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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2009.03.002 Byline: T. Fracasso (a), H. Pfeiffer (a), P. Pellerin (b), B. Karger (a) Keywords: Burn injuries; Morphology; Burning agent; Forensic Abstract: The morphology of burn injuries in 120 consecutive patients from the Department of Plastic and Reconstructive Surgery, CHR, Hospital B in Lille was correlated to the etiology and type of heat. Analysis identified five typical patterns of cutaneous burn injuries. Jet of flame-pattern from methylated spirits and gasoline detonations: superficial burn injuries; sparing of skin wrinkles and the submental region; absence or small amounts of soot; preference of exposed body regions, esp. the face and hands. Explosion-pattern from explosions and electrothermal injuries: superficial burn injuries; sparing of skin wrinkles but not of the submental region; soot; preference of exposed body regions. Alveolar soot arrangement and metallisation in electrothermal injuries. Considerable third-degree burns in dust explosions. Flame-pattern from direct flame effects due to burning gasoline or oil, open fires or ignited clothing: nonuniform depth including large third-degree burns; no sparing of the submental region; soot; preference of body regions covered by clothing. Immersion-pattern: superficial (bullous) injuries; blurred junction between scalded and unscalded areas; extremities, buttocks, and back are favourite sites; cave child abuse: waterlines and zebra-burns. Spilling-pattern: superficial injuries; sharp junction between scalded and unscalded areas; head, anterior trunk, and upper extremities are favourite sites; running off and splashing stains. Consideration of these patterns can assist the reconstruction in fire investigations or unclear scaldings. In cases of suspected arson, a typical burn injury pattern or a single finding not compatible with the rest of the pattern can disprove a suspect or raise the level of suspicion. Author Affiliation: (a) Institute of Legal Medicine, University Hospital, Rontgenstr. 23, 48149 Munster, Germany (b) Department of Plastic and Reconstructive Surgery, CHR, Hospital B, 2 Av. Oscar Lambret, 59037 Lille Cedex, France Article History: Received 14 October 2008; Revised 5 February 2009; Accepted 2 March 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2008.09.019 Byline: Douglas H. Ubelaker Keywords: Burning; Skeletal; Thermal Abstract: In recent years, research and case experience have greatly augmented knowledge regarding the effects of extreme heat on skeletal remains. As a result of this effort, enhanced interpretation is now possible on such issues as the extent of recovery, reconstruction, trauma, individual identification, size reduction, thermal effects on histological structures, color variation, the determination if remains were burned with or without soft tissue, DNA recovery and residual weight. The rapidly growing literature in this area of forensic science includes experimental research that elucidates the dynamics of the thermal impact on skeletal structure and morphology. Author Affiliation: Department of Anthropology, Smithsonian Institution, NMNH, MRC 112, Washington, DC 20560-0112, United States Article History: Received 17 September 2008; Accepted 25 September 2008

