Preoperative planning of the surgical approach for cervical spondylotic myelopathy (CSM) is central to precision medicine. This study used supervised machine learning (SML) to build a predictive model for surgical approach selection in CSM and applied unsupervised machine learning (UML) to explore clinical heterogeneity. In this retrospective study, a development cohort of 884 surgically treated patients with CSM was used for model development after exclusion of patients with incomplete perioperative data. Variables showing significant between-group differences were entered into four supervised machine-learning algorithms, including support vector machine (SVM), extreme gradient boosting (XGBoost), random forest (RF), and generalized linear model (GLM), for feature screening and model development. In addition, an exploratory unsupervised clustering analysis was performed in patients undergoing anterior surgery on the basis of perioperative profile variables to characterize clinical heterogeneity. An independent external validation cohort of 200 patients was further used to evaluate the discrimination, calibration, and clinical utility of the final model. The final prediction model for surgical approach incorporated four key variables: American Spinal Injury Association impairment scale (ASIA), eosinophils (EOS), total protein (TP), and albumin (Alb), with an area under the curve (AUC) of 0.811 in the development cohort. Model scores were significantly correlated with perioperative indicators. UML identified two exploratory subgroups among patients receiving anterior surgery, indicating distinct perioperative profiles. In the external validation cohort, the model achieved an AUC of 0.726 (95

Background SCSEH ( Spontaneous cervical spinal epidural hematoma) is a rare yet serious clinical entity characterized by idiopathic, non-traumatic, and non-iatrogenic accumulation of blood in the cervical epidural space. For patients who experience sudden neck pain and nerve root pain symptoms, acute cervical spinal epidural hematoma should be regarded as a possible differential diagnosis cas.In recent years, such cases have been reported globally, yet treatment strategies remain heterogeneous with inconclusive efficacy evidence. While surgical decompression is widely advocated for optimal neurological recovery, conventional protocols lack specificity regarding optimal intervention timing.Over a 13-year period, we surgically managed 36 SCSEH cases. This study analyzes the intervals from symptom onset to hospital admission and admission to surgical intervention, with comparative assessment of postoperative neurological outcomes. Methods A retrospective study was conducted on 36 patients (23 males and 13 females; mean age 48.43 ± 2.17 years) diagnosed with SSCEH between January 2006 and January 2019. All patients presented with varying degrees of neurological deficits upon admission and underwent single-stage surgical intervention comprising cervical spinal canal decompression, epidural hematoma evacuation, and internal fixation. Patients were categorized based on the time interval from symptom onset to surgery.Clinical outcomes were assessed using the Japanese Orthopaedic Association (JOA) score, Visual Analog Scale (VAS), and American Spinal Injury Association (ASIA) Impairment Scale. All patients achieved a minimum follow-up of 12 months (mean 16.4 ± 2.17 months). Radiographs, CT(computed tomography ), and MRI(magnetic resonance imaging ) were utilized to evaluate fusion status and spinal stability. Results All 36 patients exhibited statistically significant improvements (P < 0.05) in ASIA grade, VAS score, and JOA score at the final follow-up compared to preoperative assessments. Functional recovery was comparable between patients undergoing surgery within 8 hours of symptom onset and those operated between 8 and 24 hours post-onset, with no statistically significant difference in postoperative functional outcomes (p > 0.05). However, patients receiving surgical intervention within 24 hours demonstrated significantly superior functional recovery compared to those operated beyond 24 hours (P < 0.05). The postoperative follow-up imaging results indicated no rebleeding, no significant loss of cervical curvature, no collapse of the bone graft or no displacement of the implant, and good spinal canal volume. Conclusions Patients with SCSEH undergoing surgery within 8 hours of symptom onset demonstrated comparable postoperative functional recovery to those operated between 8–24 hours. However, subjects receiving intervention within 24 hours collectively showed superior functional outcomes compared to those undergoing surgery beyond 24 hours Trial registration: The studies involving humans were approved by the Ethics Committee of People's Hospital of Guangxi Zhuang Autonomous Regionl. The studies were conducted in accordance with the local legislation and institutional require ments. Written informed consent for participation was not required from the participants or the participants’ legal guardians/next of kin in accordance with the national legislation and institutional requirements.

