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Background: Lateral femoral cutaneous nerve (LFCN) injury has been widely reported as one of the most common complications of direct anterior approach (DAA) hip arthroplasty. Bikini incision is considered to increase the incidence of this complication.Methods: A prospective randomized study was conducted after including ninety-nine bikini and ninety-six longitudinal incision DAA cases from May to November 2020. The occurrence of LFCN was examined using ultrasound before and after surgery. The recovery of injury symptoms was evaluated by continuous clinical follow-up until six months, and the patients were treated with mecobalamin and/or celecoxib. Sensory conduction velocity and sensory action potential amplitude of the LFCN were measured after surgery in symptomatic patients.Results: Eighty five (43.6%), sixty seven (34.4%), and forty three (22.0%) cases of LFCN were of the anterior trunk, posterior trunk, and fan types, respectively, before surgery. All one hundred ninety five patients completed the follow-up period. Fifty-seven patients had symptoms of LFCN injury, including thirty six and twenty one patients in the bikini group and longitudinal group, respectively, with significantly different incidence rates (36.4% and 21.9%, respectively; P < .05). Of these, thirty two (56.1%), thirteen (22.8%), and twelve (21.1%) cases were of the anterior trunk, posterior trunk, and fan types, respectively. Sensory conduction velocity and sensory action potential amplitude significantly decreased after surgery in both groups (P < .05). Seventeen cases showed reduction of symptoms within three months. Forty six cases showed self-recovery within six months and eleven cases showed persistent symptoms at the final follow-up.Conclusion: Bikini incision DAA hip arthroplasty may increase the incidence of LFCN injury, and the anterior trunk distribution type is most likely to be affected. (Clinical Trial Registration Number: CHICTR2000035107). [ABSTRACT FROM AUTHOR]

We aimed to identify RNA N6-methyladenosine methylation associated genes in osteoarthritis (OA), and to explore possible regulatory mechanisms of these RNA methylation associated genes. Bioinformatics analyses, including differential expression analysis, functional enrichment analysis, verification analysis, and box plot analysis, were conducted based on different datasets from OA and non-OA patients. Gene expression at mRNA and protein levels was determined by quantitative reverse transcription PCR, western blot and immunofluorescence. Interleukin 1β (IL-1β)-treated SW1353 cells was used as cell model. Lentiviral vector was used for over-expression METTL3 in vitro. CCK-8 assay kit was used to determine cell viability and inflammatory cytokines (IL-1α, IL-6, IL-8, IL-10 and TNF-α) was detected using ELISA kits. Bioinformatics analysis showed that METTL3 expression was decreased in OA group, which was confirmed in clinical samples. Expression of METTL3 was also reduced in IL-1β-treated cells. Levels of inflammatory cytokines were obviously reduced in the METTL3 overexpression group, while IL-1β treatment reversed such decrease caused by METTL3 overexpression (p < 0.05). Both METTL3 overexpression and IL-1β treatment promoted expression of p65 protein and p-ERK (p < 0.01). Additionally, increased expression of MMP1 and MMP3 , and decreased expression of MMP13 , TIMP-1 , and TIMP-2 at both mRNA and protein levels were observed in the METTL3 overexpression group when compared with the control group (p < 0.01). Expression of m6A methylation gene METTL3 was reduced in OA. METTL3 is involved in OA probably by regulating the inflammatory response. METTL 3 overexpression may affect extracellular matrix degradation in OA by adjusting the balance between TIMPs and MMPs. • METTL3 and YTHDC2 were identified as m6A methylation-related genes in OA. • METTL3 may be involved in OA by regulating the inflammatory response. • METTL3 overexpression may affect ECM degradation in OA. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) has traditionally been defined as a non-inflammatory disease. Recently, many studies have demonstrated that OA also has an inflammatory component. BRD4, a member of the Bromodomain and Extra-Terminal Domain family, has emerged as an important regulator of some chronic inflammatory diseases. JQ1, an antagonist of BRD4, modulates transcription of several genes. Our study demonstrated that BRD4 is up-regulated in articular cartilage of OA. BRD4 inhibition attenuated the inflammation and catabolism of chondrocytes and suppressed NF-κB signalling pathway activation. In addition, BRD4 inhibition abolished the transcriptional activity of High Mobility Group Protein B1 (HMGB1). We identified HMGB1 as a direct target of BRD4. Genetic and pharmacological inhibition of BRD4 suppressed IL-1β-induced expression and translocation of HMGB1. Chromatin immunoprecipitation (ChIP) showed the enrichment of BRD4 around the HMGB1 upstream non-promoter region, which diminished with JQ1 treatment. Finally, haematoxylin & eosin and Safranin o/Fast Green staining demonstrated that JQ1 attenuates cartilage destruction in mice with anterior cruciate ligament transection without significant toxic effects. These studies highlighted the importance of BRD4 in the chronic inflammatory reactions of OA, which, as far as we know, was the first report of this finding, and suggested that BRD4 might be a novel potential therapeutic target for the treatment of OA. [ABSTRACT FROM AUTHOR]