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1.
  • Class, Quetzal A., et al. (författare)
  • Outcome-dependent associations between short interpregnancy interval and offspring psychological and educational problems : a population-based quasi-experimental study
  • 2018
  • Ingår i: International Journal of Epidemiology. - Stockholm : Oxford University Press. - 0300-5771 .- 1464-3685. ; 47:4, s. 1159-1168
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Causal interpretation of associations between short interpregnancy interval (the duration from the preceeding birth to the conception of the next-born index child) and the offspring's psychological and educational problems may be influenced by a failure to account for unmeasured confounding.Methods: Using population-based Swedish data from 1973-2009, we estimated the association between interpregnancy interval and outcomes [autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), severe mental illness, suicide attempt, criminality, substance-use problem and failing grades] while controlling for measured covariates. We then used cousin comparisons, post-birth intervals (the interval between the second-and third-born siblings to predict second-born outcomes) and sibling comparisons to assess the influence of unmeasured confounding. We included an exploratory analysis of long interpregnancy interval.Results: Interpregnancy intervals of 0-5 and 6-11 months were associated with higher odds of outcomes in cohort analyses. Magnitudes of association were attenuated following adjustment for measured covariates. Associations were eliminated for ADHD, severe mental illness and failing grades, but maintained magnitude for ASD, suicide attempt, criminality and substance-use problem in cousin comparisons. Post-birth interpregnancy interval and sibling comparisons suggested some familial confounding. Associations did not persist across models of long interpregnancy interval.Conclusions: Attenuation of the association in cousin comparisons and comparable post-birth interval associations suggests that familial genetic or environmental confounding accounts for a majority of the association for ADHD, severe mental illness and failing grades. Modest associations appear independently of covariates for ASD, suicide attempt, criminality and substance-use problem. Post-birth analyses and sibling comparisons, however, show some confounding in these associations.
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2.
  • Långström, Niklas, et al. (författare)
  • Sexual offending runs in families : a 37-year nationwide study
  • 2015
  • Ingår i: International Journal of Epidemiology. - Stockholm : Karolinska Institutet, Dept of Medical Epidemiology and Biostatistics. - 0300-5771 .- 1464-3685.
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Sexual crime is an important public health concern. The possible causes of sexual aggression, however, remain uncertain. METHODS: We examined familial aggregation and the contribution of genetic and environmental factors to sexual crime by linking longitudinal, nationwide Swedish crime and multigenerational family registers. We included all men convicted of any sexual offence (N = 21,566), specifically rape of an adult (N = 6131) and child molestation (N = 4465), from 1973 to 2009. Sexual crime rates among fathers and brothers of sexual offenders were compared with corresponding rates in fathers and brothers of age-matched population control men without sexual crime convictions. We also modelled the relative influence of genetic and environmental factors to the liability of sexual offending. RESULTS: We found strong familial aggregation of sexual crime [odds ratio (OR) = 5.1, 95% confidence interval (CI) = 4.5-5.9] among full brothers of convicted sexual offenders. Familial aggregation was lower in father-son dyads (OR = 3.7, 95% CI = 3.2-4.4) among paternal half-brothers (OR = 2.1, 95% CI = 1.5-2.9) and maternal half-brothers (OR = 1.7, 95% CI = 1.2-2.4). Statistical modelling of the strength and patterns of familial aggregation suggested that genetic factors (40%) and non-shared environmental factors (58%) explained the liability to offend sexually more than shared environmental influences (2%). Further, genetic effects tended to be weaker for rape of an adult (19%) than for child molestation (46%). CONCLUSIONS: We report strong evidence of familial clustering of sexual offending, primarily accounted for by genes rather than shared environmental influences. Future research should possibly test the effectiveness of selective prevention efforts for male first-degree relatives of sexually aggressive individuals, and consider familial risk in sexual violence risk assessment.
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3.
  • Viktorin, Alexander, et al. (författare)
  • Selective serotonin re-uptake inhibitor use during pregnancy : association with offspring birth size and gestational age
  • 2016
  • Ingår i: International Journal of Epidemiology. - Oxford, United Kingdom : Oxford University Press. - 0300-5771 .- 1464-3685. ; 45:1, s. 170-177
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Depression around the time of pregnancy affects at least 1 in 8 women and treatment with selective serotonin re-uptake inhibitors (SSRIs) in pregnant women has been increasing, but research on adverse effects on the fetus have so far commonly used designs unable to account for confounding. We aimed to examine the effects of prenatal SSRI exposure on offspring size outcomes and gestational age, and disentangle whether associations observed were due to the medication or other factors.Methods: We used a Swedish population-based cohort of 392,029 children and national registers to estimate the associations between prenatal exposure to SSRIs and depression on the outcomes birthweight, birth length, birth head circumference, gestational age at birth and preterm birth. A sub-sample of 1007 children was analysed in a within-family design that accounts for unmeasured parental genetic and environmental confounders.Results: Crude analyses revealed associations between prenatal SSRI exposure, and offspring birth size and gestational age. However, in the within-family analyses, only the association between SSRI exposure and reduced gestational age (-2.3 days; 95% confidence interval -3.8 to -0.8) was observed.Conclusions: This study indicates that prenatal SSRI exposure may not be causally related to offspring birth size. Rather, our analyses suggest that the association could be caused by other underlying differences instead of the medication per se. A small reduction of gestational age was associated with SSRI exposure in the within-family analysis and could be due to either the exposure, or other factors changing between pregnancies.
