complement, especially when CD4(+) T and NK cell-deficient mice were treated with imipenem. These improvements were nearly identical to those observed in mice depleted only of NK cells. These studies show that CD4(+) T cells do not seem to play a critical role in facilitating the early inflammatory response caused by CLP.

Inducible satellite cell depletion attenuates skeletal muscle regrowth following a scald-burn injury

Abstract: Key points Severe burns result in significant skeletal muscle cachexia that impedes recovery. Activity of satellite cells, skeletal muscle stem cells, is altered following a burn injury and likely hinders regrowth of muscle. Severe burn injury induces satellite cell proliferation and fusion into myofibres with greater activity in muscles proximal to the injury site. Conditional depletion of satellite cells attenuates recovery of myofibre area and volume following a scald burn injury in mice. Skeletal muscle regrowth following a burn injury requires satellite cell activity, underscoring the therapeutic potential of satellite cells in the prevention of prolonged frailty in burn survivors. Abstract Severe burns result in profound skeletal muscle atrophy; persistent muscle atrophy and weakness are major complications that hamper recovery from burn injury. Many factors contribute to the erosion of muscle mass following burn trauma, and we have previously shown concurrent activation and apoptosis of muscle satellite cells following a burn injury in paediatric patients. To determine the necessity of satellite cells during muscle recovery following a burn injury, we utilized a genetically modified mouse model (Pax7CreER-DTA) that allows for the conditional depletion of satellite cells in skeletal muscle. Additionally, mice were provided 5-ethynyl-2′-deoxyuridine to determine satellite cell proliferation, activation and fusion. Juvenile satellite cell-wild-type (SC-WT) and satellite cell-depleted (SC-Dep) mice (8 weeks of age) were randomized to sham or burn injury consisting of a dorsal scald burn injury covering 30% of total body surface area. Both hindlimb and dorsal muscles were studied at 7, 14 and 21 days post-burn. SC-Dep mice had >93% depletion of satellite cells compared to SC-WT (P < 0.05). Burn injury induced robust atrophy in muscles located both proximal and distal to the injury site (∼30% decrease in fibre cross-sectional area, P < 0.05). Additionally, burn injury induced skeletal muscle regeneration, satellite cell proliferation and fusion. Depletion of satellite cells impaired post-burn recovery of both muscle fibre cross-sectional area and volume (P < 0.05). These findings support an integral role for satellite cells in the aetiology of lean tissue recovery following a severe burn injury.