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  1. How to write an abstract Kristina Wasson-Blader, PhD, ELS Editor in Residence Office of Research Administration

  2. WHY ARE ABSTRACTS WRITTEN? • Submission requests for scientific conferences, congresses and meetings • Part of a manuscript for publication • Part of qualifying exams and dissertations • Project summaries for research grant proposals

  3. AN ABSTRACT • Is an original document • Summarize your work • Contains only information presented • Gives the reader enough information to decide if they want to learn more about your work • Provides language appropriate for the target audience

  4. AN ABSTRACT • States your question being addressed—goals and scope of work (introduction) • Describes what was done to answer your question (methods) • Provides your data to answer your question (results) • Provides your answer (conclusions)

  5. AN ABSTRACT • Does NOT provide an extensive review of the literature • Does NOT provide text copied from another section of the document • Does NOT include figures or tables • Does NOT contain references • Use: “Watson and Crick demonstrated that DNA is a double helix.” • Don’t use: “DNA is a double helix (Watson and Crick, Nature (1953), 171:737.”

  6. GENERAL PROCESS • Read The Instructions: • Due Date • Format • Word Limit • Write The Abstract • Revise, Modify, Amend • Get Comments From Mentors & Co-authors • Revise, Modify, Amend • Proofread, proofread, proofread (Grammeradn spelling miss steaks make you bad look. • Submit

  7. ANATOMY OF AN ABSTRACT • Title • Introduction • Methods • Results • Conclusions

  8. TITLES • Should accurately, completely, and specifically identify the main topic • Be clear • Be concise • Begin with an important word to engage the reader • Should use words suitable for indexing

  9. TITLES • Should AVOID • Too scholarly or too “cute” titles • Hines, G.A., K.M. Wasson and S.A. Watts. 1995. One fish, two fish...girl fish, guy fish... Social environment and gonadal steroidogenesis in tilapia. • Acronyms • Subtitles, whenever possible • Roman numerals • Abbreviations • Noun clusters • e.g. Bacteria Isolation Technique For Human Cardiac Cell ELISA. • Do NOT use jargon

  10. INTRODUCTION • States your question being addressed—your principal objectives and scope of work • May include a briefoverview of what is known

  11. METHODS • Describes what was done to answer your question • Give a brief overview for standard methods • Give more details if the techniques are novel

  12. RESULTS • Provide your data to answer your question • Make sure to present the data that answer your question • May provide specifics or only general terms • Do NOT include discussion/interpretation

  13. CONCLUSIONS • Provide your answer to your question based on the data presented • State how your findings will impact the field and how they could guide future studies

  14. HOW DO YOU WRITE AN ABSTRACT? • Use an abstract worksheet • Write 1-3 sentences for each section that summarize the important points of each section • Revise, modify, and amend with the goal of inserting transitions so the abstract flows logically

  15. ABSTRACT WORKSHEET Title: (Informative and concise) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Introduction: (What is being tested and why?) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Methods: (How was the study performed?) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Results: (What were the data?) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Conclusions: (What do the data say and what are their consequences) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________

  16. EXAMPLES OF ABSTRACTS

  17. Parasite Modulation of Gene Expression We wanted to prove that cytokine upregulation, organelle redistribution, and apoptosis blocking are due to changes in gene expression. Heretofore, we examined with arrays the response of cells to Toxo infection. We found that lots of genes were differentially regulated and some were rapidly and very strongly upregulated independently of infection but others could only be upregulated later. While some of these modulated genes were already shown to be upregulate, our data that previously unknown genes were upregulated indicates that we didn’t know much about the interaction between Toxoplasma and its host cell.

  18. Parasite Modulation of Gene Expression We wanted to prove that cytokine upregulation, organelle redistribution, and apoptosis blocking are due to changes in gene expression. Heretofore, we examined with arrays the response of cells to Toxo infection. We found that lots of genes were differentially regulated and some were rapidly and very strongly upregulated independently of infection but others could only be upregulated later. While some of these modulated genes were already shown to be upregulate, our data that previously unknown genes were upregulated indicates that we didn’t know much about the interaction between Toxoplasma and its host cell. • TITLE • Not informative • String of nouns • Can you tell if the genes from the host or parasite are being studied? • Are you excited enough from this title to read • this paper, go to this talk/poster, or fund it

  19. Parasite Modulation of Gene Expression We wanted to prove that cytokine upregulation, organelle redistribution, and apoptosis blocking are due to changes in gene expression. Heretofore, we examined with arrays the response of cells to Toxo infection. We found that lots of genes were differentially regulated and some were rapidly and very strongly upregulated independently of infection but others could only be upregulated later. While some of these modulated genes were already shown to be upregulate, our data that previously unknown genes were upregulated indicates that we didn’t know much about the interaction between Toxoplasma and its host cell. • INTRODUCTION • Poor grammar • No statement of importance • What question is being asked • NEVER state that you want to • prove something is true

