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様式C-1919科学研究費補助金研究成果報告書科学研究費補助金研究成果報告書平成２２年６月１日現在研究成果の概要（和文）：可燃性フィルムの素材に関する実験、調査、研究、分析を十分に実施することができ、日本における映画フィルム保存の基盤をさらに広げることに成功した。

特に近赤外線機器を使用することで、瞬時に可燃性か不燃性かの判別することが可能であることが明らかなった。

また、可燃性フィルムを保存・復元というテーマについても、アナログ的な側面では染色調色の実験を日本ではじめて実施し、またデジタル的な技術を使った長期保存の可能性についても検討することができた。

研究成果の概要（英文）：I accomplished several researches of nitrate materials and improved technical aspects of long-term film preservation. Using the near-infrared spectroscopy machine, it is found out that I can easily distinguish the material of each film base (nitrate or acetate) in an instance. Concerning the preservation and restoration of nitrate films, both new experiments of analog and digital restoration has been executed. On Analog theme, I was able to test the restoration of tinting and toning by traditional way.交付決定額（金額単位：円）直接経費間接経費合計 2008 年度 1,800,000 540,000 2,340,0002009 年度 1,200,000 360,000 1.560.000 年度年度年度総計 3,000,000 900,000 3,900,000研究分野：総合領域科研費の分科・細目：文化財科学キーワード：映画、フィルム、復元、保存、可燃性、アーカイブ１．研究開始当初の背景現在、世界中の多くのフィルム・アーカイブでは、もっとも資料的価値の高い可燃性フィルムを安全に保存できる専用の保存庫を設研究種目：若手研究（B）研究期間：2008～2009課題番号：20700666研究課題名（和文）可燃性フィルムの安全保存に関する基礎的研究研究課題名（英文） Fundamental study of nitrate film materials for safe preserving研究代表者板倉史明(ITAKURA Fumiaki)独立行政法人国立美術館東京国立近代美術館・フィルムセンター・研究員研究者番号：20415623置している。

论文翻译——精选推荐

澳大利亚公司碳排放披露分析Bo Bae Choi, Doowon Lee and Jim PsarosNewcastle Business School, University of Newcastle, Newcastle, Australia摘要目的——本研究旨在报告主要的澳大利亚公司在2006到2008年自愿碳排放披露程度。

本文提供当代关于澳大利亚碳排放报告的数据与解释。

此外，本文的目的是确定可以解释碳信息披露程度的变量。

设计/方法/途径——碳信息披露得分是直接从个体公司的年度报告和可持续发展报告测量得到的。

建立检查表是为了确定公开报道的气候变化与碳排放相关的信息的广度和深度。

调查结果——在作者研究阶段，整体的碳信息披露得分在明显增加。

此外，回归结果表明，具有较高的知名度大型企业倾向更多全面的碳披露。

总的来说，这一结果表明，有可能是该澳国2007年的温室气体与能源法案立法（澳国家温室气体和能源报告法）增强了2008年的自愿碳排放披露，尽管该法案到2009财政年度才生效。

创新点/价值——以前关于澳大利亚环境信息披露的研究都是在还没有引起公众广泛讨论以及对气候变化和碳排放感兴趣之前的基础上进行的。

本文在调查大型澳大利亚公司自愿性信息披露的同事，介绍了强制性排放报告方案，本文研究突出讨论和即将实施的强制性环境信息披露有没有引起更大程度上自愿碳披露。

研究结果可以帮助监管者制定针对行业和具体行为的适当法律，因为披露对利益相关者具有莫大的重要性。

此外，了解是谁和为什么存在披露碳气体排放信息可以帮助绿色团体和其他利益相关者适当地理解关于这种披露的动机。

关键词：碳排放，澳国家温室气体和能源法案，自愿披露，碳排放披露，信息披露，澳大利亚论文类型：研究报告引言全球气候变暖已成为大多数国家越来越重要的政治和商业问题。

已经有来自环保，商业和政治领导人的强烈呼吁，要应对全球变暖带来的威胁及无数挑战。

挑战的一部分是需要各单位的理解和沟通他们对全球变暖的碳排放做出的贡献。

《2024年认知负荷模式下汉英交传策略研究》范文

《认知负荷模式下汉英交传策略研究》篇一一、引言随着全球化的推进，跨文化交流与翻译的频率逐渐增加，汉语与英语之间的交流也变得越来越频繁。

在这一背景下，认知负荷成为了翻译过程中一个重要的研究领域。

认知负荷是指在进行信息处理、记忆和决策时，大脑所需投入的心理资源量。

在汉英交传过程中，认知负荷的合理分配和调控直接影响到翻译的效率和准确性。

因此，本文旨在探讨认知负荷模式下汉英交传的策略，以提升翻译工作的效率和准确性。

二、文献综述在认知负荷模式下进行汉英交传的研究已经引起了广泛的关注。

过去的研究主要集中在翻译过程中认知负荷的来源、分类及影响上。

近年来，研究者开始关注如何通过调整翻译策略来降低认知负荷。

已有研究表明，适当的策略可以帮助翻译者在高认知负荷的情境下提高翻译效率和准确性。

如使用短时记忆技巧、上下文信息预测、词汇和句法结构分析等策略，可以有效降低翻译过程中的认知负荷。

三、汉英交传的认知负荷特点汉英交传过程中，翻译者需要同时处理语言和文化层面的差异，这无疑增加了认知负荷。

首先，汉语和英语在词汇、句法和语篇结构等方面存在差异，这要求翻译者具备扎实的语言基础和良好的语言转换能力。

其次，文化差异也是影响认知负荷的重要因素，翻译者需要具备跨文化交际能力和文化敏感性。

因此，在汉英交传过程中，翻译者需要合理分配注意力资源，以应对高认知负荷的挑战。

四、认知负荷模式下的汉英交传策略针对汉英交传过程中的认知负荷问题，本文提出以下策略：1. 短时记忆技巧：在翻译过程中，利用短时记忆技巧，如关键词记忆、句法结构分析等，帮助翻译者快速捕捉并处理关键信息，降低认知负荷。

2. 上下文信息预测：通过分析上下文信息，预测即将出现的词汇和句法结构，有助于翻译者提前做好准备，减少临时处理信息的压力。

3. 词汇和句法结构分析：对源语言和目标语言的词汇和句法结构进行深入分析，有助于翻译者更好地理解原文含义，提高翻译准确性。

4. 跨文化交际能力：培养翻译者的跨文化交际能力，使其能够更好地理解和表达不同文化背景下的信息，降低因文化差异引起的认知负荷。

Convergence of the NF-kappaB and IRF pathways in the regulation of the innate antiviral response

