Background and purpose: Gene chip is a nucleic acid sequence analysis method which is based on hybridization. It is a high-through put assay which can widely detect the level of gene expression in different tissues and cell types. This study aimed to compare and bioinformatically analyze differentially expressed genes between higher malignant degree of prostate cancer tissues and prostate inflammation tissues. Methods: The total RNAs were isolated from tissues of prostate cancer and prostate inflammation by TRIzol method and then purified, reversely tran-scribed to cDNA with incorporating biotin labeling probe, hybridized with Affymetrix Human U133 Plus 2.0 (covering 47000 transcripts,representing 38500 distinct genes). Picture signals of fluorescence in gene array were scanned and differential expression of gene in two tissues were compared by Command Console Software 4.0. These differential expressed genes were analyzed by bioinformatics methods finally. Results: According to the fold change ≥2, P<0.05, 1819 differential expression genes including 1025 up-regulated genes and 794 down-regulated genes were discovered. GO enrichment analysis displayed that these differentially expressed genes were mainly involved in cell cycle, cell metabolism, etc. KEGG pathway analysis found that these genes were mainly involved in some metabolism pathways including purine nucleotide metabolism. The interactions between the proteins encoded by these genes were analyzed by STING. Twenty key nodes genes including TPX2, ANLN, NUSAP1, MELK, DLGAP5, KIF11, TOP2A, RRM2 were dis-covered. Then this study revealed CEP55 and ANLN might be related to the occurrence and metastasis of prostate cancer by looking through literature. Conclusion: During the development of prostate cancer, the activation of genes related to cell cycle and cell migration, the abnormalities of genes related to metabolism and the inhibition of genes related to cell adhesion play critical roles in the development of prostate cancer. CEP55 and ANLN were related to the occurrence and prognosis of prostate cancer by systematic analysis which provided a valuable clue for the next experiment.

Objective To investigate the influence of early growth response gene-1 (EGR1) on the autophagy of host cells following infection with human T cell leukemia virus type 1 (HTLV-1).MethodsA HTLV-1-positive cell line MT2 was co-cultured with HeLa cells for 24 h to construct the virus early infection model.Immunoblotting assay was used to detect the expression of HTLV-1 core protein p19 and EGR1.Luciferase reporter gene analysis was used to detect the transcriptional activity of 5′-regulatory sequence of EGR1 at different time points after co-culturing.An effective small interfering RNA (siRNA) targeting EGR1 was screened out and transfected into HeLa cells by Lipofectamine 2000.Then the transfected HeLa cells were co-cultured with the HTLV-1-positive cell line MT2 for 24 h.Immunoblotting assay was used to detect HTLV-1 core protein p19, EGR1 and autophagy-related protein LC3.Real-time PCR was performed to detect viral load.Autophagosome was analyzed by immunofluorescence after co-culturing.Results The expression of EGR1 and the transcriptional activity of pEGR1-luc gradually increased after co-culturing HeLa cells with MT2 cells for 8 h (P<0.01).The expression of EGR1 was positively correlated with host cell autophagy following HTLV-1 infection.The effective siRNA for silencing the expression of EGR1 was obtained and named as siE2.The viral load, the expression of HTLV-1 core protein p19 and the proportion of LC3B/LC3A in the co-culture model were markedly down-regulated by RNA interference with siE2, which was concomitant with a persistent decrease of intracellular autophagosome (P<0.01).Conclusion EGR1 is associated with host cell autophagy and viral replication in HTLV-1 infection.