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  • Accordini, S., et al. (författare)
  • A three-generation study on the association of tobacco smoking with asthma
  • 2018
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 47:4, s. 1106-1117
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Mothers' smoking during pregnancy increases asthma risk in their offspring. There is some evidence that grandmothers' smoking may have a similar effect, and biological plausibility that fathers' smoking during adolescence may influence offspring's health through transmittable epigenetic changes in sperm precursor cells. We evaluated the three-generation associations of tobacco smoking with asthma. Methods: Between 2010 and 2013, at the European Community Respiratory Health Survey III clinical interview, 2233 mothers and 1964 fathers from 26 centres reported whether their offspring (aged <= 51 years) had ever had asthma and whether it had coexisted with nasal allergies or not. Mothers and fathers also provided information on their parents' (grandparents) and their own asthma, education and smoking history. Multilevel mediation models within a multicentre three-generation framework were fitted separately within the maternal (4666 offspring) and paternal (4192 offspring) lines. Results: Fathers' smoking before they were 15 [relative risk ratio (RRR) = 1.43, 95% confidence interval (CI): 1.01-2.01] and mothers' smoking during pregnancy (RRR = 1.27, 95% CI: 1.01-1.59) were associated with asthma without nasal allergies in their offspring. Grandmothers' smoking during pregnancy was associated with asthma in their daughters [odds ratio (OR) = 1.55, 95% CI: 1.17-2.06] and with asthma with nasal allergies in their grandchildren within the maternal line (RRR = 1.25, 95% CI: 1.02-1.55). Conclusions: Fathers' smoking during early adolescence and grandmothers' and mothers' smoking during pregnancy may independently increase asthma risk in offspring. Thus, risk factors for asthma should be sought in both parents and before conception.
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7.
  • Adami, HO, et al. (författare)
  • Epidemiology, medicine and public health
  • 1999
  • Ingår i: International journal of epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 28:5, s. S1005-S1008
  • Tidskriftsartikel (refereegranskat)
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  • Agardh, E.E, et al. (författare)
  • Socio-economic position at three points in life in association with type 2 diabetes and impaired glucose tolerance in middle-aged Swedish men and women
  • 2007
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 36:1, s. 84-92
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundIt has been suggested that low socio-economic position(SEP) during childhood and adolescence predicts risk of adulttype 2 diabetes. We investigated the associations between type2 diabetes and childhood SEP (fathers’ occupational position),participants’ education and adult SEP (participants’occupational position). To determine possible independent associationsbetween early SEP (fathers’ occupational position andparticipants’ education) and disease, we adjusted foradult SEP and factors present in adult life associated withtype 2 diabetes. MethodsThis cross-sectional study comprised 3128 men and 4821women aged 35–56 years. All subjects have gone througha health examination and answered a questionnaire on lifestylefactors. At the health centre, an oral glucose tolerance testwas administered and identified 55 men and 52 women with previouslyundiagnosed type 2 diabetes. Relative risks (RRs) with 95% CIswere calculated in multiple logistic regression analyses. ResultsThe age-adjusted RRs of type 2 diabetes if having afather with middle occupational position were 2.3 [Confidenceinterval (CI:1.0–5.1) for women and, 2.0 (CI:0.7–5.6)for men]. Moreover, low education was associated with type 2diabetes in women, RR = 2.5 (CI:1.2–4.9). Low occupationalposition in adulthood was associated with type 2 diabetes inwomen, RR = 2.7 (CI:1.3–5.9) and men, RR = 2.9 (CI:1.5–5.7).The associations between early SEP and type 2 diabetes disappearedafter adjustment for adult SEP and factors associated with type2 diabetes. ConclusionThe association between type 2 diabetes and low SEPduring childhood and adolescence in middle-aged Swedish subjectsdisappeared after adjustment for adult SEP and adult risk factorsof diabetes.
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10.
  • Agardh, Emilie, et al. (författare)
  • Type 2 diabetes incidence and socio-economic position : a systematic review and meta-analysis
  • 2011
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 40:3, s. 804-818
  • Forskningsöversikt (refereegranskat)abstract
    • Background We conducted a systematic review and meta-analysis, the first to our knowledge, summarizing and quantifying the published evidence on associations between type 2 diabetes incidence and socio-economic position (SEP) (measured by educational level, occupation and income) worldwide and when sub-divided into high-, middle- and low-income countries. Methods Relevant case-control and cohort studies published between 1966 and January 2010 were searched in PubMed and EMBASE using the keywords: diabetes vs educational level, occupation or income. All identified citations were screened by one author, and two authors independently evaluated and extracted data from relevant publications. Risk estimates from individual studies were pooled using random-effects models quantifying the associations. Results Out of 5120 citations, 23 studies, including 41 measures of association, were found to be relevant. Compared with high educational level, occupation and income, low levels of these determinants were associated with an overall increased risk of type 2 diabetes; [relative risk (RR) = 1.41, 95% confidence interval (CI): 1.28-1.51], (RR = 1.31, 95% CI: 1.09-1.57) and (RR = 1.40, 95% CI: 1.04-1.88), respectively. The increased risks were independent of the income levels of countries, although based on limited data in middle- and low-income countries. Conclusions The risk of getting type 2 diabetes was associated with low SEP in high-, middle- and low-income countries and overall. The strength of the associations was consistent in high-income countries, whereas there is a strong need for further investigation in middle- and low-income countries.
