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Background: Burn injuries occurring due to thermal, electrical, flame-related, and chemical causes result in acute and chronic wounds. Platelet-rich plasma (PRP) and platelet-rich fibrin (PRF) are both autologous platelet concentrates (APCs) that may augment wound healing. We conducted a systematic review to examine patient outcomes when this biologic technology is used in the management of burn wounds. Methods: The following databases were queried to identify relevant articles used for literature review: PubMed, Embase, and Scopus. The main outcome measures of this review were efficacy of PRP and PRF for use in primary burn wounds, skin graft donor site wounds, and skin graft adherence. Results: Our review identified 14 eligible articles, reporting on a total of 781 patients. Included studies investigated PRP (n = 12) and PRF (n = 2) in the context of primary burn wounds and skin grafting. Overall, PRP and PRF were shown to accelerate burn wound re-epithelialization and healing, though there was less consensus with regards to the effects on scar quality. Additionally, PRP and PRF were demonstrated to improve graft take and skin graft donor site healing. No significant adverse events or reactions were reported in the literature. However, prolonged operative time, the necessity for multiple venipunctures, and a lack of significant improvement in healthcare costs present notable limitations of this therapy. Conclusions: PRP and PRF may improve wound healing and may be considered as adjunct therapies in the treatment of primary burn wounds and skin graft donor site wounds. We encourage future, high-quality, prospective studies to be conducted to help fill these knowledge gaps and improve clinicians' understanding of the use of PRP and PRF for burn wound and skin graft donor wound healing. Level of Evidence: Not ratable [ABSTRACT FROM AUTHOR]

Background  Living donor liver transplantation (LDLT) has expanded the availability of liver transplant but has been associated with early technical complications including the devastating complication of hepatic artery thrombosis (HAT), which has been reported to occur in 14% to 25% of LDLT using standard anastomotic techniques. Microvascular hepatic artery reconstruction (MHAR) has been implemented in an attempt to decrease rates of HAT. The purpose of this study was to review the available literature in LDLT, specifically related to MHAR to determine its impact on rates of posttransplant complications including HAT. Methods  A systematic review was conducted using PubMed/Medline and Web of Science. Case series and reviews describing reports of microscope-assisted hepatic artery anastomosis in adult patients were considered for meta-analysis of factors contributing to HAT. Results  In all, 462 abstracts were screened, resulting in 20 studies that were included in the meta-analysis. This analysis included 2,457 patients from eight countries. The pooled rate of HAT was 2.20% with an overall effect size of 0.00906. Conclusion  Systematic literature review suggests that MHAR during LDLT reduces vascular complications and improves outcomes posttransplant. Microvascular surgeons and transplant surgeons should collaborate when technical challenges such as small vessel size, short donor pedicle, or dissection of the recipient vessel wall are present. [ABSTRACT FROM AUTHOR]

The NLRP3 inflammasome senses diabetic metabolites and initiates inflammation implicated in diabetic complications and neurodegeneration. No studies have investigated NLRP3 in diabetic bladder dysfunction (DBD), despite a high clinical prevalence. In vitro, we found that numerous diabetic metabolites activate NLRP3 in primary urothelial cells. In vivo, we demonstrate NLRP3 is activated in urothelia from a genetic type 1 diabetic mouse (Akita) by week 15. We then bred an NLRP3-/- genotype into these mice and found this blocked bladder inflammation and cystometric markers of DBD. Analysis of bladder innervation established an NLRP3-dependent decrease in overall nerve density and Aδ-fibers in the bladder wall along with an increase in C-fiber populations in the urothelia, which potentially explains the decreased sense of bladder fullness reported by patients and overactivity detected early in DBD. Together, the results demonstrate the role of NLRP3 in the genesis of DBD and suggest specific NLRP3-mediated neuronal changes can produce specific DBD symptoms. [ABSTRACT FROM AUTHOR]