introduction写作方法及技巧

1、科技学术论文 Introduction引言的主要内容是交代此项研究的来龙去脉， 简要说明课题的缘起与背景， 性质与意义， 动 机与目的、 主要理论根据及其基本原理等， 同时指出相关领域内前任的研究成果、 存在问题 和知识空白， 以表明本项研究的连续性和需要性， 叙述有关本课题的历史沿革是为了温故而 知新， 但应注意掌握适当的范围和尺度， 一般来说仅需要介绍极密切的有关史料即可， 不宜 泛泛赘述大量历史文献，否则会造成 Introduction 长而乏味。first ：提出研究现状和此研究的重要性 second：强调有必要解决存在的问题 third：介绍作者自己的研究内容、提出创新性逻辑的连贯内

2、容的创新词汇简洁时态1. What is an introduction?The introduction section shows the questions that should be answered for the readers once they finish reading the “ Introduction ” .2. What s the purpose of the introduction?The introduction comes at the start of a piece of writing. Without this part, the reader

3、cannot easily understand the more detailed information about the research that comes later in the thesis.It introduces:（1）.the research by situating it （by giving background）,（2）.presenting the research problem , and saying how and why this problem will be solved ,（3）.explaining why the research is

4、being done. （rationale） which is crucial for the reader to understand the significance of the study.3. How should I start?You may want to start your introduction by describing the problem you are trying to solve, or the aim of your work4. How to build a model of introduction?Read the following intro

5、duction and decide what the author tells us in each sentence.5. The model of introduction.(1) establishes the importance of this research topic 确立研究主题的重要性(2) provides general background information for the reader. 为读者提供总体的背景信息(3) in a more specific/detailed way, using research references to support

6、both the background facts and the claim for significance.与第 1、 2句的做法一样，但是更具体(4) describes the general problem area or the current research focus of the field. 描述了所研究领域的一般性问题或当前的研究焦点(5) provides a transition between the general problem area and the literature review 提供了总体问题领域到文献综述之间的一个过渡(6) provides

7、a brief overview of key research projects in this area. 概述了此研究领域重要的研究项目(7) describes a gap in the research 描述了已有研究的空白(8) describes the paper itself 描述了论文本身的工作(9) gives details about the methodology 详细描述了论文中所用的方法(10) announces the findings 公布了论文的结论6. Four components of a model.(1) Establish the impor

8、tance of your fieldProvide background/ facts/information (possibly from research)Define the terminology in the title/key wordsPresent the problem area/current research focus 确立研究领域的重要性提供背景事实或信息(有可能来自现有文献) 定义题目或关键词中的术语给出所研究问题的范畴或目前的研究重点(2) Previous and/or current research and contributions 前期的研究或目前的研

9、究及其贡献(3) Locate a gap in the researchDescribe the problem you will address Present a prediction to be tested 确定已有研究工作的空白；描述你要解决的问题 呈现要验证的预测(4) Describe the present paper 描述现在的论文7. Grammar and writing skills.语法 时态 写作技巧8. Vocabulary词汇的简洁举例三篇文章： 1.Gene expression profiling and pathway analysis of hepat

10、otoxicity induced by triptolide in Wistar rats在 Wistar 大鼠中，通过基因表达谱和通路分析由雷公藤甲素诱导的肝毒性 引言的主要内容是交代此项研究的来龙去脉，例如本文中，简要说明课题的缘起与背景，TP 的性质Triptolide (diterpenoid triepoxide, TP), purified from the shrublike vine Tripterygium wilfondii Hook F (TWHF)与药理学意义possesses anti-inflammatory, anti-fertility, anti-neopl

11、astic and immunosuppressive activities 实验的动机However, clinical use of TWHF or TP has been limited due to severe adverse reactions, such as gastrointestinal upset, diarrhea, reproductive toxicity and problems associated with circulatory systems目的we hypothesized that liver is a major toxic target of TP

12、 treatment. Thus, it is essential to elucidate the mechanism of TP-induced hepatotoxicity from a safety point of view.the aim of our study was to identify candidate genes associated with TP treatment and to provide novel insights to better elucidate the mechanisms of toxic effects of TP.主要理论根据及其基本原理

13、Considering that microarray technology is recognized as a reliable toxicologica method to determine mechanisms of drug-induced toxicity, identify biomarkers and to predict chemical toxicity.Therefore, the aim of our study was to identify candidate genes associated with TP treatment and to provide no

14、vel insights to better elucidate the mechanisms of toxic effects of TP.同时指出相关领域内前任的研究成果possesses anti-inflammatory, anti-fertility, anti-neoplastic and immunosuppressive activities (Chen, 2001; Huynh et al., 2000; Panichakul et al., 2006).have emerged as treatments of rheumatoid arthritis, systemic

