There have been a number of reviews on this topic over the past decade, starting with Carlsen et al. and including Irvine et al. and Murray et al., concerning declining male fertility. The most exhaustive has perhaps been that of Toppari et al. The main findings of these reviews are: (1) that in some countries of the world sperm production has halved in the last 60 years, (2) rates of testicular cancer have doubled, (3) rates of malformation of the male reproductive tract, such as hypospadias, have doubled, (4) rates of testicular maldescent have risen sharply and (5) these effects are largely linked geographically. Typically, endocrine disrupting chemicals (EDCs) in the environment have been regarded as the main candidates for these effects. A consistent problem with the field, however, is the difficulty in determining the accuracy of data relating to changes in men's health over the latter half of the 20th century. Advances in diagnosis and changing attitudes to the emotive issues surrounding deformity and male infertility inevitably render some of the mass of collected data suspect. Indeed a recent review of testicular and prostate cancer concluded that while the incidence of prostate cancer had increased, the epidemiological data were not suitable for concrete conclusions about causation to be drawn. However, in the case of testicular cancer the data suggested a limited number of major risk factors. In addition, assessing urogenital malformation retrospectively from patient notes is subject to considerable variation in classification. A recent review does however find evidence to suggest that trends of increasing incidences of hypospadias on a temporal and geographical basis may reflect an actual increase in incidence and require further study. On the other hand, there is a considerable body of evidence for EDC disruption of reproduction in wildlife (reviewed by Guillette & Gunderson, 2001).

The aim of preimplantation genetic diagnosis (PGD) is to give couples at risk of passing on a genetic disorder an alternative to standard prenatal diagnosis by enabling them to start a pregnancy that is known to be free of the familial disease. This can be achieved by generating embryos in vitro by standard in vitro fertilization (IVF) techniques and then removing one to two of the cells from the early embryo (embryo biopsy). Single cell polymerase chain reaction (PCR) or fluorescence in situ hybridization (FISH) can then be used to diagnose single gene defects or chromosomal abnormalities respectively. Those embryos diagnosed as free from disease can then be considered for transfer to the womb and so the pregnancy is started knowing that the fetus is unaffected. This avoids the need to consider pregnancy termination in the quest for a healthy child. Originally it was thought that the major reason for referral would be the risk of passing on a single abnormal gene but an increasing proportion of couples are requesting PGD because of recurrent miscarriage due to parental chromosomal abnormality.

The closing years of the 20th Century saw an unprecedented explosion in the knowledge base of reproductive medicine. In turn, this knowledge has led to new approaches to the diagnosis and treatment of disease. The scientific foundation of reproductive medicine continues to expand rapidly in the “post-genomic” era, but at the same time there is an urgent need to translate scientific advances into clinical practice.

Fertilization and early embryo development take place in the oviduct in vivo. Relative to studies in other reproductive organs, the importance of the oviduct has been ignored for many years because pregnancies can be obtained in assisted reproduction treatment using in-vitro fertilization (IVF) and embryo transfer to the uterus without involving the Fallopian tube. After the reports on the beneficial effect of oviductal cells on embryo development in sheep and subsequently in human, and a practical need to improve the success rates in clinical assisted reproduction, there was a period when more research was performed on the Fallopian tube. Many of these studies used in vitro coculture systems to emulate the in vivo environment in vitro, and to search for oviduct-derived embryotrophic factors. With the recent development of sequential culture to improve embryo development in vitro, the use of coculture in assisted reproduction and its related research declined because routine use of coculture is laborious and experience-dependent.

Interest in the investigation of male erectile dysfunction and male factor infertility has risen in recent years, due in part to the increased sophistication and high profile of new treatments associated with these conditions. The assessment and management of men presenting with erectile or fertility problems are usually achieved by collaboration between urology and other specialties. A radiologist is often a vital member of this multidisciplinary team. This article will review the imaging modalities currently available and discuss their current role in the investigation of these two key areas of andrology.

Estrogens are essential regulators of female fertility. Estrogen biosynthesis is dependent upon expression of the cytochrome P450 aromatase, the highest levels of expression of which are detected in the human placenta and the granulosa cells of the mature ovarian follicle. Consistent with this pattern of expression, in non-pregnant premenopausal women, the ovaries have been shown to be the primary source of estradiol. In recent years there has also been an increased interest in the role(s) played by estrogens in regulation of adipose tissue, the vasculature and bone and as paracrine regulators of tissue function in postmenopausal women. In the premenopausal years the uterus is a target for estrogen and the cyclical event of menstruation is a consequence of the sequential exposure of the endometrium to estrogen and progesterone (reviewed in references 5 and 6). Endometrial breakdown occurs as a consequence of progesterone withdrawal with the demise of the corpus luteum (CL) in the absence of pregnancy.

Prolactin is a pleiotrophic hormone that is associated with over 300 biological functions. These functions can be broadly classified into growth and development, immune regulation, metabolism, behaviour and reproduction. The human prolactin gene is located on chromosome 6 and is composed of 6 exons. The gene is approximately 10 kilobases (kb) long whereas the mature prolactin mRNA is about 1 kb in length. Prolactin is encoded by 199 amino acids and the protein is approximately 23 kDa in size. Sequence analysis revealed that prolactin is 40% homologous to growth hormone and placental lactogen. These three proteins are thought to have arisen by duplication of an ancestral gene 400 million years ago. The high sequence homology of these proteins enables prolactin, human growth hormone and placental lactogens to bind the prolactin receptor and activate prolactin intracellular signalling pathways.

