​​ABSTRACT SUBMISSION GUIDELINES

Deadline for submission – Midnight on 20th July 2023
Word limit – 300 words (not including authors and affiliations)
Presentation types
There are two possible types of presentations, oral and poster. The conference scientific committee will make the final decision on presentation format.
If the abstract is accepted for either oral or poster presentation, at least one author MUST register for the conference.
Preparation of the abstract

1. All abstracts must be submitted in English.
2. The title should succinctly describe the work encompassed within the abstract. Use of upper case for the title is strongly discouraged.  Capitalize only the first letter of the first word of the title (unless for abbreviations or proper nouns) and do not end the title with a period (“.”)
3. Abstract text should be a summary of the research in its entirety. One author is allowed to submit multiple abstracts. Each abstract should contain concise complete information sufficient to convey why the work was done, how it was done, and the key findings and implications and a complete data set.
4. No tables, images, or references (either in text or as bibliography) to be submitted.
5. The submitter is responsible for ensuring that all authors have read the abstract and agreed to be co-authors, for submitting Name, Affiliation, City, and country and for clearly indicating the presenting author. Underline the name of the presenting author.
6. Authors are encouraged to have their abstract checked for grammar and spelling.

 
Follow the sample abstract exactly for formatting style, font size, author names and affiliations. 

ABSTRACT SAMPLE

​Trophoblast derived extracellular vesicles specifically alter the transcriptome of endometrial cells and may constitute a critical component of embryo-maternal communication
Kasun Godakumara1,2, James Ord1, Freddy Lättekivi1, Keerthie Dissanayake1,2, Janeli Viil1, Ülle Jaakma2, Andres Salumets3, Alireza Fazeli1,2,4
1- Department of Pathophysiology, Institute of Biomedicine and Translational Medicine, Faculty of Medicine, Tartu University, Tartu, Estonia. 2- Institute of Veterinary Medicine and Animal Sciences, Estonian University of Life Sciences, Tartu, Estonia. 3 - Competence Centre on Health Technologies, Tartu, Estonia. 4 - Academic Unit of Reproductive and Developmental Medicine, Department of Oncology and Metabolism, Medical School, University of Sheffield, Sheffield, UK

The period when the embryo and the endometrium undergo significant morphological alterations to facilitate a successful implantation - known as “window of implantation” - is a critical moment in human reproduction.  Embryo and the endometrium communicate extensively during this period, and lipid bilayer bound nanoscale extracellular vesicles (EVs) are purported to be integral to this communication. To investigate the nature of the EV-mediated embryo-maternal communication, we have supplemented trophoblast analogue spheroid (JAr) derived EVs to an endometrial analogue (RL 95-2) cell layer and characterized the transcriptomic alterations using RNA sequencing. EVs derived from non-trophoblast cells (HEK293) were used as a negative control. The cargo of the EVs were also investigated through mRNA and miRNA sequencing. Trophoblast spheroid derived EVs induced drastic transcriptomic alterations in the endometrial cells while the non-trophoblast cell derived EVs failed to induce such changes demonstrating functional specificity in terms of EV origin. Through gene set enrichment analysis (GSEA), we found that the response in endometrial cells was focused on extracellular matrix remodeling and G protein-coupled receptors’ signaling, both of which are of known functional relevance to endometrial receptivity. Approximately 9% of genes downregulated in endometrial cells were high-confidence predicted targets of miRNAs detected exclusively in trophoblast analogue-derived EVs, suggesting that only a small proportion of reduced expression in endometrial cells can be attributed directly to gene silencing by miRNAs carried as cargo in the EVs. Our study reveals that trophoblast derived EVs can modify the endometrial gene expression, potentially with functional importance for embryo-maternal communication during implantation, although the exact underlying signaling mechanisms remain to be elucidated.