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  • Airaksinen, Jaakko, et al. (författare)
  • The effect of smoking cessation on work disability risk : a longitudinal study analysing observational data as non-randomized nested pseudo-trials
  • 2019
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 48:2, s. 415-422
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundSmoking increases disability risk, but the extent to which smoking cessation reduces the risk of work disability is unclear. We used non-randomized nested pseudo-trials to estimate the benefits of smoking cessation for preventing work disability.MethodsWe analysed longitudinal data on smoking status and work disability [long-term sickness absence (≥90 days) or disability pension] from two independent prospective cohort studies—the Finnish Public Sector study (FPS) (n = 7393) and the Health and Social Support study (HeSSup) (n = 2701)—as ‘nested pseudo-trials’. All the 10 094 participants were smokers at Time 1 and free of long-term work disability at Time 2. We compared the work disability risk after Time 2 of the participants who smoked at Time 1 and Time 2 with that of those who quit smoking between these times.ResultsOf the participants in pseudo-trials, 2964 quit smoking between Times 1 and 2. During the mean follow-up of 4.8 to 8.6 years after Time 2, there were 2197 incident cases of work disability across the trials. Quitting smoking was associated with a reduced risk of any work disability [summary hazard ratio = 0.89, 95% confidence interval (CI) 0.81–0.98]. The hazard ratio for the association between quitting smoking and permanent disability pension (928 cases) was of similar magnitude, but less precisely estimated (0.91, 95% CI 0.81–1.02). Among the participants with high scores on the work disability risk score (top third), smoking cessation reduced the risk of disability pension by three percentage points. Among those with a low risk score (bottom third), smoking cessation reduced the risk by half a percentage point.ConclusionsOur results suggest an approximately 10% hazard reduction of work disability as a result of quitting smoking.
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  • Alcala, Karine, et al. (författare)
  • The relationship between blood pressure and risk of renal cell carcinoma
  • 2022
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 51:4, s. 1317-1327
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The relation between blood pressure and kidney cancer risk is well established but complex and different study designs have reported discrepant findings on the relative importance of diastolic blood pressure (DBP) and systolic blood pressure (SBP). In this study, we sought to describe the temporal relation between diastolic and SBP with renal cell carcinoma (RCC) risk in detail.METHODS: Our study involved two prospective cohorts: the European Prospective Investigation into Cancer and Nutrition study and UK Biobank, including >700 000 participants and 1692 incident RCC cases. Risk analyses were conducted using flexible parametric survival models for DBP and SBP both separately as well as with mutuality adjustment and then adjustment for extended risk factors. We also carried out univariable and multivariable Mendelian randomization (MR) analyses (DBP: ninstruments = 251, SBP: ninstruments = 213) to complement the analyses of measured DBP and SBP.RESULTS: In the univariable analysis, we observed clear positive associations with RCC risk for both diastolic and SBP when measured ≥5 years before diagnosis and suggestive evidence for a stronger risk association in the year leading up to diagnosis. In mutually adjusted analysis, the long-term risk association of DBP remained, with a hazard ratio (HR) per standard deviation increment 10 years before diagnosis (HR10y) of 1.20 (95% CI: 1.10-1.30), whereas the association of SBP was attenuated (HR10y: 1.00, 95% CI: 0.91-1.10). In the complementary multivariable MR analysis, we observed an odds ratio for a 1-SD increment (ORsd) of 1.34 (95% CI: 1.08-1.67) for genetically predicted DBP and 0.70 (95% CI: 0.56-0.88) for genetically predicted SBP.CONCLUSION: The results of this observational and MR study are consistent with an important role of DBP in RCC aetiology. The relation between SBP and RCC risk was less clear but does not appear to be independent of DBP.
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15.
  • Aleksandrova, Krasimira, et al. (författare)
  • Physical activity, mediating factors and risk of colon cancer : insights into adiposity and circulating biomarkers from the EPIC cohort
  • 2017
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 46:6, s. 1823-1835
  • Tidskriftsartikel (refereegranskat)abstract
    • There is convincing evidence that high physical activity lowers the risk of colon cancer; however, the underlying biological mechanisms remain largely unknown. We aimed to determine the extent to which body fatness and biomarkers of various biologically plausible pathways account for the association between physical activity and colon cancer. We conducted a nested case-control study in a cohort of 519 978 men and women aged 25 to 70 years followed from 1992 to 2003. A total of 713 incident colon cancer cases were matched, using risk-set sampling, to 713 controls on age, sex, study centre, fasting status and hormonal therapy use. The amount of total physical activity during the past year was expressed in metabolic equivalent of task [MET]-h/week. Anthropometric measurements and blood samples were collected at study baseline. High physical activity was associated with a lower risk of colon cancer: relative risk a parts per thousand91 MET-h/week vs < 91 MET-h/week = 0.75 [95% confidence interval (CI): 0.57 to 0.96]. In mediation analyses, this association was accounted for by waist circumference: proportion explained effect (PEE) = 17%; CI: 4% to 52%; and the biomarkers soluble leptin receptor (sOB-R): PEE = 15%; 95% CI: 1% to 50% and 5-hydroxyvitamin D (25[OH]D): PEE = 30%; 95% CI: 12% to 88%. In combination, these factors explained 45% (95% CI: 20% to 125%) of the association. Beyond waist circumference, sOB-R and 25[OH]D additionally explained 10% (95% CI: 1%; 56%) and 23% (95% CI: 6%; 111%) of the association, respectively. Promoting physical activity, particularly outdoors, and maintaining metabolic health and adequate vitamin D levels could represent a promising strategy for colon cancer prevention.
