Many studies have reported the good outcomes of percutaneous endoscopic lumbar discectomy (PELD) for the treatment of lumbar disc herniation (LDH). However, the majority of published studies on PELD showed an average hospital stay of 2 to 5 days. Thus, the purpose of this retrospective study was to evaluate and compare the clinical outcomes of patients undergoing PELD for LDH as day surgery with the outcomes of patients managed as inpatients. A total of 402 patients who underwent PELD for single-level LDH were included. The visual analog scale score (VAS) for leg and back pain, Oswestry Disability Index (ODI) score, and Macnab criteria were evaluated preoperatively and at 2 years postoperatively (final follow-up). Operation time, duration of hospital stay, cost, postoperative complications, and the rates of and reasons for delayed discharge and readmission were recorded and analyzed. The mean operative time was 45.8 ± 8.4 minutes in the PELD-A (nonday surgery mode) group and 41.3 ± 8.7 minutes in the PELD-D (day surgery mode) group (P = .63). The average duration of hospital stay was 2.8 ± 1.1 days in the PELD-A group and 3.2 ± 0.9 hours in the PELD-D group (P < .001). The average hospitalization expenses of the PELD-A and PELD-D groups were 28,090 ± 286 RMB and 24,356 ± 126 RMB (P = .03), respectively. In both groups, the mean VAS and ODI scores improved significantly postoperatively compared with the preoperative scores. The satisfactory result rate was 89.8% in the PELD-D group and 91.0% in the PELD-A group, without a significant difference (P = .68). The delayed discharge rate in the PELD-A and PELD-D groups was 8.20% and 8.43%, respectively (P = .93). The main reasons for delayed discharge were dysesthesia, neurologic deficit, nausea, headache and residential distance from the hospital. The overall readmission rates were 5.99% and 5.53% in the PELD-A and PELD-D groups, respectively (P = .85). The most common reasons for readmission were reherniation, sequestered herniation and pain. In conclusion, PELD is safe and effective for the treatment of LDH and can reduce medical costs as day surgery, and it thus warrants increased attention.

Lidocaine is one of the most common local anesthetics (LA) used in clinical practice and it is neurotoxic. Recent studies suggested that LA, including lidocaine, could exert protective effect over neurotoxicity by promoting autophagy. However, the underlying mechanism was not sufficiently elucidated. This study aimed to explore the mechanism behind. Human neuroblastoma cell line SH-SY5Y was used throughout the whole study. The effect of lidocaine on viability, toxicity of SH-SY5Y cells were analyzed by MTT and lactate dehydrogenase (LDH) assays, respectively. The relative expression of miR-145 was assessed by quantitative reverse transcription-polymerase chain reaction. The impact which lidocaine brought on PI3K/AKT/mTOR pathway and autophagy-related proteins were examined by the western blot assay. LC3B was assessed by immunofluorescence staining. The interaction between miR-145 and AKT3 was conducted by the dual-luciferase reporting assay. Lidocaine inhibited viability of SH-SY5Y cells in a time and dose dependent manner and enhanced the release of LDH in SH-SY5Y cells. Furthermore, the expression of miR-145 and autophagy were enhanced by lidocaine. Transfection with miR-145 inhibitor inhibited the release of LDH and autophagy. miR-145 targeted AKT3 to inhibit PI3K/AKT/mTOR pathway. Finally, lidocaine inactivated PI3K/AKT/mTOR pathways via upregulation of miR-145, and it subsequently promoted autophagy of SH-SY5Y cells. However, silence of miR-145 could reverse the promotion of the autophagy of SH-SY5Y cells. Our results showed that lidocaine promoted autophagy of nerve cells via regulating miR-145 expression and further inactivation of PI3K/AKT/mTOR signaling pathway.

No abstract

Spinal cord injury (SCI) is a serious disorder of the central nervous system with a high disability rate. Long noncoding RNAs (lncRNAs) are reported to mediate many biological processes. The aim of this study was to explore lncRNA and mRNA expression profiles and functional networks after SCI. Differentially expressed genes between SCI model rats and sham controls were identified by microarray assays and analyzed by functional enrichment. Key lncRNAs were identified using a support vector machine- (SVM-) recursive feature elimination (RFE) algorithm. A trans and cis regulation model was used to analyze the regulatory relationships between lncRNAs and their targets. An lncRNA-related ceRNA network was established. We identified 5465 differentially expressed lncRNAs (DE lncRNAs) and 8366 differentially expressed mRNAs (DE mRNAs) in the SCI group compared with the sham group ( fold   change > 2.0 , p < 0.05 ). Four genes were confirmed by qRT-PCR which were consistent with the microarray data. GSEA analysis showed that most marked changes occurred in pathways related to immune inflammation and nerve cell function, including cytokine-cytokine receptor interaction, neuroactive ligand-receptor interaction, and GABAergic synapse. Enrichment analysis identified 30 signaling pathways, including those associated with immune inflammation response. A total of 40 key lncRNAs were identified using the SVM-RFE algorithm. A key lncRNA-mRNAs coexpression network was generated for 230 951 lncRNA-mRNA pairs with half showing positive correlations. Several key DE lncRNAs were predicted to have “cis”- or “trans”-regulated target genes. The transcription factors, Sp1, JUN, and SOX10, may regulate the interaction between XR_001837123.1 and ETS 1. In addition, five pairs of ceRNA regulatory sequences were constructed. Many mRNAs and lncRNAs were found to be dysregulated after SCI. Bioinformatic analysis showed that DE lncRNAs may play crucial roles in SCI. It is anticipated that these findings will provide new insights into the underlying mechanisms and potential therapeutic targets for SCI.

Background CircRNAs are involved in the pathogenesis of several central nervous system diseases. However, their functions and mechanisms in spinal cord injury (SCI) are still unclear. Therefore, the purpose of this study was to evaluate circRNA and mRNA expression profiles in the pathological setting of SCI and to predict the potential function of circRNA through bioinformatics. Methods A microarray-based approach was used for the simultaneous measurement of circRNAs and mRNAs, together with qPCR, fluorescence in situ hybridization, western immunoblotting, and dual-luciferase reporter assays to investigate the associated regulatory mechanisms in a rat SCI model. Results SCI was found to be associated with the differential expression of 414 and 5337 circRNAs and mRNAs, respectively. Pathway enrichment analyses were used to predict the primary function of these circRNAs and mRNAs. GSEA analysis showed that differentially expressed mRNAs were primarily associated with inflammatory immune response activity. Further screening of these inflammation-associated genes was used to construct and analyze a competing endogenous RNA network. RNO_CIRCpedia_4214 was knocked down in vitro, resulting in reduced expression of Msr1, while the expression of RNO-miR-667-5p and Arg1 was increased. Dual-luciferase assays demonstrated that RNO_CIRCpedia_4214 bound to RNO-miR-667-5p. The RNO_CIRCpedia_4214/RNO-miR-667-5p/Msr1 axis may be a potential ceRNA that promotes macrophage M2-like polarization in SCI. Conclusion Overall, these results highlighted the critical role that circRNAs may play in the pathophysiology of SCI and the discovery of a potential ceRNA mechanism based on novel circRNAs that regulates macrophage polarization, providing new targets for the treatment of SCI.