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Background: Coronary heart disease (CHD) is primarily caused by atherosclerosis of coronary arteries. It is largely an inflammatory disease of the vascular wall. The inflammation is related to DNA methylation. Angiopoietin-like protein 2 (ANGPTL2) has various functions in several chronic inflammatory diseases. Macrophage-derived ANGPTL2 was reported to accelerate CHD development. It is reported that DNA hypomethylation in the promoter region of ANGPTL2 gene was associated with acute coronary syndrome (ACS), a type of CHD. Our objective was to explore the correlation between promoter methylation of the ANGPTL2 gene and CHD, and to investigate the association between methylation status and clinical characteristics of CHD patients., Methods: Firstly, we collected 122 CHD patients and 58 non-CHD participants from Han Chinese population and purified the peripheral blood DNA. The purified DNA was subjected to bisulfite modification. After bisulfite conversion, the target DNA locus was amplified using polymerase chain reaction (PCR), and the PCR products were measured by pyrosequencing. Finally, the methylation level was calculated according to the sequencing result, and the data were analyzed using xx software., Results: CHD patients had a relatively lower methylation levels (P50: 7.67% [P25: 6.22%, P75: 10.43%]) in the ANGPTL2 promoter region than did controls (P50: 8.25% [P25: 5.46%, P75: 17.98%], P = 0.001), indicating an association between ANGPTL2 promoter methylation and CHD (OR: 0.890; 95% CI, 0.832-0.953; adjusted P = 0.001). A breakdown analysis by gender showed that ANGPTL2 promoter methylation was associated with CHD in females (adjusted P = 0.002) but not in males (adjusted P = 0.404). We found no correlation between gene methylation and other clinical characteristics., Conclusions: The present work provides evidence to support an association between ANGPTL2 promoter DNA methylation status and the risk profile of CHD in females. Our data indicated that in females, promoter DNA hypomethylation of the ANGPTL2 gene is associated with an increased risk of CHD., (© 2018 Wiley Periodicals, Inc.)

Objectives: To examine the effects of carbendazim on Arabidopsis genomic DNA methylation and gene expression., Results: Carbendazim caused widespread changes in gene loci methylation and gene expression. With 0.1 mM (D2) and 0.2 mM (D3) carbendazim, there were, respectively, 1522 and 2278 demethylated sites and 1541 and 2790 methylated sites. A total of 279 and 505 genes were up-regulated by more than 300 % and 175 and 609 genes were down-regulated by 67 % in D2 and D3 treatments, respectively, compared with the control. Conjoint analysis showed that 20 and 39 demethylated genes were up-regulated >300 % and 21 and 24 methylated genes were down-regulated <67 % in D2 and D3, respectively., Conclusions: Carbendazim causes methylation or demethylation of certain genes and changes the expression of these genes. These findings provide a theoretical basis for novel epigenetics-based methods to detect organic food and a new interpretation for the degradation of crop varieties.

Background: Abnormal DNA methylation is one of the most general epigenetic modifications in hepatocellular carcinoma (HCC). Recent research showed that DNA methylation was a prognostic indicator of all‐cause HCC and nonviral HCC. However, whether DNA methylation‐driver genes could be used for predicting survival, the probability of hepatitis‐positive HCC remains unclear. Methods: In this study, DNA methylation‐driver genes (MDGs) were screened by a joint analysis of methylome and transcriptome data of 142 hepatitis‐positive HCC patients. Subsequently, a prognostic risk score and nomogram were constructed. Finally, correlation analyses between the risk score and signaling pathways and immunity were conducted by GSVA and CIBERSORT. Results: Through random forest screening and Cox progression analysis, 10 prognostic methylation‐driver genes (AC008271.1, C11orf53, CASP8, F2RL2, GBP5, LUCAT1, RP11‐114B7.6, RP11‐149I23.3, RP11‐383 J24.1, and SLC35G2) were screened out. As a result, a prognostic risk score signature was constructed. The independent value of the risk score for prognosis prediction were addressed in the TCGA‐HCC and the China‐HCC cohorts. Next, clinicopathological features were analyzed and HBV status and histological grade were screened to construct a nomogram together with the risk score. The prognostic efficiency of the nomogram was validated by the calibration curves and the concordance index (C index: 0.829, 95% confidence interval: 0.794–0.864), while its clinical application ability was confirmed by decision curve analysis (DCA). At last, the relationship between the risk score and signaling pathways, as well as the correlations between immune cells were elucidated preliminary. Conclusions: Taken together, our study explored a novel DNA methylation‐driver gene risk score signature and an efficient nomogram for long‐term survival prediction of hepatitis‐positive HCC patients. [ABSTRACT FROM AUTHOR]