46 research outputs found

    Expose Yourself to Art : Towards a Critical Epistemology of Embarrassment

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    This thesis investigates the negative affect of ‘spectatorial embarrassment’, a feeling of exposure and discomfort sometimes experienced when looking at art. Two particular characteristics of embarrassment figure in the methodology and the outcome of this enquiry; firstly that embarrassment is marginal, of little orthodox value, and secondly, it is a personal experience of aversive self-consciousness. The experiential nature of embarrassment has been adopted throughout as a methodology and the embarrassments analysed are, for the most part, my own and based on ‘true’ experience. Precedent for this is drawn from ‘anecdotal theory’, which uses event and occasion in the origination of a counter-theory that values minor narratives of personal experience in place of the generalising and abstract tendencies of theory-proper. The context is a series of encounters with artworks by Gilbert & George, Jemima Stehli, Franko B, Adrian Howells, and Sarah Lucas. They are connected by their contemporaneity, their ‘British-ness’, and that they allow the spectator no comfortable position to look from. This enquiry engages with theories of ‘the gaze’ (as both aesthetic disinterest and a dubious sign of cultural competence) and the challenge to aesthetic disinterest made by ‘transgressive art’ which may provoke a more engaged, even embodied response. Each encounter sparks consideration of differing causes and outcomes of embarrassment that resonate beyond art to broader sociocultural territories particularly in terms of gender and class. The approach taken is inherently interdisciplinary, situated within the affective turn, and engaging with feminist and queer discourses. Moments of embarrassment as ‘thinking-feeling’ are finally configured as a critical epistemology, or a ‘body of knowledge’ offering the opportunity to value the singular truth of embarrassment as an embodied criticality that is critical of coercive patterns of social ‘okayness’ and belonging

    3D morphometry of De Geer Moraines and Crevasse-Squeeze Ridges: Differentiating between pushing and squeezing mechanisms from remotely sensed data

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    De Geer Moraines (DGM) and Crevasse-Squeeze Ridges (CSR) are important landforms that can provide useful insights regarding palaeo-glacial processes. Specifically, these landforms can provide information concerning ice-marginal dynamics, and/or subglacial processes, depending on the context in which they are formed. The extraction of 3D morphometric data from these ridges can help to elucidate their formational processes, and potentially enable landform differentiation. We develop a new Python-based ArcGIS toolbox that can automatically extract 3D morphometric data from large sample sets of linear features. The morphometry toolbox may be applied to a wide range of research disciplines that are concerned with quantifying the morphometry of any elongated landforms. This is particularly useful for DGM and CSR studies, where visual similarities can result in confusion over landform type and/or formation. Here we present a case study from southwest Finland and the Northwest Territories, Canada, whereby high-resolution 3D morphometric data is used to analyse and classify DGMs and CSRs. The results reveal key differences in morphometric properties between the landforms which enables a quantified foundation by which to differentiate them. The studied CSRs are found to be higher, wider, steeper, more symmetrical, less sinuous and more voluminous than the studied prominent DGM. In contrast, a tendency for cross-sectional asymmetry in DGM supports an origin by ice-marginal pushing, rather than basal squeeze-up into crevasses. This is further supported by CSRs being less sinuous than DGM due to them being constrained to the dimensions and planform of the (relatively straight) host crevasses, whereas DGM follow a more sinuous path related to the ice margin shape. Future work should include sedimentological and geophysical studies to constrain DGM internal architecture and formation processes. The results may then be used to validate the application of DGM for detailed ice marginal reconstructions

    Exploring face perception in disorders of development: evidence from Williams syndrome and autism

