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21.
Common variation in three genes, including a noncoding variant in CFH, strongly influences risk of age-related macular degeneration 总被引:12,自引:0,他引:12
Maller J George S Purcell S Fagerness J Altshuler D Daly MJ Seddon JM 《Nature genetics》2006,38(9):1055-1059
Age-related macular degeneration (AMD) is a common, late-onset disease with seemingly typical complexity: recurrence ratios for siblings of an affected individual are three- to sixfold higher than in the general population, and family-based analysis has resulted in only modestly significant evidence for linkage. In a case-control study drawn from a US-based population of European descent, we have identified a previously unrecognized common, noncoding variant in CFH, the gene encoding complement factor H, that substantially increases the influence of this locus on AMD, and we have strongly replicated the associations of four other previously reported common alleles in three genes (P values ranging from 10(-6) to 10(-70)). Despite excellent power to detect epistasis, we observed purely additive accumulation of risk from alleles at these genes. We found no differences in association of these loci with major phenotypic categories of advanced AMD. Genotypes at these five common SNPs define a broad spectrum of interindividual disease risk and explain about half of the classical sibling risk of AMD in our study population. 相似文献
22.
裂纹在面内剪切荷载作用下,宏观应力场呈反对称分布,微观应力场将不再具有反对称性,可能是面内拉伸与面内剪切的混合型分布.另外,考虑微观裂纹前还有一个刃型位错区,据此建立起一个多尺度嵌套的裂纹模型,可以描述从原子尺度下的刃型位错区过渡到Ⅰ、Ⅱ复合型微观裂纹,再过渡到Ⅱ型宏观裂纹.材料不同尺度下的损伤,通过约束过渡区相连接,引入尺度变换因子的概念,并利用位移连续性条件与应力场匹配条件,求解出多尺度耦合问题的闭合形式的解.通过数值计算,讨论了材料宏观力学性能对不同尺度下各影响因素的的敏感性.研究结果表明,材料破坏机理非常复杂,与作用荷载、不同尺度下缺陷的几何形状、尺寸及材料性能等因素相关. 相似文献
23.
粒子物理学家倾向于把自然界视为具体化的数学 ;而固体物理学家则认为 ,从超导体和超流体等奇异形态到晶体和金属等常见形态 ,物质的许多形式都不能用基本粒子的相互作用来描述 相似文献
24.
L Feliubadaló M Font J Purroy F Rousaud X Estivill V Nunes E Golomb M Centola I Aksentijevich Y Kreiss B Goldman M Pras D L Kastner E Pras P Gasparini L Bisceglia E Beccia M Gallucci L de Sanctis A Ponzone G F Rizzoni L Zelante M T Bassi A L George M Manzoni A De Grandi M Riboni J K Endsley A Ballabio G Borsani N Reig E Fernández R Estévez M Pineda D Torrents M Camps J Lloberas A Zorzano M Palacín 《Nature genetics》1999,23(1):52-57
25.
设R是一个环,G是一个有限群,本文定义了一个R上带因子组f的投射群环RG_f,证明了如果RG_f是R的Galois扩张带由G导出的内Galois群G,使得R的中心C是R的C-直和项,则CG_f是C上中心Galois代数;还将F.R.DeMeyer关于Azumaya投射群代数的刻划推广到投射群环RG_f。 相似文献
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Worobey M Santiago ML Keele BF Ndjango JB Joy JB Labama BL Dhed'A BD Rambaut A Sharp PM Shaw GM Hahn BH 《Nature》2004,428(6985):820
Despite strong evidence to the contrary, speculation continues that the AIDS virus, human immunodeficiency virus type 1 (HIV-1), may have crossed into humans as a result of contamination of the oral polio vaccine (OPV). This 'OPV/AIDS theory' claims that chimpanzees from the vicinity of Stanleyville--now Kisangani in the Democratic Republic of Congo--were the source of a simian immunodeficiency virus (SIVcpz) that was transmitted to humans when chimpanzee tissues were allegedly used in the preparation of OPV. Here we show that SIVcpz is indeed endemic in wild chimpanzees of this region but that the circulating virus is phylogenetically distinct from all strains of HIV-1, providing direct evidence that these chimpanzees were not the source of the human AIDS pandemic. 相似文献
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Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity 总被引:1,自引:0,他引:1
Um SH Frigerio F Watanabe M Picard F Joaquin M Sticker M Fumagalli S Allegrini PR Kozma SC Auwerx J Thomas G 《Nature》2004,431(7005):200-205
Elucidating the signalling mechanisms by which obesity leads to impaired insulin action is critical in the development of therapeutic strategies for the treatment of diabetes. Recently, mice deficient for S6 Kinase 1 (S6K1), an effector of the mammalian target of rapamycin (mTOR) that acts to integrate nutrient and insulin signals, were shown to be hypoinsulinaemic, glucose intolerant and have reduced beta-cell mass. However, S6K1-deficient mice maintain normal glucose levels during fasting, suggesting hypersensitivity to insulin, raising the question of their metabolic fate as a function of age and diet. Here, we report that S6K1-deficient mice are protected against obesity owing to enhanced beta-oxidation. However on a high fat diet, levels of glucose and free fatty acids still rise in S6K1-deficient mice, resulting in insulin receptor desensitization. Nevertheless, S6K1-deficient mice remain sensitive to insulin owing to the apparent loss of a negative feedback loop from S6K1 to insulin receptor substrate 1 (IRS1), which blunts S307 and S636/S639 phosphorylation; sites involved in insulin resistance. Moreover, wild-type mice on a high fat diet as well as K/K A(y) and ob/ob (also known as Lep/Lep) mice-two genetic models of obesity-have markedly elevated S6K1 activity and, unlike S6K1-deficient mice, increased phosphorylation of IRS1 S307 and S636/S639. Thus under conditions of nutrient satiation S6K1 negatively regulates insulin signalling. 相似文献