Metallurgy: high nickel release from 1- and 2-euro coins

The amount of nickel is regulated in European products that come into direct and prolonged contact with human skin because this metal may cause contact allergy, particularly hand eczema. Here we show that 1- and 2-euro coins induce positive skin-test reactions in sensitized individuals and release 240-320-fold more nickel than is allowed under the European Union Nickel Directive. A factor contributing to this high release of nickel is corrosion due to the bimetallic structure of these coins, which generates a galvanic potential of 30-40 mV in human sweat.     

神经模糊网络自适应模糊控制研究

提出了一种由样品辨识、模糊推理和控制处理 3个子网模块构成的基于知识的多层神经网络 .这种网络由各子网分别构成并按照最初的模糊控制结构适当连接而建立 ,具有明确区分各组成子网功能及其知识流结构 .由于综合了模糊逻辑的推理过程及神经网络的学习能力 ,使它能够在其结构中以模糊规则的形式引入语言知识并通过网络的训练及自学习对这些知识进行加工 ,从而实现了真正意义上的自适应模糊控制器 .最后还讨论了这种 NFN网络在动态过程控制中的应用     

Loss-of-function mutations in LEMD3 result in osteopoikilosis, Buschke-Ollendorff syndrome and melorheostosis

Osteopoikilosis, Buschke-Ollendorff syndrome (BOS) and melorheostosis are disorders characterized by increased bone density. The occurrence of one or more of these phenotypes in the same individual or family suggests that these entities might be allelic. We collected data from three families in which affected individuals had osteopoikilosis with or without manifestations of BOS or melorheostosis. A genome-wide linkage analysis in these families, followed by the identification of a microdeletion in an unrelated individual with these diseases, allowed us to map the gene that is mutated in osteopoikilosis. All the affected individuals that we investigated were heterozygous with respect to a loss-of-function mutation in LEMD3 (also called MAN1), which encodes an inner nuclear membrane protein. A somatic mutation in the second allele of LEMD3 could not be identified in fibroblasts from affected skin of an individual with BOS and an individual with melorheostosis. XMAN1, the Xenopus laevis ortholog, antagonizes BMP signaling during embryogenesis. In this study, LEMD3 interacted with BMP and activin-TGFbeta receptor-activated Smads and antagonized both signaling pathways in human cells.     

An endoribonuclease-prepared siRNA screen in human cells identifies genes essential for cell division

RNA interference (RNAi) is an evolutionarily conserved defence mechanism whereby genes are specifically silenced through degradation of messenger RNAs; this process is mediated by homologous double-stranded (ds)RNA molecules. In invertebrates, long dsRNAs have been used for genome-wide screens and have provided insights into gene functions. Because long dsRNA triggers a nonspecific interferon response in many vertebrates, short interfering (si)RNA or short hairpin (sh)RNAs must be used for these organisms to ensure specific gene silencing. Here we report the generation of a genome-scale library of endoribonuclease-prepared short interfering (esi)RNAs from a sequence-verified complementary DNA collection representing 15,497 human genes. We used 5,305 esiRNAs from this library to screen for genes required for cell division in HeLa cells. Using a primary high-throughput cell viability screen followed by a secondary high content videomicroscopy assay, we identified 37 genes required for cell division. These include several splicing factors for which knockdown generates mitotic spindle defects. In addition, a putative nuclear-export terminator was found to speed up cell proliferation and mitotic progression after knockdown. Thus, our study uncovers new aspects of cell division and establishes esiRNA as a versatile approach for genomic RNAi screens in mammalian cells.