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Sökning: LAR1:uu > Karolinska Institutet > Pedersen Nancy L

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1.
  • Albrecht, Eva, et al. (författare)
  • Telomere length in circulating leukocytes is associated with lung function and disease
  • 2014
  • Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 43:4, s. 983-992
  • Tidskriftsartikel (refereegranskat)abstract
    • Several clinical studies suggest the involvement of premature ageing processes in chronic obstructive pulmonary disease (COPD). Using an epidemiological approach, we studied whether accelerated ageing indicated by telomere length, a marker of biological age, is associated with COPD and asthma, and whether intrinsic age-related processes contribute to the interindividual variability of lung function. Our meta-analysis of 14 studies included 934 COPD cases with 15 846 controls defined according to the Global Lungs Initiative (GLI) criteria (or 1189 COPD cases according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria), 2834 asthma cases with 28 195 controls, and spirometric parameters (forced expiratory volume in is (FEV1), forced vital capacity (PVC) and FEV1/FVC) of 12 595 individuals. Associations with telomere length were tested by linear regression, adjusting for age, sex and smoking status. We observed negative associations between telomere length and asthma (beta= -0.0452, p= 0.024) as well as COPD (beta= -0.0982, p=0.001), with associations being stronger and more significant when using GLI criteria than those of GOLD. In both diseases, effects were stronger in females than males. The investigation of spirometric indices showed positive associations between telomere length and FEV1 (p=1.07 x 10(-7)), FVC (p=2.07 x 10(-5)), and FEV1/FVC (p =5.27 x 10(-3)). The effect was somewhat weaker in apparently healthy subjects than in COPD or asthma patients. Our results provide indirect evidence for the hypothesis that cellular senescence may contribute to the pathogenesis of COPD and asthma, and that lung function may reflect biological ageing primarily due to intrinsic processes, which are likely to be aggravated in lung diseases.
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2.
  • Arpegard, Johannes, et al. (författare)
  • Cystatin C Predicts Incident Cardiovascular Disease in Twins
  • 2016
  • Ingår i: Journal of the American Heart Association. - 2047-9980 .- 2047-9980. ; 5:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Background - Cystatin C is associated with both renal function and atherosclerotic cardiovascular disease (ASCVD). We have previously shown a genetic correlation between cystatin C and prevalent ASCVD. The objective of this article is to study whether variation in cystatin C or creatinine predicts incident ASCVD when controlled for genetic factors.Methods and Results - The predictive value of cystatin C and creatinine for incident ASCVD was studied in 11 402 Swedish twins, free of CVD at baseline, in an adjusted Cox-regression model during a median follow-up of 71 months. Twin pairs discordant for incident stroke, myocardial infarction and ASCVD during follow-up were identified and within-pair comparisons regarding cystatin C and creatinine levels were performed. We also investigated whether contact frequency and degree of shared environment influences were associated with similarity in cystatin C levels. In univariate analysis, cystatin C predicted incident ASCVD hazard ratio 1.57, 95% CI 1.47-1.67. When adjusted for traditional Framingham risk factors as covariates, cystatin C remained a predictor of incident stroke hazard ratio 1.45, 95% CI (1.25-1.70), ASCVD hazard ratio 1.26, 95% CI (1.13-1.41), and myocardial infarction hazard ratio 1.16, 95% CI (1.01-1.33). In twins discordant for incident stroke, cystatin C at baseline was higher in the twin who experienced a stroke compared to the healthy co-twin (1.11 +/- 0.3 mg/L versus 1.06 +/- 0.3 mg/L), whereas creatinine was lower in the twin who developed CVD compared to their healthy co-twins (76.1 +/- 16.9 mu mol/L versus 79.4 +/- 20.3 mu mol/L).Conclusions - Variation in cystatin C relates to incident ASCVD and to stroke when adjusted for genetic confounding. In identical twins, cystatin C may be a sensitive marker of early hypertensive end-organ damage and small-vessel disease, whereas creatinine level may reflect nutritional status. The findings in disease-discordant monozygotic twins indicate that unique, possibly preventable, environmental factors are important.
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3.
