Institution
Shriners Hospitals for Children - Galveston
Healthcare•Galveston, 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 published on a yearly basis
Papers
More filters
••
TL;DR: It is demonstrated that early institution of enteral feeding can attenuate the stress response, abate hypermetabolism, and improve patient outcome in the burn patient.
Abstract: Significant weight loss is a common complication of a major burn injury. Before the modern era of early enteral nutrition support, such a complication contributed significantly to impaired wound healing, raised risk of infectious morbidity, and ultimately increased mortality. Nutrition management of the burn patient is designed to promote wound healing while minimizing loss of lean body mass. The burn patient characteristically demonstrates an increase in energy expenditure after the initial injury and period of resuscitation. Studies have demonstrated that early institution of enteral feeding can attenuate the stress response, abate hypermetabolism, and improve patient outcome.
41 citations
••
TL;DR: The increased susceptibility of mice, 10–30 days after burn injury to MRSA infection, may be controlled through the intervention of CCL1 production by M2bMΦ appearing in association with severe burn injuries.
Abstract: Patients with 10-30 days postburn injury are greatly susceptible to infections. M1M (IL-10(-)IL-12(+) M) are essential cells in host antibacterial innate immunity against MRSA infections. However, these effector cells are not easily generated in hosts who are carriers of M2bM (IL-12(-)IL-10(+)CCL1(+)LIGHT(+) M). M2bM are inhibitory on M1M generation. In this study, the antibacterial resistance of mice, 10-30 days postburn injury against MRSA infection, was improved by the modulation of M2bM activities. Unburned mice inoculated with M preparations from mice, 10-30 days after burn injury, were susceptible to MRSA infection, whereas unburned mice, inoculated with M preparations from the same mice that were previously treated with CCL1 antisense ODN, were resistant to the infection. M2bM, isolated from Day 15 burn mice, lost their M2bM properties 3 days after cultivation under frequent medium changes, whereas their M2bM properties remained in the same cultures supplemented with rCCL1. In cultures, M preparations from Day 15 burn mice treated with CCL1 antisense ODN did not produce CCL1 and did convert to M1M after heat-killed MRSA stimulation. Also, Day 15 burn mice treated with the ODN became resistant against MRSA infection. These results indicate that CCL1 released from M2bM is essentially required for the maintenance of their properties. The increased susceptibility of mice, 10-30 days after burn injury to MRSA infection, may be controlled through the intervention of CCL1 production by M2bM appearing in association with severe burn injuries.
40 citations
••
TL;DR: Respiratory capacity and function of skeletal muscle mitochondria in healthy individuals and in burn victims for up to 2 years postinjury are determined and quantitative and qualitative derangements in skeletal muscle bioenergetics likely contribute to the long-term pathophysiological stress response to burn trauma.
Abstract: The long-term impact of burn trauma on skeletal muscle bioenergetics remains unknown. Here, the authors determined respiratory capacity and function of skeletal muscle mitochondria in healthy individuals and in burn victims for up to 2 years postinjury. Biopsies were collected from the m. vastus lateralis of 16 healthy men (26 ± 4 years) and 69 children (8 ± 5 years) with burns encompassing ≥30% of their total BSA. Seventy-nine biopsies were collected from cohorts of burn victims at 2 weeks (n = 18), 6 months (n = 18), 12 months (n = 25), and 24 months (n = 18) postburn. Hypermetabolism was determined by the difference in predicted and measured metabolic rate. Mitochondrial respiration was determined in saponin-permeabilized myofiber bundles. Outcomes were modeled by analysis of variance, with differences in groups assessed by Tukey-adjusted contrasts. Burn patients were hypermetabolic for up to 2 years postinjury. Coupled mitochondrial respiration was lower at 2 weeks (17 [8] pmol/sec/mg; P < .001), 6 months (41 [30] pmol/sec/mg; P = .03), and 12 months (35 [14] pmol/sec/mg; P < .001) postburn compared with healthy controls (58 [13] pmol/sec/mg). Coupled respiration was greater at 6, 12, and 24 months postburn vs 2 weeks postburn (P < .001). Mitochondrial adenosine diphosphate and oligomycin sensitivity (measures of coupling control) were lower at all time-points postburn vs control (P < .05), but greater at 6, 12, and 24 months postburn vs 2 weeks postburn (P < .05). Muscle mitochondrial respiratory capacity remains significantly lower in burn victims for 1-year postinjury. Mitochondrial coupling control is diminished for up to 2 years postinjury in burn victims, resulting in greater mitochondrial thermogenesis. These quantitative and qualitative derangements in skeletal muscle bioenergetics likely contribute to the long-term pathophysiological stress response to burn trauma.
