The Promising Biomarker for Multiple Clinical Situations 2 1 596 2 Biomarkers have achieved broad logical and clinical attention in diverse disciplines such as screening, diagnosis, prognosis, recurrence prediction and therapeutic monitoring of diseases in modern medicine. Due to lack of direct access to the function of reproductive organs and their malfunction especially in women, most of data are received through application of sensitive and specific biomarkers. These biomarkers have been developed and validated over time. An ideal and specific biomarker should be non-invasive, easy to detect, inexpensive with acceptable precision and reliability and able to detect early onset of changes in associated organ. Anti-mullerian hormone (AMH), also known as mullerian inhibiting substance (MIS) is a biomarker indicative of above features. AMH, discovered in 1947 by Alfred Jost, is a dimeric glycoprotein member of TGF-β superfamily. It is known for its primary role in Mullerian duct regression in embryonic genital tract. Sertoli cells and granulosa cells are the main sources of AMH production in male and female gonads, respectively. The AMH secretion starts from 36 weeks of pregnancy in preantral and early antral follicles smaller than 4 mm. It reaches peak levels after puberty and steadily decreases until menopause. Development of antral follicles leads to the decrease in AMH and finally stops its secretion in follicles larger than 8 mm and atretic follicles. AMH levels are stable during the menstrual cycle. However, its level declines during pregnancy due to placental inhibition of ovaries and increases rapidly after delivery (1). It is well known that AMH is a key factor in regulation of ovarian function during folliculogenesis and oocyte maturation. The beginning of the development of primordial follicles and sensitivity of granulosa cells to FSH are regulated through AMH. The outcome of its activity on follicles leads to drive a large number of developing follicles to atresia process and finally selection of a graafian follicle in each cycle (1). Regarding the role of AMH in folliculogenesis and ovarian function, at present, it is applied as an excellent biomarker for assessing a broad range of physiologic and pathologic conditions of female fertility. AMH is a candidate biomarker for PCOS diagnosis. Impaired oocyte maturation in these patients leads to accumulation of large number of pre-antral and small antral follicles that subsequently raise serum levels of AMH. Increased level of AMH in PCOS has strong correlation with the Rotterdam diagnostic criteria. Serum AMH may be used as a marker to identify candidates of PCOS and normal ovulatory women for in vitro maturation program (2). The serum AMH level has a close correlation with oocyte and embryo quality and blastocyst formation rate in IVF/ICSI cycles; however, live birth rate and clinical pregnancy rate have only correlation with AMH concentration in follicular fluid. Serum level of AMH is a valuable marker for prediction of oocytes number retrieved after stimulation cycles in aged women. The cut-off of 1.0 ng/ml can be used to predict poor responder patients. This cut-off level can be useful to predict the probability of embryo transfer, without predictive value for clinical pregnancy. Receiver operating characteristic (ROC) analyses showed that different cut-off for serum levels of AMH are good predictors of oocytes numbers retrieved in controlled ovarian stimulation cycles (3). Serum AMH is a sensitive biomarker for monitoring cancer chemotherapy and gonadotoxic treatment on ovarian follicular reserve of young women. It is a good indicator for comparison and determination of gonadotoxicity in different chemotherapy regimens (4). AMH is also proposed as a therapeutic agent for endometriosis. AMH is expressed in normal endometrium and suggested to negatively regulate cellular viability via paracrine function. Recent data indicates that AMH will be the frontline hormone for treatment of endometriosis in future; therefore, it will reduce high recurrence rates of current surgical and medical treatments strategies (5). However, several other new clinical applications are suggested for AMH such as a tumor marker of granulosa cell tumor, diagnosis of precocious puberty, delayed onset of puberty, anorchidism, intersex disorders and control of spermatogenesis (1). Therefore, AMH is the most excellent marker of ovarian reserve in different clinical conditions (especially infertility), in prediction of reproductive lifespan, ovarian dysfunction (PCOS) and ovarian damages of cancer therapy or surgical treatment. Despite the above benefits, AMH measurement has broad variation in different storage and handling conditions. Therefore, improved assay validity and standardization, reference preparation and compatibility with international guideline for laboratories are critical tasks to maximize the clinical utility of this promising biomarker in future. 