569 research outputs found

    Locating and mitigating risks to children associated with major sporting events

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    Despite recent efforts to blend sport and human rights, activism for children's rights in sport has historically been marginalised. The positive 'social legacy' of sport events frequently masks more problematic issues, including child exploitation. We argue that harms to children in hosting communities of major sporting events (MSEs) should be a focus for both research and intervention since the plight of such children is currently a political blind spot. The article examines the evidence for four major sources of risk for children associated with such events: child labour, displacement resulting from forced evictions for infrastructure development and street clearance, child sexual exploitation, and human trafficking affecting children. The weakness of the resulting evidence is explained in relation to the methodological and ethical difficulties of conducting research on such hidden and marginal populations and to the fact that risks to children are often masked by adult social problems. It is argued that much more robust research designs, focused specifically on children, are essential in order to verify the many assertions made about risks to children associated with MSEs. Some mitigating interventions are briefly examined and an action plan for risk-mitigation work at future MSEs is proposed. Finally, drawing on wider debates about Centres and Peripheries in social and economic theory, we question whether major international sport organisations might choose to engage with projects like child protection for strategic rather than humanitarian reasons, using them as a kind of ethical fig leaf in order to bolster their power bases against threats from the margins. © 2014 © 2014 Taylor & Francis.The Oak Foundation under Grant code OCAY-13-052

    Making a national atlas of population by computer

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    This paper describes the conceptual and practical problems encountered and solved in producing a multi-colour atlas of population characteristics in Great Britain. The atlas itself is in A4 format; it consists of some thirty-four maps of Great Britain in four colours and the same number of regional maps, together with descriptive text. All maps were plotted on a laser plotter with a resolution of 127 microns. The paper describes how mapping of ratios, such as percentages, was found to be highly misleading and describes the novel probability mapping solution adopted, based on the signed chi-square statistic. In addition, the rationale for selecting the class intervals and for selecting colour schemes is described

    Local lung responses following endobronchial elastase and lipopolysaccharide instillation in sheep

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    Chronic lipopolysaccharide (LPS) exposure may contribute to the pathogenesis of a number of lung diseases including COPD and emphysema. We sought to develop a large- animal model of emphysema using repeated LPS administration into sheep lung segments. An experimental protocol was designed to facilitate comparisons with elastase-treated and control segments within the same lung of individual sheep. Histopathologic evaluation of segments treated with LPS demonstrated low-grade inflammation characterized by an increase in the number of intra-alveolar macrophages and lymphocytes. Treated segments demonstrated a significant reduction in airspace surface area (ASA), an increase in percent disrupted alveolar attachments and the distance between normal alveolar attachments, and a reduction in the number of normal alveolar attachments surrounding nonrespiratory bronchioles. Coefficient of variation of individual ASA measurements in elastase-treated segments was indicative of a heterogeneous parenchymal response, in contrast to that associated with chronic LPS treatment. Our results demonstrate that chronic LPS treatment of individual lung segments in sheep induces microscopic emphysema qualitatively and quantitatively consistent with both accepted pathologic definitions of this condition and with that produced by airway instillation of elastolytic enzymes. Development of this phenotype is associated with evidence of downregulated activation of transforming growth factor beta
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