Hyaluronic acid might be beneficial for patients after knee arthroscopy. However, the results remain controversial. A systematic review and meta-analysis was conducted to explore the efficacy of hyaluronic acid following knee arthroscopy. Randomized controlled trials assessing the effect of hyaluronic acid in knee arthroscopy were included. Compared with control intervention after knee arthroscopy, hyaluronic acid treatment was found to significantly improve Western Ontario and McMaster Universities Osteoarthritis Index scores and decrease pain on motion, but had no substantial influence on pain scores at 2, 6 and 12 weeks after knee arthroscopy. Objective: To investigate the effect of hyaluronic acid on functional recovery and pain control in patients following knee arthroscopy. Design: A systematic review and meta-analysis was conducted to explore the efficacy of hyaluronic acid following knee arthroscopy. Subjects and methods: Randomized controlled trials (RCTs) assessing the effect of hyaluronic acid in knee arthroscopy were included. A meta-analysis was performed using the random-effect model. Results: Six RCTs involving 310 patients were included in the meta-analysis. Overall, compared with control intervention following knee arthroscopy, hyaluronic acid treatment was found to significantly increase Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores (mean difference 11.43; 95% confidence intervals (95% CI) 1.39-21.47; p = 0.03), but had no impact on pain scores at 2 weeks (mean difference-0.16; 95% CI-0.81-0.49; p = 0.63), pain scores at 6 weeks (mean difference 0.01; 95% CI-0.86-0.89; p = 0.98), pain scores at 12 weeks (mean difference-0.51; 95% CI-1.56-0.53; p = 0.34). In addition, pain on motion was significantly reduced after knee arthroscopy (risk ratio (RR) 0.22; 95% CI 0.06-0.79; p = 0.02). Conclusion: Compared with control intervention after knee arthroscopy, hyaluronic acid treatment was found to significantly improve WOMAC score and decrease pain on motion, but had no substantial influence on pain scores at 2, 6 and 12 weeks after knee arthroscopy.

Tastin might be involved in tumorigenesis, but its role in non-small-cell lung cancer (NSCLC) has not been adequately explored. This work aimed to examine tastin’s role in NSCLC and to explore the underlying mechanism. The Gene Expression Omnibus (GEO), Gene Expression Database of Normal and Tumor tissues (GENT), and Cancer Genome Atlas (TCGA) databases were used. Four GEO datasets (GSE81089, GSE40419, GSE74706, and GSE19188) containing gene expression data for NSCLC and normal tissue samples were analyzed for tastin mRNA expression. Tastin expression levels in different tissues were compared using the GENT website. TCGA biolinks were used to download gene expression quantification ( n = 594) and overall survival data ( n = 535). In total, 30 lung adenocarcinoma and 25 lung squamous cell carcinoma cases were enrolled. In addition, four-week-old male BALB/c nude mice ( n = 9/group) were used to establish xenograft mouse models. Furthermore, cultured HEK293T, A549, and NCI-H226 cells assessed. Immunoblot, hematoxylin and eosin (H&E) staining, immunohistochemistry, real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), fluorescence microscopy, flow cytometry, lentiviral transduction, and MTT, colony formation, wound healing, and Transwell assays were carried out. Tastin expression levels were markedly increased in NSCLC tumor tissue specimens and correlated with a poorer prognosis. Silencing of tastin inhibited the proliferative and migratory abilities of NSCLC cells. Bioinformatic analysis suggested that tastin interacts with ErbB4. The PI3K/AKT and ERK1/2 downstream pathways were suppressed in tastin-deficient cells. In conclusion, tastin might be involved in NSCLC growth and invasion and is a potential therapeutic target in NSCLC.