Nature Human Behaviour最新文献

Healthcare use among adolescents after vaccination against SARS-CoV-2 is unknown. In a real-life register-based cohort study (trial NCT04786353), healthcare use was compared among Pfizer-BioNTech BNT162b2 COVID-19 vaccinated and unvaccinated 12–18-year-olds. First-dose-vaccinated (between 1 May and 30 September 2021) adolescents were sex and age matched 1:1 with unvaccinated adolescents. Outcomes were visits to emergency rooms, hospitalization, and visits to general practitioners and specialist practitioners. The prior event rate ratio (PERR) was applied. The study finds that boys had fewer visits to general practitioners (PERR 0.93, 95% confidence interval (CI) 0.89–0.99) after the first vaccine. Up to 56 days after the second dose, vaccinated boys had lower rates of visits to specialist practitioners (0.88, 95% CI 0.79–0.99); after 57–182 days, vaccinated girls and boys had higher rates of visits to emergency rooms (1.22, 95% CI 1.08–1.39; 1.17, 95% CI 1.07–1.31) and to general practitioners (1.17, 95% CI 1.12–1.21; 1.17, 95% CI 1.13–1.22). Furthermore, vaccinated boys had higher rates of visits to specialist practitioners (1.23, 95% CI 1.08–1.39). Estimates were close to one and do not indicate that BNT162b2 leads to a practically meaningful increase in healthcare use among vaccinated adolescents.

Science is crucial for evidence-based decision-making. Public trust in scientists can help decision makers act on the basis of the best available evidence, especially during crises. However, in recent years the epistemic authority of science has been challenged, causing concerns about low public trust in scientists. We interrogated these concerns with a preregistered 68-country survey of 71,922 respondents and found that in most countries, most people trust scientists and agree that scientists should engage more in society and policymaking. We found variations between and within countries, which we explain with individual- and country-level variables, including political orientation. While there is no widespread lack of trust in scientists, we cannot discount the concern that lack of trust in scientists by even a small minority may affect considerations of scientific evidence in policymaking. These findings have implications for scientists and policymakers seeking to maintain and increase trust in scientists.

Women in academia face a double bind. To be successful, they must embrace a highly competitive and individualistic work culture, and turn a blind eye to the systemic disparities that have historically disadvantaged them^1,2. Yet, at the same time, women academics are expected to pave the way for gender equality by actively helping other women to achieve their goals³.

The ‘queen bee phenomenon’ (QBP) describes the behaviour of some women in organizations dominated by men, who — rather than challenging the status quo — make deliberate efforts to fit in⁴. Although representation of women in academia has increased in the past decades, recent research shows that the QBP remains just as prevalent and visible as it was 15 years ago⁵. The persistence of the QBP is not surprising — academia remains a prime example of an organization in which men are the default. Women academics receive less recognition, support and resources (for example, research funding, salary and promotions)⁶. Moreover, behaviours associated with men and masculinity (for example, competition and self-promotion) are rewarded over behaviours associated with women and femininity (for example, teamwork and mentoring)⁷. Although all are expected to play by these masculine rules, women must also defy gender stereotypes that depict them as less competitive, driven and brilliant than men⁸ and demonstrate that they do not fit the stereotype — that, unlike other women, they have what it takes to be successful.

Correction to: Nature Human Behaviour https://doi.org/10.1038/s41562-024-02070-9, published online 23 December 2024.

The biology underlying the connection between social relationships and health is largely unknown. Here, leveraging data from 42,062 participants across 2,920 plasma proteins in the UK Biobank, we characterized the proteomic signatures of social isolation and loneliness through proteome-wide association study and protein co-expression network analysis. Proteins linked to these constructs were implicated in inflammation, antiviral responses and complement systems. More than half of these proteins were prospectively linked to cardiovascular disease, type 2 diabetes, stroke and mortality during a 14 year follow-up. Moreover, Mendelian randomization (MR) analysis suggested causal relationships from loneliness to five proteins, with two proteins (ADM and ASGR1) further supported by colocalization. These MR-identified proteins (GFRA1, ADM, FABP4, TNFRSF10A and ASGR1) exhibited broad associations with other blood biomarkers, as well as volumes in brain regions involved in interoception and emotional and social processes. Finally, the MR-identified proteins partly mediated the relationship between loneliness and cardiovascular diseases, stroke and mortality. The exploration of the peripheral physiology through which social relationships influence morbidity and mortality is timely and has potential implications for public health.

Genome-wide association studies (GWASs) have reported multiple risk loci for schizophrenia (SCZ). However, the majority of the associations were from populations of European ancestry. Here we conducted a large-scale GWAS in Eastern Asian populations (29,519 cases and 44,392 controls) and identified ten Eastern Asian-specific risk loci, two of which have not been previously reported. A further cross-ancestry GWAS meta-analysis (96,806 cases and 492,818 controls) including populations from diverse ancestries identified 61 previously unreported risk loci. Systematic variant-level analysis, including fine mapping, functional genomics and expression quantitative trait loci, prioritized potential causal variants. Gene-level analyses, including transcriptome-wide association study, proteome-wide association study and Mendelian randomization, nominated the potential causal genes. By integrating evidence from layers of different analyses, we prioritized the most plausible causal genes for SCZ, such as ACE, CNNM2, SNAP91, ABCB9 and GATAD2A. Finally, drug repurposing showed that ACE, CA14, MAPK3 and MAPT are potential therapeutic targets for SCZ. Our study not only showed the power of cross-ancestry GWAS in deciphering the genetic aetiology of SCZ, but also uncovered new genetic risk loci, potential causal variants and genes and therapeutic targets for SCZ.

Goal-directed behaviour requires humans to constantly manage and switch between multiple, independent and conflicting sources of information. Conventional cognitive control tasks, however, only feature one task and one source of distraction. Therefore, it is unclear how control is allocated in multidimensional environments. To address this question, we developed a multidimensional task-set interference paradigm, in which people need to manage distraction from three independent dimensions. We use this task to test whether people adapt to previous conflict by enhancing task-relevant information or suppressing task-irrelevant information. Three experiments provided strong evidence for the latter hypothesis. Moreover, control adaptation was highly dimension specific. Conflict from a given dimension only affected processing of that same dimension on subsequent trials, with no evidence for generalization. A new neural network model shows that our results can only be simulated when including multiple independent conflict-detector units. Our results call for an update to classic models of cognitive control and their neurocomputational underpinnings.