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  • Anantharaman, Devasena, et al. (författare)
  • Combined effects of smoking and HPV16 in oropharyngeal cancer
  • 2016
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 45:3, s. 752-761
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Although smoking and HPV infection are recognized as important risk factors for oropharyngeal cancer, how their joint exposure impacts on oropharyngeal cancer risk is unclear. Specifically, whether smoking confers any additional risk to HPV-positive oropharyngeal cancer is not understood.Methods: Using HPV serology as a marker of HPV-related cancer, we examined the interaction between smoking and HPV16 in 459 oropharyngeal (and 1445 oral cavity and laryngeal) cancer patients and 3024 control participants from two large European multicentre studies. Odds ratios and credible intervals [CrI], adjusted for potential confounders, were estimated using Bayesian logistic regression.Results: Both smoking [odds ratio (OR [CrI]: 6.82 [4.52, 10.29]) and HPV seropositivity (OR [CrI]: 235.69 [99.95, 555.74]) were independently associated with oropharyngeal cancer. The joint association of smoking and HPV seropositivity was consistent with that expected on the additive scale (synergy index [CrI]: 1.32 [0.51, 3.45]), suggesting they act as independent risk factors for oropharyngeal cancer.Conclusions: Smoking was consistently associated with increase in oropharyngeal cancer risk in models stratified by HPV16 seropositivity. In addition, we report that the prevalence of oropharyngeal cancer increases with smoking for both HPV16-positive and HPV16-negative persons. The impact of smoking on HPV16-positive oropharyngeal cancer highlights the continued need for smoking cessation programmes for primary prevention of head and neck cancer.
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  • Andersson, REB, et al. (författare)
  • Incidence of appendicitis during pregnancy
  • 2001
  • Ingår i: International journal of epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 30:6, s. 1281-1285
  • Tidskriftsartikel (refereegranskat)
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19.
  • Andersson, T, et al. (författare)
  • Community-based prevention of perinatal deaths : lessons from nineteenth-century Sweden.
  • 2000
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 29:3, s. 542-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Poor reproductive history, particularly previously high perinatal mortality, is associated with high perinatal mortality. Midwifery-assisted at home deliveries successfully reduced perinatal mortality.
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  • Aradhya, Siddartha, et al. (författare)
  • Maternal age and the risk of low birthweight and pre-term delivery : a pan-Nordic comparison
  • 2022
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 52:1, s. 156-164
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Advanced maternal age at birth is considered a risk factor for adverse birth outcomes. A recent study applying a sibling design has shown, however, that the association might be confounded by unobserved maternal characteristics.Methods: Using total population register data on all live singleton births during the period 1999–2012 in Denmark (N = 580 133; 90% population coverage), Norway (N = 540 890) and Sweden (N = 941 403) and from 2001–2014 in Finland (N = 568 026), we test whether advanced maternal age at birth independently increases the risk of low birthweight (LBW) (<2500 g) and pre-term birth (<37 weeks gestation). We estimated within-family models to reduce confounding by unobserved maternal characteristics shared by siblings using three model specifications: Model 0 examines the bivariate association; Model 1 adjusts for parity and sex; Model 2 for parity, sex and birth year.Results: The main results (Model 1) show an increased risk in LBW and pre-term delivery with increasing maternal ages. For example, compared with maternal ages of 26–27 years, maternal ages of 38–39 years display a 2.2, 0.9, 2.1 and 2.4 percentage point increase in the risk of LBW in Denmark, Finland, Norway and Sweden, respectively. The same patterns hold for pre-term delivery.Conclusions: Advanced maternal age is independently associated with higher risk of poor perinatal health outcomes even after adjusting for all observed and unobserved factors shared between siblings.
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  • Arden, R, et al. (författare)
  • Authors' Response to Kaufman and Muntaner
  • 2016
  • Ingår i: International journal of epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 45:2, s. 578-579
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Aschard, Hugues, et al. (författare)
  • Evidence for large-scale gene-by-smoking interaction effects on pulmonary function
  • 2017
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 46:3, s. 894-904
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Smoking is the strongest environmental risk factor for reduced pulmonary function. The genetic component of various pulmonary traits has also been demonstrated, and at least 26 loci have been reproducibly associated with either FEV1 (forced expiratory volume in 1 second) or FEV1/FVC (FEV1/forced vital capacity). Although the main effects of smoking and genetic loci are well established, the question of potential gene-by-smoking interaction effect remains unanswered. The aim of the present study was to assess, using a genetic risk score approach, whether the effect of these 26 loci on pulmonary function is influenced by smoking.METHODS: We evaluated the interaction between smoking exposure, considered as either ever vs never or pack-years, and a 26-single nucleotide polymorphisms (SNPs) genetic risk score in relation to FEV1 or FEV1/FVC in 50 047 participants of European ancestry from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) and SpiroMeta consortia.RESULTS: We identified an interaction (βint = -0.036, 95% confidence interval, -0.040 to -0.032, P = 0.00057) between an unweighted 26 SNP genetic risk score and smoking status (ever/never) on the FEV1/FVC ratio. In interpreting this interaction, we showed that the genetic risk of falling below the FEV 1: /FVC threshold used to diagnose chronic obstructive pulmonary disease is higher among ever smokers than among never smokers. A replication analysis in two independent datasets, although not statistically significant, showed a similar trend in the interaction effect.CONCLUSIONS: This study highlights the benefit of using genetic risk scores for identifying interactions missed when studying individual SNPs and shows, for the first time, that persons with the highest genetic risk for low FEV1/FVC may be more susceptible to the deleterious effects of smoking.
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25.
