Background: Numerous studies have illustrated the association between Helicobacter pylori (H pylori) infection and acute coronary syndrome (ACS). However, the results are contradictory. Therefore, we conducted the meta-analysis to identify the association between H pylori and ACS. Methods: We performed a systematic search through electronic databases (Excerpta Medica Database, PubMed, Cochrane Library, and Web of Science). Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated with a random effect model. We also carried out the sensitivity analysis and publication bias. Results: Forty-four eligible studies involving 7522 cases and 8311 controls were included. The pooled result showed that H pylori infection was associated with an increase risk of ACS (OR = 2.03, 95% CI 1.66–2.47). In addition, similar results were obtained in subgroups of study quality, area, human development index, and H pylori detection method. The OR for developing countries was significantly higher than developed countries (OR = 2.58 vs OR = 1.69). Moreover, H pylori with cytotoxin-associated antigen A was also significantly associated with an increase risk of ACS (OR = 2.39, 95% CI 1.21–4.74). Conclusion: The meta-analysis suggested that H pylori infection was associated with an increased risk of ACS, especially in developing countries. H pylori is easily screened and can be treated with a wide range of drugs. Thus, more high-quality and well-designed studies are needed to confirm whether the treatment of H pylori is an effective way to reduce ACS risk.
Background:Many studies have reported that the IL-1β + 3954C/T polymorphism (rs1143634) is related to myocardial infarction (MI). To classify the association between IL-1β + 3954C/T and MI susceptibility, we performed a meta-analysis.Methods:We retrieved relevant literature from electronic databases (Embase, PubMed, Cochrane, and Web of Science). Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated with a fixed effect model or a random effect model. Sensitivity analysis and publication bias results are also presented.Results:Nine eligible studies (2299 controls and 2203 cases) were included. The pooled results showed a significant relationship between MI and IL-1β + 3954C/T in an allelic comparison (T vs C: OR = 1.13, 95% CI 1.02–1.25, I2 = 0%, PH = .448) and in a dominant model (TC + TT vs CC: OR = 1.15, 95% CI 1.02–1.30, I2 = 0%, PH = .880). Ethnic subgroup analysis showed similar results in Caucasian populations: an allelic comparison (T vs C: OR = 1.16, 95% CI 1.04–1.29, I2 = 0%, PH = .701), homozygote model (TT vs CC: OR = 1.36, 95% CI 1.04–1.79, I2 = 0%, PH = .673), and dominant model (TC + TT vs CC: OR = 1.17, 95% CI 1.02–1.33, I2 = 0%, PH = .851). In addition, similar effects remained in subgroups analyses of high-quality studies and PCR-RFLP (restriction fragment length polymorphism) data.Conclusion:Our meta-analysis proved that IL-1β + 3954C/T is associated with MI susceptibility, especially among Caucasian populations.
Background and aims The number of hypertensive population rises year by year recently, and their age becomes more youthful. For a long time, hypertension has long been regarded as a multi-factorial disease. In addition to smoking, genetics, diet and other factors, helicobacter pylori (H. pylori) had been regarded as a potential risk factor for hypertension in recent years. However, most studies had certain limitations and their results were inconsistent. Thus, it is necessary for us to assess the impact of H. pylori on hypertension through meta-analysis. Methods We searched all published relevant literature through multiple databases by July 23, 2021. Pooled results were calculated under the random effect model. Heterogeneity was evaluated by the Q statistic and the I2 statistic. The risk of bias was evaluated via ROBINS-I tool. Publication bias was evaluated by the Egger test and Begg funnel plot. Results 6 eligible studies involving 11317 hypertensive patients and 12765 controls were selected from 20767 retrieval records. Our research confirmed that H. pylori significantly increased the probability of suffering from hypertension in the random effect model (OR:1.34, 95% CI:1.10–1.63, P = 0.002, I2 = 74%). The same results were also found in both Asian population and developing country (OR:1.28, 95%CI:1.05–1.55, P = 0.003, I2 = 78.5%). Conclusions Our results confirmed that H. pylori was a vital risk factor for hypertension. H. pylori-infected people were 13.4% higher risk for hypertension than uninfected individuals. In addition, it will be a new method to prevent and treat hypertension by eradicating H. pylori. Trial registration The registration number for systematic review in PROSPERO CRD42021279677.
