Objective:To analyze the effect of comprehensive nursing education on anxiety, depression, quality of life and survival of patients with hepatocellular carcinoma (HCC) after surgery.Methods:A total of 136 HCC patients were randomly divided into two groups: general nursing education group and comprehensive nursing education group. The comprehensive nursing education group carried out 12 months of health belief education, psychological care, care activities and telephone condolence. The routine nursing group received basic education for 12 months. The changes of anxiety and depression were assessed by hospital anxiety and depression scale (HADS). The quality of life (QOL) of participants within 12 months was assessed using the European research and treatment cancer quality of life questionnaire (QLQ-C30). The 3-year survival of the two groups was compared.Results:There was no significant difference between the two groups in baseline data. At the 9th and 12th month, the HADS-A score of the comprehensive nursing education group was significantly lower than that of the general nursing group ( P< 0.05). In the 12th month, the overall health of QLQ-C30 in the comprehensive nursing education group was better than that in the general nursing group ( P<0.05). The QLQ-C30 function score of the comprehensive nursing education group at the 12th month was better than that of the general nursing group ( P<0.05). There was no significant difference in QLQ-C30 symptom scores between the two groups at all time points ( P>0.05). The overall survival of the patients in the comprehensive nursing education group was better than that in the general nursing group ( P=0.026). Conclusion:the comprehensive nursing education can reduce the anxiety and depression of HCC patients after surgery, and can improve their quality of life and survival.

Objective To evaluate the effects of N-acetycysteine on the expression of caveolin-3 (Cav-3) during myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods Twenty-four pathogenfree healthy adult male Sprague-Dawley rats,weighing 230-270 g,were divided into 3 groups (n =8 each) using a random number table:myocardial I/R group (group I/R),diabetes mellitus plus myocardial I/R group (group D) and N-acetycysteine group (group NAC).Diabetes mellitus was induced by injection of streptozotocin 60 mg/kg via the tail vein and confirmed by blood glucose ≥ 16.7 mmol/L 3 days later.At 1 week after successful establishment of the model,N-acetycysteine 1.5 g · kg-1 · d-1 was injected through a gastric tube into stomach for 4 consecutive weeks in group NAC,and the equal volume of normal saline was given for 4 consecutive weeks in I/R and D groups.Myocardial I/R was then induced by 30 min ligation of the left anterior descending branch of the coronary artery followed by 2 h of reperfusion.At the end of reperfusion,the myocardial infarct size was determined by triphenyl tetrazolium chloride staining,the levels of serum creatine kinase-MB (CK-MB) and 15-F2t-Isoprostane were measured by enzyme-linked immunosorbent assay,and the expression of myocardial Cav-3,Akt,phosphor-Akt (p-Akt),endothelial nitric oxide synthase (eNOS) and phosphor-eNOS (p-eNOS) was detected by Western blot.Results Compared with group I/R,the myocardial infarct size and levels of serum CK-MB and 15-F2t-Isoprostane were significantly increased,and the myocardial Cav-3,p-Akt and p-eNOS expression and NO level were decreased in group D (P＜0.05).Compared with group D,the myocardial infarct size and levels of serum CK-MB and 15-F2t-Isoprostane were significantly decreased,and the myocardial Car-3,p-Akt and p-eNOS expression and NO level were increased in group NAC (P＜0.05).Conclusion N-acetycystein can activate Akt/eNOS/NO signaling pathway through up-regulating myocardial Cav-3 expression,thus reducing myocardial I/R injury in diabetic rats.