Convergence of the NF-k B and IRF pathways in the regulationof the innate antiviral responseJohn HiscottLady Davis Institute for Medical Research -Jewish General Hospital,Departments of Microbiology &Immunology,Medicine and Oncology,McGill University,Montreal,Canada H3T 1E2Available online 13August 2007AbstractThe type I interferon (IFN)a and b promoters have been a leading paradigm of virus-activated transcriptional regulation for more than two decades,and have contributed substantially to our understanding of virus-inducible gene regulation,the coordinated activities of NF-k B and IRF transcription factors,the temporal and spatial recruitment of co-activators to the enhanceosome,and signaling pathways that trigger the innate antiviral response.In 2003,the ISICR Milstein Award was presented to John Hiscott of McGill University and Tom Maniatis of Harvard University for their ongoing research describing the mechanisms of regulation of type 1interferon genes and speciﬁcally for the identiﬁcation of key signaling kinases involved in phosphorylation of the transcription factors IRF-3and IRF-7.The speciﬁc roles played by IRFs and the IKK-related kinases TBK1and IKK e are now recognized within the broader framework of TLR and RIG-I signaling pathways.This review summarizes the unique features of the IKK-related kinases and offers a summary of recent advances in the regulation of the early host response to virus infection.#2007Elsevier Ltd.All rights reserved.Keywords:NF-k B;Type 1interferon;IRFs1.Regulation of type 1IFN transcription by the IRFsThe type 1interferon (IFN)a and b genes are normally silent in mammalian cells,but in response to virus infection or other pathogenic stimuli,are induced rapidly and transiently at the transcriptional level through a combination of distinct mechanisms.Transcription of IFN-b requires the formation of a large,high-order multi-protein complex termed the enhanceosome,which consists of multiple promoter-speciﬁc transcription factors,associated structural components and basal transcription machinery bound to enhancer DNA [1–4].A 60bp DNA fragment,located À110and À36relative to the transcription start site,is a virus-inducible molecular switch composed of four positive regulatory domains (PRDI-IV).The IFN-b gene is activated by the cooperative binding of three transcription factorfamilies (NF-k B,IRFs,and ATF-2/c-Jun),and an archi-tectural protein (HMG I(Y)),to the nucleosome-free PRD regions of the promoter [4].The enhanceosome modiﬁes and repositions a nucleosome that blocks the formation of a transcriptional preinitiation complex on the IFN-b promo-ter;this is accomplished by the ordered recruitment of HATs,SWI/SNF,and basal transcription factors to the virus-inducible enhancer.Acetylation of the nucleosome by the GCN5HAT-containing complex is followed by the recruitment of the CBP-PolII holoenzyme.Next,nucleo-some structure is altered by the SWI/SNF remodeling machine,thus permitting the recruitment of TFIID to the TATA element [5,6].The DNA bending induced upon TFIID binding to the promoter causes sliding of the SWI/SNF-modiﬁed nucleosome to a new position 36bp downstream,thus allowing the initiation of transcription [5].Speciﬁcity of type I IFN induction is achieved by members of the IRF transcription factor family [7,8].In all,nine human IRFs have been identiﬁed (IRF-1–IRF-9);each/locate/cytogfrCytokine &Growth Factor Reviews 18(2007)483–490E-mail address:john.hiscott@mcgill.ca.1359-6101/$–see front matter #2007Elsevier Ltd.All rights reserved.doi:10.1016/j.cytogfr.2007.06.002member shares extensive homology in the N-terminal DNA-binding domain(DBD),characterized byﬁve tryptophan repeat elements located within theﬁrst150aa of the protein.The IRF DNA-binding domain mediates speciﬁc binding to GAAANN and AANNNGAA sequences,termed the IFN-stimulated regulatory element (ISRE)in IFN-stimulated genes(ISGs).In addition to their role in immune regulation,IRFs are also involved in regulation of cell cycle,apoptosis and tumor suppression [8].Each IRF contains a unique C-terminal domain,termed the IRF-association domain(IAD);the unique function of a particular IRF is accounted for by the ability of the IAD to interact with other members of the IRF family and other factors,its intrinsic transactivation potential,and cell type-speciﬁc expression of the IRFs.Interferon regulatory protein-3(IRF-3),a critical player in the induction of type I IFNs following virus infection,is a constitutively expressed phosphoprotein of427aa[9]. Transcriptional activity of IRF-3is controlled by virus and dsRNA induced,carboxyl-terminal phosphorylation events on serines385and386,as well as the serine/threonine cluster between aa396and405[10–13],mediated by the IKK-related kinases—TBK-1and IKK e[14,15].Based on available biochemical data,a model for IRF-3activation proposes that C-terminal phosphorylation induces a con-formational change in IRF-3that allows homo-and hetero-dimerization,nuclear localization,and association with the co-activator CBP/p300[16].Inactive IRF-3constitutively shuttles into and out of the nucleus,whereas phosphoryla-tion-dependent association with CBP/p300retains IRF-3in the nucleus and induces transcription of IFN-b and other genes[17].IRF-7wasﬁrst described to bind and repress the Epstein Bar Virus(EBV)Qp promoter regulating EBV nuclear antigen1(EBV A1)[18]but its importance in virus-induced IFN-a gene regulation was quickly recognized[19–21]. IRF-7is a multifunctional protein with transcriptional activity that,like IRF-3,depends on C-terminal phosphor-ylation[19,22].However,constitutive IRF-7expression is restricted to B cells and dendritic cells;in other cells,IRF-7 is virus and IFN-inducible.Also distinct from IRF-3,IRF-7 has a half-life of approximately30min,which may represent a mechanism that ensures transient IFN induction [19–21].In addition to the DBD,IRF-7contains multiple regulatory domains in the C-terminal region that regulate its activity(reviewed in[17]).In particular,the C-terminal region between aa471and487is the target of virus-induced phosphorylation.Whereas C-terminal phosphorylation modulates the transactivation function of IRF-7[22,23], IFN and virus treatments modulate transcription of the IRF-7gene[24],making IRF-7regulation dually dependent on stimuli.Serines471/472and477/479appear to be important residues of activation;[19,25]substitution of the Ser477/479 with the phosphomimetic Asp also leads to the generation of a constitutively active IRF-7[25].2.The virus activated,IKK-related kinases:TBK-1 and IKKThe requirement for NF-k B activation as a component of IFN-b regulation was recognized[26–28]soon after the initial discovery of NF-k B[29–31]and predated many important discoveries concerning the myriad roles of NF-k B in immunomodulation,lymphocyte development,cell growth,inﬂammation and cancer[32–34].Inducible activation of canonical NF-k B signaling requires phosphor-ylation of the I k B inhibitor by the700–900kDa multi-protein canonical IKK complex[35],composed of two catalytic kinase subunits,IKK a and IKK b,and a non-enzymatic regulatory subunit NF-k B Essential Modulator (NEMO)or IKK g.Based on sequence homology and the potential to stimulate NF-k B signaling,the family of IKK kinases expanded with the discovery of two additional IKKs members—TBK-1/NAK/T2K and IKK e/IKKi(reviewed in [36]).Inducible IKK(IKK e/IKKi)was isolated using a subtractive hybridization technique from LPS-stimulated RAW264.7murine macrophages[37],as well as from an EST database search for IKK homologues[38].The TBK-1/ NAK/T2K kinase was characterized as an IKK homologue involved in TNF a-mediated NF-k B activation[39,40], acting upstream of IKK b[41].Despite the homology and functional similarities between TBK-1and IKK e,the expression patterns of these two IKK related kinases are distinct.TBK-1expression is ubiquitous and constitutive in a wide variety of cells,while IKK e expression is relegated to cells of the immune compartment[36,37],but is inducible in non-hematopoietic cells by stimulation with activating agents such as TNF, PMA,LPS and virus infection[37,42,43]through an NF-k B-dependent mechanism involving upregulation of IKK e expression by C/EBP d and C/EBP b[44].A schematic representation of the IKK kinase family is detailed in Fig.1.Like the classical IKK kinases IKK a and IKK b,the IKK-related kinases IKK e and TBK-1contain a catalytic kinase domain,a leucine zipper domain and a helix-loop-helix domain involved in protein–protein inter-actions[36,37,39,41].IKK e and TBK-1are64%homo-logous to each other,but exhibit limited homology to the classical IKK a and b kinases,with about33%sequence identity within the kinase domain[37–39,41].IKK e and TBK-1also possess a kinase activation loop located between kinase subdomains VII and VIII;serine phosphorylation within the activation loop is required for kinase autopho-sphorylation and induction of enzymatic activity[37,38,45]. In contrast to IKK a and IKK b,the primary amino acid sequence of the IKK e and TBK-1activation loop does notﬁt a canonical MEK consensus motif[37,38,45];that is,the Ser-176residue is replaced with glycine–172SXXXG176 sequence–and a S172A mutation abolishes IKK e and TBK-1catalytic activation.Differences within the activation loop sequence are consistent with the failure of MEKK1or NIK expression to augment IKK-related kinase activity,as occursJ.Hiscott/Cytokine&Growth Factor Reviews18(2007)483–490 484with canonical IKK[37].In contrast to IKK a and IKK b,a S172E phosphomimetic mutation does not generate a constitutively active IKK e and TBK-1kinase,but decreases catalytic activity[37,38].The distinct homologies between the canonical and non-canonical kinases suggested,in retrospect,unique functions for TBK-1and IKK e.Both of the IKK-related kinases were shown early on to phosphorylate in vitro only one of the two critical serine residues(Ser-36)within the signal response domain of I k B a,suggesting that I k B a was not a physio-logical substrate for these IKKs[37,38,40].Nevertheless, TBK-1/NAP1/T2K knockout mice[40]showed striking phenotypic similarities to other mice disrupted in NF-k B signaling components[36].That is,TBK-1À/Àmice were embryonic lethal,and died at E14.5of massive liver degeneration and apoptosis,a result that prompted the idea that IKK e/TBK-1represented upstream components of the IKK complex[36].Both TBK-1and IKK e interact with the TNF-receptor-associated factor(TRAF)-interacting protein/TRAF family member-associated NF-k B activator(I-TRAF/TANK)pro-tein,a modulator of TNF a-induced NF-k B activation[46]. Overexpression of IKK e or TBK-1induces phosphorylation of I-TRAF/TANK,which results in its dissociation from TRAF2and subsequent activation of NF-k B transcription through the classical IKK pathway[39,47].The NAK Associated Protein1(NAP1),a homologue of I-TRAF/ TANK,has also been shown to directly interact with TBK-1 and IKK e[48].Overexpression of NAP1speciﬁcally enhances cytokine induction of an NF-k B-dependent reporter gene,while in vivo depletion of NAP1reduces NF-k B-dependent reporter gene expression and sensitizes cells to TNF a-induced apoptosis[48].It is possible that I-TRAF/TANK or NAP1,or perhaps both,regulate a TBK-1 and IKK e complex through an essential adaptor function, much like NEMO regulates the classical IKK complex[49–52].Physical association between TANK and NEMO suggest that the canonical IKK complex and the IKK-related kinases may exist as a physically associated signaling complex responsible for phosphorylation of additional transcription factors[53,54].Analysis of mouse embryonicﬁbroblasts derived from TBK-1knockout mice demonstrated that TBK-1expression was dispensable for signal-responsive I k B a degradation and NF-k B DNA-binding induction,but was required for NF-k B-dependent gene transcription in the nucleus[39,40]. It was proposed that IKK e and TBK-1regulate NF-k B activation at the level of C-terminal phosphorylation of the NF-k B DNA-binding subunits[36].Recent studies have in fact demonstrated that TBK-1and IKK e directly phosphor-ylate the C-terminal transactivation domain of RelA and c-Rel,which modulates their subcellular localization and transactivation potential[55,56].3.Triggering the interferon antiviral response through an IKK-related pathwayAn important breakthrough in the understanding of the physiological function of TBK-1and IKK e was theJ.Hiscott/Cytokine&Growth Factor Reviews18(2007)483–490485 parison of the family of I k B kinases.The catalytic kinase domain,leucine zipper and helix-loop-helix domain are represented.The four IKK kinases are classiﬁed into two subgroups,based on sequence homology and substrate speciﬁcity.Canonical IKK kinases–IKK a and IKK b–share52%overall homology to each other and phosphorylate both serine residues within the S32xxxS36motif of I k B a.The IKK-related kinases IKK e and TBK-1share61% overall homology to each other and phosphorylate only the Ser36residue of I k B a.Homology between the subgroups is limited,with27%overall homology and 33%homology within the catalytic kinase domain.The position of critical residues involved in catalytic activity are represented.Mutation K44A(IKK a and IKK b)or K38A(IKK e and TBK-1)within the ATP-binding pocket of the kinase domain generates a dominant negative kinase;phosphomimetic mutations S176/180E(IKK a)or S177/181E(IKK b)within the kinase activation loop generates a constitutively active kinase.demonstration that IRF-3and IRF-7are primary in vivo targets of the IKK-related kinases[14,15].These observa-tions culminated a long and often frustrating search for V AK –an acronym for‘the virus-activated kinase’–that involved the use of pharmacological inhibitors,biochemical puriﬁca-tion,yeast-two hybrid screening,and‘best guess’dominant negative kinase constructs.In the end,it was the commitment and hard work of Sonia Sharma,Benjamin tenOever,Nathalie Grandvaux,Professor Rongtuan Lin and previously Marc Servant that led back to the IKK-related kinase activity[14,57].Both TBK-1and IKK e directly phosphorylate IRF-3 and IRF-7at key resides within their C-terminal signal-responsive domain in vitro[25,58]and both kinases target identical serine residues[25,59].Alignment of the primary sequence of the C-terminal domains of IRF-3and IRF-7 revealed an extended SxSxxxS consensus motif that appears to be the target for TBK-1and IKK e[59]. Importantly,expression of the IKK-related kinases is essential to initiate IRF signaling in response to de novo Sendai,VSVor measles virus infection,and treatment with RNAi directed against either IKK e or TBK-1reduces VSV-inducible IRF-3phosphorylation and IRF-dependent gene expression in human cells.Furthermore,expression of the IKK-related kinases generates an IRF-3-dependent anti-viral state in vivo that inhibits de novo VSV replication [14,25].Subsequent analysis in TBK1À/Àand IKK eÀ/Àmice demonstrated that TBK-1is principally involved in down-stream signaling to IRF-3and IRF-7phosphorylation and development of the antiviral response[43,60].Recent experiments however demonstrate that IKK e selectively regulates a subset of IFN responsive antiviral genes during virus infection[61,62].Mice lacking IKK e produced normal amounts of IFN-b,but were hypersusceptible to viral infection because of a defect in the IFN signaling pathway.Speciﬁcally,a subset of type I IFN-stimulated genes were not activated in the absence of IKK e because the interferon-stimulated gene factor3complex(ISGF3)failed to bind to the promoters of the affected genes.About30%of the IFN-inducible ISGs were poorly induced in IkbkeÀ/ÀEFs,including Adar1,Iﬁt3,and Iﬁ203,whereas other ISGs such as Irf7,Prkra(RNA-activated protein kinase),and Stat1,were unaffected.ISGF3binding to IKK e-dependent promoters was subsequently shown to require IKK e kinase activity and in vitro phosphorylation with recombinant IKK e followed by mass spectrometry revealed that IKK phosphorylates Ser708,Ser744,and Ser747[62].The structural and functional consequences of this phosphor-ylation remain to be determined,although it is suggested that IKK e-dependent phosphorylation of STAT1appears to guide the transcriptional machinery to a subset of ISGs required for the direct antiviral response,whereas the IKK-independent genes may function in regulating the IFN signaling required for integration of innate and adaptive immune systems.4.The IKK-related kinases integrate TLR-dependent and-independent signaling pathways Although viral and microbial pathogens are detected by the Toll-like receptor(TLR)family via the recognition of PAMPs,viral infection is also detected through TLR-independent mechanisms[63].Early viral replicative intermediates are detected by two recently characterized cytosolic viral RNA receptors RIG-I[64]and Mda5 [65].Both are DExD/H box RNA helicases,and RIG-I speciﬁcally recognizes50triphosphate containing viral RNA and transmits signals that induce type I IFN-mediated host protective innate immunity against viral infection[66,67]. Structurally,RIG-I contains two caspase activation and recruitment domains(CARD)at its N-terminus and DExD box RNA helicase activity in the C-terminus[64].The importance of the RIG-I pathway in antiviral immunity was conﬁrmed with the generation of RIG-I-deﬁcient mice[68], which revealed that RIG-I and not the TLR system played an essential role in the IFN antiviral response in most cell types—ﬁbroblastic,epithelial and conventional dendritic cells.In contrast,pDCs utilize TLR-mediated signaling in preference to RIG-I[68].Furthermore,MDA5and RIG-I recognize different types of dsRNAs:MDA5recognizes poly(I:C),and RIG-I detects in vitro transcribed dsRNAs. RIG-I is essential for the production of IFN in response to RNAviruses including paramyxoviruses,inﬂuenza virus and Japanese encephalitis virus,whereas MDA5is critical for picornavirus detection.RIG-IÀ/Àand MDA5À/Àmice are highly susceptible to infection with these respective RNA viruses compared to control mice,thus illustrating that these two important RNA sensors are not functionally redundant [69].The adaptor molecule providing a link between RIG-I sensing of incoming viral RNA and downstream activation events was independently elucidated as mitochondrial antiviral signaling adapter(MAVS),also known as(IPS-1/VISA/Cardif)[70–73];like RIG-I,MAVS consists of an amino-terminal CARD domain and a C-terminal transmem-brane domain that localized MAVS to the mitochondrial membrane.MAVS expression activated the IFN-a,IFN-b, and NF-k B promoters in a TBK1-dependent manner[71]. MA VS interacts with RIG-I and recruits IKK e through its C-terminal region;knockdown by siRNA inhibited RIG-I-dependent antiviral responses[73,74].Importantly,MA VS–termed Cardif by Meylan et al.–was cleaved at its C-terminal end,adjacent to the mitochondrial targeting domain—by the NS3-4A protease of Hepatitis C virus[73], arguing that disruption of the mitochondrial association of MA VS was part of the innate immune evasion strategy used by HCV[74–76].The generation of MAVS-deﬁcient mice demonstrated that loss of MA VS abolishes viral induction of IFN and prevents activation of NF-k B and IRF3in multiple cell types,except pDCs[70,77].MAVS is critically required for the host response to RNA viruses but is not required for IFNJ.Hiscott/Cytokine&Growth Factor Reviews18(2007)483–490 486production by cytosolic DNA[78]or by Listeria mono-cytogenes.Mice lacking MA VS are viable and fertile,but are severely compromised in immune defense against viral infection.These results provide in vivo evidence that viral signaling through mitochondrial bound MA VS is speciﬁ-cally required for innate immune responses against viral infection[70,77].5.TRIM25a enters the pictureA recent study demonstrates that TRIM25a,a member of the tripartite motif(TRIM)protein family involved in various cellular processes including cell proliferation and antiviral activity,is crucial for RIG-I-mediated signaling events through its E3ubiquitin ligase activity[79]. TRIM25a contains a RING-ﬁnger domain,aB box/ coiled-coil domain and a SPRY domain and induces robust ubiquitination of the CARD domains of RIG-I.The carboxy-terminal SPRY domain of TRIM25a interacts with the N-terminal CARDs of RIG-I;this interaction effectively delivers the Lys63-linked ubiquitin moiety to the N-terminal CARDs of RIG-I,resulting in a marked increase in RIG-I downstream signaling activity.The Lys172residue of RIG-I is critical for efﬁcient TRIM25a-mediated ubiquitination and for MAVS binding,as well as the ability of RIG-I to induce antiviral signal transduction.Further-more,gene targeting demonstrated that TRIM25a is essential not only for RIG-I ubiquitination but also for RIG-I-mediated IFN production and antiviral activity in response to RNA virus infection.As observed with the ubiquitin-dependent interaction between RIP-1and NEMO [80],TRIM25a-mediated ubiquitination of RIG-I appears to facilitate interaction with MAVS,which ultimately leads to downstream signal transduction.6.Finding NEMOZhao et al.[54]have demonstrated that the NEMO/IKK g adapter also bridges the NF-k B and IRF signaling pathways and promotes cross-talk between the two pathways duringJ.Hiscott/Cytokine&Growth Factor Reviews18(2007)483–490487Fig.2.Schematic model of RNA virus-triggering of the RIG-I/MA VS signaling pathway.The speciﬁc details of the model are described in the text.virus-and RIG-I-mediated signaling to IFN activation. NEMO acts downstream of MA VS and RIG-I,and physically interacts with the TANK adapter to mediate recruitment of TBK1and IKK e to the RIG-I–MA VS complex.Virus-mediated production of endogenous IFN and IFN-inducible gene expression is severely impaired in IkbkgÀ/ÀMEFs and expression of MAVS or D RIG-I in IkbkgÀ/ÀMEFs fails to stimulate IFN signaling.Further-more,NEMO mutants lacking the TANK-binding domain fail to interact with IKK e and TBK1or transduce virus-and MA VS-mediated signals.Knockdown of TANK expression also inhibits SV-mediated ISRE activity and expression of the genes encoding ISG56and RIG-I[54].NEMO mutations have been directly linked to rare human genetic disorders,including incontinentia pigmenti (IP)and ectodermal dysplasia with immunodeﬁciency(ED-ID)[81,82](reviewed in[83–85].Most IP patients have an identical genomic deletion from exon4to10(loss-of function)in NEMO[82],whereas ED-ID patients carry NEMO hypomorphic mutations that impair but do not abolish NF-k B activation.NEMO mutations result in ED-ID patients with a combined,variable but profound immuno-deﬁciency characterized by increased susceptibility to bacterial and viral infections[86–89].Strikingly,most NEMO mutations associated with ED-ID were also severely impaired in their ability to activate the RIG-I signaling pathway[54].These observations raise the intriguing possibility that NEMO mutations with impaired production of type I IFN via the RIG-I pathway contribute to the immunodeﬁciency observed in ED-ID patients.Altogether,these recent studies support a model of cytosolic signaling(Fig.2)and response to RNA virus infection in which RIG-I senses virus-encoded50-tripho-sphate RNA at a early stage after infection through its helicase domain.K63-linked ubiquitination of RIG-I at Lys172via TRIM25a mediates downstream interaction with the mitochondrial MAVS adapter.TRAF3and/or TRAF6are also recruited to MAVS through a direct interaction with a TRAF-interaction motif within MAVS. NEMO association with the adapter TANK facilitates the recruitment of TBK1and IKK e to the MAVS-TRAF complex and results in activation of TBK1and IKK e. Activated TBK1and IKK e phosphorylate IRF3and IRF7, which provoke IFN expression and development of an antiviral state.MAVS-TRAF complexes also activate the canonical NEMO-IKK a-IKK b complex which phosphor-ylates the inhibitory subunit I k B a,resulting in the release of NF-k B and activation of proinﬂammatory gene transcrip-tion.In conclusion,studies in this rapidly movingﬁeld during the past3years have deﬁned a dynamic cytosolic,virus recognition pathway that triggers a robust innate immune response to RNA virus infection;already emerging are the strategies used by different viruses to thwart these defense mechanisms.Future research in this domain will contribute to an understanding of the molecular aspects of viral pathogenesis and promote strategic development of vaccines and antiviral agents.AcknowledgementsThis research was supported by grants from Canadian Institutes of Health Research,the National Cancer Institute of Canada,with the support of the Canadian Cancer Society and CANFAR,the Canadian Foundation for AIDS Research. 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陈攀康英文翻译摘要doc

The operational principle and methods of prevention and treatment of ARP worm virusAbstract: with the rapid development of computer network technology, cyber sources have been fully shared among people. However, at the same time ,when the Internet has brought a lot of convenience, the network seurity has bacome an un avoidable topic. The problems of network security rushed into the network headlines , inculding E-mail security, IP security , Database security, operating system security,and so on. But the root cause of the problem is the basis of moden computer network—the system of TCP/IP . Because at the beginning of its design ,we only considered the application but ignored a lot of security problems and there were a number of flaws and vuinerabilities, which gave the attackers the opportunity to attack the system of computer. Nowadays, ARP worm virus which spreads in the local area network is exactly uses the defects of ARP agreement of TCP/IP system to attck computer. ARP worm virus is not the new type virus, on the contrary, it is the typical virus that employs the operation and mode of tansmission to achieve an aim of ARP cheating. Therefore, the thesis mainly studies the process of ARPcheating, the operational principle and methods of prevention and treatment of ARP worm virus.The thesis is divided into seven chapters to study ARP worm virus. Firstly, the research briefiy introduce the ARP agreement. Secondly , itmakes a key description of the process of ARP cheating and some kinds of attacking patterns. Thirdly, It presents the media that achieves ARPcheating. The fourth chapter persents the operational principle of ARP worm virus. The fifth chapter persents some phenomena of computer system attacked by ARP virus. The sixth chapter presents methods of prevention and treatment of ARP worm virus in precaution and management. The seventh chapter persents the meaning and limitations of the thesis.Key words: ARP agreement; TCP/IP agreement; ARP cheating; worm virus；Foreword: there are a large number of types of computer virus, among which, worm virus has been one of the most furious virus over the past few years. The worm virus boasts the following shared characters: spreading via the leak of computer system and replicating itself in large number, which is injurious to computer system. And ARP virus is not concrete virus definition comparing with worm virus, instead, it is just a general definition of the virus that uses the leak of ARP agreement to attack computer system. Generally speaking, all of ARP virus carries features of worm virus. In a word, ARP worm virus is not the new type virus but a class of virus that applies operational and spearing ways of worm virus to achieve ARP cheating.。

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3640 Med. Phys. 33 „10…, October 2006
II. EXACT FAN-BEAM LT FORMULA Let S represent the unit circle in R2. Assume that ⌫2 ʚ R2 is a 2D differentiable curve parameterized by a͑t͒ , t ෈ R , f is a 2D bounded function with a compact support ⍀2 ʚ R2 \ ⌫2, and a fan-beam projection of f along a scanning trajectory ⌫ 2, D f ͑a, ␪͒ =
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论文翻译

监测焚风的无线传感器网络实时技术文摘。

在台湾因为地理因素，焚风是一种常见的气候现象。

焚风相关的气候表现是高温和低湿度,这常常会导致植物死亡,甚至会导致严重的森林火灾。

自然灾害救助基金在台湾已覆盖焚风造成的财务损失的地区。

然而,没有已开发的焚风监控系统,所以农民不能够立即获得信息和相关的焚风激活的必要减灾计划。

该研究旨在焚风检测和使用无线传感器网络技术构建一个实时系统监控焚风。

因为无线传感器网络的特点低成本,无人控制和传输距离可达80米,是可行的应用网络环境监测。

当焚风发生,无线通信设备在拟议的监测系统将传输的温度和湿度监测收集的信息传到网关模块,和喷水灭火模块行动立即冷却和增加湿度来保护由焚风引起的植物果皮损伤或落果现象。

1引言台湾位于西太平洋,在日本和菲律宾之间的中间, 在夏季和秋季该地区经常遭受台风的侵袭,每年产生巨大的生命损失和财产损失,甚至大大影响农业生产。

台风不仅带来强风和暴雨, 当台风吹过山的时候还导致焚风。

受大气低压影响，大量温暖潮湿的空气吹过迎风山坡，让大量水分落在山坡上这导致了焚风的出现。

当空气流动到山的顶部时,它变得干燥和寒冷，空气中的水分变成了雨水。

因此,当空气到达山腰的时候变得温暖比等效标高迎风坡自大气压力增加。

在台湾,焚风是经常发生在台东地区著名的甜苹果产区,因为这里的空气主要来自北方。

处于受西南风力影响的中央山脉到台东地区范围。

温度和湿度会影响到当地作物的生长和授粉时机;骤降湿度将导致减少水果生产,温度也会影响花粉活力。

因此, 焚风造成的炎热和干燥的天气将严重影响当地的作物以至于影响到当地的经济增长[1]。

在本研究中,我们使用无线传感器网络技术来构建系统它包括各种监控模块,网关模块和实时检测到焚风造成的火灾时的灭火装置,因为这很难用人工来执行。

监控模块包括温度/湿度传感器和章鱼II传感器节点，章鱼II传感器节点是用来监控温度和湿度,并发送数据到数据网关模块。

传感信息会被发送到数据库和手机，农民通过全球移动通信系统可以检查焚风相关信息通过全球移动通信系统。

谈英汉励志谚语互译学位论文

论文编号：华南师范大学增城学院本科毕业论文（设计）题目：谈英汉励志谚语互译姓名：黄静文学号：050114224系别：外语系专业班级：商务英语05级B班指导教师：翁涛2009年 4 月23 日On Translation of English-ChineseEncouraging ProverbsA Thesis Submittedto the Department of Foreign Languages Zengcheng College of South China Normal University in Partial Fulfillment of the Requirementsfor the Degree of Bachelor of ArtsBy Huang JingwenTutor：Weng TaoApril 23,2009Table of ContentsAbstract (i)中文摘要......................................................................................................................................... i i1. Introduction (1)2. The Definition of Proverbs and Encouraging Proverbs (1)3. The Origins (1)3.1 Origins from the folk (1)3.2 Origins from the Bible (2)3.3 Origins from Shakespeare’s works (2)3.4 Origins from Aesop’s Fables (2)3.5Origins from other languages (2)4. The Contents (2)5. Differences between Chinese and English in Encouraging Proverbs (3)5.1 Differences of historical stories (3)5.2 Differences of meanings of words (3)5.3 Differences of language application (5)5.4 Differences of geographic politics and social life (5)5.5 Differences of production way (5)5.6 Differences of religious belief (6)6.The Principles of Translation (6)7. The Translation Methods and Relevant Examples (6)7.1 Literal translation (6)7.2 Paraphrasing (8)7.3 Combination of literal translation and paraphrasing (10)7.4 Borrowing (10)8. Items to Be Focused (10)8.1 Establish image (10)8.2 National and cultural color (11)8.3 Features of language form (11)8.4 Art of language (12)8.5 Abbreviation forms (12)9. Conclusion (12)10. Bibliography (13)11. Acknowledgement (14)AbstractThis paper contains nine parts. They are introduction, the definition of proverbs and encouraging proverbs, the origins, the main contents, differences between Chinese and English in encouraging proverbs, translation principles, translation methods, items to be focused and conclusion.Firstly, introduce the main idea and writing purpose of the essay.Secondly, proverbs are some concise and vivid phrases and sentences descending in the folk with relatively stable forms which summarize the experience of people’s life and work and have the function of teaching and persuading.Thirdly, to be concrete, proverbs are from the folk life, the Bible, Shakespeare’s works, Aesop’s Fables and other languages. They are the summary of people experience in everyday life, so they originated from people’s daily life and experience. Proverbs have a long history.Fourth, the main contents of proverbs are exploring life philosophy and summary of social experience.Fifth, differences between Chinese and English in encouraging proverbs are differences of semantic association, pragmatics, geographic politics and social life, production way, religious belief and historical stories.Sixth, foreignization and domestication are the two translation principles.Seventh, there are four translation methods. They are literal translation, paraphrasing, combination of literal translation and paraphrasing and borrowing.Eighth, some attention should be drawn on how to translate English and Chinese proverbs.Ninth, draw a conclusion of the essay. After reading this paper, one may translate the encouraging proverbs properly.Key words: proverbs; translation principles; translation methods中文摘要这篇论文包括了九个部分。

