Mean waiting time approximation for a real time polling system

This paper considers a novel polling system with two classes of message which can experience an upper bounded time before being served. The station serves these two classes with mixed service discipline, one class with exhaustive service discipline, and the other with gated service discipline. Using iterative method, we have developed an approximation method to obtain the mean waiting time for each message class. The performance of approximation has been compared with the simulation results. The expression for the upper bound of waiting time is given too.     

基于AST的克隆序列与克隆类识别

为了减少代码冗余,改善程序结构,提出一种新的基于抽象语法的代码克隆识别方法,归纳出常见的代码克隆形式并给出相应的重构技术.用二叉树表示源程序的抽象语法(BAST),逐条判断各语句BAST子树的同构性,识别出相似的语句序列作为克隆序列;根据子树同构识别一元克隆类,然后通过克隆类的连接操作,逐步识别二元及任意元数的克隆类.实验分析了多个开源软件,识别出了其中的克隆序列以及克隆类,从中归纳出4种常见的代码克隆,其基本特征分别为:相同的程序点访问同类对象的不同属性、部分变量名不同、针对不同的数据类型实施相同的操作、修改克隆区域外定义的变量,并对这4种代码有效地实施了重构.     

置换群作用于一类映射集的等价类的计数

应用Burnside-Polya计数定理与容斥原理等组合分析方法研究置换群作用于一类映射集的等价类的计数,具体得到循环置换群与二面体置换群作用下的一类映射集的等价类的显式计数公式及其相关的平面环型错排、空间环型错排的计数公式以及组合恒等式,拓展了已有文献的研究结果。     

基于工业基础类标准的参数化实体模型数据交互技术

针对已有技术参数化程度低、信息易丢失的缺陷,提出了基于工业基础类(IFC)标准的参数化实体模型数据交互技术.确立了实体模型IFC格式文件的基本框架,研究了实体模型各类信息的参数化IFC格式数据表达方法,并通过软件编程实现.结果表明,该参数化实体模型数据交互技术可准确描述复杂实体模型,生成的IFC格式文件可在各主流BIM...     

Role of Nef in primate lentiviral immunopathogenesis

More than a decade ago it was established that intact nef genes are critical for efficient viral persistence and greatly accelerate disease progression in SIVmac-infected rhesus macaques and in HIV-1-infected humans. Subsequent studies established a striking number of Nef functions that evidently contribute to the maintenance of high viral loads associated with the development of immunodeficiency in the 'evolutionary-recent' human and the experimental macaque hosts. Recent data show that many Nef activities are conserved across different lineages of HIV and SIV. However, some differences also exist. For example, Nef alleles from most SIVs that do not cause disease in their natural monkey hosts, but not those of HIV-1 and its simian precursors, down-modulate TCR-CD3 to suppress T cell activation and programmed death. This evolutionary loss of a specific Nef function may contribute to the high virulence of HIV-1 in humans.     

The specificity of binding of glycoprotein hormones to their receptors

The glycoprotein hormone receptor family is peculiar because, in contrast to other G protein-coupled receptors, a large N-terminal extracellular ectodomain is responsible for hormone recognition. Hormone-receptor pairs have evolved in such a manner that a limited number of positions both at the 'seat-belt' domain of the hormone and the leucine-rich repeats of the receptor, play attractive and repulsive interactions for binding and specificity, respectively. Surprisingly, the constitutive activity of the receptor, mostly modulated by highly conserved amino acids within the heptahelical domain of the receptor (i.e., outside the hormone binding region), also regulates effectiveness of hormone recognition by the extracellular part. In this review we analyze, at the molecular level, these important discriminating determinants for selective binding of glycoprotein hormones to their receptors, as well as natural mutations, observed in patients with gestational hyperthyroidism or ovarian hyperstimulation syndrome, that modify the selectivity of binding.     

Understanding BACE1: essential protease for amyloid-β production in Alzheimer’s disease

The identification of the aspartic protease BACE1 (β-secretase) was a defining event in research aimed at understanding the molecular mechanisms that underlie Alzheimer’s disease (AD) pathogenesis. This is because BACE1 catalyses the rate limiting step in the production of amyloid-β (Aβ) the principal component of plaque pathology in AD, the excessive production of which is believed to be a primary cause of neurodegeneration, and cognitive dysfunction in AD. Subsequent discoveries showed that genetic deletion of BACE1 completely abolishes Aβ production and deposition in vivo, and that BACE1 activity is significantly increased in AD brain. In this review we present current knowledge on BACE1, discussing its structure, function and complex regulation with a view to understanding BACE1 function in the brain, and BACE1 as a target in blocking aberrant Aβ production in AD. Received 15 May 2008; received after revision 13 June 2008; accepted 18 June 2008     

Structural biology of the purine biosynthetic pathway

Purine biosynthesis requires ten enzymatic transformations to generate inosine monophosphate. PurF, PurD, PurL, PurM, PurC, and PurB are common to all pathways, while PurN or PurT, PurK/PurE-I or PurE-II, PurH or PurP, and PurJ or PurO catalyze the same steps in different organisms. X-ray crystal structures are available for all 15 purine biosynthetic enzymes, including 7 ATP-dependent enzymes, 2 amidotransferases and 2 tetrahydrofolate-dependent enzymes. Here we summarize the structures of the purine biosynthetic enzymes, discuss similarities and differences, and present arguments for pathway evolution. Four of the ATP-dependent enzymes belong to the ATP-grasp superfamily and 2 to the PurM superfamily. The amidotransferases are unrelated, with one utilizing an N-terminal nucleophileglutaminase and the other utilizing a triad glutaminase. Likewise the tetrahydrofolate-dependent enzymes are unrelated. Ancestral proteins may have included a broad specificity enzyme instead of PurD, PurT, PurK, PurC, and PurP, and a separate enzyme instead of PurM and PurL. Received 26 May 2008; received after revision 30 June 2008; accepted 9 July 2008     

Two-tiered hypotheses for Duchenne muscular dystrophy

New approaches to understanding and designing treatments for Duchenne muscular dystrophy (DMD) may emerge from two hypotheses outlined here. The proposal that growing skeletal muscle is more susceptible to necrosis than adult muscle raises the possibility that less intensive treatments may be sufficient to protect muscles during the adult phase. The second proposal is that a different balance of cell and molecular events contributes to acute necrosis (e.g. resulting from exercise) compared with chronic damage of dystrophic muscle. Validation of such differences presents the potential for more specific targeting of drugs or nutritional interventions to events downstream of the dystrophin deficiency. A deeper understanding of the events arising as an early consequence of dystrophin deficiency in these two situations may strengthen approaches to therapy for DMD designed to improve muscle function and the quality of life. Received 18 December 2007; received after revision 9 January 2008; accepted 25 February 2008