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11.
  • Szatmari, Peter, et al. (författare)
  • Mapping autism risk loci using genetic linkage and chromosomal rearrangements.
  • 2007
  • Ingår i: Nature Genetics. - 1061-4036. ; 39:3, s. 319-328
  • Tidskriftsartikel (refereegranskat)abstract
    • Autism spectrum disorders (ASDs) are common, heritable neurodevelopmental conditions. The genetic architecture of ASDs is complex, requiring large samples to overcome heterogeneity. Here we broaden coverage and sample size relative to other studies of ASDs by using Affymetrix 10K SNP arrays and 1,168 families with at least two affected individuals, performing the largest linkage scan to date while also analyzing copy number variation in these families. Linkage and copy number variation analyses implicate chromosome 11p12-p13 and neurexins, respectively, among other candidate loci. Neurexins team with previously implicated neuroligins for glutamatergic synaptogenesis, highlighting glutamate-related genes as promising candidates for contributing to ASDs.
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12.
  • Chen, Gongbo, et al. (författare)
  • Mortality risk attributable to wildfire-related PM2·5 pollution : a global time series study in 749 locations
  • 2021
  • Ingår i: The Lancet Planetary Health. - 2542-5196. ; 5:9, s. e579-e587
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Many regions of the world are now facing more frequent and unprecedentedly large wildfires. However, the association between wildfire-related PM2·5 and mortality has not been well characterised. We aimed to comprehensively assess the association between short-term exposure to wildfire-related PM2·5 and mortality across various regions of the world.METHODS: For this time series study, data on daily counts of deaths for all causes, cardiovascular causes, and respiratory causes were collected from 749 cities in 43 countries and regions during 2000-16. Daily concentrations of wildfire-related PM2·5 were estimated using the three-dimensional chemical transport model GEOS-Chem at a 0·25° × 0·25° resolution. The association between wildfire-related PM2·5 exposure and mortality was examined using a quasi-Poisson time series model in each city considering both the current-day and lag effects, and the effect estimates were then pooled using a random-effects meta-analysis. Based on these pooled effect estimates, the population attributable fraction and relative risk (RR) of annual mortality due to acute wildfire-related PM2·5 exposure was calculated.FINDINGS: 65·6 million all-cause deaths, 15·1 million cardiovascular deaths, and 6·8 million respiratory deaths were included in our analyses. The pooled RRs of mortality associated with each 10 μg/m3 increase in the 3-day moving average (lag 0-2 days) of wildfire-related PM2·5 exposure were 1·019 (95% CI 1·016-1·022) for all-cause mortality, 1·017 (1·012-1·021) for cardiovascular mortality, and 1·019 (1·013-1·025) for respiratory mortality. Overall, 0·62% (95% CI 0·48-0·75) of all-cause deaths, 0·55% (0·43-0·67) of cardiovascular deaths, and 0·64% (0·50-0·78) of respiratory deaths were annually attributable to the acute impacts of wildfire-related PM2·5 exposure during the study period.INTERPRETATION: Short-term exposure to wildfire-related PM2·5 was associated with increased risk of mortality. Urgent action is needed to reduce health risks from the increasing wildfires.
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13.
  • Djoussé, Luc, et al. (författare)
  • Evidence for a modifier of onset age in Huntington disease linked to the HD gene in 4p16.
