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Träfflista för sökning "WFRF:(Ohman I) srt2:(2010-2014)"

Sökning: WFRF:(Ohman I) > (2010-2014)

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  • Aad, G., et al. (författare)
  • 2014
  • Ingår i: Journal of High Energy Physics. - 1029-8479 .- 1126-6708. ; :9
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2014
  • Tidskriftsartikel (refereegranskat)
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  • Golkar, A, et al. (författare)
  • Other people as means to a safe end: vicarious extinction blocks the return of learned fear
  • 2013
  • Ingår i: Psychological science. - : SAGE Publications. - 1467-9280 .- 0956-7976. ; 24:11, s. 2182-2190
  • Tidskriftsartikel (refereegranskat)abstract
    • Information about what is dangerous and safe in the environment is often transferred from other individuals through social forms of learning, such as observation. Past research has focused on the observational, or vicarious, acquisition of fears, but little is known about how social information can promote safety learning. To address this issue, we studied the effects of vicarious-extinction learning on the recovery of conditioned fear. Compared with a standard extinction procedure, vicarious extinction promoted better extinction and effectively blocked the return of previously learned fear. We confirmed that these effects could not be attributed to the presence of a learning model per se but were specifically driven by the model’s experience of safety. Our results confirm that vicarious and direct emotional learning share important characteristics but that social-safety information promotes superior down-regulation of learned fear. These findings have implications for emotional learning, social-affective processes, and clinical practice.
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  • Lindblom, P, et al. (författare)
  • Tesaglitazar, a dual PPAR-α/γ agonist, hamster carcinogenicity, investigative animal and clinical studies
  • 2012
  • Ingår i: Toxicologic pathology. - : SAGE Publications. - 1533-1601 .- 0192-6233. ; 40:1, s. 18-32
  • Tidskriftsartikel (refereegranskat)abstract
    • Tesaglitazar was developed as a dual peroxisome proliferator–activated receptor (PPARα/γ). To support the clinical program, a hamster carcinogenicity study was performed. The only neoplastic findings possibly related to treatment with tesaglitazar were low incidences of hemangioma and hemangiosarcoma in the liver of male animals. A high-power, two-year investigative study with interim necropsies was performed to further elucidate these findings. Treatment with tesaglitazar resulted in changes typical for exaggerated PPARα pharmacology in rodents, such as hepatocellular hypertrophy and hepatocellular carcinoma, but not an increased frequency of hemangiosarcomas. At the highest dose level, there was an increased incidence of sinusoidal dilatation and hemangiomas. No increased endothelial cell (EC) proliferation was detected in vivo, which was confirmed by in vitro administration to ECs. Immunohistochemistry and gene expression analyses indicated increased cellular stress and vascular endothelial growth factor (VEGF) expression in the liver, which may have contributed to the sinusoidal dilatation. A two-fold increase in the level of circulating VEGF was detected in the hamster at all dose levels, whereas no effect on VEGF was observed in patients treated with tesaglitazar. In conclusion, investigations have demonstrated that tesaglitazar does not produce hemangiosarcomas in hamster despite a slight effect on vascular morphology in the liver.
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