Objective:To investigate whether cachexia affects the treatment effect of immune checkpoint inhibitors for non-small cell lung cancer (NSCLC).Methods:The prognosis of 62 patients with advanced NSCLC who received anti-programmed cell death-1 (PD-1) in Henan Provincial People′s Hospital from 2019 to 2021 were retrospectively analyzed. The cachexia was evaluated before and after the second course of immunotherapy. Kaplan-Meier and Log rank methods were used for survival analysis, Cox regression model was used for multivariate analysis, and Spearman′s correlation analysis was used for correlation analysis.Results:After the second course of immunotherapy, psoas major muscle area (PMMA) values of the cachexia group and the control group were (14.10±4.09) and (11.66±3.22) cm 2 respectively, with statistics significance ( P=0.001). The level of Prealbumin and body weight were correlated with cachexia ( P<0.05). The 6-month and 1-year survival rates of 62 cases in the whole group were 58.6% and 42.5%, respectively. The progression-free survival (PFS) in the control group (7.6 months) was higher than that in the cachexia group (3.8 months, P=0.006). The PFS in patients with high expression of PD-L1 (7.1 months) was longer than that of patients with low expression (3.8 months, P=0.009). The overall survival (OS) in the cachexia group (6.3 months) was lower than that in the control group (18.2 months, P=0.006). The OS in patients with high expression of PD-L1 (14.5 months) was longer than that of patients with low expression (1 months, P=0.038). The level of Prealbumin, the level of PD-L1 expression and the change rate of PMMA were related to the OS of the patients ( P<0.05). The level of Prealbumin and the change rate of PMMA were the independent influencing factors of the OS ( P<0.05). The PMMA and the level of Prealbumin were negatively correlated ( r=-0.003 8, P<0.05). Conclusion:Cachexia has a negative impact on the outcomes of patients who received anti-PD-1 immune checkpoint inhibitor therapy.

Objective:To investigate whether cachexia affects the treatment effect of immune checkpoint inhibitors for non-small cell lung cancer (NSCLC).Methods:The prognosis of 62 patients with advanced NSCLC who received anti-programmed cell death-1 (PD-1) in Henan Provincial People′s Hospital from 2019 to 2021 were retrospectively analyzed. The cachexia was evaluated before and after the second course of immunotherapy. Kaplan-Meier and Log rank methods were used for survival analysis, Cox regression model was used for multivariate analysis, and Spearman′s correlation analysis was used for correlation analysis.Results:After the second course of immunotherapy, psoas major muscle area (PMMA) values of the cachexia group and the control group were (14.10±4.09) and (11.66±3.22) cm 2 respectively, with statistics significance ( P=0.001). The level of Prealbumin and body weight were correlated with cachexia ( P<0.05). The 6-month and 1-year survival rates of 62 cases in the whole group were 58.6% and 42.5%, respectively. The progression-free survival (PFS) in the control group (7.6 months) was higher than that in the cachexia group (3.8 months, P=0.006). The PFS in patients with high expression of PD-L1 (7.1 months) was longer than that of patients with low expression (3.8 months, P=0.009). The overall survival (OS) in the cachexia group (6.3 months) was lower than that in the control group (18.2 months, P=0.006). The OS in patients with high expression of PD-L1 (14.5 months) was longer than that of patients with low expression (1 months, P=0.038). The level of Prealbumin, the level of PD-L1 expression and the change rate of PMMA were related to the OS of the patients ( P<0.05). The level of Prealbumin and the change rate of PMMA were the independent influencing factors of the OS ( P<0.05). The PMMA and the level of Prealbumin were negatively correlated ( r=-0.003 8, P<0.05). Conclusion:Cachexia has a negative impact on the outcomes of patients who received anti-PD-1 immune checkpoint inhibitor therapy.