  • 2004
  • Ingår i: Neurogenetics. - 1364-6745 .- 1364-6753. ; 5:2, s. 109-14
  • Tidskriftsartikel (refereegranskat)abstract
    • Huntington disease (HD) is a neurodegenerative disorder caused by the abnormal expansion of CAG repeats in the HD gene on chromosome 4p16.3. A recent genome scan for genetic modifiers of age at onset of motor symptoms (AO) in HD suggests that one modifier may reside in the region close to the HD gene itself. We used data from 535 HD participants of the New England Huntington cohort and the HD MAPS cohort to assess whether AO was influenced by any of the three markers in the 4p16 region: MSX1 (Drosophila homeo box homologue 1, formerly known as homeo box 7, HOX7), Delta2642 (within the HD coding sequence), and BJ56 ( D4S127). Suggestive evidence for an association was seen between MSX1 alleles and AO, after adjustment for normal CAG repeat, expanded repeat, and their product term (model P value 0.079). Of the variance of AO that was not accounted for by HD and normal CAG repeats, 0.8% could be attributed to the MSX1 genotype. Individuals with MSX1 genotype 3/3 tended to have younger AO. No association was found between Delta2642 (P=0.44) and BJ56 (P=0.73) and AO. This study supports previous studies suggesting that there may be a significant genetic modifier for AO in HD in the 4p16 region. Furthermore, the modifier may be present on both HD and normal chromosomes bearing the 3 allele of the MSX1 marker.
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14.
  • Flexeder, Claudia, et al. (författare)
  • Second-hand smoke exposure in adulthood and lower respiratory health during 20 year follow up in the European Community Respiratory Health Survey
  • 2019
  • Ingår i: Respiratory Research. - : BioMed Central. - 1465-9921 .- 1465-993X. ; 20
  • Tidskriftsartikel (refereegranskat)abstract
    • Early life exposure to tobacco smoke has been extensively studied but the role of second-hand smoke (SHS) for new-onset respiratory symptoms and lung function decline in adulthood has not been widely investigated in longitudinal studies. Our aim is to investigate the associations of exposure to SHS in adults with respiratory symptoms, respiratory conditions and lung function over 20 years. We used information from 3011 adults from 26 centres in 12 countries who participated in the European Community Respiratory Health Surveys I-III and were never or former smokers at all three surveys. Associations of SHS exposure with respiratory health (asthma symptom score, asthma, chronic bronchitis, COPD) were analysed using generalised linear mixed-effects models adjusted for confounding factors (including sex, age, smoking status, socioeconomic status and allergic sensitisation). Linear mixed-effects models with additional adjustment for height were used to assess the relationships between SHS exposure and lung function levels and decline. Reported exposure to SHS decreased in all 26 study centres over time. The prevalence of SHS exposure was 38.7% at baseline (1990-1994) and 7.1% after the 20-year follow-up (2008-2011). On average 2.4% of the study participants were not exposed at the first, but were exposed at the third examination. An increase in SHS exposure over time was associated with doctor-diagnosed asthma (odds ratio (OR): 2.7; 95% confidence interval (95%-CI): 1.2-5.9), chronic bronchitis (OR: 4.8; 95%-CI: 1.6-15.0), asthma symptom score (count ratio (CR): 1.9; 95%-CI: 1.2-2.9) and dyspnoea (OR: 2.7; 95%-CI: 1.1-6.7) compared to never exposed to SHS. Associations between increase in SHS exposure and incidence of COPD (OR: 2.0; 95%-CI: 0.6-6.0) or lung function (beta: - 49 ml; 95%-CI: -132, 35 for FEV1 and beta: - 62 ml; 95%-CI: -165, 40 for FVC) were not apparent. Exposure to second-hand smoke may lead to respiratory symptoms, but this is not accompanied by lung function changes.
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15.
