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The new edition of this canonical text on male reproductive medicine will cement the book's market-leading position. Practitioners across many specialties - including urologists, gynecologists, reproductive endocrinologists, medical endocrinologists and many in internal medicine and family practice – will see men with suboptimal fertility and reproductive problems. The book provides an excellent source of timely, well-considered information for those training in this young and rapidly evolving field. While several recent books provide targeted 'cookbooks' for those in a male reproductive laboratory, or quick reference for practising generalists, the modern, comprehensive reference providing both a background for male reproductive medicine as well as clinical practice information based on that foundation has been lacking until now. The book has been extensively revised with a particular focus on modern molecular medicine. Appropriate therapeutic interventions are highlighted throughout.
Human semen is ejaculated into the anterior vagina and, within minutes, spermatozoa enter the cervix by traversing the cervical mucus. Human sperm capacitation is initiated when the male gamete traverses the cervical mucus, with the removal of inhibitory factors from the seminal plasma. Studies performed in several mammalian species have shown that sperm cells that have completed capacitation first bind to the zona pellucida (ZP) and undergo acrosomal exocytosis (AE). Acrosome-reacted spermatozoa penetrate the ZP, reach the perivitelline space, and bind and fuse to the egg plasma membrane. Sperm-ZP binding involves the interaction of ZP components with sperm surface proteins of capacitated cells, known as primary binding. The evaluation of the subfertile male should include a basic semen analysis, followed by bioassays aimed at assessing sperm functional competence. Many of the molecular mechanisms underlying mammalian sperm capacitation, AE, and fusion with the egg modulate somatic cell functions.
This chapter discusses the development of the adult population of Leydig cells from the stem cell precursor through the progenitor and immature Leydig cell stages. The morphogenetic events of early testis differentiation are controlled by the Sry (sex-determining region on the Y chromosome) gene. Lack of luteinizing hormone (LH) stimulation results in reduced steroidogenic enzyme activities and in Leydig cell atrophy. As men age, progressive decreases in serum concentrations of testosterone occur. Associated with these decreases are significant health consequences, including reduced sexual function, energy, muscle function, and bone density, and increased frailty and cognitive impairment. A number of hypotheses have been put forward over the years to explain changes that occur in aging cells, including late-onset gene expression, telomere shortening, gene modifications, changes in the immune system, and accumulated reactive oxygen-induced damage to DNA, lipids, and/or proteins.