http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Wind pressure coefficients on low-rise structures and codification
Letchford, Chris,Holmes, J.D.,Hoxey, Roger,Robertson, Adam Techno-Press 2005 Wind and Structures, An International Journal (WAS Vol.8 No.4
This paper describes the work of the Working Group on wind pressure coefficients on low-rise structures, one of the groups set up by the International Association of Wind Engineering in 1999. General aspects of wind loading on low-rise structures are summarized. The definition, derivation and codification of loading coefficients is described. Comparisons of pressure coefficients on low rise structures are made between a selection of wind loading standards. Recommendations for consistency and for the harmonization of these coefficients are given.
Horikoshi, Momoko,Pasquali, Lorenzo,Wiltshire, Steven,Huyghe, Jeroen R.,Mahajan, Anubha,Asimit, Jennifer L.,Ferreira, Teresa,Locke, Adam E.,Robertson, Neil R.,Wang, Xu,Sim, Xueling,Fujita, Hayato,Hara IRL Press 2016 Human molecular genetics Vol.25 No.10
<P>To gain insight into potential regulatory mechanisms through which the effects of variants at four established type 2 diabetes (T2D) susceptibility loci (<I>CDKAL1</I>, <I>CDKN2A-B</I>, <I>IGF2BP2</I> and <I>KCNQ1</I>) are mediated, we undertook transancestral fine-mapping in 22 086 cases and 42 539 controls of East Asian, European, South Asian, African American and Mexican American descent. Through high-density imputation and conditional analyses, we identified seven distinct association signals at these four loci, each with allelic effects on T2D susceptibility that were homogenous across ancestry groups. By leveraging differences in the structure of linkage disequilibrium between diverse populations, and increased sample size, we localised the variants most likely to drive each distinct association signal. We demonstrated that integration of these genetic fine-mapping data with genomic annotation can highlight potential causal regulatory elements in T2D-relevant tissues. These analyses provide insight into the mechanisms through which T2D association signals are mediated, and suggest future routes to understanding the biology of specific disease susceptibility loci.</P>