Scientific Reading and Writing in English

1. Scientific Reading and Writing in English • Lectures on: 12/11 “Abstract” 12/18 “References, Acknowledgements, and Front page” 12/25 “Cover letter” • Readings: “How to Write & Publish a Scientific Paper” by Robert A. Day, 5th Edition • Pin Ling (凌 斌), Ph.D. Department of Microbiology & Immunology, NCKU ext 5632 lingpin@mail.ncku.edu.tw

2. How to prepare the abstract? • Definition and function of the abstract • Organization of the abstract • Tips for writing the abstract • Example and practice Your involvement is the key to success in this lecture.

3. Read them first and decide to read the rest or not The Structure of A Paper

4. What is the abstract? • Ab, out + trahere, to pull: to pull out To pull out the key points from the paper • An abstract can be viewed as a mini-version of the paper. • Two common types of Abstracts - Informative abstracts: most research papers (five elements) -Indicative (Descriptive) abstracts: review articles

5. A Good Abstract The Whole Paper The Whole Paper A Poor Abstract X The function of the abstract • the first contact to readers Readers A good abstract delivers the paper’s key points “Concisely and Precisely”.

6. How to prepare the abstract? • Definition and function of the abstract • Organization of the abstract • Tips for writing the abstract • Example and practice

7. The Organization of the abstract (I) • The organization of the (informative) abstract is similar to the organization of the paper. • It includes the key information from the paper : - Introduction - Purpose (Key Question) - Materials & Methods (What was done) - Results (What was found) - Conclusions & Discussion (Answer & Implication)

8. Introduction & Purpose Materials & Methods Abstract(one paragraph) Title (a sentence) Results & Figures Conclusions & Discussion The Organization of the abstract (II) • Pull out the key information from each part to form a paragraph.

9. How to prepare the abstract? • Definition and function of the abstract • Organization of the abstract • Tips for writing the abstract • Example and practice

10. Tips for writing the abstract • Timing to write the abstract • Length • Sentence structure & word choice • Other issues

11. The Structure of A Paper

12. Introduction & Purpose Title (One sentence) Abstract (One paragraph) Materials & Methods Results & Figures Conclusions & Discussion Main text Overview sections The order to write a paper Write the main text first and then the overview sections

13. The length of the abstract • One paragraph • Most journals limit the length within 250 words. Some are even lesser. *Check the journal submission rules • Do not add unimportant details or unnecessary words to fill up the space. • Add more details => Out of => Lost the "Focus" "Big Picture"

16. Sentence structure • Write short and simple sentences • Short sentences are easy for readers to follow up. • By contrast, long sentences tend to make readers lost.

17. Word choice & Abbreviations • Use simple words. Avoid jargon. • Avoid noun clusters (try your best) e.g. Real-time quantitative polymerase chain reaction (qPCR) • Rules of using abbreviations: Use standard (std) abbreviations => units of measurement, e.g. microgram (mg) => widely accepted, e.g. DNA & NF-kB Define a non-std abbreviation the first time you use it. e.g. Epidermal Growth Factor Receptor (EGFR), c-Jun N-terminal Kinase (JNK)

18. Other issues for writing the abstract • Verb tenses in the abstract = those in the paper. Present tense => Question & Answer Past tense => What was done & What was found • Continuity Keep clear continuity throughout the abstract • Signaling Topics Signal the parts of an abstract by starting a new sentence, and by stating the topic at the beginning of the sentence.

19. How to prepare the abstract? • Definition and function of the abstract • Organization of the abstract • Tips for writing the abstract • Example and practice

20. Example of an informative abstract Regulation of IkB Kinase (IKK)g/NEMO Function by IKKb-mediated Phosphorylation* Shashi Prajapati and Richard B. Gaynor‡ J Biol Chem. 2002 Jul 5;277(27):24331-9. From the Division of Hematology-Oncology, Department of Medicine, Harold Simmons Cancer Center, University of TexasSouthwestern Medical Center, Dallas, Texas 75390 The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha and IKKbeta in addition to the scaffold protein IKKgamma/NEMO. Increases in the activity of the IKK complex result in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB pathway. Recent data indicate that the constitutive activation of the NF-kappaB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKgamma/NEMO by IKKbeta. To address further the significance of IKKbeta-mediated phosphorylation of IKKgamma/NEMO, we determined the sites in IKKgamma/NEMO that were phosphorylated by IKKbeta, and we assayed whether IKKgamma/NEMO phosphorylation was involved in modulating IKKbeta activity. IKKgamma/NEMO is rapidly phosphorylated following treatment of cells with stimuli such as tumor necrosis factor-alpha and interleukin-1 that activate the NF-kappaB pathway. By using both in vitro and in vivo assays, IKKbeta was found to phosphorylate IKKgamma/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKgamma/NEMO to stimulate IKKbeta kinase activity. These results indicate that the differential phosphorylation of IKKgamma/NEMO by IKKbeta and perhaps other kinases may be important in regulating IKK activity. One paragraph, 201 words