Objective:To establish training system for postoperative delirium (POD) assessment and evaluate the efficacy of training for anesthesia nurses.Methods:Sixteen nurse anesthetists of both sexes in our hospital were selected and received the systemic training for POD assessment.The training system included questionnaire survey, theoretical teaching, simulated visit, clinical observation, independent evaluation, centralized question-answering, evaluation of efficacy and random inspection.The level of POD knowledge tests were performed before the training and at the end of the fourth week of independent evaluation, respectively.At week 1 and 4 of independent evaluation, the diagnostic rate of POD and sensitivity and specificity of the assessment were calculated, and Kappa consistency analysis was used to assess the consistency between anesthesia nurses and training group in diagnosis of POD.In the first week of the third month after the end of training, the evaluation results were randomly inspected, the POD diagnosis rate was calculated between the anesthesia nurses and the training group, and the consistency analysis was conducted.Results:Compared with the scores of POD knowledge questionnaire and sensitivity of the assessment of the anesthesia nurses in the first week of training, the scores were significantly increased ( P<0.05), and no significant change was found in the POD diagnosis rate in the fourth week of training ( P>0.05). Compared with the training group, the diagnosis rate of POD of anesthesia nurses was significantly decreased in the first week of training ( P<0.05), and no significant change was found at the fourth week of training ( P>0.05). In the first and fourth weeks of training, the Kappa value of anesthesia nurses and the training group was 0.676 and 0.954 ( P<0.001), respectively.In the first week of the third month after the end of training, the Kappa value between anesthesia nurses and the training group in diagnosis of POD was 0.862 ( P<0.05). Conclusion:The training system of POD assessment has been successfully established, and the standardized anesthesia nurses training of POD has been achieved with good results.

Objective To investigate whether high glucose-induced vascular calcification is associated with WNT signaling pathway. Methods An in vitro model of human vascular smooth muscle cell (VSMC) calcification was induced by exposure of the cells to high glucose. The expressions of WNT signal molecules and bone-related proteins including Cbfa1, Osx, OCN and BMP2 were analyzed with qRT-PCR, and the cell calcification was assessed by alizarin red staining. The effect of Dkk1, a WNT signaling inhibitor, on high glucose-induced cell calcification was tested with alizarin red staining and calcium content analysis. Results High glucose activated WNT signaling pathway in human VSMCs by up-regulating the expressions of WNT signal molecules including Wnt3a, Wnt7a, Fzd4 and Wisp1 mRNA by 1.86, 1.68, 2.1, and 2.3 folds, respectively, and by promoting the phosphorylation ofβ-catenin (2.70±0.22, P<0.05), a key mediator of WNT signaling pathway. Inhibition of WNT signaling pathway by Dkk1 attenuated high glucose-induced VSMC calcification and down-regulated the expression of bone-related proteins Cbfa1, Osx, OCN, and BMP2 by (51 ± 9)%, (58 ± 11)%, (56 ± 10)%, and (62 ± 10)% (P<0.01). Conclusion WNT signaling pathway is involved in high glucose-induced VSMC calcification.

Objective To investigate whether high glucose-induced vascular calcification is associated with WNT signaling pathway. Methods An in vitro model of human vascular smooth muscle cell (VSMC) calcification was induced by exposure of the cells to high glucose. The expressions of WNT signal molecules and bone-related proteins including Cbfa1, Osx, OCN and BMP2 were analyzed with qRT-PCR, and the cell calcification was assessed by alizarin red staining. The effect of Dkk1, a WNT signaling inhibitor, on high glucose-induced cell calcification was tested with alizarin red staining and calcium content analysis. Results High glucose activated WNT signaling pathway in human VSMCs by up-regulating the expressions of WNT signal molecules including Wnt3a, Wnt7a, Fzd4 and Wisp1 mRNA by 1.86, 1.68, 2.1, and 2.3 folds, respectively, and by promoting the phosphorylation ofβ-catenin (2.70±0.22, P<0.05), a key mediator of WNT signaling pathway. Inhibition of WNT signaling pathway by Dkk1 attenuated high glucose-induced VSMC calcification and down-regulated the expression of bone-related proteins Cbfa1, Osx, OCN, and BMP2 by (51 ± 9)%, (58 ± 11)%, (56 ± 10)%, and (62 ± 10)% (P<0.01). Conclusion WNT signaling pathway is involved in high glucose-induced VSMC calcification.