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1.
Chinese Medical Ethics ; (6): 770-776, 2023.
Article in Chinese | WPRIM | ID: wpr-1005665

ABSTRACT

【Objective:】 Evaluating the service quality and medical experience of elderly-friendly medical institutions from the perspective of elderly patients and their accompanying relatives and friends is a specific measure and work focus to promote the construction of elderly-friendly medical institutions, optimize the medical procedures for the elderly, solve the intelligent technology difficulties encountered in the medical process for the elderly, promote public hospitals to fully implement preferential policies for elderly medical services, and continuously improve the health and well-being of the elderly. 【Methods:】 Based on literature analysis and expert consultation, the satisfaction evaluation indicators for elderly-friendly medical institutions were formed. The Analytic Hierarchy Process was used to assign weights to the indicators. And then, the satisfaction evaluation index system for elderly-friendly medical institutions was formed. 【Results:】 After two rounds of Delphi method, and the scoring and demonstration of 15 experts, four primary indicators and 21 secondary indicators were finally formed, and then, assigned weight coefficients to them through analysis. 【Conclusion:】 After the expert demonstration, the satisfaction evaluation system for elderly-friendly medical institutions has good reliability and validity, providing the basis for the construction of elderly-friendly medical institutions and contributing to the formation of a sustainable, systematic, and diversified elderly-friendly service system.

2.
Chinese Journal of Lung Cancer ; (12): 323-330, 2021.
Article in Chinese | WPRIM | ID: wpr-880276

ABSTRACT

BACKGROUND@#MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression, influence cellular processes, and promote disease development. Variations in miRNA expression have been observed in many diseases, including hepatitis, cardiovascular disease, and cancer. The aim of this study is to investigate the effect of miR-144-3p on the invasion and metastasis of lung adenocarcinoma by targeting recombinant insulin receptor substrate 1 (IRS1).@*METHODS@#The expression of miR-144-3p in patients with lung adenocarcinoma was queried through bioinformatics database. MirTarPathway was used to analyze the KEGG enrichment pathway of miRNA. The expression and plasmid transfection efficiency of miR-144-3p in lung adenocarcinoma cell lines were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Transwell assay was used to detect the changes of cell invasion and migration ability in different groups. Bioinformatics determined the key genes (Hub genes) of miR-144-3p; Double luciferase target assay was used to detect the mutual binding of miR-144 and IRS1. Western blot assay was used to detect the expression of IRS1 in different cell lines and the expression of after overexpression of miR-144.@*RESULTS@#The expression of miR-144-3p in lung adenocarcinoma tissues was decreased, qRT-PCR results indicated that the expression of miR-144-3p in lung adenocarcinoma cell A549 was significantly decreased (P<0.05), and the overexpressed plasmid was successfully transfected (P<0.05). Overexpression of miR-144 decreased the ability of cell migration and invasion (P<0.05). The expression of IRS1 was up-regulated in lung adenocarcinoma tissues. Survival analysis showed that patients with lung adenocarcinoma with high IRS1 expression had a poor prognosis (P<0.05). Double luciferase assay results showed that miR-144 could specifically identify 3'-UTR of IRS1 and inhibit reporter enzyme expression (P<0.05). Western blot indicated that the expression of IRS1 was increased in A549 cells (P<0.05). After overexpression of miR-144, the expression level of IRS1 protein was decreased (P<0.05). Transwell experiment proved that miR-144-3p could inhibit invasion and metastasis of lung adenocarcinoma cells by targeting IRS1 (P<0.05).@*CONCLUSIONS@#MiR-144-3p inhibits the invasion and migration of A549 cells through targeted regulation of IRS1, thus playing an anticancer role in tumors.

