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Träfflista för sökning "WFRF:(Simon Gunnel) srt2:(2010-2014)"

Sökning: WFRF:(Simon Gunnel) > (2010-2014)

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1.
  • Knapstad, Marit, et al. (författare)
  • Previous sickness absence and current low perceived social support at work among employees in the general population: a historical cohort study
  • 2014
  • Ingår i: BMJ Open. - : BMJ. - 2044-6055. ; 4:10
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Although sickness absence often is a process over time, most studies have treated the phenomenon as a discrete event and focused more on its causes than its consequences. We aimed to examine whether various patterns of previous long-term sickness absence were associated with current low perceived social support at work. METHOD: This is a historical cohort study based on data from a population-based survey among Swedish employees (n=2581). The survey data were linked to official registries yielding data on sickness absence 1-7 years prior to the survey. RESULTS: The main finding was that previous sickness absence was associated with current low perceived social support at work. The highest odds for low social support were found among those who had a stable high level of sickness absence. The two indicators of perceived social support employed were somewhat differently associated with previous sickness absence: Recency of absence showed to be of importance for general support at the workplace and the relationship with colleagues and superiors. Experiencing that one's immediate superior rarely or never regards one's view was, on the other hand, mainly related to having had a high level of sickness absence, irrespective of recency. CONCLUSIONS: Our results indicate that recency and extent of previous sickness absence are related to perceived social support at work. Future research on the relationship between social support and sickness absence should use repeated measurements and acknowledge the possible bidirectional relationship.
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2.
  • Knapstad, Marit, et al. (författare)
  • Shame among long-term sickness absentees: Correlates and impact on subsequent sickness absence.
  • 2014
  • Ingår i: Scandinavian journal of public health. - : SAGE Publications. - 1651-1905 .- 1403-4948. ; 42:1, s. 96-103
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: The contribution of general psychological aspects, such as emotions, has received little focus in research on sickness absence. We wanted to study the relationship between shame and sickness absence, which factors that explained differences in levels of shame, and if shame predicted subsequent sickness absence. Methods: We employed a Swedish population-based cohort of current sickness absentees (19-64 years old), responding to a mailed questionnaire in 2008. Data was linked to national registries on sickness absence.Results: The young, those born outside the Nordic countries, those on lower incomes and those with higher level of education reported being more ashamed of their sickness absence. Those with more sickness absence in the past were also more likely to report higher levels of shame. Level of shame was not associated with gender or occupational class. Compared to those absent for a somatic cause, mental or co-morbid illness was associated with higher levels of shame. Those reporting high level of shame were more likely to have prolonged sickness absence the following year. Symptoms of depression at baseline only partly explained these associations. Conclusions: Our results suggest that shame might prolong sickness absence. Increased understanding of the impact of social and emotional aspects around sickness absence could be an important source for improved quality of rehabilitation.
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3.
  • Lessard, Christopher J., et al. (författare)
  • Variants at multiple loci implicated in both innate and adaptive immune responses are associated with Sjogren's syndrome
  • 2013
  • Ingår i: Nature Genetics. - : NATURE PUBLISHING GROUP, 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA. - 1061-4036 .- 1546-1718. ; 45:11, s. 1284-
  • Tidskriftsartikel (refereegranskat)abstract
    • Sjogrens syndrome is a common autoimmune disease (affecting similar to 0.7% of European Americans) that typically presents as keratoconjunctivitis sicca and xerostomia. Here we report results of a large-scale association study of Sjogrens syndrome. In addition to strong association within the human leukocyte antigen (HLA) region at 6p21 (P-meta = 7.65 x 10(-114)), we establish associations with IRF5-TNPO3 (P-meta = 2.73 x 10(-19)), STAT4 (Pmeta = 6.80 x 10-15), IL12A (P-meta = 1.17 x 10(-10)), FAM167ABLK (P-meta = 4.97 x 10(-10)), DDX6-CXCR5 (P-meta = 1.10 x 10(-8)) and TNIP1 (P-meta = 3.30 x 10(-8)). We also observed suggestive associations (P-meta andlt; 5 x 10(-5)) with variants in 29 other regions, including TNFAIP3, PTTG1, PRDM1, DGKQ, FCGR2A, IRAK1BP1, ITSN2 and PHIP, among others. These results highlight the importance of genes that are involved in both innate and adaptive immunity in Sjogrens syndrome.
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4.
  • Nordmark, Gunnel, et al. (författare)
  • Association of Genes in the NF-κB Pathway with Antibody-Positive Primary Sjögren's Syndrome
  • 2013
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 0300-9475 .- 1365-3083. ; 78:5, s. 447-454
  • Tidskriftsartikel (refereegranskat)abstract
    • Primary Sjogrens syndrome (SS) is a systemic autoimmune inflammatory disease characterized by focal lymphocytic infiltrates in the lachrymal and salivary glands and autoantibodies against the SSA/Ro and SSB/La antigens. Experimental studies have shown an activation of NF-B in primary SS. NF-B activation results in inflammation and autoimmunity and is regulated by inhibitory and activating proteins. Genetic studies have shown an association between multiple autoimmune diseases and TNFAIP3 (A20) and TNIP1 (ABIN1), both repressors of NF-B and of IKBKE (IKK epsilon), which is an NF-B activator. The aim of this study was to analyse single nucleotide polymorphisms (SNPs) in the IKBKE, NFKB1, TNIP1 and TNFAIP3 genes for association with primary SS. A total of 12 SNPs were genotyped in 1105 patients from Scandinavia (Sweden and Norway, n=684) and the UK (n=421) and 4460 controls (Scandinavia, n=1662, UK, n=2798). When patients were stratified for the presence of anti-SSA and/or anti-SSB antibodies (n=868), case-control meta-analysis found an association between antibody-positive primary SS and two SNPs in TNIP1 (P=3.4x10(-5), OR=1.33, 95%CI: 1.16-1.52 for rs3792783 and P=1.3x10(-3), OR=1.21, 95%CI: 1.08-1.36 for rs7708392). A TNIP1 risk haplotype was associated with antibody-positive primary SS (P=5.7x10(-3), OR=1.47, 95%CI: 1.12-1.92). There were no significant associations with IKBKE, NFKB1 or TNFAIP3 in the meta-analysis of the Scandinavian and UK cohorts. We conclude that polymorphisms in TNIP1 are associated with antibody-positive primary SS.
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