Comparison of microendoscopic discectomy and percutaneous transforaminal endoscopic discectomy for upper lumbar disc herniation: A protocol for a systematic review and meta-analysis.

BACKGROUND: Microendoscopic discectomy (MED) and percutaneous transforaminal endoscopic discectomy (PTED), as two alternative surgical techniques in minimally invasive spine surgery (MISS), are widely conducted in the treatment of upper lumbar disc herniation (ULDH). This study will systematically assess and compare the clinical outcomes of MED and PTED in treating ULDH combining with the meta-analysis. METHODS: All the randomized controlled trials (RCTs) will be searched at the databases including PubMed, EMBASE, Cochrane Library and Web of Science, China National Knowledge Infrastructure (CNKI), Chinese Biomedical Literature Database (CBM), Chinese Scientific Journal Database (VIP), and WANFANG Database from inception to December 2025. The primary outcome will involve Japanese Orthopedic Association (JOA), Oswestry disability index (ODI), and visual analog scale (VAS) scores. The secondary outcomes will be the short-form 36-item (SF-36) health survey questionnaire and the modified MacNab criterion. We will perform data synthesis, subgroup analysis, sensitivity analysis, meta-regression analysis, and the assessment of reporting bias using RevMan 5.3 software. RESULTS: This systematic review will comprehensively evaluate the clinical outcomes of comparison of MED and PTED in the treatment of ULDH and provide a reliable and high-quality evidence. CONCLUSION: The conclusion of this study will elucidate the clinical outcomes of MED compared with PTED and clarify whether PTED generates better clinical effects than MED in treating ULDH. PROSPERO REGISTRATION NUMBER: CRD 42021244204.

Circadian clock protein CRY1 prevents paclitaxel­induced senescence of bladder cancer cells by promoting p53 degradation.

Bladder cancer is a common tumor type of the urinary system, which has high levels of morbidity and mortality. The first­line treatment is cisplatin­based combination chemotherapy, but a significant proportion of patients relapse due to the development of drug resistance. Therapy­induced senescence can act as a 'back­up' response to chemotherapy in cancer types that are resistant to apoptosis­based anticancer therapies. The circadian clock serves an important role in drug resistance and cellular senescence. The aim of the present study was to investigate the regulatory effect of the circadian clock on paclitaxel (PTX)­induced senescence in cisplatin­resistant bladder cancer cells. Cisplatin­resistant bladder cancer cells were established via long­term cisplatin incubation. PTX induced apparent senescence in bladder cancer cells as demonstrated via SA­ß­Gal staining, but this was not observed in the cisplatin­resistant cells. The cisplatin­resistant cells entered into a quiescent state with prolonged circadian rhythm under acute PTX stress. It was identified that the circadian protein cryptochrome1 (CRY1) accumulated in these quiescent cisplatin­resistant cells, and that CRY1 knockdown restored PTX­induced senescence. Mechanistically, CRY1 promoted p53 degradation via increasing the binding of p53 with its ubiquitin E3 ligase MDM2 proto­oncogene. These data suggested that the accumulated CRY1 in cisplatin­resistant cells could prevent PTX­induced senescence by promoting p53 degradation.