  • Aulchenko, Yurii S, et al. (författare)
  • Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts
  • 2009
  • Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 41:1, s. 47-55
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent genome-wide association (GWA) studies of lipids have been conducted in samples ascertained for other phenotypes, particularly diabetes. Here we report the first GWA analysis of loci affecting total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides sampled randomly from 16 population-based cohorts and genotyped using mainly the Illumina HumanHap300-Duo platform. Our study included a total of 17,797-22,562 persons, aged 18-104 years and from geographic regions spanning from the Nordic countries to Southern Europe. We established 22 loci associated with serum lipid levels at a genome-wide significance level (P < 5 x 10(-8)), including 16 loci that were identified by previous GWA studies. The six newly identified loci in our cohort samples are ABCG5 (TC, P = 1.5 x 10(-11); LDL, P = 2.6 x 10(-10)), TMEM57 (TC, P = 5.4 x 10(-10)), CTCF-PRMT8 region (HDL, P = 8.3 x 10(-16)), DNAH11 (LDL, P = 6.1 x 10(-9)), FADS3-FADS2 (TC, P = 1.5 x 10(-10); LDL, P = 4.4 x 10(-13)) and MADD-FOLH1 region (HDL, P = 6 x 10(-11)). For three loci, effect sizes differed significantly by sex. Genetic risk scores based on lipid loci explain up to 4.8% of variation in lipids and were also associated with increased intima media thickness (P = 0.001) and coronary heart disease incidence (P = 0.04). The genetic risk score improves the screening of high-risk groups of dyslipidemia over classical risk factors.
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4.
  • Beijer, Kristina, et al. (författare)
  • Interaction between physical activity and television time on blood pressure level : cross-sectional data from 45000 individuals
  • 2018
  • Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 36:5, s. 1041-1050
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives:The aim was to investigate if there is an interaction between sitting time and leisure time physical activity on blood pressure and if there are age differences and sex differences in this respect.Methods:Linear regression analysis on cross-sectional data was performed in more than 45000 men and women from two Swedish cohort studies, EpiHealth (45-75 years) and LifeGene (18-45 years). Self-reported leisure time physical activity was given in five levels from low (level 1) to vigorous physical activity (level 5) and television time was used as a proxy measure of sitting time.Results:High physical activity was associated with lower DBP (P=0.001), but not SBP. Active middle-aged men had lower DBP (-1.1mmHg; 95% CI -1.7 to -0.4) compared with inactive participants. Prolonged television time was associated with higher SBP (P<0.001) and DBP (P=0.011) in both sexes and in most age groups. Watching 3h instead of 1h television per day was associated with higher SBP in middle-aged women (SBP: 1.1mmHg; 95% CI 0.7-1.4) and men (SBP: 1.2mmHg; 95% CI 0.8-1.6). Only in young men, a high physical activity (level 4 instead of level 1) could compensate for a prolonged television time (3h per day) in terms of DBP.Conclusion:Prolonged television time was associated with higher SBP and DBP in both sexes and at most ages, whereas an increased physical activity was mainly associated with a lower DBP. Only in young men, a high physical activity could compensate for prolonged television time regarding DBP.
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5.
  • Beijer, Kristina, et al. (författare)
  • Physical activity may compensate for prolonged TV time regarding pulse rate-a cross-sectional study
  • 2018
  • Ingår i: Upsala Journal of Medical Sciences. - : Uppsala Medical Society. - 0300-9734 .- 2000-1967. ; 123:4, s. 247-254
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Regular exercise reduces pulse rate, but it is less clear how prolonged sitting time affects pulse rate. Our hypothesis was that high physical activity could compensate for prolonged sitting time regarding the pulse rate.Methods: Regression analysis was performed on cross-sectional data including 47,457 men and women based on two Swedish cohort studies, EpiHealth (18–45 years) and LifeGene (45–75 years). Self-reported leisure time physical activity was given in five levels, from low (level 1) to vigorous (level 5), and television time was used as a proxy of sitting time.Results: A higher physical activity (level 4 compared to level 1) was associated with a lower pulse rate in middle-aged females (-2.7 beats per minute [bpm]; 95% CI -3.3 to -2.2) and males (-4.0 bpm; 95% CI -4.7 to -3.4). The relationship between physical activity and pulse rate was strongest in the young. A prolonged television time (3 h compared to 1 h per day) was associated with a slightly higher pulse rate in middle-aged females (+0.6 bpm; 95% CI +0.3 to +0.8) and males (+0.9 bpm; 95% CI +0.7 to +1.2). Among participants with a prolonged television time (3 h), those with a high physical activity (level 4) had a lower pulse rate compared to those with a low physical activity (level 1).Conclusions: A prolonged television time was associated with a high pulse rate, while high physical activity was associated with a low pulse rate. The results suggest that a high physical activity could compensate for a prolonged television time regarding pulse rate.