21. Dissection of the abstract The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha and IKKbeta in addition to the scaffold protein IKKgamma/NEMO. Increases in the activity of the IKK complex result in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB pathway. Recent data indicate that the constitutive activation of the NF-kappaB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKgamma/NEMO by IKKbeta. To address further the significance of IKKbeta-mediated phosphorylation of IKKgamma/NEMO, we determined the sites in IKKgamma/NEMO that were phosphorylated by IKKbeta, and we assayed whether IKKgamma/NEMO phosphorylation was involved in modulating IKKbeta activity. IKKgamma/NEMO is rapidly phosphorylated following treatment of cells with stimuli such as tumor necrosis factor-alpha and interleukin-1 that activate the NF-kappaB pathway. By using both in vitro and in vivo assays, IKKbeta was found to phosphorylate IKKgamma/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKgamma/NEMO to stimulate IKKbeta kinase activity. These results indicate that the differential phosphorylation of IKKgamma/NEMO by IKKbeta and perhaps other kinases may be important in regulating IKK activity. Introduction (Background)

22. Dissection of the abstract The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha and IKKbeta in addition to the scaffold protein IKKgamma/NEMO. Increases in the activity of the IKK complex result in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB pathway. Recent data indicate that the constitutive activation of the NF-kappaB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKgamma/NEMO by IKKbeta. To address further the significance of IKKbeta-mediated phosphorylation of IKKgamma/NEMO, we determined the sites in IKKgamma/NEMO that were phosphorylated by IKKbeta, and we assayed whether IKKgamma/NEMO phosphorylation was involved in modulating IKKbeta activity. IKKgamma/NEMO is rapidly phosphorylated following treatment of cells with stimuli such as tumor necrosis factor-alpha and interleukin-1 that activate the NF-kappaB pathway. By using both in vitro and in vivo assays, IKKbeta was found to phosphorylate IKKgamma/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKgamma/NEMO to stimulate IKKbeta kinase activity. These results indicate that the differential phosphorylation of IKKgamma/NEMO by IKKbeta and perhaps other kinases may be important in regulating IKK activity. Purpose (Question)

23. Dissection of the abstract The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha and IKKbeta in addition to the scaffold protein IKKgamma/NEMO. Increases in the activity of the IKK complex result in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB pathway. Recent data indicate that the constitutive activation of the NF-kappaB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKgamma/NEMO by IKKbeta. To address further the significance of IKKbeta-mediated phosphorylation of IKKgamma/NEMO, we determined the sites in IKKgamma/NEMO that were phosphorylated by IKKbeta, and we assayed whether IKKgamma/NEMO phosphorylation was involved in modulating IKKbeta activity. IKKgamma/NEMO is rapidly phosphorylated following treatment of cells with stimuli such as tumor necrosis factor-alpha and interleukin-1 that activate the NF-kappaB pathway. By using both in vitro and in vivo assays, IKKbeta was found to phosphorylate IKKgamma/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKgamma/NEMO to stimulate IKKbeta kinase activity. These results indicate that the differential phosphorylation of IKKgamma/NEMO by IKKbeta and perhaps other kinases may be important in regulating IKK activity. J Biol Chem. 2002 Jul 5;277(27):24331-9. What was done

24. Dissection of the abstract The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha and IKKbeta in addition to the scaffold protein IKKgamma/NEMO. Increases in the activity of the IKK complex result in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB pathway. Recent data indicate that the constitutive activation of the NF-kappaB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKgamma/NEMO by IKKbeta. To address further the significance of IKKbeta-mediated phosphorylation of IKKgamma/NEMO, we determined the sites in IKKgamma/NEMO that were phosphorylated by IKKbeta, and we assayed whether IKKgamma/NEMO phosphorylation was involved in modulating IKKbeta activity. IKKgamma/NEMO is rapidly phosphorylated following treatment of cells with stimuli such as tumor necrosis factor-alpha and interleukin-1 that activate the NF-kappaB pathway. By using both in vitro and in vivo assays, IKKbeta was found to phosphorylate IKKgamma/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKgamma/NEMO to stimulate IKKbeta kinase activity. These results indicate that the differential phosphorylation of IKKgamma/NEMO by IKKbeta and perhaps other kinases may be important in regulating IKK activity. What was found

