Overexpression of rice OsLOL2 gene confers disease resistance in tobacco to Pseudomonas syringae pv. Tabaci

LSD1-related proteins of Arabidopsis with LSD1-like zinc finger domains regulate disease resistance and programmed cell death(PCD). We cloned a rice OsLOL2 gene, orthologous to LSDI of Arabidopsis and expressed it in a tobacco plant. Transgenic tobacco lines displayed enhanced disease resistance to a virulent bacterium Pseudomonas syringae pv. tabaci (Pst). RT-PCR analysis showed that overexpression of OsLOL2 in transgenic tobacco lines resulted in upregulation of two pathogenesis-related (PR) protein genes, PR2 and PR5. Our results suggest that overexpression of OsLOL2 in transgenic tobacco enhances the resistance through the induction of PR pro-teins and hypersensitive response-like reaction.     

Isochorismate synthase is required to synthesize salicylic acid for plant defence.

Salicylic acid (SA) mediates plant defences against pathogens, accumulating in both infected and distal leaves in response to pathogen attack. Pathogenesis-related gene expression and the synthesis of defensive compounds associated with both local and systemic acquired resistance (LAR and SAR) in plants require SA. In Arabidopsis, exogenous application of SA suffices to establish SAR, resulting in enhanced resistance to a variety of pathogens. However, despite its importance in plant defence against pathogens, SA biosynthesis is not well defined. Previous work has suggested that plants synthesize SA from phenylalanine; however, SA could still be produced when this pathway was inhibited, and the specific activity of radiolabelled SA in feeding experiments was often lower than expected. Some bacteria such as Pseudomonas aeruginosa synthesize SA using isochorismate synthase (ICS) and pyruvate lyase. Here we show, by cloning and characterizing an Arabidopsis defence-related gene (SID2) defined by mutation, that SA is synthesized from chorismate by means of ICS, and that SA made by this pathway is required for LAR and SAR responses.     

Overexpression of rice OsLOL2 gene confers disease resistance in tobacco to Pseudomonas syringae pv. Tabaci

LSD1-related proteins of Arabidopsis with LSDl-like zinc finger domains regulate disease resistance and programmed cell death （PCD）. We cloned a rice OsLOL2 gene, orthologous to LSD1 of Arabidopsis and expressed it in a tobacco plant. Transgenic tobacco lines displayed enhanced disease resistance to a virulent bacterium Pseudomonas syringae pv. tabaci （Pst）. RT-PCR analysis showed that overexpression of OsLOL2 in transgenic tobacco lines resulted in upregulation of two pathogenesis-related （PR） protein genes, PR2 and PR5. Our results suggest that overexpression of OsLOL2 in transgenic tobacco enhances the resistance through the induction of PR proteins and hypersensitive response-like reaction.     

有局域场的三能级∧系统的瞬态解析结果

考虑Lorentz局域场效应的影响，我们在Liouville运动方程的基础上用微扰理论分析了一个三能级系统的非线性响应．在非线性光学响应中，两波矢分别为k1，k2的连续相干脉冲将会在新的方向产生新的光波．计算之后，我们给出四波混频信号关于Lorentz局域场因子l的表达式，发现负时间延迟时在2k2-k1方向仍有四波混频信号，四波混频信号的频率也有所改变．     

改善机载雷达方位聚焦的成像处理试验研究

雷达（SAR）信号相位的稳定性对于成像处理后图像的方位向分辨率的高低有至关重要的影响．由于飞行平台运动误差或湍流大气中微波传播的影响会直接导致信号相位的波动,机载SAR的方位聚焦一直是SAR成像研究中的重要内容．这里介绍一种基于相位梯度自动聚焦矫正信号相位的高分辨率机载SAR成像处理方法,利用这种方法,对真实的机载SAR信号实验数据进行成像处理．试验表明：在缺乏机载平台运动补偿系统提供飞机运动状况信息的情况下,该成像方法能够有效地估计和补偿相位误差,从而可获得方位向分辨率明显提高的机载SAR图像．     

