Browsing by Subject "Burn"

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    A Prospective, Randomized, Controlled Study to Evaluate the Effectiveness of a Fabric-Based Wireless Electroceutical Dressing Compared to Standard-of-Care Treatment Against Acute Trauma and Burn Wound Biofilm Infection
    (Mary Ann Liebert, 2024) Chan, Rodney K.; Nuutila, Kristo; Mathew-Steiner, Shomita S.; Diaz, Victoria; Anselmo, Kristin; Batchinsky, Maria; Carlsson, Anders; Ghosh, Nandini; Sen, Chandan K.; Roy, Sashwati; Surgery, School of Medicine
    Objective: Despite advances in the use of topical and parenteral antimicrobial therapy and the practice of early tangential burn wound excision to manage bacterial load, 60% of the mortality from burns is attributed to bacterial biofilm infection. A low electric field (∼1 V) generated by the novel FDA-cleared wireless electroceutical dressing (WED) was previously shown to significantly prevent and disrupt burn biofilm infection in preclinical studies. Based on this observation, the purpose of this clinical trial was to evaluate the efficacy of the WED dressing powered by a silver–zinc electrocouple in the prevention and disruption of biofilm infection. Approach: A prospective, randomized, controlled, single-center clinical trial was performed to evaluate the efficacy of the WED compared with standard-of-care (SoC) dressing to treat biofilms. Burn wounds were randomized to receive either SoC or WED. Biopsies were collected on days 0 and 7 for histology, scanning electron microscopy (SEM) examination of biofilm, and for quantitative bacteriological analyses. Results: In total, 38 subjects were enrolled in the study. In 52% of the WED-treated wounds, little to no biofilm could be detected by SEM. WED significantly lowered or prevented increase of biofilm in all wounds compared with the pair-matched SoC-treated wounds. Innovation: WED is a simple, easy, and rapid method to protect the wound while also inhibiting infection. It is activated by a moist environment and the electrical field induces transient and micromolar amounts of superoxide anion radicals that will prevent bacterial growth. Conclusion: WED decreased biofilm infection better compared with SoC. The study was registered in clinicaltrials.gov as NCT04079998.
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    Molecular Mechanisms Responsible for the Rescue Effects of Pamidronate on Muscle Atrophy in Pediatric Burn Patients
    (Frontiers, 2019-08-07) Pin, Fabrizio; Bonetto, Andrea; Bonewald, Lynda F.; Klein, Gordon L.; Anatomy and Cell Biology, School of Medicine
    Not only has pamidronate been shown to prevent inflammation associated bone resorption following burn injury, it also reduces protein breakdown in muscle. The aim of this study was to identify the molecular mechanisms responsible for muscle mass rescue in pamidronate treated compared to placebo/standard of care-treated burn patients. Mature myotubes, generated by differentiating murine C2C12 myoblasts, were exposed for 48 h to 1 or 5% serum obtained from 3 groups of children: normal unburned, burned receiving standard of care, and burned receiving standard of care with pamidronate. Exposure to serum from burned patients caused dose-dependent myotube atrophy compared to normal serum as expected based on previous observations of muscle atrophy induced by burn injury in humans and animals. The size of C2C12 myotubes was partially protected upon exposure to the serum from patients treated with pamidronate correlating with the rescue of muscle size previously observed in these patients. At the molecular signaling level, serum from both pamidronate and non-pamidronate-treated burn patients increased pSTAT3/STAT3 and pERK1/2/ERK1/2 compared to normal serum with no significant differences between the two groups of burn patients indicating elevated production of inflammatory cytokines. However, serum from pamidronate-treated patients restored the phosphorylation of AKT and mTOR and reduced protein ubiquitination when compared to burn serum alone, suggesting a prevention of muscle catabolism and a restoration of muscle anabolism. Myotube atrophy induced by burn serum was partially rescued after exposure to a pan anti-TGFβ-1/2/3 antibody, suggesting that this signaling pathway is partially responsible for the atrophy and that bisphosphonate protection of bones from resorption during burn injury prevents the release of muscle pro-catabolic factors such as TGFβ into the circulation.