15、lupus erythematosus, nephritis, leprosy and asthma (Lipsky and Tao, 1997; Liu et al., 2005; Zhang et al., 2010).clinical use of TWHF or TP has been limited due to severe adverse reactions, such as gastrointestinal upset, diarrhea, reproductive toxicity and problems associated with circulatory system

16、s (Hikim et al., 2000; Ni et al., 2008; Yang et al., 2012; Zhang et al., 2011).Recently, hepatotoxicity induced by various extracts of TWHF in animals and humans has been reported by many researches (He et al., 2006; Mei et al., 2005; Wang et al., 2007)To date, only mitochondrial respiratory chain i

17、nhibition, lipid peroxidation, DNA damage and hepatocyte apoptosis were proposed to be involved in TP-induced liver injury (Fu et al., 2011; Mei et al., 2005; Yao et al., 2008). 等存在问题和知识空白Hepatic differential gene expression was analyzed using oligonucleotide microarray analysis for over-represented

18、 functions and phenotypically anchored to complementary histopathologic, biochemical, and dosimetry data in the liver. The results indicate that TP affects diverse cellular pathways, including insulin signaling pathway, glucose metabolism, cell cycling, oxidative stress and apoptosis. These data pro

19、vide a clearer understanding of the molecular mechanisms of TP-induced hepatotoxicity, as well as useful information for predicting drug hepatotoxicity.以表明本项研究的连续性和需要性，叙述有关本课题的历史沿革是为了温故而知新，Triptolide (diterpenoid triepoxide, TP), purified from the shrublike vine Tripterygium wilfondii Hook F (TWHF),

20、 possesses anti-inflammatory, anti-fertility, anti-neoplastic and immunosuppressive activities (Chen, 2001; Huynh et al., 2000; Panichakul et al., 2006). Recently, the methanol/chloroform (T2) and ethyl acetate (EA) extracts of TWHF, in which TP was identified as the principal active compound, have

21、emerged as treatments of rheumatoid arthritis, systemic lupus erythematosus, nephritis, leprosy and asthma (Lipsky and Tao, 1997; Liu et al., 2005; Zhang et al., 2010). However, clinical use of TWHF or TP has been limited due to severe adverse reactions, such as gastrointestinal upset, diarrhea, rep

22、roductive toxicity and problems associated with circulatory systems (Hikim et al., 2000; Ni et al., 2008; Yang et al., 2012; Zhang et al., 2011).Recently, hepatotoxicity induced by various extracts of TWHF in animals and humans has been reported by many researches (He et al., 2006; Mei et al., 2005;

23、 Wang et al., 2007). Besides, Liu et al., (2010) found that potential hepatotoxicity in rats treated with TP for 28 days was associated with increasing levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (Liu et al., 2010). Moreover, it was reported that oral administ

24、ration of TP to rats could lead to liver injury or even death (Fu et al., 2011). In addition to this, our previous investigation showed that the concentration of TP found in liver exceeds those observed in other tissues, such as spleen, lung, heart, and kidney (unpublished data). On account of this,

25、 we hypothesized that liver is a major toxic target of TP treatment. Thus, it is essential to elucidate the mechanism of TP-induced hepatotoxicity from a safety point of view.Unfortunately, its underling mechanisms are still insufficiently recognized. To date, only mitochondrial respiratory chain in

26、hibition, lipid peroxidation, DNA damage and hepatocyte apoptosis were proposed to be involved in TP-induced liver injury (Fu et al., 2011; Mei et al., 2005; Yao et al., 2008). Considering that microarray technology is recognized as a reliable toxicologica method to determine mechanisms of drug-indu

27、ced toxicity, identify biomarkers and to predict chemical toxicity (Lee et al., 2010; Wang et al., 2011). Therefore, the aim of our study was to identify candidate genes associated with TP treatment and to provide novel insights to better elucidate the mechanisms of toxic effects of TP.Here, we desc

28、ribe genome-wide gene expression in the TP-exposed Wistar female rat liver. Differential gene expression was evaluated in 6-week-old female Wistar rat livers following 14 days of continuous exposure to large doses of TP. Hepatic differential gene expression was analyzed using oligonucleotide microar

29、ray analysis for over-represented functions and phenotypically anchored to complementary histopathologic, biochemical, and dosimetry data in the liver. The results indicate that TP affects diverse cellular pathways, including insulin signaling pathway, glucose metabolism, cell cycling, oxidative str

