Evolutionary relationship and species separation of four morphologically similar stichotrichous ciliates （Protozoa, Ciliophora）

Phylogenetic and taxonomic studies on ciliate protists using molecular approaches have been demonstrated to be very reliable to form strong conclusions and results. In the present work, species separation of some morphologically similar stichotrichous ciliates, two species of Pseudokeronopsis and two species of Apokeronopsis, was reexamined using amplified ribosomal DNA restriction analysis (PCRRFLP). Five of 10 restriction enzymes revealed species-specific polymorphic patterns, of which four similar stichotrichs could be significantly separated and identified. Among them, EcoR I offered almost no significantly different restriction fragment patterns, but the four species could be separated from one another and identified with Hae III. Distinctly different restriction digestion haplotypes and similarity indices separated the species, and were used to construct a phylogeny. Phylogenies based on ITS2 nucleotide sequences and ITS2 secondary structures supported the separation of Pseudokeronopsis and Apokeronopsis using RFLP analysis, although three Pseudokeronopsis carnea populations did not cluster together. In addition, phylogenetic analyses using multiple algorithms confirmed that these two genera formed two distinct groups within the urostylids.     

Action Research: Its Foundations in Open Systems Thinking and Relationship to the Scientific Method

This paper considers those interpretations of action research that can be traced to Kurt Lewin at the Research Center for Group Dynamics at the University of Michigan, and the work in social ecology by Emery and Trist at the Tavistock Institute. It locates the logical basis of these interpretations in the philosophy of pragmatism, particularly as it relates to Peirce’s inferential logic and inquiry system. Drawing on this argument, and on the significant developments in approaches to systemic thinking over the past 40–50 years, a normative set of criteria is established for action research. The paper concludes that both positivist science (which relates to closed systems thinking) and action research (which relates to open systems thinking) are essential to any complete scientific approach.     

序列运算离散化过程中的误差成因及补偿

为了减少序列离散化过程导致的误差,提出几种概率补偿的方法。由误差的成因入手,分析了离散化过程的误差机理,将利用随机变量的概率分布函数离散化后所得序列,分别以修正公式、平均补偿法及比例补偿法进行补偿,推导出各种误差补偿方法下序列期望值及方差的误差估计公式。结果表明:经误差补偿后,算例中序列期望值误差下降为原误差的8%以下,而方差误差至少可降为原误差的91%。     

C2H2-2.5O2-Ar混合气体临界管径和爆轰胞格及临界能量的实验研究

建立了C2H2-2.5O2-Ar混合气体爆轰临界管径的测试系统,其中高压电火花作为起爆源.首先分别测定了C2H2-2.5O2,C2H2-2.5O2-50%Ar,C2H2-2.5O2-70%Ar三种混合气体在不同初始压力下的爆轰临界管径.结果表明:随着氩气稀释浓度的提高,在管道直径相同的条件下,可形成球形爆轰的临界压力增加,表明物质的爆轰敏感性降低.进一步探究各种物质临界管径与爆轰胞格的关系,得到了三种物质临界管径与胞格宽度的比例系数.最后分析了三种物质的临界管径和直接起爆的临界能量的关联性,并与Lee表面积能量模型对比,实验结果与理论模型基本吻合,得出C2H2-2.5O2-Ar混合气体爆轰临界管径与临界起爆能量之间的关系为Ec=16-1πρ0v2CJIdc3.     

Preface

Energy is stored and transported most easily as chemical energy. The fossil fuels represent solar energy captured and stored as chemical energy by plants over many millions of years. Modern economies depend on this finite, non-renewable energy store. The inexorable march to a global economy and the rising expectations of an expanding world population place ever greater demands on the finite resources of planet     

A novel retinoblastoma therapy from genomic and epigenetic analyses

Retinoblastoma is an aggressive childhood cancer of the developing retina that is initiated by the biallelic loss of RB1. Tumours progress very quickly following RB1 inactivation but the underlying mechanism is not known. Here we show that the retinoblastoma genome is stable, but that multiple cancer pathways can be epigenetically deregulated. To identify the mutations that cooperate with RB1 loss, we performed whole-genome sequencing of retinoblastomas. The overall mutational rate was very low; RB1 was the only known cancer gene mutated. We then evaluated the role of RB1 in genome stability and considered non-genetic mechanisms of cancer pathway deregulation. For example, the proto-oncogene SYK is upregulated in retinoblastoma and is required for tumour cell survival. Targeting SYK with a small-molecule inhibitor induced retinoblastoma tumour cell death in vitro and in vivo. Thus, retinoblastomas may develop quickly as a result of the epigenetic deregulation of key cancer pathways as a direct or indirect result of RB1 loss.