The receptor for advanced glycation end-products (RAGE), a member of the immunoglobulin superfamily, is expressed in various cell types and mediates cellular responses to a wide range of ligands. The activation of RAGE triggers complex signaling pathways that drive inflammatory, oxidative, and proliferative responses, which are increasingly implicated in the pathogenesis of skin diseases. Despite its well-established roles in conditions such as diabetes, cancer, and chronic inflammation, the contribution of RAGE to skin pathologies remains underexplored. This review synthesizes current findings on RAGE’s involvement in the pathophysiology of skin diseases, including conditions such as psoriasis, atopic dermatitis, and lichen planus, focusing on its roles in inflammatory signaling, tissue remodeling, and skin cancer progression. Additionally, it examines RAGE-modulating treatments investigated in dermatological contexts, highlighting their potential as therapeutic options. Given RAGE’s significance in a variety of skin conditions, further research into its mediated pathways may uncover new opportunities for targeted interventions in skin-specific RAGE signaling.

Breast augmentation is one of the most popular cosmetic surgery procedures in the world and it requires a comprehensive study of the methods performed. As less-invasive techniques are sought, tissue fillers have found its purpose in these procedures. However, it has been revealed that some of them may be associated with serious complications. One of them is the Aquafilling/Los Deline gel. A case report of a female patient who developed unprecedented sequelae after Aquafilling injection—distant migration of the gel in the hand—was presented in this study. The patient underwent total gel removal from the left forearm, arm, and both breasts as well as wound debridement and irrigation. We discovered a canal connecting the left breast to the left forearm, created by a polyacrylamide hydrogel dislocation. It was thoroughly revised using an endoscope. Despite the advantages of tissue fillers such as simplicity of use and less invasiveness, certain complications can occur after injection. Although a few of them have been banned due to these sequelae, new ones continue to appear. Every new product should be examined very carefully before it is introduced to the market.

Artificial intelligence (AI) is increasingly investigated as a potential adjunct in the diagnosis and staging of lung cancer, particularly through integration with bronchoscopy and endobronchial ultrasound (EBUS). Deep learning models have been applied to modalities such as white-light imaging, autofluorescence bronchoscopy, and spectroscopy, with the aim of assisting lesion detection, standardizing interpretation, and reducing interobserver variability. AI has also been explored in EBUS for lymph node assessment and guidance of transbronchial needle aspiration (EBUS-TBNA), with preliminary studies suggesting possible improvements in diagnostic yield. However, current evidence remains largely confined to small, retrospective, single-center datasets, often reporting performance under idealized conditions. External validation is rare, reproducibility is undermined by a lack of data and code availability, and workflow integration into real-world bronchoscopy practice has not been demonstrated. As such, most systems should still be regarded as experimental. Translating AI into routine thoracic oncology will require large-scale, prospective, multicenter validation studies, greater data transparency, and careful evaluation of cost-effectiveness, regulatory approval, and clinical utility.

Orthotopic liver transplantation stands as the sole curative solution for end-stage liver disease. Nevertheless, the discrepancy between the demand and supply of grafts in transplant medicine greatly limits the success of this treatment. The increasing global shortage of organs necessitates the utilization of extended criteria donors (ECD) for liver transplantation, thereby increasing the risk of primary graft dysfunction (PGD). Primary graft dysfunction (PGD) encompasses early allograft dysfunction (EAD) and the more severe primary nonfunction (PNF), both of which stem from ischemia–reperfusion injury (IRI) and mitochondrial damage. Currently, the only effective treatment for PNF is secondary transplantation within the initial post-transplant week, and the occurrence of EAD suggests an elevated, albeit still uncertain, likelihood of retransplantation urgency. Nonetheless, the ongoing exploration of novel IRI mitigation strategies offers hope for future improvements in PGD outcomes. Establishing an intuitive and reliable tool to predict upcoming graft dysfunction is vital for early identification of high-risk patients and for making informed retransplantation decisions. Accurate diagnostics for PNF and EAD constitute essential initial steps in implementing future mitigation strategies. Recently, novel methods for PNF prediction have been developed, and several models for EAD assessments have been introduced. Here, we provide an overview of the currently scrutinized predictive tools for PNF and EAD evaluation strategies, accompanied by recommendations for future studies.

Purinergic P2X7 receptors are involved in cellular processes such as inflammation, proliferation, and tissue remodeling, although their significance in human skin physiology remains poorly understood. In this study, we demonstrated strong P2X7 receptor immunoreactivity in the basal and granular layers of the epidermis. Cutaneous expression of P2X7 receptors was further confirmed at the level of specific mRNA and protein in cultured primary human keratinocytes and dermal fibroblasts. To reveal a possible role of these receptors in regulation of keratinocyte and fibroblast function, the cells were treated with a P2X7 agonist BzATP, or its selective antagonist A438079. Cell proliferation and viability were assessed using an immunofluorescence-based cell counter, and cell migration was evaluated by wound healing assay. P2X7 stimulation with BzATP significantly inhibited keratinocyte proliferation and migration, while P2X7 inhibition with A438079 significantly enhanced keratinocyte migration. In contrast, fibroblasts displayed minimal response to either treatment. These findings indicate that P2X7 regulates keratinocyte growth, and purinergic signaling may play a role in the skin. Our data also suggest that selective P2X7 inhibition may support re-epithelialization under conditions associated with impaired wound healing.