目的 探讨不同病因导致的应激性胃黏膜损伤时胃黏膜环氧化酶(cyclooxygenase,COX)-2表达强度的变化及二者的关系。 方法 通过建立急性甲胺磷中毒及急性心肌梗死动物模型,采用胃黏膜溃疡指数评定是否发生胃黏膜损伤,采用免疫组化方法测定胃黏膜COX-2的表达强度变化。 结果 ①成功建立大鼠急性甲胺磷中毒及急性心肌梗死动物模型;②在急性甲胺磷中毒及急性心肌梗死这两种应激状态下胃黏膜发生了损伤;③不同病因所致应激性胃黏膜损伤时胃黏膜COX-2表达增加。 结论 临床危重疾病可产生应激状态胃黏膜损伤,胃黏膜溃疡指数增加。不同病因所致的应激性胃黏膜损伤时胃黏膜COX-2表达增加,可能为一种保护机制。
Objective To investigate the effects of percutaneous cement discoplasty (PCD) and percutaneous cement interbody fusion (PCIF) on spinal stability by in vitro biomechanical tests. Methods Biomechanical test was divided into intact (INT) group, percutaneous lumbar discectomy (PLD) group, PCD group, and PCIF group. Six specimens of L4, 5 (including vertebral bodies and intervertebral discs) from fresh male cadavers were taken to prepare PLD, PCD, and PCIF specimens, respectively. Before treatment and after the above treatments, the MTS multi-degree-of-freedom simulation test system was used to conduct the biomechanical test. The intervertebral height of the specimen was measured before and after the axial loading of 300 N, and the difference was calculated. The range of motion (ROM) and stiffness of the spine in flexion, extension, left/right bending, and left/right rotation under a torque of 7.5 Nm were calculated. Results After axial loading, the change of intervertebral height in PLD group was more significant than that in other three groups (P<0.05). Compared with INT group, the ROM in all directions significantly increased and the stiffness significantly decreased in PLD group (P<0.05). Compared with INT group, the ROM of flexion, extension, and left/right rotation in PCD group significantly increased and the stiffness significantly decreased (P<0.05); compared with PLD group, the ROM of flexion, extension, and left/right bending in PCD group significantly decreased and the stiffness significantly increased (P<0.05). Compared with INT group, ROM of left/right bending in PCIF group significantly decreased and stiffness significantly increased (P<0.05); compared with PLD group, the ROM in all directions significantly decreased and the stiffness significantly increased (P<0.05); compared with PCD group, the ROM of flexion, left/right bending, and left/right rotation significantly decreased and stiffness significantly increased (P<0.05). Conclusion Both PCD and PCIF can provide good biomechanical stability. The former mainly affects the stiffness in flexion, extension, and bending, while the latter is more restrictive on lumbar ROM in all directions, especially in bending and rotation.
Objective To explore the role and clinical significance of cell-cycle dependent kinase 1 (CDK1) and its upstream and downstream molecules in the development of malignant peripheral nerve sheath tumor (MPNST) through the analysis of clinical tissue samples. Methods A total of 56 tumor samples from MPNST patients (“Tianjin” dataset) who underwent surgical resection, confirmed by histology and pathology between September 2011 and March 2020, along with 17 normal tissue samples, were selected as the research subjects. MPNST-related hub genes were identified through transcriptome sequencing, bioinformatics analysis, immunohistochemistry staining, and survival analysis, and their expression levels and prognostic associations were analyzed. Results Transcriptome sequencing and bioinformatics analysis revealed that upregulated genes in MPNST were predominantly enriched in cell cycle-related pathways, with CDK1 occupying a central position among all differentially expressed genes. Further differential analysis demonstrated that CDK1 mRNA expression in sarcoma tissues was significantly higher than in normal tissues [based on searching the cancer genome atlas (TCGA) dataset, P<0.05]. In MPNST tissues, CDK1 mRNA expression was not only significantly higher than in normal tissues (based on Tianjin, GSE141438 datasets, P<0.05), but also significantly higher than in neurofibromatosis (NF) and plexiform neurofibromas (PNF) (based on GSE66743 and GSE145064 datasets, P<0.05). Immunohistochemical staining results indicated that the expression rate of CDK1 protein in MPNST tissues was 40.31%. Survival analysis results demonstrated that CDK1 expression was associated with poor prognosis. The survival time of MPNST patients with high CDK1 mRNA expression was significantly lower than that of the low expression group (P<0.05), and the overall survival trend of patients with positive CDK1 protein expression was worse than that of patients with negative CDK1 expression. Additionally, differential analysis of CDK family genes (CDK1-8) revealed that only CDK1 was significantly upregulated in MPNST, NF, and PNF. Conclusion Increased expression of CDK1 is associated with poor prognosis in MPNST patients. Compared to other CDK family members, CDK1 exhibits a unique expression pattern, suggesting its potential as a therapeutic target for MPNST.