翻译文献3

JNK/SAPK activity contributes to TRAIL-induced apoptosisIngrid Herr1,Dagmar Wilhelm2,3,Eric Meyer1,4,Irmela Jeremias1,Peter Angel2andKlaus-Michael Debatin*,1,41Division of Molecular Oncology,Deutsches Krebsforschungszentrum, Heidelberg,Germany2Division of Signal Transduction,Deutsches Krebsforschungszentrum, Heidelberg,Germany3Forschungszentrum Karlsruhe,Institute of Genetics,Karlsruhe,Germany4UniversitaÈts Kinderklinik,Ulm,Germany*corresponding author:Prof.Dr.Klaus-Michael Debatin,UniversitaÈts Kinderklinik,Prittwitzstr.43,D-89075Ulm,Germany.tel:+49-731-5027701; fax:+49-731-5026681Received28.5.98;revised26.8.98;accepted13.10.98Edited by S.J.MartinAbstractWe report here that JNK/SAPKs are activated by TRAIL in parallel to induction of apoptosis in human T and B cell lines. Death signaling as well as JNK/SAPK activation by TRAIL in these cells is FADD-and caspase-dependent since dominant-negative FADD or the caspase inhibitor zVAD prevented both, apoptosis and JNK/SAPK activity.JNK/SAPK activity in response to triggering of CD95by an agonistic antibody (a APO-1)was also diminished by dominant-negative FADD or zVAD.Correspondingly,a cell line resistant to a APO-1-induced death exhibited crossresistance to TRAIL-induced apoptosis and did not upregulate JNK/SAPK activity in response to TRAIL or a APO-1.Inhibition of JNK/SAPK activity, by stably transfecting cells with a dominant-negative JNKK-MKK4construct,reduced apoptosis in response to TRAIL or a APO-1.Therefore,activation of JNK/SAPKs by TRAIL or a APO-1occurs downstream of FADD and caspases and contributes to apoptosis in human lymphoid cell lines.Keywords:apoptosis;TRAIL(APO2-L);CD95-L(APO1-L/Fas-L); JNKK-MKK4Abbreviations:JNK,c-Jun N-terminal kinase;SAPK,stress-activated protein kinase;JNKK-MKK4,c-Jun N-terminal kinase, MAP kinase kinase;DILs,Death-inducing ligands;a APO-1, agonistic CD95receptor antibody;TRAIL-R1,TRAIL Receptor1; TRAIL-R2,TRAIL Receptor2;TNF,Tumor Necrosis Factor;TNF-R1,Tumor Necrosis Factor Receptor1;SD,Standard DeviationsIntroductionTRAIL(also known as APO-2ligand)is a member of the tumor necrosis factor(TNF)family of death inducing ligands (DILs)and leads to apoptosis in a wide variety of cells.1,2 The effects of TRAIL are mediated by five distinct cell surface receptors and two of them possess an intact intracellular`death domain'.3±7Among members of the TNF receptor superfamily this intracellular`death domain'is significantly conserved and required to transduce the apoptosis-inducing signal through interaction with the `death domains'of adapter proteins.4,5,8±10FADD is a major adapter molecule which binds either directly or indirectly to the death domains of CD95receptor(CD95), TNF receptor1(TNF-R1)or TRAIL receptor1(TRAIL-R1) and TRAIL receptor2(TRAIL-R2)to transduce the apoptotic signal by activation of caspase8(FLICE)followed by sequential activation of other caspases.5,8,9,11±14The emerging model from these molecular studies is that death receptors via adapter proteins like FADD directly engage and activate apoptotic ICE family proteases.However,this model fails to explain how diverse physiologic signals like sphingosine-1-phosphate,15activation of protein kinase C by phorbol esters16or Bcl-217,18may modulate death receptor-mediated apoptosis.Cross-linking of CD95and TNF-R1can also activate the Jun N-terminal kinase/stress-activated protein kinase(JNK/ SAPK)pathway.19±24The significance of JNK/SAPK activation has been unclear.One hypothesis is that activation of the JNK/SAPK pathway contributes to CD95-and TNF-mediated apoptosis22,25,26whereas others23,24 suggested that JNK/SAPK activation is not required for TNF-R1-induced apoptosis.Recently,a novel signaling protein,DAXX was identified that binds specifically to the CD95death domain.Overexpression of DAXX enhanced CD95-mediated apoptosis by activation of the JNK/SAPK pathway in a FADD independent manner.26Correspond-ingly,activation of JNK/SAPKs by TNF-R1is described to be mediated through a TRAF2pathway which also acts independently of FADD.23,24Signaling events downstream of TRAIL receptors are largely unknown.We found an involvement of JNK/SAPKs in apoptosis signaling downstream of FADD and caspases following ligation of TRAIL and a APO-1in human lymphoid cell lines.ResultsTRAIL induces JNK/SAPK activity downstream of caspasesTo examine whether JNK/SAPKs are activated during TRAIL-induced apoptosis we analyzed JNK/SAPK activity in human T(JURKAT)and B(BJAB)cell lines following treatment with recombinant TRAIL protein.Crosslinking of TRAIL leads to a rapid induction of JNK/SAPKs within2h which parallels the onset of apoptosis(Figure1A,B).TRAIL-control supernatant from Pichia pastoris transfected with empty vector induced neither significant JNK/SAPK activity nor apoptosis.Next we measured TRAIL-induced JNK/ SAPK activity in the presence of zVAD,an inhibitory peptide substrate for caspases which also blocks the receptor proximal caspase FLICE.27Pre-incubation of JURKAT cells with zVAD completely prevented TRAIL-induced JNK/SAPK activity and cell death.In contrast,a APO-1-mediated activity of JNK/SAPKs was not totally prevented by zVAD(Figure 1D).This might be due to a cross-talk between the FADD-and DAXX-dependent signaling pathways initiated by triggering of CD95.26TRAIL-induced JNK/SAPK activity and apoptosis was also not detectable in JURKAT-derived JAPO cells.This cell line exhibits cross-resistance towards TRAIL and a APO-1-mediated apoptosis and does neither cleave caspases nor activate JNK/SAPKs although CD95 receptor is expressed(Figure1A and C and data not shown).This suggests that TRAIL induces JNK/SAPK activity downstream of FLICE/caspases in lymphoid cell lines similar as shown for CD95signaling(Figure1D).19 Therefore,a common element of the CD95and TRAIL pathway might be defective in JAPO cells which is necessary for JNK/SAPK activation.TRAIL-induced apoptosis and JNK/SAPK activity depends on intact FADD signalingTo further dissect the TRAIL-induced pathway leading to JNK/ SAPK activation we determined the effect of FADD signaling located upstream of FLICE/caspases and used a B cell line in which FADD signaling was blocked by stable transfection of a FADD dominant-negative construct(BJAB-FADD-DN cells). In BJAB-FADD-DN cells apoptosis and activation of JNK/ SAPKs induced by treatment with TRAIL was totally inhibited compared to the vector control line(Figure2A and B).The same result was obtained after ligation of CD95in mutant and control BJAB cells(Figure2C and D).Thus,death signaling downstream of TRAIL and CD95receptors may use common elements in the following sequence:death-recep-tors?FADD?caspases?JNK/SAPKs.TRAIL-induced apoptosis is attenuated in cells stably transfected with a JNKK-MKK4 dominant-negative constructTo examine more specifically whether enhanced JNK/SAPK activity might contribute to TRAIL-induced apoptosisweFigure1TRAIL-induced JNK/SAPK activity occurs downstream of caspases.(A)JURKAT(J)or a APO-1resistant JURKAT cells JAPO were incubated with 100ng/ml recombinant TRAIL protein(J/TR;JAPO/TR)or with control supernatant from Pichia pastoris transfected with empty vector(J/V;JAPO/V).Likewise, JURKAT cells were pre-incubated with50m M zVAD and subsequently treated with TRAIL or control supernatant(J/TR/zVAD;J/V/zVAD).0.5,1,2,4or8h later early apoptotic changes were measured by annexin staining using flow cytometry.(B)Cells were treated in a similar way as described in A and at the time points indicated nuclei-free supernatant was normalized for protein content and immunoprecipitated with anti-JNK/SAPK antibody-conjugated sepharose beads.GST-cJun-1-166fusion protein was added to the immuno complexes and incubated in kinase buffer in the presence of[g-32P]ATP.The phosphorylated fusion protein was resolved by10%SDS±PAGE and visualized by autoradiography.(C and D)Cells were treated and analyzed as described in(A and B)except that cells were treated with a APO-1agonistic antibody(a APO-1,2m g/ml)instead of TRAIL.The results depicted are the mean of three separate experiments+S.D.inhibited JNK/SAPK activity by transfecting JURKAT cells with a dominant-negative JNKK-MKK4construct which partially inhibits JNK/SAPK activity.28JNKK-MKK4has been shown to be a direct activator for JNK/SAPKs.29Cotransfec-tion with the gene for the GFP marker protein enabled separate forward side scatter FACScan analysis of trans-fected cells.However,using this treatment,cell death induced by stimulation with TRAIL or a APO-1for8and24h, respectively,was not significantly influenced compared to empty vector transfected control cells(Figure3A).The same result was found using CEM leukemic T cells.However, detection of cell death by gating on GFP-cotransfected cells is less sensitive than measuring apoptosis.Furthermore,an enhancement of TRAIL and/or CD95-induced apoptosis could not be recorded in transfectants which died already.Therefore we selected stably transfected cells by continuous culture in G418.This treatment strongly diminished activity of JNK-SAPKs compared to empty vector transfected cells as examined by a kinase assay(Figure3B).In control experiments we detected expression of a-Tubulin and the amount of phosphorylated ERK protein by Western blot. Whereas a-Tubulin was found to be equal expressed in both cell lines phosphorylation of ERKs in cells with a repressed JNK/SAPK activity was induced.This is in line with the recent finding that a balance between JNK/SAPK and ERK affects the apoptotic outcome since activation of the JNK/SAPK pathway in combination with a repressed growth factor activated ERK-cascade was required for apoptosis.30 Correspondingly,apoptosis induced by stimulation with TRAIL or a APO-1for4and8h,respectively,was strongly diminished in cells with a repressed JNK/SAPK activity compared to empty vector transfected control cells as detected by annexin-staining and flow cytometry(Figure 3C).The same result was found in HeLa cells stably transfected with JNKK-MKK4dominant-negative or empty vector.Therefore,activation of JNK/SAPKs contributes to apoptosis signaling downstream of death receptors.DiscussionIn the present study we demonstrate that JNK/SAPKs are activated in response to treatment of leukemic T cell lines with TRAIL in a similar kinetic as found for cross-linking of CD95. Both,TRAIL-and CD95-induced JNK/SAPK activity was inhibited by preventing signaling of FADD or caspases. Furthermore,inhibition of JNK/SAPKs in cells stably transfected with dominant-negative JNKK-MKK4diminished TRAIL or a APO-1-mediated apoptosis.Therefore,activation of JNK/SAPKs may contribute to apoptosis signaling down-stream of death receptors.However,death signaling in lymphoid cell lines seems to differ from the pathway initiated in HeLa,293or MCF7cells since in these systems a dichotomy upstream of FADD leading to JNK/SAPK activity was described.Thus,crosslinking of CD95or TNF-R1inFigure2TRAIL-induced apoptosis and JNK/SAPK activity depends on intact FADD signaling in human B cells.Human B lymphoma BJAB cells stably transfected with pcDNA3carrying the cDNA for inactive FADD-WT(B-WT)or a pcDNA3-FADD-DN construct(B-DN)were treated with TRAIL or a APO-1and analyzed as described in Figure1HeLa,293or MCF7cells seems to engage predominantly the death domain adapter proteins DAXX and TRAF2,respec-tively which define a pathway distinct from FADD/FLICE/caspases to activate JNK/SAPKs.23,24,26,31DAXX-signaling might also contribute to CD95-mediated JNK/SAPK activity in lymphoid cells since we observed that inhibition of caspases prevented not in all cases a APO-1-mediated activity of these kinases.In contrast,TRAIL-induced JNK/SAPK activity was totally blocked by zVAD,dominant-negative FADD and in a APO-1-resistant JAPO cells suggesting that FADD is a critical element for activation of JNK/SAPKs by TRAIL.However,the contribution of the individual receptors for TRAIL in induction of JNK/SAPK activity remains to be further highlighted.The precise role of JNK/SAPK activation following direct triggering of death receptors is unclear.Our data correspond to the recent findings that JNK/SAPK activation contributes to CD95-mediated apoptosis since counter-acting activation of JNK/SAPKs by sphingosine-1-phos-phate inhibits CD95-induced cell death in some cells 15and activation of JNK/SAPKs by overexpression of DAXX induces apoptosis.26Furthermore,activity of ASK-1,an apoptosis signal-regulating kinase of the JNK/SAPK path-way which can be activated by DAXX is both sufficient to mediate apoptosis and required for TNF-a -induced cell death.32,33Paradoxically,JNK/SAPK activation in response to various stimuli was also demonstrated to be dispensable for apoptosis or even to prevent this process.23,24,34,Thus,the JNK/SAPK pathway might directly or indirectly counter-act the expression of survival factors,such as NF-k B 24orBcl-2.35Correspondingly,activation of the JNK/SAPK pathway in combination with a repressed growth factor activated ERK-cascade has been shown to be required for apoptosis and a balance between JNK/SAPK and ERK has been found to be critical in affecting the apoptotic outcome.30In addition,JNK/SAPK activity may also occur independently of death receptor triggering as described in response to cellular stress.36In contrast to direct triggering of death receptors inhibition of caspases by zVAD did not prevent but even superinduced activity of JNK/SAPKs in response to cellular stress in lymphoid cells.37Thus,the co-operation of multiple signaling pathways as well as cell type-specific variations allows fine-tuned,targeted regulation and creates multiple checkpoints for the modulation of death signals.Materials and MethodsReagents and cell lineszVAD (Enzyme Systems Products,Dublin,USA)stock was dissolved in dimethylsulfoxide and stored in aliquots at 7208C.Final concentrations of the solvent in medium were 0.1%.Anti-CD95-agonistic antibody (a APO-1)and recombinant TRAIL were prepared as previously described.14,38Stock solutions were dissolved in PBS.The following human cell lines were used:Apoptosis-sensitive JURKAT (acute human T cell leukemia)cells which rapidly die in response to treatment with a APO-1.An a APO-1-resistant subclone (JAPO)has been selected by continuous culture of the parental JURKAT cells in increasing doses of a APO-1during a period of 1yearFigure 3TRAIL-induced apoptosis in transiently and stably transfected cells harboring dominant-negative JNKK-MKK4.(A )JURKAT cells were transfected with empty vector (pSV,white bars)or vector containing the cDNA for JNKK-MKK4dominant-negative (JNKK-DN,black bars)and cotransfected with pEGFP as described in Materials and Methods.Seventy-two hours after transfection cells were stimulated with recombinant TRAIL protein (100ng/ml)or a APO-1(1m g/ml).Eight or 24h later cell death was measured by forward side scatter analysis by gating at GFP-positive cells using a FACScan cytometer.The percentage of GFP-positive cells 72h after transfection was 26%(pSV)and 23%(JNKK-DN).(B )JNK/SAPK activity of untreated JURKAT cells stably transfected with empty vector (pSV)or vector containing the cDNA for JNKK-MKK4-dominant-negative (JNKK-DN)was examined by kinase assay as described in Figure 1B and D and Materials and Methods.In addition,the amount of phosphorylated ERK or the expression of a -Tubulin proteins was examined by Western blot using extracts from the same cells.(C )JURKAT cells stably transfected with empty vector (pSV,white bars)or vector containing the cDNA for JNKK-MKK4dominant-negative (JNKK-DN,black bars)were stimulated with recombinant TRAIL protein (100ng/ml)or a APO-1(1m g/ml).After 4or 8h apoptosis was analyzed by annexin-staining and flow cytometry.The results depicted are the mean of three separate experiments performed in duplicates +S.D.(starting with doses of10ng and ending at10m g/ml).BJAB is a human B lymphoma cell line stably transfected with pcDNA3vector carrying the cDNA for inactive FADD-WT(BJAB-WT)or a pcDNA3-FADD-DN construct(BJAB-FADD-DN)as described.39All cell lines were grown in RPMI-1640medium supplemented with10%FCS (Biochrom,Hamburg,Germany),100U/ml penicillin,100m g/ml streptomycin,25mM HEPES and2mM L-glutamine(all from Boehringer Ingelheim,Germany).For selection of stably transfected JURKAT cells25m g of either pSV empty vector or a JNKK-MKK4 dominant-negative expression construct were transfected by electro-poration(975m F,220V).Transfected cells were resuspended in 10ml fresh medium and living cells were selected by continuous culture in G418(Calbiochem,California,USA).Measurement of apoptosisEarly apoptotic changes were identified by staining of cells with fluoresceinthiocyanate(FITC)-conjugated annexin V(Bender Med Systems,Vienna,Austria)and analyzed by flow cytometry(FACScan, Becton Dickinson,Heidelberg,Germany)as described.36JNK/SAPK assayJNK/SAPKs were immunoprecipitated with polyclonal antibodies raised against JNK1(C-17,Santa Cruz,USA)and JNK2(FL-18, Santa Cruz,USA)and activity was detected using GST-Jun1/166as substrate as described.28,36Western blotExpression of a-Tubulin and the amount of phosphorylated ERK proteins was detected by Western blotting as described.36a-Tubulin was stained with a mouse monoclonal antibody obtained from Calbiochem(California,USA).Phosphorylated ERK was detected using a specific mouse monoclonal antibody(Santa Cruz,California, USA).Bound antibodies were detected by anti-mouse/horseradish peroxidase conjugates(Santa Cruz,California,USA).Enhanced chemiluminescence system(Amersham,Braunschweig,Germany) was used for detection.Transient transfections16108JURKAT cells were pelleted,resuspended in200m l PBS and transfected with25m g expression construct and5m g GFP construct by electroporation(975m F,220V).After transfection the cells were separated by Ficoll-gradient centrifugation and resuspended in fresh medium at56105/ml.Twenty-four hours later living cells were Ficoll-separated again and resuspended in fresh medium at56105/ml. 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Human Cytomegalovirus Infection Alters the Expression of Cellular

