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Sökning: WFRF:(Ek Åsa) > (2015-2019)

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1.
  • Ek, Weronica E, et al. (författare)
  • Genome-wide DNA methylation study identifies genes associated with the cardiovascular biomarker GDF-15
  • 2016
  • Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 25:4, s. 817-827
  • Tidskriftsartikel (refereegranskat)abstract
    • Growth-differentiation factor 15 (GDF-15) is expressed in low to moderate levels in most healthy tissues and increases in response to inflammation. GDF-15 is associated with cardiovascular dysfunction and over-expressed in the myocardium of patients with myocardial infarction (MI). However, little is known about the function of GDF-15 in cardiovascular disease, and the underlying regulatory network of GDF-15 is not known. To investigate a possible association between GDF-15 levels and DNA methylation, we performed a genome-wide DNA methylation study of white blood cells in a population-based study (N = 717). Significant loci where replicated in an independent cohort (N = 963). We also performed a gene ontology (GO) enrichment analysis. We identified and replicated 16 CpG-sites (false discovery rate [FDR] < 0.05), at 11 independent loci including MIR21. MIR21 encodes a microRNA (miR-21) that has previously been shown to be associated with the development of heart disease. Interestingly, GDF15 mRNA contains a binding site for miR-21. Four sites were also differentially methylated in blood from participants previously diagnosed with MI and 14 enriched GO terms (FDR < 0.05, enrichment > 2) were identified, including 'cardiac muscle cell differentiation'. This study shows that GDF-15 levels are associated with differences in DNA methylation in blood cells, and a subset of the loci are also differentially methylated in participants with MI. However, there might be interactions between GDF-15 levels and methylation in other tissues not addressed in this study. These results provide novel links between GDF-15 and cardiovascular disease.
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2.
  • Ek, Weronica E., et al. (författare)
  • Tea and coffee consumption in relation to DNA methylation in four European cohorts
  • 2017
  • Ingår i: Human Molecular Genetics. - : Oxford University Press. - 0964-6906 .- 1460-2083. ; 26:16, s. 3221-3231
  • Tidskriftsartikel (refereegranskat)abstract
    • Lifestyle factors, such as food choices and exposure to chemicals, can alter DNA methylation and lead to changes in gene activity. Two such exposures with pharmacologically active components are coffee and tea consumption. Both coffee and tea has been suggested to play an important role in modulating disease-risk in humans by suppressing tumour progression, decreasing inflammation and influencing estrogen metabolism. These mechanisms may be mediated by changes in DNA methylation.To investigate if DNA methylation in blood is associated with coffee and tea consumption we performed a genome-wide DNA methylation study for coffee and tea consumption in four European cohorts (N = 3,096). DNA methylation was measured from whole blood at 421,695 CpG sites distributed throughout the genome and analysed in men and women both separately and together in each cohort. Meta-analyses of the results and additional regional-level analyses were performed.After adjusting for multiple testing, the meta-analysis revealed that two individual CpG-sites, mapping to DNAJC16 and TTC17, were differentially methylated in relation to tea consumption in women. No individual sites were associated in men or in the sex-combined analysis for tea or coffee. The regional analysis revealed that 28 regions were differentially methylated in relation to tea consumption in women. These regions contained genes known to interact with estradiol metabolism and cancer. No significant regions were found in the sex-combined and male-only analysis for either tea or coffee consumption.
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3.
  • Ahsan, Muhammad, et al. (författare)
  • The relative contribution of DNA methylation and genetic variants on protein biomarkers for human diseases.
  • 2017
  • Ingår i: PLOS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 13:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Associations between epigenetic alterations and disease status have been identified for many diseases. However, there is no strong evidence that epigenetic alterations are directly causal for disease pathogenesis. In this study, we combined SNP and DNA methylation data with measurements of protein biomarkers for cancer, inflammation or cardiovascular disease, to investigate the relative contribution of genetic and epigenetic variation on biomarker levels. A total of 121 protein biomarkers were measured and analyzed in relation to DNA methylation at 470,000 genomic positions and to over 10 million SNPs. We performed epigenome-wide association study (EWAS) and genome-wide association study (GWAS) analyses, and integrated biomarker, DNA methylation and SNP data using between 698 and 1033 samples depending on data availability for the different analyses. We identified 124 and 45 loci (Bonferroni adjusted P < 0.05) with effect sizes up to 0.22 standard units' change per 1% change in DNA methylation levels and up to four standard units' change per copy of the effective allele in the EWAS and GWAS respectively. Most GWAS loci were cis-regulatory whereas most EWAS loci were located in trans. Eleven EWAS loci were associated with multiple biomarkers, including one in NLRC5 associated with CXCL11, CXCL9, IL-12, and IL-18 levels. All EWAS signals that overlapped with a GWAS locus were driven by underlying genetic variants and three EWAS signals were confounded by smoking. While some cis-regulatory SNPs for biomarkers appeared to have an effect also on DNA methylation levels, cis-regulatory SNPs for DNA methylation were not observed to affect biomarker levels. We present associations between protein biomarker and DNA methylation levels at numerous loci in the genome. The associations are likely to reflect the underlying pattern of genetic variants, specific environmental exposures, or represent secondary effects to the pathogenesis of disease.
