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Xinwang Chen, Xiao Jia, Jie Qiao, Youfei Guan and Jihong Kang

Introduction Polycystic ovary syndrome (PCOS) is one of the most common causes of female infertility, which affects 5–10% of women of reproductive age. It is a heterogeneous syndrome with the characteristics of hirsutism, acne, anovulation

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Muraly Puttabyatappa and Vasantha Padmanabhan

Excess and the Polycystic Ovary Syndrome Society (AE-PCOS) is a threshold setting of >25 follicles, when scanned with transducer frequency ≥8 MHz ( Dewailly et al. 2014 ). Most studies addressing follicular number and distribution have involved single

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L J Moran, P A Mundra, H J Teede and P J Meikle

Introduction Polycystic ovary syndrome (PCOS) is the most common cause of anovulatory infertility in reproductive-aged women affecting 12–18% of women ( March et al . 2010 ). It is a reproductive, metabolic and psychological condition

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FY Diao, M Xu, Y Hu, J Li, Z Xu, M Lin, L Wang, Y Zhou, Z Zhou, J Liu and J Sha

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders; it is characterized by polycystic ovaries, hyperandrogenism and chronic anovulation. To obtain a global view of those genes that might be involved in the development of this complex clinical disorder, we used recently developed cDNA microarray technology to compare differential gene expressions between normal human ovary and ovaries from PCOS patients. A total of 9216 clones randomly selected from a commercial human ovary cDNA library were screened. Among them, 290 clones showed differential expressions, including 119 known genes and 100 known or unknown expressed sequence tags (ESTs). Among 119 known genes, 88 were upregulated and 31 downregulated in the PCOS ovary, as compared with normal human ovary. These differentially expressed genes are involved in various biologic functions, such as cell division/apoptosis, regulation of gene expression and metabolism, reflecting the complexity of clinical manifestations of PCOS. The molecular characteristics established from our study will further our understanding of the pathogenesis of PCOS and help us to identify new targets for further studies and for the development of new therapeutic interventions.

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Xiaoxia Che, Fangfang Jian, Chen Chen, Chang Liu, Gedan Liu and Weiwei Feng

Introduction Polycystic ovary syndrome (PCOS), characterized by oligo/anovulation, hyperandrogenism and polycystic-appearing ovaries, is the most common endocrine disorder among reproductive-age women. Complex interrelationships between

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W Arlt, P Neogi, C Gross and WL Miller

Thiazolidinediones improve insulin sensitivity in type 2 diabetes mellitus by acting as peroxisome proliferator-associated receptor gamma (PPARgamma) agonists, and decrease circulating androgen concentrations in polycystic ovary syndrome by unknown mechanisms. Some thiazolidinediones directly inhibit the steroidogenic enzymes P450c17 and 3beta-hydroxysteroid dehydrogenase type II (3betaHSDII) by distinct mechanisms. We synthesized five novel thiazolidinediones, CLX-M1 to -M5 by linking a 2,4-thiazolidinedione moiety to a substituted alpha-phenyl cinnamic acid previously shown to have glucose-lowering effects. Using yeast microsomes expressing human P450c17 and 3betaHSDII we found that cinnamic acid methyl esters with a double bond in the thiazolidinedione core structure (M3, M5) were stronger inhibitors of P450c17 than methyl esters with the conventional core (M1, M4). These four compounds inhibited 3betaHSDII equally well, while the free cinnamic acid analog (M2) did not inhibit either enzyme. Thus, the inhibition of P450c17 and 3betaHSDII by these novel thiazolidinediones reveals structure-activity relationships independent of PPARgamma transactivation. PPARgamma transactivation was moderate (M1), weak (M2, M3) or even absent (M4, M5). While the PPARgamma agonist activity of M1 was only 3% of that of rosiglitazone, both increased glucose uptake by 3T3-L1 adipocytes and reduced serum glucose levels in ob/ob and db/db mice to a similar extent. The similar glucose-lowering effects of M1 and rosiglitazone, despite their vast differences in PPARgamma agonist activity, suggests these two actions may occur by separate mechanisms.

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Jessica K Devin, Joyce E Johnson, Mesut Eren, Linda A Gleaves, William S Bradham, John R Bloodworth Jr and Douglas E Vaughan

with polycystic ovary syndrome. Journal of Clinical Endocrinology and Metabolism 90 1929 –1935. Atiomo WU , Bates SA, Condon JE, Shaw S, West JH & Prentice AG 1998 The plasminogen activator system in women with

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Salman Azhar, Dachuan Dong, Wen-Jun Shen, Zhigang Hu and Fredric B Kraemer

polycystic ovary syndrome (PCOS) also leads to infertility. Testis  Leydig Cells LH Testosterone Testosterone is synthesized in men by the testicular Leydig cells and in women either directly by the adrenals and ovaries, or by

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J M Young and A S McNeilly

rates of follicle activation and lead to premature loss of primordial follicles. In polycystic ovary syndrome (PCOS), follicle development is stalled, and a major characteristic is the presence of excess androgens that are produced by an intrinsic

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Robin Haring, Henri Wallaschofski, Alexander Teumer, Heyo Kroemer, Angela E Taylor, Cedric H L Shackleton, Matthias Nauck, Uwe Völker, Georg Homuth and Wiebke Arlt

serum adrenal hormones among African-American men ( Wilborn et al . 2006 ), Finnish prepubertal children ( Utriainen et al . 2012 ), or white women with polycystic ovary syndrome (PCOS; Goodarzi et al . 2007 ). The latter study found only one