双前置罩式辐射测温原理

在环境辐射及物体发射率未知的情况下,直接用辐射测温仪测出物体的真实温度,是长期以来未解决的问题。本文假定将两个具有给定温度及发射率的罩子罩在物体上,并利用安装在罩子顶上开孔处的二台辐射测温仪分别测得两个表现信号,利用这两个信号及我们推得的公式,可实时测出物体的发射率及真实温度。本文还给出了前置罩式辐射测温仪的信噪比及灵敏度公式。     

黄海周边河流的稀土元素地球化学及沉积物物源示踪

黄海周边的中韩主要河流悬浮沉积物中稀土元素组成不同, 韩国河流的稀土元素分异强于中国长江、黄河和鸭绿江, 表现为上陆壳标准化模式上明显的轻稀土相对富集. 不同级别的流域内源岩组成差异是形成这些河流稀土元素组成差异的主要因素. 稀土元素分异参数(La/Yb)_UCC和(Gd/Yb)_UCC, 以及稳定的La/Sc和Th/Sc元素比是识别进入黄海的中韩河流沉积物的可靠指标, 可以用于中国边缘海沉积物物源研究和古环境分析.     

基于全球超导重力仪观测资料考虑液核近周日共振效应的固体潮实验模型

基于全球地球动力学合作观测网络20个台站28个系列的高精度每分钟高密度采样超导重力仪观测数据, 精密测定了地球液核近周日共振参数(包括共振周期, 共振强度和品质因子). 研究了共振周期与理论值间的差异, 用重力手段证明了真实地球液核动力学扁率要比流体静力平衡假设下获得的动力学扁率大约5%的重要结论. 构制了考虑液核共振效应的重力固体潮汐实验模型, 3个实验模型间的差异小于0.1%, 与目前广泛使用的Dehant(1999)和Mathews(2001)理论模型间的最大差异仅为0.4%, 可为全球固体潮、大地测量研究和空间技术等提供最新的重力潮汐实测参考模型.     

Microarray-Based Differential Expression Monitoring of 79 Novel Genes in Human Fetal Tissues

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不同应力路径下含瓦斯煤的声发射特性与能量演化规律

为了研究含瓦斯煤在不同扰动作用下的声发射特性和能量演化规律,利用多场煤与瓦斯突出过程宏细观试验系统,开展6种应力路径下的含瓦斯煤轴向加卸载试验,分析应力路径对含瓦斯煤声发射特性和变形特性的影响,并得到含瓦斯煤在循环加卸载过程中的能量演化特征及储能规律。研究结果表明：含瓦斯煤在吸附过程中的振铃计数随吸附时间增长而减少,根据出气口压力变化趋势将吸附过程分为3个阶段,分别为外扩散阶段、内扩散阶段和吸附饱和阶段;含瓦斯煤在加卸载过程中的振铃计数主要分布在应力上升区段,出现了明显的Kaiser效应,累计振铃计数在循环加卸载路径下呈“阶梯”形增长,且随着循环次数增加和应力路径延长而增大;含瓦斯煤在不同循环加卸载路径下的能量演化规律具有一致性,各能量密度均随着轴向应力增加而呈现二次函数型增长,并经历了减速增长、线性增长和加速增长的3个阶段;同时,弹性能密度和总输入能密度之间存在线性关系,储能系数为定值且均在50%以上。     

Mutations in GRIN2A and GRIN2B encoding regulatory subunits of NMDA receptors cause variable neurodevelopmental phenotypes

N-methyl-D-aspartate (NMDA) receptors mediate excitatory neurotransmission in the mammalian brain. Two glycine-binding NR1 subunits and two glutamate-binding NR2 subunits each form highly Ca2(+)-permeable cation channels which are blocked by extracellular Mg2(+) in a voltage-dependent manner. Either GRIN2B or GRIN2A, encoding the NMDA receptor subunits NR2B and NR2A, was found to be disrupted by chromosome translocation breakpoints in individuals with mental retardation and/or epilepsy. Sequencing of GRIN2B in 468 individuals with mental retardation revealed four de novo mutations: a frameshift, a missense and two splice-site mutations. In another cohort of 127 individuals with idiopathic epilepsy and/or mental retardation, we discovered a GRIN2A nonsense mutation in a three-generation family. In a girl with early-onset epileptic encephalopathy, we identified the de novo GRIN2A mutation c.1845C>A predicting the amino acid substitution p.N615K. Analysis of NR1-NR2A(N615K) (NR2A subunit with the p.N615K alteration) receptor currents revealed a loss of the Mg2(+) block and a decrease in Ca2(+) permeability. Our findings suggest that disturbances in the neuronal electrophysiological balance during development result in variable neurological phenotypes depending on which NR2 subunit of NMDA receptors is affected.     

ATM mutations that cause ataxia-telangiectasia are breast cancer susceptibility alleles

We screened individuals from 443 familial breast cancer pedigrees and 521 controls for ATM sequence variants and identified 12 mutations in affected individuals and two in controls (P = 0.0047). The results demonstrate that ATM mutations that cause ataxia-telangiectasia in biallelic carriers are breast cancer susceptibility alleles in monoallelic carriers, with an estimated relative risk of 2.37 (95% confidence interval (c.i.) = 1.51-3.78, P = 0.0003). There was no evidence that other classes of ATM variant confer a risk of breast cancer.     

Systematic mapping of genetic interactions in Caenorhabditis elegans identifies common modifiers of diverse signaling pathways

Most heritable traits, including disease susceptibility, are affected by interactions between multiple genes. However, we understand little about how genes interact because very few possible genetic interactions have been explored experimentally. We have used RNA interference in Caenorhabditis elegans to systematically test approximately 65,000 pairs of genes for their ability to interact genetically. We identify approximately 350 genetic interactions between genes functioning in signaling pathways that are mutated in human diseases, including components of the EGF/Ras, Notch and Wnt pathways. Most notably, we identify a class of highly connected 'hub' genes: inactivation of these genes can enhance the phenotypic consequences of mutation of many different genes. These hub genes all encode chromatin regulators, and their activity as genetic hubs seems to be conserved across animals. We propose that these genes function as general buffers of genetic variation and that these hub genes may act as modifier genes in multiple, mechanistically unrelated genetic diseases in humans.