目的 探討不同病因導致的應激性胃黏膜損傷時胃黏膜環氧化酶(cyclooxygenase,COX)-2表達強度的變化及二者的關系。 方法 通過建立急性甲胺磷中毒及急性心肌梗死動物模型,采用胃黏膜潰瘍指數評定是否發生胃黏膜損傷,采用免疫組化方法測定胃黏膜COX-2的表達強度變化。 結果 ①成功建立大鼠急性甲胺磷中毒及急性心肌梗死動物模型；②在急性甲胺磷中毒及急性心肌梗死這兩種應激狀態下胃黏膜發生了損傷；③不同病因所致應激性胃黏膜損傷時胃黏膜COX-2表達增加。 結論 臨床危重疾病可產生應激狀態胃黏膜損傷,胃黏膜潰瘍指數增加。不同病因所致的應激性胃黏膜損傷時胃黏膜COX-2表達增加,可能為一種保護機制。
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.