34 research outputs found

    Current perspectives of the signaling pathways directing neural crest induction

    Get PDF
    The neural crest is a migratory population of embryonic cells with a tremendous potential to differentiate and contribute to nearly every organ system in the adult body. Over the past two decades, an incredible amount of research has given us a reasonable understanding of how these cells are generated. Neural crest induction involves the combinatorial input of multiple signaling pathways and transcription factors, and is thought to occur in two phases from gastrulation to neurulation. In the first phase, FGF and Wnt signaling induce NC progenitors at the border of the neural plate, activating the expression of members of the Msx, Pax, and Zic families, among others. In the second phase, BMP, Wnt, and Notch signaling maintain these progenitors and bring about the expression of definitive NC markers including Snail2, FoxD3, and Sox9/10. In recent years, additional signaling molecules and modulators of these pathways have been uncovered, creating an increasingly complex regulatory network. In this work, we provide a comprehensive review of the major signaling pathways that participate in neural crest induction, with a focus on recent developments and current perspectives. We provide a simplified model of early neural crest development and stress similarities and differences between four major model organisms: Xenopus, chick, zebrafish, and mouse

    Myo-inositol therapy for poor-responders during IVF: a prospective controlled observational trial

    No full text
    BACKGROUND: The overall incidence of poor ovarian response in IVF cycles has been reported to be between 9 and 24 %. The management of these patients remains a significant challenge in assisted reproduction. The aim of the present study was to evaluate the effect of myo-inositol (MI) on ovarian function in poor responders undergoing ICSI. METHODS: The study is a prospective controlled observational trial, that involved 72 poor responders included in an ICSI program and divided into two groups; group A: 38 patients who have been assuming MI (4 g) + folic acid (FA) (400 μg) for the previous 3 months before the enrollment day; group B: 38 patients assuming FA (400 μg) alone for the same period. COH was carried out in the same manner in the two groups. The main goal was the assessment of oocytes retrieved number and quality; secondary endpoints were the Ovarian Sensitivity Index (OSI: n° oocytes retrieved/total Gonadotropins units × 1000), oestradiol levels on the day of hGC, fertilization rate, implantation rate, ongoing pregnancy rate. RESULTS: There was no significant difference between the two groups regarding oestradiol level, but total rec-FSH units were significantly lower (p = 0.004) and M2 oocytes rate significantly higer (p = 0.01) in group A. The ovarian sensitivity index was higher, reaching a statistical significance (p < 0.05), in the group of patients pre-treated with MI, showing an improvement in ovarian sensibility to gonadotropin. CONCLUSIONS: Our results suggest that MI therapy in poor responders results in an increased of the number of oocytes recovered in MII and of the gonadotropin Ovarian Sensitivity Index (OSI), suggesting a MI role in improving ovarian response to gonadotropins. Therefore MI seems to be helpful in “poor responders” undergoing IVF cycles
    corecore