306 research outputs found

    Correcting fake news headlines after repeated exposure: memory and belief accuracy in younger and older adults

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    The efficacy of fake news corrections in improving memory and belief accuracy may depend on how often adults see false information before it is corrected. Two experiments tested the competing predictions that repeating fake news before corrections will either impair or improve memory and belief accuracy. These experiments also examined whether fake news exposure effects would differ for younger and older adults due to age-related differences in the recollection of contextual details. Younger and older adults read real and fake news headlines that appeared once or thrice. Next, they identified fake news corrections among real news headlines. Later, recognition and cued recall tests assessed memory for real news, fake news, if corrections occurred, and beliefs in retrieved details. Repeating fake news increased detection and remembering of corrections, correct real news retrieval, and erroneous fake news retrieval. No age differences emerged for detection of corrections, but younger adults remembered corrections better than older adults. At test, correct fake news retrieval for earlier-detected corrections was associated with better real news retrieval. This benefit did not differ between age groups in recognition but was greater for younger than older adults in cued recall. When detected corrections were not remembered at test, repeated fake news increased memory errors. Overall, both age groups believed correctly retrieved real news more than erroneously retrieved fake news to a similar degree. These findings suggest that fake news repetition effects on subsequent memory accuracy depended on age differences in recollection-based retrieval of fake news and that it was corrected

    High levels of contact dermatitis and decreased mobility in broiler breeders, but neither have a relationship with floor eggs

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    Contact dermatitis, both on the foot pads and hocks, is a well-known health issue in broilers. Less is known about contact dermatitis in broiler breeders, however, although they have many risk factors for developing leg health problems in common with broilers. This study aimed to describe the prevalence and severity of contact dermatitis during the production cycle in 5 lines of broiler breeders, investigate possible causes of contact dermatitis, and study its relationship with gait, egg production, and floor egg percentage. Five commercially available genetic lines of broiler breeders were housed in 21 pens of 550 females and 50 males from 20 to 60 wk of age. Every 10 wk litter quality, leg health measurements (foot pad dermatitis, hock burn, and gait) and body weight were assessed of 50 random hens per pen. Total number of eggs, number of eggs laid outside the nest (floor eggs), and mortality were recorded daily per pen. Prevalence of foot pad dermatitis, hock burn, and gait problems increased with age. Litter quality started to decrease at 50 wk of age. Prevalence of foot pad dermatitis was affected by litter quality, whereas genetic line had little effect. One genetic line was more prone to developing hock burns, though generally the prevalence of hock burn (13%) was much lower than that of foot pad dermatitis (74%). The percentage of broiler breeders with gait problems increased up to 24% with age, but this was not related to the prevalence of contact dermatitis. The lines differed in body weight from 32 wk of age onwards, and a higher body weight was related to lower egg production and higher cumulative mortality. The percentage of floor eggs was not related to leg health parameters or genetic line. Broiler breeders thus have similar leg health problems as broilers, but these problems are not related to the percentage of floor eggs, suggesting that other factors are involved in the undesirable behavior of floor laying.</p

    Changes in social groups across reintroductions and effects on post-release survival

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    Reintroductions, essential to many conservation programmes, disrupt both abiotic and social environments. Despite growing recognition that social connections in animals might alter survival (e.g. social transmission of foraging skills, or transmission of disease), there has thus far been little focus on the consequences of social disruption during reintroductions. Here we investigate if moving familiar social groups may help a threatened species to adjust to its new environment and increase post-release survival. For a reintroduction of 40 juvenile hihi Notiomystis cincta (a threatened New Zealand passerine), we observed social groups before and after translocation to a new site and used social network analysis to study three levels of social change: overall group structure, network associations and individual sociality. We also tested alternate translocation strategies where birds were kept temporarily in aviaries in either a familiar group, or where their prior association was mixed. Although social structure remained similar among juveniles that remained at the source site, we detected significant changes in translocated birds at both the group- and individual- level post-release. However, our holding treatments did not affect these social bonds so we remain unable to maintain or manipulate social groups during translocation. Crucially, there was a small tendency for translocated juveniles that gained more associates during re-assortment of social groups to be more likely to survive their first year post-release. We suggest that prior sociality may not be important during translocations, but rather individuals that are most able to adapt and form associations at a new site are most likely to be the surviving founders of reintroduced populations.Peer reviewe

    Changes in synaptic transmission and protein expression in the brains of adult offspring after prenatal inhibition of the kynurenine pathway

