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The main functions of the male reproductive system are the synthesis and secretion of male sex steroids (androgens), production of male gametes (spermatozoa), and transport of sperm into the female genital tract. The development, maturation, and normal function of male fertility are mainly under the control of the hypothalamic-pituitary-testicular axis, which constitutes the hormonal component of an interplaying and intercommunicating neuronal and endocrine system, that will be explained in this chapter.
In this review we reflect on the many attempts highlighting key achievements in the field of in vitro spermatogenesis made so far. The research in this field is at a crucial juncture. The evolving technologies (like biofabricated 3D organoids, 3D bioprinting, microfluidics, or organ-on-a-chip) may offer excellent tools and in vitro testicular model systems to advance our understanding and bridge the existing knowledge gaps. Each of these culture systems offers unique advantages and may complement each other to address the common goal of achieving primate spermatogenesis in vitro. There are various possibilities and future scenarios for applying in vitro spermatogenesis as a tool for research and clinical applications in the future.
This chapter introduces medical students, residents, fellows, and practicing urologists to surgical syndromes that can affect a man's reproductive potential. The most widely accepted theory of how varicocele affects testicular function is that of elevated testicular temperature. When obstructive azoospermia is present, sperm production by the testis remains normal and often epididymal tubules become quite dilated. The yield of sperm from the epididymis is logarithmically higher than the yield of sperm from the testis. The anatomy of the male reproductive tract is such that sperm exit the testes, travel through the epididymis, and enter the vas deferens. The vas deferens travels into the inguinal canal with the spermatic cord and then dives posteromedially to fuse with the seminal vesicles at the ampulla of the vas deferens. Any serious medical illness or surgery can result in impaired testicular function and disruption of normal ejaculatory function.
This chapter discusses the current knowledge of hormonal suppression as a means to preserve or restore fertility in males. The seminiferous tubules contain the germ cells, which consist of stem and differentiating spermatogonia, spermatocytes, spermatids and sperm and the sertoli cells, which support and regulate germ cell differentiation. The eventual recovery of sperm production depends on the survival of the spermatogonial stem cells and their ability to differentiate after exposure to cytotoxic agents. Several studies support the conclusion that gonadotropin suppression does not protect spermatogenesis in mice from damage. Seven clinical trials have been performed in attempts to demonstrate protection of spermatogenesis in humans by hormone suppression treatment before and during cytotoxic therapy, but six indicated no protection. One contribution to the difference in the stimulation of recovery by hormone suppression after cytotoxic treatment may be the interspecies differences in the block in differentiation of spermatogonia.
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