This year all of our poster winners will be presenting at the COM Dean’s Distinguished Lecturer Series on May 3, 2018, from 12:00 - 1:00 PM in the Pavilion A Auditorium.
The primary objective of the University of Kentucky College of Medicine Trainees in Research Advisory Committee (TRAC) is to develop the trainee community in the College. The TRAC is comprised of faculty, administrative staff, and postdoctoral and graduate student representatives who serve as resources to enhance the training environment for all trainees in the basic and clinical sciences. In addition to the Poster Competition, TRAC programs include a Career Development Seminar Series and a Research Seminar Series designed to support trainee career development.
As a postdoc, we invite you to participate in the 10th Annual Postdoctoral Poster Session. In order to provide an opportunity for presentation of data and development of presentation skills, the TRAC has instituted a peer-reviewed poster session. This unique opportunity permits scholars across diverse disciplines to present their work in progress in a friendly environment for constructive feedback. This event will provide the presenters direct feedback on the organization and presentation of their posters. Generous awards will be presented to the best poster presentations. All postdoctoral fellows and scholars are encouraged to participate. Each participant is limited to one poster. Early submissions are encouraged, and abstracts must be submitted by March 9, 2018, to be considered. This is a wonderful opportunity to showcase your research and compete for awards.
Abstracts may be submitted on any aspect of original research performed by the postdoctoral scholar or fellow at the UK College of Medicine. This includes both basic and clinical research, epidemiological studies, and outcomes research. Abstracts and posters may describe work that has been or will be submitted at other meetings. This is an excellent opportunity to receive feedback on the presentation of data for a meeting in the near future. Abstracts are NOT restricted to work that is completed or near completion. Poster presentations describing the design of new studies and work in progress can and should be submitted as well. Presentation of such data or experimental plans to peers offers an opportunity for the establishment of collaborations.
Who may submit?
All postdoctoral scholars and fellows in the UK College of Medicine may participate. Trainees within seven years of earning their terminal degree who may have other title designations may apply.
Abstracts may describe work that has been or will be submitted at other meetings. There is NO fee for participation in this unique opportunity; however there is a limited number of spaces available. Submitted abstracts will be compiled and distributed to attendees.
Posters cannot be larger than 36" high and 54" wide. The abstract itself should follow the format below and be in Arial, size 12. They should be sent to firstname.lastname@example.org in a .doc or .docx format with the subject line "Poster Session Abstract".
Abstracts are due to the above e-mail address by March 9, 2018.
Secretogranin II is a novel periovulatory gene that is induced by human chorionic gonadotropin in human and rodent granulosa cells
Patrick R. Hannon 1 ● Linah Al-Alem 1 ● Katherine L. Rosewell 1 ● James W. Akin 2 ● Thomas E. Curry, Jr. 2
1 Department of Obstetrics & Gynecology, University of Kentucky ●
2 Bluegrass Fertility Center, Lexington, KY
The events that occur in the ovary following the luteinizing hormone (LH) surge leading to ovulation are paramount for fertility, so much so that defects in ovulation are the leading cause of female infertility. Thus, there is an urgent need to elucidate the mechanisms that control ovulation, including a more thorough understanding of the mediators of ovulation. Evidence from our laboratory suggests that secretogranin II (SCG2) is a potential mediator of ovulation across species. In other tissues, SCG2 is involved in hormone packaging and secretion, or is cleaved to peptides that promote leukocyte migration and angiogenesis. These processes are vital for ovulation; however, the characterization and regulation of SCG2 in ovarian function and ovulation is unstudied. Our hypothesis is that the LH surge increases SCG2 levels in human and rodent granulosa cells, via classic LH receptor signaling pathways, to serve as a mediator of ovulation. To test this, women undergoing tubal sterilization were recruited into this study and monitored by transvaginal ultrasound for 2-3 menstrual cycles. The dominant follicle was surgically excised at the preovulatory phase or women were given 250μg hCG and dominant follicles were collected at one of three time intervals after hCG: early ovulatory (12-18h), late ovulatory (18-34h) and postovulatory (44-70h). Granulosa cells were isolated and processed for mRNA analysis or whole follicles were processed for immunohistochemistry. Our results indicated that hCG significantly increased the mRNA levels of SCG2 in early (15 fold increase), late (19 fold increase), and postovulatory (15 fold increase) granulosa cells when compared to the preovulatory granulosa cells in vivo (n=3-6 patients; p≤0.05). In the whole follicle in vivo, SCG2 protein staining was rather prominent in the theca and stroma across the periovulatory period, but increased dramatically in the granulosa cells with hCG treatment. In order to examine the regulation of SCG2 induction, a validated model of cultured granulosa-lutein cells (GLCs) from IVF patients was utilized. GLCs were collected on the day of oocyte retrieval and were allowed to acclimate in culture for 6 days to regain LH/hCG responsiveness. The GLCs were then treated with vehicle control (DMSO), AG1478 (5µM; EGF receptor antagonist), hCG (1 IU), and hCG+AG1478 for 0, 6, 12, and 24h. Similar to the results in vivo, hCG significantly increased the mRNA levels of SCG2 at the 6 (9 fold increase) and 12h (8 fold increase) timepoints when compared to controls; however, the mRNA levels of SCG2 in the hCG+AG1478 groups were significantly reduced by 50% when compared to the hCG group (n=7-10 patients; p≤0.05). To further test our hypothesis in the rodent, the well-characterized immature rodent PMSG/hCG model was utilized. Following 0, 4, 8, 12, and 24h of hCG treatment, ovaries were removed, and follicles were punctured to collect granulosa cells for qPCR analysis in vivo. In mouse granulosa cells, hCG significantly increased the mRNA levels of Scg2 at 4, 8, and 12h when compared to the 0h group (n=5-6 mice; p≤0.05). In rat granulosa cells, hCG significantly increased the mRNA levels of Scg2 at 8 and 12h when compared to the 0h group (n=5-6 rats; p≤0.05). These data are the first to demonstrate that SCG2 is induced by hCG in the human and rodent periovulatory granulosa cell, and that EGF receptor signaling partially mediates the hCG-induced increase in human periovulatory SCG2 expression. Supported by P01HD071875, HD057446, and the Lalor Foundation Postdoctoral Fellowship.
Judging and Awards
Each poster and presentation will be evaluated separately by at least 2 faculty judges from the College of Medicine on the basis of: (1) abstract, (2) poster quality, (3) oral presentation of poster and research.Judging criteria will be adjusted to take into account the time the presenter has been in postdoctoral status as well as the time spent on the specific project. Cash prizes in amounts of $700, $500, and $300 will be awarded to the top three posters. These presenters will also have the opportunity to present at the Dean's Distinguished Lecture Series on May 3, 2018. Participants are required to be present in the judging of their poster.