30、ess and apoptosis. These data provide a clearer understanding of the molecular mechanisms of TP-induced hepatotoxicity, as well as useful information for predicting drug hepatotoxicity.2.综述Blood vessels, a potential therapeutic target in rheumatoid arthritis? 血管，类风湿性关节炎潜在的治疗靶标？IntroductionRheumatoid

31、 arthritis (RA) can be defined as a disease of the blood vessels, both micro- and macro-vessels. The formation of new micro-vessels is in fact necessary to afford the nutritional supply to proliferating synovial pannus, while macro-vessels are the site where accelerated atherosclerosis driven by dis

32、ease s systemic inflammation develops. New vessels formation on one side, and atherosclerotic plaque progression on the other, might seem two different biological phenomena, the first related to the articular involvement of the disease, the second to its main systemic complication. In this context,

33、targeting blood vessels in RA might mean either attempting to reduce synovial vascular supply starving the synovial pannus limiting its proliferation or, in the other case, trying to limit macro-vessels damage outside the joint. In this review we will analyse the possibility of targeting synovial mi

34、crovessels to treat rheumatoid arthritis, but we will discuss as well the evidence supporting a link between micro- and macro-vascular involvements in RA. 综述的介绍，介绍所提到物质的基本概念，简要说明课题的缘起与背景， RA 与血管生成相 关，与血管生成的必要性，在这里， 说明该文章立题的主要依据与主要原理，并提出在此综 述中接下来会说到的内容， 如：作者将分析滑膜微血管治疗类风湿关节炎的可能性， 且讨论， 血管与 RA 微观和宏观之间联系

35、的证据。 概念由浅入深， 词汇简介，介绍基本概念时使用一 般时态，提到文章后续会介绍的内容时使用将来时，对未来内容的展望。3.介绍功能性文章Dissection of TNF Receptor 1 Effector Functions: JNK Activation Is Not Linked to Apoptosis While NF-kB Activation Prevents Cell Death肿瘤坏死因子受体 1 的效应功能： NF-kB 的活化阻止细胞死亡， JNK 活化未关联凋亡这篇文章的简介有 1318词，系统的介绍了 TNF 的含义，分类，受体类型，相关的两个转录 因子， A

36、P-1、 NF-kB 、TNF 所经过的通路，通路中所涉及的许多其他细胞因子，由于是介 绍功能性文章，这样的背景知识很重要，所以虽然 Introduction 很长，但是有意义。 逻辑连贯由各部分功能连接到总体功能，均采用一般时介绍，时态统一。Tumor necrosis factor (TNF) is a cytokine produced by many cell types, including macrophages, monocytes, lymphoid cells, and fibroblasts, in response to inflamma-tion, infection,

37、 and other environmental challenges (Tra-cey and Cerami, 1993). TNF elicits a wide spectru of organismal and cellular responses, including fever, shock, tissue injury, tumor necrosis, anorexia, induction inof other cytokines and immunoregulatory molecules cell proliferation, differentiation, and apo

38、ptosis (Tracey and Cerami, 1993; Vandenabeele et al., 1995). These responses are elicited by TNF-induced trimerization of two distinct cell surface receptors, TNFR1 (p55) and TNFR2 (p75), at least one of which is present in almost every cell type (Tartaglia and Goeddel, 1992; Smith et al., 1994; Van

39、denabeele et al., 1995). The structural simi- larity between the two TNF receptors is limited to their extracellular domains (Tartaglia and Goeddel, 1992). The TNFR ectodomains are related to those of CD30, CD40, CD27, and Fas, all of which belong to the TNF receptor difsuperfamily (Smith et al., 19

40、94). The ligands for these receptors are structurally related to TNF, and many of them are cell-surface anchored (Smith et al., 1994). Al- though most of the biological activities of TNF appear to be transduced by TNFR1, many can also be mediated by TNFR2 (Tartaglia and Goeddel, 1992; Smith et al.,1

41、994; Vandenabeele et al., 1995). TNFR2,however, is a poor inducer of apoptosis Exposure to TNF results in activation of two transcription factors, AP-1 (Brenner et al., 1989) and NF-kB (Osborn et al., 1989). These transcription factors mediate induction of other cytokine and immunoregulatorygenes, a

42、s well as metalloproteinases.Several second messengers have been proposed tomediate the biological effects of TNFR ligation, including various phospho lipid breakdown products, arachidonic acid metabolites, free radicals, and increased intracellular Ca21 (reviewed by Beyaert and Fiers, 1994). Howeve

43、r, as discussed by Beyaert and Fiers, (1994), it is not clear whether these are true second messengers or secondary effects of TNFR activation. Several protein kinases were found to be activated rapidly in response to TNF, including yettigated to-be-identified ceramide-activated kinase (Weigmann et