  • Kuiper, Ingrid Nordeide, et al. (författare)
  • Lung health in adulthood after childhood exposure to air pollution and greenness
  • 2018
  • Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • Background: Little is known on childhood exposure to air pollution and adult chronic respiratory outcomes.Aim: To investigate associations between air pollution and greenness in childhood and adult lung health.Methods: In selected centres of the RHINESSA study (age 18-52) we analysed the outcomes respiratory symptoms (≥3 symptoms), severe wheeze (wheeze last year with breathlessness, no cold) and late onset asthma (>10 years). We calculated mean annual exposures of PM2.5, PM10, NO2 (µg/m³) and greenness (Normalized Difference Vegetation Index, 100m buffer) from offspring's birth till age 18, categorised into mean exposure <10 years and 11-18 years. We performed multilevel logistic regression clustered by family, stratified by centre and adjusted for childhood passive smoke and parental asthma.Results: 12% had ≥3 respiratory symptoms, 7.7% severe wheeze, and 9.4% late onset asthma. Overall estimates: greenness was associated with less respiratory symptoms, PM2.5 and NO2 with more late onset asthma. Exposure <10 years: Greenness was associated with less wheeze in Tartu (OR 0.29, 95%CI 0.11-0.73). PM2.5 (OR 1.22, 95%CI 1.00-1.48) and NO2 (OR 1.06, 95%CI 1.01-1.11) were risk factors for late onset asthma in Bergen. PM10 was a risk factor for respiratory symptoms (OR 1.21, 95%CI 1.04-1.41) in Uppsala and late onset asthma (OR 1.23, 95%CI 1.02-1.45) in Bergen. Exposure 11-18 years: Greenness was protective for respiratory symptoms (OR 0.29, 95%CI 0.10-0.86) and wheeze (OR 0.39, 95%CI 0.19-0.80) in Tartu.Conclusions: Childhood exposure to greenness was associated with less respiratory symptoms, while air pollutants were associated with more respiratory symptoms (some centres) and late onset asthma.
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16.
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17.
  • Matheson, Melanie Claire, et al. (författare)
  • Early-life risk factors and incidence of rhinitis : Results from the European Community Respiratory Health Study - an international population-based cohort study
  • 2011
  • Ingår i: Journal of Allergy and Clinical Immunology. - 0091-6749 .- 1097-6825. ; 128:4, s. 816-823.e5
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Rhinitis is an increasingly common condition with a heavy health care burden, but relatively little is known about its risk factors. Objective: To examine the association between early-life factors and the development of rhinitis in the European Community Respiratory Health Study (ECRHS). Methods: In 1992-1994, community-based samples of 20-44-year-old people were recruited from 48 centers in 22 countries. On average, 8.9 years later, 28 centers reinvestigated their samples. Onset of rhinitis was reported by 8486 participants in interviewer-led questionnaires. Cox regression was used to assess independent predictors of rhinitis at ages <= 5, 6-10, 11-20, and >= 21 years. Results: The crude lifelong incidence of rhinitis was 7.00/1000/year (men) and 7.95/1000/year (women) (P = .002). Women developed less rhinitis in later childhood (hazard ratios [HR], 0.63; 95% CI, 0.47-0.85) and more rhinitis in adulthood (HR, 1.36; 95% CI, 1.11-1.66) than did men. In atopic subjects, siblings were associated with lower risk of rhinitis throughout life (pooled HR, 0.94; 95% CI, 0.91-0.98 per 1 sibling). Early contact with children in the family or day care was associated with less incidence of rhinitis, predominantly before age 5 years (HR, 0.84; 95% CI, 0.72-0.99). Early childhood pets or growing up on a farm was associated with less incidence of rhinitis in adolescence (HR, 0.50; 95% CI, 0.37-0.68). Combining these factors showed evidence of a dose-response relationship (trend P = .0001). Conclusions: Gender is a strong risk factor for rhinitis, with age patterns varying according to atopic status. Protective effects of early contact with children and animals were suggested for incident rhinitis, with risk patterns varying by age window and atopic status.
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18.
