276 research outputs found

    Psychopathic traits influence amygdala-anterior cingulate cortex connectivity during facial emotion processing

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    There is accumulating evidence that youths with antisocial behavior or psychopathic traits show deficits in facial emotion recognition, but little is known about the neural mechanisms underlying these impairments. A number of neuroimaging studies have investigated brain activity during facial emotion processing in youths with Conduct Disorder (CD) and adults with psychopathy, but few of these studies tested for group differences in effective connectivity – i.e., changes in connectivity during emotion processing. Using functional magnetic resonance imaging and psycho-physiological interaction methods, we investigated the impact of CD and psychopathic traits on amygdala activity and effective connectivity in 46 male youths with CD and 25 typically-developing controls when processing emotional faces. All participants were aged 16-21 years. Relative to controls, youths with CD showed reduced amygdala activity when processing angry or sad faces relative to neutral faces, but the groups did not significantly differ in amygdala-related effective connectivity. In contrast, psychopathic traits were negatively correlated with amygdala-ventral anterior cingulate cortex connectivity for angry versus neutral faces, but were unrelated to amygdala responses to angry or sad faces. These findings suggest that CD and psychopathic traits have differential effects on amygdala activation and functional interactions between limbic regions during facial emotion processing

    Intact priors for gaze direction in adults with high-functioning autism spectrum conditions

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    This research was supported by the UK Medical Research Council under project code MC-A060-5PQ50 (Andrew J. Calder). IM was supported by a Leverhulme Trust Project Grant. CC was supported by an Australian Research Council Future Fellowship. SBC was supported by the MRC, the Wellcome Trust and the Autism Research Trust during the period of this work. The research was also supported by the National Institute for Health Research (NIHR) Collaboration for Leadership in Applied Health Research and Care East of England at Cambridgeshire and Peterborough NHS Foundation Trust

    A systematic review of oil tanker truck disasters: Identifying prevention targets

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    Introduction: Oil tanker truck disasters have been reported worldwide; however, the circumstances, causes, and health effects of these disasters have not been described. To address this gap, we performed a systematic review using PRISMA criteria to better understand this public health problem and identify prevention targets. Methods: The academic and lay literatures were systematically searched for terms related to oil tanker truck disasters. Reports about civilian oil tanker truck disasters that occurred from 1997–2017 were included. Details about the disasters were summarized, including circumstances, identifiable causes, and health effects. Results: The search yielded 4713 Nexis Uni articles, 199 Google results, and one PubMed article; 951 records met inclusion criteria, describing 224 oil tanker truck explosions or fires. At least 2909 people died as a result of these disasters, and 3038 additional people were hospitalized. Almost all deaths (94%) occurred in low- and low-middle-income countries (LMIC). This may largely be due to scooping – the practice of collecting spilled oil from disabled tanker trucks for use or resale. Using the Haddon matrix, potential targets for future disaster prevention were identified. Conclusions: These data highlight the circumstances, causes, and health burden related to oil tanker truck disasters. Most began as collisions or rollovers, but nearly half of the fatalities involved scooping. The findings suggest opportunities to promote road safety, improve scene safety and security protocols used by drivers and first responders, and promote public understanding of the dangers of scooping to prevent mass casualty disasters from disabled tanker trucks, particularly in LMIC

    Forum: Parental education and child mortality

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    A Two-Gene Balance Regulates Salmonella Typhimurium Tolerance in the Nematode Caenorhabditis elegans

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    Lysozymes are antimicrobial enzymes that perform a critical role in resisting infection in a wide-range of eukaryotes. However, using the nematode Caenorhabditis elegans as a model host we now demonstrate that deletion of the protist type lysozyme LYS-7 renders animals susceptible to killing by the fatal fungal human pathogen Cryptococcus neoformans, but, remarkably, enhances tolerance to the enteric bacteria Salmonella Typhimurium. This trade-off in immunological susceptibility in C. elegans is further mediated by the reciprocal activity of lys-7 and the tyrosine kinase abl-1. Together this implies a greater complexity in C. elegans innate immune function than previously thought

    Adapting effects of emotional expression in anxiety: evidence for an enhanced late positive potential

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    An adaptation paradigm was used to investigate the influence of a previously experienced visual context on the interpretation of ambiguous emotional expressions. Affective classification of fear-neutral ambiguous expressions was performed following repeated exposure to either fearful or neutral faces. There was a shift in the behavioural classification of morphs towards ‘fear’ following adaptation to neutral compared to adaptation to fear with a non-significant trend towards the high anxiety group compared to the low being more influenced by the context. The event-related potential (ERP) data revealed a more pronounced late positive potential (LPP), beginning at ~400 ms post-stimulus onset, in the high but not the low anxiety group following adaptation to neutral compared to fear. In addition, as the size of the behavioural adaptation increased there was a linear increase in the magnitude of the late-LPP. However, context-sensitivity effects are not restricted to trait anxiety, with similar effects observed with state anxiety and depression. These data support the proposal that negative moods are associated with increased sensitivity to visual contextual influences from top-down elaborative modulations, as reflected in an enhanced late positive potential deflection

