硫酸钛为钛源制备二氧化钛的实验条件研究

实验以硫酸钛为钛源、尿素为沉淀剂、聚乙二醇600为分散剂,采用均匀沉淀法制备二氧化钛粉末。主要讨论了影响沉淀形成时间的主要因素:尿素的用量及加入方法、聚乙二醇的用量、以及水浴的温度等。实验结果表明,以硫酸钛为钛源、尿素为沉淀剂、聚乙二醇600为分散剂,采用均匀沉淀法制备二氧化钛粉末最佳反应条件为:在水浴加热343 K条件下,将尿素缓慢滴加到硫酸钛和聚乙二醇600的混合液中,硫酸钛和聚乙二醇600的混合液在磁力搅拌器搅拌时滴加尿素,用硫酸调节pH在1.5~2,保持硫酸钛、尿素和聚乙二醇600的摩尔比1∶12∶0.01。     

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.     

New crystal structure of molecular complex 1-piperidine carboxylate-piperidinium-H<Subscript>2</Subscript>O studied by X-ray single crystal diffraction

Piperidine absorbs CO2 and H2O in air to form a molecular complex： piperidium-l-piperidinecarboxylate-H2O. The structure of the complex was characterized by X-ray single crystal diffraction. The crystal structure was determined to be triclinic, space group P1^-with a=0.648 6（8） nm, b=0.809 200） nm, c= 1.357 1（16） nm, a=96.96706）°, β =102.506（15）°,γ=104.202 05）°, Z=2. The complex is stabilized via five hydrogen bonds between the three components, N-O electrostatic interaction and O-O interaction （electron transfer） betweenl-piperidinecarboxylate and H2O. Due to electron transference of carbamate ion, the oxygen atom in water molecule is strongly negatively charged and the O-H bond is considerably shorter than that of the free molecule of water. The formation of the molecular complex is a reversible process and will decompose upon heating. The mechanism of formation and stabilization is further investigated herein.     

二维可控细胞自动机伪随机序列发生方法研究

提出了一种新的细胞自动机———二维可控细胞自动机。根据二维可控细胞自动机的性质,提出了一 种具有梯型结构的二维可控细胞自动机的伪随机序列发生方法。计算机模拟表明,具有梯型结构的二维可控细 胞自动机伪随机序列发生器实现简单,产生的序列具有速度高、统计特性好等优点。新的细胞自动机在对称密 码学中有广泛地应用。     

２００３年SARS对中国交通客运量影响的后评价研究 ———基于本底趋势线全国２８个省（市）自治区的分析与估算

２００３年SARS是中国公众健康的“灾难”,交通旅客运输因此蒙受巨大损失。依据本底趋势线理论, 对此次危机的交通客运量损失进行了定量估算。结果显示：２００３年SARS共造成交通旅客损失１０畅０７亿人次,其 中,公路损失８畅８８亿人次,铁路损失１畅０５亿人次,航空损失１６１１畅７万人次,水运损失１９４３万人次;危机的生命 周期从２００３年４月开始,５～６月全面爆发,７～８月消减衰退,１１～１２月有一定的补偿;由于交通区位和SARS 疫情的差异,全国２８个省（市）自治区客运量损失可划分为４个等级,其中,广东、     

用逻辑方法验证移动Ad Hoc网络协议

针对移动Ad Hoc网络节点移动和无线广播通信特征,引入移动算子和广播算子,扩展形式逻辑LS2,提出了建模和分析移动Ad Hoc网络安全系统的逻辑ELS2.ELS2把网络模型化为不同位置上执行程序的线程复合,把攻击者模型化为与协议参与方并发运行的线程.ELS2中提出网络迹概念,描述网络节点内部计算和外部交互,以及节点移...