25 resultados para Sander, Nicholas, 1530?-1581.

em QUB Research Portal - Research Directory and Institutional Repository for Queen's University Belfast


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This article offers a reconsideration of planning and development in
English towns and cities after the Black Death (1348). Conventional historical
accounts have stressed the occurrence of urban ‘decay’ in the later fourteenth and fifteenth centuries. Here, instead, a case is made that after 1350 urban planning continued to influence towns and cities in England through the transformation of their townscapes. Using the conceptual approaches of urban morphologists in particular, the article demonstrates that not only did the foundation of new towns and creation of new suburbs characterize the period 1350–1530, but so too did the redevelopment of existing urban landscapes through civic improvements and public works. These reveal evidence for the particular ‘agents of change’ involved in the planning and development process, such as surveyors, officials, patrons and architects, and also the role played by maps and drawn surveys. In this reappraisal, England’s urban experiences can be seen to have been closely connected with those instances of urban planning after the Black Death occurring elsewhere in contemporary continental Europe.

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Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated 1/42,000, 1/43,700 and 1/49,500 SNPs explained 1/421%, 1/424% and 1/429% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/I 2-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.

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Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10(-8)), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

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