激光引起金属靶层裂的实验研究

激光引起金属靶的层裂,目前国外只有少量文献有报道,并主要集中在铝、铜材料。由于脉冲强激光能产生10~7s~(-1)以上的超高应变率,它为在实验室内研究这样极端条件下的材料的断裂行为和机理,提供了几乎唯一的加载手段。本文简要报道我们在中国科技大学“华光”10~(10)W钕玻璃激光器上所做的铝和铁靶层裂实验的初步结果。这是我国首次利用强激光装置实现金属层裂的尝试,为强激光破坏效应的研究提供了现实的前景。     

后表面声阻抗匹配对钛相变动力学的影响

基于磁驱动装置CQ-4开展了金属钛的斜波压缩相变实验,研究了窗口特性对钛相变动力学的影响.实验结果显示,钛后表面为较低声阻抗(自由面和Li F窗口)时,相变起始对应的粒子速度特征拐点约408.9 m/s,而高阻抗蓝宝石窗口时约373.9 m/s,这一速度特征拐点对应的压力并不是相变压力.结合基于热力学Helmholtz自由能的多相状态方程和非平衡相变速率模型开展了钛的相变动力学数值模拟研究,计算结果与三种情况的实验结果都基本吻合.计算结果显示,样品在加载面附近速度波形相同,在后表面附近由于阻抗匹配不同,波形幅值差异较大.钛的相变压力为10.5 GPa,且为率相关的非平衡相变.在压力-比容热力学平面,相变前准等熵线与冲击绝热线基本重合,相变过程在一定的压力区间内完成,进入新相后准等熵线在冲击绝热线下方.进入相变后有明显的声速下降,这是由于相变引起的比容间断造成的,相变完成后恢复到体波声速.     

Enhanced performance of nano-sized SiC reinforced Al metal matrix nanocomposites synthesized through microwave sintering and hot extrusion techniques

In the present study, nano-sized SiC (0, 0.3, 0.5, 1.0 and 1.5 vol%) reinforced aluminum (Al) metal matrix composites were fabricated by microwave sintering and hot extrusion techniques. The structural (XRD, SEM), mechanical (nanoindentation, compression, tensile) and thermal properties (co-efficient of thermal expansion- CTE) of the developed Al-SiC nanocomposites were studied. The SEM/EDS mapping images show a homogeneous distribution of SiC nanoparticles into the Al matrix. A significant increase in the strength (compressive and tensile) of the Al-SiC nanocomposites with the addition of SiC content is observed. However, it is noticed that the ductility of Al-SiC nanocomposites decreases with increasing volume fraction of SiC. The thermal analysis indicates that CTE of Al-SiC nanocomposites decreases with the progressive addition of hard SiC nanoparticles. Overall, hot extruded Al 1.5 vol% SiC nanocomposites exhibited the best mechanical and thermal performance as compared to the other developed Al-SiC nanocomposites.     

A second generation human haplotype map of over 3.1 million SNPs

We describe the Phase II HapMap, which characterizes over 3.1 million human single nucleotide polymorphisms (SNPs) genotyped in 270 individuals from four geographically diverse populations and includes 25-35% of common SNP variation in the populations surveyed. The map is estimated to capture untyped common variation with an average maximum r2 of between 0.9 and 0.96 depending on population. We demonstrate that the current generation of commercial genome-wide genotyping products captures common Phase II SNPs with an average maximum r2 of up to 0.8 in African and up to 0.95 in non-African populations, and that potential gains in power in association studies can be obtained through imputation. These data also reveal novel aspects of the structure of linkage disequilibrium. We show that 10-30% of pairs of individuals within a population share at least one region of extended genetic identity arising from recent ancestry and that up to 1% of all common variants are untaggable, primarily because they lie within recombination hotspots. We show that recombination rates vary systematically around genes and between genes of different function. Finally, we demonstrate increased differentiation at non-synonymous, compared to synonymous, SNPs, resulting from systematic differences in the strength or efficacy of natural selection between populations.     

Genome-wide detection and characterization of positive selection in human populations

With the advent of dense maps of human genetic variation, it is now possible to detect positive natural selection across the human genome. Here we report an analysis of over 3 million polymorphisms from the International HapMap Project Phase 2 (HapMap2). We used 'long-range haplotype' methods, which were developed to identify alleles segregating in a population that have undergone recent selection, and we also developed new methods that are based on cross-population comparisons to discover alleles that have swept to near-fixation within a population. The analysis reveals more than 300 strong candidate regions. Focusing on the strongest 22 regions, we develop a heuristic for scrutinizing these regions to identify candidate targets of selection. In a complementary analysis, we identify 26 non-synonymous, coding, single nucleotide polymorphisms showing regional evidence of positive selection. Examination of these candidates highlights three cases in which two genes in a common biological process have apparently undergone positive selection in the same population:LARGE and DMD, both related to infection by the Lassa virus, in West Africa;SLC24A5 and SLC45A2, both involved in skin pigmentation, in Europe; and EDAR and EDA2R, both involved in development of hair follicles, in Asia.     

