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The Winograd technique is the most commonly used surgical treatment for ingrown toenails. We describe a novel modified approach, more effective and simpler to perform with a better cosmetic outcome. We retrospectively included 45 and 39 patients with 67 and 58 ingrown toenails who underwent our modified Winograd technique and the Winograd technique, respectively, from July 2017 to June 2020, and obtained data after 3, 6, and 12 months of follow-up. No significant differences in the postoperative time taken to return to regular activities in the modified Winograd and traditional Winograd groups (p = 0.103) and regarding the recurrence in both groups (p = 0.055) were found. The extent of proximal germinal matrix exposure with the modified Winograd technique was significantly more clearly revealed than in the traditional Winograd method contextually (p < 0.05). The postoperative appearance satisfaction rate was significantly higher in the modified Winograd group than in the traditional Winograd group (p = 0.029). The modified Winograd technique is effective in treating ingrown toenails. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the effects of E26-transformation-specific variant-2 (ETV2) overexpression on wound healing in a cutaneous wound (CW) model and clarify associated mechanisms. pLVX-ETV2 lentivirus expressing ETV2 was constructed and infected into BMSCs to generate ETV2-overexpressed BMSCs (BMSCs+pLVX+ETV2). The RT-PCR assay was applied to amplify ETV2, VE-cadherin, vWF, ARG-1, IL-6, iNOS, TGF-β, IL-10, TNF-α. Western blot was used to determine expression of VE-cadherin and vWF. ETV2 induced differentiation of BMSCs into ECs by increasing CDH5/CD31, triggering tube-like structures, inducing Dil-Ac-LDL positive BMSCs. ETV2 overexpression increased the gene transcription and expression of VE-cadherin and vWF (P<0.01). Transcription of M1 phenotype specific iNOS gene was lower and transcription of M2 phenotype specific ARG-1 gene was higher in the RAW264.7+BMSCs+ETV2 group compared to the RAW264.7+BMSCs+pLVX group (P<0.01). ETV2 overexpression (RAW264.7+BMSCs+ETV2) downregulated IL-6 and TNF-α, and upregulated IL-10 and TGF-β gene transcription compared to RAW264.7+BMSCs+pLVX group (P<0.01). ETV2-overexpressed BMSCs promoted wound healing in CW mice and triggered the migration of BMSCs to the wound region and macrophage activation. ETV2-overexpressed BMSCs promoted collagen fibers and blood vessel formation in the wound region of CW mice. In conclusion, this study revealed a novel biofunction of ETV2 molecule in the wound healing process. ETV2 overexpression in BMSCs promoted wound healing in CW mice by triggering BMSCs differentiation into endothelial cells and modulating the transformation of M1 pro-inflammatory and M2 anti-inflammatory macrophages in vitro and in vivo. • ETV2 induces BMSCs differentiation into endothelial cells and triggers BMSCs migration to wound region. • ETV2-overexpressed BMSCs promotes wound healing of cutaneous wound mice. • ETV2-overexpressed BMSCs promotes collagen fibers and blood vessels formation. • ETV2-overexpressed BMSCs modulates transformation of M1 and M2 phenotype macrophages. [ABSTRACT FROM AUTHOR]

Irisin, a myokine derived from proteolytic cleavage of the fibronectin type III domain-containing protein 5 (FNDC5) protein, is crucial in protecting tissues and organs from ischemia-reperfusion (I/R) injury. However, the underlying mechanism of its action remains elusive. In this study, we investigated the expression patterns of genes associated with FNDC5 knockout to gain insights into its molecular functions. We employed a mouse model of skeletal muscle I/R injury with FNDC5 knockout to examine the transcriptional profiles using RNA sequencing. Differentially expressed genes (DEGs) were identified and subjected to further analyses, including gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, protein-protein interaction (PPI) network analysis, and miRNA-transcription factor network analysis. The bioinformatics findings were validated using qRT-PCR and Western blotting. Comparative analysis of skeletal muscle transcriptomes between wild-type (WT; C57BL/6), WT-I/R, FNDC5 knockout (KO), and KO-I/R mice highlighted the significance of FNDC5 in both physiological conditions and I/R injury. Through PPI network analysis, we identified seven key genes (Col6a2, Acta2, Col4a5, Fap, Enpep, Mmp11, and Fosl1), which facilitated the construction of a TF-hub genes-miRNA regulatory network. Additionally, our results suggested that the PI3K-Akt pathway is predominantly involved in FNDC5 deletion-mediated I/R injury in skeletal muscle. Animal studies revealed reduced FNDC5 expression in skeletal muscle following I/R injury, and the gastrocnemius muscle with FNDC5 knockout exhibited larger infarct size and more severe tissue damage after I/R. Moreover, Western blot analysis confirmed the upregulation of Col6a2, Enpep, and Mmp11 protein levels following I/R, particularly in the KO-I/R group. Furthermore, FNDC5 deletion inhibited the PI3K-Akt signaling pathway. This study demonstrates that FNDC5 deletion exacerbates skeletal muscle I/R injury, potentially involving the upregulation of Col6a2, Enpep, and Mmp11. Additionally, the findings suggest the involvement of the PI3K-Akt pathway in FNDC5 deletion-mediated skeletal muscle I/R injury, providing novel insights into the molecular mechanisms underlying FNDC5's role in this pathological process. • Our study revealed 102 differentially expressed genes associated with FNDC5 knockout and highlighted seven essential genes (Col6a2, Acta2, Col4a5, Fap, Enpep, Mmp11, and Fosl1) through bioinformatics analysis. • FNDC5 knockout significantly exacerbated skeletal muscle injury, potentially by upregulating the expression of Col6a2, Enpep, and Mmp11. • Moreover, we revealed the importance of the PI3K-Akt signaling pathway in regulating skeletal muscle I/R injury by FNDC5. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a common degenerative joint disorder. Currently, the underlying etiology of OA is still far from fully elucidated and there is no cure for OA progression. Previous studies have demonstrated that oxymatrine (OMT) could inhibit inflammation and oxidative stress in several animal models. However, the potential effects of OMT on OA remain largely elusive. The aim of the study is to investigate the anti-inflammatory and chondrocyte protective effect of OMT, and delineate the potential mechanism in vitro and in vivo. Western blotting, RT-PCR, ELISA and tissue staining were employed to explore the mechanisms by which OMT exerted a protective effect on IL-1β-induced production of pro-inflammation cytokines and extracellular matrix (ECM) degradation in primary murine chondrocytes and DMM mouse models. The results showed that OMT reduced the IL-1β-induced over-production of pro-inflammation cytokines and ECM degradation. Mechanistically, OMT inhibited the NF-κB pathway via activating Nrf2. In vivo studies also demonstrated that OMT ameliorated OA progression. OMT reduced pro-inflammation cytokines, ECM degradation and OA progression via activating Nrf2 and inhibiting NF-κB pathway. • Oxymatrine (OMT) reduced the IL-1β-induced over-production of pro-inflammation cytokines and ECM degradation. • OMT inhibited the NF-κB pathway via activating Nrf2 in IL-1β-stimulated chondrocytes. • OMT ameliorated OA progression in DMM mouse models. • OMT can be used as a new drug for the treatment of OA. [ABSTRACT FROM AUTHOR]