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The vanishing twin syndrome is a relatively frequent finding, especially since the widespread use of assisted reproductive technology (ART). Both an earlier follow-up of pregnancy and the use of transvaginal ultrasound, providing a better ultrasound resolution, have brought us closer to the real incidence of this phenomenon, which was underestimated prior to the introduction of these techniques. Thanks to this, we can establish the real incidence of early embryonic loss, from its early ultrasound identification, as well as study the incidence of complications, clinical management, and perinatal prognosis associated with these pregnancies.

Epidemiological studies on male mediated developmental toxicity may focus on links between environmental exposure of the male and pregnancy failures or disorders in the offspring. Alternatively, the focus may be on biological markers of male fecundity and developmental disorders. The study design only rarely allows for a combination of these two approaches. Demonstration of effects of male exposure on the male reproductive system, and subsequent demonstration of links between observed abnormalities of the male system with abnormalities of foetal and childhood development in the offspring would provide strong evidence for causal associations between exposure and outcomes.

In this work we analise the effects of ionizing radiation in prepubertal and adult female rats, using as parameters, implantation sites, embryonic loss, and synaptonemal complex (SC) analysis of the female F1 of the pregnant rats. Our preliminary results show a decrease statisticaly significant in fertility of irradiated groups, but cytogenetic analysis did not shown any inherited damage atributed to radiation. At the same time, our results seem to indicate a higher resistance of oocytes from prepubertal rats and support the possible use of GnRH agonists as oestrus cycle supressors to turn adult rats into gonadal quiescence.

Human gametes are frequently aneuploid. It is estimated that approximately 2% of sperm, 18% of eggs and 20% of conceptuses have extra or missing chromosomes (Burgoyne et al., 1991). This condition of genetic imbalance accounts for much of the embryonic loss during development, and for various disabling syndromes in liveborn. Paternal contributions to the aneuploidy load are less than those which are maternally-mediated; nevertheless, they are substantial. Roughly 6% of individuals with Trisomy 21, the most common aneuploidy condition, are thought to have inherited the extra chromosome from their father (Sherman et al., 1991). In regard to sex chromosome aneuploidies, all of the XYY trisomies, most of the XO monosomies, and half of the XXY trisomies are considered to be of paternal origin (reviewed by May et al., 1990).

Existing models used to analyze uterine receptivity to blastocyst attachment have thus far failed to account for non-genotypic embryonic loss following in vitro fertilization and embryo transfer in any species. Although application of the technology for biochemistry and molecular biology has yielded useful information about the uterus at a molecular level, the regulatory mechanisms of ovoreceptivity and implantation remain elusive.