  • Moitra, Subhabrata, et al. (författare)
  • Effect of asthma on the development of obesity among adults : Results of the European Community Respiratory Health Survey (ECRHS)
  • 2018
  • Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • Introduction: Obesity has been associated with asthma, however the reverse relation has recently been observed among children.Objective: To investigate whether asthma contributes to obesity incidence in adults.Methods: The ECRHS is a cohort study with two follow-ups around, 10-years (ECRHS-II) and 20-years (ECRHS-III) after enrolment. Participants with obesity (BMI>30kg/m2) at baseline were excluded (n=957), leaving 8618 non-obese subjects who participated in at least one follow-up. Asthmatics were described if the subjects reported ever having asthma and had an asthma attack or woke up by an attack of shortness of breath in last 12 months or on current asthma medication. We evaluated the association between: (1) asthma at baseline (ECRHS-I) and obesity at ECRHS-II; and (2) newly reported asthma at ECRHS-II and obesity at ECRHS-III.Results: 10.2% of asthmatics at baseline developed obesity after 10 years compared to 7.7% of non-asthmatics (Age, sex & country-adjusted relative risk: 1.26; 95% confidence interval: 1.03-1.55). Further adjustment for BMI at baseline slightly reduced this risk (RR:1.2; 95%CI: 1.0-1.4). Obesity risk was highest for those developing asthma in adulthood (RR:1.37; 95%CI: 1.01-1.86) compared to those with childhood onset asthma (RR: 1.13; 95%CI: 0.83-1.53). Asthmatics who were non-atopic at baseline had a higher risk of developing obesity at 1st follow up (RR: 1.47; 95%CI: 1.15-1.86). Similar trend was observed in newly reported asthmatics in ECRHS-II and increased obesity risk at the final follow up ECRHS-III (RR: 1.22; 95%CI: 0.86-1.73).Conclusion: These results suggest that asthmatics are at a higher risk of developing obesity.
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19.
  • Peralta, Gabriela P., et al. (författare)
  • Body mass index and weight change are associated with adult lung function trajectories : the prospective ECRHS study
  • 2020
  • Ingår i: Thorax. - : BMJ Publishing Group Ltd. - 0040-6376 .- 1468-3296. ; 75:4, s. 313-320
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Previous studies have reported an association between weight increase and excess lung function decline in young adults followed for short periods. We aimed to estimate lung function trajectories during adulthood from 20-year weight change profiles using data from the population-based European Community Respiratory Health Survey (ECRHS).METHODS: We included 3673 participants recruited at age 20-44 years with repeated measurements of weight and lung function (forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1)) in three study waves (1991-93, 1999-2003, 2010-14) until they were 39-67 years of age. We classified subjects into weight change profiles according to baseline body mass index (BMI) categories and weight change over 20 years. We estimated trajectories of lung function over time as a function of weight change profiles using population-averaged generalised estimating equations.RESULTS: In individuals with normal BMI, overweight and obesity at baseline, moderate (0.25-1 kg/year) and high weight gain (>1 kg/year) during follow-up were associated with accelerated FVC and FEV1 declines. Compared with participants with baseline normal BMI and stable weight (±0.25 kg/year), obese individuals with high weight gain during follow-up had -1011 mL (95% CI -1.259 to -763) lower estimated FVC at 65 years despite similar estimated FVC levels at 25 years. Obese individuals at baseline who lost weight (<-0.25 kg/year) exhibited an attenuation of FVC and FEV1 declines. We found no association between weight change profiles and FEV1/FVC decline.CONCLUSION: Moderate and high weight gain over 20 years was associated with accelerated lung function decline, while weight loss was related to its attenuation. Control of weight gain is important for maintaining good lung function in adult life.
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20.
  • Peralta, Gabriela P., et al. (författare)
  • Body mass index trajectories during adult life and lung function decline
  • 2018
  • Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
  • Tidskriftsartikel (övrigt vetenskapligt)abstract
    • Body mass index (BMI) has been associated with lung function. Whether distinct BMI trajectories during adult life affect lung function differently is unknown. We assessed associations of BMI trajectories from 34 to 54 years with lung function decline over the same period of time in the ECRHS cohort.BMI trajectories were developed using Group-Based Trajectory Modeling on data collected at least twice between ECRHS I and ECRHS III (n=9327). Associations of these trajectories with lung function decline were assessed using mixed linear regression models (adjusted for sex, age, age2, height, smoking status and baseline lung function) in a subgroup (n=3534) with lung function data at ECRHS I and III. As sex-specific analyses showed similar findings, males and females were combined.Four parallel trajectories were identified: ‘normal’, ‘overweight’, ‘obese’ and ‘morbidly obese’ (Fig. 1). Those with higher BMI trajectories had greater decline of FEV1 and FVC than those with ‘normal BMI’ trajectory (Fig. 2).Overweight and obese trajectories of BMI during adult life were associated with greater lung function decline in the ECRHS cohort.
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