Background Stress, both acute and chronic, can impair cutaneous wound repair, which has previously been mechanistically ascribed to stress-induced elevations of cortisol. Here we aimed to examine an alternate explanation that the stress-induced hormone epinephrine directly impairs keratinocyte motility and wound re-epithelialization. Burn wounds are examined as a prototype of a high-stress, high-epinephrine, wound environment. Because keratinocytes express the [beta]2-adrenergic receptor ([beta]2AR), another study objective was to determine whether [beta]2AR antagonists could block epinephrine effects on healing and improve wound repair. Methods and Findings Migratory rates of normal human keratinocytes exposed to physiologically relevant levels of epinephrine were measured. To determine the role of the receptor, keratinocytes derived from animals in which the ([beta]2AR had been genetically deleted were similarly examined. The rate of healing of burn wounds generated in excised human skin in high and low epinephrine environments was measured. We utilized an in vivo burn wound model in animals with implanted pumps to deliver ([beta]2AR active drugs to study how these alter healing in vivo. Immunocytochemistry and immunoblotting were used to examine the up-regulation of catecholamine synthetic enzymes in burned tissue, and immunoassay for epinephrine determined the levels of this catecholamine in affected tissue and in the circulation. When epinephrine levels in the culture medium are elevated to the range found in burn-stressed animals, the migratory rate of both cultured human and murine keratinocytes is impaired (reduced by 76%, 95% confidence interval [CI] 56%-95% in humans, p < 0.001, and by 36%, 95% CI 24%-49% in mice, p-0.001), and wound re-epithelialization in explanted burned human skin is delayed (by 23%, 95% CI 10%-36%, p-0.001), as compared to cells or tissues incubated in medium without added epinephrine. This impairment is reversed by ([beta]2AR antagonists, is absent in murine keratinocytes that are genetically depleted of the ([beta]2AR, and is reproduced by incubation of keratinocytes with other ([beta]2AR-specific agonists. Activation of the ([beta]2AR in cultured keratinocytes signals the down-regulation of the AKT pathway, accompanied by a stabilization of the actin cytoskeleton and an increase in focal adhesion formation, resulting in a nonmigratory phenotype. Burn wound injury in excised human skin also rapidly up-regulates the intra-epithelial expression of the epinephrine synthesizing enzyme phenylethanolamine-N- met hyltransferase, and tissue levels of epinephrine rise dramatically (15-fold) in the burn wounded tissue (values of epinephrine expressed as pg/ug protein [+ or -] standard error of the mean: unburned control, 0.6 [+ or -] 0.36; immediately postburn, 9.6 [+ or -] 1.58; 2 h postburn, 3.1 [+ or -] 1.08; 24 h post-burn, 6.7 [+ or -] 0.94). Finally, using an animal burn wound model (20% body surface in mice), we found that systemic treatment with [beta]AR antagonists results in a significant increase (44%, 95% CI 27%-61%, p < 0.00000001) in the rate of burn wound re-epithelialization. Conclusions This work demonstrates an alternate pathway by which stress can impair healing: by stress-induced elevation of epinephrine levels resulting in activation of the keratinocyte ([beta]2AR and the impairment of cell motility and wound re-epithelialization. Furthermore, since the burn wound locally generates epinephrine in response to wounding, epinephrine levels are locally, as well as systemically, elevated, and wound healing is impacted by these dual mechanisms. Treatment with beta adrenergic antagonists significantly improves the rate of burn wound re-epithelialization. This work suggests that specific ([beta]2AR antagonists may be apt, near-term translational therapeutic targets for enhancing burn wound healing, and may provide a novel, low-cost, safe approach to improving skin wound repair in the stressed individual., Introduction Major burn injury, characterized by burns of greater than 20% of body surface area, is associated with significant multisystem dysfunction [1]. The absence of a protective epithelium in the [...]

Hypertrophic scar formation is a major clinical problem in the developing and industrialized worlds. Burn injuries, traumatic injuries, and surgical procedures can give rise to exuberant scarring that results in [...]

Severe burn trauma is generally followed by a catabolic response that leads to muscle wasting and weakness affecting skeletal musculature. Here, we perform whole-genome expression and in vivo NMR spectroscopy studies to define respectively the full set of burn-induced changes in skeletal muscle gene expression and the role of mitochondria in the altered energy expenditure exhibited by burn patients. Our results show 1,136 genes differentially expressed in a mouse hind limb burn model and identify expression pattern changes of genes involved in muscle development, protein degradation and biosynthesis, inflammation, and mitochondrial energy and metabolism. To assess further the role of mitochondria in burn injury, we performed in vivo [sup.31]P NMR spectroscopy on hind limb skeletal muscle, to noninvasively measure high-energy phosphates and the effect of magnetization transfer on inorganic phosphate (Pi) and phosphocreatine (PCr) resonances during saturation of [gamma]ATP resonance, mediated by the ATP synthesis reactions. Although local burn injury does not alter high-energy phosphates or pH, apart from PCr reduction, it does significantly reduce the rate of [gamma]ATP synthesis, to further implicate a role for mitochondria in burn trauma. These results, in conjunction with our genomic results showing down-regulation of mitochondrial oxidative phosphorylation and related functions, strongly suggest alterations in mitochondrial-directed energy expenditure reactions, advancing our understanding of skeletal muscle dysfunction suffered by burn injury patients. mitochondria | mitochondrial oxidative phosphorylation | muscle dysfunction | nuclear magnetic resonance