Background In recent years, some researchers have reported the learning curves of TLIF, MIS-TLIF, and OLIF. However, there were few reports about the learning curve of PE-LIF. Methods Data for consecutive patients with single-segment lumbar spondylolisthesis or lumbar spinal stenosis who had undergone PE-LIF with percutaneous pedicle screw fixation from January 2022 to September 2023 were retrospectively collected. We tried to divide the entire surgical process into different time segments according to surgical steps and the learning curves of each time frame were plotted out and further studied. We also reported the initial clinical results to provide experience of the safety, accuracy, and efficiency of PE-LIF directly. Results A total of 42 patients was included in the study, of which 2 patients were lost to follow-up and were excluded from the scope of the study. The duration of the surgery and each corresponding step decreased while the number of cases increased. Yet, the slope of whole operative time and each corresponding step flattened at quite different case numbers. The VAS score in low-back pain, leg pain and ODI score improved significantly for all patients after surgery and continued to improve throughout the entire follow-up. At the 1-year follow-up, excellent modified Macnab outcomes were achieved at 26 patients, good at 13, and fair at 1. The incidence rate of complications in the series was 7.5%: 1 case of cage retropulsion, 1 case of cage subsidence, 1 case of dural matter tear and no intraoperative neurovascular injury. Conclusions It is technically feasible and safe to implant an interbody fusion cage device directly through an endoscopic working cannula. It may be accelerated the process of endplates preparation under the endoscopy by introducing endplate handling equipment used in open surgery.

Autophagy is a promising therapeutic target for intervertebral disc degeneration (IDD). Previous study has shown down-regulation of activator protein 2α (AP-2α) promoted proliferation and inhibited senescence and apoptosis of rat nucleus pulposus (NP) cells in IDD. This study aimed to investigate the involvement of autophagy in IDD and the regulatory mechanism of AP-2α on autophagy. Rat NP cells were exposed to varying concentrations of H2O2. A rat IDD model was constructed and injected with AP-2α low expression adeno-associated virus. To study the role of AP-2α and autophagy in IDD, we constructed an IDD cell model using H2O2 and treated NP cells with AP-2α low expression adeno-associated virus, autophagy activator rapamycin (RA) and autophagy inhibitor 3MA. In vitro, AP-2α (TFAP2A), LC3 (MAP1LC3A/B), Beclin-1 (BECN1), and p62 (Sequestosome 1, SQSTM1) levels were up-regulated after H₂O₂ treatment. In vivo, IDD increased the apoptosis degree of NP cells, but apoptosis was reduced after knockdown of AP-2α. Additionally, IDD increased AP-2α, LC3 II/I, Beclin-1, and p62 levels, but knockdown of AP-2α unblocked the autophagy flow. In vitro, H₂O₂ treatment increased AP-2α, LC3 II/I, Beclin-1, and p62 levels and NP cell apoptosis. Treatment with RA and its combined knockdown of AP-2α alleviated the dysfunction of autophagy flow and reduced the degree of apoptosis. Treatment with 3MA aggravated the dysfunction of autophagy flow and apoptosis, which can be alleviated by knockdown of AP-2α. Together, AP-2α regulated autophagy to participate in the development of IDD in vivo and rat NP cell model of IDD in vitro.

Objective: Our study aims to develop a deep learning-based Ankylosing Spondylitis (AS) diagnostic model that achieves human expert-level performance using only a minimal amount of labeled samples for training, in regions with limited access to expert resources. Methods: Our semi-supervised diagnostic model for AS was developed using 5389 pelvic radiographs (PXRs) from a single medical center, collected from March 2014 to April 2022. The dataset was split into a training set and a validation set with an 8:2 ratio, allocating 431 labeled images and the remaining 3880 unlabeled images for semi-supervised learning. The model’s performance was evaluated on 982 PXRs from the same center, assessing metrics such as AUC, accuracy, precision, recall, and F1 scores. Interpretability analysis was performed using explainable algorithms to validate the model’s clinical applicability. Results: Our semi-supervised learning model achieved accuracy, recall, and precision values of 0.891, 0.865, and 0.859, respectively, using only 10% of labeled data from the entire training set, surpassing human expert performance. Extensive interpretability analysis demonstrated the reliability of our model’s predictions, making the deep neural network no longer a black box. Conclusion: This study marks the first application of semi-supervised learning to diagnose AS using PXRs, achieving a 90% reduction in manual annotation costs. The model showcases robust generalization on an independent test set and delivers reliable diagnostic performance, supported by comprehensive interpretability analysis. This innovative approach paves the way for training high-performance diagnostic models on large datasets with minimal labeled data, heralding a cost-effective future for medical imaging research in big data analytics.