25. Dissection of the abstract The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha and IKKbeta in addition to the scaffold protein IKKgamma/NEMO. Increases in the activity of the IKK complex result in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB pathway. Recent data indicate that the constitutive activation of the NF-kappaB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKgamma/NEMO by IKKbeta. To address further the significance of IKKbeta-mediated phosphorylation of IKKgamma/NEMO, we determined the sites in IKKgamma/NEMO that were phosphorylated by IKKbeta, and we assayed whether IKKgamma/NEMO phosphorylation was involved in modulating IKKbeta activity. IKKgamma/NEMO is rapidly phosphorylated following treatment of cells with stimuli such as tumor necrosis factor-alpha and interleukin-1 that activate the NF-kappaB pathway. By using both in vitro and in vivo assays, IKKbeta was found to phosphorylate IKKgamma/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKgamma/NEMO to stimulate IKKbeta kinase activity. These results indicate that the differential phosphorylation of IKKgamma/NEMO by IKKbeta and perhaps other kinases may be important in regulating IKK activity. Answer & Implication

26. Suggestions for the abstract The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha and IKKbeta in addition to the scaffold protein IKKgamma/NEMO. Increases in the activity of the IKK complex result in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB pathway. Recent data indicate that the constitutive activation of the NF-kappaB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKgamma/NEMO by IKKbeta. To address further the significance of IKKbeta-mediated phosphorylation of IKKgamma/NEMO, we determined the sites in IKKgamma/NEMO that were phosphorylated by IKKbeta, and we assayed whether IKKgamma/NEMO phosphorylation was involved in modulating IKKbeta activity. IKKgamma/NEMO is rapidly phosphorylated following treatment of cells with stimuli such as tumor necrosis factor-alpha and interleukin-1 that activate the NF-kappaB pathway. By using both in vitro and in vivo assays, IKKbeta was found to phosphorylate IKKgamma/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKgamma/NEMO to stimulate IKKbeta kinase activity. These results indicate that the differential phosphorylation of IKKgamma/NEMO by IKKbeta and perhaps other kinases may be important in regulating IKK activity.

27. Tips for the abstract Use simple words and define abbreviations Write short and simple sentences Verb tenses Continuity Signal Topics

28. Define the Abbreviations

29. Tips for the abstract

30. The Revised Abstract The IkappaB kinase (IKK) complex includes the catalytic components IKKalpha (IKKa) and IKKbeta (IKKb) in addition to the scaffold protein IKKgamma (IKKg)/NEMO. Activation of the IKK complex results in the phosphorylation and subsequent degradation of IkappaB and the activation of the NF-kappaB (NF-kB) pathway. Recent data indicate that the constitutive activation of the NF-kB pathway by the human T-cell lymphotrophic virus, type I, Tax protein leads to enhanced phosphorylation of IKKg/NEMO by IKKb. To address the significance of IKKb-mediated phosphorylation of IKKg/NEMO, we determined the sites in IKKg/NEMO that were phosphorylated by IKKb. We also assayed whether IKKg/NEMO phosphorylation was involved in modulating IKKb activity. Our result showed that IKKg/NEMO was rapidly phosphorylated following stimulation by tumor necrosis factor-alpha and interleukin-1 that activate the NF-kB pathway. IKKb was found to phosphorylate IKKg/NEMO predominantly in its carboxyl terminus on serine residue 369 in addition to sites in the central region of this protein. Surprisingly, mutation of these carboxyl-terminal serine residues increased the ability of IKKg/NEMO to stimulate IKKb kinase activity. These results indicate that the differential phosphorylation of IKKg/NEMO by IKKb and perhaps other kinases may be important in regulating IKK activity. • Use simple words & abbreviations • Write short and simple sentences • Verb tenses • Signal Topics One paragraph, 201=>191 words

31. Common Problems in Abstracts • Excessive details (length) => make the abstract unreadable (the trees overshadow the forest) • Omitting the question or Stating the question vaguely => No goal for this work • Answer not stated => No ending

33. Abstracts for conferences (I) • Abstracts for conferences • show a valuable contribution • lure audiences to your talk • Follow the most of guidelines as abstracts of research papers. • To encourage speculation, alternative theories, and suggestion for further research, the conference abstract is not as strict as the abstract for research papers.

34. Abstracts for conferences (II) • Several differences as below: => include more details for methods => display data in a table or a graph sometimes => include more implications (to indicate the importance of the work) • Abstracts for conferences self-destruct after a year. • If the paper is not published eventually, the details and data in the conference abstract can not be used because of no validation.

