Background Enhanced recovery after surgery (ERAS) pathway in spine surgery is increasingly popular which can reduce the length of hospital stay (LOS). However, there are few studies on the safety and effectiveness of ERAS pathway in the treatment of single-level lumbar disc herniation (LDH) by percutaneous endoscopic transforaminal discectomy (PETD). The aim of this study was to investigate whether ERAS can reduce LOS of patients with single segment LDH treated by PETD. Methods We reviewed the outcomes of all LDH patients (L4/5) who had been treated with PETD at our institution. Quasi-experimental study was adopted between patients treated in an ERAS after PETD with those rehabilitated on a traditional pathway. The two groups were analyzed for LOS, operation time, complications, visual analog scale (VAS), Oswestry Dysfunction Index (ODI), hospitalization expenses (HE), and improved MacNab efficacy assessment criteria (MacNab). Results A total of 120 single segment LDH patients (ERAS pathway 60 cases, traditional care pathway 60 cases) who were selected from January 2019 to January 2021 met the inclusion criteria. There was a significant difference in mean LOS postoperative VAS scores and ODI on the 3rd day after surgery between the two groups (P < 0.05). The incidence of complications and HE were similar in the two groups (P > 0.05). The mean LOS decreased from 3.47 ± 1.14 days to 5.65 ± 1.39 days after application of ERAS pathway (P < 0.05). Conclusions The ERAS pathway reduced LOS without resulting in additional complications after PETD. These findings support the application of the perioperative ERAS pathway in the treatment of single-level LDH with PETD. Level of evidence Level IV, therapeutic

Purpose. To investigate the relationship between serum cotinine and lumbar bone mineral density (BMD) among 7905 participants aged 30 years and over. Method. A total of 3945 men and 3960 women from the National Health and Nutrition Examination Survey 2011–2018 were included in this cross-sectional analysis. Independent variable was serum cotinine, which is a biomarker of cigarette exposure. The outcome variable was lumbar BMD. We investigated the associations of serum cotinine levels and lumbar BMD using multivariable linear regression models. Results. Serum cotinine concentration was negatively associated with lumbar BMD after adjustment of relevant covariables (β = −0.039, 95% CI: −0.078 to −0.014, P = 0.005 ). However, in the subgroup analysis stratified by gender, this negative association remained only in women (β = −0.072, 95% CI: −0.132 to −0.012, P = 0.019 ). Conclusion. Our study suggested that elevated serum cotinine level correlated with decreased lumbar BMD, especially in women. This finding indicated that reducing cigarette exposure and maintaining serum cotinine at a low level may be beneficial to bone health for adults.

Background Neurofilament light chain (NEFL) has been identified as a biomarker for spinal cord injury (SCI), but its effect and underlying mechanism in SCI remain unclear. Methods SCI rat models were established for in vivo studies. Lipopolysaccharide (LPS)‐induced cell models were used for in vitro studies. The protein and mRNA expression levels of genes were evaluated by western blotting and reverse transcription‐quantitative polymerase chain reaction (RT‒qPCR). The pathological changes in rats after SCI were subjected to histological examinations. The interaction of NEFL and upstream miRNAs was explored using dual‐luciferase reporter gene assays. Results NEFL was highly expressed in SCI rat spinal cord tissues and LPS‐stimulated PC12 cells. NEFL silencing showed an inhibitory effect on the morphological changes of SCI rats and the secretion of inflammatory factors and facilitated functional recovery of SCI rats. MiR‐30b‐5p was demonstrated to target NEFL and negatively regulate NEFL mRNA and protein levels. Downregulation of miR‐30b‐5p in SCI cell and rat models was demonstrated. MiR‐30b‐5p alleviated the inflammatory response in SCI rat models and LPS‐stimulated PC12 cells and promoted functional recovery in rats by targeting NEFL. NEFL activated mTOR signaling. MiR‐30b‐5p inactivated mTOR signaling by negatively regulating NEFL. Conclusion MiR‐30b‐5p alleviated the inflammatory response and facilitated the functional recovery of SCI rats by targeting NEFL to inactivate the mTOR pathway.

Background As a natural process of aging, intervertebral disc degeneration is more prone to degeneration, with limited repair ability, which is closely related to ageing and excessive manual labor. The main manifestations include the formation of fissures in the annulus fibrosus, the reduction of water in the intervertebral disc, and the decrease of elasticity. However, the molecular mechanism of intervertebral disc degeneration is still unclear. Methods In this study, key biomarkers in intervertebral disc degeneration were identified through bioinformatics. GSE70362 and GSE56081 were downloaded from the GEO database, and then the two datasets were differentially analyzed and validated for their expression, immune infiltration analysis, functional enrichment analysis, and potential drug prediction through the Connectivity Map (CMap) database. Results A total of 352 and 9815 differential genes were identified by GSE70362, GSE56081, respectively. The up-regulated and down-regulated genes of the two datasets were intersected with ferroptosis genes to obtain five key genes that were significantly correlated with immune cell content, namely AKR1C3, CKB, KRT19, MT1G and MUC1. The ROC results showed that the five core genes could well predict the occurrence and development of the disease. In addition, the results of CMap suggested that four drugs, including 1-Phenylbiguanide, LY-2183240, Flubendazole and Penciclovir, have the potential to reverse intervertebral disc degeneration. Conclusion Exploring the expression levels of five key genes in intervertebral disc degeneration is conductive to providing new ideas for the prevention and treatment of intervertebral disc degeneration. Moreover, Flubendazole and Penciclovir have the potential to provide options for clinical treatment of intervertebral disc degeneration.