J OURNAL OF V IROLOGY,Sept.2008,p.9065–9074Vol.82,No.18 0022-538X/08/$08.00ϩ0doi:10.1128/JVI.00961-08Copyright©2008,American Society for Microbiology.All Rights Reserved.Human Cytomegalovirus Infection Alters the Expression of Cellular MicroRNA Species That Affect Its ReplicationᰔFu-Zhang Wang,1†Frank Weber,2Carlo Croce,3Chang-Gong Liu,3Xudong Liao,4and Philip E.Pellett1,5*Departments of Molecular Genetics1and Molecular Cardiology4and the Genomic Medicine Institute,2Lerner Research Institute, Cleveland Clinic,Cleveland,Ohio44195;Human Cancer Genetics Program,Comprehensive Cancer Center, Ohio State University,Columbus,Ohio432103;and Department of Immunology and Microbiology,Wayne State University School of Medicine,Detroit,Michigan482015Received8May2008/Accepted24June2008The human genome encodes over500microRNAs(miRNAs),small RNAs(19to26nucleotides[nt])thatregulate the expressions of diverse cellular genes.Many cellular processes are altered through a variety ofmechanisms by human cytomegalovirus(HCMV)infection.We asked whether HCMV infection leads tochanges in the expression of cellular miRNAs and whether HCMV-regulated miRNAs are important for HCMVreplication.Levels of most miRNAs did not change markedly during infection,but some were positively ornegatively regulated.Patterns of miRNA expression were linked to the time course of infection.Some similarlyreregulated miRNAs share identical or similar seed sequences,suggesting coordinated regulation of miRNAspecies that have shared targets.miRNAs miR-100and miR-101were chosen for further analyses based ontheir reproducible changes in expression after infection and on the basis of having predicted targets in the3؅untranslated regions(3؅-UTR)of genes encoding components of the mammalian target of rapamycin(mTOR)pathway,which is important during HCMV infection.Reporter genes that contain the3؅-UTR of mTOR(predicted targets for miR-100and miR-101)or raptor(a component of the mTOR pathway;predicted site formiR-100)were constructed.Mimics of miR-100and miR-101inhibited expression from the mTOR construct,while only miR-100inhibited the raptor construct.Together,miR-100and miR-101reduced mTOR proteinlevels.While the miR-100and miR-101mimics individually modestly inhibited production of infectiousprogeny,much greater inhibition was achieved with a combination of both(33-fold).Our keyﬁnding is thatHCMV selectively manipulates the expression of some cellular miRNAs to help its own replication.MicroRNAs(miRNAs)are small(ϳ21-nucleotide[nt]) RNA species that are expressed from specialized genes and have important roles in the regulation of cellular gene expres-sion,including the regulation of development,the differentia-tion of hematopoietic stem cells,apoptosis,and the develop-ment of cancer(reviewed in references16,25,and26). miRNA-mediated gene regulation is related to cellular de-fenses that are mediated via very similar mechanisms(small interfering RNA)but target exogenous mRNAs,such as those expressed by viruses.The human genome contains perhaps500 distinct miRNA genes(1,33).miRNAs are initially expressed as5Ј-capped and polyadenylated RNA polymerase II tran-scripts(4,31).They are expressed either as individually regu-lated genes or as clusters of miRNAs that are expressed and then processed from a single primary transcript that might contain several miRNAs(22,29,49).After cytoplasmic pro-cessing to theϳ21-nt single-stranded mature form by the en-zyme Dicer,miRNAs associate with the RNA-induced silenc-ing complex.miRNA-mediated RNA interference is manifest as reduced levels of translation from the targeted mRNAs.This translational silencing comes in two forms:(i)by inhibit-ing protein synthesis after binding via incomplete base pairing to the3Јuntranslated regions(3Ј-UTR)of target mRNAs,and (ii)by binding to mRNAs with perfect complementarity,which leads to cleavage of the targeted mRNA.One important con-sequence of miRNA-mediated inhibition of gene expression via imperfect base pairing is that individual miRNAs can po-tentially regulate many cellular targets.Further,individual genes can be targeted by multiple miRNAs.There are connections between viruses and the miRNA world.Simian virus40,human immunodeﬁciency virus type1 (HIV-1),herpes simplex virus type1,Marek’s disease virus, murine cytomegalovirus,human cytomegalovirus(HCMV), Epstein-Barr virus,and human herpesvirus8encode sets of miRNAs(3,12,18,40,42,44,48,53).HCMV encodes at least 12miRNAs that are expressed as immediate early or early viral genes in infected cells;their abundance increases for at least 72h after infection(12,18,41).Similarly,a herpes simplex virus type1viral miRNA encoded upstream of the latency-associated transcript also persisted at high levels until late in infection(9).Thus,the miRNA machinery remains opera-tional in cells infected by these viruses.While functions have yet not been ascribed to most of the virally encoded miRNAs, HCMV-miR-UL112inhibits NK cell killing by reducing major histocompatibility complex class I chain-related molecule B protein levels(46),the simian virus40miRNA plays a role in preventing the immune recognition of infected cells by reduc-ing the production of some viral proteins(47),several human*Corresponding author.Mailing address:Department of Immunology and Microbiology,Wayne State University School of Medicine,540East Canﬁeld Avenue,6225Scott Hall,Detroit,MI48201.Phone:(313)577-6494.Fax:(313)577-1155.E-mail:ppellett@.†Present address:Lineberger Comprehensive Cancer Center,Uni-versity of North Carolina at Chapel Hill,Chapel Hill,NC27599.ᰔPublished ahead of print on2July2008.9065herpesvirus 8-encoded viral miRNAs target cellular genes that may be relevant to pathogenesis (45),and an HIV-1-encoded viral miRNA suppresses nef gene expression (40).In addition to encoding miRNAs,viruses can interact with host miRNAs or affect their regulation.Nuclear export of miRNA precursors is inhibited by the adenovirus VA1non-coding RNA (35).Accumulation of primate foamy virus type 1is inhibited by a cellular miRNA (miR-32),and the virus en-codes a protein that suppresses miRNA silencing in mamma-lian and plant cells (30).In addition,a cellular miRNA (miR-122)that targets the 5Јend of the hepatitis C virus genome facilitates viral replication (24).Transfection of HeLa cells with HIV-1leads to a substantial alteration in the expression of cellular miRNAs,with many of them being downregulated (54).Moreover,HIV-1infection downregulates cellular miRNAs that repress viral growth (50).HCMV exerts diverse and profound effects on the regulation of host cell metabolism,including altering levels of cellular transcripts,perturbing the cell cycle,and inhibiting infection-triggered apoptosis (reviewed in reference 39),and the ma-chinery for miRNA biosynthesis and activity is functional in HCMV-infected cells.Thus,we asked whether HCMV infec-tion results in altered expression of cellular miRNA species.We found that levels of most miRNA species do not change dramatically during infection,but several species were mark-edly up-or downregulated,indicating that HCMV infection leads to speciﬁc changes in the expression of some cellular miRNAs.Further,we identiﬁed cellular targets for two of the virally regulated miRNAs and found that synthetic mimics of these miRNAs can inhibit viral replication.MATERIALS AND METHODSCells and virus.MRC-5,HeLa,and 293T cells were obtained from the Amer-ican Type Culture Collection (Manassas,VA)and maintained in Earle’s modi-ﬁed Eagle’s medium containing 10%fetal bovine serum (HyClone,Logan,UT),2mM L -glutamine,0.1mM nonessential amino acids,and 1mM sodium pyru-vate.T-BACwt (a gift from Hua Zhu)is a derivative of the HCMV Towne strain that has several nonessential genes (US1through half of US12)replaced with a gene encoding a green ﬂuorescence protein and was used in all experiments (38).Virus stocks were prepared in MRC-5cells infected with T-BACwt at a multi-plicity of infection (MOI)of 0.01,fresh culture medium was added when the cells showed Ͼ90%cytopathic effects,and the cells were harvested after 3to 4days.Harvested cells were resuspended in a thrice-autoclaved mixture of 50%fat-free milk and 50%culture medium and then frozen in aliquots at Ϫ80°C.Viral titers were determined by a plaque-forming assay done in triplicate in 48-well ﬂat-bottom plates (Corning Incorporated,Corning,NY).RNA preparation.MRC-5cells were infected at an MOI of 2in 100-mm cell culture dishes (Becton Dickinson,Franklin Lakes,NJ).Total RNA was extracted at 6,24,48,and 96,or 120h postinfection (hpi)with Trizol reagent (Invitrogen,Carlsbad,CA).Brieﬂy,the culture medium was removed and the cells were lysed with 6ml of Trizol reagent and then frozen at Ϫ80°C.The RNA phase was partitioned with 6ml of chloroform,precipitated with 3ml of isopropyl alcohol,washed,and resuspended in DNase/RNase-free sterile water and then stored at Ϫ80°C.RNA quality was veriﬁed by electrophoresis in agarose gels.miRNA microarray.miRNA microarray analysis was performed as described previously (34),using an updated version of the chip (human and mouse miRNA 11K version 2chip).Arrays included 40-mer oligomers with sequences corre-sponding to 250human miRNAs and their precursors known at the time this work was initiated.The chips also included a series of well-tested control probes with sequences corresponding to human tRNA and GAPDH (glyceraldehyde-3-phosphate dehydrogenase)that served as positive controls and numerous ran-dom sequences that served as negative controls.Each probe was printed in quadruplicate on activated Amersham CodeLink slides (Amersham,Piscataway,NJ).Five micrograms of total RNA was labeled with biotin by reverse transcrip-tion (RT),and the labeled cDNA was hybridized to the printed chips.Bound sequences were detected with a streptavidin-Alexa647conjugate.After process-ing,data were collected using an Axon 4000B scanner and the Genepix Pro 6.0software package (Molecular Devices,Sunnyvale,CA).miRNA data analysis.Microarray data were analyzed with BRB-ArrayTools (version 3.4_Beta_1a,National Cancer Institute,Rockville,MD).In the initial data ﬁltering,spots were excluded if the minimum ﬂuorescence intensity was Յ10or if there was insufﬁcient agreement among the quadruplicate spots.The mean ﬂuorescence intensities (MFI)of the quadruplicate spots were log 2trans-formed and then normalized using the median-centering array procedure.miRNAs were excluded if one of the expression values was less than 20%or had a 1.5-fold change in either direction from the averaged median value (34).For each miRNA for which data of sufﬁcient quality were available,array intensities from each time point after HCMV infection were compared with those of mock-infected MRC-5cells.qRT-PCR.Short RNAs (Յ200nt)were separated from total RNA prepara-tions (described above)by use of the mirVanaTM miRNA isolation kit (Ambion,Austin,TX)according to the manufacturer’s directions,beginning with 50␮g of total RNA that had been treated with 10units of DNase at 37°C for 30min.Levels of miRNA expression at different times after HCMV infection were determined by quantitative RT-PCR (qRT-PCR)from 10-ng aliquots of short RNA by using the mirVanaTM qRT-PCR miRNA detection kit (Ambion,Austin,TX)and primers for speciﬁc miRNAs (Applied Biosystems,Foster City,CA).miRNA target veriﬁcation.Fragments containing the 3Ј-UTR of mTOR and raptor that contain predicted targets of miR-100and/or miR-101were cloned from MRC-5cells by use of the following primers,each of which contains a NotI site (italicized):5Ј-GCGGCCGC AGATGTGCCCATCACGTT-3Јand 5Ј-GCG GCCGC TGATGTCATTTATTGGCACA-3Ј(mammalian target of rapamycin [mTOR],NM_004958),and 5Ј-GCGGCCGC CCTGCTACTCGCTTTTGTC-3Јand 5Ј-GCGGCCGC TTTCCCGAATTTCCAGTGTC-3Ј(raptor,NM_020761).The mTOR primers amplify a 927-bp fragment located 11to 937bp downstream of the stop codon,and the raptor primers amplify a 406-bp fragment located 143to 557bp downstream of the stop codon.Cloned sequences were conﬁrmed and the fragments were transferred to the NotI site in the 3Јmultiple cloning se-quence of pHygEGFP (BD Biosciences,Palo Alto,CA),which is located down-stream of the stop codon of a gene encoding a fusion protein of hygromycin and enhanced green ﬂuorescent protein (EGFP)to produce pHygEGFP-mTOR and pHygEGFP-raptor.HeLa cells were cotransfected with reporter genes andmim-parison of results from two independent miRNA microarray experiments.RNA was prepared from MRC-5ﬁbroblasts mock infected or infected with HCMV T-BACwt (MOI of 2)at 6,24,and 48hpi plus 96hpi (experiment 1)or 120hpi (experiment 2).These RNAs were used as probes on miRNA microarrays,as described in Materials and Methods.Data that passed the quality control criteria were compared with the BRB-ArrayTools software.9066WANG ET AL.J.V IROL .ics of miR-100,miR-101,or a negative-control miRNA mimic (Dharmacon,Lafayette,CO)by use of Lipofectamine 2000(Invitrogen,Carlsbad,California)as described previously (10).At 15to 24h after transfection,digital pictures of the cells were taken with a Leica (DM IRB)UV microscope system with a Q-Imaging camera at 100ϫmagniﬁcation,and EGFP expression levels were determined using Image-Pro Plus software (version 6.1).HCMV growth in the presence of miR-100and miR-101mimics.MRC-5cells were grown in 48-well plates (Becton Dickinson,Franklin Lakes,NJ)to 40to 50%conﬂuence and transfected using Lipofectamine 2000with miR-100,miR-101,or a negative-control miRNA mimic.Two days after transfection,the cells were serum starved for 48h and then infected with T-BACwt (MOI of 2).Four days after infection,virus titers in culture supernatants were determined by standard serial dilution on MRC-5cells.Immunoblot analyses.Cells from six-well plates were collected and lysed on ice in lysis buffer (50mM Tris-HCl [pH 8.0],150mM NaCl,1%Triton X-100[vol/vol],10%glycerol [vol/vol],and 1%protease inhibitor cocktail).After clar-iﬁcation by centrifugation,100␮g of protein lysate was separated in a gradient (4to 20%)polyacrylamide-sodium dodecyl sulfate gel and then transferred to a membrane (Immobilon-P;Millipore Corp.,Billerica,MA).The membrane was preincubated in blocking buffer containing 5%fat-free milk in Tris-buffered saline containing 0.1%Tween 20(pH 7.6).The membrane was probed with a rabbit anti-mTOR antibody (2972;Cell Signaling Technology,Inc.,Beverly,MA)overnight at 4°C and then with a horseradish peroxidase-conjugated anti-rabbit secondary antibody for 1h at room temperature with chemiluminescent detec-tion (Millipore Corp.).Bands were scanned and then quantiﬁed using Image-Pro Plus software (version 6.1).Statistical analysis.The two-tailed Student’s t test was used to analyze the effects of miRNA mimics on reporter assays and viral replication.The samples were treated as having equal variances (43,52).RESULTSBased on the abundant observations that HCMV employs a variety of mechanisms to regulate cellular processes,we hy-pothesized that (i)cellular miRNAs play a signiﬁcant role in CMV biology and (ii)HCMV regulates cellular miRNA pop-ulations,collectively or individually.miRNA microarray analysis.(i)Experimental design.To gain an overview of the impact of HCMV infection on host cellular miRNA expression,MRC-5cells that had been con-ﬂuent for 3days were infected at an MOI of 2with HCMV strain T-BACwt.In this way,we excluded the effects of cell replication and ensured the synchronous infection of the met-abolically synchronized cells (2,55).The HCMV strain we used has an integrated GFP gene so that infection efﬁciency can be conveniently monitored,as infected cells show green ﬂuorescence from 48hpi.Two independent experiments were done in which total RNA samples were extracted from mock-infected cells and cells that had been infected for 6,24,and 48h plus a 96-h time point in experiment 1and a 120-h time point in experiment 2,thus enabling analysis of early and late stages of infection.The rationale for this design was that in previous global analyses of host cellular gene expression,the number of affected cellular genes increased with time after HCMV infection,and groups of genes associated with different cellular activities,such as innate immune responses andcellFIG.2.Impact of HCMV infection on the expression proﬁle of cellular miRNA.(A)Comparison of miRNA expression levels at dif-ferent times after HCMV infection with levels in mock-infected cells.(B)Cluster analyses and heat map showing the expression levels of probes representing miRNAs with high-quality data available for every time point.The heat map is based on center-normalized MFI for each miRNA probe.Black bars denote probes for which signal intensities were below the level of quantitation.V OL .82,2008HCMV AND CELLULAR miRNA EXPRESSION 9067cycle regulation,were affected at different times after infection (2,21).The miRNA microarray chips used in this study are well established and have been used in many studies of cancer and cellular differentiation(5,7,8,13,17,20,34,51,52).The array results passed the standard blank,negative,and positive qual-ity controls.(ii)Similar results in experiments1and2.Results of two independent experiments(experiment1and experiment2)at each time point were compared to evaluate their reproducibil-ity.For the scatterplots shown in Fig.1,the analysis was re-stricted to probes that met the quality control criteria;because of the variability in the data for spots with very lowﬂuores-cence signals,signals ofՅ64ﬂuorescence units are not repre-sented in the scatterplots.These species are considered to be negative for expression in our experiments;probes for153of the250miRNAs were negative at all time points in both experiments.There was generally good agreement between the two experiments.The correlation coefﬁcients(r)wereϾ0.9at all time points.The similarity between results obtained at the 96-hpi and120-hpi time points(rϭ0.93)is consistent with the cells being in the late phase of the replication cycle.Because of the high agreement between the two experiments,further anal-yses were based on experiment2.(iii)miRNA expression after HCMV infection.The scatter-plots in Fig.2A are comparisons of the expressions of individ-ual miRNAs at each time point with mock-infected cells.Two general observations are apparent from these plots:(i)there is no global unidirectional change in miRNA expression,and(ii) the expression levels of individual miRNAs may be unaffected by infection or may be positively or negatively regulated after infection.Table1shows the changes relative to levels for mock-infected cells for a set of miRNAs for which high-quality data(as deﬁned in Materials and Methods)were available from every time point.In the comparison with mock-infected cells at the6-hpi time point,the miRNA expression proﬁles are very similar;only one cellular miRNA was upregulated,but none were downregulated by more than twofold.At24hpi, three cellular miRNA species were upregulated by more than twofold and none were downregulated(one of the miRNAs was targeted by probes for two precursor forms;thus,it shows up in the plot as two points).Especially manifest at48hpi and 120hpi is a progressive change in the expression of individual miRNAs relative to what was seen for mock-infected cells, such that the differences in expression levels of most miRNAs are readily visible.In total,2and8miRNA species wereTABLE1.Human miRNA expression patterns afterHCMV infection amiRNA ID b Mock MFI(ϮSD)cRatio of infected cell MFI tomock MFI at d:6hpi24hpi48hpi120hpimiRNAs withՆ2-folddecrease-10p3,022Ϯ2490.8**0.7***0.4**0.6*-214,286Ϯ274 1.10.9*0.5***0.4** -29p2,366Ϯ128 1.20.8*0.5***0.5** -34p1,112Ϯ3710.7*0.5***0.4*** -99p7,208Ϯ80910.8**0.4***0.5** -1009,842Ϯ63210.70.4**0.1*** -101p2,558Ϯ17110.8*0.4***0.4*** -1051,412Ϯ135 1.10.7*0.4**0.4*** -125p9,903Ϯ173 1.2*0.80.6***0.5** -1331,127Ϯ73 1.10.9*0.6**0.5** -145p2,442Ϯ184 1.20.8*0.5**0.5** -146p873Ϯ56 1.10.90.5**0.5** -155p4,035Ϯ2520.9**0.8**0.4**0.4** -181p2,445Ϯ114 1.10.7**0.4**0.3*** -1815,051Ϯ42510.6**0.3**0.3** -181p1,943Ϯ49 1.10.80.5***0.4** -1921,844Ϯ21910.7***0.5**0.4*-194963Ϯ4610.7**0.5**0.4** -213p4,350Ϯ250 1.10.6***0.4***0.3** -221p24,951Ϯ98210.90.5***0.5** -222p31,697Ϯ5890.90.7*0.4***0.4*** -223p2,847Ϯ510.90.8*0.5***0.4*** -3201,970Ϯ145 1.20.8**0.5**0.4** -3213,449Ϯ259 1.10.9*0.6**0.4** -3351,170Ϯ7010.6**0.5**0.5** miRNAs with nochanges ofϾ2-fold(up ordown)-let-7p944Ϯ53 1.9* 1.10.8*1-16856Ϯ69 1.110.9 1.4-32p927Ϯ54 1.11 1.1 1.4*** -34311Ϯ15 1.2 1.10.9*0.8*-93p955Ϯ431 1.2* 1.1 1.9** -148331Ϯ11010.90.8 1.1-191p2,137Ϯ1191 1.11 1.7*** -1961,481Ϯ272 1.5*0.80.70.7-206p1,146Ϯ91 1.8* 1.3**11-210p819Ϯ48 1.10.90.7*0.6** -212p1,537Ϯ48 1.9* 1.7 1.3 1.8-215p271Ϯ30 1.4*** 1.4* 1.6* 1.5*-220p1,896Ϯ113 1.2*10.6**0.6** -324596Ϯ58 1.30.9*0.7*0.6** miRNAs withՆ2-foldincrease-1p302Ϯ11 1.5* 2.1* 1.4* 1.1-1227Ϯ5 1.3 2.7*** 1.6 1.2-17p1,008Ϯ581 1.2* 1.3 2.3*** -20p792Ϯ781 1.1 1.2* 2.4** -33p453Ϯ24 2.2* 1.20.91-92p13,751Ϯ6160.9* 1.1 1.12**-95p1,745Ϯ1361 1.2 1.22**-106p807Ϯ56 1.1 1.2* 1.2 2.1** -132p404Ϯ38 1.4* 2.7**2** 1.7*-197p1,287Ϯ167 1.2 1.1 1.12*-2195,463Ϯ689 1.8** 1.5* 1.9*2*-203p196Ϯ15 1.1 1.7* 2.3** 3.5*** a Array data for human miRNAs with high-quality data(as deﬁned in Materials and Methods)at every time point.Data from a representative probe are shown if similar results were obtained with multiple probes for the same miRNA species.b miRNA names are for human miRNAs as listed in the Sanger miRNA registry.The sufﬁx“p”denotes species for which the array probe targeted the precursor form of the miRNA.c MFI and SD of mock-infected cells are shown to give baselines for inter-preting the change levels.d At each time point,the MFI for each probe was compared with the corre-sponding value from mock-infected cells with the two-tailed Student t test, considering the samples as paired.*,PՅ0.01;**,PՅ0.001;***,PՅ0.0001.parison of microarray and qRT-PCR results miRNA and test aFold change at b:6hpi24hpi48hpi120hpi miR-223Microarray0033 qRT-PCR0023 miR-101Microarray0034 qRT-PCR0088 miR-181Microarray0047 qRT-PCR0224 miR-100Microarray00334 qRT-PCR00416a Short RNAs(Յ200nt)isolated from the same RNA preparations used in microarray analysis were reverse transcribed and then analyzed by qRT-PCR.b The change is the ratio of threshold cycles(CT),C T mock to C T infected,for each time point.Results are shown from a subset of downregulated miRNAs.9068WANG ET AL.J.V IROL.upregulated by more than twofold at 48and 120hpi,respec-tively,and 22and 24miRNAs were downregulated by more than twofold at 48and 120hpi,respectively.In many instances,changes of 20%to 30%were statistically signiﬁcant at a P value of Ͻ0.01,and all of the changes of at least twofold were signiﬁcant at that or higher levels (Table 1).qRT-PCR was used to conﬁrm the microarray data for selected miRNAs;as shown in Table 2,the two methods were in good agreement.To compare the expression patterns of individual miRNAs over the time course of the experiment,we did a cluster anal-ysis based on the MFI for 64probes for which high-quality data were available for every time point (Fig.2B).From the den-drogram and the associated heat maps,it is apparent that changes in miRNA expression levels link to the infection time course.The heat maps reveal coherent temporal linkages from time point to time point.Thus,the mock and 6-hpi time points are closely related to each other,as are the 48-and 120-h time points,with the 24-h time point being related to the 48-and 120-h time points.From the heat maps,persistent and tran-sient effects on the expression levels of individual miRNAs are apparent.The expression levels of some species progressively changed from high to low over the experimental time course;conversely,the expression levels of some species changed from low to high.The expression levels of some species transiently increased,especially at the 6-and 24-h time points.Speciﬁc examples of the types of changes mentioned above are shown in Fig.3.Cellular miRNAs were upregulated in three general patterns:persistent increases beginning from 6hpi (Fig.3A),transient increases in expression that peaked at 24hpi (Fig.3B),and late increases (Fig.3C).Some miRNAs were downregulated,with their levels decreasing until 48hpi with little change thereafter (Fig.3D).Interestingly,some miRNAs with the same seed sequence (residues 2to 8)had similar patterns of changes in expression after HCMV infection.This included miR-99and miR-100,which have identical seed sequences and have only a single-nucleotide difference elsewhere.In addition,of the nine miRNAs upregulated at 120hpi,four (miR-17,-20,-93,and -106)have identical seed sequences and only 2-to 3-nt se-quence differences elsewhere (11).These miRNAs are en-coded on different chromosomes.Thus,some groups of unique miRNA species that have similar targets are coordinately reg-ulated after infection.(iv)Selection of miRNAs for functional analyses.After the initial data quality ﬁltering described above,we applied a series of additional ﬁlters to identify the miRNA species whose ex-pression levels were most profoundly and reproducibly changed after HCMV infection.This involved identifying miRNAs for which there was at least a twofold change in the expression level (up or down),MFI of Ն1,024ﬂuorescence units at least one time point,and concordance between exper-iments 1and 2.Species that passed these ﬁlters are miR-21,-99,-100,-101,-155,-181,-213,-222,-223,and -320(down-regulated)and miR-17,-20,-106,and -219(upregulated).Interestingly,many of these species have been identiﬁed by others as playing possible roles in cell differentiation or onco-genesis (reviewed in references 16,25,and 26),and some are known to target cellular regulators that may be important during infection.miR-100and miR-101interact with components of the mTOR pathway.For the miRNA species that had the most consistent and signiﬁcant changes in expression following HCMV infection,we examined lists of targets predicted by MIRANDA and TargetScan (19,32).miR-100and miR-101have predicted targets on the mTOR pathway,which is impor-tant in regulating the translation of capped mRNAs,cell size,cell growth,cell cycle,cell survival,and cytoskeletal organiza-tion (37)(Fig.4A).Speciﬁcally,miR-100and miR-101each have a predicted target in the mTOR 3Ј-UTR.In addition,miR-100has a predicted target in the 3Ј-UTR of raptor,whichFIG.3.Patterns of changes in cellular miRNA expression after HCMV infection.Cellular miRNAs were upregulated in three general patterns:gradual upregulation over the time course of infection (A),transient upregulation that peaked at 24hpi (B),and late increases (C).There was only one pattern for downregulated cellular miRNAs (D).V OL .82,2008HCMV AND CELLULAR miRNA EXPRESSION 9069is a partner of mTOR,and miR-101has two predicted targets in the 3Ј-UTR of another mTOR partner,rictor (Fig.4B).To determine whether miR-100and miR-101interact with components of the mTOR pathway,we constructed reporter genes containing segments of the 3Ј-UTR from the mTOR and raptor genes downstream of the EGFP reading frame (pHygEGFP-mTOR and pHygEGFP-raptor)(Fig.5A and 6A).Cells transfected with the reporter genes express EGFP,and the effects of miRNAs on EGFP expression can be as-sessed by comparing ﬂuorescence intensities in the presence or absence of synthetic miRNA mimics or a negative-control miRNA mimic (Fig.5B).The miRNA mimics are able to be processed by Dicer and produce stable and active silencing of their cognate targets.For pHygEGFP-mTOR,the cloned region contains pre-dicted targets for miR-100and miR-101(Fig.5A).At 25nM,the miR-100mimic alone inhibited EGFP expression by 35%,while the miR-101mimic alone had no effect.At 50nM,the miR-100mimic alone inhibited EGFP expression by 60%,and the miR-101mimic alone inhibited it by 38%;the combination of 25nM of each of the miR-100and miR-101mimics (50nM total)inhibited EGFP by 48%(Fig.5C).The raptor 3Ј-UTR fragment contains a predicted target for miR-100but has none for miR-101.Consistent with this,in experiments performed in parallel to those for which results are shown in Fig.5B and C,miR-100inhibited pHygEGFP-raptor by about 50%,but nei-ther miR-101nor the negative-control miRNA mimic had an effect (Fig.6B).In addition,the miR-100and miR-101mimics had no effect on the parental EGFP vector,which lacks the mTOR and raptor 3ЈUTR (Fig.6B).We extended this to an analysis of the effects of miR-100and miR-101on the expres-sion of the mTOR protein in 293T cells.As shown in Fig.5D,a combination of the two miRNAs (6.25nM of each)reduced mTOR expression by 41%relative to what was seen for the transfection control,an effect greater than that seen for either of the mimics alone at 12.5nM;the control miRNA had a negligible effect.Note that the levels of miRNA mimics re-quired to achieve silencing of the EGFP reporter constructs (Fig.5A to C)and mTOR protein expressed at its native levels (Fig.5D)are not directly comparable,due to the high level of reporter gene transcripts expressed from the HCMV immedi-ate early promoter in the transfected HeLa cells and the rel-atively low level of mTOR expressed from its native transcript in 293T cells and possibly to differences in silencing resulting from differences in the overall structure of the mTOR 3ЈUTR reporter transcript versus that of the native mTOR transcript.To summarize,two of the miRNAs reregulated after HCMV infection interact speciﬁcally with the 3Ј-UTR of at least two members of the mTOR pathway and can reduce the expression of mTOR at the protein level.miR-100and miR-101inhibit HCMV replication.We tested the hypothesis that if levels of a cellular miRNA are reduced following HCMV infection,their absence might be helpful for viral replication.Therefore,by supplementing intracellular lev-els of the miRNA by exogenous addition of the miRNA,viral replication might be suppressed.First,we directly compared miR-100and miR-101.Based on work from Kudchodkar and colleagues,subconﬂuent human ﬁbroblasts (28)were transfected with the mimics of miR-100and miR-101individually and as equimolar mixtures (10).Two days after transfection,the cells were serum starved for two more days and then infected with the T-BACwt virus at an MOI of 2.Virus titers in the culture supernatant on the fourth day after infection are shown in Fig.7A.Individual mimics reduced virus titers by about one-half of a log at concentrations from 25to 100nM.Equimolar mixes of the two mimics were much more potent (Ͼ10-fold reduction)than individual mim-ics at the same total molar concentration.Inhibition by the 25nM mixture (12.5nM of each species)was Ͼ4-fold greater than that in the presence of 100nM of either species alone.These inhibitory effects were veriﬁed and extended in an in-dependent experiment that included a commercial miRNA mimic as a negative control (Fig.7B).In this experiment,miR-100and miR-101,either alone or in combination,reduced the amount of infectious HCMV in the culture supernatants at 4days after infection to levels similar to those shown inFig.FIG.4.Predicted targets of miR-100and miR-101in the 3Ј-UTR of members of the mTOR pathway.(A)Schematic of the mTOR signaling pathway.mTOR functions by partnering with either raptor or rictor and controls mRNA translation or cell growth and survival,respectively.Rapamycin inhibits the function of the mTOR/raptor complex,while the function of Akt,the only known target of the mTOR/rictor complex,can be inhibited by caffeine.PI3K,phosphati-dylinositol 3-kinase.(B)Predicted targets.For each duplex,the upper sequence is from the predicted target and the lower sequence is the mature form of the indicated miRNA.For mTOR at least,the pre-dicted target sequences are highly conserved among diverse mamma-lian species.9070WANG ET AL.J.V IROL .。

