多相滤波器组的ZFFT算法在轨道电路信号检测中的应用

针对轨道电路信号(FSK信号)的检测提出了基于多相滤波器组的频谱细化(ZFFT)分析方法,该方法利用多相滤波器组将待分析的移频信号按照不同载频分解成多个子带,经过子带选择,再进行FFT,与传统的信号检测算法相比,这种算法可以提高信号检测精度和实时性.     

Rag mutations reveal robust alternative end joining

Mammalian cells repair DNA double-strand breaks (DSBs) through either homologous recombination or non-homologous end joining (NHEJ). V(D)J recombination, a cut-and-paste mechanism for generating diversity in antigen receptors, relies on NHEJ for repairing DSBs introduced by the Rag1-Rag2 protein complex. Animals lacking any of the seven known NHEJ factors are therefore immunodeficient. Nevertheless, DSB repair is not eliminated entirely in these animals: evidence of a third mechanism, 'alternative NHEJ', appears in the form of extremely rare V(D)J junctions and a higher rate of chromosomal translocations. The paucity of these V(D)J events has suggested that alternative NHEJ contributes little to a cell's overall repair capacity, being operative only (and inefficiently) when classical NHEJ fails. Here we find that removing certain portions of murine Rag proteins reveals robust alternative NHEJ activity in NHEJ-deficient cells and some alternative joining activity even in wild-type cells. We propose a two-tier model in which the Rag proteins collaborate with NHEJ factors to preserve genomic integrity during V(D)J recombination.     

等离子驱动微小碎片加速器机理及运行参数

毫米以下尺寸微小碎片在近地空间存在数量大, 对航天器暴露材料的长期累积侵蚀作用成为影响航天器寿命和可靠性的重要因素, 在航天器的空间环境适应性设计中必须予以考虑. 为了模拟研究空间微小碎片对航天器材料的撞击效应, 研制了等离子体驱动的微小碎片加速器. 本文对加速器的核心过程—— 等离子体的加速、压缩进而形成超高速等离子体射流的物理过程建立了物理模型, 并进行了计算以及与实验结果的对比分析, 揭示了加速过程的物理机制, 为加速器的优化设计提供了依据. 同时, 通过一系列实验研究, 确定了加速器运行的最佳工作参数, 并初步获得了加速器的加速能力范围.     

大壁虎脚趾运动和感觉的分区分级调控

近年来, 爬壁机器人是机器人领域研究和开发的一个热点课题. 大壁虎是研究爬墙机器人的理想模型. 在仿壁虎机器人的研制过程中, 脚掌(趾)的设计是关键技术之一. 采用高速摄像和电生理学方法, 观测了大壁虎前、后脚在不同界面爬行时不同的运动模式; 研究了5个脚趾的黏-脱附运动及其感觉信息传入的神经支配; 发现了5个脚趾运动和感觉功能的不同分区, 黏附和脱附行为及其感受传入的分级调控现象. 这些结果为当前仿壁虎机器人, 以及其他4足和多足机器人脚掌(趾)的结构和运动控制系统的设计提供重要的信息和理念.     

广角光接收机研究进展

广角光接收机在无线光通信、传感和检测系统中有明显的优势和广泛的应用前景. 然而, 当它采用传统光器件来实现时, 其视场角会受到这些组件内在矛盾的限制, 而传统的视场角扩展机制无法从根本上打破这些束缚. 为此, 提出金属等离子表面波(SPP)作为有效实现广角接收机的潜在机制. 文中列举了两个SPP的应用实例, 生动地说明了它可以破解一些传统方法无法克服的矛盾, 提供意想不到的解决方案; 而且, 在某些情况下, 为了利用SPP, 人们需要探索一些不寻常的条件. 探讨了SPP在光异常透射效应中的几种机制, 并认为与入射角度无关的局域金属等离子表面波(localized SPP)最适合用来实现广角接收. 还报道了关于斜入射空间光激励SPP的结构优化的一些最新进展.     

