This chapter reviews the key roles of the different layers of the maternofetal interface in supplying essential nutrients to the developing fetus before the placental circulations are fully established. Focal trophoblastic oxidative damage and progressive villous degeneration trigger the formation of the fetal membranes that remodel the uteroplacental interface. The distribution of the placental-specific protein human chorionic gonadotrophin (hCG) in yolk sac and coelomic fluid samples, and the absence of hCG mRNA expression in yolk sac tissue, suggests the secondary yolk sac (SYS) has an absorptive function. During the 10th week of gestation, the yolk sac starts to degenerate and rapidly ceases to function. The anatomy of the materno-fetal interface in the first trimester is the result of the need for a delicate balance between the metabolic requirements of the developing fetus and the potential harmful effects of oxygen during embryogenesis and organogenesis.

This chapter compares the role of human menopausal gonadotrophin (hMG), follicle-stimulating harmone (FSH) agonist/antagonist and recombinant/urinary human chorionic gonadotrophin (hCG)/luteinizing hormone (LH)/gonadotrophin-releasing hormone agonist (GnRHa) in triggering ovulation. With the use of GnRHa, hCG was necessary to induce final follicular maturation and triggering of ovulation. Accordingly, in the 1980s, the use of gonadotrophins, GnRHa, and hCG became a standard successful protocol for ovulation induction in assisted conception cycles. The GnRH antagonists emerged as an alternative to GnRHa in preventing premature LH surges. Recombinant FSH (recombinant-human FSH), which is free of LH activity, is used in many cases of controlled ovarian hyperstimulation (COH) after downregulation with long protocol. The conclusions of the meta-analyses are that there is no advantage for either recombinant FSH or urinary FSH concerning the clinical pregnancy rate, miscarriage rate, or ovarian hyperstimulation syndrome (OHSS) rate.