At present, the impact of cuproptosis-related genes in the study of osteosarcoma is largely unknown. Genome-wide data of osteosarcoma and controls were downloaded from 3 different databases, and specific diagnostic models associated with cuproptosis in osteosarcoma were constructed by support vector machines with artificial intelligence, random forest trees and LASSO regression. Differential analysis of immune cell infiltration was examined using routine blood data from 25,665 cases. Differential expression was examined using immunohistochemistry and PCR. PDHA1 and CDKN2A were obtained as specific cuproptosis-related biomarkers for osteosarcoma after artificial intelligence analysis. PDHA1, CDKN2A and neutrophils were differentially expressed in OS and control groups. PDHA1 and CDKN2A are significantly dysregulated in OS and are able to serve as biomarkers of OS.

目的 研究Mfn2对椎间盘退变大鼠髓核细胞内质网应激及细胞凋亡的作用及机制.方法 离体培养正常大鼠NP细胞为control组,离体培养椎间盘退变大鼠NP细胞分为model组、OE-Mfn2组、OE-NC组及4-PBA组.Western blot法检测Mfn2、PERK、p-PERK、eIF2α、p-eIF2α、ATF4、CHOP、GRP78、Bcl-2、Bax、caspase-3的蛋白水平;qRT-PCR检测Mfn2、PERK、eIF2α、ATF4mRNA水平;免疫共沉淀实验验证Mfn2与PERK互作关系;MTT检测细胞活力;流式细胞术检测细胞凋亡率.结果 Mfn2可特异性结合PERK;与model组比较,OE-Mfn2组Mfn2、Bcl-2水平及细胞活力增加(P<0.05),PERK、p-PERK、eIF2α、p-eIF2α、ATF4、CHOP、GRP78、Bax、caspase-3水平及凋亡率降低(P<0.05).结论 Mfn2可通过降低ERS抑制椎间盘退变大鼠NP细胞凋亡.

Intervertebral disc degeneration (IDD) is considered the basis of serious clinical symptoms, especially for low back pain (LBP). Therefore, it is essential to explore the regulatory role and diagnostic performance of dysregulated genes and potential drugs in IDD. Through WGCNA co-expression analysis, 36 co-expression modules were obtained. Among them, MidnightBlue and Red modules were the most related to IDD. Functional enrichment analysis showed that the Red module was mainly related to neutrophil activation and regulation of cytokine-mediated signaling pathway and apoptosis, whereas the MidnightBlue module was mainly related to extracellular matrix organization, bone development, extracellular matrix, extracellular matrix component, and other extracellular matrices. Furthermore, 356 genes highly related to the module were screened to construct a protein interaction network. Network degree distribution analysis showed that the known IDD-related genes had a higher degree of distribution. Enrichment analysis demonstrated that these genes were enriched in MAPK_SIGNALING_PATHWAY (FDR = 0.012), CHEMOKINE_SIGNALING_PATHWAY, and some other pathways. By constructing a disease-gene interaction network, three disease-specific genes were finally identified. Through combining with the drug-target gene interaction network, two potential therapeutic drugs, entrectinib and larotrectinib, were determined. Finally, based on these genes, the diagnostic model in the training dataset, test dataset, and verification dataset all showed a high diagnostic performance. The findings of this study contributed to the diagnosis of IDD and personalized treatment of IDD.

目的 探讨miR-422a调控骨肉瘤细胞自噬及凋亡的作用和机制及其与靶基因ATG12的关系.方法 采用瞬时转染miR-422a模拟物和抑制物分别上调或下调骨肉瘤细胞的miR-422a表达水平,采用MTT法检测各时间点骨肉瘤细胞的增殖能力,瞬时转染miR-422a后采用流式细胞术检测骨肉瘤细胞凋亡情况,采用实时荧光定量聚合酶链式反应(RT-qPCR)检测转染miR-422a对靶基因mRNA的影响.结果 RT-qPCR结果 显示,miR-422a在肿瘤组织及细胞中均高表达,ATG12在肿瘤组织及细胞中均低表达.MTT法结果 显示,miR-422a-mimic组吸光度值明显升高,miR-422a-inhibitor组吸光度值明显降低(P<0.05).流式细胞术检测结果 显示,miR-422a-inhibitor组细胞凋亡率高于空白组与NC组(P<0.0001).Western blot检测结果 显示,miR-422a-mimic组细胞中ATG12、LC3-Ⅱ和LC3-Ⅰ蛋白量明显低于空白组与NC组(P<0.05);miR-422a-inhibitor组细胞中ATG12、LC3-Ⅱ蛋白量明显高于空白组与NC组,LC3-Ⅰ蛋白量明显低于空白组与NC组(P<0.05);miR-422a-inhibitor组细胞中LC3-Ⅱ/Ⅰ明显高于空白组与NC组(P<0.05).结论 miR-422a/ATG12信号轴可能调控骨肉瘤细胞的自噬及凋亡.