40 citations
••
TL;DR: The recent rediscovery of BAT depots in adult humans has rekindled scientific interest in the manipulation of mitochondrial uncoupling reactions as a means to increase metabolic rate, thereby counteracting obesity and its associated metabolic phenotype.
Abstract: Obesity and its metabolic consequences represent a significant clinical problem. From a thermodynamic standpoint, obesity results from a discord in energy intake and expenditure. To date, lifestyle interventions based on reducing energy intake and/or increasing energy expenditure have proved ineffective in the prevention and/or treatment of obesity, owing to poor long-term adherence to such interventions. Thus, an effective strategy to prevent or correct obesity is currently lacking. As the combustion engines of our cells, mitochondria play a critical role in energy expenditure. At a whole-body level, approximately 80% of mitochondrial membrane potential generated by fuel oxidation is used to produce ATP, and the remaining 20% is lost through heat-producing uncoupling reactions. The coupling of mitochondrial respiration to ATP production represents an important component in whole-body energy expenditure. Brown adipose tissue (BAT) is densely populated with mitochondria containing the inner mitochondrial proton carrier uncoupling protein 1 (UCP1). UCP1 uncouples oxidative phosphorylation, meaning that mitochondrial membrane potential is dissipated as heat. The recent rediscovery of BAT depots in adult humans has rekindled scientific interest in the manipulation of mitochondrial uncoupling reactions as a means to increase metabolic rate, thereby counteracting obesity and its associated metabolic phenotype. In this article, we discuss the evidence for the role BAT plays in metabolic rate and glucose and lipid metabolism in humans and the potential for UCP1 recruitment in the white adipose tissue of humans. While the future holds much promise for a therapeutic role of UCP1 expressing adipocytes in human energy metabolism, particularly in the context of obesity, tissue-specific strategies that activate or recruit UCP1 in human adipocytes represent an obligatory translational step for this early promise to be realized.
39 citations
••
TL;DR: Prescription and follow-up assessment of cardiopulmonary endurance training are inconsistent among institutions, underscoring the need for greater awareness of the importance of exercise in any burn rehabilitation program.
Abstract: Exercise programs capable of contributing positively to the long-term rehabilitation of burn patients should be included in outpatient rehabilitation programs. However, the extent and intensity of the resistance and cardiopulmonary exercise prescribed are unclear. This study was conducted to investigate the existence, design, content, and prescription of outpatient cardiopulmonary and resistance exercise programs within outpatient burn rehabilitation. A survey was designed to gather information on existing exercise programs for burn survivors and to assess the extent to which these programs are included in overall outpatient rehabilitation programs. Three hundred and twenty-seven surveys were distributed in the licensed physical and occupational therapists part of the American Burn Association Physical Therapy/Occupational Therapy Special Interest Group. One hundred and three surveys were completed. Eighty-two percent of respondents indicated that their institutions offered outpatient therapy after discharge. The frequency of therapists' contact with patients during this period varied greatly. Interestingly, 81% of therapists stated that no hospital-based cardiopulmonary endurance exercise programs were available. Patients' physical function was infrequently determined through the use of cardiopulmonary parameters (oxygen consumption and heart rate) or muscle strength. Instead, more subjective parameters such as range of motion (75%), manual muscle testing (61%), and quality of life (61%) were used. Prescription and follow-up assessment of cardiopulmonary endurance training are inconsistent among institutions, underscoring the need for greater awareness of the importance of exercise in any burn rehabilitation program. Identification of cardiopulmonary and progressive resistance parameters for establishing and tracking exercise training is also needed to maximize exercise-induced benefits.
39 citations
Authors
Showing all 250 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert R. Wolfe | 124 | 566 | 54000 |
Csaba Szabó | 123 | 958 | 61791 |
David N. Herndon | 108 | 1227 | 54888 |
Steven E. Wolf | 74 | 419 | 21329 |
Blake B. Rasmussen | 65 | 152 | 18951 |
Marc G. Jeschke | 64 | 174 | 13903 |
Daniel L. Traber | 62 | 629 | 14801 |
Nicole S. Gibran | 60 | 273 | 14304 |
Donald S. Prough | 58 | 508 | 11644 |
David L. Chinkes | 56 | 151 | 11871 |
Labros S. Sidossis | 53 | 224 | 11636 |
Robert E. Barrow | 51 | 130 | 7114 |
Ashok K. Chopra | 49 | 199 | 7568 |
James A. Carson | 49 | 157 | 7554 |
Celeste C. Finnerty | 48 | 172 | 10647 |