Profiles

Gustav Nilsonne

Gustav Nilsonne

Forskare

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Arbetar vid Psykologiska institutionen
Telefon 08-553 789 34
E-post gustav.nilsonne@su.se
Besöksadress Frescati Hagväg 16 A
Rum 334
Postadress Psykologiska institutionen 106 91 Stockholm

Om mig

Gustav Nilsonne är forskare i neurovetenskap och metavetenskap. Hans forskning i neurovetenskap handlar om sömn och dygnsrytmer, och om hjärnans kommunikation med immunsystemet. Med hjälp bland annat av magnetkamerateknik och av analys av stora öppna datamängder undersöks effekter av sömnbrist och tid på dygnet, med mera. Hans forskning i metavetenskap handlar om reproducerbarhet och öppenhet inom vetenskapen.

Publikationer

I urval från Stockholms universitets publikationsdatabas
  • 2019. Karin Lodin (et al.).

    This study investigated associations between inflammatory markers, sickness behaviour, health anxiety and self-rated health in 311 consecutive primary care patients. Poor self-rated health was associated with high sickness behaviour (rho = 0.28, P < 0.001; rho = 0.42, P = 0.003) and high health anxiety (rho = 0.31, P < 0.001; rho = -0.32, P = 0.003). High levels of interleukin 6 were associated with poor self-rated health in men (rho = 0.26, P = 0.009). Low levels of interleukin-6 were associated with poor self-rated health in women (rho = -0.15, P = 0.04), but this association was non-significant when adjusted for health anxiety (rho = -0.08, P = 0.31). These results are consistent with the theory that interoceptive processes draw on both inflammatory mediators and the state of sickness behaviour in inferring health state.

  • 2019. Gustav Nilsonne.

    Nyligen meddelade Bibsam-konsortiet, som för svenska lärosätens räkning förhandlar om vetenskapliga tidskriftsprenumerationer, att man nått ett nytt avtal med Elsevier. Därmed slutar det avtalslösa tillstånd som rått i bortåt ett och ett halvt år, då svenska forskare inte fått tillgång till aktuella artiklar i Elseviertidskrifter. Det nya avtalet är transformativt. Detta innebär att det innehåller publicering med öppen tillgång för svenska forskare utan att forskaren eller lärosätet behöver betala en avgift för varje artikel. Fler artiklar kommer därmed att bli omedelbart öppet tillgängliga.

    Det gamla avtalet med Elsevier kostade 14 miljoner euro 2017, samtidigt som tidskrifterna också tog betalt per artikel för publicering med öppen tillgång. Det var helt nödvändigt att bryta den skenande kostnadsökningen, och Bibsamkonsortiet ska ha all heder av sitt beslut att inte fortsätta med samma typ av avtal som förut.

    Men det transformativa avtalet med Elsevier är en pyrrhusseger. Problemet med det nya avtalet är att det cementerar låsningen till en föråldrad publiceringskultur. Förlaget tillåts fortfarande ta dubbelt betalt: både för att vi ska få läsa andra länders artiklar, och för att publicera svenska artiklar med öppen tillgång – fastän båda kostnaderna är inbakade i samma avtal. Vi får alltså betala först för att de reser en brandvägg framför vetenskapens landvinningar, och sedan igen för att få spika upp våra egna alster på väggens utsida.

    Öppna arkiv på internet gör att vetenskapliga resultat kan publiceras till mycket låg kostnad, och utan den fördröjning som tidskrifternas granskning innebär. Systematiska metoder för att granska kvaliteten efter publicering har potential att ersätta den traditionella referentgranskningen, som ofta åberopas som kvalitetshöjande, men som i allmänhet försiggår i det fördolda och inte i sig kan granskas. Tidskrifternas roll som förvaltare av ett prestigekapital som snedvrider forskningsprocessen behöver brytas.