基于六自由度定位的SAR阵元位置误差校正

为了能够消除采用阶跃调频连续波体制的地面合成孔径雷达(GB-SAR)由于偏离理想航线产生的误差,提出了一种基于六自由度电磁敏感度定位系统测量SAR精确航线的方法,对雷达自身的位置进行定位、校正。使系统定位距离误差小于1 cm,角度误差小于1,°但仍然对成像效果有一定影响。因此,对于由定位系统产生的阵元误差采用对信号导向矢量的绝对相位进行最小二乘线性拟合,进而估计出阵元位置误差的方法,并对其进行校正。仿真的成像结果表明,不需迭代运算即可完成对阵元位置误差的有效校正,具有较低的运算复杂度和较高的估计精度。     

基于MA的可生存系统基本服务模型

可生存性系统是指当系统面临外部的攻击与入侵,内部的错误与紊乱时,仍能继续履行事先确定好的基本服务,直到入侵结束,系统恢复正常运行为止.可生存性系统最显著的特点是,系统处于危机情况时,系统的基本服务仍能继续履行.因此,在可生存性系统中怎样保障基本服务的继续履行就变的非常重要.Mobile Agent作为一项新的技术,除了具有反应性、自治性、面向目标性等Agent的基本特点外,还有其独特性,即具有移动性的特点.在分析了可生存性理论和Mobile Agent的特点基础之上,笔者提出了基于Mobile Agent的移动性,来保障可生存性系统中基本服务继续履行的模型--MESMMA(A Model For Essential Services Mobility Based On Mobile Agent),并且着重探讨了MESMMA系统的结构设计、运行过程和各种Mobile Agent的功能.     

一种无线异构网络的垂直切换算法

针对移动台在异构网络之间切换性能不理想的问题,提出基于通用移动通信系统(UMTS)和无线局域网(WLAN)构建的具有接入控制单元(ACU)的异构网络模型.采用描述网络性能和服务质量的代价函数选择首选网络;利用一种基于信号强度累积量和距离准则的联合优化策略进行垂直切换判决,进一步对该方案进行切换率和丢包率的分析.仿真结果表明,该算法可以在维持较小丢包率的情况下,有效地减少切换次数,消除“乒乓效应”,改善切换呼叫阻塞率,取得较好的切换性能.     

FGF-induced vesicular release of Sonic hedgehog and retinoic acid in leftward nodal flow is critical for left-right determination

The precise specification of left-right asymmetry is an essential process for patterning internal organs in vertebrates. In mouse embryonic development, the symmetry-breaking process in left-right determination is initiated by a leftward extraembryonic fluid flow on the surface of the ventral node. However, it is not known whether the signal transduction mechanism of this flow is chemical or mechanical. Here we show that fibroblast growth factor (FGF) signalling triggers secretion of membrane-sheathed objects 0.3-5 microm in diameter termed 'nodal vesicular parcels' (NVPs) that carry Sonic hedgehog and retinoic acid. These NVPs are transported leftward by the fluid flow and eventually fragment close to the left wall of the ventral node. The silencing effects of the FGF-receptor inhibitor SU5402 on NVP secretion and on a downstream rise in Ca2+ were sufficiently reversed by exogenous Sonic hedgehog peptide or retinoic acid, suggesting that FGF-triggered surface accumulation of cargo morphogens may be essential for launching NVPs. Thus, we propose that NVP flow is a new mode of extracellular transport that forms a left-right gradient of morphogens.     

53BP1 promotes non-homologous end joining of telomeres by increasing chromatin mobility

