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Sökning: WFRF:(Böttcher Gerhard)

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1.
  • Böttcher, Johanna, et al. (författare)
  • Adding a smartphone app to internet-based self-help for social anxiety : A randomized controlled trial
  • 2018
  • Ingår i: Computers in human behavior. - : Elsevier BV. - 0747-5632 .- 1873-7692. ; 87, s. 98-108
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Increasing access to treatment via smartphone apps is an important topic in Social Anxiety Disorder (SAD). ‘Challenger’ is an app promoting exposure exercises in daily life. The present study evaluated the additional benefit of using the app as adjunct to Internet-based unguided self-help for SAD. In a second step, we also tested how the app and the self-help programme (SH) should best be combined.Method: 209 patients diagnosed with SAD were randomly allocated to three groups. Group 1 received the app and the self-help programme for six weeks (parallel treatment), group 2 first received SH for six weeks and then the app for six weeks (sequential treatment). Group 3 was a wait-list group. Comparisons were made at week 7 evaluating the potential add-on effect of the app (SH plus app versus SH only) and at week 14 comparing the parallel to the sequential treatment. Participants filled in questionnaires prior, during, and post treatment, and at 4- and 12- months follow-up.Results: Intention-to-treat analyses showed no significant effect of adding the app to Internet-based self-help. However, among participants actively using the app, adding Challenger to self-help resulted in significantly less social anxiety (d = 0.30). At week 14, decreases in social anxiety were large for both the parallel and the sequential group with no differences between the active groups (dwithin = 1.12–1.19). Changes were maintained throughout the follow-up period.Conclusion: Results of the current study cautiously support the notion of adding a smartphone app to unguided self-help for SAD. Future studies should investigate how patients can be motivated to use the app more frequently.
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2.
  • Carlbring, Per, et al. (författare)
  • Adding a Smartphone App to Bibliotherapy for Social Anxiety : A Randomized Controlled Comparison
  • 2017
  • Ingår i: Applying CBT in Diverse Contexts: 51st Annual Convention. ; , s. 394-394
  • Konferensbidrag (refereegranskat)abstract
    • The efficacy of Internet-based treatments and bibliotherapy for Social Anxiety Disorder is well established. The next step is to evaluate smartphone supported interventions. ‘Challenger’ is a recently developed facilitating the implementation of exposure exercises in daily life. The present study evaluates the efficacy of the combination of Challenger and bibliotherapy for Social Anxiety Disorder. A total of 209 patients with Social Anxiety Disorder were randomly allocated to three groups. The first group received app and bibliotherapy for six weeks (parallel design) and the second group received first bibliotherapy for six weeks and then the app for another six weeks (sequential design). The third group was a wait-list control group. Participants filled in questionnaires on primary and secondary outcomes post treatment as well as at 4 and 12 months follow-up. Participants using both app and bibliotherapy showed somewhat larger reductions in social fears after six weeks of treatment compared to participants using only bibliotherapy (d=0.25). Decreases in social anxiety were large for both groups after 12 weeks of treatment (d= 1.11-1.20) and were maintained throughout the follow-up period. Results of the current study support the notion of adding a smartphone app to bibliotherapy for Social Anxiety Disorder. Future study should investigate the potential of the app in different treatment settings.
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3.
  • Dohi, Takaaki, et al. (författare)
  • Enhanced thermally-activated skyrmion diffusion with tunable effective gyrotropic force
  • 2023
  • Ingår i: Nature Communications. - : Springer Nature. - 2041-1723. ; 14:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Magnetic skyrmions, topologically-stabilized spin textures that emerge in magnetic systems, have garnered considerable interest due to a variety of electromagnetic responses that are governed by the topology. The topology that creates a microscopic gyrotropic force also causes detrimental effects, such as the skyrmion Hall effect, which is a well-studied phenomenon highlighting the influence of topology on the deterministic dynamics and drift motion. Furthermore, the gyrotropic force is anticipated to have a substantial impact on stochastic diffusive motion; however, the predicted repercussions have yet to be demonstrated, even qualitatively. Here we demonstrate enhanced thermally-activated diffusive motion of skyrmions in a specifically designed synthetic antiferromagnet. Suppressing the effective gyrotropic force by tuning the angular momentum compensation leads to a more than 10 times enhanced diffusion coefficient compared to that of ferromagnetic skyrmions. Consequently, our findings not only demonstrate the gyro-force dependence of the diffusion coefficient but also enable ultimately energy-efficient unconventional stochastic computing.
