Objective To explore whether PERK is involved in the regulation of arsenite-induced autophagy.Methods Human hepatoma cells HepG2 were cultured and treated with arsenite.The expression level of autophagic hallmarks and the activation status of PERK were detected by Western blotting.The transactivation of p53 and the induction of its downstream target genes expression were also detected by Western blotting after knockdown of PERK expression.Transactivity of p53 was detected by dual luciferase reporter assay after knockdown of PERK expression.Results An increase in the LC3BII:I ratio,the induction of Beclin-1 expression and the degradation of p62 were readily observed in arsenite-treated HepG2 cells,but the effects were abolished after knockdown of PERK expression.Furthermore,phosphorylation of p53 at Ser15 and Ser392,transactivation of p53 and the induction of its downstream target gene DAPK1 expression were effectively inhibited under the same PERK knockdown conditions.Conclusion PERK regulates arsenite-induced autophagy by activating p53-dependent DAPK1 upregulation.

目的探讨后外侧小切口行全髋置换术(THA)后患者康复护理。方法后外侧入路小切口患者45例48髋,经精心护理后与常规THA患者在手术切口、围手术期出血量、术后疼痛、住院天数、早期活动方面比较。结果在相同条件下,小切口手术患者减少围手术期出血量、术后疼痛、住院天数及术后早期康复快,缩短住院时间。结论康复护理有助于THA患者的恢复。

Objective: To develop the outcome evaluation index system for home care service of disabled elderly based on the long-term care insurance in Guangzhou. Methods: Delphi method was used to develop the outcome evaluation index system for home care service of disabled elderly under the long-term care insurance in Guangzhou. The Analytic Hierarchy Process was used to determine the weights of all indexes. Results: After two rounds of expert consultation, questionnaire response rates were 86.67%, 100%; expert authority coefficients were 0.843, 0.858; coefficients of variation ranged from 0.07 to 0.23 and 0.00 to 0.14; coordination coefficients ranged from 0.221 to 0.355 and 0.379 to 0.433 (P<0.01). The final index system consisted of 5 first-level indicators, 17 second-level indicators, and 59 third-level indicators. The analytic hierarchy process was used to determine the weights of all indexes, and the consistency test (CR<0.1) was performed. Conclusions The outcome evaluation index system for home care service of disabled elderly under the long-term care insurance in Guangzhou was scientific and reliable, the weights of all indexes were reasonable, which could provide reference for the designated service institution on evaluation and improvement of the effect of home care service of long-term care insurance for disabled elderly.

OBJECTIVE: To analyze the differentially expressed genes (DEGs) between lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) with bioinformatics analysis and search for potential biomarkers for clinical diagnosis of nonsmall cell lung cancer (NSCLC). METHODS: The gene expression profiling datasets of LUAD and LUSC were acquired. The transcriptome differences between LUAD and LUSC were identified using R language processing and t-test analysis. The differential expressions of the genes were shown by Venn diagram. The DEGs identified by GEO2R were analyzed with DAVID and Ingenuity Pathway Analysis (IPA) to identify the signaling pathways and biomarkers that could be used for differential diagnosis of LUAD and LUSC. The TCGA data and the biomarker expression data from clinical lung cancer samples were used to verify the differential expressions of the Osteoarthritis pathway and LXR/RXR between LUAD and LUSC. We further examined the differential expressions of miR-181 and its two target genes, and , in 23 clinical specimens of lung squamous cell carcinoma and the paired adjacent tissues. RESULTS: GEO data analysis identified 851 DEGs (including 276 up-regulated and 575 down-regulated genes) in LUAD and 885 DEGs (including 406 up-regulated and 479 down-regulated genes) in LUSC. DAVID and IPA analysis revealed that leukocyte migration and inflammatory responses were more abundant in LUAD than in LUSC. Osteoarthritis pathway was inhibited in LUAD and activated in LUSC. IPA analysis showed that transcription factors (GATA4, RELA, YBX1, TP63 and MBD2), cytokines (WNT5A and IL1A) and microRNAs (miR-34a, miR-181b and miR-15a) differed significantly between LUAD and LUSC. miR-34a with IL-1A, miR-15a with YBX1, and miR-181b with WNT5A and MBD2 could serve as the paired microRNA and mRNA targets for differential diagnosis of NSCLC subtypes. Analysis of the clinical samples showed an increased expression of miR-181b-5p and the down-regulation of WNT5A, which could be used as molecular markers for the diagnosis of LUSC. CONCLUSIONS Through transcriptome analysis, we identified candidate genes, paired microRNAs and pathways for differentiating LUAD and LUSC, and they can provide novel differential diagnosis and therapeutic strategies for LUAD and LUSC.
Adenocarcinoma of Lung ; Carcinoma, Non-Small-Cell Lung ; Carcinoma, Squamous Cell ; Humans ; Lung Neoplasms ; MicroRNAs ; Y-Box-Binding Protein 1