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, Autism, Health care, Cohort study
Papers published on a yearly basis
Papers
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TL;DR: Reliability was tested between pairs of therapists for 168 children between 4 and 18 years and between 25 parents and their children's therapists, demonstrating that MACS has good validity and reliability.
Abstract: The Manual Ability Classification System (MACS) has been developed to classify how children with cerebral palsy (CP) use their hands when handling objects in daily activities. The classification is designed to reflect the child's typical manual performance, not the child's maximal capacity. It classifies the collaborative use of both hands together. Validation was based on the experience within an expert group, a review of the literature, and thorough analysis of children across a spectrum of function. Discussions continued until consensus was reached, first about the constructs, then about the content of the five levels. Parents and therapists were interviewed about the content and the description of levels. Reliability was tested between pairs of therapists for 168 children (70 females, 98 males; with hemiplegia [n=52], diplegia [n=70], tetraplegia [n=19], ataxia [n=6], dyskinesia [n=19], and unspecified CP [n=2]) between 4 and 18 years and between 25 parents and their children's therapists. The results demonstrated that MACS has good validity and reliability. The intraclass correlation coefficient between therapists was 0.97 (95% confidence interval 0.96-0.98), and between parents and therapist was 0.96 (0.89-0.98), indicating excellent agreement.
1,778 citations
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TL;DR: This document is an update of Guidelines published in 2005 and now includes scientific publications through to May 2010 that provides evidence-based recommendations for the most common management questions occurring in routine clinical practice in the management of adult patients with LRTI.
768 citations
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TL;DR: The disease risk of RF-seropositive RA associated with one of the classic genetic risk factors for immune-mediated diseases (the SE of HLA-DR) is strongly influenced by the presence of an environmental factor (smoking) in the population at risk.
Abstract: Objective
The main genetic risk factor for rheumatoid arthritis (RA) is the shared epitope (SE) of HLA–DR, while smoking is an important environmental risk factor. We studied a potential gene–environment interaction between SE genes and smoking in the etiology of the 2 major subgroups of RA: rheumatoid factor (RF)–seropositive and RF-seronegative disease.
Methods
A population-based case–control study involving incident cases of RF-seropositive and RF-seronegative RA (858 cases and 1,048 controls) was performed in Sweden. Cases and controls were classified according to their cigarette smoking status and HLA–DRB1 genotypes. The relative risk of developing RA was calculated for different gene/smoking combinations and was compared with the relative risk in never smokers without SE genes.
Results
The relative risk of RF-seropositive RA was 2.8 (95% confidence interval [95% CI] 1.6–4.8) in never smokers with SE genes, 2.4 (95% CI 1.3–4.6) in current smokers without SE genes, and 7.5 (95% CI 4.2–13.1) in current smokers with SE genes. Smokers carrying double SE genes displayed a relative risk of RF-seropositive RA of 15.7 (95% CI 7.2–34.2). The interaction between smoking and SE genes was significant, as measured by the attributable proportion due to interaction, which was 0.4 (95% CI 0.2–0.7) for smoking and any SE, and 0.6 (95% CI 0.4–0.9) for smoking and a double SE. Neither smoking nor SE genes nor the combination of these factors increased the risk of developing RF-seronegative RA.
Conclusion
The disease risk of RF-seropositive RA associated with one of the classic genetic risk factors for immune-mediated diseases (the SE of HLA–DR) is strongly influenced by the presence of an environmental factor (smoking) in the population at risk.
667 citations
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TL;DR: Adaptions of cognitive behavioural therapy elements that are feasible to implement for those facing changed work schedules and requirements, those with health anxiety and those handling childcare and home‐schooling are suggested, whilst also recognizing the general limitations imposed on physical exercise and social interaction.
Abstract: In the current global home confinement situation due to the COVID-19 outbreak, most individuals are exposed to an unprecedented stressful situation of unknown duration. This may not only increase daytime stress, anxiety and depression levels, but also disrupt sleep. Importantly, because of the fundamental role that sleep plays in emotion regulation, sleep disturbance can have direct consequences upon next day emotional functioning. In this paper, we summarize what is known about the stress-sleep link and confinement as well as effective insomnia treatment. We discuss those effects of the current home confinement situation that can disrupt sleep but also those that could benefit sleep quality. We suggest adaptions of cognitive behavioural therapy elements that are feasible to implement for those facing changed work schedules and requirements, those with health anxiety and those handling childcare and home-schooling, whilst also recognizing the general limitations imposed on physical exercise and social interaction. Managing sleep problems as best as possible during home confinement can limit stress and possibly prevent disruptions of social relationships.
660 citations
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United States Department of Health and Human Services1, Erasmus University Rotterdam2, University of California, Berkeley3, Johns Hopkins University4, Icahn School of Medicine at Mount Sinai5, University of Southern California6, Duke University7, University of Bristol8, University Medical Center Groningen9, University of California, San Francisco10, North Carolina State University11, Karolinska Institutet12, Pompeu Fabra University13, University of Paris14, University of Memphis15, Centre Hospitalier Universitaire de Grenoble16, University of Bergen17, Isfahan University of Medical Sciences18, Brigham and Women's Hospital19, Oslo University Hospital20, Utrecht University21, French Institute of Health and Medical Research22, Norwegian Institute of Public Health23, Johns Hopkins University School of Medicine24, Harvard University25, International Agency for Research on Cancer26, Paris Descartes University27, Michigan State University28, Centre national de la recherche scientifique29, Fred Hutchinson Cancer Research Center30, Swiss Tropical and Public Health Institute31, University of Basel32, Stockholm County Council33, University of Southampton34
TL;DR: This large scale meta-analysis of methylation data identified numerous loci involved in response to maternal smoking in pregnancy with persistence into later childhood and provide insights into mechanisms underlying effects of this important exposure.
Abstract: Epigenetic modifications, including DNA methylation, represent a potential mechanism for environmental impacts on human disease. Maternal smoking in pregnancy remains an important public health problem that impacts child health in a myriad of ways and has potential lifelong consequences. The mechanisms are largely unknown, but epigenetics most likely plays a role. We formed the Pregnancy And Childhood Epigenetics (PACE) consortium and meta-analyzed, across 13 cohorts (n = 6,685), the association between maternal smoking in pregnancy and newborn blood DNA methylation at over 450,000 CpG sites (CpGs) by using the Illumina 450K BeadChip. Over 6,000 CpGs were differentially methylated in relation to maternal smoking at genome-wide statistical significance (false discovery rate, 5%), including 2,965 CpGs corresponding to 2,017 genes not previously related to smoking and methylation in either newborns or adults. Several genes are relevant to diseases that can be caused by maternal smoking (e.g., orofacial clefts and asthma) or adult smoking (e.g., certain cancers). A number of differentially methylated CpGs were associated with gene expression. We observed enrichment in pathways and processes critical to development. In older children (5 cohorts, n = 3,187), 100% of CpGs gave at least nominal levels of significance, far more than expected by chance (p value < 2.2 × 10(-16)). Results were robust to different normalization methods used across studies and cell type adjustment. In this large scale meta-analysis of methylation data, we identified numerous loci involved in response to maternal smoking in pregnancy with persistence into later childhood and provide insights into mechanisms underlying effects of this important exposure.
646 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 |