Institution
Stockholm County Council
Government•Stockholm, Sweden•
About: Stockholm County Council is a government organization based out in Stockholm, Sweden. It is known for research contribution in the topics: Population & Poison control. The organization has 1410 authors who have published 2429 publications receiving 78936 citations.
Topics: Population, Poison control, Health care, Autism, Cohort study
Papers published on a yearly basis
Papers
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TL;DR: It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification to enhance the understanding of role of environmental factors in the etiology of ASD.
Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental condition of heterogeneous etiology. While it is widely recognized that genetic and environmental factors and their interactions contribute to autism phenotypes, their precise causal mechanisms remain poorly understood. This article reviews our current understanding of environmental risk factors of ASD and their presumed adverse physiological mechanisms. It comprehensively maps the significance of parental age, teratogenic compounds, perinatal risks, medication, smoking and alcohol use, nutrition, vaccination, toxic exposures, as well as the role of extreme psychosocial factors. Further, we consider the role of potential protective factors such as folate and fatty acid intake. Evidence indicates an increased offspring vulnerability to ASD through advanced maternal and paternal age, valproate intake, toxic chemical exposure, maternal diabetes, enhanced steroidogenic activity, immune activation, and possibly altered zinc–copper cycles and treatment with selective serotonin reuptake inhibitors. Epidemiological studies demonstrate no evidence for vaccination posing an autism risk. It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification. Our understanding of autism etiology could be advanced by research aimed at disentangling the causal and non-causal environmental effects, both founding and moderating, and gene–environment interplay using twin studies, longitudinal and experimental designs. The specificity of many environmental risks for ASD remains unknown and control of multiple confounders has been limited. Further understanding of the critical windows of neurodevelopmental vulnerability and investigating the fit of multiple hit and cumulative risk models are likely promising approaches in enhancing the understanding of role of environmental factors in the etiology of ASD.
259 citations
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Erasmus University Medical Center1, University of Porto2, University of Western Australia3, Stockholm County Council4, Paris Descartes University5, Maastricht University6, French Institute of Health and Medical Research7, National and Kapodistrian University of Athens8, University Medical Center Groningen9, University of Valencia10, University of Southampton11, Liverpool School of Tropical Medicine12, Université de Sherbrooke13, Norwegian Institute of Public Health14, University of Bologna15, University of Crete16, University Hospital Southampton NHS Foundation Trust17, Ludwig Maximilian University of Munich18, Nofer Institute of Occupational Medicine19, University of California20, Harvard University21, University of Illinois at Chicago22, National Institutes of Health23, Wageningen University and Research Centre24, University of Turku25, Helmholtz Centre for Environmental Research - UFZ26, Jagiellonian University Medical College27, Åbo Akademi University28, Harokopio University29, University College Dublin30, University of Calgary31, Boston Children's Hospital32, University of Copenhagen33, University College Cork34, VU University Medical Center35, University of Helsinki36, University of Turin37, Radboud University Nijmegen38, University of Trieste39, University of Bergen40, Slovak Medical University41, Utrecht University42, Pompeu Fabra University43, Bradford Royal Infirmary44, University of Bristol45
TL;DR: In this paper, the separate and combined associations of maternal pre-pregnancy body mass index (BMI) and gestational weight gain with the risks of pregnancy complications and their population impact were assessed.
258 citations
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Finnish Institute of Occupational Health1, University of Helsinki2, Stockholm County Council3, University College London4, Federal Institute for Occupational Safety and Health5, Université libre de Bruxelles6, Ghent University7, University of Düsseldorf8, University of Duisburg-Essen9, RMIT University10, University of Tampere11, Mid Sweden University12, Stockholm University13, University of Copenhagen14, German Institute for Economic Research15, University of Turku16, Max Planck Society17, Uppsala University18
TL;DR: In this article, a systematic review and meta-analysis of published studies and unpublished individual participant data was conducted to quantify the association between long working hours and alcohol use, showing that individuals whose working hours exceed standard recommendations are more likely to increase their alcohol use to levels that pose a health risk.
Abstract: Objective: To quantify the association between long working hours and alcohol use. Design: Systematic review and meta-analysis of published studies and unpublished individual participant data. Data sources: A systematic search of PubMed and Embase databases in April 2014 for published studies, supplemented with manual searches. Unpublished individual participant data were obtained from 27 additional studies. Review methods: The search strategy was designed to retrieve cross sectional and prospective studies of the association between long working hours and alcohol use. Summary estimates were obtained with random effects meta-analysis. Sources of heterogeneity were examined with meta-regression. Results: Cross sectional analysis was based on 61 studies representing 333 693 participants from 14 countries. Prospective analysis was based on 20 studies representing 100 602 participants from nine countries. The pooled maximum adjusted odds ratio for the association between long working hours and alcohol use was 1.11 (95% confidence interval 1.05 to 1.18) in the cross sectional analysis of published and unpublished data. Odds ratio of new onset risky alcohol use was 1.12 (1.04 to 1.20) in the analysis of prospective published and unpublished data. In the 18 studies with individual participant data it was possible to assess the European Union Working Time Directive, which recommends an upper limit of 48 hours a week. Odds ratios of new onset risky alcohol use for those working 49-54 hours and ≥55 hours a week were 1.13 (1.02 to 1.26; adjusted difference in incidence 0.8 percentage points) and 1.12 (1.01 to 1.25; adjusted difference in incidence 0.7 percentage points), respectively, compared with working standard 35-40 hours (incidence of new onset risky alcohol use 6.2%). There was no difference in these associations between men and women or by age or socioeconomic groups, geographical regions, sample type (population based v occupational cohort), prevalence of risky alcohol use in the cohort, or sample attrition rate. Conclusions: Individuals whose working hours exceed standard recommendations are more likely to increase their alcohol use to levels that pose a health risk.
