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General Guidelines on Preparing an Abstract
Title
1.
2.
3.
4.
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6.
Choose with care
Not too long or too short
Not too broad or too explicit
Attention getting, but without sounding like a headline from the "National Inquirer"
Take care with technical words and abbreviations. Some acronyms are not common usage and
may mean different things to different people. "HPL" or "DNA" is fine - "MLCK" is not. Never
make up your own acronym and use it in the title!
Some people are irritated by titles phrased as questions
Author
The first author will usually be assumed to be the person presenting the poster
Body
1.
2.
3.
4.
5.
The Introduction section should be 10% (you have to assume some knowledge). It must be clear
what question is being addressed
The Methods section should comprise about 15%. Provide only the essential features, not the
details
The Results section includes usually a qualitative description only. You may well elect to omit the
actual numbers generated by your experiments
The Conclusions section is usually 25% and should reflect the question asked in the introduction
Do not use these section markers in the abstract itself - they are a guide to the format only
Note: These percentages are not written in stone - they provide a rough guide only. For
example, if the work is mostly concerned with a novel methodology, the "Methods" section
should be increased accordingly.
6.
7.
8.
Do not say "…will be discussed"
Do not list references. If there is one key reference, it should usually be given in an abbreviated
form just sufficient to locate it, in parentheses within the body of the text.
Read what you have written and make sure that it reads smoothly
Acknowledgement
1.
Author’s stipend support and funding support for the project
Size
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2.
Do not exceed the marked area. If you have to reduce the amount, it is usually best to eliminate
one entire finding, rather than rephrase. By all means, remove superfluous phrases ("…in point of
fact", "…it is thus not unreasonable to suppose that…"), but make sure that the abstract is still
intelligible.
Use the available space. A couple of blank lines at the foot of the abstract are fine, however an
abstract that only occupies half the available space looks unprofessional.
Sample below on next page
Abstract Example
AKT NEGATIVELY REGULATES PHOSPHORYLATION OF AMP-ACTIVATED
PROTEIN KINASE TO PROMOTE CARDIAC HYPERTROPHY
Anita Y.M. Chan, Suzanne Kovacic, Carrie-Lynn M. Soltys, Amy J. Barr, Ichiro Shiojima, Kenneth Walsh, and
Jason R.B. Dyck
Akt and AMP-activated protein kinase (AMPK) are serine/threonine protein kinases with diverse physiological roles
affecting a number of cellular processes. For instance, Akt has been shown to contribute to cardiac hypertrophy
while AMPK is a stress related kinase involved in the control of cardiac energy substrate utilization. Despite these
diverse roles, a number of common signaling pathways do exist for these kinases, which suggest Akt can regulate
the activity of AMPK. Indeed, mouse hearts perfused in the presence of insulin displayed increased Akt
phosphorylation and decreased AMPK phosphorylation at its major regulatory site, threonine 172 of the  catalytic
subunit, as compared to non-insulin perfused hearts. Transgenic mice over-expressing a constitutively active mutant
form of Akt1 in a cardiac specific manner also showed a decreased phosphorylation of cardiac -AMPK. In
addition, isolated neonatal rat cardiac myocytes infected with an adenovirus expressing constitutively active Akt1
suppressed AMPK phosphorylation. Our hypothesis is that Akt regulates the activity of AMPK. To investigate the
importance of this relationship between Akt1 and AMPK in cardiac hypertrophy, neonatal rat cardiac myocytes
were infected with constitutively active Akt1 and contributors of the hypertrophic response – such as protein
synthesis and intracellular signaling pathways – were measured. Expression of constitutively active Akt1 resulted in
increased protein synthesis and increased phosphorylation and activation of p70S6 kinase, a promoter of selective
translation of mRNA that encode for ribosomal proteins and elongation factors. Furthermore, eukaryotic elongation
factor 2 (eEF2), a major regulator of protein translation, exhibited decreased phosphorylation at threonine 56
resulting in the activation of its activity. However, pharmacological activation of AMPK by metformin or AICAR
in myocytes with Akt1 over-expression completely negated the effects of Akt1 on protein synthesis as well as p70S6
kinase and eEF2 phosphorylation. Taken together, our data suggest that a contributing factor to Akt1 induced
hypertrophy may be the reduction of a protein synthesis inhibitor such as AMPK. In addition, our data suggest that
pharmacological activation of AMPK may prevent cardiac hypertrophy.
Supervisor: Dr. J.R.B. Dyck, Depts. of Pediatrics and Pharmacology, U of A
Funding for this Project Provided By CIHR and Heart and Stroke Foundation of Canada
Stipend Support for Anita Chan Provided by
An AHFMR Summer Studentship