  • Ashfaq, Awais, 1990-, et al. (författare)
  • Data resource profile : Regional healthcare information platform in Halland, Sweden
  • 2020
  • Ingår i: International Journal of Epidemiology. - Oxford : Oxford University Press. - 0300-5771 .- 1464-3685. ; 49:3, s. 738-739f
  • Tidskriftsartikel (refereegranskat)abstract
    • Accurate and comprehensive healthcare data coupled with modern analytical tools can play a vital role in enabling care providers to make better-informed decisions, leading to effective and cost-efficient care delivery. This paper describes a novel strategic healthcare analysis and research platform that encapsulates 360-degree pseudo-anonymized data covering clinical, operational capacity and financial data on over 500,000 patients treated since 2009 across all care delivery units in the county of Halland, Sweden. The over-arching goal is to develop a comprehensive healthcare data infrastructure that captures complete care processes at individual, organizational and population levels. These longitudinal linked healthcare data are a valuable tool for research in a broad range of areas including health economy and process development using real world evidence.Key messagesStructured and standardized variables have been linked from different regional healthcare sources into a research information platform including all healthcare visits in the county of Halland in Sweden, from 2009 to date.Since 2015, the regional information platform integrates a cost component to each healthcare visit: thus being able to quantify patient level value, safety and cost efficiency across the continuum of care. © The Author(s) 2020; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association
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26.
  • Astell-Burt, Thomas, et al. (författare)
  • More green, less lonely? : A longitudinal cohort study
  • 2022
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 51:1, s. 99-110
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundUrban greening may reduce loneliness by offering opportunities for solace, social reconnection and supporting processes such as stress relief. We (i) assessed associations between residential green space and cumulative incidence of, and relief from, loneliness over 4 years; and (ii) explored contingencies by age, sex, disability and cohabitation status.MethodsMultilevel logistic regressions of change in loneliness status in 8049 city-dwellers between 2013 (baseline) and 2017 (follow-up) in the Household, Income and Labour Dynamics in Australia study. Associations with objectively measured discrete green-space buffers (e.g. parks) (<400, <800 and <1600 m) were adjusted for age, sex, disability, cohabitation status, children and socio-economic variables. Results were translated into absolute risk reductions in loneliness per 10% increase in urban greening.ResultsThe absolute risk of loneliness rose from 15.9% to 16.9% over the 4 years; however, a 10% increase in urban greening within 1.6 km was associated with lower cumulative incident loneliness [odds ratio (OR) = 0.927, 95% confidence interval (CI) = 0.862 to 0.996; absolute risk reduction = 0.66%]. Stronger association was observed for people living alone (OR = 0.828, 95% CI = 0.725 to 0.944). In comparison to people with <10% green space, the ORs for cumulative incident loneliness were 0.833 (95% CI = 0.695 to 0.997), 0.790 (95% CI = 0.624 to 1.000) and 0.736 (95% CI = 0.549 to 0.986) for 10–20%, 20–30% and >30% green space, respectively. Compared with the <10% green-space reference group with 13.78% incident loneliness over 4 years and conservatively assuming no impact on incident loneliness, associations translated into absolute risk reductions of 1.70%, 2.26% and 2.72% within populations with 10–20%, 20–30% and >30% green space, respectively. These associations were stronger again for people living alone, with 10–20% (OR = 0.608, 95% CI = 0.448 to 0.826), 20–30% (OR = 0.649, 95% CI = 0.436 to 0.966) and >30% (OR = 0.480, 95% CI = 0.278 to 0.829) green space within 1600 m. No age, sex or disability-related contingencies, associations with green space within 400 or 800 m or relief from loneliness reported at baseline were observed.ConclusionsA lower cumulative incidence of loneliness was observed among people with more green space within 1600 m of home, especially for people living alone. Potential biopsychosocial mechanisms warrant investigation.
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  • Battram, Thomas, et al. (författare)
  • Appraising the causal relevance of DNA methylation for risk of lung cancer
  • 2019
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 48:5, s. 1493-1504
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: DNA methylation changes in peripheral blood have recently been identified in relation to lung cancer risk. Some of these changes have been suggested to mediate part of the effect of smoking on lung cancer. However, limitations with conventional mediation analyses mean that the causal nature of these methylation changes has yet to be fully elucidated.Methods: We first performed a meta-analysis of four epigenome-wide association studies (EWAS) of lung cancer (918 cases, 918 controls). Next, we conducted a two-sample Mendelian randomization analysis, using genetic instruments for methylation at CpG sites identified in the EWAS meta-analysis, and 29 863 cases and 55 586 controls from the TRICL-ILCCO lung cancer consortium, to appraise the possible causal role of methylation at these sites on lung cancer.Results: Sixteen CpG sites were identified from the EWAS meta-analysis [false discovery rate (FDR) < 0.05], for 14 of which we could identify genetic instruments. Mendelian randomization provided little evidence that DNA methylation in peripheral blood at the 14 CpG sites plays a causal role in lung cancer development (FDR > 0.05), including for cg05575921-AHRR where methylation is strongly associated with both smoke exposure and lung cancer risk.Conclusions: The results contrast with previous observational and mediation analysis, which have made strong claims regarding the causal role of DNA methylation. Thus, previous suggestions of a mediating role of methylation at sites identified in peripheral blood, such as cg05575921-AHRR, could be unfounded. However, this study does not preclude the possibility that differential DNA methylation at other sites is causally involved in lung cancer development, especially within lung tissue.
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31.