3.
Chinese Journal of Lung Cancer ; (12): 638-645, 2020.
Article in Chinese | WPRIM | ID: wpr-826917

ABSTRACT

BACKGROUND@#Derlin 3 (DERL3) is downregulated in colorectal cancer (CRC) samples. Its level is closely linked to lymphatic metastasis or distant metastasis rate in CRC patients. However, its biological behavior in lung adenocarcinoma were rarely reported. The aim of this study is to investigate the ectopic expression of DERL3 in lung adenocarcinoma tissues and its effect on the invasion and metastasis of lung adenocarcinoma A549 cell line to reveal the possible mechanism of invasion and metastasis of lung adenocarcinoma.@*METHODS@#Lung adenocarcinoma microarray gene chip data included 3 cases of lymph node metastasis and 3 cases of lung adenocarcinoma tissue without lymph node metastasis. The GEDS and Kaplan-Meier plot queries the survival curve and expression level of DERL3. Western blot was used to detect the expression of DERL3 in lung adenocarcinoma cells. The efficiency of knockdown DERL3 gene was detected by Western blot assay. Transwell detected the number of cells passing through the basement membrane of the transwell. EDU assay detected cell proliferation ability. Western blot detected the expression of epithelial-mesenchymal transition related proteins E-cadherin and Vimentin.@*RESULTS@#The microarray gene chip results showed that compared with lung adenocarcinoma tissues without lymph node metastasis, 1,314 mRNAs in lung adenocarcinoma tissues with lymph node metastasis were up-regulated, 400 mRNAs were down (P<0.05). The expression of DERL3 increased in lung adenocarcinoma (P<0.05). The results of survival curve showed that the lung cancer patients with high expression of DERL3 with poor prognosis (P<0.05). Western blot results indicated that plasmid transfection was successful. Knockdown of DERL3 suppressed the ability of proliferation, invasion and migration in A549 cells (P<0.05). After knockdown of DERL3, the expression level of Vimentin was decreased, while E-cadherin expression increased (P<0.05).@*CONCLUSIONS@#Knockdown of DERL3 inhibited the proliferation, invasion and metastasis of A549 cells.

4.
Journal of Southern Medical University ; (12): 869-875, 2020.
Article in Chinese | WPRIM | ID: wpr-828891

ABSTRACT

OBJECTIVE@#To investigate the effect of miR-204 on the invasion and metastasis of breast cancer by targeted regulation of HNRNPA2B1.@*METHODS@#The bioinformatics database was used to obtain data of the expressions of miR-204 in breast cancer patients and the survival rate of the patients. RT-qPCR was used to detect the expression of miR-204 in breast cancer cell lines. The expression vector GV369-miR-204 was used to overexpress miR-204 in MDA-MB-231 cells. Transwell assay was performed to detect the effect of miR-204 on the migration and invasion ability of the breast cancer cells. The key genes (hub genes) of miR-204 were determined by bioinformatics method. A dual luciferase assay was used to analyze the targeting relationship between miR-204 and HNRNPA2B1. The expression of HNRNPA2B1 in MDA-MB-231 cells after miR-204 overexpression was detected by Western blotting, and Transwell assay was used to examine the changes in the cell invasion ability.@*RESULTS@#The expression of miR-204 was decreased in both breast cancer tissues, and was significantly lower in breast cancer MDA-MB-231 cells than in MCF-10A cells ( < 0.05). The decreased expression of miR-204 was associated with poorer prognosis of breast cancer patients ( < 0.05). Upregulation of miR-204 in MDA-MB-231 cells significantly inhibited the invasion and migration of the cells ( < 0.05). Analysis of the data from the Starbase revealed that the expression of miR-204-5p was negatively correlated with the expression of HNRNPA2B1, and the expression of HNRNPA2B1 was increased in breast cancer patients ( < 0.05) in association with a poorer prognosis of the patients ( < 0.05). Dual luciferase assay demonstrated that miR-204 could bind to HNRNPA2B1 in a target-specific manner. Western blotting and Transwell assay showed that miR-204 significant inhibited the migration and invasion ability of breast cancer cells by targeting HNRNPA2B1 ( < 0.05).@*CONCLUSIONS@#miR-204 expression is decreased in breast cancer tissues and cells, and its overexpression can inhibit the invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1.


Subject(s)
Humans , Breast Neoplasms , Cell Line, Tumor , Cell Movement , Cell Proliferation , Gene Expression Regulation, Neoplastic , MicroRNAs , Genetics , Neoplasm Invasiveness , Neoplasm Metastasis
5.
Journal of Medical Informatics ; (12): 29-32, 2015.
Article in Chinese | WPRIM | ID: wpr-479273

ABSTRACT

The paper summarizes application of new media in patient informatization services in hospitals, introduces exploration and practices made by Children′s Hospital of Shanghai on new media informatization platform construction from such aspects of OA system-basedwindowservice platform,order typeservice model provided to the public onMicroblogandWeChatplatforms andex-press typemobile network terminal service for hospital staffs.The service effects are summarized at last.

6.
International Journal of Pediatrics ; (6): 238-241,244, 2011.
Article in Chinese | WPRIM | ID: wpr-564347

ABSTRACT

Specific immunotherapy(SIT)is the most effective therapy for allergies.Although specific immunotherapy has existed for more than 90 years and has made a great progress,its mechanism is not well defined.Early studies focused on the circulating antibodies and effector cells.At present.the research of the mechanism mainly concentrates on the immune therapy on T cells role and a series of cytokines arising from the change,CD4+ regulatory T cells subsets,modified APC induction of immune tolerance,aggregation mechanism of immune effector cells,restructuring allergens under the support of monoclonal antibody technique,allergens DNA vaccines,allergens coupling adjuvants.This essay is a review of progress in mechanism of specific immunotherapy.

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