散射和结构——量子物理学中的要点和相似性

著名物理学家卢瑟福有一句名言：“如果你不能用简单的、非技术的术语解释一个结果，你就没有真正弄懂它”。作者们认为这样一句名言最恰当地表达了他们撰写本书的目的。     

螺旋压缩机：数学模型和性能计算

本书是施普林格出版社2005年出版的一本关于螺旋压缩机的新著。螺旋式压缩机是一种最常见的用于压缩气体的机器，由于其构造简单、工作效率高而受到人们的关注。本书系统阐述了螺旋压缩机的种类、几何参数转子的设计工作原理和螺旋压缩机的计算。     

纳米技术手册

“纳米材料”是指在纳米尺度（0．1～100nm范围，1nm=10^-9m）上研究物质的特征和相互作用，以及利用纳米尺度的特征开发新产品的一门科学和技术。纳米科技包含纳米材料、纳米器件和对它们的检测与表征等应用性很强的研究和技术领域。通常说的纳米检测和表征是指在纳米尺度上分析纳米结构材料和器件的组成、构造，并且进一步探索新现象，作为发展新的器件和功能材料的手段。     

无线网络的移动管理：数据的复制和应用

在无线通讯系统中，网络通过从数据库中查找用户信息来跟踪用户，这样就需要把用户信息事先存储在大量的数据库中。本书讨论了有关在数据库中复制用户信息并更新的若干问题。     

数字通信系统 第三版

本书全面介绍了数字通信系统的理论和实际应用方法，并且包含了在数字信号传输中需要运用的关于设计、实现和测试的最新方法和技术。此书介绍的基本技术有：纠错码、多路复用、数字调制、数字用户线路、电缆调制、移动无线网络、城域网和光纤网络。新的工业标准有：声音／视频编码、SONET/SDH、DWDM、ATM、宽带无线网、网络同步和网络管理。每一章节后都有评述和参考文献和大量习题（无答案）。     

MERGING OPTIMALITY CONDITIONS WITH GENETIC ALGORITHM OPERATORS TO SOLVE SINGLE MACHINE TOTAL WEIGHTED TARDINESS PROBLEM

1.Introduction Production sequencing and scheduling is one of the most important activities in production planning and control.Sequencing is defined as the order in which the jobs are processed through the machines.The allocation of machines over time to process a collection of jobs is defined as Scheduling.Several methods have been developed to solve the scheduling problem which can be classified as follows:1)efficient optimal methods,2)implicit and explicit,or complete enumerative methods,a…     

不同降水强度4种草地群落土壤呼吸通量变化特征

利用静态暗箱法, 对内蒙古锡林河流域沿降水梯度4种半干旱草地类型进行了连续2年的野外定位试验, 对比研究了沿降水梯度4种不同草地类型土壤呼吸通量的变化特征, 统计分析了水热因子对草地土壤呼吸通量特征的可能影响, 并建立了土壤呼吸通量与水热因子间的数值关系模式, 同时利用野外连续完整的观测数据对不同草地类型土壤CO₂年排放量分别进行了估算. 结果表明: 土壤呼吸通量存在明显的季节变化规律, 沿降水梯度各草地类型土壤呼吸通量的季节变化型式基本相同, 各草地群落土壤呼吸均以春末和夏季较高, 秋冬季排放量较低, 不同草地类型冬季均观测到土壤呼吸的负通量, 对其机制的进一步研究有利于对土壤年呼吸总量的准确估算; 沿降水梯度4种草地类型土壤年(或生长季)呼吸量均沿降水梯度递减, 表现为贝加尔针茅草原>羊草草原>大针茅草原>克氏针茅草原; 不同草地类型土壤呼吸通量在植物生长季与0~10 cm以及10~20 cm土壤含水量均呈不同程度的正相关, 而与气温和表层土壤温度的相关性较弱, 4种草地类型生长季内土壤表层含水量的变化通常能解释土壤呼吸通量变异的70.2%~94.7%, 而在植物非生长季, 土壤呼吸通量更多地受气温及土壤表层地温的限制, 温度条件的变化能解释土壤呼吸通量变化的70%以上.     

Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency

Collagen VI is an extracellular matrix protein that forms a microfilamentous network in skeletal muscles and other organs. Inherited mutations in genes encoding collagen VI in humans cause two muscle diseases, Bethlem myopathy and Ullrich congenital muscular dystrophy. We previously generated collagen VI-deficient (Col6a1-/-) mice and showed that they have a muscle phenotype that strongly resembles Bethlem myopathy. The pathophysiological defects and mechanisms leading to the myopathic disorder were not known. Here we show that Col6a1-/- muscles have a loss of contractile strength associated with ultrastructural alterations of sarcoplasmic reticulum (SR) and mitochondria and spontaneous apoptosis. We found a latent mitochondrial dysfunction in myofibers of Col6a1-/- mice on incubation with the selective F1F(O)-ATPase inhibitor oligomycin, which caused mitochondrial depolarization, Ca2+ deregulation and increased apoptosis. These defects were reversible, as they could be normalized by plating Col6a1-/- myofibers on collagen VI or by addition of cyclosporin A (CsA), the inhibitor of mitochondrial permeability transition pore (PTP). Treatment of Col6a1-/- mice with CsA rescued the muscle ultrastructural defects and markedly decreased the number of apoptotic nuclei in vivo. These findings indicate that collagen VI myopathies have an unexpected mitochondrial pathogenesis that could be exploited for therapeutic intervention.     

Heritable and inducible genetic interference by double-stranded RNA encoded by transgenes

Double-stranded RNA interference (RNAi) is an effective method for disrupting expression of specific genes in Caenorhabditis elegans and other organisms. Applications of this reverse-genetics tool, however, are somewhat restricted in nematodes because introduced dsRNA is not stably inherited. Another difficulty is that RNAi disruption of late-acting genes has been generally less consistent than that of embryonically expressed genes, perhaps because the concentration of dsRNA becomes lower as cellular division proceeds or as developmental time advances. In particular, some neuronally expressed genes appear refractory to dsRNA-mediated interference. We sought to extend the applicability of RNAi by in vivo expression of heritable inverted-repeat (IR) genes. We assayed the efficacy of in vivo-driven RNAi in three situations for which heritable, inducible RNAi would be advantageous: (i) production of large numbers of animals deficient for gene activities required for viability or reproduction; (ii) generation of large populations of phenocopy mutants for biochemical analysis; and (iii) effective gene inactivation in the nervous system. We report that heritable IR genes confer potent and specific gene inactivation for each of these applications. We suggest that a similar strategy might be used to test for dsRNA interference effects in higher organisms in which it is feasible to construct transgenic animals, but impossible to directly or transiently introduce high concentrations of dsRNA.     

Mutations in the gene encoding pejvakin, a newly identified protein of the afferent auditory pathway, cause DFNB59 auditory neuropathy

Auditory neuropathy is a particular type of hearing impairment in which neural transmission of the auditory signal is impaired, while cochlear outer hair cells remain functional. Here we report on DFNB59, a newly identified gene on chromosome 2q31.1-q31.3 mutated in four families segregating autosomal recessive auditory neuropathy. DFNB59 encodes pejvakin, a 352-residue protein. Pejvakin is a paralog of DFNA5, a protein of unknown function also involved in deafness. By immunohistofluorescence, pejvakin is detected in the cell bodies of neurons of the afferent auditory pathway. Furthermore, Dfnb59 knock-in mice, homozygous for the R183W variant identified in one DFNB59 family, show abnormal auditory brainstem responses indicative of neuronal dysfunction along the auditory pathway. Unlike previously described sensorineural deafness genes, all of which underlie cochlear cell pathologies, DFNB59 is the first human gene implicated in nonsyndromic deafness due to a neuronal defect.