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6.
  • Blom, Elin Susanne, et al. (författare)
  • Does APOE explain the linkage of Alzheimer’s disease to chromosome 19q13?
  • 2008
  • Ingår i: American Journal of Medical Genetics Part B: Neuropsychiatric Genetics American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. - : Wiley. - 1552-485X. ; 147B:6, s. 778-83
  • Tidskriftsartikel (refereegranskat)abstract
    • We have studied the impact of the apolipoprotein E gene (APOE) on the chromosome 19 linkage peak from an analysis of sib-pairs affected by Alzheimer's disease. We genotyped 417 affected sib-pairs (ASPs) collected in Sweden and Norway (SWE), the UK and the USA for 10 microsatellite markers on chromosome 19. The highest Zlr (3.28, chromosome-wide P-value 0.036) from the multi-point linkage analysis was located approximately 1 Mb from APOE, at marker D19S178. The linkage to chromosome 19 was well explained by APOE in the whole sample as well as in the UK and USA subsamples, as identity by descent (IBD) increased with the number of epsilon 4 alleles in ASPs. There was a suggestion from the SWE subsample that linkage was higher than would be expected from APOE alone, although the test for this did not reach formal statistical significance. There was also a significant age at onset (aao) effect on linkage to chromosome 19q13 in the whole sample, which manifested itself as increased IBD sharing in relative pairs with lower mean aao. This effect was partially, although not completely, explained by APOE. The aao effect varied considerably between the different subsamples, with most of the effect coming from the UK sample. The other samples showed smaller effects in the same direction, but these were not significant.
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7.
  • Bogo, Renata, et al. (författare)
  • Prevalence, Incidence Proportion, and Heritability for Tinnitus : A Longitudinal Twin Study
  • 2017
  • Ingår i: Ear and Hearing. - 0196-0202 .- 1538-4667. ; 38:3, s. 292-300
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: The purpose of this longitudinal twin study was to explore the effect of tinnitus on hearing thresholds and threshold shifts over two decades and to investigate the genetic contribution to tinnitus in a male twin cohort (n = 1114 at baseline and 583 at follow-up). The hypothesis was that participants with faster hearing deterioration had a higher risk for developing tinnitus and there is an underlying role of genetic influences on tinnitus.DESIGN: Male mono- and dizygotic twin pairs, born between 1914 and 1958 were included. Mixed models were used for comparison of hearing threshold shifts, adjusted for age. A co-twin comparison was made within pairs discordant for tinnitus. The relative influence of genetic and environmental factors was estimated by genetic modeling.RESULTS: The overall prevalence of tinnitus was 13.5% at baseline (x age 50) and 34.4% at follow-up (x age 67). The overall incidence proportion was 27.8%. Participants who reported tinnitus at baseline or at both time points were older. At baseline, the hearing thresholds differed between tinnitus cases and controls at all frequencies. New tinnitus cases at follow-up had the greatest hearing threshold shift at the high-frequency area compared with the control group. Within pairs, the tinnitus twin had poorer hearing than his unaffected co-twin, more so for dizygotic than monozygotic twin pairs. The relative proportion of additive genetic factors was approximately 0.40 at both time points, and the influence of individual-specific environment was 0.56 to 0.61. The influence of genetic factors on tinnitus was largely independent of genetic factors for hearing thresholds.CONCLUSIONS: Our hypotheses were confirmed: The fastest hearing deterioration occurred for new tinnitus cases. A moderate genetic influence for tinnitus was confirmed.
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8.
