Burns : journal of the International Society for Burn Injuries
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Infection risk, sepsis and mortality after severe burn are primarily determined by patient age, burn size, and depth. Whether genetic differences contribute to otherwise unexpected variability in outcomes is unknown. We sought to determine whether there was an association between IL-6, IL-10 and IL-17 polymorphisms with cytokine production and development of sepsis. ⋯ Only IL-10 promoter -1082GG genotype was related to an increased IL-10 production in burned patients. In addition, septic subjects bearing -1082G/G genotype have shown the highest and non-septic bearing -1082A/* genotypes the lowest IL-10 serum levels. All together these data seem to indicate that genetically determined individual difference in IL-10 production might influence the susceptibility to septic complications in burned patients and suggest that these markers might be useful in burned patient management.
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Split-thickness skin autografts are the gold-standard in providing permanent acute wound closure in major burns. Split-thickness dermal grafts harvested from the same donor site may provide an additional autologous option for permanent acute coverage and increase the number of potential autologous donor sites. ⋯ Dermis grafts can provide an additional autologous option for permanent coverage in acute major burn wounds without increasing donor site size or morbidity.
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Necrotising fasciitis and sepsis caused by the infection of vibrio is a rare but dangerous clinical emergency, with a mortality of 50-100%. Early diagnosis and surgical treatment may improve the prognosis significantly. However, valid emergency operation indications are scarce and need to be explored, which will be helpful for the early recognition and selection of operational procedures in patients with vibrio necrotising fasciitis. ⋯ Rapidly progressive local damage and acute deterioration of the patients are the most distinctive clinical manifestations of vibrio necrotising fasciitis. Recognition of the signs of local skin and tissue damage in early stage is crucial for early diagnosis and surgical intervention. Emergency incision and drainage, combined with selective debridement and skin graft, could improve the prognosis of the patients, and preserve the integrity of the patient's limbs as much as possible.
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Transforming growth factor-β1 (TGF-β1) plays a key role in hypertrophic scar formation. A lot of studies have shown that TGF-β1 stimulates fibroblast proliferation, collagen production, and α-smooth muscle actin (α-SMA) expression, inhibits matrix degradation and eventually leads to scar formation. Smad proteins are important intracellular mediators of TGF-β1 signaling, and Smad ubiquitination regulatory factor 2 (Smurf2), an ubiquitin ligase for Smads, plays critical roles in the regulation of TGF-β1/Smad signaling. ⋯ In the present study, we found that hypertrophic scar fibroblasts exhibited increased Smurf2 protein and mRNA levels compared with normal fibroblasts, and the expression of Smurf2 gradually increased in hypertrophic scar fibroblasts after TGF-β1 stimulation. Furthermore, we transfected Smurf2 siRNA into hypertrophic scar fibroblasts, and we found that silencing the expression of Smurf2 in hypertrophic scar fibroblasts dramatically reduced TGF-β1 production, inhibited TGF-β1-induced α-SMA expression and inhibited TGF-β1-induced collagen I synthesis. Our results suggest that the enhanced expression of Smurf2 is involved in the progression of hypertrophic scarring.