introduction寫作方法及技巧

1、科技學術論文Introduction引言的主要內(nèi)容是交代此項研究的來龍去脈，簡要說明課題的緣起與背景，性質(zhì)與意義，動機與目的、主要理論根據(jù)及其基本原理等，同時指出相關領域內(nèi)前任的研究成果、存在問題和知識空白，以表明本項研究的連續(xù)性和需要性，敘述有關本課題的歷史沿革是為了溫故而知新，但應注意掌握適當?shù)姆秶统叨?，一般來說僅需要介紹極密切的有關史料即可，不宜泛泛贅述大量歷史文獻，否則會造成Introduction長而乏味。first:提出研究現(xiàn)狀和此研究的重要性 second：強調(diào)有必要解決存在的問題third :介紹作者自己的研究內(nèi)容、提出創(chuàng)新性邏輯的連貫 內(nèi)容的創(chuàng)新 詞匯簡潔 時態(tài)1. Wha

2、t is an introduction?The introduction section shows the questions that should be answered for the readers once they finish reading the a 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 cannot

3、easily understand the more detailed information about the research that comes later in the thesis.It introduces:11) .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 bein

4、g done. (ratio'nale) 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 intr

5、oduction and decide what the author tells us in each sentence.5. The model of introduction.(1) establishes the importance of this research topic確立研究主題的重要性(2) provides general background information for the reader.為讀者提供總體的背景信息(3) in a more specific/detailed way, using research references to support b

6、oth the background facts and the claim for significance.與第1、2句的做法一樣，但是更具體(4) describes the general problem area or the current research focus of the field.描述了所研究領域的一般性問題或當前的研究焦點(5) provides a transition between the general problem area and the literature review提供了總體問題領域到文獻綜述之間的一個過渡(6) provides a bri

7、ef overview of key research projects in this area.概述了此研究領域重要的研究項目(7) describes a gap in the research描述了已有研究的空白(8) describes the paper itself描述了論文本身的工作(9) gives details about the methodology詳細描述了論文中所用的方法(10) announces the findings公布了論文的結論6. Four components of a model.(1) Establish the importance of y

8、our fieldProvide background/ facts/information (possibly from research)Define the terminology in the title/key wordsPresent the problem area/current research focus確立研究領域的重要性提供背景事實或信息(有可能來自現(xiàn)有文獻)定義題目或關鍵詞中的術語給出所研究問題的范疇或目前的研究重點(2) Previous and/or current research and contributions前期的研究或目前的研究及其貢獻(3) Loca

9、te a gap in the researchDescribe the problem you will addressPresent a prediction to be tested確定已有研究工作的空白；描述你要解決的問題 呈現(xiàn)要驗證的預測(4) Describe the present paper描述現(xiàn)在的論文7. Grammar and writing skills.語法時態(tài)寫作技巧8. Vocabulary詞匯的簡潔舉例三篇文章：1.Gene expression profiling and pathway analysis of hepatotoxicity induced b

10、ytriptolide in Wistar rats在Wistar大鼠中，通過基因表達譜和通路分析由雷公藤甲素誘導的肝毒性引言的主要內(nèi)容是交代此項研究的來龍去脈，例如本文中，簡要說明課題的緣起與背景，TP的性質(zhì)Triptolide (diterpenoid triepoxide, TP), purified from the shrublike vine Tripterygium wilfondii Hook F (TWHF)與藥理學意義possesses anti-inflammatory, anti-fertility, anti-neoplastic and immunosuppress

11、ive activities實驗的動機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 treatment. Thus, it is e

12、ssential 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.主要理論根據(jù)及其基本原理Considering that microarr

13、ay 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 novel insights to better el

14、ucidate the mechanisms of toxic effects of TP.同時指出相關領域內(nèi)前任的研究成果possessesanti-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 lupus erythematosus, nephr

15、itis, 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 systems (Hikim et al., 2000; Ni

16、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 inhibition, lipid peroxidat

17、ion, 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).等存在問題和知識空白Hepatic differential gene expression was analyzed using oligonucleotide microarray analysis for over-represented functions and phenotypical

18、ly 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 provide a clearer understandin

19、g of the molecular mechanisms of TP-induced hepatotoxicity, as well as useful information for predicting drug hepatotoxicity.以表明本項研究的連續(xù)性和需要性，敘述有關本課題的歷史沿革是為了溫故而知新，Triptolide (diterpenoid triepoxide, TP), purified from the shrublike vine Tripterygium wilfondii Hook F (TWHF), possesses anti-inflammator