    Experimentet med ett avtalslöst tillstånd visade att svensk forskning klarade sig bra. Kostnaden för det nya avtalet är ännu inte offentliggjord, men den kvardröjande låsningen till Elsevier medför en risk för fortsatta kostnadsökningar. Det går inte att motivera att svensk forskning årligen ska dräneras på hundratals miljoner kronor för att köpa tillbaka forskningsresultat som borde varit öppet tillgängliga från början. Bibsamkonsortiet borde experimentera med att säga upp fler avtal. Inbesparade medel skulle kunna användas exempelvis till stöd för att publicera forskningsdata och andra forskningsprodukter öppet och FAIR.

  • 2019. Kristoffer N.T. Månsson (et al.). Translational Psychiatry 9

    Telomere attrition is a hallmark of cellular aging and shorter telomeres have been reported in mood and anxiety disorders. Telomere shortening is counteracted by the enzyme telomerase and cellular protection is also provided by the antioxidant enzyme glutathione peroxidase (GPx). Here, telomerase, GPx, and telomeres were investigated in 46 social anxiety disorder (SAD) patients in a within-subject design with repeated measures before and after cognitive behavioral therapy. Treatment outcome was assessed by the Liebowitz Social Anxiety Scale (self-report), administered three times before treatment to control for time and regression artifacts, and posttreatment. Venipunctures were performed twice before treatment, separated by 9 weeks, and once posttreatment. Telomerase activity and telomere length were measured in peripheral blood mononuclear cells and GPx activity in plasma. All patients contributed with complete data. Results showed that social anxiety symptom severity was significantly reduced from pretreatment to posttreatment (Cohen’s d = 1.46). There were no significant alterations in telomeres or cellular protection markers before treatment onset. Telomere length and telomerase activity did not change significantly after treatment, but an increase in telomerase over treatment was associated with reduced social anxiety. Also, lower pretreatment telomerase activity predicted subsequent symptom improvement. GPx activity increased significantly during treatment, and increases were significantly associated with symptom improvement. The relationships between symptom improvement and putative protective enzymes remained significant also after controlling for body mass index, sex, duration of SAD, smoking, concurrent psychotropic medication, and the proportion of lymphocytes to monocytes. Thus, indices of cellular protection may be involved in the therapeutic mechanisms of psychological treatment for anxiety.

  • 2019. Sandra Tamm (et al.). Royal Society Open Science 6 (3)

    Sleep restriction has been proposed to cause impaired emotional processing and emotional regulation by inhibiting top-down control from prefrontal cortex to amygdala. Intentional emotional regulation after sleep restriction has, however, never been studied using brain imaging. We aimed here to investigate the effect of partial sleep restriction on emotional regulation through cognitive reappraisal. Forty-seven young (age 20–30) and 33 older (age 65–75) participants (38/23 with complete data and successful sleep intervention) performed a cognitive reappraisal task during fMRI after a night of normal sleep and after restricted sleep (3 h). Emotional downregulation was associated with significantly increased activity in the dorsolateral prefrontal cortex (pFWE < 0.05) and lateral orbital cortex (pFWE < 0.05) in young, but not in older subjects. Sleep restriction was associated with a decrease in self-reported regulation success to negative stimuli (p< 0.01) and a trend towards perceiving all stimuli as less negative (p = 0.07) in young participants. No effects of sleep restriction on brain activity nor connectivity were found in either age group. In conclusion, our data do not support the idea of a prefrontal-amygdala disconnect after sleep restriction, and neural mechanisms underlying behavioural effects on emotional regulation after insufficient sleep require further investigation.

  • 2019. Igor Radun (et al.). Transportation Research Part F 60, 81-92

    The use of company employees as experimental participants when testing products, technology orparadigms developed by the same company raises questions about bias in results and researchethics. We aimed to investigate the prevalence of studies authored by car company researchers withcar company employees as participants, to assess the risk of bias in such studies, to investigatejournal editors’ opinions in the field of traffic safety regarding these procedures, and to offer ageneral discussion about ethical and methodological implications. Three types of data were

    collected. We (i) examined guidelines and recommendations for authors in eleven selected peer-reviewed journals in the area of traffic safety; (ii) surveyed editors of these journals; and (iii)