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4.
  • Lindén, Daniel, 1971, et al. (författare)
  • Pnpla3 silencing with antisense oligonucleotides ameliorates nonalcoholic steatohepatitis and fibrosis in Pnpla3 I148M knock-in mice.
  • 2019
  • Ingår i: Molecular metabolism. - : Elsevier BV. - 2212-8778. ; 22:April, s. 49-61
  • Tidskriftsartikel (refereegranskat)abstract
    • Nonalcoholic fatty liver disease (NAFLD) is becoming a leading cause of advanced chronic liver disease. The progression of NAFLD, including nonalcoholic steatohepatitis (NASH), has a strong genetic component, and the most robust contributor is the patatin-like phospholipase domain-containing 3 (PNPLA3) rs738409 encoding the 148M protein sequence variant. We hypothesized that suppressing the expression of the PNPLA3 148M mutant protein would exert a beneficial effect on the entire spectrum of NAFLD.We examined the effects of liver-targeted GalNAc3-conjugated antisense oligonucleotide (ASO)-mediated silencing of Pnpla3 in a knock-in mouse model in which we introduced the human PNPLA3 I148M mutation.ASO-mediated silencing of Pnpla3 reduced liver steatosis (p=0.038) in homozygous Pnpla3 148M/M knock-in mutant mice but not in wild-type littermates fed a steatogenic high-sucrose diet. In mice fed a NASH-inducing diet, ASO-mediated silencing of Pnpla3 reduced liver steatosis score and NAFLD activity score independent of the Pnpla3 genotype, while reductions in liver inflammation score (p=0.018) and fibrosis stage (p=0.031) were observed only in the Pnpla3 knock-in 148M/M mutant mice. These responses were accompanied by reduced liver levels of Mcp1 (p=0.026) and Timp2 (p=0.007) specifically in the mutant knock-in mice. This may reduce levels of chemokine attracting inflammatory cells and increase the collagenolytic activity during tissue regeneration.This study provides the first evidence that a Pnpla3 ASO therapy can improve all features of NAFLD, including liver fibrosis, and suppress the expression of a strong innate genetic risk factor, Pnpla3 148M, which may open up a precision medicine approach in NASH.
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5.
  • Lindgren, Anna, et al. (författare)
  • Adiponectin receptor 2 deficiency results in reduced atherosclerosis in the brachiocephalic artery in apolipoprotein e deficient mice.
  • 2013
  • Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 8:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Adiponectin has been shown to have beneficial cardiovascular effects and to signal through the adiponectin receptors, AdipoR1 and AdipoR2. The original aim of this study was to investigate the effect of combined AdipoR1 and AdipoR2 deficiency (AdipoR1(-/-)AdipoR2(-/-)) on atherosclerosis. However, we made the interesting observation that AdipoR1 (-/-) AdipoR2 (-/-) leads to embryonic lethality demonstrating the critical importance of the adiponectin signalling system during development. We then investigated the effect of AdipoR2-ablation on the progression of atherosclerosis in apolipoprotein E deficient (ApoE (-/-) ) mice. AdipoR2(-/-)ApoE(-/-) mice fed an atherogenic diet had decreased plaque area in the brachiocephalic artery compared with AdipoR2 (+/+) ApoE(-/-) littermate controls as visualized in vivo using an ultrasound biomicroscope and confirmed by histological analyses. The decreased plaque area in the brachiocephalic artery could not be explained by plasma cholesterol levels or inflammatory status. However, accumulation of neutral lipids was decreased in peritoneal macrophages from AdipoR2(-/-)ApoE(-/-) mice after incubation with oxidized LDL. This effect was associated with lower CD36 and higher ABCA1 mRNA levels in peritoneal macrophages from AdipoR2(-/-)ApoE(-/-) mice compared with AdipoR2(+/+)ApoE(-/-) controls after incubation with oxidized LDL. In summary, we show that adiponectin receptors are crucial during embryonic development and that AdipoR2-deficiency slows down the progression of atherosclerosis in the brachiocephalic artery of ApoE-deficient mice.
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