Global, Regional, and National Burdens of Ischemic Heart Disease Attributable to Smoking From 1990 to 2019

Background This study was conducted to estimate the distribution of and changes in the global disease burden of ischemic heart disease attributable to smoking between 1990 and 2019. Methods and Results Data used in this study come from the GBD 2019 (Global Burden of Disease Study 2019). Age‐standardized rates and estimated annual percentage change of age‐standardized rates were used to describe this burden and its changing trend. Pearson's correlation coefficient was used to evaluate the correlation between the sociodemographic index and changing trend. From 1990 to 2019, the burden of ischemic heart disease attributable to smoking has shown a downward trend globally; estimated annual percentage changes of age‐standardized mortality rates and age‐standardized disability‐adjusted life‐years rates were −2.012 (95% CI, −2.068 to −1.956) and −1.907 (95% CI, −1.975 to −1.838). Nineteen countries experienced an increase in disease burden, and the changes in 17 countries were not statistically significant. In addition, this burden was higher in men and older age groups. Estimated annual percentage change of the age‐standardized rates of this burden were negatively correlated with the sociodemographic index. Conclusions Although the burden of ischemic heart disease attributable to smoking has decreased in >80% of countries or regions in the past 30 years, it has remained a significant issue in low‐ and middle‐income countries, particularly among men and elderly populations. Therefore, active tobacco control measures, focusing on key populations, are required to reduce the associated burden of ischemic heart disease, especially in those countries or regions with increasing prevalence and disease burden

The Tumor Suppressive Role of MiRNA-509-5p by Targeting FOXM1 in Non-Small Cell Lung Cancer

Background/Aims: Deregulation of microRNAs (miRNAs) expression is a frequent event in cancer development and progression. Recent studies have implied that abnormal expression of miRNAs is frequently observed in non-small cell lung cancer (NSCLC). Here, we examined the levels and biological functions of miR-509-5p in NSCLC. Methods: The levels of miR-509-5p were measured by real-time quantitative PCR (RT-PCR) in NSCLC cell lines and NSCLC tissues along with adjacent normal tissues. Cell viability was analyzed by MTT and colony formation assay. Cell migration and invasion were evaluated by transwell and wound healing assay. In addition, we predicted the putative targets of miR-509-5p by bioinformatics analyses. Moreover, by luciferase-reporter assay, we analyzed the relationship between miR-509-5p and the target in NSCLC cells. Results: miR-509-5p expression was significantly reduced in NSCLC tissues compared with adjacent normal tissues. In addition, miR-509-5p decreased cell proliferation, migration and invasive capability of NSCLC cells. Moreover, we found that FOXM1 was a putative target of miR-509-5p. Enforced miR-509-5p expression in NSCLC cells reduced both mRNA and protein levels of FOXM1. Furthermore, dual-luciferase reporter assay showed miR-509-5p could bind to the 3' untranslational regions of FOXM1 mRNA. Furthermore, overexpression of FOXM1 reversed cell viability, migration, invasion and vimentin levels suppressed by miR-509-5p mimics in H1299 cells. Conclusions: miR-509-5p exerts tumor-suppressive effects by attenuating FOXM1 in NSCLC. Collectively, these findings provide further evidence that miR-509-5p may be considered as a novel and potential target for the diagnosis, prognosis and treatment of NSCLC

Additional file 8: Table S4. of AFEAP cloning: a precise and efficient method for large DNA sequence assembly

PCR thermocycling conditions. (DOCX 13 kb

Additional file 9: Table S5. of AFEAP cloning: a precise and efficient method for large DNA sequence assembly

PCR product reannealing conditions. (DOCX 14 kb

Additional file 4: Figure S2. of AFEAP cloning: a precise and efficient method for large DNA sequence assembly

Sequencing validation of number of fragments characterization. The join sites were shown as S1 to S13, and number of fragments for assembly was shown as 2 + V to 12 + V. The overhang sequences were shown. V: vector backbone. (DOCX 11884 kb

Additional file 6: of AFEAP cloning: a precise and efficient method for large DNA sequence assembly

Supporting Information. (DOCX 32 kb

Additional file 5: Figure S3. of AFEAP cloning: a precise and efficient method for large DNA sequence assembly

Sequencing validation of plasmid sizes characterization. Five join sites are S1, S2, S3, S4, and S5. (a) 11.5 kb plasmid; (b) 19.6 kb plasmid; (c) 28 kb plasmid; (d) 34.6 kb plasmid. The overhang sequences were shown. (DOCX 3815 kb

Additional file 2: Table S2. of AFEAP cloning: a precise and efficient method for large DNA sequence assembly

Primers used in this work. (DOCX 32 kb

Additional file 1: Table S1. of AFEAP cloning: a precise and efficient method for large DNA sequence assembly

Comparisons of AFEAP cloning with common DNA assembly methods. (DOCX 23 kb