256 citations
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TL;DR: The design of a large intergenerational resource for ASD research is presented, along with population-based prevalence estimates of ASD and their diagnostic validity, and findings accords with recently reported prevalence estimates from Western countries at around 1.
Abstract: OBJECTIVE: Reports of rising prevalence of autism spectrum disorders (ASD), along with their profound personal and societal burden, emphasize the need of methodologically sound studies to explore their causes and consequences. We here present the design of a large intergenerational resource for ASD research, along with population-based prevalence estimates of ASD and their diagnostic validity.METHOD: The Stockholm Youth Cohort is a record-linkage study comprising all individuals aged 0-17 years, ever resident in Stockholm County in 2001-2007 (N = 589,114). ASD cases (N = 5,100) were identified using a multisource approach, involving registers covering all pathways to ASD diagnosis and care, and categorized according to co-morbid intellectual disability. Prospectively recorded information on potential determinants and consequences of ASD were retrieved from national and regional health and administrative registers. Case ascertainment was validated through case-note review, and cross validation with co-existing cases in a national twin study.RESULTS: The 2007 year prevalence of ASD in all children and young people was 11.5 per 1,000 (95% confidence interval 11.2-11.8), with a co-morbid intellectual disability recorded in 42.6% (41.0-44.2) of cases. We found 96.0% (92.0-98.4) of reviewed case-notes being consistent with a diagnosis of ASD, and confirmed ASD in 85.2% (66.2-95.8) of affected twins.CONCLUSIONS: Findings from this contemporary study accords with recently reported prevalence estimates from Western countries at around 1%, based on valid case ascertainment. The Stockholm Youth Cohort, in light of the availability of extensive information from Sweden's registers, constitutes an important resource for ASD research. On-going work, including collection of biological samples, will enrich the study further. (Less)
254 citations
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TL;DR: Results with PCR as a rapid and sensitive tool for early diagnosis of HSE extend and confirm previous results with PCR with HSV 2 as an etiological agent.
Abstract: A herpes simplex virus type 2 (HSV 2) etiology was sought in 93 consecutive cases of herpes simplex encephalitis (HSE) in immunocompetent post neonate patients. Antibodies to HSV 2 glycoprotein G antigen were determined by an enzyme-linked immunosorbent assay (ELISA) and HSV 2 DNA in cerebrospinal fluid (CSF) by a nested polymerase chain reaction (PCR) assay with primer pairs in the glycoprotein G gene. Evidence of HSV 2 infection was found in 6 patients; HSV 2 DNA was demonstrated in CSF and the intrathecal HSV 2 antibody response confirmed the findings. Five of the 6 patients with HSV 2 encephalitis presented a clinical picture, CSF, EEG, and CT findings characteristic of severe HSE. An atypically mild clinical course was seen in one patient. HSV 2 should be considered as an etiological agent in the viral diagnosis of HSE. With a combination of nested PCR assays for HSV 1 (primer pairs in the glycoprotein D gene) and HSV 2 in 10 microliters of CSF with no other preparation than freeze-thawing, HSV 1 or HSV 2 DNA was detected in 88 out of 93 (95%) of the first CSF specimens collected after the onset of neurological HSV disease. These findings extend and confirm previous results with PCR as a rapid and sensitive tool for early diagnosis of HSE.
249 citations
Authors
Showing all 1415 results
Name | H-index | Papers | Citations |
---|---|---|---|
Lars Klareskog | 131 | 697 | 63281 |
Christopher A. Walsh | 123 | 455 | 55874 |
Jan K. Buitelaar | 123 | 1004 | 61880 |
Gerhard Andersson | 118 | 902 | 49159 |
Lars Alfredsson | 112 | 607 | 51151 |
Sarah E. Medland | 106 | 462 | 46888 |
Tomas Olsson | 105 | 677 | 39905 |
René E. M. Toes | 101 | 454 | 39812 |
Göran Pershagen | 98 | 432 | 33214 |
Juha Kere | 97 | 642 | 38403 |
Agneta Nordberg | 93 | 513 | 39763 |
Lars Farde | 90 | 446 | 28122 |
G. David Batty | 88 | 451 | 23826 |
Christer Halldin | 87 | 713 | 32079 |
Anders Ahlbom | 87 | 359 | 27369 |