There is now considerable evidence that leucocytes and their products have significant effects on the functional capacity of spermatozoa both in the male and female reproductive tract. Recent advances in the accurate detection of these leucocytes and their products using monoclonal antibodies and a parallel increase in the application of sophisticated sperm function tests has now made it possible to further determine the influence of the leucocytes on sperm function. It is therefore likely that this field of reproductive biology will be an area of considerable activity in the near future.

Over the past four years, major advances in the understanding of the aetiology and pathogenesis of the androgen insensitivity syndrome (AIS) have occurred. This review aims to summarize current information on clinical, diagnostic, therapeutic and molecular aspects of AIS.

Male infertility, while having a variety of causes, is generally discussed in terms of semen parameters. While the World Health Organization (WHO) have been able io set limits for semen parameters below which a male can be considered subfertile (20 million/ml; >50% motility; >50% morphologically normal forms), it is well documented that in vivo conceptions have been achieved where semen quality falls well outside these limits, and that infertile men may have normal semen parameters. Macleod and Gold in comparing 1000 fertile men and 1000 infertile men, found that significantly more infertile men had sperm densities below 20 million/ml, but also that 60% of infertile men had sperm densities of 60 million or more. Jouannet and Feneaux have shown that the conception rate in vivo only apparently falls significantly at sperm concentrations of less than five million/ml. Although the cause of subnormal semen analysis is unknown in the majority of cases, there is no reason to suppose that abnormal semen parameters on their own are the cause of infertility. Rather the problem may be caused by failure of sufficient numbers of sperm traversing the female tract and reaching the oocyte. Unfortunately, lack of defined diagnoses lead to a lack of direct treatment for subnormal semen parameters. The development of in vitro fertilization (IVF) resulted in a method that could be used to circumvent the problem since it requires relatively low numbers of sperm and these are placed in the immediate vicinity of the oocyte. It should also be pointed out that normal semen parameters do not imply fertility, since these parameters cannot directly identify dysfunction. IVF offers the advantage that sperm-oocyte interractions can be observed, and in cases of fertilization failure, the point at which sperm dysfunction manifests itself may potentially be identified – if not the nature of the dysfunction. Techniques have now been developed that may overcome certain types of dysfunction, using both biochemical and mechanical means.

Before sexual differentiation occurs at seven weeks, the urological ridges develop in the embryo. These contain the primitive gonads, the mesonephros (embryonic kidneys) and the paired Wolffian (mesonephric) ducts, along with the Müllerian (paramesonephric) ducts. The fundamental mechanism of fetal sexual development was elucidated by Alfred Jost and is determined by the development of the gonad: where testes form in response to the testis-determining gene, and the male testicular hormones cause development of the male phenotype. If ovaries develop or the gonads are absent, female secondary sex characteristics are produced. Recently, the cloning of the putative human testis-determining gene on the Y-chromosome was reported. Assuming this is the true controller of testicular development, an understanding of the initiation of sexual differentiation at the genetic level should emerge in the near future. Of great importance will be the isolation of the testis-determining gene product and identification of other genes that it regulates.

Embryo cryopreservation is a well established technique and is used widely for embryo banking of genetically valuable strains of mice, the transport and proliferation of farm animals and as a valuable adjunct to human in vitro fertilization (IVF). The range of methods presently used to cryopreserve human embryos has been recently reviewed. This article examines the results obtained by the established freezing techniques and developments in the new rapid cooling methods. There is a dramatic contrast in the simplicity, ease and cost between these new rapid techniques and the conventional slow cooling or equilibrium freezing methods and it is likely that the rapid freezing will replace conventional freezing by slow cooling which is presently in widespread use in IVF clinics.

Gonadotropin-releasing hormone (GnRH) is also known as luteinizing hormone-releasing hormone (LHRH), formerly luteinizing hormone releasing factor (LRF). Since this hormone regulates the secretion of both FSH and LH, we prefer to call it GnRH. GnRH antagonists, as the name implies, are a class of compounds that actively compete with GnRH for the GnRH receptor, thereby neutralizing the effects of GnRH by competitive receptor occupancy. In order to fully appreciate their potential clinical utility, it is first important to comprehend the critical role of GnRH in the regulation of the pituitary-gonadal axis and secondly to familiarize ourselves with the mechanisms of action of GnRH, GnRH agonists and GnRH antagonists.