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Abstracts

Late abstract submission deadline: 4 July 2008

GENERAL INFORMATION on ABSTRACTS

1. Abstracts should be submitted for all plenary lectures, symposia lectures and posters.
2. Abstracts will be reviewed be the EBEC 2008 Local Organizing Committee.
3. It is expected that several abstracts from each Symposium topic will be raised to 10 minute talks (plus 5 minutes for questions)[Raised Abstracts] based on the quality and novelty of the work described.
4. Authors should indicate using the numbering system below under which of the following Symposia Topics their abstracts are to be submitted:

P.  Plenary
S1. ATPsynthase and ATPases
S2. Photosystems
S3. Membrane Transporters
S4. NADH dehydrogenases
S5. Mitochondrial Biogenesis
S6. Sepsis and Mitochondrial Function
S7. Mitochondrial and Neuronal Function
S8. Cell Physiology
S9. Mitochondrial Dynamics
S10. Mitochondria and Reactive Oxygen Containing Species
S11. Terminal Oxidases
S12. Mitochondria and Disease
S13. Electron Transport Chain and Proton Pumps
S14. Mitochondria and Ageing
S15. bc1 (like) complexes
S16. Proteomics and Methods
C1. Genomics and Evolution of Energy Transducing Systems
C2. Controversial Issues in Cytochrome Oxidase



5. Abstracts are to be submitted in Word format (or equivalent) as an email attachment to ebecabs@tcd.ie
6. The word 'Abstract', the Symposium Topic number and 'Student' (where appropriate) must be included in the email Subject line.
7. Abstracts will be acknowledged and assigned an appropriate code.
8. All experimental procedures used to provide the data for the abstracts must comply with scientific best practice and ethical approval where appropriate.
9. All abstracts submitted by the deadline of 17 March 2008 will be published in a Biochimica Biophysica Acta Special Issue EBEC 2008 Short Reports by Elsevier Publications.
10. Submitted abstracts cannot be withdrawn once processed for publication.
11. All student posters will be entered in a competition. A prize will be given for the three best student posters.

ABSTRACT STRUCTURE

1. The abstract should include (a) symposium number, (b) title, (c) author(s), (d) affiliation, (e) email address of presenting author and (f) text. No figures, graphs, photographs, citations, references are to be included in the abstract.
2. The number of words including (a) symposium number, (b) title, (c) author(s), (d) affiliation, (e) email address of presenting author and (f) text, should come to no more than 250 words.
3. The abstract should be written in Times New Roman, Font size 10 and left justified. Symbols can be used in the abstract.
4. The title should be in capitals and bold
5. The remainder of the text should be in normal text.
6. The names of the authors should be of the format: full forename single letter middle name(s) and full surname
7. Superscript numbers should be used to assign authors' affiliation
8. The abstract should contain a sentence stating the aim of the study, a brief description of the methods (if pertinent), a summary of the results and a statement of the conclusion reached.
9. An example of an appropriately worked abstract is given below:

S8. THE CONTROL OF OXIDATIVE PHOSPHORYLATION IN THE ADRENAL GLAND (Y1) CELL LINE
James E.J. Murphy¹ and Richard K. Porter^1
1School of Biochemistry and Immunology, Trinity College Dublin, Ireland.
Correspondence: rkporter@tcd.ie
The aim of this study was to determine the proportion of oxygen consumption due to oxidative phosphorylation by mitochondria in the adrenal gland cell line (Y1 cells). In addition, we determined the relative proportion of in situ mitochondrial oxygen consumption attributable to (i) proton leak and (ii) ATP turnover in these cells. Our data show that resting oxygen consumptions rates of Y1 cells to be 87±7 (3) nmolO/min/10⁷ cells of which 38±3(3)% was not due to oxidative phosphorylation. We demonstrated that mitochondrial proton leak accounted for 7±3(3)% of total cellular oxygen consumption or 12±6(3)% of resting mitochondrial oxygen consumption, with ATP turnover accounting for 55±3(3)% of total cellular oxygen consumption or 78±6(3)% of mitochondrial oxygen consumption. Application of top-down elasticity analysis showed that control of resting mitochondrial oxygen consumption in Y1 cells was shared by (a) substrate oxidation flux (37±8(3)%), (b) proton leak flux (15±8(3)%) and (c) ATP turnover (56±8(3)%). The high proportion of oxygen consumption not due to oxidative phosphorylation (38%), is consistent with the observation that cancer cells have augmented monooxygenase activity. Our data demonstrate, for the first time, that the majority of oxygen consumption by resting Y1 cells is due to oxidative phosphorylation. Data are presented as mean±sem(n), where n is the number of experiments performed in triplicate.