汉语翻译

有机污染物在氮氟共掺杂二氧化钛催化剂催化下的可见光降解WANG Zheng-peng，XU Jun，CAI Wei-min ，ZHOU Bao-xue，HE Zheng-guang，CAI Chun-guang，HONG Xiao-ring(中国，上海交通大学，环境科学与工程学院E—mail：wizip@sjtu．edu．cn)摘要通过对异丁基钛和氟化铵水解产物的煅烧可以制备氮氟共掺杂二氧化钛多晶粉末。

氮和氟的掺杂导致二氧化钛的吸收频率变低。

同时发现，锐钛矿型的掺杂二氧化钛在可见光照射下降解苯酚的催化活性比市售的二氧化钛催化剂高2.4倍。

共掺杂二氧化钛粉体只有在1000℃时才含有锐钛晶型。

显然，氟化铵的加入钝化了二氧化钛粉末晶型由锐钛矿型向无定型的转变。

在共掺杂的二氧化钛多晶粉末中取代的氟和空穴氮原子可吸收可见光从而导致二氧化钛的吸收频率变低。

关键词：光催化可见光氮氟共掺杂苯酚带隙综述TiO2作为一种环保型催化剂被广泛的应用，基于此人们对它的催化性质作了大量的研究(Fujishima, 1972; Asahi, 2001)。

