Study Design. This study is a systematic literature review and meta-analysis. Objective. To evaluate the efficacy of tubular microdiscectomy (TMD) compared with conventional microdiscectomy (CMD) for lumbar disc herniation (LDH). Summary of Background Data. TMD has developed rapidly due to reduced tissue trauma by minimization of the required access to spine and disc herniation; however, CMD remains the standard of care for this patient group. To date, it remains debatable whether TMD is superior to CMD for LDH. Methods. We performed a comprehensive database search of PubMed, EMBASE, and Cochrane Central Register of Controlled Trails for prospective randomized controlled trials (RCTs), through using Medical Subject Headings (MeSH) terms “microdiscectomy,” “tubular microdiscectomy,” “minimally invasive surgery,” and “spinal disease.” The retrieved results were last updated on March 15, 2018. Two independent investigators selected qualified studies, extracted indispensable data, assessed risk of bias of original papers. The Grades of Recommendation, Assessment, Development and Evaluation (GRADE) approach was used to grade quality of evidence. If I 2 >50, the heterogeneity is considerable. Results. Four RCT studies (total n = 605), involving 610 individuals with a follow-up period of no less than 12 months, were selected for further review. We assessed these studies as low overall risk of bias. There was low-quality evidence that TMD was superior to CMD considering postoperative Oswestry Disability Index scores (SMD, –3.43, 95% CI, –4.64 to –2.21, P < 0.00001). Compared with CMD, the TMD group exhibited significantly worse Short Form-36 physical function scores (SMD, –4.83, 95% CI, –8.94 to –0.72, P = 0.02). There were no significant differences in the visual analogue scale (P = 0.30), operative time (P = 0.68), dural tear (P = 0.52), and reoperation (P = 0.98). Conclusion. The benefits 1 year after TMD were similar to that of CMD. There was no significant difference in the incidence of reoperation and dural tear. Level of Evidence: 1
This study investigated whether miR-509 plays a role in regulating autophagy and apoptosis-related caspase 3 genes, and analyzes targeted nanoparticles intervention in glioma cells. The surgically resected glioma tissue specimens were included as observation group, and control group used a 2-cm open tissue next to the glioma followed by analysis of miR-509 and caspase 3 level by qPCR. Glioma cell line U251 was divided into miRNC group, targeted nanoparticle group, siRNA-NC group, and siRNA-caspase 3 group, followed by analysis of caspase 3 expression, cell proliferation by flow cytometry, and cell invasion and metastasis by trans well. Caspase 3 mRNA expression was significantly higher in glioma tissues compared with controls. Lower miR-509 and higher caspase 3 expression were correlated with TNM stage. Caspase 3 mRNA level was significantly higher and miR-509 was lower in glioma cells or glioma ell line U251 than those in normal cells. Transfection of siRNA-caspase 3, targeted nanoparticles effectively reduced cell proliferation, metastasis, and invasion and down-regulated caspase 3 levels in U251 cells. Reduced miR-509 expression was associated with elevated caspase 3 expression and enhanced invasive metastatic capacity of glioma cells. Overexpression of miR-509 can effectively reduce cell proliferation, metastasis, and invasion by targeted nanoparticles inhibiting caspase 3 expression.
Background Protein p62 (sequestosome 1) encoded by gene SQSTM1 plays a vital role in mediating protectively selective autophagy in tumor cells under stressed conditions. CircSQSTM1 (hsa_circ_0075323) is a circular transcript generated from gene SQSTM1 (chr5:179260586–179260782) by back-splicing. However, the potential role of hsa_hsa_circ_0075323 in glioblastoma (GBM) remains unclear. Here, we aimed to explore the biological function of hsa_circ_0075323 in GBM and its relationship with autophagy regulation. Results Hsa_circ_0075323 is highly expressed in GBM cells and mainly locates in the cytoplasm. Inhibition of hsa_circ_0075323 in U87-MG and T98G cells attenuated proliferation and invasion ability significantly, while upregulation of has_ circ_0075323 enhanced proliferation and migration of U251-MG and A172 cells. Mechanistically, depletion of hsa_circ_0075323 in GBM cells resulted in impaired autophagy, as indicated by increased expression of p62 and decreased expression of LC3B. Conclusions Hsa_circ_0075323 regulates p62-mediated autophagy pathway to promote GBM progression and may serve as a prognostic biomarker potentially.
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