  • Beckley, Amber L., et al. (författare)
  • Association of height and violent criminality : results from a Swedish total population study
  • 2014
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 43:3, s. 835-842
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Violent criminality is at least moderately heritable, but the mechanisms behind this remain largely unexplained. Height, a highly heritable trait, may be involved but no study has estimated the effect of height on crime while simultaneously accounting for important demographic, biological and other heritable confounders. Methods: We linked nationwide, longitudinal registers for 760 000 men who underwent mandatory military conscription from 1980 through 1992 in Sweden, to assess the association between height and being convicted of a violent crime. We used Cox proportional hazard modelling and controlled for three types of potential confounders: physical characteristics, childhood demographics and general cognitive ability (intelligence). Results: In unadjusted analyses, height had a moderate negative relationship to violent crime; the shortest of men were twice as likely to be convicted of a violent crime as the tallest. However, when simultaneously controlling for all measured confounders, height was weakly and positively related to violent crime. Intelligence had the individually strongest mitigating effect on the height-crime relationship. Conclusions: Although shorter stature was associated with increased risk of violent offending, our analyses strongly suggested that this relationship was explained by intelligence and other confounding factors. Hence, it is unlikely that height, a highly heritable physical characteristic, accounts for much of the unexplained heritability of violent criminality.
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32.
  • Bengtsson, Tommy, et al. (författare)
  • Airborne infectious diseases during infancy and mortality in later life in southern Sweden, 1766-1894.
  • 2003
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 32:2, s. 286-294
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The importance of early life conditions and current conditions for mortality in later life was assessed using historical data from four rural parishes in southern Sweden. Both demographic and economic data are valid. Methods: Longitudinal demographic and socioeconomic data for individuals and household socioeconomic data from parish registers were combined with local area data on food costs and disease load using a Cox regression framework to analyse the 55–80 year age group mortality (number of deaths = 1398). Results: In a previous paper, the disease load experienced during the birth year, measured as the infant mortality rate, was strongly associated with old-age mortality, particularly the outcome of airborne infectious diseases. In the present paper, this impact persisted after controlling for variations in food prices during pregnancy and the birth year, and the disease load on mothers during pregnancy. The impact on mortality in later life stems from both the short-term cycles and the long-term decline in infant mortality. An asymmetrical effect and strong threshold effects were found for the cycles. Years with very high infant mortality, dominated by smallpox and whooping cough, had a strong impact, while modest changes had almost no impact at all. The effects of the disease load during the year of birth were particularly strong for children born during the winter and summer. Children severely exposed to airborne infectious diseases during their birth year had a much higher risk of dying of airborne infectious diseases in their old age. Conclusions: This study suggests that exposure to airborne infectious diseases during the first year of life increases mortality at ages 55–80.
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33.
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34.
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35.
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36.
  • Bjerg, L., et al. (författare)
  • Duration of diabetes-related complications and mortality in type 1 diabetes: a national cohort study
  • 2021
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 50:4, s. 1250-1259
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: People with type 1 diabetes often live for many years with different combinations of diabetes-related complications. We aimed to quantify how complication duration and total complication burden affect mortality, using data from national registers. Methods: This study included 33 396 individuals with type 1 diabetes, registered in the Swedish National Diabetes Register at any time between 2001 and 2012. Each individual was followed and classified according to their time-updated diabetes-related complication status. The main outcomes were all-cause mortality, cardiovascular (CV) mortality and non-CV mortality. Poisson models were used to estimate the rate of these outcomes as a function of the time-updated complication duration. Results: Overall, 1748 of the 33 396 individuals died during 198 872 person-years of follow-up. Overall, the time-updated all-cause mortality rate ratio (MRR) was 2.25 [95% confidence interval (CI): 1.99-2.54] for patients with diabetic kidney disease, 0.98 (0.82-1.18) for patients with retinopathy and 4.00 (3.56-4.50) for patients with cardiovascular disease relative to individuals without complications. The excess rate was highest in the first period after a diagnosis of CVD, with an 8-fold higher mortality rate, and stabilized after some 5 years. After diagnosis of diabetic kidney disease, we observed an increase in all-cause mortality with an MRR of around 2 compared with individuals without diabetic kidney disease, which stabilized after few years. Conclusions: In this cohort we show that duration of diabetes-related complications is an important determinant of mortality in type 1 diabetes, for example the MRR associated with CVD is highest in the first period after diagnosis of CVD. A stronger focus on time-updated information and thorough consideration of complication duration may improve risk stratification in routine clinical practice.
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37.
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38.
  • Bjørge, Tone, et al. (författare)
  • BMI and weight changes and risk of obesity-related cancers : a pooled European cohort study
  • 2019
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 48:6, s. 1872-1885
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Obesity is an established risk factor for several cancers. Adult weight gain has been associated with increased cancer risk, but studies on timing and duration of adult weight gain are relatively scarce. We examined the impact of BMI (body mass index) and weight changes over time, as well as the timing and duration of excess weight, on obesity- and non-obesity-related cancers. METHODS: We pooled health data from six European cohorts and included 221 274 individuals with two or more height and weight measurements during 1972-2014. Several BMI and weight measures were constructed. Cancer cases were identified through linkage with national cancer registries. Hazard ratios (HRs) of cancer with 95% confidence intervals (CIs) were derived from time-dependent Cox-regression models. RESULTS: During follow-up, 27 881 cancer cases were diagnosed; 9761 were obesity-related. The HR of all obesity-related cancers increased with increasing BMI at first and last measurement, maximum BMI and longer duration of overweight (men only) and obesity. Participants who were overweight before age 40 years had an HR of obesity-related cancers of 1.16 (95% CI 1.02, 1.32) and 1.15 (95% CI 1.04, 1.27) in men and women, respectively, compared with those who were not overweight. The risk increase was particularly high for endometrial (70%), male renal-cell (58%) and male colon cancer (29%). No positive associations were seen for cancers not regarded as obesity-related. CONCLUSIONS: Adult weight gain was associated with increased risk of several major cancers. The degree, timing and duration of overweight and obesity also seemed to be important. Preventing weight gain may reduce the cancer risk.
