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2007 ACVP Award Notices
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ACVP Veterinary Student Posters

ACVP is now accepting abstracts for the 2007 Veterinary Student Poster Award.

To qualify, veterinary students must submit an abstract and then present a quality poster of pathology-related research or case work material at the 2007 Annual Meeting. The posters will be judged by Student Chapter Sub-Committee representatives during the Annual Meeting in Savannah on November 10-14, 2007.

Entitled the Veterinary Student Poster Award, the criteria for submission are as follows:

  1. Be the first author of the presentation for individual entries or for group entries, a clear designation of group members who contributed equally (equivalent to first author).
  2. Should have performed the major portion of the work.
  3. May submit only one poster for consideration.
  4. Presence at the poster display is required at a time to be determined.
  5. Individuals or groups eligible for this competition must be currently enrolled veterinary students. The poster must present original work of the competitor or group completed during the period of student training.

There will be two awards in 2007 – one for an experimental disease poster and one for a clinical poster. The recipients of these awards receive a $250 monetary award (for group entries, the award is split amongst members) and an additional award of $250 will go to the ACVP-recognized Student Chapter (if the recipient/s is/are a member of a Student Chapter).

Abstracts must be submitted by August 31, 2007.  Place your abstract (no more than 300 words including title and authors) in a word document and attach it to an e-mail addressed to the ACVP Office at meetings@acvp.org.  Please include your author contact information – name and telephone number.  See the sample below for format.  Abstracts must be received by e-mail no later than 12:00 midnight CST on Friday, August 31, 2007. 

Awards will be announced at the ACVP Business Meeting, on Tuesday, November 13 in Savannah.

SAMPLE ABSTRACT

Analysis of skin defects associated with an ENU induced mutation in the p53 binding protein p53bp1.
B. Chaffee1,2, X. Zhao2, M. Morasso2, R. Tuan2, and C. Lo2.
Texas A&M University College of Veterinary Medicine, College Station, TX1 and
Laboratory of Developmental Biology, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD2.

The p53 cell signaling pathway plays a pivotal role in oncogenesis and in modulating cellular responses to genotoxic stress.  The protein p53BP1 interacts with the DNA binding domain of p53 and enhances transcriptional activation.  Mice deficient in p53BP1 are viable, but have growth retardation, immunodeficiencies, hypersensitivity to ionizing radiation and are prone to developing cancer.  We recovered an N-ethyl-N-nitrosourea (ENU) induced point mutation in p53BP1 that causes a spectrum of defect phenotypes that show overlap with DiGeorge syndrome.  Thus the mutants show craniofacial defects and cardiac defects consisting of persistent truncus arteriosus.  In addition, the mutants are growth retarded, exhibit eye defects, and have thickened skin with fewer pigmented hair follicles. To examine the skin defect phenotype in this….

 

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