Double-strand breaks activate the ataxia telangiectasia mutated (ATM) kinase, which promotes the accumulation of DNA damage factors in the chromatin surrounding the break. The functional significance of the resulting DNA damage foci is poorly understood. Here we show that 53BP1 (also known as TRP53BP1), a component of DNA damage foci, changes the dynamic behaviour of chromatin to promote DNA repair. We used conditional deletion of the shelterin component TRF2 (also known as TERF2) from mouse cells (TRF2(fl/-)) to deprotect telomeres, which, like double-strand breaks, activate the ATM kinase, accumulate 53BP1 and are processed by non-homologous end joining (NHEJ). Deletion of TRF2 from 53BP1-deficient cells established that NHEJ of dysfunctional telomeres is strongly dependent on the binding of 53BP1 to damaged chromosome ends. To address the mechanism by which 53BP1 promotes NHEJ, we used time-lapse microscopy to measure telomere dynamics before and after their deprotection. Imaging showed that deprotected telomeres are more mobile and sample larger territories within the nucleus. This change in chromatin dynamics was dependent on 53BP1 and ATM but did not require a functional NHEJ pathway. We propose that the binding of 53BP1 near DNA breaks changes the dynamic behaviour of the local chromatin, thereby facilitating NHEJ repair reactions that involve distant sites, including joining of dysfunctional telomeres and AID (also known as AICDA)-induced breaks in immunoglobulin class-switch recombination.     

显影抑制剂释放化合物的合成——2-乙酰氧基-1-苯基-2-[(1-苯基-1H-四唑-5-基)硫基]-乙酮

作者企图按专利程序制备文题所述显影抑制剂释放化合物(DIR化合物),但所得结果与报道不一致。1-苯基-2-溴-2-[(1-苯基-1 H-四唑-5-基)硫基]-乙酮与羧酸盐缩合反应的结果显示,该反应的主要产物为1-苯基-2,2-双[(1-苯基-1 H-四唑-5-基)硫基]-乙酮,而并非所期待的乙酰基化合物。最后,通过一条新的合成路线,经1-苯基-2-乙酰氧基-2-溴-乙酮与1-苯基-1H-四唑硫醇钠缩合,成功地制得了上述DIR化合物。总收率超过70%。     

Reporter-based screen for Arabidopsis mutants compromised in nonhost resistance

Plants are exposed to many potentially pathogenic microbes in the environment, but each species is only susceptible to a limited number of pathogens. The broad resistance is referred to as nonhost re-sistance. To date, little is known about the underlying mechanism of nonhost resistance and the sig-naling transduction process. Here we describe a simple method for isolating Arabidopsis nonhost re-sistance mutants against a nonadapted bacterial pathogen. A RAP2.6 promoter-driven LUC reporter system was developed to replace the tedious bacterial growth assay during the primary screening. The RAP2.6-LUC reporter gene is normally induced by the virulent bacterium Pseudomonas syringae pv tomato but not the nonadapted bacterium P. syringae pv phaseolicola. By using this method we iso-lated 4 mutants displaying strong reporter activity in response to P. syringae pv phaseolicola, which were characterized in some details. ebs1, ebs2, ebs3, and ebs4 (enhanced bacterial susceptibility) were compromised in resistance against P. syringae pv phaseolicola and/or P. syringae pv tomato. In addi-tion, ebs4 showed enhanced hypersensitive response to the incompatible bacterium P. syringae pv tomato (avrB). These results demonstrated that the method is suited for large scale screening for nonhost resistance mutants.     

Accurate localization and excision of genomic islands in four strains of <Emphasis Type="Italic">Pseudomonas aeruginosa</Emphasis> and <Emphasis Type="Italic">Pseudomonas fluorescens</Emphasis>

Mobile genomic islands (GIs) can be excised from the chromosome, then form a circular intermediate and be reintegrated into the chromosome by the GI internal integrase. Some mobile GIs can also be transferred into a new receptor cell by transformation, conjugation, or transduction. The action sites of the integrase are usually flanked direct repeats (DRs) of the GIs. Accurate localization of the flanking sequences is a precondition for determining the mobility of the GI. Mobile GIs are generally associated with transfer RNAs (tRNAs). Based on the correlation between flanking sequences and tRNA sequences, the flanking sequences of 11 putative mobile GIs in Pseudomonas aeruginosa PAO1, P. aeruginosa PA14, P. fluorescens Pf-5 and P. fluorescens Pf0-1 were identified. Among the 11 GIs, Pf0-1GI-1 is responsible for benzoate degradation. PAO1GI-1, Pf5GI-2, Pf5GI-3, and Pf5GI-4 were confirmed experimentally to be excised from a chromosome to form a circular intermediate. The action sites of the integrases are these GIs direct repeats. Due to distinct DRs, cutting sites for the internal integrase of PAO1GI-1, Pf5GI-2, Pf5GI-3 and Pf5GI-4 were determined outside the T-loop of the tRNA^Gly gene, outside the anticodon loop of the tRNA^Ser gene and tRNA^Lys gene, and at the asymmetric 3′-end of the tRNA^Leu gene, respectively. PAO1GI-1 and other mobile GIs may be transferred into many different strains that belong to different phyla because of the clear flanking sequences. This study describes basic information about the action sites of the integrases, assesses the mobility of GIs, and can help design and transfer mobile GIs to candidate strains.     

