No abstract

Based on the results above, anterior CORP and fusion is recommended for the treatment of multilevel cervical myelopathy when the involved surgical segments were <3. Given the higher rates of surgical complications and complication-related reoperation and the higher surgical trauma associated with multilevel CORP, however, it is suggested that posterior LAMP may be the preferred method of treatment for multilevel cervical myelopathy when the involved surgical segments were equal to 3 or more. In addition, taking the limitations of this study into consideration, it was still not appropriate to draw a strong conclusion claiming superiority for CORP or LAMP. A well-designed, prospective, randomized controlled trial is necessary to provide objective data on the clinical results of both procedures.

Osteoarthritis (OA) is a common degenerative joint disorder, which involves articular cartilage degeneration as well as joint inflammatory reactions. The recent studies have identified microRNA (miRNA) as one of the epigenetic mechanisms for the regulation of gene expression. Here we aim to reveal the role of miRNA in the regulation of gene expression in articular chondrocytes and its significance in the OA pathogenesis. In the present study, miRNA profiling was performed using OA cartilage and normal healthy cartilage tissues. As compared to their levels in normal cells and tissues, miR-27a expression was found to be upregulated in OA cartilage and IL-1β-treated articular chondrocytes. TUNEL staining, as well as flow cytometry with Annexin V-FITC/PI double labeling indicated that miR-27a inhibition reduced the apoptosis of IL-1β-treated articular chondrocytes. Bioinformatics prediction and the dual-luciferase reporter assay indicated that miR-27a targeted the 3′-UTR of the PI3K gene to silence it. The PI3K mRNA level in OA cartilage and IL-1β-treated articular chondrocytes was also downregulated, comparing with normal cells and tissues. Transfection of chondrocytes transfected with the miR-27a inhibitor upregulated the PI3K expression. This study demonstrated miR-27a is a regulator of the PI3K-Akt-mTOR axis in human chondrocytes and could participate in OA pathogenesis.