然而，TiO2只有在紫外线照射下才表现出活性，所以对TiO2的改性使其对可见光敏感成为光催化领域的热门课题。

在先前的研究中，不同的变价金属离子被广泛的应用以使TiO2的吸光域延伸到可见光区。

Iwasaki et al.使用溶胶-凝胶法让Co2+代替晶格点阵中的Ti4+。

他们注意到在可见光照射下，Co2+掺杂的TiO2具有更高的光催化活性。

他们认为在可见光下其高的催化活性取决于掺杂物中钴的原子价态，以及锐钛晶型中特殊表面积的比例。

因而，除个别情况外，阳离子掺杂的能大大降低紫外区的吸光频率。

这是因为掺杂后的氧化物能带变得不稳定或者空穴中心增加(Choi, 1994; Herrmann, 1984)。

近来，有文献显示阴离子掺杂的TiO2膜或粉体在可见光下具有活性。

Asahi et al.从理论上对氮原子掺杂的TiO2薄膜和粉体能带结构进行计算后认为TiO2中氧的位置被氮原子取代后在可见光下具有光活性。

文献

One dimensionally spinel NiCo 2O 4nanowire arrays:facile synthesis,water oxidation,and magnetic propertiesYu-Zhi Su,Qi-Zhi Xu,Gao-Feng Chen,Hui Cheng,Nan Li,Zhao-Qing Liu *School of Chemistry and Chemical Engineering/Guangzhou Key Laboratory for Environmentally Functional Materials and Technology,Guangzhou University,Guangzhou 510006,ChinaA R T I C L E I N F OArticle history:Received 22April 2015Received in revised form 16June 2015Accepted 20June 2015Available online 29June 2015Keywords:Oxygen evolution reaction One-dimensional Spinel NiCo 2O 4Nanowire arrays Oxygen vacanciesA B S T R A C TDevelopment of ef ﬁcient,affordable,non-precious metal oxides catalysts is critical for the oxygen evolution reaction (OER).Herein,we present a spinel NiCo 2O 4nanowire arrays (NWAs),synthesized by a simple solution route,as an inexpensive,ef ﬁcient anode electrocatalyst for water electrolysis.The as-prepared NiCo 2O 4NWAs contains Ni 2+/Ni 3+which replace Co in octahedral sites of the spinel Co 3O 4,exhibiting higher catalytic activity than that of Co 3O 4and NiO.The enhanced catalytic activity of NiCo 2O 4NWAs is correlated with a large surface area,one-dimensional (1D)architecture,high conductivity and synergistic behavior of Ni/Co bifunctional catalyst.Besides,oxygen vacancies,which favor ef ﬁcient electrons transport,supply more active sites,and assist in the adsorption of OH À,can be conducive to make high utilization of catalytic materials in the OER.Moreover,the magnetic properties of NiCo 2O 4NWAs are also investigated in detail.The results indicate that NiCo 2O 4NWAs could be a promising economical and environmentally benign bifunctional electrocatalyst for water splitting and other applications.ã2015Elsevier Ltd.All rights reserved.1.IntroductionOxygen electrochemistry plays a key role in ef ﬁcient energy conversion and storage devices,particularly in the ﬁelds of electrochemical and photoelectrochemical water splitting [1–4].Oxygen evolution reaction (OER)is considered to reach a bottleneck,severely hampered by the sluggish kinetics and low energy ef ﬁciency.Currently,the noble-metal electrocatalysts,such as IrO 2and RuO 2are normally employed as the benchmark OER catalysts,although their low abundance and exorbitant cost constrain the potential practical applications [5–7].In view of their unaffordable price and impracticable scarcity,designing and developing low-cost,earth-abundant and ef ﬁcient electrocatalysts that lower the energy barrier,improve the water oxidation ef ﬁciency,and boost the availability for large-scale application is still a crucial scienti ﬁc challenge in water electrolysis systems.Recently,many burgeoning efforts have been made to develop high ef ﬁcient and non-precious electrocatalysts based on earth-abundant elements for OER [8–10].As an important class,non-precious metal oxides with spinel structure have attracted numerous interest owing to its promising electrochemicalef ﬁciency and stability for OER in the alkaline solution [11,12].Particularly,the spinel-type Co 3O 4-based electrocatalysts involv-ing partially replacing Co with more eco-friendly and cheaper alternative metals to form MCo 2O 4(M =Mn,Ni,Cu,and Zn)have become the focus of research due to their high surface areas and enhanced conductivity [13–17].Moreover,this partial replacement was mainly motivated by the fact that Co 3O 4is slightly less active than the noble metal oxides for oxidation in alkaline solution.Thus,it is still a challenge to develop and design high activity,low-cost,and durability spinel-type MCo 2O 4electrocatalysts for water splitting.The spinel structure of NiCo 2O 4is found to be a typically mixed valence oxide,in which nickel ions occupy the octahedral sites and cobalt is distributed over both octahedral and tetrahedral sites.Meanwhile,the spinel-type NiCo 2O 4containing highly oxidized redox couples Co 3+/Co 2+and Ni 3+/Ni 2+,which are known as active centre in pared with the single Co 3O 4,NiCo 2O 4may possess a much better electronic conductivity and 2orders of magnitude higher [14,18].To date,many researchers have focused on the study of the OER activity of NiCo 2O 4nanomaterials.For example,Chen et al.[19]reported a three-dimensional (3D)nitrogen-doped graphene-NiCo 2O 4with hierarchical pores as an advanced OER electrocatalyst,which shows a superior catalytic activity that was comparable to the reported noble metal catalyst (IrO 2).And Cui et al.[20]fabricated an innovative core-ring*Corresponding author.Tel.:+862039366908;fax:+862039366908.E-mail address:lzqgzu@ (Z.-Q.Liu)./10.1016/j.electacta.2015.06.0920013-4686/ã2015Elsevier Ltd.All rights reserved.Electrochimica Acta 174(2015)1216–1224Contents lists available at ScienceDirectElectrochimica Actaj o u rn a l h o m e p a g e :w w w.e l s e v i e r.c o m /l o c a t e /e l e c t a c tananoplatelet of NiCo2O4for water splitting,exhibiting an enhanced electrocatalytic performance.However,to our knowledge,barely research is performed to examine the relationship between the morphology,composition,and the electrocatalytic activity, let alone the issues of limited surface area,oxygen vacancies and conductivity.Therefore,directly constructing one-dimension-al(1D)architecture on conductive metal substrates can partially overcome the above issues,owning to the ordered open-space structure allows for less adhesion of the gas bubble formed,and thus leading to less ohmic pared to the conventional two-dimensional(2D)planar architecture and3D porous architecture, electrodes based on1D ordered architecture can offer several critical advantages,such as facilitating electron transportation, promoting electrolyte penetration,and increasing the electro-chemically active surface area(ECSA).Recent reports have also conﬁrmed the great beneﬁt of1D architecture in enhancing the OER activity[21–23].With an aim to develop highly efﬁcient catalysts based on earth-abundant elements for OER,in this work,we focus on the NiCo2O4nanowire arrays(NWAs)as an electrocatalyst,which directly grow on conductive substrate Ti via a facile template-free solution method avoiding the above mentioned drawbacks.As expected,the as-prepared1D NiCo2O4NWAs exhibits better electrocatalytic activity than the individual Co3O4and NiO.The possible reasons for the enhanced electrochemical performance of NiCo2O4NWAs are investigated in detail with relation to morphology,charge transfer ability,oxygen vacancies,and speciﬁc surface area,etc.In addition,the magnetic properties of the1D NiCo2O4NWAs are also examined.Therefore,it is believed that the easy accessibility of1D ordered nanomaterial will provide a promising candidate for tailoring efﬁcient and durable electro-catalysts.2.Experimental2.1.Synthesis of NiCo2O4Nanowire ArraysAll the reagents used in the experiment were of analytical grade and were used without further puriﬁcation.In a typical hydro-thermal process,2mmol of Ni(NO3)2Á6H2O and4mmol of Co (NO3)2Á6H2O were dissolved into a mixed solution of40mL ofethanol and40mL of H2O at room temperature to form a clear pink solution,followed by the addition of24mmol of urea.The solution was then transferred to a100mL bottle with a cap.The Ti foil (2cmÂ1cm in rectangular shape)was immersed in a3M HCl solution for15min to get rid of the possible surface oxide layer before it was put into the bottle for reaction.The bottle was then capped and heated to90 C in an electric oven.After reaction for 8h,the sample was taken out after the solution was cooled down naturally to room temperature.After that,the Ti foil with grown products was dried at60 C.In order to get crystallized NiCo2O4 nanowires,Ti foil with the as-grown precursor was annealed at 400 C for3h.For comparison,the preparation of Co3O4and NiO used the similar synthesis procedure.2.2.CharacterizationsThe surface morphology and structure of the as-prepared samples were analyzed by usingﬁeld emission scanning electron microscopy(FE-SEM,Quanta400)and transmission electron microscopy(TEM,300kV,Tecnai TM G2F30).The as-prepared samples were also characterized by energy-dispersive X-ray spectroscopy(EDX,INCA300)to determine the deposit compo-sitions.The structure of the samples were analyzed by powder X-ray diffraction(XRD,Bruker,D8ADVANCE)with K a radiation (l=1.5418Å).The chemical-state analysis of samples was carried out by X-ray Photoelectron Spectroscopy(XPS,ESCALab250). Moreover,the BET surface area and pore volume were evaluated by using nitrogen adsorption-desorption isotherms measured at77K on an ASAP2020M instrument.The magnetic properties were studied by measuring hysteresis loops at low(5K)and room temperature(300K)using a quantum design MPMS-XL7superconducting quantum interference device(SQUID)and a vibrating sample magnetometer(VSM)from Oxford Instruments, respectively.2.3.Electrochemical measurementsThe electrochemical properties of the as-prepared samples were investigated by employing a CHI760D electrochemical workstation(Chenhua,Shanghai)in a three-compartment cell with a Pt plate counter electrode,a saturated calomel electrode (SCE)reference electrode,and a working electrode.The electrolyte was1M aqueous solution of KOH.The working electrode was prepared as follow:20mg of the catalyst were dispersed in100mL of DI water,then45mL of PTFE was added.The contents were dispersed,followed by ultrasonication for approximately30min to obtain a homogeneous suspension.0.48mL of the catalyst ink were dropped on the surface of the carbon rod(working electrode, 0.33cmÀ2)and dried at room temperature.The polarization curves were recorded with the scan rate of1mV sÀ1.The working electrodes were scanned for several times until the signals were stabilized,and then the data were collected.Cyclic voltammetry was conducted with scan rate of10mV sÀ1in the range ofÀ0.2to 0.6V.Electrochemical impedance spectroscopy(EIS)was carried out in the frequency range of0.01Hz to1MHz with an constant potential of0.6V.The stability was characterized by chronoam-perometry which was carried out at0.65V.3.Result and discussionThe X-ray diffraction(XRD)measurement was used to identify the chemical composition and phase of the as-prepared products. In order to rule out the effect of substrate,the as-prepared products were scraped off from the Ti foil.As shown in Fig.1a,all of the diffraction peaks agreed well with the standard patterns of the spinel NiCo2O4phase(JCPDF No.20-0781)with lattice constants a=b=c=8.11Å.As a comparison,the XRD patterns of the as-prepared Co3O4and NiO in the same process are shown in Fig.1a, corresponding to the cubic spinel Co3O4phase(JCPDF No.43-1003) and cubic NiO phase(JCPDF No.65-2901),respectively.All the products were highly pure since no peaks of any purity phases could be detected from the patterns.Moreover,it can be observed from(311)XRD peaks of NiCo2O4and Co3O4that the substitution of Ni for Co does not modify the general XRD pattern of Co3O4,but broadens the diffraction line of Co3O4with a slight shift in2u to lower values,indicating that the addition of Ni to Co3O4decreases both the crystallinity and the crystalline size(Fig.S1)[24].The average crystallite sizes of the composites were calculated by using the Scherer equation for the high intensity metal oxide peaks,as presented in Fig.S1(b-d).In comparison to Co3O4(3.92nm), NiCo2O4shows low crystalline size of2.29nm.Raman spectrosco-py was also used to characterize the phase composition of the NiCo2O4,Co3O4and NiO.As shown in Fig.1b,the peaks at186,469, 519,and668cmÀ1correspond to F2g,E g,F2g,and A1g models of the NiCo2O4,respectively[25].In contrast toﬁve peaks locating at188, 480,528,614,and688cmÀ1(F2g,E g,F2g,F2g,and A1g modes of Co3O4)[26],the peaks of NiCo2O4NWAs are broadened and weakened with a slight shift to lower values by the substitution of Ni for Co,consistent with the above XRD results.Furthermore,the ﬁve Raman peaks located at approximately459,526,719,998and 1076cmÀ1of NiO corresponding to theﬁrst-order transverseY.-Z.Su et al./Electrochimica Acta174(2015)1216–12241217optical (TO)and longitudinal optical (LO),2TO,2LO and 2LO phonon modes,respectively [27].The morphology and microstructures of the as-prepared products were examined by the scanning electron microscopy (SEM)and the transmission electron microscopy (TEM).As presented in Fig.2a-b,the hierarchical NiO microsphere consisted of nanosheets which have a uniform diameter of 4-5m m can be ovserved.The microstructure of these microspheres was further investigated by TEM (Fig.2c-d),where the solid microsphere with ultra-thin nanosheets can be clearly observed.And the High-resolution TEM (HRTEM)image (Fig.2e)shows lattice fringes with a d -spacing of 0.243nm,corresponding to the (111)lattice plane of NiO.In addition,the selected-area electron diffraction (SAED)pattern shown in Fig.2f also re ﬂects the polyctrystalline feature of the hierarchical sphere and can be readily indexed to (111),(200),(220),and (311)crystal planes of NiO phase.The morphology and microstructure of Co 3O 4were investigated in pared with NiO,the morphology of Co 3O 4was obviously different from NiO microspheres.Fig.3a-c exhibits panoramic and SEM images of Co 3O rge numbers of spherical urchin shape structures of Co 3O 4can be found,and the SEM image in Fig.3c clearly reveals the urchin-like Co 3O 4sphere having numerous small nanorods with 3um radially grown from the center.Fig.3d displays the TEM image of an individual urchin-like Co 3O 4sphere with a large number of nanorods (15-20nm diameter and 2-3m m length).However,the as-prepared urchin-like Co 3O 4is a solid sphere.As presented in Fig.3e,the lattice fringe with a d-spacing of 0.286nm can be well indexed to the (220)plance of Co 3O 4.The SAED pattern (Fig.3f)can be readily indexed to (220),(311),(400),(511),and (440)crystal planes of the cubic Co 3O 4phase,which is consistent with the XRD results.Similarly,the analysis of the morphology and microstructure was applied to the as-prepared NiCo 2O 4.Fig.4a-b shows typical SEM images of NiCo 2O 4NWAs.It clearly exhibits the highly ordered NiCo 2O 4NWAs uniformly grown onto the Ti foil substrates.Fig.4c-d displays the TEM image of the NiCo 2O 4nanowires with uniform diameter of 10nm and length of several micrometers.The HRTEM in Fig.4e exhibits a lattice spacing of 0.29nm,corresponding to be (220)plane of NiCo 2O 4.Additionally,the SAED pattern of NiCo 2O4Fig.1.(a)XRD patterns of NiO,Co 3O 4and NiCo 2O 4grown on Ti foil calcined at 400 C in air for 3h;(b)Raman spectra of NiO,Co 3O 4and NiCo 2O 4.Fig.2.(a-b)SEM images of NiO;(c-d)TEM images of NiO;(e)HR-TEM image of NiO and (f)SAED pattern of NiO.1218Y.-Z.Su et al./Electrochimica Acta 174(2015)1216–1224(Fig.4f)shows the well indexed (220),(311),(400),(511),and (440)planes of the spinel NiCo 2O 4.The porosity of the as-prepared samples was investigated by BET analysis as shown in Fig.5.The N 2adsorption isotherm recorded for NiCo 2O 4NWAs is type IV with a distinct hysteresis loop,typical for mesoporous inorganic oxides with good pore connectivity [28].The pore size distribution (inset in Fig.5)of the product,calculated from the desorption data using the BJH method,shows a narrow peak centered at $50nm indicating uniform mesopores of NiCo 2O 4NWAs,a lot smaller than macro-pore of Co 3O 4(177nm)and NiO (98nm).The NiCo 2O 4NWAs also possesses a high speci ﬁc surface area of 83m 2g À1and a pore volume as high as 0.36cm 3g À1,largely exceeding Co 3O 4with speci ﬁc surface area of 37m 2g À1and a pore volume of 0.21cm 3g À1prepared by same method.These results indicate that the introduction of Ni to Co 3O 4increases both speci ﬁc surface areaand pore volume.Therefore,the features may be bene ﬁcial for the transport and diffusion of electrolyte ions during OER process.X-ray photoelectron spectra (XPS)was recorded to investigate the surface chemical state of as-prepared samples.The corre-sponding survey spectra in Fig.6a,which clearly shows that the elements of Ni,Co and O are presented in NiCo 2O 4,while the elements of Co,O and Ni,O are presented in Co 3O 4and NiO,respectively.In the Ni 2p spectra,six species including two pairs of spin-orbit doublets characteristic of Ni 2+and Ni 3+and two shake-up (sat.)excitations were achieved,implying both Ni 2+and Ni 3+present in NiCo 2O 4and NiO [24,29,30].In the same way,the best deconvolution of Co 2p spectra for NiCo 2O 4and Co 3O 4(Fig.6a)were obtained under assumption of the six species including two pairs of spin-orbit doublets characteristic of Co 2+and Co 3+and two shake-up (sat.)excitations [31].The satellite peaks corresponding to Co 2+species imply a much higher Co 2+concentration in NiCo 2O4Fig.3.(a-b)SEM images of Co 3O 4;(c-d)TEM images of Co 3O 4;(e)HR-TEM image of Co 3O 4and (f)SAED pattern of spinel Co 3O 4.Fig.4.(a-b)SEM images of NiCo 2O 4;(c-d)TEM images of NiCo 2O 4;(e)HR-TEM image of NiCo 2O 4and (f)SAED pattern of spinel NiCo 2O 4.Y.-Z.Su et al./Electrochimica Acta 174(2015)1216–12241219than that in Co 3O 4.On the basis of the Gaussian ﬁtting curves,the calculated Ni 3+/Ni 2+ratios based on the area intensity are 0.988for NiCo 2O 4,while the calculated Co 3+/Co 2+ratios are 0.110and 1.873for NiCo 2O 4and Co 3O 4,respectively.In view of charge balance in the crystalline NiCo 2O 4and Co 3O 4,the theoretical molecular formulas are NiCo 2O 3.348and Co 3O 3.978for NiCo 2O 4and Co 3O 4,respectively,indicating an obvious oxygen de ﬁciency (oxygen vacancy)in NiCo 2O 4.The substitution of Ni for Co was well known to have a strong octahedral site preference [21,24].Thus,according to the XPS results,it may make a conclusion that the defects of oxygen vacancies may extensively exist in NiCo 2O 4mainly inducing by the replacement of octahedral Co sites with lower valence Ni (Ni 2+).Fig.6d exhibits the high-resolution O 1s spectrum of NiCo 2O 4,Co 3O 4and NiO with two oxygen contribu-tions denoted as 1,2and ponent O1for NiCo 2O 4located at 531.1eV can be associated with total response of metal-oxygen bonds [Ni-O (531.2eV)and Co-O (530.1eV)bonds][29,30].Component O2at 532.0eV are usually assigned to oxygen in OH Àgroups and the presence of this contribution in the O 1s spectra indicates that the surface of oxides were hydroxylated to some extent as a result of either surface oxyhydroxide or the substitution of oxygen atoms at the surface by hydroxyl ponent O3belonged to NiCo 2O 4at 532.9eV is linked with a higher number of defect sites with low oxygen coordination,further demonstrating the existence of oxygen vacancies [24].Actually,the structural change from Co 3O 4to NiCo 2O 4should result in differences in electrocatalytic performance basing on the existence of oxygen vacancies and the presence of Ni 3+/Ni 2+at octahedral sites,as will be discussed later.The as-prepared NiCo 2O 4,Co 3O 4and NiO samples were performed as anodes to demonstrate their electrocatalytic activity in OER.Cyclic voltammograms (CV),polarization curves,electro-chemical impedance spectroscopy (EIS)and chronoamperometry were obtained in a standard three-electrode cell consisting of a SCE reference electrode,a platinum foil counter electrode,and 1M aqueous KOH solution as the electrolyte.All potentials in this paper are reported with respect to the SCE reference electrode.CV measurements are served as the appropriate tool to identify Faradic and non-Faradic reaction of electrochemicalmechanismFig.5.N 2adsorption-desorption isotherms of NiO,Co 3O 4and NiCo 2O 4.The inset shows the pore size distribution curve obtained from the desorptiondata.Fig.6.(a)XPS survey spectra of NiO,Co 3O 4and NiCo 2O 4;(b)High-resolution Ni 2p XPS spectrum of NiO and NiCo 2O 4;(c)High-resolution Co 2p spectra of Co 3O 4and NiCo 2O 4;(d)High-resolution O 1s spectra of NiO,Co 3O 4and NiCo 2O 4.1220Y.-Z.Su et al./Electrochimica Acta 174(2015)1216–1224for the as-prepared materials.In Fig.7a,the CV curves reveal the measurement in 1M KOH at a scan rate of 10mV s À1for the NiCo 2O 4,Co 3O 4and NiO.The Co 3O 4shows an anodic response (0.41V)with a peak current during positive scanning from À0.2to 0.6V,corresponding to the oxidation of the Co 2+and Co 3+species.The cathodic peak around 0.37V is associated with the reduction of the Co 4+and Co 3+species on the surface of the Co 3O 4catalyst.The CV of NiO exhibits a pair of redox peaks with an anodic peak at around 0.35V and a cathodic peak at about 0.28V corresponds to the conversion between different oxidation states of Ni (Ni 2+/Ni 3+/Ni 4+).The CV curves for the NiCo 2O 4display a larger pair of redox couples (Ni 2+/Ni 3+/Ni 4+and Co 2+/Co 3+/Co 4+)[32,33]than Co 3O 4and NiO with the broad anodic peak shifted in the negative direction (0.29V).This shift with a more negative (less positive)potential can be attributed to the coef ﬁcient between the oxidation of Ni 2+and Ni 3+and the oxidation of Co 2+and Co 3+on the surface of the NiCo 2O 4.It is quite clear that the peak current density dramatically increased after the substitution of Co with Ni for Co 3O 4,resulting in much more active reactive sites,consistent with the BET and XPS results.Polarization curves of the OER on the anodes were measured to evaluate the catalytic activity.As displayed in Fig.7b,linear-sweep measurements con ﬁrm the more negative onset potential of NiCo 2O 4(about 0.50V)and the larger OER current density at 0.7V for NiCo 2O 4indicating the enhancement in OER electrocatalytic activity of NiCo 2O 4.Tafel plots derived from polarization curves were constructed (Fig.6b)to gain more insight into the OER activity.The resulting Tafel slope of NiCo 2O 4was 62mV dec À1,which is smaller than that of the Co 3O 4(67mV dec À1)and much smaller than NiO (107mV dec À1),indicating effective chargetransfers and the high ef ﬁciency of NiCo 2O 4for OER.As shown in Table S1,NiCo 2O 4NWAs in this work present superior OER activity compared to other NiCo 2O 4reported earlier,appearing the competitive performance.With the replacement of octahedral Co sites by the lower valence Ni (Ni 2+)creating oxygen de ﬁcient structure,this structural change would result in the promotion of the electrocatalytic performance depending on the existence of the oxygen vacancies in the spinel structures.The OER is generally preformed basing on the oxidation process as follow [34]:MO +OH À=MOOH +e À(1)MOOH +OH À=MO 2+H 2O +e À(2)MO 2=MO +O 2(3)4OH À=O 2+2H 2O +4e À(4)The exchange between O 2Àand O 22Àspecies (Eqs.(3)and (4))are considered to be the rate-determining step for the OER [2].Thus,the kinetic of both OH Àbonding via the oxygen vacant site on spinel structures and the above step of ion exchange need to be taken into the consideration.NiCo 2O 4possesses oxygen defect sites,in which the oxygen vacancies give the distorted structure and the molecular level oxygen porosity beyond the mesoscale porosity.Such transfer assists the adsorption of OH À,leading to the fast OER kinetics [2,35].Moreover,NiCo 2O 4NWAs alsopossessFig.7.(a)CV curves for NiO,Co 3O 4and NiCo 2O 4;(b)Polarization curves of NiO,Co 3O 4and NiCo 2O 4;(c)Tafel slopes of NiO,Co 3O 4and NiCo 2O 4derived from polarization curves and (d)EIS Nyquist plots of NiO,Co 3O 4and NiCo 2O 4.The inset in the panel (d)shows corresponding Nyquist plot at the high-frequency range.Y.-Z.Su et al./Electrochimica Acta 174(2015)1216–12241221uniform mesoporous structure resulting in the more ef ﬁcient transport of OH Àto the active sites on the catalyst than the other compositions of nickel cobaltite nanostructures.As mentioned above,Ni substitution is believed to improve Co 3O 4activity by increasing its conductivity (electronic effect),providing a number of defect sites and enlarging its speci ﬁc surface area,thereby resulting in the enhancement of OER performance.In order to go insight into the resistance of the catalysts,the electrochemical impedance spectroscopy (EIS)was conducted to assess the conductivity and charge transfer process at 0.6V.As shown in Fig.7d,the internal resistance (R s )of the NiCo 2O 4,Co 3O 4and NiO are about 6.1,7.9and 9.8V ,respectively.Meanwhile,the semicircular diameter in the electrochemical impedance spectrum (EIS)of NiCo 2O 4is much smaller than that of Co 3O 4and NiO due to smaller charge transfer impedance in NiCo 2O 4.The values of the charge transfer resistance for NiCo 2O 4,Co 3O 4and NiO are 12.1,34.4and 66.2V ,respectively.The result con ﬁrms that the conductivity of NiCo 2O 4is higher than that of Co 3O 4,which is in accord with the previous reports.The catalytic stability of the as-prepared anodes was investi-gated by chronoamperometric measurements at 0.65V (Fig.8a).The NiCo 2O 4NWAs show more stable current densities decreasing from 20.6to 17.2mA cm À2during 180min of testing,comparable toCo 3O 4(current densities decreasing from 17.1to 8.8mA cm À2)and NiO (current densities decreasing from 3.7to 1.3mA cm À2),revealing the excellent stability of NiCo 2O 4NWAs in OER conditions.Fig.8b shows the current density of the NiCo 2O 4at 0.7V derived from state polarization curves at a scan rate of 1mV s À1after given number of CV cycles between 0.2and 0.7V at a scan rate of 100mV s À1versus scan cycles.It can be clearly seen that 90.2%of the original catalytic current for NiCo 2O 4NWAs can be retained after 500scan cycles at a scan rate of 100mV s À1(the inset of Fig.8b),higher retention rate than 68.5%for Co 3O 4(Fig.S3a)and 49.2%for NiO (Fig.S3b).The enhancement of OER electrocatalytic activity and catalytic stability of the NiCo 2O 4NWAs may be mainly attributed to the advantageous morphology of NiCo 2O 4NWAs and the effect of Ni substitution of Co 3+in octahedral sites in the spinel Co 3O 4.As shown in Fig.9,the main reasons towards the enhancement of catalytic activity might be summarized in the following factors:(i)NiCo 2O 4NWAs offers several critical advantages,as the mainly advantage is the 1D ordered architecture facilitate electron transportation.The open space between NWAs facilitates the diffusion of electrolyte and the mesoporous structures with large surface areas associated with NWAs accelerate the surface reaction.(ii)The addition of Ni to the spinel lattice (more speci ﬁcally,replacing of octahedral Co sites with lower valence Ni)increases the conductivity and creates oxygen de ﬁcient structure.(iii)The Ni doped nanowire arrays increase the reaction active sites creating ef ﬁcient diffusion pathways for electrolyte ions,which signi ﬁcantly enhance the intercalation of ions and the utilization rate of the electrode material.Furthermore,the ECSA could be calculated by using cyclic voltammetry measurement.As shown in Fig.S4,with the Ni doping,the ECSA of NiCo 2O 4increases and reaches ECSA of 140cm 2,whereas that of Co 3O 4and NiO are only 112.5cm 2and 63.75cm 2,respectively.The calculated result indicates the enhancement of catalytic activity by Ni doping.(iv)The oxygen vacancies give the distorted structure and the molecular level oxygen porosity may assist the adsorption of OH À,resulting in the fast OER kinetics.In consideration of the interestingly structural defects on the surface of NiCo 2O 4NWAs,the magnetic properties of the samples were also investigated.As shown in Fig.10a,the typical magnetization hysteresis loops for NiCo 2O 4,Co 3O 4and NiO samples at 5K display that the response of Co 3O 4and NiO are typical of antiferromagnetic (AFM)materials,in which the magnetization of Co 3O 4increases almost linearly with the magnetic ﬁeld and the AFM NiO displays a hysteresis loop that can be ascribed to ﬁnite size effects,both of which are consistent with the studies reported for Co 3O 4and NiO [36,37].The spinel NiCo 2O 4shows ferrimagnetic (FM)nature with clear hysteresis loops,in which the nonlinear curves with nonzero remnant magnetization and coercivity can be clearly observed.The coercivity ﬁeld (H c )of the NiCo 2O 4NWs is 2805Oe,and the corresponding remanent magnetization (M r )is 0.019emu g À1.As have been reported that H c is likely to have two main contributions apart from magnetocrystalline anisotropy:shape anisotropy,such as FM materials are known to have magnetic disorder at the surface and AFM-FM exchange coupling,where the ferromagnetic originates from the defects of interfaces.Based on the F-center mediated bound magnetic polaron theory (FCBMP)or bound magnetic polaron (BMP)theory [38],Ni 2+ions,on substitution of Co 3+,create oxygen vacancies nearby Ni 2+in the lattice,in which an electron trapped in an oxygen vacancy (F center)couple with the magnetic spins of the nearest Ni 2+ions within the radius of the hydrogen like orbit of the F center and forms a BMP,thereby imparts ferromagnetism.Therefore,both the NWAs structure and oxygen de ﬁcient of NiCo 2O 4may contributed to increased H c at low temperatures.Fig.10b represents the ﬁeld-dependentFig.8.(a)Chronoamperometry data (j –t)recorded on NiO,Co 3O 4and NiCo 2O 4at a constant potential of 0.65V;(b)CV curves recorded at 1st cycle and 500th cycle for NiCo 2O 4.1222Y.-Z.Su et al./Electrochimica Acta 174(2015)1216–1224。

