EDR: Executive Dean for Research

Abstract Guidelines

Important Dates
  • October 31, 2019: Early Abstract Submission Deadline
  • November 30, 2019: Regular Abstract Submission Deadline

You must follow the steps described below. Your application will not be considered complete until all of the necessary materials are received. All emails should be sent to Isabel Perez.

  • Fill out the online application form.
  • Submit your abstract(s) in a MS Word Document along with the Letter of Endorsement signed by your mentor to Isabel Perez. The Letter of Endorsement Form must be signed by your research mentor or faculty advisor stating that the student submitting the abstract was responsible for the major portion of the work.
  • The abstract must conform to the following specifications (sample below). The entire abstract should be no longer than 450 words including the title.
    • Use “Times New Roman” font, point size 10 for normal text.
    • All words in the title should be in bold capital letters except abbreviations such as Ca2+ and CsA.
    • All abbreviations designated by code or initial letters in the title must be identified in the body of the abstract.
    • The presenting Author’s Name (i.e. your name) should be underlined.
    • Include the department and school or institution along with city, state and ZIP code after the authors’ names.
    • The abstract should consist of one, single-spaced solitary paragraph.
    • The abstract should contain an Introduction/Aim and a summary of Methodology, Results, and Conclusions/Discussion. (View Abstract Rubric)
  • Your abstract will be reviewed by the ESRF Executive Committee and, if deemed acceptable, you will be notified of the decision.
  • Upon acceptance to the Forum, we will respond by email with the letter of acceptance and hotel accommodation form.
  • Your abstract must be received by December 1, 2019 to be considered for acceptance.

Abstract Text Instructions

The abstract should be single-spaced and submitted as an MS Word document. This will be a brief statement of what was done in your research, along with your principal results and conclusions. Only the most important facts should be related here, in non-indented paragraph form. Please take special care to follow the format in the following abstract sample. In particular, the abstract should contain no figures or tables. There is no limit on the number of authors, but the first author must be the presenter. The abstract itself should be no longer than 450 words. Depicted below is a sample abstract in the actual format to be used for all submissions:

THE ROLE OF THE INTERLEUKIN2 RECEPTOR γc CHAIN IN THE PERIPHERAL IMMUNE RESPONSE. Jocelyn A. Hamilton and Thomas R. Malek. Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, FL 33101.

Introduction/Aim: The common gamma chain (γc) of the interleukin-2 receptor (IL-2R) is present in four other cytokine receptor complexes (IL-4R, IL-7 R, IL-9R, and IL-15R), and has been shown to be of central importance in lymphocyte development. γc has been causally associated with human X-linked severe combined immunodeficiency (X-SCID), a condition where there is a complete lack of T-lymphocytes and near normal numbers of non-functional B-lymphocytes. In addition, the γc cytokines have all been shown to be capable of supporting T cell growth, with the possible exception of IL-9, and thus, γc is thought to be highly influential in the function of the peripheral immune response. Methods: In order to further characterize the role of γc in peripheral immunity, this study used antibodies to several distinct epitopes of γc which antagonize cytokine function to inhibit immune activation in vitro. The degree of blockade by the antibodies was quantified by inhibition of allogeneic cytotoxic T lymphocyte (CTL) responses and proliferative responses to antigen and anti-CD3. Results: Anti-γc effectively blocked the generation of cytotoxic T cells, however, proliferation of T cells to antigen and anti-CD3 was not inhibited. Thus, optimal stimulation of the T cell receptor (TCR) appears to result in γc-independent proliferation. In contrast, where stimulation is suboptimal, the majority of the proliferation to anti-CD3 and to antigen was inhibited by anti-γc mAbs, but not antibodies to IL-2 and IL-4. This finding suggests that one or more of the other γc associated cytokines (IL-7, IL-9, IL-15) are important in inducing proliferation under these suboptimal conditions. Conclusion: Collectively, these results raise the possibility that the first rounds of activation and expansion of T cells may be due to stimulation through the TCR, whereas differentiation to the effector CTL phenotype is strictly cytokine dependent.

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