Syncytin-1 plays a critical role in the maintenance of normal pregnancy by mediating the formation of syncytiotrophoblasts through a fosugenic action. Encoded by the human endogenous retrovirus envelope gene HERV-W, syncytin-1 trophoblast-specific expression is controlled by epigenetic mechanisms. In non-placental tissues, the syncytin-1 gene is suppressed by hypermethylation in the LTR promoter region. Hypomethylated and activated syncytin-1 gene is found in placental trophoblast lineages and malignant cells. We here demonstrate that while syncytin-1 gene remains silenced in the eutopic endometrium from endometriotic patients, syncytin-1 mRNA and protein are detected in ectopic, endometriotic lesions; particularly the endometrioid glandular endothelial cells. LINE-1 COBRA assay and immunohistochemistry using the 5-MC-specific antibody did not detect any changes in global DNA methylation in the endometriotic tissues. However, results from COBRA and bisulfite sequencing indicated that the LTR region of the syncytin-1 promoter is hypomethylated in endometriotic tissues, highlighting the significance of DNA demethylation in syncytin-1 gene activation. Analysis of DNA methyltransferase 3B (DNMT3B) mRNA levels revealed that DNMT3B3, an isoform carrying methyltransferase activity, is downregulated; whereas DNMT3B7, the isoform without enzymatic activity, is upregulated in the endometriotic tissues, pointing to positive and negative regulatory functions, respectively, of these isoforms on syncytin-1 methylation. These results have provided the first evidence supporting the involvement of epigenetic mechanisms for syncytin-1 upregulation in endometriotic tissues. Considering recent findings on the nonfusogenic activity of syncytin-1, its expression in endometriotic tissues suggests that this multifunctional protein may be implicated in the pathogenesis and/or progression of endometriosis.

Education and training can improve the quality of health care. We evaluated a course taught by Obstetrics/Gynaecology residents on the work environment and maternal/neonatal outcomes at Orotta Maternity Hospital. Participants were given a Standardised Safety Attitudes Questionnaire (SAQ) to measure work environment before and after training. Maternal/neonatal outcomes were extracted from hospital logbooks. Neonatal quality indicators were: adverse score index, weighted score index and severity score index. SAQ response rate was 77.6% (45/58) pre-training and 95.6% (43/45) post-training. Mean total SAQ score increased from 3.07 to 3.32 out of 5 points (p < 0.05). Changes in relative risk (RR) were not statistically significant for maternal [maternal death ratio of RR (RRR) =1.08, 95% CI: 0.20-5.84 and blood transfusion RRR = 0.90, 95% CI: 0.74 -1.09] or neonatal outcomes (intrapartum death RRR = 1.24, 95% CI: 0.57-2.75, neonatal death RRR = 0.93, 95% CI: 0.26-3.24, neonatal transfer RRR = 1.02, 95% CI: 0.81-1.27, and Apgar < 7 at 5 minutes RRR = 1.20, 95% CI: 0.83-1.73). Neonatal quality indicators did not change significantly. Utilising residents to teach staff-developed training within a hospital setting was feasible and may improve the work environment. Impact on maternal/neonatal outcomes is not evident but continued follow-up is important.

No abstract