基于FPGA的SAR原始数据实时压缩系统设计与实现

文章讨论一种基于FPGA,并采用分块自适应量化(BAQ)算法的SAR原始数据实时压缩处理系统的设计方法,该设计可大大提高实时压缩处理系统的性能,降低数据率,突破卫星下传数据率的限制。BAQ模块内部采用4路并行处理的逻辑结构来计算数据块的统计特性;优化设计量化电平实时计算乘法器资源、量化比较逻辑结构;当I/Q两路采用多模块分时复用模型时,可使整个系统压缩处理能力成倍增加。通过测试表明,BAQ模块的最高运行速度可达到149 MHz,单个模块处理能力已达到1 Gbps以上,其中压缩比8/3时信号失真噪声比(SDNR)大于14 dB。     

基于小波和分形理论的多径衰落信号分析

首次将小波理论和分形理论相结合来分析多径衰落信号，从多径衰落信号产生的动力学机制出发，指出了多径衰落信号具有分形的特征，进一步研究多径衰落信道的多重分形特性，分析并指出了多重分形维数是描述无线信道传播特性的重要参数，根据多径衰落信道参数突变，首次指出了多径衰落信号具有局部奇异性，其局部奇异性对信道参数估计和信号重构有着重要的作用，中提出了短时网格分形维数的定义和给出了其计算的详细算法，用Lipschitz指数来表征局部奇异性，利用小波检测多径衰落信号奇异性和信号重构。仿真实验结果表明：小波重构后信号具有很好去噪性能；多径衰落信号不同尺度下小波变换系数具有自相似性，论证了多径衰落信号的分形特性，不同移动速度时多径衰落信号的多重分形特性仿真实验表明：随着移动速度增大，其短时网格分形维数也变大。     

移动IP在校园网的应用设计

分析了移动IP的基本原理,从实际应用的角度详细阐述了移动IP在校园网中的设计与实现过程,重点对网络架构设计、技术选择、上联方式设计等进行了分析设计。     

利用高介电材料提高胎儿磁共振射频安全性理论研究

探究应用高介电材料(HDM)降低胎儿磁共振成像(fetus MRI)扫描中组织射频能量比吸收率(SAR)在理论上的可行性。建立13周胎儿和成人女性盆腔混合数值模型。通过计算机仿真计算1.5 T和3 T场强下普通扫描及应用不同HDM时的部分身体比吸收率(partial body SAR)和局部比吸收率(local SAR)的分布规律,以及两种场强下普通扫描和应用两种形状HDM取得最佳胎儿local SAR最大值时的B+1场均匀性。通过应用合适的HDM,能够显著降低1.5 T和3 T fetus MRI中的SAR值。在1.5 T和3 T成像时当取得最佳胎儿local SAR最大值时,分别可使胎儿local SAR最大值比普通扫描时下降12.90%和24.75%。这项研究表明通过应用合适的HDM,可以降低在临床上进行fetus MRI时的SAR值来提高胎儿的安全性。     

合成孔径雷达回波信号线性调频特性分析

本文从合成孔径雷达(SAR)回波信号的特点出发,对SAR回波信号的线性调频特性、频谱特性进行了详细的分析.由于SAR回波信号的线性调频特性,对方位向和距离向的SAR信号进行脉冲压缩,可实现SAR回波数据的成像.本文首先构建了二维线性调频信号,分别通过两个一维傅立叶变换实现对信号的脉冲压缩,并对压缩后的波形进行质量评估,可以得到积分旁瓣比小于-10dB的信号质量.通过这种仿真过程,实现对SAR成像算法的进一步理解.