目的 探讨异硫氰酸苯乙酯(PEITC)联合阿霉素(ADM)诱导骨肉瘤细胞凋亡的作用.方法 选用U2-OS细胞株,根据处理方法的不同将其分为PEITC组、ADM组、PEITC+ADM组和空白对照组.采用MTT法检测不同处理组药物对U2-OS细胞增殖能力的影响.采用TUNEL法测定不同处理组U2-OS细胞的凋亡情况.采用Western blot法检测不同处理组U2-OS细胞Caspase-3、Fas、FasL蛋白的表达情况.结果 PEITC和ADM浓度对U2-OS细胞的半抑制浓度(IC50)分别为4.37μM/ml和6.61μg/ml.与单独使用PEITC或ADM处理相比,联合使用两种药物对U2-OS细胞的增殖抑制率更高(P<0.05).低剂量的PEITC联合ADM产生协同效应,而高剂量的两种药物联合产生相加效应.与单药物处理相比,PEITC联合ADM能够显著提高U2-OS细胞凋亡率(P<0.05),增加Caspase-3蛋白的活性及表达(P<0.05).结论 PEITC增强了ADM诱导骨肉瘤细胞凋亡的作用,可能与Caspase-3蛋白活性升高和表达量上调有关,这为PEITC联合ADM的临床应用提供了参考依据.

颈椎管狭窄症是脊柱外科的常见病、多发病,大多数患者临床症状明显,生活质量及生命安全受到严重影响.当临床明确诊断时,应尽早采取手术治疗.颈椎后路单开门手术是目前治疗颈椎管狭窄症常用且成熟的手术方式,本文就其治疗进展及现状进行综述.

目的 分析多节段颈椎病患者行颈椎前路椎间盘切除融合术(ACDF)前后生活质量变化及健康改善的影响因素.方法 选择2010-02～2017-02该院收治的143例行ACDF治疗的多节段颈椎病患者,采用SF-36量表对其手术前后的生活质量进行评价.分析患者术后健康改善的影响因素.结果 多节段颈椎病患者ACDF前生活质量普遍受限,ACDF可显著改善患者的生活质量.JOA评分<9分(OR=2.357)、教育程度为初中及以下(OR=1.645)、病程>6年(OR=3.122)、年龄>60岁(OR=5.049)及工作不稳定(OR=2.616)均为影响多节段颈椎病患者ACDF后健康改善的危险因素.结论 ACDF可显著改善多节段颈椎病患者的生活质量,可对具有影响术后改善相关危险因素的患者给予更多的护理措施,以有效改善其术后生活质量.

Objective: Studies have proposed the role of AP-2 alpha in human disease. However, few have focused on its effects on intervertebral disc degeneration (IDD). This study intends to discuss the role of AP-2 alpha in IDD by regulating TGF-beta 1 and Smad3 expression. Methods: The AP-2 alpha and TGF-beta 1 expression in IDD NP clinical samples was detected. Rat models of IDD were established by acupuncture. The rats were injected with AP-2 alpha low expression adeno-associated virus or TGF-beta 1 high expression adeno-associated virus to observe their effects on pathological damages, NP cell apoptosis, matrix metalloproteinase-2 (MMP-2), MMP-9, Smad3, Aggrecan and collagen (Col)-2 expression in NP tissues. The NP cells were isolated and transfected with silenced AP-2 alpha or overexpressed TGF-beta 1 vector to figure out their functions in growth, senescence and apoptosis. Results: AP-2 alpha and TGF-beta 1 were upregulated in NP tissues of patients and rats with IDD. AP-2 alpha silencing limited the activation of TGF-beta 1 signaling pathway. Reduced AP-2 alpha ameliorated pathological changes, declined MMP-2, MMP-9 and Smad3 expression and elevated Aggrecan and Col-2 expression in NP tissues of rats with IDD, and speeded up the growth and depressed senescence and apoptosis of NP cells of rats with IDD. Up-regulating TGF beta 1 weakened the effect of down-regulated AP-2 alpha on NP tissues and cells in IDD. Conclusion: Collectively, our study demonstrates that knockdown of AP-2 alpha restricts TGF-beta 1 and Smad3 expression to promote proliferation and depress senescence and apoptosis of NP cells in rats with IDD.