Prenatal exposures and exposomics of asthma

This review examines the causal investigation of preclinical development of childhood asthma using exposomic tools. We examine the current state of knowledge regarding early-life exposure to non-biogenic indoor air pollution and the developmental modulation of the immune system. We examine how metabolomics technologies could aid not only in the biomarker identification of a particular asthma phenotype, but also the mechanisms underlying the immunopathologic process. Within such a framework, we propose alternate components of exposomic investigation of asthma in which, the exposome represents a reiterative investigative process of targeted biomarker identification, validation through computational systems biology and physical sampling of environmental medi

Association between the Prevalence of Metabolic Syndrome and the Level of Coffee Consumption among Korean Women

As coffee consumption is increasing remarkably over the past decade, the health effects concerning the coffee drinking has gained a wide attention across the nation. However, there is not a true consensus regarding the effects of coffee on metabolic disease. Therefore, this study aims to examine the association between coffee intake and the risk of metabolic syndrome in Korean women.We used publicly accessible datasets collected through Korean National Health and Nutrition Examination Survey (KNHANES). Among 20,435 individuals from five consecutive years' worth of data from 2007 to 2011, only 15,691 subjects qualified for statistical analysis upon applying the exclusion criteria. We carried out the statistical analysis utilizing SPSS Statistics version 13.0 (IBM Corp., Armonk, NY.) and STATA statistical software release 13.0 (STATA Corp., College Station, TX).We found that the frequency of coffee intake inversely correlates with the prevalence of metabolic syndrome in women. Upon adjusting for life-style factors, socioeconomic status, and nutritional profile, the subjects from the highest coffee consumption quartile exhibited 40% lower odds of suffering from metabolic syndrome compared to those in the control (OR = 0.75; 95% CI = 0.67-0.84; P for trend < 0.001). Also, we observed that age- and BMI-adjusted HOMA-IR decreased as the coffee consumption increased (P for trend < 0.001).The findings of our study suggest that coffee consumption might be associated with reduction of metabolic syndrome in Korean women. To elucidate this cross-sectional association between coffee consumption and metabolic syndrome in women, cohort studies are warranted to confirm this relationship

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)