Poisson方程各向异性一阶混合元格式

研究了Poisson方程在各向异性网格下的一阶混合元格式，在不引入传统投影算子的情况下，直接利用插值技巧得到了与以往文献相同的误差估计．     

用小波变换和奇异指数表征蔡氏混沌信号键带

计算了蔡氏电路混沌信号的离散二进小波变换及奇异指数，结果发现，当尺度2∧5上的小波变换结果的模大于某一阈值时，其所对应的信号段就是键带，在混沌信号的键带处，奇异指数限大的正值，而在非键带处，奇异指数取负值或小的正值。     

论国际商事仲裁中的公共政策保留

公共政策条款是<纽约公约>中关于拒绝承认和执行外国仲裁裁决的重要抗辩理由之一,也是各国法院保护其法律制度的一道安全阀.但由于公约以及各国的立法均未对公共政策作一个明确的界定,其在实践中便存在被各国滥用的危险.随着仲裁在国际商事争议解决中的作用和价值得到越来越多国家的重视,公共政策抗辩正在呈现窄化的趋势,这将有助于仲裁在更为自由和自治的基础上继续发展.     

浅谈煤矸石在混凝土砌块中的应用

介绍了开滦煤矿马家沟矿新型建材分公司使用台式振动小型砌块成型机全自动生产线中的煤矸石的主要指标及特性,及利用煤矸石生产砌块的可行性,并分析了其产品性能。     

基于熵权法的河南省村镇建设用地集约节约利用评价

运用熵权法对河南省各地市的村镇建设用地集约节约用地水平进行评价,揭示出全省现状村镇建设用地集约节约利用的空间分异特征,进而为村镇建设用地潜力挖掘与释放提供支撑.     

Microstructure and properties of in-situ synthesized Cu-1 wt%TiC alloy followed by ECAP and post-annealing

A dispersion-strengthened copper alloy with 1 wt% TiC for commercial electrical-contact wires was prepared by in-situ reaction casting, grain-ultrafining by equal-channel angular pressing (ECAP) and subsequent annealing with aim to obtain excellent comprehensive performance. The results showed that fine TiC particles were in-situ synthesized in the as-cast Cu matrix and aggregated in clusters, and thus mechanical properties of the as-cast alloy deemed insufficient. Continued ECAP at 473 K significantly refined the grains of the as-cast alloy and improved the distribution of TiC particles. Due to multiple strengthening mechanisms, the ECAP-processed alloys maintained good conductivity with obviously enhanced tensile strength and hardness values. After post-ECAP annealing, the elongation and conductivity of the fine-grained copper alloy increased with the adequate tensile strength. The novel combined process endows the alloy appropriate performance to serve current high-frequency electrification railway systems.     

BAI1 is an engulfment receptor for apoptotic cells upstream of the ELMO/Dock180/Rac module

Engulfment and subsequent degradation of apoptotic cells is an essential step that occurs throughout life in all multicellular organisms. ELMO/Dock180/Rac proteins are a conserved signalling module for promoting the internalization of apoptotic cell corpses; ELMO and Dock180 function together as a guanine nucleotide exchange factor (GEF) for the small GTPase Rac, and thereby regulate the phagocyte actin cytoskeleton during engulfment. However, the receptor(s) upstream of the ELMO/Dock180/Rac module are still unknown. Here we identify brain-specific angiogenesis inhibitor 1 (BAI1) as a receptor upstream of ELMO and as a receptor that can bind phosphatidylserine on apoptotic cells. BAI1 is a seven-transmembrane protein belonging to the adhesion-type G-protein-coupled receptor family, with an extended extracellular region and no known ligands. We show that BAI1 functions as an engulfment receptor in both the recognition and subsequent internalization of apoptotic cells. Through multiple lines of investigation, we identify phosphatidylserine, a key 'eat-me' signal exposed on apoptotic cells, as a ligand for BAI1. The thrombospondin type 1 repeats within the extracellular region of BAI1 mediate direct binding to phosphatidylserine. As with intracellular signalling, BAI1 forms a trimeric complex with ELMO and Dock180, and functional studies suggest that BAI1 cooperates with ELMO/Dock180/Rac to promote maximal engulfment of apoptotic cells. Last, decreased BAI1 expression or interference with BAI1 function inhibits the engulfment of apoptotic targets ex vivo and in vivo. Thus, BAI1 is a phosphatidylserine recognition receptor that can directly recruit a Rac-GEF complex to mediate the uptake of apoptotic cells.     

Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia

Chromosomal aberrations are a hallmark of acute lymphoblastic leukaemia (ALL) but alone fail to induce leukaemia. To identify cooperating oncogenic lesions, we performed a genome-wide analysis of leukaemic cells from 242 paediatric ALL patients using high-resolution, single-nucleotide polymorphism arrays and genomic DNA sequencing. Our analyses revealed deletion, amplification, point mutation and structural rearrangement in genes encoding principal regulators of B lymphocyte development and differentiation in 40% of B-progenitor ALL cases. The PAX5 gene was the most frequent target of somatic mutation, being altered in 31.7% of cases. The identified PAX5 mutations resulted in reduced levels of PAX5 protein or the generation of hypomorphic alleles. Deletions were also detected in TCF3 (also known as E2A), EBF1, LEF1, IKZF1 (IKAROS) and IKZF3 (AIOLOS). These findings suggest that direct disruption of pathways controlling B-cell development and differentiation contributes to B-progenitor ALL pathogenesis. Moreover, these data demonstrate the power of high-resolution, genome-wide approaches to identify new molecular lesions in cancer.     

TPP1 is a homologue of ciliate TEBP-beta and interacts with POT1 to recruit telomerase

Telomere dysfunction may result in chromosomal abnormalities, DNA damage responses, and even cancer. Early studies in lower organisms have helped to establish the crucial role of telomerase and telomeric proteins in maintaining telomere length and protecting telomere ends. In Oxytricha nova, telomere G-overhangs are protected by the TEBP-alpha/beta heterodimer. Human telomeres contain duplex telomeric repeats with 3' single-stranded G-overhangs, and may fold into a t-loop structure that helps to shield them from being recognized as DNA breaks. Additionally, the TEBP-alpha homologue, POT1, which binds telomeric single-stranded DNA (ssDNA), associates with multiple telomeric proteins (for example, TPP1, TIN2, TRF1, TRF2 and RAP1) to form the six-protein telosome/shelterin and other subcomplexes. These telomeric protein complexes in turn interact with diverse pathways to form the telomere interactome for telomere maintenance. However, the mechanisms by which the POT1-containing telosome communicates with telomerase to regulate telomeres remain to be elucidated. Here we demonstrate that TPP1 is a putative mammalian homologue of TEBP-beta and contains a predicted amino-terminal oligonucleotide/oligosaccharide binding (OB) fold. TPP1-POT1 association enhanced POT1 affinity for telomeric ssDNA. In addition, the TPP1 OB fold, as well as POT1-TPP1 binding, seemed critical for POT1-mediated telomere-length control and telomere-end protection in human cells. Disruption of POT1-TPP1 interaction by dominant negative TPP1 expression or RNA interference (RNAi) resulted in telomere-length alteration and DNA damage responses. Furthermore, we offer evidence that TPP1 associates with the telomerase in a TPP1-OB-fold-dependent manner, providing a physical link between telomerase and the telosome/shelterin complex. Our findings highlight the critical role of TPP1 in telomere maintenance, and support a yin-yang model in which TPP1 and POT1 function as a unit to protect human telomeres, by both positively and negatively regulating telomerase access to telomere DNA.     

关于一类不定方程有解的一般性结论

用模型论的方法证明了一类不定方程a1xr11 a2xr22 ... anxrnn=bys(其中a1,...,an,b为任意整数,r1,...,rn,s为任意正整数)有解.进一步地,我们用相同的方法解决了一个猜想.