Objective To investigate the association between DNA methylation and the stable warfarin dose through genome-wide DNA methylation analysis and pyrosequencing assay. Method This study included 161 patients and genome-wide DNA methylation analysis was used to screen potential warfarin dose-associated CpGs through Illumina Infinium HumanMethylation 450 K BeadChip; then, the pyrosequencing assay was used to further validate the association between the stable warfarin dose and alterations in the methylation of the screened CpGs. GenomeStudio Software and R were used to analyze the differentially methylated CpGs. Results The methylation levels of CpGs surrounding the xenobiotic response element (XRE) within the CYP1A1 promoter, differed significantly between the different dose groups (P < 0.05), and these CpGs presented a positive correlation (r> 0, P < 0.05) with an increase in the stable dose of warfarin. At the VKORC1 promoter, two CpGs methylation levels were significantly different between the differential dose groups (P < 0.05), and one CpG (Chr16: 31106793) presented a significant negative correlation (r < 0, P < 0.05) among different dose (low, medium, and high) groups. Conclusion This is a novel report of the methylation levels of six CpGs surrounding the XRE within the CYP1A1 promoter and one differential CpG at the VKORC1 promoter associated with stable warfarin dosage; these methylation levels might be applied as molecular signatures for warfarin.
Hypertrophic cardiomyopathy (HCM), a genetically and clinically heterogeneous cardiomyopathy, is commonly caused by mutations in the MYBPC3 gene or other various sarcomeric genes. HCM patients carrying sarcomeric gene mutations may experience an asymptomatic period at early stage but still possess an escalating risk of developing adverse cardiac events including sudden cardiac death. It is crucial to determine the phenotypic and pathogenic effects of mutations in sarcomeric genes. In this study, a 65‐year‐old male was admitted with a history of chest pain, dyspnoea, and syncope and with a family history of HCM and sudden cardiac death. On admission, electrocardiogram indicated atrial fibrillation and myocardial infarction. Transthoracic echocardiography revealed left ventricular concentric hypertrophy and systolic dysfunction (48%), which were ascertained by cardiovascular magnetic resonance. With late gadolinium‐enhancement imaging, cardiovascular magnetic resonance found myocardial fibrosis on left ventricular wall. The exercise stress echocardiography test showed non‐obstructive myocardial changes. Whole‐exome sequencing analysis identified a MYBPC3 gene heterozygous nonsense variant (c.1522C>T) in the patient and one of his healthy grandnieces (18‐year‐old). The patient was diagnosed with non‐obstructive HCM, heart failure, atrial fibrillation, and so on. Medications, ICD implantation, and catheter ablation were chosen to maintain heart function. Our study provides the clinical evidence regarding the HCM pathogenicity of MYBPC3 c.1522C>T variant and highlights the significance of family genetic testing in the diagnosis and management of HCM.
Background We used bioinformatic analysis and quantitative reverse transcription polymerase chain reaction (RT-qPCR) assays to investigate the association between plasma microRNAs (miRNAs) and stable warfarin dosage in a Chinese Han population. Methods Bioinformatics analysis was used to screen out potential warfarin dose-associated miRNAs. Three plasma miRNAs were validated in 99 samples by RT-qPCR. Kruskal–Wallis test and multivariate logistic regression were used to compare differences in plasma miRNAs expression levels between three warfarin dosage groups. Results There were significant between-group differences among the three dose groups for hsa-miR-133b expression (p = 0.005), but we observed an “n-shaped” dose-dependent curve rather than a linear relationship. Expression levels of hsa-miR-24-3p (p = 0.475) and hsa-miR-1276 (p = 0.558) were not significantly different in the multivariate logistic regression. Conclusion miRNAs have received extensive attention as ideal biomarkers and possible therapeutic targets for various diseases. However, they are not yet widely used in precision medicine. Our results indicate that hsa-miR-133b may be a possible reference factor for the warfarin dosage algorithm. These findings emphasize the importance of a comprehensive evaluation of complex relationships in warfarin dose prediction models and provide new avenues for future pharmacogenomics studies.
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