    reviewed articles authored by researchers from a selected group of car manufacturers and publishedin these journals during 2011-2015. Guidelines and recommendations for authors in the includedjournals did not mention whether and under what circumstances company employees can beresearch participants, nor did publishers’ general guidelines. However, three out of the four editorswho responded to our survey believed that this issue of private company researchers usingparticipants from the same company deserves to be explicitly addressed in their journal’s guide forauthors. The total number of regular articles and conference papers during 2011-2015 in the elevenjournals reviewed was 6763; 95 (1.4%) listed at least one car manufacturer in the authors’affiliations; and out of these, nine included company employees as participants. In summary,company employees are seldom (0.13%) used as research participants in traffic safety research.Nevertheless, the use of company employees as research participants raises questions about bias inresults as well as about incursions into the participants’ autonomy.

  • 2018. Kristoffer Månsson (et al.). Biological Psychiatry 83 (9), S351-S352

    Background: Mental illness, including anxiety disorders, is linked to accelerated cell aging. This is evidenced by shorter leukocyte telomere length. Cells with critically short telomeres may undergo apoptosis. In dividing cells, telomere shortening is counteracted by the telomeraseenzyme. Telomerase is reportedly low following chronic psychological stress. We hypothesized that a psychological treatment may increase telomerase activity, less telomere attritionand greater symptom improvement.

    Methods: Forty-six patients (91% SSRI naïve) with social anxiety disorder(SAD; mean age 31, 63% females) underwent a 9-week waiting period, and 9 weeks of Internet-delivered cognitive behavior therapy(CBT). During treatment, symptoms were assessed weekly using the Liebowitz Social Anxiety Scale (LSAS-SR). Fasting blood samples were collected twice before treatment, and at post-treatment. Genomic DNA was extracted using DNeasy® Blood & Tissue Kit (Qiagene) to assess leukocyte telomere length. Telomerase activity was detected by real-time telomeric repeat amplification protocol (RT-TRAP).

    Results: Patients improved significantly on the LSAS-SR (p<.001; Cohen’s d=1.5). Pre-post changes in telomerase and telomere length correlated positively (Pearson’s r=.31, p=.05). Reduced telomerase activity (<33th percentile) was associated with less improvement and increased activity (>66th percentile) with more improvement on the LSAS-SR (Z=-2.4, p=.02).

    Conclusions: We demonstrate, to our knowledge for the first time, that altered telomerase activity is associated with clinical response to a psychological treatment in a psychiatric population. The observed CBT effect on telomerase in patients with SAD is consistent with results from animal trials and a small previous study of antidepressants in humans. Thus, telomerase activation may play an important role in clinical recovery.

  • 2018. Tom E. Hardwicke (et al.). Royal Society Open Science 5 (8)

    Access to data is a critical feature of an efficient, progressive and ultimately self-correcting scientific ecosystem. But the extent to which in-principle benefits of data sharing are realized in practice is unclear. Crucially, it is largely unknown whether published findings can be reproduced by repeating reported analyses upon shared data ('analytic reproducibility'). To investigate this, we conducted an observational evaluation of a mandatory open data policy introduced at the journal Cognition. Interrupted time-series analyses indicated a substantial post-policy increase in data available statements (104/417, 25% pre-policy to 136/ 174, 78% post-policy), although not all data appeared reusable (23/ 104, 22% pre-policy to 85/136, 62%, post-policy). For 35 of the articles determined to have reusable data, we attempted to reproduce 1324 target values. Ultimately, 64 values could not be reproduced within a 10% margin of error. For 22 articles all target values were reproduced, but 11 of these required author assistance. For 13 articles at least one value could not be reproduced despite author assistance. Importantly, there were no clear indications that original conclusions were seriously impacted. Mandatory open data policies can increase the frequency and quality of data sharing. However, suboptimal data curation, unclear analysis specification and reporting errors can impede analytic reproducibility, undermining the utility of data sharing and the credibility of scientific findings.

Visa alla publikationer av Gustav Nilsonne vid Stockholms universitet

Senast uppdaterad: 11 januari 2020

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