Transcript ABSTRACT WRITING

How to write an abstract
Kristina Wasson-Blader, PhD, ELS
Editor in Residence
Office of Research Administration
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
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
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)
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.”
GENERAL PROCESS
1. Read The Instructions:
•
•
•
2.
3.
4.
5.
6.
Due Date
Format
Word Limit
Write The Abstract
Revise, Modify, Amend
Get Comments From Mentors & Co-authors
Revise, Modify, Amend
Proofread, proofread, proofread
(Grammer adn spelling miss steaks make you bad look.
7. Submit
ANATOMY OF AN ABSTRACT
•
•
•
•
•
Title
Introduction
Methods
Results
Conclusions
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
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
INTRODUCTION
• States your question being addressed—your
principal objectives and scope of work
• May include a brief overview of what is
known
METHODS
• Describes what was done to answer your
question
– Give a brief overview for standard methods
– Give more details if the techniques are novel
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
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
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
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)
_______________________________________________________________________________________________________________________
_______________________________________________________________________________________________________________________
_______________________________________________________________________________________________________________________
EXAMPLES OF ABSTRACTS
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.
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
TITLE
infection. We found that lots of genes were differentially regulated and
•Not informative
some were rapidly and very strongly upregulated independently of
•String of nouns
infection but
others
upregulated
later.
While
•Can
youcould
tell ifonly
the be
genes
from the
host
or some of these
modulatedparasite
genes were
to be upregulate, our data that
arealready
beingshown
studied?
you excited
enough
from this
title that
to read
previously•Are
unknown
genes were
upregulated
indicates
we didn’t
this
paper,
go to thisbetween
talk/poster,
or fund
it its host cell.
know much
about
the interaction
Toxoplasma
and
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
INTRODUCTION
some were rapidly•Poor
and very
strongly upregulated independently of
grammar
infection but others
could
only be upregulated
later. While some of these
•No
statement
of importance
•What
question
asked our data that
modulated genes were
already
shownistobeing
be upregulate,
•NEVER
stateupregulated
that you want
to that we didn’t
previously unknown
genes were
indicates
prove something is true
know much about the interaction between Toxoplasma and its host cell.
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
METHODS
modulated genes
were already shown
be upregulate, our data that
•Unnecessary
bulky to
words
•Jargon
previously unknown
genes were upregulated indicates that we didn’t
•No clear description of methods
know much about the interaction between Toxoplasma and its host cell.
used in the study
RESULTS
•More detailed description of data
•Unnecessary adjectives make the sentence wordy
•Long sentence that could be broken up
•Will
the reader
excited
toupregulation,
see to the main
attraction?
We
wanted
to provebe
that
cytokine
organelle
redistribution,
WHAT WAS WRONG WITH THE
FIRST ABSTRACT?
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.
Parasite Modulation of Gene
Expression
CONCLUSION
•Doesn’t summarize data
We wanted to prove
that cytokine
upregulation, organelle redistribution,
•Run-on
sentence
•Poor grammar
and apoptosis blocking
are due to changes in gene expression.
•How do these results impact the
Heretofore, we examined
with arrays the response of cells to Toxo
field
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.
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)
_______________________________________________________________________________________________________________________
_______________________________________________________________________________________________________________________
_______________________________________________________________________________________________________________________
ABSTRACT WORKSHEET
Title: (Informative and concise)
Microarray analysis reveals previously unknown changes in Toxoplasma gondiiinfected 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.
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 hostpathogen interaction.
Microarray analysis reveals previously unknown
changes in Toxoplasma gondii-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 upregulated 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 hostpathogen interaction.
From the Journal of Biological Chemistry 2001; 276: 24223.
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
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, 0.271.10; 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
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.
SOME GENERAL WRITING TIPS
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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.”
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