20、y, 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 emerged as treatments of rh

21、eumatoid 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, reproductive toxicity and prob

22、lems 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; Wang et al., 2007). Beside

23、s, 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 administration of TP to rats could

24、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, we hypothesized that liver

25、 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 inhibition, lipid peroxidatio

26、n, 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-induced toxicity, identify biom

27、arkers 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 describe genome-wide gene expre

28、ssion 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 microarray analysis for over-repre

29、sented 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 da

30、ta provide a clearer understanding of the molecular mechanisms of TP-induced hepatotoxicity, as well as useful information for predicting drug hepatotoxicity.2綜述Blood vessels, a potential therapeutic target in rheumatoid arthritis?血管，類風濕性關節(jié)炎潛在的治療靶標？IntroductionRheumatoid arthritis (RA) can be define

31、d 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 disease ' s systemic inflamm

32、ation 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, targeting blood vessels

33、 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 microvessels to tre

34、at rheumatoid arthritis, but we will discuss as well the evidence supporting a link between micro- and macro-vascular involvements in RA. 綜述的介紹，介紹所提到物質(zhì)的基本概念，簡要說明課題的緣起與背景，RA與血管生成相關，與血管生成的必要性，在這里，說明該文章立題的主要依據(jù)與主要原理，并提出在此綜述中接下來會說到的內(nèi)容，如：作者將分析滑膜微血管治療類風濕關節(jié)炎的可能性，且討論，血管與RA微觀和宏觀之間聯(lián)系的證據(jù)。概念由淺入深，詞匯簡介，介紹基本概念時使用一般

35、時態(tài)，提到文章后續(xù)會介紹的內(nèi)容時使用將來時，對未來內(nèi)容的展望。3.介紹功能性文章Dissection of TNF Receptor 1 Effector Functions: JNK Activation Is Not Linked to Apoptosis While NF-kB Activation Prevents Cell Death腫瘤壞死因子受體1的效應功能：NF-kB的活化阻止細胞死亡，JNK活化未關聯(lián)凋亡這篇文章的簡介有1318詞，系統(tǒng)的介紹了 TNF的含義，分類，受體類型，相關的兩個轉(zhuǎn)錄 因子，AP-1、 NF-kB、TNF所經(jīng)過的通路，通路中所涉及的許多其他細胞因子，由于

36、是介 紹功能性文章，這樣的背景知識很重要，所以雖然Introduction很長，但是有意義。邏輯連貫由各部分功能連接到總體功能，均采用一般時介紹，時態(tài)統(tǒng)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, and other environmental challenges (Tra-cey

37、 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 apoptosis (Tracey and Cerami, 1993; Vandenabeel

38、e 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; Vandenabeele et al., 1995). The structural simi

39、- 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., 1994). The ligands for these receptors are str

40、ucturally 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., 1994; Vandenabeele et al., 1995). TNFR2, how

41、ever, 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 immunoregulatory genes, as well as metalloproteinases. Several sec

42、ond 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). However, as discussed by Beyaert and Fiers, (1

43、994), 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 al., 1994), IkB kinase (DiDonato et al.,

44、 1996), and a TNFR1-associated serine/threonine kinase (VanArsdale and Ware, 1994), as well as the molecularly identified Raf-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 kinase results in NF-kB actiTRAF2 vatio

45、n (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 has been placed on the potential rol

46、e 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., 1996) and apoptosis (Obeid et al., 19

47、93). 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 TNFR2, following ligand inof duced tr

48、imerization (Rothe et al., 1994, 1995a; Hsu et al., 1995). While activation ofTNFRIresults 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 (TRAF1 and TRAF2; Rothe et al., 1994),

49、as well as c-IAP1 and c-IAP2 (Rothe et al., 1995a). Recently TRADD was shown to 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 receptors can elicit certain ove

50、rlapping responses, despite having dif ferent cytoplasmic 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 identified as a protein that intera

51、cts 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 receptors mediates protein -protein i

52、nteractions 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; Hsu et al., 1996b). Originally

53、 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 for induction of apoptosis b

54、y 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 activity is mediated by the FADDN-te

55、rminal 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 proteaseMACH (for MORT1-associati

56、ng CED homolog) or FLICE (for FADD-like interleukin-1b-convertingenzyme ICE), which appears to be a direct activator of theapoptotic.These results suggest the protein-recruitment model for TNFR1 signaling that is illustrated in Figure 1. TNF induced trimerization of TNFR1 results in recruitment of T

57、RADD 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 and its t