35. A Example of the Conference Abstract

36. Indicative (Descriptive) Abstracts • Usually for the review articles • Tell readers what information the article contains • Include the purpose, methods, and scope of the article • Do not provide results, conclusions, or recommendations

37. A Example of an indicative abstract

41. What you should include in the abstract section…5 elements • The goal is to include all the important • information in the paper. • Background (B) • Purpose (P) • Method (M) • Results (R) • Conclusion (C) • Sometimes, sentences with the combination • of two elements have to be used. (the shortest abstract I have seen: 2-3 paragraphs)

42. Two common forms of abstract • A “structured” abstract includes headings that • reflect the main elements of the paper. More • explicit details are usually required. • A single-paragraph abstract includes all the • contents in a single text block.

43. Structured Abstract Prognostic Value of Myeloperoxidase in Patients with Chest Pain NEJM 349:1595-1604October 23, 2003 Background Inflammation is linked to adverse outcomes in acute coronary syndromes. Myeloperoxidase, an abundant leukocyte enzyme, is elevated in culprit lesions that have fissured or ruptured in patients with sudden death from cardiac causes. Numerous lines of evidence suggest mechanistic links between myeloperoxidase and both inflammation and cardiovascular disease. (In this example, purpose and methods are combined) Methods We assessed the value of plasma levels of myeloperoxidase as a predictor of the risk of cardiovascular events in 604 sequential patients presenting to the emergency department with chest pain. Results Initial plasma myeloperoxidase levels predicted the risk of myocardial infarction, even in patients who are negative for troponin T (<0.1 ng per milliliter) at base line (P<0.001). Myeloperoxidase levels at presentation also predicted the risk of major adverse cardiac events (myocardial infarction, the need for revascularization, or death) within 30 days and 6 months after presentation (P<0.001). In patients without evidence of myocardial necrosis (defined as those who were negative for troponin T), the base-line myeloperoxidase levels independently predicted the risk of major adverse coronary events at 30 days (unadjusted 2nd, 3rd, and 4th quartile odds ratios, 2.2 [95 percent confidence interval, 1.1 to 4.6], 4.2 [95 percent confidence interval, 2.1 to 8.4], and 4.1 [95 percent confidence interval, 2.0 to 8.4], respectively) and at 6 months. Conclusions A single initial measurement of plasma myeloperoxidase independently predicts the early risk of myocardial infarction, as well as the risk of major adverse cardiac events in the ensuing 30-day and 6-month periods. Myeloperoxidase levels, in contrast to troponin T, creatine kinase MB isoform, and C-reactive protein levels, identified patients at risk for cardiac events in the absence of myocardial necrosis, highlighting its potential usefulness for risk stratification among patients who present with chest pain.

44. Example of an informative abstract

45. Informative Abstract • communicate specific information from the article • include the purpose, methods, and scope of the article. • provide the article's results, conclusions, and recommendations. • are short -- from a paragraph to a page or two. Usually informative abstracts are 10% or less of the length of the original piece. • allow readers to decide whether they want to read the article

46. A single-paragraph abstractIndicative and informative abstracts • Indicative (Descriptive) abstracts, stating what • the paper is about, are usually for long review • papers. (contain descriptive info: illustration of • previous and current concepts) • Informative abstracts are for most research • papers (five elements).

47. Writing an Informative Abstract • Be orderly, succinct, and concrete • Use active verbs such as “report”, “propose”, and • “analyze” rather than static verbs such as “is”, • “are”, and “appears to be”. • State the core issue, research question, or • objective of the research • Briefly describe the methods. • Interpret the results (supporting or against the • hypothesis) • Draw conclusions and state implications

48. Format A Introductory statement, including motivation/ problem statement (sometimes not needed) 2. Approach : research methodology 3. Results or other main points (absolutely essential) 4. Concluding statement, telling what the results mean Note: including all the keywords in the abstract.

49. Format B Re-establish the topic of the research 2. Give the research problem and/or main objective of the research (this usually comes first) 3. Indicate the methodology used 4. Present the main findings 5. Present the main conclusions

50. Styles 1. Single paragraph, and concise. 2. As a summary of work done, it is always written in past tense. 3. An abstract should stand on its own, and not refer to any other part of the paper such as a figure or table. 4. Focus on summarizing results---limit background info to a sentence or two, if absolutely necessary. 5. What you report in an abstract must be consistent with what you reported in the paper. 6. Correct spelling, clarity of sentences and phrases, and proper reporting of quantities are just as important in an abstract as they are anywhere else.