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

Subclassification of tumors based on molecular features may facilitate therapeutic choice and increase the response rate of cancer patients. However, the highly complex cell origin involved in osteosarcoma (OS) limits the utility of traditional bulk RNA sequencing for OS subclassification. Single-cell RNA sequencing (scRNA-seq) holds great promise for identifying cell heterogeneity. However, this technique has rarely been used in the study of tumor subclassification. By analyzing scRNA-seq data for six conventional OS and nine cancellous bone (CB) samples, we identified 29 clusters in OS and CB samples and discovered three differentiation trajectories from the cancer stem cell (CSC)-like subset, which allowed us to classify OS samples into three groups. The classification model was further examined using the TARGET dataset. Each subgroup of OS had different prognoses and possible drug sensitivities, and OS cells in the three differentiation branches showed distinct interactions with other clusters in the OS microenvironment. In addition, we verified the classification model through IHC staining in 138 OS samples, revealing a worse prognosis for Group B patients. Furthermore, we describe the novel transcriptional program of CSCs and highlight the activation of EZH2 in CSCs of OS. These findings provide a novel subclassification method based on scRNA-seq and shed new light on the molecular features of CSCs in OS and may serve as valuable references for precision treatment for and therapeutic development in OS.

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.