Objective To identify main factors affecting the research capacity of nursing staff for efficient elevation of such a capacity. Methods 1000 persons were chosen in a random coded sampling for completion of questionnaires, including a general information questionnaire, research capacity self-assessment questionnaire, nursing professional value scale and work satisfaction scale for nursing staff. Results Main factors for the research capacity range from high to low the following: education, work satisfaction, training involvement, cognitive value, and nature of their employer. Beta values of such factors are found to be 0. 323, 0. 234, 0. 182,0. 064, and 0. 062 respectively. Conclusion Administrators of nursing staff need to focus on the development of the work values and satisfaction of nursing staff, on top of developing their research methodology and knowledge. This approach may encourage them to proactively involve in research activities.

Objective:To explore the effects of sulforaphane (SFN), an activator of Nrf2, on anxiety and fear memory in Alzheimer's disease(AD) model mice and mechanism.Methods:The AD mice and wild type (WT) mice with the same background were randomly divided into four groups ( n=12 for each group): wild type + normal saline group (WT+ NS), wild type + sulforaphane (WT+ SFN), AD model + normal saline group (AD+ NS) and AD model + sulforaphane group (AD+ SFN). SFN was dissolved in normal saline (0.9% NaCl) and prepared solution with concentration of 1 g/L.According to body weight, mice in WT+ SFN group and AD+ SFN group were intraperitoneally injected with SFN (10 mg/kg), and mice in WT+ NS group and AD+ NS group were intraperitoneally injected with the same volume of normal saline once a day for 30 days.The open field test was used to detect the autonomous exploration ability and anxious behavior of mice.The elevated cross maze was used to detect the anxiety of mice.Conditional fear test was used to test the fear memory behavior of mice.Finally, the expression of superoxide dismutase(SOD) and malondialdehyde(MDA) in the hippocampus and cerebral cortex were detected by ELISA.Two-way ANOVA analysis was performed using GraphPad Prism 8.0.2 software. Results:In the open field test, the percentage of time in central region in AD+ SFN group ((9.99+ 0.37)%) was higher than that of AD+ NS group ((8.47+ 0.42)%) ( q=3.842, P<0.05). In the elevated cross maze, the percentage of time in open arm of AD+ SFN group ((26.2±1.6)%) was higher than that in AD+ NS group ((15.8±1.0)%) ( q=7.452, P<0.01). In the conditional fear test, all the mice of the four groups developed the fear memory, but AD+ SFN group showed higher freezing time ratio ((64.5±3.8)%) than AD+ NS group ((51.0±4.3)%)( q=5.266, P<0.01) in the testing stage.After SFN intervention, the important indicator of oxidative stress, the expression levels of SOD in hippocampus ( q=6.370, P<0.01) and cortex ( q=7.858, P<0.01) of AD mice increased, while the level of MDA in hippocampus ( q=5.146, P<0.05) and cortex ( q=5.833, P<0.01) decreased. Conclusion:SFN may inhibit oxidative stress through Nrf2 pathway, thereby improving anxiety and fear memory in AD mice.

BACKGROUND:Studies have found that glucagon-like peptide-1 and its analogues have a significant neuroprotective effect,and some drugs have been applied to the clinical stage Ⅲ study of Alzheimer's disease.However,the mechanism of its neuroprotective effect is still unclear,which needs to be further explored and clarified. OBJECTIVE:To screen out the genes related to the pathogenesis of Alzheimer's disease and the related targets of semaglutide for the treatment of Alzheimer's disease based on bioinformatics and network pharmacology analyses,to identify the potential target genes by comprehensive analysis of the two and to verify them at the cellular level. METHODS:Using DisGeNET database,differentially expressed genes between Alzheimer's disease patients and healthy population were screened out.The chemical structure formula and two-dimensional structure diagram of semaglutide were obtained using PubChem online database.GO/KEGG enrichment analysis was performed using DAVID online database.A protein-protein interaction network was constructed by using the STRING database.The HPA database was used to determine the distribution characteristics of the target proteins in various human tissues.Finally,western blot was used to detect relevant protein expression in HT22 cells after semaglutide intervention. RESULTS AND CONCLUSION:With the dataset in DisGeNET database,3 374 differentially expressed genes between Alzheimer's disease patients and healthy people were obtained,and meanwhile,101 target genes of semaglutide potential drugs were obtained.There were 23 intersection genes between them.Ten key genes were identified based on the protein-protein interaction network,which were silent information regulator 1(SIRT1),CASP9,CCND1,CASP1,KEAP1,DLG4,CASP4,GRB2,GRIA1,and EDNRA.The results of GO gene functional annotation analysis of key genes showed that the positive regulatory activity of cysteine endopeptidase,the positive regulation of proteolysis,and the positive regulation of cysteine endopeptidase involved the cytoplasmic part of the apoptotic activity process;AMPA glutamate receptor complex,inflammatory complex,CARD domain binding,cysteine endopeptidase activity,and cysteine endopeptidase activity were involved in the apoptotic process.The results of KEGG signaling pathway analysis indicated that colorectal cancer,non-small cell carcinoma,and endometrial carcinoma were related to immune infiltration,inflammation and autophagic apoptosis.In addition,according to the association ranking of key genes and their distribution in different tissues of HPA online database,SIRT1 was identified as the most significant differential gene.The expression level of SIRT1 protein was significantly down-regulated in HT22 cells after β-amyloid protein 1-42 treatment,but it could be significantly increased after being treated with semaglutide.To conclude,SIRT1 may be a target gene for semaglutide in the treatment of Alzheimer's disease.