带原文的文献翻译报告

带原⽂的⽂献翻译报告NaCaPO4-SiO2系统硅酸盐-磷酸盐玻璃的直接结晶摘要这项研究的主题是硅酸盐-磷酸盐玻璃NaCaPO4-SiO2系统，它们是玻璃的前⾝-结晶材料。

玻璃-通过NaCaPO4-SiO2系统结晶获得结晶材料玻璃属于⼀类叫做⽣物活性的材料。

为了获得玻璃-结晶材料和预先建⽴的参数，让玻璃结晶在特殊条件在实验是必须的。

为了设计直接结晶过程正常，有必要知道玻璃状前体的结构和微结构。

微观观查显⽰，熔析发⽣在所有的玻璃研究中。

基于DSC检查，它已经发现的该结晶NaCaPO4-SiO2系统的玻璃是⼀个多步骤的过程。

测试玻璃中，在DSC曲线存在⼏个明显分开放热的峰值，使它可能结晶只与分离的相矩阵剩余⾮晶反之亦然。

开展材料的详细X射线和光谱研究通过加热的梯度炉（DSC中的基础上指定的温度）得到的结果表明分离相与基体分别结晶。

因此，⽣物活性玻璃-结晶材料可由于得到的相分离现象和结晶相的预先建⽴的⼤⼩的存在。

关键词：玻璃-结晶材料，直接结晶，硅酸盐-磷酸盐玻璃第1章绪论玻璃和NaCaPO4-SiO2系统的玻璃结晶材料属于⼀组⽣理活性的材料，能够形成与组织结合[1-10]。

使⽤玻璃作为⽣物材料使得有可能采取的优点的玻璃态的特定属性，即易于获得的⼏乎任何形状，缓和通过控制属性化学组合物的适当的选择，以应⽤可能性各种加⼯⽅法，以及各向同性性能。

然⽽，在硅酸盐 - 磷酸盐玻璃的主要特征也是它的脆弱性，这显著限制了它们的⽤途如⽣物材料。

⼀种最好的⽅法就是提⾼眼镜的机械性能的最佳⽅式是执⾏部分结晶（失透），以获得玻璃 - 结晶材料。

这种材料的特点是⾮常的存在的结晶相的细晶体，随机分布在在玻璃状基质的其余部分[11,12]。

这使得组合两个玻璃和晶体材料的优点（⾼机械强度）。

其结果，玻璃的结晶材料的特点是⾼得多的机械强度相⽐玻前体。

然⽽，⼀个问题结晶相⽣长的出现会对玻璃的⽣物活性产⽣不利影响[13,14] 。

在极端的情况下，不受控制的结晶可导致转换⽣物活性玻璃成完全惰性材料[14]。

《认知负荷理论视角下汉语无主句的英译同传策略研究》范文

《认知负荷理论视角下汉语无主句的英译同传策略研究》篇一一、引言随着全球化进程的加速，翻译在跨文化交流中的地位愈发重要。

其中，汉语无主句作为汉语特有的一种句式，在英译过程中往往存在一定难度。

本篇论文旨在从认知负荷理论的角度出发，探讨汉语无主句的英译同传策略。

通过对认知负荷理论的运用，寻求更为有效的翻译方法，提高同声传译的效率和质量。

二、认知负荷理论概述认知负荷理论认为，在信息处理过程中，人们的信息处理能力是有限的。

因此，翻译过程中需考虑认知负荷对翻译效果的影响。

翻译时，译者的认知负荷主要来源于语言转换的复杂性、信息处理的难度以及记忆负担等。

而针对汉语无主句的英译过程，译者的认知负荷更是成为制约翻译质量和效率的重要因素。

三、汉语无主句的特点及翻译难点汉语无主句是汉语中常见的句式，其特点在于省略了主语或没有显性的主语。

这种句式在表达上具有简洁、含蓄的特点，但在英译过程中却存在一定难度。

由于英语和汉语在句式结构、语法规则等方面存在差异，直接将汉语无主句翻译成英语往往会导致语义不清、结构混乱等问题。

因此，如何在保证语义准确的前提下，降低认知负荷，成为汉语无主句英译的关键。

四、认知负荷理论下的英译同传策略针对汉语无主句的英译同传过程，本文提出以下策略：1. 理解与预测：在同传过程中，译者需充分理解源语信息，预测可能出现的无主句结构。

这需要译者具备扎实的汉语功底和丰富的英语表达经验。

通过理解与预测，可以有效降低认知负荷，提高翻译效率。

2. 语境还原：在翻译过程中，译者应尽量还原语境，明确无主句所表达的具体含义。

这有助于减少信息损失，使译文更加准确、流畅。

3. 转换表达方式：针对汉语无主句的特殊性，译者可采取转换表达方式的方法，如增补主语、改变语序等，以适应英语的表达习惯。

这样可以在保证语义准确的前提下，降低认知负荷。

4. 借助记忆辅助工具：在同传过程中，可使用记忆辅助工具（如笔记、记忆卡片等）来帮助记忆关键信息。

初中生优秀议论文：做一个扬长避短的人

做一个扬长避短的人
富兰克林曾说过：“宝贝放错了地方便是废物”。

这是说在某一方面很有用的东西一旦用错了时间或是地点就不起丝毫作用了，这对人也是一样。

有的人明明精通某项技能，却从事着自己不擅长的工作，英雄无用武之地，岂不悲哉。

所以我们要发扬古人所说的：“扬长避短。

”
经营自己的长处，是许多成功人士的经验之道。

美国微软公司总裁比尔盖茨没有完成哈弗大学的学业就去经营他的电脑公司了，这正是由于他发现了自己的兴趣和长处，所以他成为世界首富就不足为奇了。

因为兴趣为动力长处为优势二者兼而有之，做事岂会不全力以赴，披荆斩棘？
反之，如果人们站错了位置，用自己的短处做事，那恐怕前途坎坷了。

记得曾康一个80/20的原则，其实很简单，就是用80%的时间去做只能见效20%的事，不如用20%的时间去做可以见效80%的事，这不正好说明扬长避短的好处吗？
也许有的人会说儒家经典语论调：“知其不可而为之”来证明挑战自我的勇气，甚至认为避短是懦弱的表现，其实不知“扬长避短”正是对于自身正确的评估。

广袤星空中，每颗星都有自己运行的轨道，茫茫人海中，每个人都有自己生活的位置，社会360行行行出状元，尺有所短，寸有所长。

擅于发现自己的长处，你就是那名状元郎。

扬长避短岂不美哉？
莎士比亚曾说：“人的青春是短暂的，但是，如果卑劣地度过这短暂的青春，就显得太多了
----------后记。

言词证据的分析与判断——以言词证据的结构分析为路径

言词证据的分析与判断——以言词证据的结构分析为路径曾康
【期刊名称】《西南政法大学学报》
【年(卷),期】2009(011)005
【摘要】言词证据是一类重要的诉讼证据,但是由于它以人的言词陈述为表现形式,因而通常被认为稳定性较差,证明力较弱.然而,如果我们能够认识到它的内在结构,透过其表面上的不稳定性,会发现言词证据是可以被把握的,其作用可以得到充分的发挥.
【总页数】7页(P69-75)
【作者】曾康
【作者单位】重庆市沙坪坝区人民法院,重庆,400038
【正文语种】中文
【中图分类】DF713
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文献回顾各解释变结果(1)