  • Bogo, Renata, et al. (författare)
  • The Role of Genetic Factors for Hearing Deterioration Across 20 Years : A Twin Study
  • 2015
  • Ingår i: The journals of gerontology. Series A, Biological sciences and medical sciences. - : Oxford University Press (OUP). - 1079-5006 .- 1758-535X. ; 70:5, s. 647-653
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Hearing deterioration at advanced ages is associated with environmental exposures (eg, to noise and solvents) and genetic influences may also be important. Little is known about the role of genetic influences on hearing when evaluated longitudinally. We sought to investigate longitudinal hearing loss in a cohort of adult male twins to evaluate the importance of genetic and environmental factors for hearing deterioration over time. Methods. Hearing using conventional clinical audiometry was assessed in 583 male twins (128 monozygotic twin pairs and 111 dizygotic twin pairs) aged 34-79 at baseline and again two decades later. The hearing thresholds at two time points were compared at each frequency and in two different frequency regions. Genetic analyses were based on structural equation models. Bivariate Cholesky decomposition was used for longitudinal analysis. Results. The prevalence of hearing loss increased over time in better and worse ear. The hearing threshold shift was more pronounced in the high-frequency region, especially at 8000 Hz. Genetic influences were moderate (heritability: 53%-65%) for pure-tone averages at both lower and higher frequencies, and were of equal magnitude at baseline and follow-up. In contrast, environmental influences were of substantial importance (55%-88%) for rate of change of the hearing threshold over the 18-year period. Conclusions. Genetic factors are of considerable importance for level of hearing acuity, but environmental factors are more important for rate of change over an 18-year period.
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9.
  • Bruder, Carl E G, et al. (författare)
  • Phenotypically concordant and discordant monozygotic twins display different DNA copy-number-variation profiles
  • 2008
  • Ingår i: American Journal of Human Genetics. - : Elsevier BV. - 0002-9297 .- 1537-6605. ; 82:3, s. 763-71
  • Tidskriftsartikel (refereegranskat)abstract
    • The exploration of copy-number variation (CNV), notably of somatic cells, is an understudied aspect of genome biology. Any differences in the genetic makeup between twins derived from the same zygote represent an irrefutable example of somatic mosaicism. We studied 19 pairs of monozygotic twins with either concordant or discordant phenotype by using two platforms for genome-wide CNV analyses and showed that CNVs exist within pairs in both groups. These findings have an impact on our views of genotypic and phenotypic diversity in monozygotic twins and suggest that CNV analysis in phenotypically discordant monozygotic twins may provide a powerful tool for identifying disease-predisposition loci. Our results also imply that caution should be exercised when interpreting disease causality of de novo CNVs found in patients based on analysis of a single tissue in routine disease-related DNA diagnostics.
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10.
  • Cornelis, Marilyn C, et al. (författare)
  • Genome-wide association study of caffeine metabolites provides new insights to caffeine metabolism and dietary caffeine-consumption behavior
  • 2016
  • Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 25:24, s. 5472-5482
  • Tidskriftsartikel (refereegranskat)abstract
    • Caffeine is the most widely consumed psychoactive substance in the world and presents with wide interindividual variation in metabolism. This variation may modify potential adverse or beneficial effects of caffeine on health. We conducted a genome-wide association study (GWAS) of plasma caffeine, paraxanthine, theophylline, theobromine and paraxanthine/caffeine ratio among up to 9,876 individuals of European ancestry from six population-based studies. A single SNP at 6p23 (near CD83) and several SNPs at 7p21 (near AHR), 15q24 (near CYP1A2) and 19q13.2 (near CYP2A6) met GW-significance (P < 5 × 10(-8)) and were associated with one or more metabolites. Variants at 7p21 and 15q24 associated with higher plasma caffeine and lower plasma paraxanthine/caffeine (slow caffeine metabolism) were previously associated with lower coffee and caffeine consumption behavior in GWAS. Variants at 19q13.2 associated with higher plasma paraxanthine/caffeine (slow paraxanthine metabolism) were also associated with lower coffee consumption in the UK Biobank (n = 94 343, P < 1.0 × 10(-6)). Variants at 2p24 (in GCKR), 4q22 (in ABCG2) and 7q11.23 (near POR) that were previously associated with coffee consumption in GWAS were nominally associated with plasma caffeine or its metabolites. Taken together, we have identified genetic factors contributing to variation in caffeine metabolism and confirm an important modulating role of systemic caffeine levels in dietary caffeine consumption behavior. Moreover, candidate genes identified encode proteins with important clinical functions that extend beyond caffeine metabolism.
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