Objective:To assess the effects of intervention measures on the quality control of health examination institutions in Dalian City.Methods:This cross-sectional study encompassed a comprehensive evaluation of 40 physical examination institutions in Dalian City. Interrupted time series analysis was employed to examine the changes in level and slope of processing rates for significant abnormal health examination results, chief inspection physician qualification rates, and completion rates of basic health examination items before (January 2020 to July 2021) and after (August 2021 to July 2022) intervention. An interrupted time series analysis diagram was generated.Results:After the implementation of intervention measures, the processing rate of significant abnormal results in public physical examination institutions reached 93.52%, while the qualification rate of chief inspection physicians was as high as 98.86%. And completion rate of basic health examination items was 93.86%. The rates of handling important abnormal results in health check-ups at private healthcare institutions before intervention, 1 month after intervention, and long-term intervention showed an upward trend of 1.374%, 0.229%, and 0.664%, respectively ( t=8.61, 12.21, and 108.61, all P<0.05). The qualification rate of chief inspection physicians in public physical examination institutions exhibited an increase of 0.227% and 0.155% before and after the intervention respectively ( t=6.74 and 617.67, all P<0.05). The completion rates of basic health check-up items in public healthcare institutions showed an upward trend before intervention, 1 month after intervention, and long-term intervention, with a rate of 0.446%, 0.067%, and 0.745%, respectively ( t=24.95, 3.25, 138.80, all P<0.05). Conclusions:The implementation of quality control intervention measures for health check-ups has significantly improved the quality control of health examination institutions in Dalian City.

ObjectiveTo study the regulatory effect of the partial sequence within the 3’ untranslated region （3’UTR） of slit guidance ligand 1 （Slit1） （Slit1-3’UTR） on the fibrotic phenotypes of cardiac fibroblasts （CFs） and its potential mechanism. MethodsThe adenovirus vector was used to overexpress the 1526nt sequence of Slit1-3’UTR in ICR neonatal mouse CFs （mCFs）. The expression of fibrosis-related genes in mCFs， such as collagen type 1 alpha1（COL1A1）， collagen type 3 alpha3 （COL3A1） and alpha smooth muscle actin （α-SMA） were detected by Western blot assay. The effect of Slit1-3’UTR 1526nt on the proliferation and migration of mCFs was assessed by EdU staining and Trans-well assays. Angiotensin Ⅱ （Ang Ⅱ） was used to treat mCFs， and the impact of Slit1-3’UTR 1526nt on the fibrotic phenotypes of Ang Ⅱ-induced mCFs was evaluated. After overexpression of Slit1-3’UTR 1526nt， miR-34a-5p mimic was transfected into mCFs， followed by actinomycin D treatment to detect the mRNA stability of Slit1-3’UTR 1526nt， and the levels of miR-34a-5p and its target gene SIRT1（si-SIRT1） in mCFs were determined. The effects of miR-34a-5p and small interfering RNA targeting SIRT1 on the Slit1-3’UTR 1526nt-mediated regulation of fibrotic phenotypes were also determined. ResultsAdenovirus-mediated overexpression of Slit 1-3’UTR 1526nt was achieved in mCFs. Overexpression of Slit 1-3’UTR 1526nt markedly inhibited the expression of the fibrosis-related genes， proliferation and migration of mCFs and fibrotic phenotypes of Ang Ⅱ. The results of actinomycin D assay showed that miR-34a-5p inhibited the stability of Slit1-3’UTR 1526nt in mCFs， while the level of miR-34a-5p was reduced in mCFs with overexpression of Slit1-3’UTR 1526nt. Transfection of miR-34a-5p promoted the fibrotic phenotypes， and reversed the inhibitory effect of Slit1-3’UTR 1526nt on the fibrotic phenotypes of mCFs. Overexpression of Slit1-3’UTR 1526nt significantly increased the level of miR-34a-5p target gene SIRT1 in mCFs. Transfection of miR-34a-5p and si-SIRT1 consistently reversed the inhibitory effects of Slit1-3’UTR 1526nt on the fibrotic phenotypes of mCFs. ConclusionSlit1-3’UTR1526nt inhibits the fibrotic phenotypes of mCFs by binding to miR-34a-5p and increasing the expression of its target gene of SIRT1.