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39.
  • Bjørge, Tone, et al. (författare)
  • Metabolic risk factors and ovarian cancer in the metabolic syndrome and cancer project
  • 2011
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 40:6, s. 1667-1677
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: No studies have so far evaluated the impact of the metabolic syndrome (MetS) as an entity on ovarian cancer risk. The authors aimed to examine the association between factors in the MetS, individually and combined, and risk of ovarian cancer incidence and mortality. METHODS: Altogether, 290 000 women from Austria, Norway and Sweden were enrolled during 1974-2005, with measurements taken of height, weight, blood pressure and levels of glucose, cholesterol and triglycerides. Relative risks (RRs) of ovarian cancer were estimated using Cox regression for each MetS factor in quintiles and for standardized levels (z-scores), and for a composite z-score for the MetS. RRs were corrected for random error in measurements. RESULTS: During follow-up, 644 epithelial ovarian cancers and 388 deaths from ovarian cancer were identified. There was no overall association between MetS and ovarian cancer risk. Increasing levels of cholesterol [RR 1.52, 95% confidence interval (95% CI) 1.01-2.29, per 1-U increment of z-score] and blood pressure (RR 1.79, 95% CI 1.12-2.86) conferred, however, increased risks of mucinous and endometrioid tumours, respectively. In women below the age of 50 years, there was increased risk of ovarian cancer mortality for MetS (RR 1.52, 95% CI 1.00-2.30). Increasing levels of BMI (RR 1.17, 95% CI 1.01-1.37) conferred increased risk of ovarian cancer mortality in women above the age of 50 years. CONCLUSION: There was no overall association between MetS and ovarian cancer risk. However, increasing levels of cholesterol and blood pressure increased the risks of mucinous and endometrioid tumours, respectively. Increasing levels of BMI conferred an increased risk of ovarian cancer mortality in women above the age of 50 years.
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40.
  • Björkenstam, Emma, et al. (författare)
  • Juvenile delinquency, social background and suicide-a Swedish national cohort study of 992 881 young adults
  • 2011
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 40:6, s. 1585-1592
  • Tidskriftsartikel (refereegranskat)abstract
    • Background As the suicide rates in young adults do not show a clear decline, it is important to elucidate possible risk factors. Juvenile delinquency has been pointed out as a possible risk behaviour. Methods This register-based cohort study comprises the birth cohorts between 1972 and 1981 in Sweden. We followed 992 881 individuals from the age of 20 years until 31 December 2006, generating 10 210 566 person-years and 1482 suicides. Juvenile delinquency was defined as being convicted of a crime between the ages of 15 and 19 years. Estimates of risk of suicide were calculated as incidence rate ratio (IRR) with 95% confidence intervals (CIs) using Poisson regression analysis with adjustment for potential confounding by their own and their parents' mental illness or substance abuse, parental education, single parenthood, social assistance, adoption and foster care. Results Among females, 5.9%, and among males, 17.9%, had at least one conviction between the ages 15 and 19 years. In the fully adjusted model, females with one conviction had a suicide risk of 1.7 times higher (95% CI 1.2-2.4), the corresponding IRR for men was 2.0 (95% CI 1.7-2.4) and 5.7 (95% CI 2.5-13.1) and 6.6 (95% CI 5.2-8.3), for women and men with five or more convictions. The effect of severe delinquency on suicide was independent of parental educational level. Conclusions This study supports the hypothesis that individuals with delinquent behaviour in late adolescence have an increased risk of suicide as young adults. Regardless of causality issues, repeated juvenile offenders should be regarded by professionals in health, social and correctional services who come into contact with this group as a high-risk group for suicide.
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41.
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42.
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43.
  • Boudigaard, S. H., et al. (författare)
  • Occupational exposure to respirable crystalline silica and risk of autoimmune rheumatic diseases: a nationwide cohort study
  • 2021
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 50:4, s. 1213-1226
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Exposure to respirable crystalline silica is suggested to increase the risk of autoimmune rheumatic diseases. We examined the association between respirable crystalline silica exposure and systemic sclerosis, rheumatoid arthritis, systemic lupus erythematosus and small vessel vasculitis. Methods: In a cohort study of the total Danish working population, we included 1 541 505 male and 1 470 769 female workers followed since entering the labour market 1979-2015. Each worker was annually assigned a level of respirable crystalline silica exposure estimated with a quantitative job exposure matrix. We identified cases of autoimmune rheumatic diseases in a national patient register and examined sex-specific exposure-response relations by cumulative exposure and other exposure metrics. Results: We identified 4673 male and 12 268 female cases. Adjusted for age and calendar year, men exposed to high levels of respirable crystalline silica compared with non-exposed showed increased incidence rate ratio (IRR) for the four diseases combined of 1.53 [95% confidence interval (CI): 1.39-1.69], for systemic sclerosis of 1.62 (1.08-2.44) and rheumatoid arthritis of 1.57 (1.41-1.75). The overall risk increased with increasing cumulative exposure attained since entering the workforce [IRR: 1.07 (1.05-1.09) per 50 mu g/m(3)-years]. Female workers were less exposed to respirable crystalline silica, but showed comparable risk patterns with overall increased risk with increasing cumulative exposure [IRR: 1.04 (0.99-1.10) per 50 mu g/m(3)-years]. Conclusions: This study shows an exposure-dependent association between occupational exposure to respirable crystalline silica and autoimmune rheumatic diseases and thus suggests causal effects, most evident for systemic sclerosis and rheumatoid arthritis.
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44.
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45.
