The image acquisition and time-lapse analysis system makes it possible to determine exact timing of embryo cleavages in a clinical setting. We propose a multivariable model based on our findings to classify embryos according to their probability of implantation. The efficacy of this classification will be evaluated in a prospective randomized study that ultimately will determine if implantation rates can be improved by time-lapse analysis.

This controlled-randomized, clinical trial confirmed the effectiveness of oocyte cryo-storage in an ovum donation programme, failing to demonstrate the superiority of using fresh oocytes with respect to the use of vitrified egg-banked ones in terms of OPR. Instead, the non-inferiority of vitrified oocytes was confirmed. These findings involve highly relevant issues that may open a new range of possibilities in ART.

At least 8-10 metaphase II oocytes are necessary to achieve reasonable success. Numbers should be individualized in women >36 years old. We suggest encouraging women who are motivated exclusively by a desire to postpone childbearing because of age, to come at younger ages to increase success possibilities.

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Disorders of sex development (DSDs) and the testicular dysgenesis syndrome (TDS) seem to result from maldevelopment of the fetal testis. TDS seems to be associated with the development of testicular germ cell tumors in young adulthood. Current knowledge of normal and disrupted testicular development has been largely derived from rodent models. Immature testis tissue from several primate species has been grafted into a nude mouse host, resulting in full spermatogenesis in the grafted tissue. However, rodents do not develop testicular germ cell tumors equivalent to those occurring in human beings, suggesting fundamental differences in fetal testis development between primates and rodents. Previous studies show limited survival of human testis xenografts when postnatal tissue is grafted. The lack of an appropriate human model system has hampered efforts to study mechanisms of human germ cell differentiation and to investigate the origins of DSDs and TDS.The present study evaluated the use of human fetal testis xenografting as a technique to recapitulate normal fetal testis development and differentiation.First-trimester (9 weeks, n ϭ 4) and second-trimester (14-18 weeks, n ϭ 6) human fetal testes were grafted into castrated male nude mice for 6 weeks. Mice with second-trimester xenografts were treated with human chorionic gonadotropin (hCG), or received 0.9% saline or the vehicle 7 days after the graft. Immunohistochemistry, triple immunofluorescence, and testosterone assay were used for quantification of germ cell differentiation and proliferation. Cellular development and function within the xenografts were compared with those of age-matched controls.Graft survival rates were Ͼ75% with normal morphology. Seminiferous cord formation was initiated in the first-trimester xenografts. Expression of cell-specific and differentiation-specific protein markers in first-and second-trimester grafts demonstrated normal functional development of Sertoli, Leydig, and peritubular myoid cells. Differentiation and functional activation of Leydig cells in second-trimester hCG-exposed grafts indicated induction of steroidogenesis. In hosts bearing second-trimester xenografts, treatment with hCG resulted in nearly a 10-fold increase in serum testosterone levels compared with vehicle-treated hosts. Germ cell differentiation during the grafting period was similar to that occurring normally in the intact testis and was equivalent to that of age-matched controls This was established by quantification of the loss of expression of the gonocyte pluripotency marker OCT4 after grafting coincident with emerging expression of the protein VASA, which is associated with normal differentiation into prespermatogonia.These findings suggest that this in vivo system has the potential to investigate mechanisms of normal human fetal testis development and to study mechanisms of disruption associated with DSDs and TDS or with exposure to environmental chemicals and other exogenous factors. EDITORIAL COMMENT(For the most part, the reports in the SURVEY ha...

No abstract

Elevated serum progesterone levels on the day of hCG administration is associated with reduced ongoing pregnancy rates. In particular, serum progesterone levels of >1.5 ng/ml were associated with lower ongoing pregnancy rates following IVF/ICSI cycles irrespective of the GnRH analogue used for pituitary down-regulation.

Expression of MUC1 in endometrial epithelium has been suggested to create a barrier to embryo attachment that must be lifted at the time of implantation. In this study, we investigated the hormonal regulation of human endometrial MUC1 in hormone replacement therapy cycles and in the human blastocyst. We also analyzed the embryonic regulation of MUC1 in human endometrial epithelial cells (EECs) during the apposition and adhesion phases of human implantation using two different in vitro models. Our results indicate that endometrial MUC1 mRNA and immunoreactive protein increase in receptive endometrium compared to nonreceptive endometrium. Human blastocysts express MUC1, as demonstrated by reverse transcription-polymerase chain reaction and immunocytochemistry, localized at the trophectoderm. In vitro, MUC1 was present at the surface of primary cultures of human EEC, and presence of a human blastocyst (i.e., apposition phase) increases EEC MUC1 protein and mRNA compared to control EEC lacking embryos. Interestingly, when human blastocysts were allowed to attach to the EEC monolayer (i.e., adhesion phase), MUC1 was locally removed in a paracrine fashion on EEC at the implantation site. These results demonstrate a coordinated hormonal and embryonic regulation of EEC MUC1. Progesterone combined with estradiol priming induces an up-regulation of MUC1 at the receptive endometrium. During the apposition phase, presence of a human embryo increases EEC MUC1. However, at the adhesion phase, the embryo induces a paracrine cleavage of EEC MUC1 at the implantation site. These findings strongly suggest that MUC1 may act as an endometrial antiadhesive molecule that must be locally removed by the human blastocyst during the adhesion phase.