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    Individuals with Williams syndrome (WS) and autism are characterized by different social phenotypes but have been said to show similar atypicalities of face-processing style. Although the structural encoding of faces may be similarly atypical in these two developmental disorders, there are clear differences in overall face skills. The inclusion of both populations in the same study can address how the profile of face skills varies across disorders. The current paper explored the processing of identity, eye-gaze, lip-reading, and expressions of emotion using the same participants across face domains. The tasks had previously been used to make claims of a modular structure to face perception in typical development. Participants with WS (N=15) and autism (N=20) could be dissociated from each other, and from individuals with general developmental delay, in the domains of eye-gaze and expression processing. Individuals with WS were stronger at these skills than individuals with autism. Even if the structural encoding of faces appears similarly atypical in these groups, the overall profile of face skills, as well as the underlying architecture of face perception, varies greatly. The research provides insights into typical and atypical models of face perception in WS and autism

    The interplay between structure and agency in shaping the mental health consequences of job loss

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    Main themes that emerged from the qualitative exploration of the psychological distress of job loss included stress, changes to perceived control, loss of self-esteem, shame and loss of status, experiencing a grieving process, and financial strain. Drawing on two models of agency we identified the different ways workers employed their agency, and how their agency was enabled, but mainly constrained, when dealing with job loss consequences. Respondents’ accounts support the literature on the moderating effects of economic resources such as redundancy packages. The results suggest the need for policies to put more focus on social, emotional and financial investment to mediate the structural constraints of job loss. Our study also suggests that human agency must be understood within an individual’s whole of life circumstances, including structural and material constraints, and the personal or interior factors that shape these circumstances.The authors acknowledge support from the National Health and Medical Research Council Capacity Building Grant (324724). The research was supported by the SA Department of Health and the SA Department of Families and Communities through the Human Services Research and Innovation Program (HSRIP), and the Australian Research Council Linkage Program (LP0562288), with the Department of Health (DOH) serving as Industry Partner. Professor Fran Baum was supported by an ARC Federation Fellowship and Drs Newman and Ziersch by the SA Premier’s Science and Research Fund

    Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

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    Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

    Analysis of shared heritability in common disorders of the brain

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    ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

    Repeated nebulisation of non-viral CFTR gene therapy in patients with cystic fibrosis:a randomised, double-blind, placebo-controlled, phase 2b trial

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    Background: Lung delivery of plasmid DNA encoding the CFTR gene complexed with a cationic liposome is a potential treatment option for patients with cystic fibrosis. We aimed to assess the efficacy of non-viral CFTR gene therapy in patients with cystic fibrosis. Methods: We did this randomised, double-blind, placebo-controlled, phase 2b trial in two cystic fibrosis centres with patients recruited from 18 sites in the UK. Patients (aged ≥12 years) with a forced expiratory volume in 1 s (FEV1) of 50–90% predicted and any combination of CFTR mutations, were randomly assigned, via a computer-based randomisation system, to receive 5 mL of either nebulised pGM169/GL67A gene–liposome complex or 0·9% saline (placebo) every 28 days (plus or minus 5 days) for 1 year. Randomisation was stratified by % predicted FEV1 (<70 vs ≥70%), age (<18 vs ≥18 years), inclusion in the mechanistic substudy, and dosing site (London or Edinburgh). Participants and investigators were masked to treatment allocation. The primary endpoint was the relative change in % predicted FEV1. The primary analysis was per protocol. This trial is registered with ClinicalTrials.gov, number NCT01621867. Findings: Between June 12, 2012, and June 24, 2013, we randomly assigned 140 patients to receive placebo (n=62) or pGM169/GL67A (n=78), of whom 116 (83%) patients comprised the per-protocol population. We noted a significant, albeit modest, treatment effect in the pGM169/GL67A group versus placebo at 12 months' follow-up (3·7%, 95% CI 0·1–7·3; p=0·046). This outcome was associated with a stabilisation of lung function in the pGM169/GL67A group compared with a decline in the placebo group. We recorded no significant difference in treatment-attributable adverse events between groups. Interpretation: Monthly application of the pGM169/GL67A gene therapy formulation was associated with a significant, albeit modest, benefit in FEV1 compared with placebo at 1 year, indicating a stabilisation of lung function in the treatment group. Further improvements in efficacy and consistency of response to the current formulation are needed before gene therapy is suitable for clinical care; however, our findings should also encourage the rapid introduction of more potent gene transfer vectors into early phase trials
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