哈特曼装置上粉尘浓度的测量

粉尘浓度和湍流速度对粉尘爆炸猛烈程度和粉尘云最小着火能的测试有很大影响.针对1.2 L哈特曼装置上的粉尘浓度进行了测量研究,并对测量数据进行了分析讨论,得到了1.2 L哈特曼管上不同位置高度的粉尘浓度随时间的变化曲线.粉尘浓度随哈特曼管高度位置分布很不均匀.对于哈特曼管电极位置高度,当点火延迟时间170 ms、计算浓度为500 g/m3时,其粉尘测量浓度近似等于计算浓度;当计算浓度低于500 g/m3时,其测量浓度高于计算浓度.当计算浓度大于500 g/m3时,测量浓度低于计算浓度.哈特曼管上粉尘浓度随高度分布的获得,为最小着火能在不同装置上的测试比较提供了数据,为粉尘爆炸数学模型的检验提供了...     

星系的生命和呼吸

<正>科学家追踪气体随时间和空间的变化,探寻恒星群出生及死亡的方式。天文学家对宇宙的大部分了解来自他们能够看到的东西,因此,他们的理论总是偏爱明亮的恒星和星系。然而,宇宙中的大部分常规物质都是以昏暗的气体形式存在的。称作星系际介质的气体充满星系间的空间;而环星系介质的气体则环绕在星系附近。这两个区域的气体管控星系诞生、成长和死亡,也详细记录了整个宇宙的     

西北地区人口-经济-水环境质量耦合协调发展研究

基于2005～2014年西北五省人口-经济-水环境质量相关数据,构建耦合协调评价指标体系。运用统计学和GIS方法对近10年来西北地区人口-经济-水耦合协调发展的时空演变进行分析,发现2005～2014年,耦合类别变化情况为勉强耦合-初级耦合-中级耦合,耦合协调度持续上升表明三个子系统之间的协调促进作用增强,系统逐步由无序走向有序;近10年来,西北五省耦合协调度均有不同程度提升,其中青海省提升幅度最大,达到了0.44,陕西省提升幅度为0.044,是五省中提升幅度最小的省区;不论是区域整体还是区域内部各个省份,经济和人口对系统的推动作用均逐步增强,而水环境质量则逐步失去对各区域发展的推动力,表明区域发展的动力逐步由资源转向经济和人口,发展的可持续性增强。     

量子全加法器的修改和算法研究

通过与经典全加器的基本模型进行比较后,讨论了一个改进后的量子平面加法器的基本构型.对其原理、组件和算法进行了研究,比较了本加法器两个主要组件与一般量子加法器的不同.作为应用的例,设计了一个n比特量子全加法器的模型,对其具体运算过程和基本功能进行了说明.     

Memory

Memories become stabilized through a time-dependent process that requires gene expression and is commonly known as consolidation. During this time, memories are labile and can be disrupted by a number of interfering events, including electroconvulsive shock, trauma and other learning or the transient effect of drugs such as protein synthesis inhibitors. Once consolidated, memories are insensitive to these disruptions. However, they can again become fragile if recalled or reactivated. Reactivation creates another time-dependent process, known as reconsolidation, during which the memory is restabilized. Here we discuss some of the questions currently debated in the field of memory consolidation and reconsolidation, the molecular and anatomical requirements for both processes and, finally, their functional relationship.     

Galectin-7

Galectins are a family of animal lectins with an affinity for β-galactosides. They are differentially expressed by various tissues and appear to be functionally multivalent, exerting a wide range of biological activities both during development and in adult tissue. Galectin-7, a member of this family, contributes to different events associated with the differentiation and development of pluristratified epithelia. It is also associated with epithelial cell migration, which plays a crucial role in the re-epithelialization process of corneal or epidermal wounds. In addition, recent evidence indicates that galectin-7, designated as the product of the p53-induced gene 1 (PIG1), is a regulator of apoptosis through JNK activation and mitochondrial cytochrome c release. Defects in apoptosis constitute one of the major hallmarks of human cancers, and galectin-7 can act as either a positive or a negative regulatory factor in tumour development, depending on the histological type of the tumour. Received 30 October 2005; received after revision 15 November 2005; accepted 25 November 2005     

Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis

Atopic disease, including atopic dermatitis (eczema), allergy and asthma, has increased in frequency in recent decades and now affects approximately 20% of the population in the developed world. Twin and family studies have shown that predisposition to atopic disease is highly heritable. Although most genetic studies have focused on immunological mechanisms, a primary epithelial barrier defect has been anticipated. Filaggrin is a key protein that facilitates terminal differentiation of the epidermis and formation of the skin barrier. Here we show that two independent loss-of-function genetic variants (R510X and 2282del4) in the gene encoding filaggrin (FLG) are very strong predisposing factors for atopic dermatitis. These variants are carried by approximately 9% of people of European origin. These variants also show highly significant association with asthma occurring in the context of atopic dermatitis. This work establishes a key role for impaired skin barrier function in the development of atopic disease.     

ANG mutations segregate with familial and 'sporadic' amyotrophic lateral sclerosis

We recently identified angiogenin (ANG) as a candidate susceptibility gene for amyotrophic lateral sclerosis (ALS), a neurodegenerative disorder characterized by adult-onset loss of motor neurons. We now report the finding of seven missense mutations in 15 individuals, of whom four had familial ALS and 11 apparently 'sporadic' ALS. Our findings provide further evidence that variations in hypoxia-inducible genes have an important role in motor neuron degeneration.     

Analysis of the human protein interactome and comparison with yeast, worm and fly interaction datasets

We present the first analysis of the human proteome with regard to interactions between proteins. We also compare the human interactome with the available interaction datasets from yeast (Saccharomyces cerevisiae), worm (Caenorhabditis elegans) and fly (Drosophila melanogaster). Of >70,000 binary interactions, only 42 were common to human, worm and fly, and only 16 were common to all four datasets. An additional 36 interactions were common to fly and worm but were not observed in humans, although a coimmunoprecipitation assay showed that 9 of the interactions do occur in humans. A re-examination of the connectivity of essential genes in yeast and humans indicated that the available data do not support the presumption that the number of interaction partners can accurately predict whether a gene is essential. Finally, we found that proteins encoded by genes mutated in inherited genetic disorders are likely to interact with proteins known to cause similar disorders, suggesting the existence of disease subnetworks. The human interaction map constructed from our analysis should facilitate an integrative systems biology approach to elucidating the cellular networks that contribute to health and disease states.     

Genome-wide genetic association of complex traits in heterogeneous stock mice

Difficulties in fine-mapping quantitative trait loci (QTLs) are a major impediment to progress in the molecular dissection of complex traits in mice. Here we show that genome-wide high-resolution mapping of multiple phenotypes can be achieved using a stock of genetically heterogeneous mice. We developed a conservative and robust bootstrap analysis to map 843 QTLs with an average 95% confidence interval of 2.8 Mb. The QTLs contribute to variation in 97 traits, including models of human disease (asthma, type 2 diabetes mellitus, obesity and anxiety) as well as immunological, biochemical and hematological phenotypes. The genetic architecture of almost all phenotypes was complex, with many loci each contributing a small proportion to the total variance. Our data set, freely available at http://gscan.well.ox.ac.uk, provides an entry point to the functional characterization of genes involved in many complex traits.