Catastrophic flooding origin of shelf valley systems in the English Channel

Megaflood events involving sudden discharges of exceptionally large volumes of water are rare, but can significantly affect landscape evolution, continental-scale drainage patterns and climate change. It has been proposed that a significant flood event eroded a network of large ancient valleys on the floor of the English Channel-the narrow seaway between England and France. This hypothesis has remained untested through lack of direct evidence, and alternative non-catastrophist ideas have been entertained for valley formation. Here we analyse a new regional bathymetric map of part of the English Channel derived from high-resolution sonar data, which shows the morphology of the valley in unprecedented detail. We observe a large bedrock-floored valley that contains a distinct assemblage of landforms, including streamlined islands and longitudinal erosional grooves, which are indicative of large-scale subaerial erosion by high-magnitude water discharges. Our observations support the megaflood model, in which breaching of a rock dam at the Dover Strait instigated catastrophic drainage of a large pro-glacial lake in the southern North Sea basin. We suggest that megaflooding provides an explanation for the permanent isolation of Britain from mainland Europe during interglacial high-sea-level stands, and consequently for patterns of early human colonisation of Britain together with the large-scale reorganization of palaeodrainage in northwest Europe.     

Corridors of migrating neurons in the human brain and their decline during infancy

The subventricular zone of many adult non-human mammals generates large numbers of new neurons destined for the olfactory bulb. Along the walls of the lateral ventricles, immature neuronal progeny migrate in tangentially oriented chains that coalesce into a rostral migratory stream (RMS) connecting the subventricular zone to the olfactory bulb. The adult human subventricular zone, in contrast, contains a hypocellular gap layer separating the ependymal lining from a periventricular ribbon of astrocytes. Some of these subventricular zone astrocytes can function as neural stem cells in vitro, but their function in vivo remains controversial. An initial report found few subventricular zone proliferating cells and rare migrating immature neurons in the RMS of adult humans. In contrast, a subsequent study indicated robust proliferation and migration in the human subventricular zone and RMS. Here we find that the infant human subventricular zone and RMS contain an extensive corridor of migrating immature neurons before 18 months of age but, contrary to previous reports, this germinal activity subsides in older children and is nearly extinct by adulthood. Surprisingly, during this limited window of neurogenesis, not all new neurons in the human subventricular zone are destined for the olfactory bulb--we describe a major migratory pathway that targets the prefrontal cortex in humans. Together, these findings reveal robust streams of tangentially migrating immature neurons in human early postnatal subventricular zone and cortex. These pathways represent potential targets of neurological injuries affecting neonates.     

Extremely low-coverage sequencing and imputation increases power for genome-wide association studies

Genome-wide association studies (GWAS) have proven to be a powerful method to identify common genetic variants contributing to susceptibility to common diseases. Here, we show that extremely low-coverage sequencing (0.1-0.5×) captures almost as much of the common (>5%) and low-frequency (1-5%) variation across the genome as SNP arrays. As an empirical demonstration, we show that genome-wide SNP genotypes can be inferred at a mean r(2) of 0.71 using off-target data (0.24× average coverage) in a whole-exome study of 909 samples. Using both simulated and real exome-sequencing data sets, we show that association statistics obtained using extremely low-coverage sequencing data attain similar P values at known associated variants as data from genotyping arrays, without an excess of false positives. Within the context of reductions in sample preparation and sequencing costs, funds invested in extremely low-coverage sequencing can yield several times the effective sample size of GWAS based on SNP array data and a commensurate increase in statistical power.     

CCDC103 mutations cause primary ciliary dyskinesia by disrupting assembly of ciliary dynein arms

Cilia are essential for fertilization, respiratory clearance, cerebrospinal fluid circulation and establishing laterality. Cilia motility defects cause primary ciliary dyskinesia (PCD, MIM244400), a disorder affecting 1:15,000-30,000 births. Cilia motility requires the assembly of multisubunit dynein arms that drive ciliary bending. Despite progress in understanding the genetic basis of PCD, mutations remain to be identified for several PCD-linked loci. Here we show that the zebrafish cilia paralysis mutant schmalhans (smh(tn222)) encodes the coiled-coil domain containing 103 protein (Ccdc103), a foxj1a-regulated gene product. Screening 146 unrelated PCD families identified individuals in six families with reduced outer dynein arms who carried mutations in CCDC103. Dynein arm assembly in smh mutant zebrafish was rescued by wild-type but not mutant human CCDC103. Chlamydomonas Ccdc103/Pr46b functions as a tightly bound, axoneme-associated protein. These results identify Ccdc103 as a dynein arm attachment factor that causes primary ciliary dyskinesia when mutated.