  20. Parasite Modulation of Gene Expression We wanted to prove that cytokine upregulation, organelle redistribution, and apoptosis blocking are due to changes in gene expression. Heretofore, we examined with arrays the response of cells to Toxo infection. We found that lots of genes were differentially regulated and some were rapidly and very strongly upregulated independently of infection but others could only be upregulated later. While some of these modulated genes were already shown to be upregulate, our data that previously unknown genes were upregulated indicates that we didn’t know much about the interaction between Toxoplasma and its host cell. • METHODS • Unnecessary bulky words • Jargon • No clear description of methods • used in the study

  21. RESULTS • More detailed description of data • Unnecessary adjectives make the sentence wordy • Long sentence that could be broken up • Will the reader be excited to see to the main attraction? WHAT WAS WRONG WITH THE FIRST ABSTRACT? We wanted to prove that cytokine upregulation, organelle redistribution, and apoptosis blocking are due to changes in gene expression. Heretofore, we examined with arrays the response of cells to Toxo infection. We found that lots of genes were differentially regulated and some were rapidly and very strongly upregulated independently of infection but others could only be upregulated later. While some of these modulated genes were already shown to be upregulate, our data that previously unknown genes were upregulated indicates that we didn’t know much about the interaction between Toxoplasma and its host cell.

  22. Parasite Modulation of Gene Expression • CONCLUSION • Doesn’t summarize data • Run-on sentence • Poor grammar • How do these results impact the field We wanted to prove that cytokine upregulation, organelle redistribution, and apoptosis blocking are due to changes in gene expression. Heretofore, we examined with arrays the response of cells to Toxo infection. We found that lots of genes were differentially regulated and some were rapidly and very strongly upregulated independently of infection but others could only be upregulated later. While some of these modulated genes were already shown to be upregulate, our data that previously unknown genes were upregulated indicates that we didn’t know much about the interaction between Toxoplasma and its host cell.

  23. ABSTRACT WORKSHEET Title: (Informative and concise) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Introduction: (What is being tested and why?) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Methods: (How was the study performed?) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Results: (What were the data?) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ Conclusions: (What do the data say and what are their consequences) _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________

  24. ABSTRACT WORKSHEET Title: (Informative and concise) Microarray analysis reveals previously unknown changes in Toxoplasmagondii-infected human cells. Introduction: (What is being tested and why?) Cells infected with the intracellular protozoan parasite Toxoplasma gondii undergo up-regulation of pro-inflammatory cytokines, organelle redistribution, and protection from apoptosis. Methods: (How was the study performed?) To examine the molecular basis of these and other changes, gene expression profiles of human foreskin fibroblasts infected with Toxoplasma were studied using human cDNA microarrays consisting of ~22,000 known genes and uncharacterized expressed sequence tags.

  25. ABSTRACT WORKSHEET Results: (What were the data?) Early during infection (1-2 h), <1% of all genes show a significant change in the abundance of their transcripts. Of the 63 known genes in this group, 27 encode proteins associated with the immune response. These genes are also up-regulated by secreted, soluble factors from extracellular parasites indicating that the early response does not require parasite invasion. Later during infection, genes involved in numerous host cell processes, including glucose and mevalonate metabolism, are modulated. Many of these late genes are dependent on the direct presence of the parasite; i.e. secreted products from either the parasite or infected cells are insufficient to induce these changes. Conclusions: (What do the data say and what are their consequences) These results reveal several previously unknown effects on the host cell and lay the foundation for detailed analysis of their role in the host-pathogen interaction.

  26. Microarray analysis reveals previously unknown changes in Toxoplasmagondii-infected human cells Cells infected with the intracellular protozoan parasite Toxoplasma gondii undergo up-regulation of pro-inflammatory cytokines, organelle redistribution, and protection from apoptosis. To examine the molecular basis of these and other changes, gene expression profiles of human foreskin fibroblasts infected with Toxoplasma were studied using human cDNA microarrays consisting of ~22,000 known genes and uncharacterized expressed sequence tags. Early during infection (1-2 h), <1% of all genes show a significant change in the abundance of their transcripts. Of the 63 known genes in this group, 27 encode proteins associated with the immune response. These genes are also up-regulated by secreted, soluble factors from extracellular parasites indicating that the early response does not require parasite invasion. Later during infection, genes involved in numerous host cell processes, including glucose and mevalonate metabolism, are modulated. Many of these late genes are dependent on the direct presence of the parasite; i.e. secreted products from either the parasite or infected cells are insufficient to induce these changes. These results reveal several previously unknown effects on the host cell and lay the foundation for detailed analysis of their role in the host-pathogen interaction. From the Journal of Biological Chemistry 2001; 276: 24223.

