BackgroundThe common and effective treatment for degenerative lumbar diseases is lumbar spinal fusion. Controversy still exists on the choice for instrumentation with spinal fusion procedures. Therefore, we conducted this meta-analysis exclusively of RCTs to compare the clinical outcomes of patients receiving bilateral versus unilateral pedicle screw fixation (PSF).Material/MethodsAfter systematic review of published and unpublished literature, a meta-analysis was conducted to compare the 2 treatment strategies. The methodological quality of the literature was assessed using the PEDro critical appraisal tool.ResultsData synthesis showed less blood loss (P<0.001) and shorter operative time (P<0.001) in patients receiving unilateral PSF compared to bilateral PSF. However, there was no significant difference in fusion rates and functional outcomes between the 2 groups.ConclusionsThe meta-analysis indicated no significant difference in fusion rates and functional outcomes between the 2 treatment procedures, but unilateral PS fixation reduced blood loss and operative time.
Emerging evidence has demonstrated that the dysregulation of microRNA (miRNA/miR) serves a crucial role in the tumorigenesis and tumor development of osteosarcoma (OS), primarily by affecting various pathological behaviors. Therefore, better knowledge of miRNA in OS may provide novel insights into the pathogenesis of OS, and may facilitate the development of promising therapeutics for patients with this disease. MiRNA-944 is frequently dysregulated in human cancers. However, the expression levels, functions and underlying mechanisms of miR-944 in OS remain largely elusive. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect miR-944 expression in OS tissues and cell lines. The regulatory influence of miR-944 in OS proliferation and invasion was determined with MTT and Transwell invasion assays. In addition, the mechanisms underlying the action of miR-944 in OS cells were elucidated through a series of experiments, including bioinformatics analysis, luciferase reporter assay, RT-qPCR and western blot analysis. Spearman's correlation analysis was utilized to examine the relationship between miR-944 and VEGF expression levels, and rescue experiments were applied to further verify whether VEGF mediates the role of miR-944 in OS. The results demonstrated that miR-944 was downregulated in cancer tissues and cell lines. Furthermore, exogenous miR-944 expression inhibited cell proliferation and invasion in OS in vitro. Vascular endothelial growth factor (VEGF) was identified as a direct target of miR-944 in OS and was overexpressed in cancer tissues. VEGF expression was inversely correlated with miR-944 expression in cancer tissues. Rescue experiments demonstrated that overexpression of VEGF partially prevented the miR-944-induced inhibition of OS cell proliferation and invasion. These results suggested that miR-944 may serve a tumor suppressive role in OS by directly targeting VEGF. Therefore, miR-944 may be a promising target in the treatment of OS.
Background: Spinal cord injury (SCI) is a destructive trauma accompanying with local injury, half of which cause chronic paralysis. Ginsenoside Rg1 exerts anti-apoptosis and anti-autophagy properties. Therefore, our goal was to study the protective mechanism of Rg1 in attenuating cell injury. Methods: MiR-216a-5p inhibitor was transfected into PC-12 cells, then cells were pre-treated by Rg1 and treated with 300 μ M hydrogen peroxide (H 2 O 2 ) for 24 h. CCK-8 and apoptosis experiments were done to test cell activity and apoptosis respectively. Expression of miR-216a-5p and cell damage relative factors was tested via qRT-PCR and western blot experiments, respectively. Results: H 2 O 2 induced cell activity suppression, apoptosis and autophagy well at the concentration of 300 μ M, leading cell injury. Rg1 could attenuate cell injury induced by H 2 O 2 at the working concentration of 200 μ M that it elevated cell activity, attenuated apoptosis and autophagy and activated PI3K/AKT and AMPK signal pathways. Further, miR-216a-5p was up-regulated by Rg1. Rg1 played its role in relieving cell injury by positively regulating miR-216a-5p. Conclusion:Our study demonstrated that Rg1 attenuated H 2 O 2 -caused cell injury through positively regulated miR-216a-5p.
BackgroundSpinal cord injury (SCI) is a destructive trauma accompanying with local injury, half of which cause chronic paralysis. Ginsenoside Rg1 exerts anti-apoptosis and anti-autophagy properties. Therefore, our goal was to study the protective mechanism of Rg1 in attenuating cell injury.MethodsMiR-216a-5p inhibitor was transfected into PC-12 cells, then cells were pre-treated by Rg1 and treated with 300 μM hydrogen peroxide (H2O2) for 24 h. CCK-8 and apoptosis experiments were done to test cell activity and apoptosis respectively. Expression of miR-216a-5p and cell damage relative factors was tested via qRT-PCR and western blot experiments, respectively.ResultsH2O2 induced cell activity suppression, apoptosis and autophagy well at the concentration of 300 μM, leading cell injury. Rg1 could attenuate cell injury induced by H2O2 at the working concentration of 200 μM that it elevated cell activity, attenuated apoptosis and autophagy and activated PI3K/AKT and AMPK signal pathways. Further, miR-216a-5p was up-regulated by Rg1. Rg1 played its role in relieving cell injury by positively regulating miR-216a-5p.ConclusionOur study demonstrated that Rg1 attenuated H2O2-caused cell injury through positively regulated miR-216a-5p.
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