氟氯共存体系锡在流/熔体相间分配的实验研究

为深入了解与含氟花岗岩有关锡矿床的成矿机制, 在温度为850℃, 压力为100 MPa, 氧逸度接近NNO的条件下开展了氟氯共存体系锡在花岗质熔体相和共存流体相间分配行为的实验研究. 实验通过改变液相中HCl浓度和熔体的铝饱和指数ASI及F含量来观察锡的分配行为. 研究结果显示, 在氟氯共存的花岗质岩浆体系中: (1) 熔体ASI值越高相应锡在流/熔体相间的分配系数D_Sn越大, 过铝质熔体有利于锡分配进入流体相; (2) 流体相中HCl浓度越大越有利于锡分配进入流体相中; (3) 实验固相产物熔体相中氯含量随体系氟氯含量的增大而升高, 且熔体相中氟氯含量具有正相关关系; (4) 含F高的熔体(F含量约大于1 wt%)有利于锡在熔体相中富集从而可为锡矿的形成提供物质来源, 当熔体相中氟含量从约1 wt%左右逐渐减小后锡的分配系数明显增大, 流体相中HCl浓度越高D_Sn增涨幅度越大越明显, 即氟含量减小后有利于锡分配进入富氯液相中, 从而有助于热液型锡矿床的形成.     

DNA damage defines sites of recurrent chromosomal translocations in B lymphocytes

Recurrent chromosomal translocations underlie both haematopoietic and solid tumours. Their origin has been ascribed to selection of random rearrangements, targeted DNA damage, or frequent nuclear interactions between translocation partners; however, the relative contribution of each of these elements has not been measured directly or on a large scale. Here we examine the role of nuclear architecture and frequency of DNA damage in the genesis of chromosomal translocations by measuring these parameters simultaneously in cultured mouse B lymphocytes. In the absence of recurrent DNA damage, translocations between Igh or Myc and all other genes are directly related to their contact frequency. Conversely, translocations associated with recurrent site-directed DNA damage are proportional to the rate of DNA break formation, as measured by replication protein A accumulation at the site of damage. Thus, non-targeted rearrangements reflect nuclear organization whereas DNA break formation governs the location and frequency of recurrent translocations, including those driving B-cell malignancies.     

The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers

Colorectal tumours that are wild type for KRAS are often sensitive to EGFR blockade, but almost always develop resistance within several months of initiating therapy. The mechanisms underlying this acquired resistance to anti-EGFR antibodies are largely unknown. This situation is in marked contrast to that of small-molecule targeted agents, such as inhibitors of ABL, EGFR, BRAF and MEK, in which mutations in the genes encoding the protein targets render the tumours resistant to the effects of the drugs. The simplest hypothesis to account for the development of resistance to EGFR blockade is that rare cells with KRAS mutations pre-exist at low levels in tumours with ostensibly wild-type KRAS genes. Although this hypothesis would seem readily testable, there is no evidence in pre-clinical models to support it, nor is there data from patients. To test this hypothesis, we determined whether mutant KRAS DNA could be detected in the circulation of 28 patients receiving monotherapy with panitumumab, a therapeutic anti-EGFR antibody. We found that 9 out of 24 (38%) patients whose tumours were initially KRAS wild type developed detectable mutations in KRAS in their sera, three of which developed multiple different KRAS mutations. The appearance of these mutations was very consistent, generally occurring between 5 and 6 months following treatment. Mathematical modelling indicated that the mutations were present in expanded subclones before the initiation of panitumumab treatment. These results suggest that the emergence of KRAS mutations is a mediator of acquired resistance to EGFR blockade and that these mutations can be detected in a non-invasive manner. They explain why solid tumours develop resistance to targeted therapies in a highly reproducible fashion.     

Identification of hundreds of conserved and nonconserved human microRNAs

MicroRNAs are noncoding RNAs of approximately 22 nucleotides that suppress translation of target genes by binding to their mRNA and thus have a central role in gene regulation in health and disease. To date, 222 human microRNAs have been identified, 86 by random cloning and sequencing, 43 by computational approaches and the rest as putative microRNAs homologous to microRNAs in other species. To prove our hypothesis that the total number of microRNAs may be much larger and that several have emerged only in primates, we developed an integrative approach combining bioinformatic predictions with microarray analysis and sequence-directed cloning. Here we report the use of this approach to clone and sequence 89 new human microRNAs (nearly doubling the current number of sequenced human microRNAs), 53 of which are not conserved beyond primates. These findings suggest that the total number of human microRNAs is at least 800.     

Model uncertainty and policy choice: A plea for integrated subjectivism

A question at the intersection of scientific modeling and public choice is how to deal with uncertainty about model predictions. This “high-level” uncertainty is necessarily value-laden, and thus must be treated as irreducibly subjective. Nevertheless, formal methods of uncertainty analysis should still be employed for the purpose of clarifying policy debates. I argue that such debates are best informed by models which integrate objective features (which model the world) with subjective ones (modeling the policy-maker). This integrated subjectivism is illustrated with a case study from the literature on monetary policy. The paper concludes with some morals for the use of models in determining climate policy.