附表一文獻回顧各解釋變數結果(1)補習與教育成就補習教育、文化資本與教育取得家庭、學校與補習作者羅淇孫清山、黃毅志章英華、伊慶春年份2003 1996 2001樣本母體台灣成年人口20~64歲在台出生的樣本台北、宜蘭地區國三學生樣本數年輕1,257 國中1,247 全部樣本2,653 年長1,306 高中855 自願補習1,945被解釋變數分類分為校內補習與校外補習分為校內課業輔導上補習班與家教分為校內補習、校外補習、自願補習樣本分組方式1935~1963年與1978~1984年兩組分為升高中職與大學兩組性別1978~1984年組女多於男男性進補習班機會高、補習項數多高中請家教機會高女性自願補習者多於男性出生年次類別以1944、1954年為界分三組(僅限1935~1963年組)民國年次結果較年長者補習機率低年輕人國中時各種補習機會多學校類別類別公立、私立結果讀公立國中者補習機會高城鄉類別類別學校位置是否在直省縣轄市按出生地分八等級按學校所在地北縣市各分三地區宜縣分為城鄉兩組結果都市地區補習機會高都會區：校外補習鄉村：校內補習宜縣城鎮、較台北新興區顯著補習與教育成就補習教育、文化資本與教育取得家庭、學校與補習作者羅淇孫清山、黃毅志章英華、伊慶春年份2003 1996 2001班級課程分類類別升學班與否(僅限1935~1963年組)結果升學班學生補習機會高個人成績類別前五名、6~10名11~20名、21~30名30名以後結果各組較30名以後校外補習機率高國小補習或安親國小有補習者國中階段亦會補習參加校內課輔參加者亦會再參加校外補習自己期望升大學與校外補習呈現正向顯著兄弟姐妹數目與校外補習負向顯著相關與校外補習呈現負向顯著家庭所得類別實際每月所得每月總收入分五組結果不顯著不顯著經濟評估類別很大幫助至很大限制分為五組結果幫助愈大愈易參加校外補習家庭情況類別完整或破碎(離婚分居)家庭結果家庭破碎者校外補習傾向弱補習與教育成就補習教育、文化資本與教育取得家庭、學校與補習作者羅淇孫清山、黃毅志章英華、伊慶春年份2003 1996 2001 父母補習重考不顯著父親省籍類別外省籍與否閩南、客家外省、原住民結果僅上一代外省人有較多校外補習機會外省籍、客家籍讀書環境較佳父母教育程度類別採用年數計算國初中、高中大專以上三組結果教育年數愈多子女補習時間增加(高中)大專畢者校外與自願補習者高父母職業類別公教人員與否雇主、自營商結果公教人員子女較有補習機會雇主子女補習項數較多父母教育期望類別國中以上分為六組結果期望高者不參加補習機會低附表二文獻回顧各解釋變數結果(2)補習在台灣的變遷效能與階層化台灣高中生參加補習之效益分析Shadow Education andAllocation in FormalSchooling：Transition toUniversity in Japan作者劉正林大森、陳憶芬Stevenson, David L. and David P. Baker年份2006 2006 1992樣本母體90學年度就讀的國中生92學年度大一新生1980、1982年日本高中生樣本數 33,9597,240被解釋變數分類補習與否補習總科目模擬考班、函授家教、一般補習班與重考班樣本分組方式性別分組社會與自然兩組性別不顯著不顯著女性較偏好家教男性較女性偏好模擬考班、函授重考班家庭排行老二以上較老大補習機率低獨生子女與否不顯著城鄉類別類別按學校所在地分為鄉村城鎮都市北、中、南、東部離島五區域城市或鄉村結果都市學校補習機率較鄉村顯著中部社會組較北部少東部自然組較北部多僅函授部份城鄉無顯著差異補習在台灣的變遷效能與階層化台灣高中生參加補習之效益分析Shadow Education andAllocation in FormalSchooling：Transition toUniversity in Japan作者劉正林大森、陳憶芬Stevenson, David L. and David P. Baker年份2006 2006 1992班級課程分類類別學科課程與否結果除家教外參與學科課程參與其他補習機率高自己成績類別結果學業成績愈好補習機率愈高自己期望升大學期望者補習機率高兄弟姐妹數目社會組呈顯著負相關家庭所得類別每月總收入分六組年收入分為六組結果5~15萬收入家庭補習機率大於2萬以下家庭114萬元以下補習項數小於151~300萬元家庭情況類別分為雙親、單親與未與父母同住結果其他家庭皆較雙親家庭補習機率低補習在台灣的變遷效能與階層化台灣高中生參加補習之效益分析Shadow Education andAllocation in FormalSchooling：Transition toUniversity in Japan作者劉正林大森、陳憶芬Stevenson, David L. and David P. Baker年份2006 2006 1992父母教育程度類別國中以下、高中職科大、大學、研究所教育年數結果高中以上至大學補習機率顯著大於國中以下教育年數愈高補習項數愈多教育年數愈高各項補習機率愈多父母職業類別分為七等級分為六組結果各工作皆較待業者補習機率高農工階級補習項數低於技術員與教師父母教育期望類別大學學歷與否結果期望者補習機率高。

政论文本翻译

政论文本翻译政论汉翻译出现的差异（一）思维方式和社会价值观的不同摘要: 英汉民族长期处于不同的生活环境，其民族历史积淀着不同的文化，显现出不同的思维方式、思维特征与思维风格。

思维上的差异，反映着操某一种语言的民族群体千万年以来形成的语言心理倾向。

思维方式、思维特征和思维风格是语言生成的哲学机制。

语言实际上是紧紧地附着在思维这个有无限纵深的基础之上的结构体，语言受思维的支配，它是处在交际中的人的思维载体。

我们在翻译中遇到的许多困难，正是由于思维对语言的支配作用而造成的。

然而，在以往的翻译探讨中，我们对思维在翻译活动中的作用却未予以足够的重视。

本文通过对比英汉思维方式的差异在语言上的表现，揭示英汉思维方式差异对翻译的影响，进而探索避免汉英思维方式差异影响翻译的途径。

价值观是帮助人们辨别好与坏、美与丑、正确与错误、真实与虚假等的标准。

不同的国家有不同的文化规范价值观念，这种差异是导致中西方思想沟通困难，从而产生误解和冲突的主要因素。

认识和掌握跨文化差异对世界文化交流有重要意义。

本文先介绍了中西方价值观差异的成因，然后阐述了这种差异在诸多方面的表现，有助于读者更深入地了解中西方在文化方面的不同。

关键词：思维方式；文化；价值观；差异一、引言“思维方式是主体在反映客体的思维过程中，定型化了的思维形式、思维方法和思维程序的综合和统一。

”思维是语言产生的基础，它支配着语言。

语言依附于思维，它是思维的载体。

在一种语言向另一种语言的转换的翻译过程中，原作与译者的沟通依靠共同的思维规律。

思维活动的规律及内容制约着确译活动的全过程。

因此对翻译的研究离不开对人脑思维的研究, 深入、系统地探讨不同民族思维方式的个性即差异性可以帮我们更好了解语言表达上不同的深层原因，这对翻译实践有所启发和指导。

二、英汉思维方式差异的表现思维与语言存在一定的对应关系，思维方式决定着语言形式，东西方不同的思维方式不仅表现在语言内也表现在语言结构上。

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表面涂层工艺包埋渗工艺制备铝改性硅化物涂层应用于铌基超高温合金摘要：为制备覆有铝改性硅化物涂层的铌基超高温合金，需要应用两阶段包埋渗技术和共包埋渗技术。

两阶段过程包括样品在1150℃渗硅化4小时，然后在800℃—1000℃渗铝化4小时。

渗硅化的涂层由厚的(Nb.X)Si2(X代表Ti、Cr和Hf)外层和薄的(Nb.X)5Si2过渡层构成，渗硅化的样品在860℃进行铝化，(Nb.Ti)3Si5Al2层在涂层表面形成，并且，在860℃渗铝过程中，于(Nb.X)5Si3涂层及底层之间形成新的(Nb.Ti)2Al涂层，但是当在900℃—1000℃进行铝化时，新的涂层是(Nb.Ti)Al3。

共包埋渗过程由样品在1000℃—1150℃进行硅和铝的不同的包埋，并且发现，与包埋组成相比，涂层的结构更明显的受到共包埋温度的影响。

铝改性的硅化物涂层的表层由(Nb.X)5Si3、(Nb.X)Si2、(Nb.Ti)Al3组成，且表层由硅和铝在1050℃共包埋获得。

介绍由于铌基合金的低密度、高熔点、和高拉伸强度等优点，它适合于做高温结构材料，但较差的耐氧化性能成为在高温实际应用中的主要障碍。

机械特征与高温环境下的耐氧化性能之间的平衡还无法在铌基合金中实现，因此为了在高温环境下使用，需要一种保护性涂层。

保护性的涂层应该能够可以缓慢形成SiO2或者Al2O3来充当一种阻碍防止氧气的渗入，而且，能够紧紧的吸附住底层。

不同的涂层通过改变外部的底层来形成强而均一的金属连接的涂层。

卤化物包埋技术制成的扩散涂层，普遍应用与金属材料的保护。

铌基硅化物可用作涂层材料，但是简在氧化环境中，对于简单的双重铌基硅化物有限的耐氧化性能对于Nb2O5。

因此，目前有大量研究致力于制成改性的硅化物涂层，然而很少有公开的报道是关于铝改性硅化物涂层应用于铌基合金。

近年来，Murakami已经证实，Nb3Si5Al2在1100℃—1300℃的超高耐氧化性能优于简单的NbSi2，这是由于在Nb3Si5Al2氧化过程中形成了薄Al2O3保护层。

所以本文章主旨在于通过HAPC技术制备覆有Nb3Si5Al2表层的铝改性硅化物涂层，并将其应用于铌基合金。

实验过程通过真空自耗电弧方法制备的多组分组成(24%Nb、16%Ti、6%Si、4%Cr、3%Hf、1.5%Al、0.05%B)的铌基超高温合金用作为涂层实验的基层物。

通过电化学放电加工工艺，将样品制成8nm ×8nm×8nm方块。

使用1000规格的SiC细砂纸将其抛光，然后经过超高温丙酮浴，干燥处理。

应用两种不同的包埋渗工艺来制备铝改性硅化物涂层。

其中之一是：两阶段的包埋渗工艺；另一种是：共沉积包埋渗工艺。

两阶段的包埋渗工艺包括在1050℃渗硅化和在800℃—1000℃的渗铝化过程。

包混合物的组成和沉积条件如表格1所列。

由Al2O3、NaF、Al或者硅粉组成的包混合物通过称重、球滚3.5h而混合。

包埋粉填充满氧化铝器皿中样品，然后用氧化铝盖子封存。

包埋达到负荷后，熔炉腔经过抽真空到 2.6×10-2pa，熔炉内温度以每分钟16℃升温。

抽真空系统需在保护性气体氩气纯度达到99.99%时停止，温度为700℃。

涂层样品经过X射线衍射分析和扫描电子显微镜分析。

EDS数据经过被刻蚀的样品检测，腐蚀剂的组成是60%H2O、37.5%HNO3、12.5%HF结果分析3.1两阶段制备涂层第一步，渗硅化，在样品表面形成一硅化的涂层。

图一显示涂层的扫描电子显微图像。

大概50um厚，而且几乎看不见缝隙。

EDS检测显示涂层由48um厚外层和2um的过渡层构成，表面XRD(X射线衍射分析)显示外层是(Nb.X)Si2(X代表Ti、Cr和Hf)，过渡层是43.97%Si、28.78%Nb、21.23%Ti、3.48%Cr、2.08%Hf、0.46%Al。

在样品剥除48um形成的新的表层的Ｘ射线衍射显示：过渡层主要由(Nb.X)5Si3构成。

第二步，使已经渗硅化的样品进行渗铝化。

发现，随着渗铝化的温度的升高，铝在表层的比例也增加，如图2所示。

在800℃和830℃制备的铝改性硅化物涂层，与硅化物涂层相比，有相似的结构及相似的形态学特征；但是在860℃、900℃、1000℃制备的涂层，与硅化物涂层相比，却有不同的结构和形态学特征。

图3表征860℃渗铝化的硅化样品SEM（扫描电子显微图像）。

发现在涂层的表层出现特征区域，如图三所示。

特征区域是由45.43%Si、24.93%Al、19.05%Nb、9.46%Ti、0.72%Cr、0.42%Hf 组成。

表层X射线衍射谱图显示，涂层的外层是由(Nb.X)Si2、(Nb.Ti)3Si5Al2构成。

故可得出结论：特征区域就是(Nb.Ti)3Si5Al2。

除此之外还发现新的表层是在（Nb.X)5Si3层和底层之间形成。

表层B是非连续的，它由（Nb.X)5Si3阻断。

表层B的组成是44.06%Nb、29.21%Al、15.69%Ti、2.45%Si、7.46%Cr、1.13%Hf，而这和(Nb.Ti)2Al的分子构成相同。

图3中的表层A 则是（Nb.X)5Si3和Al，其组成是37.76%Si、31.77%Nb、15.50%Ti、9.14%Al、3.87%Cr、1.97%Hf。

铝在（Nb.X)5Si3中的溶解度和参考文献8中报道的8%-—12%的溶解度一致。

在此实验中，可得出结论，当铝蒸汽环境的沉积量超过铝在硅化物表层的溶解度时，表层B就会形成。

于900℃渗铝化的硅化样品涂层的结构如图5显示，硅和铝的线性扫描结果也如图5所示。

涂层含有50um的外层和90um内层。

图4中样品红外谱图显示，外层的构成是(Nb.X)Si2、(Nb.Ti)3Si5Al2其组成相同于在860形成的渗铝化的硅化物涂层样品；内层的红外谱图显示（经过剥除60um原始表层而形成的新的表层的红外检测）：内层主要是由(Nb.Ti)Al3构成，EDS分析证实：内层的基体构成是66.21%Al、14.01%Nb、10.13%Ti、8.16%Si、0.50%Cr、1.08%Hf 这和(Nb.Ti)Al3的分子构成相同。

在内部的分散层是富含硅的沉淀物，其组成是36.02%Si、16.94%Nb、10.18%Ti、33.69%Al、1.90%Cr、1.27%Hf。

内层的组成是由于向内部扩散的铝和底层的在(Nb.X)Si2低溶解度的铝共同反应形成的。

据此可猜测：由于高含量的活泼铝，内层可以充当第二层的防氧化层。

在1000℃制备的渗铝化硅化物涂层，与900℃制备的渗铝化的硅化物涂层(除开在制备过程中形成裂纹的涂层）相比，有着相似结构和形态学特征。

3.2Si—Al共沉积涂层3.2.1Si—Al共沉积涂层的结构在相同温度下（都在1050℃和1100℃），经过Si—Al共沉积来制备涂层，但是包埋物组成却不相同（质量比为10%Si、x%Al、5%NaF、85%—x%Al2O3,x代表2.5和10）。

经过对比，共沉积的温度对涂层的结构有很大影响。

图6表征在不同温度下，由Si—Al共沉积制备的涂层的扫描电子图像，其中包埋组成是质量比为10%Si、10%Al、5%NaF、75%Al2O3,所有的涂层都有多层结构。

图7中表层X射线分析显示，在不同温度下的不同涂层的的结构。

图6（a）表征在1000℃下，由Si—Al共沉积制备的涂层的扫描电子图像。

涂层具有25um 外层和5um的内层，内层由于(Nb.X)5Si3的阻断而成为不连续态。

图7X射线衍射分析显示涂层外层由(Nb.Ti)Al3和少量的(Nb.X)5Si3组成，经过EDS分析外层中Si含量为2.32%，现今还无法判定外层的Si是来自于气象沉积还是源于底层物。

从图6中还可以得出：和Al的成分一样，Cr的含量明显高于其它区的含量。

同样可知，在1050℃—1100℃下制备的涂层，可以发现富含Cr的表层。

图6（b）表征在1050℃，由Si—Al共沉积制备的涂层的扫描电子图像。

图7（b）X射线衍射表征外层主要有(Nb.X)Si2、(Nb.Ti)3Si5Al2、(Nb.Ti)Al3。

因此，在高温氧化环境中，SiO2和Al2O3更易形成。

外层大概9um。

在外层下部，有8um的(Nb.X)5Si3中间层，其组成为45.35%Si、2.19%Al、29.78%Nb、19.25%Ti、1.72%Cr、1.17%Hf，而内层是2—4um，组成富含Cr和Al。

图6（c）表征在1100℃和1150℃下，由Si—Al共沉积制备的涂层的扫描电子图像。

图7（c)和（d）X射线衍射表征外层的组成都是(Nb.X)Si2。

EDS分析证实(Nb.X)Si2中Al含量在2.35%—3.71%。

在1100℃和1150℃制备的(Nb.X)Si2厚度分别为20um和45um。

同样，在外层下面，也出现(Nb.X)5Si3中间层，其组成为46.03%Si、1.05%Al、29.43%Nb、19.16%Ti、3.00%Cr、1.33%Hf，两者中间层厚度都为6um，两者的内层厚度为4—7um。

从图6可知，在不同的涂层的内层都有相似的结构。

X射线衍射和EDS分析显示：上述四种共沉积制备的涂层都有两层，一层是较高的Al含量和较低的Cr含量（3.76%Si、60.45%Al、24.23%Nb、7.15%Ti、3.96%Cr、0.45%Hf），另一层是较高的Cr含量和较低的Al含量（1.32%Si、40.27%Al、23.33%Nb、12.39%Ti、21.38%Cr、1.31%Hf）。

根据文献10，含量Al较高的层主要在金属间的(Nb.Ti)Al3；根据文献11，含量Cr较高的层是（Cr.Al)2(Nb.Ti)。

图8表征在1050℃下，Si—Al共沉积制备的涂层的背散射电子和X射线衍射谱图。

谱图表明，灰色基质层是(Nb.Ti)Al3，白色圆柱层是(Cr.Al)2(Nb.Ti)。

内层的组成是由于Al在气象沉积过程而形成，这与文献8中报道的一致：额外的Al有助于在Nb—Si—Cr体系中熔岩象的形成，而且Al在Cr2Nb 中溶解度高达45%。

3.2.2共沉积涂层的结构组成HAPC（卤化物包埋技术）是化学气象沉积过程，因为在包埋渗过程中，金属—卤素气象成分会沉积。

化学物促使金属—卤素气象扩散而形成表面的沉积。

为了在单过程中获得两象及更多成分，卤素气象压力应该控制在可比较的范围。

在此研究共沉积过程中，NaF和Si及Al的反应产生了氟化物，如AlF3、AlF2、AlF、AlF4以及SiF、SiF2、SiF3、SiF4等。

通过查找JANAF中热化学数据，所有的反应速率常数(kp)都可以计算得出，通过氟元素和钠元素的元素守恒定理，可以推导出氟化物的分子组成。