  27. TYPES OF ABSTRACTS • Unstructured – Paragraph format. • Structured – Section format; different journals use different section heading but all include in one form or another • Introduction • Methods • Results • Conclusions

  28. STRUCTURED ABSTRACT • Journal of American Medical Association Context Comorbidities may increase the negative effects of specific anticancer treatments such as androgen suppression therapy (AST). Objectives To compare 6 months of AST and radiation therapy (RT) to RT alone and to assess the interaction between level of comorbidity and all-cause mortality. Design, Setting, and Patients At academic and community-based medical centers in Massachusetts, between December 1, 1995, and April 15, 2001, 206 men with localized but unfavorable-risk prostate cancer were randomized to receive RT alone or RT and AST combined. All-cause mortality estimates stratified by randomized treatment group and further stratified in a postrandomization analysis by the Adult Comorbidity Evaluation 27 comorbidity score were compared using a log-rank test. Main Outcome Measure Time to all-cause mortality. Results As of January 15, 2007, with a median follow-up of 7.6 (range, 0.5-11.0) years, 74 deaths have occurred. A significant increase in the risk of all-cause mortality (44 vs 30 deaths; hazard ratio [HR], 1.8; 95% confidence interval [CI], 1.1-2.9; P=.01) was observed in men randomized to RT compared with RT and AST. However, the increased risk in all-cause mortality appeared to apply only to men randomized to RT with no or minimal comorbidity (31 vs 11 deaths; HR, 4.2; 95% CI, 2.1-8.5; P.001). Among men with moderate or severe comorbidity, those randomized to RT alone vs RT and AST did not have an increased risk of all-cause mortality (13 vs 19 deaths; HR, 0.54; 95% CI, 0.27-1.10; P=.08). Conclusions The addition of 6 months of AST to RT resulted in increased overall survival in men with localized but unfavorable-risk prostate cancer. This result may pertain only to men without moderate or severe comorbidity, but this requires further assessment in a clinical trial specifically designed to assess this interaction. JAMA. 2008;299(3):296-307

  29. STRUCTURED ABSTRACT Investigative Ophthalmology and Visual Science PURPOSE. Retinal pigmented epithelial (RPE) cells may contribute to retinal immune privilege. Daily phagocytosis and degradation of photoreceptor cell outer segment tips by RPE provide substantial amounts of retinal autoantigens for potential MHC occupancy. RPE are well placed to modulate antigen (Ag)- specific activation of T cells in the outer retina under conditions in which inflammatory mediators may upregulate major histocompatibility complex (MHC) on RPE cells. The Ag-presenting ability of RPE cells was examined to determine whether they induce Ag-dependent modulation of CD4 T-cell activity. METHODS. The effects of RPE on Ag-specific activation of naive, Ag-specific CD4 T cells were tested in cultures with immortalized, syngeneic murine RPE cells. Flow cytometry, proliferation, and cytokine production were used to assess T-cell activation and phenotype. RESULTS. Naive CD4 T cells exposed to peptide-pulsed RPE upregulated expression of CD25, CD69, and CD44, showing receptor ccupancy. However, T-cell proliferation and production of IL-2, IL-17, and IFN- were severely depressed. Provision of whole -gal, as opposed to -gal peptide, gave no evidence of T-cell activation. T cells recovered from RPE cocultures were hyporesponsive to restimulation with splenic APC and Ag, but did not exhibit significant regulatory activity. Although CD25 was upregulated on RPE-activated T cells, expression of FoxP3 was similar to that found after activation with splenic APC and Ag. The inhibitory activity of RPE was dominant, since T-cell activation remained inhibited if splenic APCs were included in the cocultures. CONCLUSIONS. RPE cells directly presented extracellular peptides through MHC class II to naive CD4 T cells, leading to an anergic state in the T cells. The anergic T cells survived, but were not immunoregulatory. The ability to modulate T-cell responsiveness in this manner may underlie the contribution of the RPE to immune privilege. IOVS. 2007;48:4654-4663.

  30. SOME GENERAL WRITING TIPS • Use one thought per sentence • Use active voice whenever possible • Use simple words • Be succinct by limiting adjectives • Use short sentences (~22 words) • Use simple sentences • subject—verb—object construction • “One hundred isolates were tested and 6 contained mutations.” vs. “ Six mutations were determined to be present out of the 100 isolates that were tested.”

  31. RESOURCES • Chest Journal has monthly scientific writing tips (www.chestjournal.org) • http://www.texasheart.org/AboutUs/Depart/scipub.cfm • Robert A Day and Barbara Gastel. 2006. How to Write and Publish a Scientific Paper. 6th Edition. Greenwood Press. • Mimi Zeiger. 2000.Essentials of Writing Biomedical Research Papers. 2nd Edition. McGraw-Hill. • Read other published abstracts in your field