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Sperm morphology assessed by strict criteria, along with other male-factor analyses, was reported to be a good predictor of fertilization. Strict criteria for sperm morphology have been widely accepted, their usefulness remains an issue of contention. Sperm morphology assessed by strict criteria, along with other male-factor analyses, was reported to be a good predictor of fertilization. Improved sperm morphology observed surgical correction of varicocele, is probably the result of influencing spermatogenesis. Sperm morphology tends to vary less than sperm count and sperm motility in the same male. Morphology, count, and motility may be likened to a fingerprint, except when some acute process produces a temporary change, and morphology may therefore be an indicator of the health of the germinal epithelium. In the absence of other male or female factors, a very high percentage of spermatozoa need to be abnormal before strict criteria can provide a definitive assessment of infertility.
The Sertoli cell is implicated centrally in spermatogenesis, organogenesis, male phenotypic development, and the hypothalamic-pituitary-gonadal axis. The cytoskeletal architecture of the Sertoli cell, as in many other cells, consists of actin filaments, intermediate filaments, and microtubules. The interaction of adjoining Sertoli cells with each other and with the basement membrane is crucially important to the function of the Sertoli cell: tight junctions and adherens junctions between Sertoli cells allow for the creation of an immunologically privileged space within the seminiferous tubule. This barrier, created by Sertoli cells and the basement membrane, is known as the blood-testis barrier. This chapter provides a brief discussion spermiogenesis and spermiation. Sertoli cells in adult mammals exist as a terminally differentiated, postmitotic population. Regulation of the Sertoli cell in its function as "nurse cell" for developing spermatogenic cells is obviously multifaceted and complex.
The X chromosome may be as important as the Y in determining male fertility potential. By refining the analysis of the particular recombination abnormalities in infertile men, this study confirmed that there may be decreased chromosomal pairing quality as well as recombination frequencies in men with non-obstructive azoospermia. Documentation of the normal variability in recombination is a prerequisite for the understanding of changes observed in abnormal situations, such as non-disjunction or a chromosome re-arrangement. It appears that G-group as well as sex chromosomes are most susceptible to having no recombination foci and thus are more susceptible to non-disjunction during spermatogenesis. The growing knowledge of the close relationship between germ cells and stem cells, and the successful manipulation of these cells in vitro, has tremendous implications not only for the treatment and cure of male infertility but also for a host of other medical diseases in the future.
In mammals, spermatogenesis begins with diploid stem cells that resemble other somatic cells; it ends with highly specialized motile haploid cells that are remarkably unique in appearance and function. Continuous production of spermatozoa throughout life requires that spermatogonia replenish themselves. Type B spermatogonia undergo mitosis to give rise to diploid primary spermatocytes. The spermatocytes then cross the blood-testis barrier formed by the Sertoli tight junctions to the adluminal compartment. Spermiogenesis refers to the acquisition by the germ cell of several organelles and accessory structures such as the acrosome and the flagellum. Testosterone and follicle-stimulating hormone (FSH) are the two major regulatory hormones of spermatogenesis. FSH binding to its receptor activates adenylate cyclase, and the resultant rise in cAMP triggers binding of cAMP response element modulator (CREM) to ACT (activator of CREM). The complex then acts as a molecular master-switch for a number of genes involved in spermatogenesis.
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