384 research outputs found

    Rational Fictions and Imaginary Systems: Cynical Ideology and the Problem Figuration and Practise of Public Housing

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    This paper aims to show how Van Wel's theory of problem figuration, Carlen's concept of imaginary systems and Zizek's notion of cynical ideology may advance our theoretical and empirical understanding of the contemporary construction of housing policy narratives and embedded localised housing practise. Applying this theoretical framework to a case study of responses to homelessness in Scotland and further illustrative examples from the UK and the USA, the paper examines how housing practise is constituted through different imaginaries of housing systems. These are based on fictional as well as rational elements, located within a form of cynical ideology whereby actors act ‘as if’ the realities of the present housing crisis are distanced from the imagined intended functioning of housing systems. This masks alternative social realities and denies an explicitly articulated politics of housing which would reveal new processes of capitalism, generational and class realignments and a reframing of the role of government itself

    How accurate is patients' anatomical knowledge: a cross-sectional, questionnaire study of six patient groups and a general public sample

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    <p>Abstract</p> <p>Background</p> <p>Older studies have shown that patients often do not understand the terms used by doctors and many do not even have a rudimentary understanding of anatomy. The present study was designed to investigate the levels of anatomical knowledge of different patient groups and the general public in order to see whether this has improved over time and whether patients with a specific organ pathology (e.g. liver disease) have a relatively better understanding of the location of that organ.</p> <p>Methods</p> <p>Level of anatomical knowledge was assessed on a multiple-choice questionnaire, in a sample of 722 participants, comprising approximately 100 patients in each of 6 different diagnostic groups and 133 in the general population, using a between-groups, cross-sectional design. Comparisons of relative accuracy of anatomical knowledge between the present and earlier results, and across the clinical and general public groups were evaluated using Chi square tests. Associations with age and education were assessed with the Pearson correlation test and one-way analysis of variance, respectively.</p> <p>Results</p> <p>Across groups knowledge of the location of body organs was poor and has not significantly improved since an earlier equivalent study over 30 years ago (χ<sup>2 </sup>= 0.04, df = 1, ns). Diagnostic groups did not differ in their overall scores but those with liver disease and diabetes were more accurate regarding the location of their respective affected organs (χ<sup>2 </sup>= 18.10, p < 0.001, df = 1; χ<sup>2 </sup>= 10.75, p < 0.01, df = 1). Age was significantly negatively correlated (r = -0.084, p = 0.025) and education was positively correlated with anatomical knowledge (F = 12.94, p = 0.000). Although there was no overall gender difference, women were significantly better at identifying organs on female body outlines.</p> <p>Conclusion</p> <p>Many patients and general public do not know the location of key body organs, even those in which their medical problem is located, which could have important consequences for doctor-patient communication. These results indicate that healthcare professionals still need to take care in providing organ specific information to patients and should not assume that patients have this information, even for those organs in which their medical problem is located.</p

    Hundreds of variants clustered in genomic loci and biological pathways affect human height

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    Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

    New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

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    Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes
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