ABSTRACT
AIM: To construct an evaluation indicator system for nursing multi-disciplinary team (MDT) clinical practice in China and to provide quantifiable indicators for MDT clinical teaching courses. METHODS: Based on relevant literature retrieval and analysis, a evaluation indicator system of nursing MDT clinical teaching quality was preliminarily constructed using the Donabedian. Structure-Process-Outcome model as theoretical guidance. Then, a final indicators content was formed after two rounds of expert consultation and Analytic Hierarchy Process (AHP) was used to determine the weight of indicators at all levels. RESULTS: The effective response rate of the questionnaires in two rounds were 95.23% (20/21) and 100% (20/20) respectively, the expert authority coefficient (Cr) were 0.838 and 0.853 respectively and the Kendall's coefficient of concordance (Kendall's W) of indicators at all levels were 0.137-0.612 (P < 0.05). The final evaluation index system consisted of three one-class indicators, 8 s-class indicators and 28 third-class indicators. CONCLUSION: The study constructed a comprehensive set of evaluation indicator system of nursing MDT clinical practice, which was scientific and reliable and provides reference for the clinical teaching quality evaluation of MDT nursing.
Subject(s)
Delphi Technique , China , Humans , Surveys and QuestionnairesABSTRACT
Background: It was reported that circular RNA (circRNA) circCTNNA1 plays an oncogenic role in colorectal cancer, while its role in mantle cell lymphoma (MCL) is unknown. This study aimed to explore the role of circCTNNA1 in MCL. Methods: Samples of B lymphocytes were collected from 56 MCL patients and 56 healthy controls. The expression of circCTNNA1 and miR-34a in these samples were determined by RT-qPCR. The direct interaction between circCTNNA1 and miR-34a in MCL cells was detected using RNA-RNA pulldown assay. Overexpression assays were performed to study the interactions between circCTNNA1 and miR-34a. Cell proliferation was assessed with BrdU assay. Results: The results showed that circCTNNA1 was upregulated in MCL and high expression levels of circCTNNA1 predicted the poor survival of MCL patients. MiR-34a was downregulated in MCL and inversely correlated with circCTNNA1. CircCTNNA1 was predicted to interact with miR-34a, and the interaction between them was confirmed by RNA pull-down assay. Interestingly, overexpression of circCTNNA1 and miR-34a did not affect the expression of each other. Cell proliferation analysis showed that overexpression of circCTNNA1 reversed the inhibitory effects of overexpression of miR-34a on cell proliferation. Conclusion: Upregulation of circCTNNA1 in MCL predicts poor survival of patients and it may sponge miR-34a to promote cancer cell proliferation.
ABSTRACT
BACKGROUND: Acute myeloid leukemia (AML) is recognized as a hematological neoplasm with heterogenetic cytology and short-term outcome. HCP5 has been proven to be related with the pathogenesis of AML. However, the underlying mechanism of HCP5 in AML remains unclear. METHODS: Clinical profiles of AML patients were downloaded from TCGA and GTEx databases. LncBase and TargetScan online tools were utilized to predict potential targets, and dual-luciferase reporter assay was performed to verify the association between miR-1291 and HCP5 or PIK3R5. Cell Counting Kit 8 and flow cytometry tests were implemented to evaluate the effects of HCP5/miR-1291/PIK3R5 axis in AML cells. Quantitative RT-PCR and Western blot were conducted to detect the expression levels of genes. RESULTS: HCP5 and PIK3R5 were significantly increased in AML tissue samples compared with healthy controls. HCP5 facilitated AML cells viability and inhibited apoptosis. There was a positive relationship between HCP5 and PIK3R5, but miR-1291 negatively regulated PIK3R5. Overexpression of PIK3R5 enhanced the promoting effect of HCP5 in the development of AML, while weakened the suppression of miR-1291 to AML progression. CONCLUSION: Our findings manifested that HCP5 was remarkably upregulated in AML and upregulated HCP5 promoted the malignant behaviors of AML cells by mediating miR-1291/PIK3R5 axis, which would provide a new insight for the treatment of AML.