  • Bouras, Emmanouil, et al. (författare)
  • Identification of potential mediators of the relationship between body mass index and colorectal cancer : a Mendelian randomization analysis
  • 2024
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 53:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Colorectal cancer (CRC) is the third-most-common cancer worldwide and its rates are increasing. Elevated body mass index (BMI) is an established risk factor for CRC, although the molecular mechanisms behind this association remain unclear. Using the Mendelian randomization (MR) framework, we aimed to investigate the mediating effects of putative biomarkers and other CRC risk factors in the association between BMI and CRC.Methods: We selected as mediators biomarkers of established cancer-related mechanisms and other CRC risk factors for which a plausible association with obesity exists, such as inflammatory biomarkers, glucose homeostasis traits, lipids, adipokines, insulin-like growth factor 1 (IGF1), sex hormones, 25-hydroxy-vitamin D, smoking, physical activity (PA) and alcohol consumption. We used inverse-variance weighted MR in the main univariable analyses and performed sensitivity analyses (weighted-median, MR–Egger, Contamination Mixture). We used multivariable MR for the mediation analyses.Results: Genetically predicted BMI was positively associated with CRC risk [odds ratio per SD (5 kg/m2) ¼ 1.17, 95% CI: 1.08–1.24, P-value ¼ 1.4 × 10−5] and robustly associated with nearly all potential mediators. Genetically predicted IGF1, fasting insulin, low-density lipoprotein cholesterol, smoking, PA and alcohol were associated with CRC risk. Evidence for attenuation was found for IGF1 [explained 7% (95% CI: 2–13%) of the association], smoking (31%, 4–57%) and PA (7%, 2–11%). There was little evidence for pleiotropy, although smoking was bidirectionally associated with BMI and instruments were weak for PA.Conclusions: The effect of BMI on CRC risk is possibly partly mediated through plasma IGF1, whereas the attenuation of the BMI–CRC association by smoking and PA may reflect confounding and shared underlying mechanisms rather than mediation.
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46.
  • Brew, Bronwyn K., et al. (författare)
  • Longitudinal depression or anxiety in mothers and offspring asthma : a Swedish population-based study
  • 2018
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 47:1, s. 166-174
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Previous research has found that maternal stress during pregnancy increases the risk of offspring asthma. However, whether this association is consistent with a causal interpretation has never been tested. The objective is to determine whether there is a critical exposure period for maternal depression or anxiety on offspring asthma or whether cumulative exposure is most important, and to investigate evidence of confounding.Methods: The study population included all children born in Sweden from July 2006 to December 2009 (n = 360 526). Information about childhood asthma, maternal depression or anxiety (diagnosis or medication) and covariates was obtained from the Swedish national health registers. The associations between exposure periods (pre-conception, pregnancy, postnatal or current) and childhood asthma were estimated using structured life course approach hypothesis testing. Paternal and cousin analyses were used to test for evidence of confounding from shared genes and environment.Results: For childhood asthma, cumulative exposure best described the effect of exposure to maternal depression or anxiety up to a maximum of any two exposure periods [adjusted odds ratio 1.44, 95% confidence interval (CI) 1.38, 1.52]. The hypotheses of a critical period were not supported. The paternal and cousin analyses indicated minimal influence from familial confounding.Conclusions: These findings support an association between cumulative exposure to maternal depression or anxiety and asthma development in offspring. This association is unique for maternal depression or anxiety and not due to familial confounding. The clinical implication is that effective psychological management of women with chronic distress may reduce offspring asthma risk.
  •  
47.
  • Brew, BK, et al. (författare)
  • Modelling paternal exposure as a negative control
  • 2020
  • Ingår i: International journal of epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 49:3, s. 1053-1054
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
  •  
48.
  • Brännström, Inger, 1945-, et al. (författare)
  • Changing social patterns of risk factors for cardiovascular disease in a Swedish community intervention programme
  • 1993
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press. - 0300-5771 .- 1464-3685. ; 22:6, s. 1026-1037
  • Tidskriftsartikel (refereegranskat)abstract
    • Since 1985 a small-scale community-based cardiovascular disease (CVD) preventive programme has been in operation in an inland municipality, Norsjö, in Northern Sweden. The aim of this study was to assess the development of the relationship between social position and CVD risk factors in repeated cross-sectional surveys (1985-1990) among all men and women aged 30, 40, 50 and 60 years in the study area, using an age-stratified random sample from the Northern Sweden MONICA Study of 1986 and 1990 as reference population. These multiple cross-sectional surveys comprised a self-administered questionnaire and a health examination. Of the study population 95% (n = 1499) and 80% of those in the reference area (n = 3208) participated. Subjects were classified with regard to demographic, structural and social characteristics in relation to CVD risk factors and self-reported health status. Time trends in classical risk factor occurrence were assessed in terms of age- and sex- adjusted odds ratios using Mantel-Haenszel procedures. When simultaneously adjusting for several potential confounders we used a logistic regression analysis. Initially, more than half of the study population, both males and females, had and elevated (> or = 6.5 mmol/l) serum cholesterol level. After adjustments had been made for age and social factors it was found that the relative risk of hypercholesterolaemia dropped substantially and significantly among both sexes during the 6 years of CVD intervention in the study area. However, the probability of being a smoker was significantly reduced only in highly educated groups. Among other risk factors no single statistically significant change over time could be found. In the reference area there were no changes over time for the selected CVD risk factors. People in the study area had a less favourable perception of their health than those in the reference area. Social differences were found when perceived good health was measured, especially in variables indicating emotional and social support. When sex, age and social factors had been accounted for there was not clear change over the years in perceived good health.
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