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4.
  • Andersson, Linda, et al. (författare)
  • The Swedish flex-fuel failure
  • 2016
  • Ingår i: BEHAVE 2016.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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5.
  • Andersson, Linda, et al. (författare)
  • Why flex-fuel failed? : A household perspective
  • 2016
  • Ingår i: Meeting Sweden's current and future energy challenges, Luleå: Luleå tekniska universitet, 2016. - Luleå : Luleå tekniska universitet.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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7.
  • Aulin, Radhlinah, et al. (författare)
  • Underlying Causes for Risk Taking Behaviour Among Construction Workers
  • 2019
  • Ingår i: 10th Nordic Conference on Construction Economics and Organization. - 2516-2853. - 9781838670511 ; 2, s. 419-426
  • Konferensbidrag (refereegranskat)abstract
    • Purpose – This paper will examine the unsafe work practices that are plaguing the construction industry. Statistics show that four out of five of all workplace accidents are attributed to unsafe behaviour. Research studies have sought to understand worker self-protection. For example, it is difficult to make predictions of conditions that influenced worker’s behaviour to act unsafely or safely in a given work situation. It is evidentthere is a gap in the literature in this area of research, most notably failing to understand the underlying “why” factors. The aim of the study is to identify and examine the proximate set of contributing factors most likely to have an influence on workers’ decisions about participation in unsafe behaviour.Design/Methodology/Approach – To perform the study, questionnaires were adopted, and 225construction workers from 9 construction companies participated in the study.Findings – Results showed that both underlying organisational factors and individual factors could affect the risk aversion among construction workers. The paper also highlights measures to create a safe work environment to minimise unsafe behaviour among construction workers. Results from the study are important to help organisation to systematically plan for a good working environment.Research limitations – As the results were based only from the questionnaires, a deeper understanding behind the workers’ responses was not probed.Practical implications – Construction companies should work at several organisational levels at thesame time. It is necessary to include levels such as individual, group, workplace and management levels, thus taking a systemperspective on risk behaviour and safety.
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8.
  • Bal, Anjali S., et al. (författare)
  • You know you've got to, express yourself : A comparative study of self-expression through brand, women in six Asian nations
  • 2015
  • Ingår i: The Sustainable Global Marketplace. - Cham : Encyclopedia of Global Archaeology/Springer Verlag. - 9783319108728 - 9783319108735 ; , s. 165-
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Consumers express themselves in a multitude of ways; one expression mechanism is brand consumption. Self-expression can be an important driver of consumer preference and choice. Despite the importance of self-expression, additional research is needed as to how brands are used as a means of self-expression. Previous studies indicate that the importance of brands for self-expression can differ across cultures. This study explores how female consumers in six Asian nations differ in the extent to which they express themselves through the use of their favorite brands.
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9.
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10.
  • Ek, Amanda, 1981-, et al. (författare)
  • Physical inactivity and smoking after myocardial infarction as predictors for readmission and survival : results from the SWEDEHEART-registry.
  • 2019
  • Ingår i: Clinical Research in Cardiology. - : Springer. - 1861-0684 .- 1861-0692. ; 108:3, s. 324-332
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Physical activity (PA) and smoking cessation are included in the secondary prevention guidelines after myocardial infarction (MI), but they are still underutilised. This study aims to explore how PA level and smoking status (6-10 weeks post-MI) were associated with 1-year readmission and mortality during full follow-up time, and with the cumulative 5-year mortality.METHODS: A population-based cohort of all hospitals providing MI-care in Sweden (SWEDEHEART-registry) in 2004-2014. PA was expressed as the number of exercise sessions of ≥ 30 min in the last 7 days: 0-1 (low), 2-4 (medium) and 5-7 (high) sessions/week. Individuals were categorised as smokers, former smokers or never-smokers. The associations were analysed by unadjusted and adjusted logistic and Cox regressions.RESULTS: During follow-up (M = 3.58 years), a total of 1702 deaths occurred among 30 644 individuals (14.1 cases per 1000 person-years). For medium and high PA, the hazard ratios (HRs) for mortality were 0.39 and 0.36, respectively, compared with low PA. For never-smokers, the HR was 0.45 and former smokers 0.56 compared with smokers. Compared with low PA, the odds ratios (ORs) for readmission in medium PA were 0.65 and 0.59 for CVD and non-CVD causes, respectively. For high PA, the corresponding ORs were 0.63 and 0.55. The association remained in adjusted models. There were no associations between smoking status and readmission.CONCLUSIONS: The PA level and smoking status are strong predictors of mortality post-MI and the PA level also predicts readmission, highlighting the importance of adherence to the secondary prevention guidelines.
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