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Träfflista för sökning "WFRF:(Christensen Marit) srt2:(2012-2014)"

Sökning: WFRF:(Christensen Marit) > (2012-2014)

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1.
  • Christensen, Marit, et al. (författare)
  • Building engagement and healthy organisations : Validation of the Nordic Questionnaire on Positive Organisational Psychology (N-POP). The Third Report from the Nordic Project
  • 2012
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • The main aim of the project was to investigate the predictors of positive work-related states and attitudes, e.g. work engagement, meaning at work and personal growth, and healthy organisations. A questionnaire on these positive factors at work were pilot-tested through a data collection in chosen companies in Norway and Sweden. The results of these studies were used as a base for a preliminary validation of the Nordic Questionnaire on Positive Organisational Psychology (N-POP) published in this report. It is concluded that the N-POP constitutes a reliable and valid instrument. The concluding summary suggests that the concepts of work environment, health and productivity do indeed seem able to flow together to reach an optimal point at which well-being at the individual level is coexistent with efficient and productive work organisations.
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2.
  • Flannick, Jason, et al. (författare)
  • Loss-of-function mutations in SLC30A8 protect against type 2 diabetes.
  • 2014
  • Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 46:4, s. 357-357
  • Tidskriftsartikel (refereegranskat)abstract
    • Loss-of-function mutations protective against human disease provide in vivo validation of therapeutic targets, but none have yet been described for type 2 diabetes (T2D). Through sequencing or genotyping of ∼150,000 individuals across 5 ancestry groups, we identified 12 rare protein-truncating variants in SLC30A8, which encodes an islet zinc transporter (ZnT8) and harbors a common variant (p.Trp325Arg) associated with T2D risk and glucose and proinsulin levels. Collectively, carriers of protein-truncating variants had 65% reduced T2D risk (P = 1.7 × 10(-6)), and non-diabetic Icelandic carriers of a frameshift variant (p.Lys34Serfs*50) demonstrated reduced glucose levels (-0.17 s.d., P = 4.6 × 10(-4)). The two most common protein-truncating variants (p.Arg138* and p.Lys34Serfs*50) individually associate with T2D protection and encode unstable ZnT8 proteins. Previous functional study of SLC30A8 suggested that reduced zinc transport increases T2D risk, and phenotypic heterogeneity was observed in mouse Slc30a8 knockouts. In contrast, loss-of-function mutations in humans provide strong evidence that SLC30A8 haploinsufficiency protects against T2D, suggesting ZnT8 inhibition as a therapeutic strategy in T2D prevention.
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