Robust associations of four new chromosome regions from genome-wide analyses of type 1 diabetes

The Wellcome Trust Case Control Consortium (WTCCC) primary genome-wide association (GWA) scan on seven diseases, including the multifactorial autoimmune disease type 1 diabetes (T1D), shows associations at P < 5 x 10(-7) between T1D and six chromosome regions: 12q24, 12q13, 16p13, 18p11, 12p13 and 4q27. Here, we attempted to validate these and six other top findings in 4,000 individuals with T1D, 5,000 controls and 2,997 family trios independent of the WTCCC study. We confirmed unequivocally the associations of 12q24, 12q13, 16p13 and 18p11 (P(follow-up) 相似文献   

是什么控制着细胞周期

尽管使细胞诞生的事实已知之甚详,但如今的生物学家也只是了解到那是如何调节的,实际上,有一种蛋白质是所有的生物机体的主要调节者. 19世纪初,科学家已经认识到细胞周期这一基本事实——单细胞成长并分裂为子细胞.直到最近才知道调节着这一周期的是什么.而人类的这一周期是充满活力的,不但进行生殖而且也在生长,进行组织修复、免疫和其它过程.     

生物工程领域的就业前景

工业生物工程协会(1984)对生物技术所下的直接定义是“用以制成商业产品的生物有机体利用”.按此,任何直接或间接涉及到诸如试验或分配这些产品之活动的公司皆被称作生物工程公司. 给定这样广涵的定义,生物工程作为一门表征着一些分支门类的生物学分支学科来说便不足为奇了.     

Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Mitochondria play a critical role in mediating both apoptotic and necrotic cell death. The mitochondrial permeability transition (mPT) leads to mitochondrial swelling, outer membrane rupture and the release of apoptotic mediators. The mPT pore is thought to consist of the adenine nucleotide translocator, a voltage-dependent anion channel, and cyclophilin D (the Ppif gene product), a prolyl isomerase located within the mitochondrial matrix. Here we generated mice lacking Ppif and mice overexpressing cyclophilin D in the heart. Ppif null mice are protected from ischaemia/reperfusion-induced cell death in vivo, whereas cyclophilin D-overexpressing mice show mitochondrial swelling and spontaneous cell death. Mitochondria isolated from the livers, hearts and brains of Ppif null mice are resistant to mitochondrial swelling and permeability transition in vitro. Moreover, primary hepatocytes and fibroblasts isolated from Ppif null mice are largely protected from Ca2+-overload and oxidative stress-induced cell death. However, Bcl-2 family member-induced cell death does not depend on cyclophilin D, and Ppif null fibroblasts are not protected from staurosporine or tumour-necrosis factor-alpha-induced death. Thus, cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.     

Another continental pool in the terrestrial silicon cycle

Silicon is the second most abundant element on Earth. It is an important nutrient for phytoplankton and is readily absorbed by terrestrial vegetation; it also assists the removal of carbon dioxide from the atmosphere through the weathering of silicates. But the continental cycle of silicon is not well known, and only a few studies have attempted to use silicon stable isotopes (28Si, 29Si and 30Si) to quantify the continental silicon reservoirs. Dissolved silicon in sea and river waters forms a reservoir of mean isotopic value +1.1 per thousand (refs 7, 10). It is enriched in 30Si with respect to the igneous rocks reservoir, which has a mean isotopic value of -0.3 per thousand (refs 4, 9). This enrichment can only be produced by a major fractionation during weathering, and should result in the formation of a continental 30Si-depleted reservoir. Such a reservoir, however, has not been identified to date. Here we analyse silicon isotopes of in situ quartz from a sandstone series in France, using a new-generation secondary ion mass spectrometry apparatus. We show that quartz that precipitates as siliceous cements forms a strongly 30Si-depleted reservoir with isotopic values down to -5.7 per thousand, a more negative value than any previously published for terrestrial samples. Our findings suggest that quartz re-precipitation plays an important role in the biogeochemical cycle of silicon.     

Predictive models of molecular machines involved in Caenorhabditis elegans early embryogenesis

Although numerous fundamental aspects of development have been uncovered through the study of individual genes and proteins, system-level models are still missing for most developmental processes. The first two cell divisions of Caenorhabditis elegans embryogenesis constitute an ideal test bed for a system-level approach. Early embryogenesis, including processes such as cell division and establishment of cellular polarity, is readily amenable to large-scale functional analysis. A first step toward a system-level understanding is to provide 'first-draft' models both of the molecular assemblies involved and of the functional connections between them. Here we show that such models can be derived from an integrated gene/protein network generated from three different types of functional relationship: protein interaction, expression profiling similarity and phenotypic profiling similarity, as estimated from detailed early embryonic RNA interference phenotypes systematically recorded for hundreds of early embryogenesis genes. The topology of the integrated network suggests that C. elegans early embryogenesis is achieved through coordination of a limited set of molecular machines. We assessed the overall predictive value of such molecular machine models by dynamic localization of ten previously uncharacterized proteins within the living embryo.