1. Regulation of Ovulation Rate.- 2. Dynamics of Follicle Development in the Human Ovary.- 3. The Molecular Basis of Ovarian Cell Death.- 4. Polycystic Ovary Syndrome (PCOS): The Possible Roles of Apoptosis in Human Granulosa Cells.- 5. Potential Role of the Renin-Angiotensin System in Polycystic Ovaries.- 6. Dysregulation of Androgen Secretion and Steroid Metabolism in Polycystic Ovary Syndrome.- 7. Adrenocortical Dysfunction in the Polycystic Ovary Syndrome.- 8. Insulin Resistance in the Polycystic Ovary Syndrome.- 9. Beta-Cell Function in Polycystic Ovary Syndrome.- 10. Luteinizing Hormone and Growth Factor Control of the Thecal Cell.- 11. Comparative Androgen Production from Theca Cells of Normal Women and Women with Polycystic Ovaries.- 12. Development of a Human Thecal Tumor Cell Model: Regulation of Steroidogenesis and Enzyme Expression.- 13. Development of Human Granulosa Cell Lines.- 14. Suppression of Aromatase Activity in Polycystic Ovary Syndrome.- 15. The Insulin-Like Growth Factor (IGF) System in Human Ovary and Its Relevance to Polycystic Ovarian Syndrome.- 16. Hyperinsulinemic Androgenism: A Pathophysiologic Paradox.- 17. Hypothalamic-Pituitary Dynamics in Polycystic Ovary Syndrome.- 18. Aspects of Ovulation Induction in Polycystic Ovary Syndrome.- 19. Polycystic Ovary Syndrome, Fertilization, and Early Embryonic Development.- 20. In Vitro Fertilization in Polycystic Ovary Syndrome.- 21. Surgical Approaches to Ovulation Induction: The Laparoscopic Experience.- 22. Androgens, Lipids, Insulin Resistance, and Cardiovascular Risk.- 23. A Unifying Concept for Polycystic Ovary Syndrome.- Author Index.
The term polycystic ovary syndrome (peOS) is meant to describe a clinical endocrinopathy characterized by menstrual irregularity and evidence of hyperandrogenism. While recognized since the 1800s, a clinical composite was not constructed until 1935 when Stein and Leventhal reported their findings of seven women with infertility, menstrual dysfunction, hirsutism, and enlarged ovaries. Notably, the ovaries contained numerous multiple cysts and the ovarian capsule was thickened. At the time, this preciseness of definition was sufficient to entitle the entity Stein-Leventhal syndrome. Subsequently, over the intervening years as investigators attempted to un ravel the pathophysiology and genesis of this disorder and the number of reported studies increased, there ensued a gradual and distinct terminologic conversion to polycystic ovary syndrome, which, whether intentional or not, connoted a less well-defined condition. Perhaps this is appropriately so, given the seemingly broadening spectrum of clinical presentations and the continuing debate over what constitutes peos. The expansive new knowledge about peos was discussed to a significant degree at an international symposium organized by Serono Symposia USA and held in Boston in the late spring of 1995. Ovarian physiology, including the fate of the follicular unit, was a central focus with several presentations on the genesis, growth, and death of ovarian cellular components. A discus sion of the regulation of ovarian cell function was also highlighted and comprised a major portion of the program.
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