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2018 North Dakota INBRE Annual Symposium Abstract Submission

Call for Abstracts

2018 Abstract Submission Form

The scientific program highlighting North Dakota INBRE investigators will consist of both invited oral presentations and Core Facility poster presentations.  All authors may submit their abstracts by following the directions below.  The deadline for submission of abstracts is on October 8 at noon. Please limit abstracts to 250 words or less.

Abstract Submission Deadline: October 8, 2018, at noon.
If you would like your abstract in the Symposium booklet, your abstract needs to be
submitted by October 3, 2018.


Guidelines and Rules for Submission

It is the author's responsibility to see that the following guidelines and instructions are followed to ensure optimal results.

1. Size. The entire abstract, including title, author(s), university, department and text must fit on half a sheet of (8.5" x 11") paper. The body of the abstract may have no more than 250 words, including any footnotes or acknowledgements.

2. Format. Use an Arial 11 pt. font; set 1" margins on all sides; single space only; do not use text boxes, tables, figures or diagrams.

3. Title. The title should be brief, clearly indicating the nature of the presentation. The title should be in bold type.

4. Authors. Include all author's first name, middle initial, and last name. The presenting author's name should be listed first and underlined. Include all authors' department and university affiliations. If there are multiple authors with multiple affiliations (i.e. universities/departments) indicate affiliations according to the sample below.

SAMPLE ABSTRACT SUBMISSION (taken from 2016 program):

Differential Gene Expression of Grin2c, Grin2d, and Bax in the Hippocampi of Mice with Constitutive α1A-Adrenergic Receptors
Tyler Fahy3, Zachary O Dent1, Nicholas A Smith1, Joseph P Biggane1, Dianne M Perez2, Van A Doze1
1University of North Dakota School of Medicine and Health Sciences; 2Cleveland Clinic Foundation; Dakota College at Bottineau

This study identified differentially expressed genes that are affected by constitutive activation of the α1A-adrenergic receptor (α1A-AR) in adult mice. Previous studies in this lab have associated α1A-AR stimulation with increased neurogenesis, learning, and memory. Genes we hypothesized to be respondent to α1A-AR activation were studied in this study; these genes included Grin2c, Grin2d, and Bax. Grin2c and Grin2d encode ionotropic glutamate receptor, NMDA (N-methyl-D-aspartate), subunit 2c and subunit 2d. NMDA receptors are ionotropic glutamate receptors and are highly expressed in the central nervous system. NMDA receptors are an important modulator of intracellular calcium influx, which is a key aspect underlying long-term potentiation. Bax encodes the BCL2 associated x protein, which can be a common apoptotic activator. This protein has been known to interact with the P53 and can be involved in P53-mediated apoptosis. Grin2c and Grin2d were both hypothesized to be upregulated because previous research in the Doze lab showed that constitutively active α1A-ARs can invoke an increase in long-term potentiation. Bax was hypothesized to be downregulated because it is an apoptotic activator. A transgenic mouse model that expresses a constitutively active mutant (CAM) α1A-AR was used to identify the role of α1A-AR activity in the expression of the aforementioned genes. We compared differential gene expression of Grin2c, Grin2d, and Bax in the hippocampi of CAM α1A-AR and wild-type mouse brains. Gene expression was determined by utilizing real-time quantitative polymerase chain reaction (RT-qPCR). Initial findings of this experiment found that Grin2c was downregulated (p-value: 0.006), Grin2d had no significant change in transcription (p-value: 0.504), and Bax was up regulated (p-value: 0.048).

5. No fax copies will be accepted in lieu of electronic submission.

6. Deadline: Submit your abstract by noon on October 8, 2018. Abstracts received after the deadline will not be accepted.
If you would like your abstract in the Symposium booklet, your abstract needs to be
submitted by October 3, 2018.