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.

Brown adipose tissue is linked to a distinct thermoregulatory response to mild cold in people

Abstract: Brown adipose tissue (BAT) plays an important role in thermoregulation in rodents. Its role in temperature homeostasis in people is less studied. To this end, we recruited 18 men [8 subjects with no/minimal BAT activity (BAT-) and 10 with pronounced BAT activity (BAT+)]. Each volunteer participated in a 6 h, individualized, non-shivering cold exposure protocol. BAT was quantified using positron emission tomography/computed tomography. Body core and skin temperatures were measured using a telemetric pill and wireless thermistors, respectively. Core body temperature decreased during cold exposure in the BAT- group only (-0.34°C, 95% CI: -0.6 to -0.1, p = 0.03), while the cold-induced change in core temperature was significantly different between BAT+ and BAT- subjects (BAT+ vs. BAT-, 0.43°C, 95% CI: 0.20-0.65, p = 0.0014). BAT volume was associated with the cold-induced change in core temperature (p = 0.01) even after adjustment for age and adiposity. Compared to the BAT- group, BAT+ subjects tolerated a lower ambient temperature (BAT-: 20.6 ± 0.3°C vs. BAT+: 19.8 ± 0.3°C, p = 0.035) without shivering. The cold-induced change in core temperature (r = 0.79, p = 0.001) and supraclavicular temperature (r = 0.58, p = 0.014) correlated with BAT volume, suggesting that these non-invasive measures can be potentially used as surrogate markers of BAT when other methods to detect BAT are not available or their use is not warranted. These results demonstrate a physiologically significant role for BAT in thermoregulation in people. This trial has been registered with Clinaltrials.gov: NCT01791114 (https://clinicaltrials.gov/ct2/show/NCT01791114).

Human Mitochondrial Oxidative Capacity Is Acutely Impaired After Burn Trauma

Abstract: Background Mitochondrial proteins and genes are damaged after burn injury in animals and are assessed in human burn patients in this study. Methods The rates of maximal muscle mitochondrial oxidative capacity (adenosine triphosphate production) and uncoupled oxidation (heat production) for both palmitate and pyruvate were measured in muscle biopsies from 40 children sustaining burns on more than 40% of their body surface area and from 13 healthy children controls. Results Maximal mitochondrial oxidation of pyruvate and palmitate were reduced in burn patients compared with controls (4.0 ± .2:1.9 ± .1 μmol O 2 /citrate synthase activity/mg protein/min pyruvate; control:burn; P 2 /citrate synthase activity/mg protein/min palmityl CoA; control:burn; P = .003). Uncoupled oxidation was the same between groups. Conclusions The maximal coupled mitochondrial oxidative capacity is severely impaired after burn injury, although there are no alterations in the rate of uncoupled oxidative capacity. It may be that the ratio of these indicates that a larger portion of energy production in trauma patients is wasted through uncoupling, rather than used for healing.

Extracorporeal membrane oxygenation in the treatment of respiratory failure in pediatric patients with burns.

Abstract: Extracorporeal membrane oxygenation (ECMO) as a treatment for pulmonary failure from postshock respiratory distress in burned children recently has been shown to salvage patients who were thought to have more than a 90% chance of dying. We describe five burned children in whom severe respiratory failure--not responsive to medical management and maximal ventilatory support--developed, and who underwent ECMO treatment. Three (60%) cases involved flame burns, with significant inhalation injury as diagnosed after a bronchoscopy; mean age was 3 years (2 to 4 years), with a mean total body surface area (TBSA) burn of 32% (15% to 53%), mean third-degree burns of 25% (5% to 53%). Two (40%) cases involved scald burns; mean age was 6 years (7 months to 11 years), with a mean TBSA burn of 56.5% (43% to 70%), mean third-degree burns of 40% (10.5% to 70%). Outcome was poor for those burned children who received ECMO therapy after prolonged ventilatory support for smoke inhalation injury. Children who experience perfusion/reperfusion shock injury to the lungs as a result of delayed resuscitation of scald burns may have an improved chance of survival with short courses of ECMO regardless of the burn size.

PPAR-α agonism improves whole body and muscle mitochondrial fat oxidation, but does not alter intracellular fat concentrations in burn trauma children in a randomized controlled trial

Abstract: Insulin resistance is often associated with increased levels of intracellular triglycerides, diacylglycerol and decreased fat β-oxidation. It was unknown if this relationship was present in patients with acute insulin resistance induced by trauma. A double blind placebo controlled trial was conducted in 18 children with severe burn injury. Metabolic studies to assess whole body palmitate oxidation and insulin sensitivity, muscle biopsies for mitochondrial palmitate oxidation, diacylglycerol, fatty acyl Co-A and fatty acyl carnitine concentrations, and magnetic resonance spectroscopy for muscle and liver triglycerides were compared before and after two weeks of placebo or PPAR-α agonist treatment. Insulin sensitivity and basal whole body palmitate oxidation as measured with an isotope tracer increased significantly (P = 0.003 and P = 0.004, respectively) after PPAR-α agonist treatment compared to placebo. Mitochondrial palmitate oxidation rates in muscle samples increased significantly after PPAR-α treatment (P = 0.002). However, the concentrations of muscle triglyceride, diacylglycerol, fatty acyl CoA, fatty acyl carnitine, and liver triglycerides did not change with either treatment. PKC-θ activation during hyper-insulinemia decreased significantly following PPAR-α treatment. PPAR-α agonist treatment increases palmitate oxidation and decreases PKC activity along with reduced insulin sensitivity in acute trauma, However, a direct link between these responses cannot be attributed to alterations in intracellular lipid concentrations.