44、al., 1994), IkB kinase (DiDonato et al., 1996), and aTNFR1-associated serine/threonine kinase(VanArsdale and Ware, 1994), as well as the molecularly identifiedRaf-1 (Belka et al., 1995),Jun N-terminal kinases (JNKs; Minden et al., 1994), and p38/Mpk2 (Raingeaud et al.1995). Activation of the IkB kin

45、ase results in NF-kB actiTRAF2 vation (Verma et al., 1995; DiDonato et al., 1996), while Raf-1, JNK, and p38/Mpk2 activation contribute to in duction of AP-1 activity (Karin, 1995). The pathways by which TNFR ligation causes activation of these protein kinases are not clear. Recently, much emphasis

46、has been placed on the potential role of ceramide as a mediator of TNF signaling. TNF-induced phospholipid hydro- introduction lysis can result in ceramide production (Kolesnick and Golde, 1994), and exogenous ceramide can lead to acti vation of NF-kB(Weigmann et al., 1994) and JNK (Verhei et al., 1

47、996) and apoptosis (Obeid et al., 1993). However, it is also possible that ceramide is produced as a result of TNF-induced cell death (Beyaert and Fiers, 1994).A major advance in understanding early events in TNF signaling was the identification of protein molecules that are recruited to TNFR1 and T

48、NFR2, following ligand inof duced trimerization(Rothe et al., 1994, 1995a; Hsu et al., 1995). While activation ofTNFR1results in recruitment of the TNFR1-associated death domain protein (TRADD; Hsu et al., 1995, 1996a), occupancy of TNFR2 leads to recruitment of TNFR-associated proteins 1 and 2 (TRA

49、F1 and TRAF2; Rothe et al., 1994), as well as c-IAP1and c-IAP2 (Rothe et al., 1995a). Recently TRADD was shownto interact directly with two other proteins, TRAF2 and Fas-associated protein with death domain (FADD; Hsu et al., 1996a). The recruitment of TRAF2 to both TNFR1 and TNFR2 explains why both

50、 receptors can elicit certain overlapping responses, despite having differentcytoplasmic domains. Indeed, TRAF2 appears to mediate NF-kB activation by both TNFR1 and TNFR2 as well as by the related CD40 receptor (Rothe et al., 1995b; Hsu et al., 1996a). FADD (also known as MORT1) was originally iden

51、tified as a protein that interacts with the cytoplasmic domain of Fas (Boldin et al., 1995; Chinnaiyan et al., 1995), which is structurally related to the cytoplasmic domain of TNFR1 (Itoh and Nagata, 1993; Tartaglia et al., 1993a). The death domain present in the cytoplasmic portions of both recept

52、ors mediates protein protein interactions with other death domain containing proteins, such as TRADD (Hsu et al., 1995) and FADD (Boldin et al., 1995; Chinnaiyan et al., 1995). Another death domain protein is the serine/threonine kinase RIP (for receptor-interacting protein; Stanger et al., 1995; Hs

53、u et al., 1996b). Originally identified by its interaction with Fas (Stanger et al., 1995), RIP was recently shown to be recruited to the TNFR1 signaling complex via TRADD and to participate in NF-kB activation (Hsu et al., 1996b). The use of dominant-negative mutants suggests that TRADD is required

54、 for induction of apoptosis by TNFR1 (Hsu et al., 1996a, 1996b) and expression of both TRADD and RIP death domains is sufficient to activate this process (Hsu et al., 1995, 1996b; Stanger et al., 1995). Apoptosis induction by TNFR1 also appears to require FADD, but unlike TRADD and RIP, this activit

55、y is mediated by the FADDN-terminal domain rather than its death domain (Chinnaiyan et al., 1995;Hsu et al., 1996a). In fact, the FADD death domain blocks TNF-induced apoptosis (Hsu et al., 1996a; Chinnaiyan et al., 1996). The N-terminal death effector domain of FADD interacts with the ICE-like prot

56、easeMACH (for MORT1-associating CED homolog) or FLICE (for FADD-like interleukin-1b-converting enzyme ICE), which appears to be a direct activator of the apoptotic.These results suggest the protein-recruitment model for TNFR1 signaling that is illustrated in Figure 1. TNF induced trimerization of TN

57、FR1 results in recruitment of TRADD and RIP via death domain interactions. The TNFR1 TRADD complex then recruits at least three other signaling proteins: RIP, FADD, and TRAF2. While FADD activates the apoptotic machinery, TRAF2 and RIP mediate NF-kB activationThese results, however, provide no clue to themechanism by which TNFR1 can activate the JNK and p38 mitogen-activated protein kinase (MAPK) cascades or stimulate AP-1 activity. Furthermore, it was recently sug gested that JNK an