[Objective] To investigate the effects and mechanisms of Nrf2-ARE (nuclear factor erythroid-2 related factor-anti-oxidant response element) pathway on uremic serum-mediated endothelial dysfunction in human aortic endothelial ceils.[Methods] Human aortic endothelial cells were incubated in endothelial cell medium containing 10％ normal serum,10％ non-diabetic nuremic serum or 10％ diabetic uremic serum respectively,and 20 μmol/L tertiary butyl hydroquinone (tBHQ) were pretreated with cells to active Nrf2-ARE pathway.The cells apoptosis rate were measured by flow cytometry,and the synthesis of NO was detected by flow cytometry and immune fluorescent confocal,while the expression of P-eNOSer1177/eNOS,and quinone oxidoreductase-1 (NQO1) were measured by western blotting.The levels of malondialdehyde,superoxide dismutase,eatalase,and glutathione in these cells were also measured with kits.[Results] Aortic endothelial cells incubated with uremic serum had a higher level of apoptosis rate and MDA (P ＜ 0.05),and a lower level of NO systhesis,P-eNOSSer1177/eNOS expression,CAT,SOD,GSH (P ＜ 0.05).Pretreated with tBHQ can reduce the apoptosis rate and MDA level (P ＜ 0.05),improve the amount of NO systhesis,the expression of P-eNOSSer1177/eNOS,the levels of CAT,SOD,and GSH in these cells (P ＜ 0.05).[Conclusion] Activation of Nrf2-ARE pathway can improve endothelial dysfunction in aortic endothelial cells induced by uremic serum,and its mechanism might be related with enhancement of the antioxidant stress.

Nasopharyngeal carcinoma is a common malignant tumor in southern China, and its occurrence and development mechanism are still not fully understood. However, a large number of studies have shown that DNA methylation has important clinical application value in the screening, diagnosis, treatment and prognosis evaluation of nasopharyngeal carcinoma. DNA methylation affects the division cycle, growth, invasion and migration of nasopharyngeal carcinoma cells by regulating the transcription and protein expression levels of genes associated with tumorigenesis and development. In addition, there are significant differences in DNA methylation expression levels in different stages of nasopharyngeal carcinoma, which provides theoretical guidance and clinical reference for the early diagnosis, timely treatment and response evaluation of nasopharyngeal carcinoma. Current studies have shown that DNA methylation detection may provide a simple and efficient early screening method for nasopharyngeal carcinoma, and can also explore new ideas for the development of non-invasive screening methods.

Objective     To explore the role of versican (VCAN) in ESCC prognosis based on bioinformatics data. Methods    First, three RNA microarray datasets of ESCC were downloaded from GEO database, which were then integrated and used to explore differentially expressed genes (DEGs). The subsequent analysis was conducted based on the results of these DEGs: (1) The STRING database was used to construct a protein-protein interaction (PPI) network;(2) molecular complex detection software was used to analyze the modules of the PPI network, of which the most significant modules were chosen, and hub genes were the genes included in the chosen modules; (3) high-throughput RNA sequencing data from TCGA and GTEx databases were used to verify the expression of these hub genes to confirm whether they were differentially expressed; (4) the survival curve analysis of confirmed DEGs was conducted to select genes that had significant influence on the survival of ESCC; (5) TIMER database was used to analyze the relationship between the gene expression of VCAN and the abundance of tumor-infiltrating immune cells (TIICs) and gene markers in these cells; (6) Targetscan and miRDB software were used to predict the miRNAs that could regulate VCAN, and Cytoscape software was used to construct the regulatory network. Results    A total of 630 DEGs and 32 hub genes were found, of which VCAN was an up-regulated DEG, and high expression of VCAN was significantly associated with poor prognosis of ESCC. Moreover, VCAN could also play a role in the immune microenvironment of ESCC, which was mainly manifested by a significant positive correlation between the abundance of VCAN and the abundance of M2 macrophages gene markers, some of which had been reported to be associated with poor prognosis of ESCC. Finally, we also found that VCAN could be regulated by 15 miRNAs in ESCC, some of which had been reported to be associated with ESCC prognosis. Conclusion    This study provides direct and indirect comprehensive evidence for the role of VCAN in ESCC prognosis. The direct evidence is that the survival curve shows that highly expressed VCAN is significantly associated with the poor prognosis of ESCC, and the indirect evidence is that VCAN is positively related to some markers which indicate poor prognosis in the ESCC immune microenvironment, and VCAN can be regulated by some prognostic miRNAs in ESCC.