Meta-analysis of 28,141 individuals identifies common variants within five new loci that influence uric acid concentrations

Elevated serum uric acid levels cause gout and are a risk factor for cardiovascular disease and diabetes. To investigate the polygenetic basis of serum uric acid levels, we conducted a meta-analysis of genome-wide association scans from 14 studies totalling 28,141 participants of European descent, resulting in identification of 954 SNPs distributed across nine loci that exceeded the threshold of genome-wide significance, five of which are novel. Overall, the common variants associated with serum uric acid levels fall in the following nine regions: SLC2A9 (p = 5.2x10(-201)), ABCG2 (p = 3.1x10(-26)), SLC17A1 (p = 3.0x10(-14)), SLC22A11 (p = 6.7x10(-14)), SLC22A12 (p = 2.0x10(-9)), SLC16A9 (p = 1.1x10(-8)), GCKR (p = 1.4x10(-9)), LRRC16A (p = 8.5x10(-9)), and near PDZK1 (p = 2.7x10(-9)). Identified variants were analyzed for gender differences. We found that the minor allele for rs734553 in SLC2A9 has greater influence in lowering uric acid levels in women and the minor allele of rs2231142 in ABCG2 elevates uric acid levels more strongly in men compared to women. To further characterize the identified variants, we analyzed their association with a panel of metabolites. rs12356193 within SLC16A9 was associated with DL-carnitine (p = 4.0x10(-26)) and propionyl-L-carnitine (p = 5.0x10(-8)) concentrations, which in turn were associated with serum UA levels (p = 1.4x10(-57) and p = 8.1x10(-54), respectively), forming a triangle between SNP, metabolites, and UA levels. Taken together, these associations highlight additional pathways that are important in the regulation of serum uric acid levels and point toward novel potential targets for pharmacological intervention to prevent or treat hyperuricemia. In addition, these findings strongly support the hypothesis that transport proteins are key in regulating serum uric acid levels.

Manifestação solicitada pelo TCU à CONOF/CD acerca de relatório preliminar, relativo à consulta sobre a aplicação da Lei Complementar nº 141, de 2012, formulada pela Comissão de Seguridade Social e Família/CD : TC 046.061/2012‐6

Avalia o relatório elaborado pelo TCU acerca da consulta formulada pela CSSF/CD(TC 046.061/2012‐6). Procura a pacificação de entendimento no âmbito do Congresso Nacional.

HIV蛋白酶抑制剂与细胞凋亡

　HIV 感染人体后造成大量CD4 + T 淋巴细胞的凋亡, 从而破坏免疫系统,使机体无法抵抗病毒的入侵,导致免疫 缺陷。目前的药物靶点都针对病毒本身,无法清除体内储存 病毒的感染细胞,而HIV 蛋白酶抑制剂治疗HIV/ AIDS 患 者后可以减少HIV 感染引起的细胞凋亡,帮助机体恢复免 疫功能,并且这种作用与其抑制病毒的作用是相独立的,这 提示了可以通过免疫重建的策略来治疗AIDS。本文综述了 HIV 蛋白酶抑制剂的研究和发展概况,其作用特点以及对细 胞凋亡的影响。明确HIV 蛋白酶抑制剂与细胞凋亡的关 系,可以启发新的思路从细胞着手,通过恢复机体的免疫能 力来对抗病毒,从根本上治疗AIDS。

抗对虾白斑综合症病毒的单链抗体A1的表达和生物化学特性

用噬菌体展示技术制备了抗对虾白斑综合症病毒(WSSV)的单链抗体A1。该抗体在30℃培养条件下诱导表达20h后,其蛋白表达量可达总菌体蛋白的3.67%。用亲和层析柱和SephadexG-100层析柱可将单链抗体A1纯化为一条单电泳条带,其分子量约为31.5kD。用等电聚焦电泳测定,其等电点为pH5.8。ELISA测定表明冻干的单链抗体A1在室温储藏4年后与WSSV结合仍具有较高的活力。

从CLEO’97会议看光电子学进展

于2010-11-23批量导入

~(143)Dy和~(141)Dy的β缓发质子衰变与自旋指认

分析了143Dy和141Dy的β缓发质子衰变的数据,对比计算了这两种核的核位能面。从中看到了143Dy的衰变包括有1/2+基态和11/2-同核异能态的两种衰变成分,并且确定了它们的半衰期分别为(6.0±1.5)s和(3.0±0.5)s。同时也测定了141Dy的半衰期为(0.9±0.2)s,并指认了它的自旋宇称为9/2-。

~(140)Tb和~(141)Dy的β缓发质子衰变以及~(143)Dy的自旋宇称

利用40Ca+106Cd融合蒸发反应产生了近质子滴线核140Tb和141Dy,配合氦喷嘴带传输系统采用“质子-γ”符合方法观测了它们的β缓发质子衰变,其中包括半衰期、质子能谱和衰变到第二代子核不同低位态的分支比．通过统计理论拟合提取了140Tb和141Dy的基态自旋宇称分别为7±和9／2±．另一方面,用Woods-Saxon Strutinsky方法计算了这两种核限制组态的势能面,由此得到140Tb和141Dy的基态自旋宇称分别为7+和9／2-．此外用同一方法还计算了143Dy的核势能面,从中看出143Dy存在有自旋宇称为1／2+的基态和一个激发能为198keV的11／2-的同质异能态．该结果与2003年Eur．Phys．J． A16:347-351中的143Dy衰变实验数据相符．

~(141)Nd激发态的在束γ谱学研究

通过1 3 0 Te(1 6O ,5nγ) 1 4 1 Nd反应布居了1 4 1 Nd的高自旋态能级 .对反应产生的在束γ射线进行了γ射线单谱和γ -γ符合测量 .建立了激发能达 76 1 4 .5keV的1 4 1 Nd能级纲图 ,新发现了 1 2条γ射线和 1 5个能级 .基于实验测量的γ跃迁各向异性 ,建议了1 4 1 Nd部分能级的自旋值 .用一个h1 1 2 价中子空穴与1 4 2 Nd核芯晕态的耦合可以定性地解释1 4 1 Nd的能级结构