    Separated and overlapping neural coding of face and body identity

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    Recognising a person's identity often relies on face and body information, and is tolerant to changes in low-level visual input (e.g., viewpoint changes). Previous studies have suggested that face identity is disentangled from low-level visual input in the anterior face-responsive regions. It remains unclear which regions disentangle body identity from variations in viewpoint, and whether face and body identity are encoded separately or combined into a coherent person identity representation. We trained participants to recognise three identities, and then recorded their brain activity using fMRI while they viewed face and body images of these three identities from different viewpoints. Participants' task was to respond to either the stimulus identity or viewpoint. We found consistent decoding of body identity across viewpoint in the fusiform body area, right anterior temporal cortex, middle frontal gyrus and right insula. This finding demonstrates a similar function of fusiform and anterior temporal cortex for bodies as has previously been shown for faces, suggesting these regions may play a general role in extracting high-level identity information. Moreover, we could decode identity across fMRI activity evoked by faces and bodies in the early visual cortex, right inferior occipital cortex, right parahippocampal cortex and right superior parietal cortex, revealing a distributed network that encodes person identity abstractly. Lastly, identity decoding was consistently better when participants attended to identity, indicating that attention to identity enhances its neural representation. These results offer new insights into how the brain develops an abstract neural coding of person identity, shared by faces and bodies

    Genome-Wide Gene Expression Analysis in Response to Organophosphorus Pesticide Chlorpyrifos and Diazinon in C. elegans

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    Organophosphorus pesticides (OPs) were originally designed to affect the nervous system by inhibiting the enzyme acetylcholinesterase, an important regulator of the neurotransmitter acetylcholine. Over the past years evidence is mounting that these compounds affect many other processes. Little is known, however, about gene expression responses against OPs in the nematode Caenorhabditis elegans. This is surprising because C. elegans is extensively used as a model species in toxicity studies. To address this question we performed a microarray study in C. elegans which was exposed for 72 hrs to two widely used Ops, chlorpyrifos and diazinon, and a low dose mixture of these two compounds. Our analysis revealed transcriptional responses related to detoxification, stress, innate immunity, and transport and metabolism of lipids in all treatments. We found that for both compounds as well as in the mixture, these processes were regulated by different gene transcripts. Our results illustrate intense, and unexpected crosstalk between gene pathways in response to chlorpyrifos and diazinon in C. elegans

    Caenorhabditis elegans Semi-Automated Liquid Screen Reveals a Specialized Role for the Chemotaxis Gene cheB2 in Pseudomonas aeruginosa Virulence

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    Pseudomonas aeruginosa is an opportunistic human pathogen that causes infections in a variety of animal and plant hosts. Caenorhabditis elegans is a simple model with which one can identify bacterial virulence genes. Previous studies with C. elegans have shown that depending on the growth medium, P. aeruginosa provokes different pathologies: slow or fast killing, lethal paralysis and red death. In this study, we developed a high-throughput semi-automated liquid-based assay such that an entire genome can readily be scanned for virulence genes in a short time period. We screened a 2,200-member STM mutant library generated in a cystic fibrosis airway P. aeruginosa isolate, TBCF10839. Twelve mutants were isolated each showing at least 70% attenuation in C. elegans killing. The selected mutants had insertions in regulatory genes, such as a histidine kinase sensor of two-component systems and a member of the AraC family, or in genes involved in adherence or chemotaxis. One mutant had an insertion in a cheB gene homologue, encoding a methylesterase involved in chemotaxis (CheB2). The cheB2 mutant was tested in a murine lung infection model and found to have a highly attenuated virulence. The cheB2 gene is part of the chemotactic gene cluster II, which was shown to be required for an optimal mobility in vitro. In P. aeruginosa, the main player in chemotaxis and mobility is the chemotactic gene cluster I, including cheB1. We show that, in contrast to the cheB2 mutant, a cheB1 mutant is not attenuated for virulence in C. elegans whereas in vitro motility and chemotaxis are severely impaired. We conclude that the virulence defect of the cheB2 mutant is not linked with a global motility defect but that instead the cheB2 gene is involved in a specific chemotactic response, which takes place during infection and is required for P. aeruginosa pathogenicity

    A Genome-Wide Collection of Mos1 Transposon Insertion Mutants for the C. elegans Research Community

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    Methods that use homologous recombination to engineer the genome of C. elegans commonly use strains carrying specific insertions of the heterologous transposon Mos1. A large collection of known Mos1 insertion alleles would therefore be of general interest to the C. elegans research community. We describe here the optimization of a semi-automated methodology for the construction of a substantial collection of Mos1 insertion mutant strains. At peak production, more than 5,000 strains were generated per month. These strains were then subject to molecular analysis, and more than 13,300 Mos1 insertions characterized. In addition to targeting directly more than 4,700 genes, these alleles represent the potential starting point for the engineered deletion of essentially all C. elegans genes and the modification of more than 40% of them. This collection of mutants, generated under the auspices of the European NEMAGENETAG consortium, is publicly available and represents an important research resource
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