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    During early brain development, N-methyl-d-aspartate (NMDA) receptors are involved in cell migration, neuritogenesis, axon guidance and synapse formation, but the mechanisms which regulate NMDA receptor density and function remain unclear. The kynurenine pathway of tryptophan metabolism includes an agonist (quinolinic acid) and an antagonist (kynurenic acid) at NMDA receptors and we have previously shown that inhibition of the pathway using the kynurenine-3-monoxygenase inhibitor Ro61-8048 in late gestation produces rapid changes in protein expression in the embryos and effects on synaptic transmission lasting until postnatal day 21 (P21). The present study sought to determine whether any of these effects are maintained into adulthood. After prenatal injections of Ro61-8048 the litter was allowed to develop to P60 when some offspring were euthanized and the brains removed for examination. Analysis of protein expression by Western blotting revealed significantly reduced expression of the GluN2A subunit (32%) and the morphogenetic protein sonic hedgehog (31%), with a 29% increase in the expression of doublecortin, a protein associated with neurogenesis. No changes were seen in mRNA abundance using quantitative real-time polymerase chain reaction. Neuronal excitability was normal in the CA1 region of hippocampal slices but paired-pulse stimulation revealed less inhibition at short interpulse intervals. The amount of long-term potentiation was decreased by 49% in treated pups and recovery after low-frequency stimulation was delayed. The results not only strengthen the view that basal, constitutive kynurenine metabolism is involved in normal brain development, but also show that changes induced prenatally can affect the brains of adult offspring and those changes are quite different from those seen previously at weaning (P21). Those changes may be mediated by altered expression of NMDAR subunits and sonic hedgehog

    An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

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    For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

    CSF1R inhibitor JNJ-40346527 attenuates microglial proliferation and neurodegeneration in P301S mice

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    Neuroinflammation and microglial activation are significant processes in Alzheimer's disease pathology. Recent genome-wide association studies have highlighted multiple immune-related genes in association with Alzheimer's disease, and experimental data have demonstrated microglial proliferation as a significant component of the neuropathology. In this study, we tested the efficacy of the selective CSF1R inhibitor JNJ-40346527 (JNJ-527) in the P301S mouse tauopathy model. We first demonstrated the anti-proliferative effects of JNJ-527 on microglia in the ME7 prion model, and its impact on the inflammatory profile, and provided potential CNS biomarkers for clinical investigation with the compound, including pharmacokinetic/pharmacodynamics and efficacy assessment by TSPO autoradiography and CSF proteomics. Then, we showed for the first time that blockade of microglial proliferation and modification of microglial phenotype leads to an attenuation of tau-induced neurodegeneration and results in functional improvement in P301S mice. Overall, this work strongly supports the potential for inhibition of CSF1R as a target for the treatment of Alzheimer's disease and other tau-mediated neurodegenerative diseases

    Inflammatory biomarkers in Alzheimer&apos;s disease plasma

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    Introduction: Plasma biomarkers for Alzheimer's disease (AD) diagnosis/stratification are a \u201cHoly Grail\u201d of AD research and intensively sought; however, there are no well-established plasma markers. Methods: A hypothesis-led plasma biomarker search was conducted in the context of international multicenter studies. The discovery phase measured 53 inflammatory proteins in elderly control (CTL; 259), mild cognitive impairment (MCI; 199), and AD (262) subjects from AddNeuroMed. Results: Ten analytes showed significant intergroup differences. Logistic regression identified five (FB, FH, sCR1, MCP-1, eotaxin-1) that, age/APO\u3b54 adjusted, optimally differentiated AD and CTL (AUC: 0.79), and three (sCR1, MCP-1, eotaxin-1) that optimally differentiated AD and MCI (AUC: 0.74). These models replicated in an independent cohort (EMIF; AUC 0.81 and 0.67). Two analytes (FB, FH) plus age predicted MCI progression to AD (AUC: 0.71). Discussion: Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. Further replication is needed before clinical translation

    Meta-analysis of Genome-Wide Association Studies for Extraversion: Findings from the Genetics of Personality Consortium

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    Extraversion is a relatively stable and heritable personality trait associated with numerous psychosocial, lifestyle and health outcomes. Despite its substantial heritability, no genetic variants have been detected in previous genome-wide association (GWA) studies, which may be due to relatively small sample sizes of those studies. Here, we report on a large meta-analysis of GWA studies for extraversion in 63,030 subjects in 29 cohorts. Extraversion item data from multiple personality inventories were harmonized across inventories and cohorts. No genome-wide significant associations were found at the single nucleotide polymorphism (SNP) level but there was one significant hit at the gene level for a long non-coding RNA site (LOC101928162). Genome-wide complex trait analysis in two large cohorts showed that the additive variance explained by common SNPs was not significantly different from zero, but polygenic risk scores, weighted using linkage information, significantly predicted extraversion scores in an independent cohort. These results show that extraversion is a highly polygenic personality trait, with an architecture possibly different from other complex human traits, including other personality traits. Future studies are required to further determine which genetic variants, by what modes of gene action, constitute the heritable nature of extraversion
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