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Barrow, Robert E.; Dasu, Mohan; Ferrando, Arny A.; Spies, Marcus; Thomas, Stephen B.; Perez-Polo, J.; Herndon, David N.

doi:10.1097/00000658-200303000-00018

Cited by 7 publications

(5 citation statements)

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“…50nM of insulin treatment improved myotube fusion and creatine kinase activity in C2C12 cell lines through NF-κB/MAPKs pathways (33). Oxandrolone administration was shown to increase muscle myogenesis with MRF4 gene expression action in pediatric burn patients (34). These data provide fundamental evidence to link tissue metabolic status and cellular homeostasis in response to severe injury.…”

Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Loss is Associated with TNF Mediated Insufficient Skeletal Myogenic Activation After Burn

Song

Saeman

Libero

et al. 2015

Shock

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Muscle loss accompanies severe burn; in this hyper-catabolic state, muscle undergoes atrophy through protein degradation and disuse. Muscle volume is related to the relative rates of cellular degradation and myogenesis. We hypothesize that muscle atrophy after injury is in part due to insufficient myogenesis associated with the hyper-inflammatory response. The aim of the study is to investigate the role of skeletal myogenesis and muscle cell homeostasis in response to severe burn. Twenty-eight male C57BL6 mice received 25% TBSA scald. Gluteus muscle from these animals was analysed at day 1, 3, 7 and 14 after injury. Six additional animals without burn served as controls. We showed muscle wet weight and protein content decreased at day 3 and 7 after burn, with elevated TNF mRNA expression (p< 0.05). Increased cell death was observed through TUNEL staining, and cleaved caspase-3 levels reached a peak in muscle lysate at day 3 (p < 0.05). The cell proliferation marker PCNA significantly increased after burn, associated with increased gene and protein expression of myogenesis markers Pax7 and myogenin. However, desmin mRNA expression and the ratio of desmin to PCNA protein expression significantly decreased at day 7 (p < 0.05). In vitro, the ratio of desmin to PCNA protein expression significantly decreased in C2C12 murine myoblasts after TNF-α stimulation for 24 hours. We showed that severe burn induces both increased cell death and proliferation. However, myogenesis does not counterbalance increased cell death after burn. Data suggest insufficient myogenesis might be associated with pro-inflammatory mediator TNF activity.

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Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Loss is Associated with TNF Mediated Insufficient Skeletal Myogenic Activation After Burn

Song

Saeman

Libero

et al. 2015

Shock

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“…Oxandrolone administered at 0.1 mg/kg twice daily has been shown to enhance protein synthesis and upregulate anabolic genes in acute pediatric burn patients [160], and similarbenefits have also been demonstrated in adult patients [161]. Long-term benefits include increased bone mineral density and LBM up to 12 months post burn [161].…”

Section: Clinical Managementmentioning

confidence: 99%

Alcohol Modulation of the Postburn Hepatic Response

Chen

Carter

Curtis

et al. 2017

Journal of Burn Care & Research

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The widespread and rapidly increasing trend of binge drinking is accompanied by a concomitant rise in the prevalence of trauma patients under the influence of alcohol at the time of their injury. Epidemiologic evidence suggests up to half of all adult burn patients are intoxicated at the time of admission and the presence of alcohol is an independent risk factor for death in the early stages post burn. As the major site of alcohol metabolism and toxicity, the liver is a critical determinant of post burn outcome and experimental evidence implies an injury threshold exists beyond which burn-induced hepatic derangement is observed. Alcohol may lower this threshold for post burn hepatic damage through a variety of mechanisms including modulation of extrahepatic events, alteration of the gut-liver axis, and changes in signaling pathways. The direct and indirect effects of alcohol may prime the liver for the second-hit of many overlapping physiologic responses to burn injury. In an effort to gain a deeper understanding of how alcohol potentiates post burn hepatic damage, we summarize possible mechanisms by which alcohol modulates the post burn hepatic response.

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“…Oxandrolone has been used in acute and rehabilitating adult burn patients with promising results with regard to weight gain, net protein synthesis in the muscle, and LBM [65, 66]. When treated orally with 0.1 mg/kg oxandrolone twice daily, acute pediatric burn patients exhibit enhanced protein anabolism and upregulation of anabolic genes in the muscle [67, 68]. Oxandrolone affects LBM and bone mineral density not only in the acute setting, but also up to 12 months post burn [68].…”

Section: Current Therapies Administered To Counteract Specific Aspmentioning

confidence: 99%

Burns: an update on current pharmacotherapy

Rojas¹,

Finnerty

Radhakrishnan³

et al. 2012

Expert Opinion on Pharmacotherapy

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Introduction The world-wide occurrence of burn injuries remains high despite efforts to reduce injury incidence through public awareness campaigns and improvements in living conditions. In 2004, almost 11 million people experienced burns severe enough to warrant medical treatment. Advances over the past several decades in aggressive resuscitation, nutrition, excision, and grafting have reduced morbidity and mortality. Incorporation of pharmacotherapeutics into treatment regimens may further reduce complications of severe burn injuries. Areas covered Severe burn injuries, as well as other forms of stress and trauma, trigger a hypermetabolic response that, if left untreated, impedes recovery. In the past two decades, use of anabolic agents, beta adrenergic receptor antagonists, and anti-hyperglycemic agents has successfully counteracted post-burn morbidities including catabolism, the catecholamine-mediated response, and insulin resistance. Here we review the most up-to-date information on currently used pharmacotherapies in the treatment of these sequelae of severe burns and the insights that have expanded our understanding of the pathophysiology of severe burns. Expert opinion Existing drugs offer promising advances in the care of burn injuries. Continued gains in our understanding of the molecular mechanisms driving the hypermetabolic response will enable the application of additional existing drugs to be broadened to further attenuate the hypermetabolic response.

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Abstract: DNA microarray technology will help identify molecular changes that can serve as targets for new therapies to attenuate muscle wasting in severely burned children and thus improve recovery and early rehabilitation.

Cited by 7 publications

References 0 publications

Skeletal Muscle Loss is Associated with TNF Mediated Insufficient Skeletal Myogenic Activation After Burn

Skeletal Muscle Loss is Associated with TNF Mediated Insufficient Skeletal Myogenic Activation After Burn

Alcohol Modulation of the Postburn Hepatic Response

Burns: an update on current pharmacotherapy

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