Burns in the Elderly: Potential Role of Stem Cells.

Burns in the elderly continue to be a challenge despite advances in burn wound care management. Elderly burn patients continue to have poor outcomes compared to the younger population. This is secondary to changes in the quality of the aged skin, leading to impaired wound healing, aggravated immunologic and inflammatory responses, and age-related comorbidities. Considering the fast-growing elderly population, it is imperative to understand the anatomic, physiologic, and molecular changes of the aging skin and the mechanisms involved in their wound healing process to prevent complications associated with burn wounds. Various studies have shown that stem cell-based therapies improve the rate and quality of wound healing and skin regeneration; however, the focus is on the younger population. In this paper, we start with an anatomical, physiological and molecular dissection of the elderly skin to understand why wound healing is delayed. We then review the potential use of stem cells in elderly burn wounds, as well as the mechanisms by which mesenchymal stem cell (MSCs)-based therapies may impact burn wound healing in the elderly. MSCs improve burn wound healing by stimulating and augmenting growth factor secretion and cell proliferation, and by modulating the impaired elderly immune response. MSCs can be used to expedite healing in superficial partial thickness burns and donor site wounds, improve graft take and prevent graft breakdown.

Return-to-work challenges following a work-related mild TBI: The injured worker perspective.

PRIMARY OBJECTIVE: To explore how individuals with work-related mild traumatic brain injury (wrMTBI) experience return-to-work (RTW) processes when returning to the workplace where the injury occurred. DESIGN: RTW experiences were explored using in-depth interviews and an inductive analytic approach. Qualitative analysis guided by the research question moved through phases of line-by-line and thematic coding through which categories and the interaction between categories emerged. PARTICIPANTS: Twelve workers diagnosed with a wrMTBI reported on their RTW experiences following wrMTBIs that occurred 3-5 years prior to the time of the interview. MAIN OUTCOMES AND RESULTS: Participants perceived employer and workers' compensation factors as profoundly influencing their RTW experiences. Participants consistently reported that employers and workers' compensation representatives had an inadequate understanding of wrMTBI sequelae. Six of 12 participants were re-injured following their wrMTBI, with three of these injuries occurring at work. CONCLUSION: Employers, co-workers and workers' compensation representatives should be aware of wrMTBI sequelae so injured workers can receive appropriate supports and both stigmatization and re-injury can be mitigated. Greater attention to the structural and social elements of workplace and compensation environments could inform strategies to break down barriers to successful return-to-work following a wrMTBI.

Hydrogen sulfide is an endogenous stimulator of angiogenesis.

The goal of the current study was to investigate the role of exogenous and endogenous hydrogen sulfide (H(2)S) on neovascularization and wound healing in vitro and in vivo. Incubation of endothelial cells (ECs) with H(2)S enhanced their angiogenic potential, evidenced by accelerated cell growth, migration, and capillary morphogenesis on Matrigel. Treatment of chicken chorioallantoic membranes (CAMS) with H(2)S increased vascular length. Exposure of ECs to H(2)S resulted in increased phosphorylation of Akt, ERK, and p38. The K(ATP) channel blocker glibenclamide or the p38 inhibitor SB203580 abolished H(2)S-induced EC motility. Since glibenclamide inhibited H(2)S-triggered p38 phosphorylation, we propose that K(ATP) channels lay upstream of p38 in this process. When CAMs were treated with H(2)S biosynthesis inhibitors dl-propylargylglycine or beta-cyano-L-alanine, a reduction in vessel length and branching was observed, indicating that H(2)S serves as an endogenous stimulator of the angiogenic response. Stimulation of ECs with vascular endothelial growth factor (VEGF) increased H(2)S release, while pharmacological inhibition of H(2)S production or K(ATP) channels or silencing of cystathionine gamma-lyase (CSE) attenuated VEGF signaling and migration of ECs. These results implicate endothelial H(2)S synthesis in the pro-angiogenic action of VEGF. Aortic rings isolated from CSE knockout mice exhibited markedly reduced microvessel formation in response to VEGF when compared to wild-type littermates. Finally, in vivo, topical administration of H(2)S enhanced wound healing in a rat model, while wound healing was delayed in CSE(-/-) mice. We conclude that endogenous and exogenous H(2)S stimulates EC-related angiogenic properties through a K(ATP) channel/MAPK pathway.