In frozen embryo transfer, artificial cycles were associated with more early pregnancy loss and lower live birth rate than stimulated cycles.
Throughout the entire first trimester of pregnancy, fetal growth is sustained by endometrial secretions, i.e histiotrophic nutrition. Endometrial stromal cells (EnSCs) accumulate and secrete a variety of nutritive molecules which are absorbed by trophoblastic cells and transmitted to the fetus. Glycogen appears to have a critical role in the early stages of fetal development, since infertile women have low endometrial glycogen levels. However, the molecular mechanisms underlying glycogen metabolism and trafficking at the fetal-maternal interface have not yet been characterized. Among the various factors acting at the fetal-maternal interface, we focused on adiponectin - an adipocyte-secreted cytokine involved in the control of carbohydrate and lipid homeostasis. Our results clearly demonstrated that adiponectin controls glycogen metabolism in EnSCs by (i) increasing glucose transporter 1 expression (ii) inhibiting glucose catabolism via a decrease in lactate and ATP productions (iii) increasing glycogen synthesis, (iv) promoting glycogen accumulation via phosphoinositide-3 kinase activation, and (v) enhancing glycogen secretion. Furthermore, our results revealed that adiponectin significantly limits glycogen endocytosis by human VTs. Lastly, we demonstrated that once glycogen has been endocytosed into placental cells, it is degraded into glucose molecules in lysosomes. Taken as a whole, the present results demonstrate that adiponectin exerts a dual role at the fetal-maternal interface by promoting glycogen synthesis in the endometrium and conversely reducing trophoblastic glycogen uptake. We conclude that adiponectin may be involved in feeding the conceptus during the first trimester of pregnancy by controlling glycogen metabolism in both the uterus and the placenta.
onographic techniques, including transvaginal sonography, have been proven effective in identifying disorders responsible for gynecologic emergencies. 1,2 In women presenting to emergency departments (EDs) because of symptoms in the first trimester of pregnancy, sonography is recommended as part of the initial workup. 3,4 According to a recent systematic review, the use of sonography in gynecologic EDs decreases the risk of missed ectopic pregnancy, time to surgery for ectopic pregnancy, and length of stay in patients with normal pregnancies and may be more cost-effective than diagnostic strategies requiring formal sonography. 5 Abbreviations ED, emergency department; Ob/Gyn, obstetrics and gynecology S ©2015 by the American Institute of Ultrasound in Medicine | J Ultrasound Med 2015; 34:829-835 | 0278-4297 | www.aium.org ORIGINAL RESEARCH Objectives-To assess the impact of an educational intervention based on an original accreditation training program on the quality of emergency sonography performed by obstetrics and gynecology (Ob/Gyn) residents. Methods-We conducted a prospective before-after study on residents who performed bedside standardized sonographic examinations as first-line investigations in patients seen at our gynecologic emergency department. In both periods, the residents followed a 1-hour class taught by a board-certified Ob/Gyn sonography expert (opinion leader) and received a written standardized imaging protocol. An accreditation training process was implemented for the new residents at the beginning of the second period: 5 complete sonographic examinations were required for each resident, and facilitated feedback from the opinion leader was performed using a dedicated sonographic quality score. During both periods, all consecutive sonograms were collected and stored. The primary outcome was the sonographic quality score. A mixed model for repeated measures was used to compare scores in both periods from 20 consecutive sonographic examinations performed by 5 residents who were different in each period. Results-The mixed model analysis showed an increase in quality scores in the post-accreditation training compared to the pre-accreditation training period (estimated coefficient ± SD, 4.13 ± 0.51; t = 8.16). The sonographic examination order also had a significant effect in both periods (estimated coefficient ± SD, 0.11 ± 0.03; t = 3.99). Conclusions-An accreditation training process including facilitated feedback from a local opinion leader improved the quality of sonographic examinations performed by Ob/Gyn residents in women presenting to a gynecologic emergency department.
Background Successful human embryo implantation requires the differentiation of endometrial stromal cells (ESCs) into decidual cells during a process called decidualization. ESCs express specific markers of decidualization, including prolactin, insulin-like growth factor-binding protein-1 (IGFBP-1), and connexin-43. Decidual cells also control of trophoblast invasion by secreting various factors, such as matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases. Preimplantation factor (PIF) is a recently identified, embryo-derived peptide with activities at the fetal-maternal interface. It creates a favorable pro-inflammatory environment in human endometrium and directly controls placental development by increasing the human trophoblastic cells’ ability to invade the endometrium. We hypothesized that PIF’s effects on the endometrium counteract its pro-invasive effects. Methods We tested sPIF effect on the expression of three decidualization markers by RT-qPCR and/or immunochemiluminescence assay. We examined sPIF effect on human ESC migration by performing an in vitro wound healing assay. We analyzed sPIF effect on endometrial control of human trophoblast invasion by performing a zymography and an invasion assay. Results Firstly, we found that a synthetic analog of PIF (sPIF) significantly upregulates the mRNA expression of IGFBP-1 and connexin-43, and prolactin secretion in ESCs - suggesting a pro-differentiation effect. Secondly, we showed that the HTR-8/SVneo trophoblastic cell line’s invasive ability was low in the presence of conditioned media from ESCs cultured with sPIF. Thirdly, this PIF’s anti-invasive action was associated with a specifically decrease in MMP-9 activity. Conclusion Taken as a whole, our results suggest that PIF accentuates the decidualization process and the production of endometrial factors that limit trophoblast invasion. By controlling both trophoblast and endometrial cells, PIF therefore appears to be a pivotal player in the human embryo implantation process.
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