Angiogenesis is defined as the formation of new blood vessels from the existing vasculature. Angiogenesis occurs regularly in the endometrium throughout the reproductive life of females as part of the rapid growth and regression of this tissue that occurs during the menstrual cycle. It is now clearly evident that angiogenesis plays a key role in reproductive processes such as embryo implantation, placentation, endometrial regeneration after menstruation, and in the ovary during folliculogenesis and corpus luteum formation. Given the complexity and continual change of the endometrial milieu, it seems highly likely that aberrations in the angiogenic process may contribute to various disorders, including endometrial cancer, endometriosis, menorrhagia and breakthrough bleeding – all significant and common gynaecological pathologies. This review provides an update on the mechanisms and regulation of endometrial angiogenesis, with particular reference to the role of angiogenesis in implantation and placentation, as well as two endometrial pathologies – endometriosis and breakthrough bleeding.

Only 50% of all conceptions result in a live birth (Figure 1). Human reproduction can therefore be viewed as being remarkably inefficient. However, the diametrically opposite opinion that it is in fact a very efficient and selective process, designed to optimize the outcome of pregnancy, deserves to be stated.

Between 65% and 90% of clinically recognized miscarriages are due to chromosome abnormalities, the occurrence of which is more closely related to basal follicle-stimulating hormone (FSH) levels rather than to maternal age alone. In contrast to women suffering a sporadic miscarriage, women who recurrently miscarry often, but not exclusively, lose pregnancies with a normal chromosome content. Using a combination of conventional Geimsa banding and the recently introduced technique of comparative genomic hybridization it has been reported that 54% of pregnancy losses amongst women with recurrent miscarriage are euploid. The challenge we face is to identify the causes of pregnancy loss amongst those couples who recurrently lose such euploid conceptions.

Whilst many conventionally held beliefs as to the aetiology and treatment of women with recurrent miscarriage have not withstood critical scrutiny, significant progress has been made. This progress is the subject of this review, which will also highlight potential areas of future research.

Malignant tumours of the female reproductive tract in childhood and adolescence are rare. The comparative frequencies of tumours in adults and children may be related to the relative accumulation of exposure to environmental factors. An example might be the relationship between exposure to human papillomavirus and the development of vulval, vaginal and cervical cancers. Some cancers in childhood are associated with factors specific to the time of life. Examples include in-utero stilboestrol exposure related to clear cell carcinoma and teenage pregnancy associated with gestational trophoblastic tumours. In childhood and adolescence, 67% of all ovarian tumours are germ cell in origin. This differs significantly to the distribution of ovarian tumours in adults.

Percutaneous trans-catheter embolization has been practised by radiologists for well over 20 years. In many different clinical situations a great variety of embolization materials or agents has been used in all parts of the body, but generally these procedures have been performed rarely. An important indication is severe bleeding not responding to conservative measures, where the alternative treatment would involve major surgery. Embolization has also been used in tumours, particularly where they are hypervascular, when the role has often been to debulk and devascularize immediately prior to surgery. The third main indication is in arteriovenous malformations and fistulae. Thus, it is somewhat surprising that it was not until 1995 that uterine artery embolization (UAE) was first advocated as a treatment for uterine fibroid disease.

Thyroid disorders are common in young women and are, therefore, amongst the commonest endocrine disorders to be encountered in pregnancy. Pregnancy outcomes for mother and fetus are usually good, but assessment and monitoring are required, often in conjunction with an endocrinologist, and, occasionally, serious complications are encountered.

Embryonic stem (ES) cells are a primitive cell type derived from the inner cell mass (ICM) of the developing embryo. When cultured for extended periods, ES cells maintain a high telomerase activity, normal karyotype and the pluripotential developmental capacity of their ICM derivatives. Such capacity is best demonstrated by mouse ES cells which can contribute to all tissues of the developing embryo following either their injection into host blastocysts or tetraploid embryo complimentation (for a review see Robertson). For both practical and ethical reasons it is not possible to inject human ES cells into blastocysts for the development of a term fetus. However, when injected beneath the testicular capsule of severe combined immunodeficient (SCID) mice, human ES cells form teratomas comprising tissue representatives of all three embryonic germ layers (ectoderm, mesoderm and endoderm) thus attesting to their pluripotency. Based upon morphological criteria, neuronal, cardiac, bone, squamous epithelium, skeletal muscle, gut and respiratory epithelia are readily identifiable within the human ES-cell-derived teratomas. With the demonstrated capability to isolate and maintain pluripotent human ES cells in vitro, their ability to give rise to tissue representatives of all three embryonic germ layers and the technical advances made possible by research on mouse ES cells, a rapid increase in human ES cell research aimed at drug discovery and human cell and gene therapies has occurred. Indeed in the mouse, dissociated embryoid bodies (EBs) have already been demonstrated capable of repopulating the haematopoietic system of recipient animals (for a review see Keller) and mouse ES cells are currently being used in attempts to repair mouse neural degenerative lesions.