121 122 Mohammad Reza MR Sadeghi محمدرضا صادقی Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR Iran sadeghi@avicenna.ac.ir No Keyword 596.pdf Broer SL, Broekmans FJ, Laven JS, Fauser BC. Anti-Mullerian hormone: ovarian reserve testing and its potential clinical implications. Hum Reprod Update. 2014 May 12. [Epub ahead of print]##Sahmay S, Aydin Y, Oncul M, Senturk LM. Diagnosis of Polycystic Ovary Syndrome: AMH in combination with clinical symptoms. J Assist Reprod Genet. 2014;31(2):213-20.##Lin WQ, Yao LN, Zhang DX, Zhang W, Yang XJ, Yu R. The predictive value of anti-Mullerian hormone on embryo quality, blastocyst development, and pregnancy rate following in vitro fertilization-embryo transfer (IVF-ET). J Assist Reprod Genet. 2013;30(5):649-55.##Peigne M, Decanter C. Serum AMH level as a marker of acute and long-term effects of chemotherapy on the ovarian follicular content: a systematic review. Reprod Biol Endocrinol. 2014;12:26.##Signorile PG, Petraglia F, Baldi A. Anti-mullerian hormone is expressed by endometriosis tissues and induces cell cycle arrest and apoptosis in endometriosis cells. J Exp Clin Cancer Res. 2014;33:46.##

Role of Postnatal Expression of Fgfr1 and Fgfr2 in Testicular Germ Cells on Spermatogenesis and Fertility in Mice 2 1 586 2 Background: Fibroblast growth factor (FGF) signaling is thought to play diverse roles in the male reproductive system. However, its role in testicular cells for spermatogenesis and fertility remains unclear. Methods: In this study, the expression and localization of Fgfr 1 (FGF Receptor) and Fgfr 2 in the postnatal mouse testes were examined by RT-PCR, Western blotting and immunohistochemistry. The in vivo function of each receptor in testicular germ cells was determined using germ cell-specific Fgfr mutant animals, Tex101-iCre;Fgfr flox/flox and Tex101-iCre;Fgfrflox/flox mice. The results were analyzed by Kruskal-Wallis test and Dunn's Post-test. Results: Both Fgfr1 and Fgfr2 were expressed in the testis throughout the entire postnatal development. Prominent immunostaining of these FGFRs was observed in interstitial and peritubular cells with little or no changes in all phases during postnatal development. Positive staining of these receptors was also detected in germ cells including elongated spermatids and spermatozoa. Germ cell-specific Fgfr1 or Fgfr2 mutant mice were viable with no developmental abnormalities in the testes and accessory sex organs. Fertility studies showed that the fecundity of both mutant mouse lines did not significantly differ from wild-type siblings (n=4, p>0.05). Further analysis indicated the presence of other Fgfrs in testicular germ cells including Fgfr 3, 4 and 5. Conclusion: The results demonstrated that Fgfr1 and 2 are expressed in all testicular cell types and that neither Fgfr1 nor Fgfr2 in testicular germ cells is essential for spermatogenesis and fertility. Future studies are needed to investigate the potential functional redundancy among five Fgfrs in male germ cells for spermatogenesis and fertility. 122 134 Shengqiang Sh Li Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine USA Zi-jian Z Lan Division of Life Sciences, Alltech Division of Life Sciences, Alltech USA Xian X Li Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine USA Jing J Lin Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine USA Zhenmin Zh Lei Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine Department of Obstetrics/Gynecology and Women’s Health, University of Louisville, School of Medicine USA zhenmin.lei@louisville.edu Conditional gene knockoutFertilityFGFFgfrSpermatogenesisTestis 586.pdf Cotton LM, O'Bryan MK, Hinton BT. 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Biol Reprod. 2003;68(6):2314-21.##Hirai K, Sasaki H, Yamamoto H, Sakamoto H, Kubota Y, Kakizoe T, et al. HST-1/FGF-4 protects male germ cells from apoptosis under heat-stress condition. Exp Cell Res. 2004;294(1):77-85.##El Ramy R, Verot A, Mazaud S, Odet F, Magre S, Le Magueresse-Battistoni B. Fibroblast growth factor (FGF) 2 and FGF9 mediate mesenchymal epithelial interactions of peritubular and Sertoli cells in the rat testis. J Endocrinol. 2005;187(1):135-47.##Abd-Elmaksoud A, Sinowatz F. Expression and localization of growth factors and their receptors in the mammalian testis. Part I: Fibroblast growth factors and insulin-like growth factors. Anat Histol Embryol. 2005;34(5):319-34.##Kim Y, Bingham N, Sekido R, Parker KL, Lovell-Badge R, Capel B. Fibroblast growth factor receptor 2 regulates proliferation and Sertoli differentiation during male sex determination. Proc Natl Acad Sci U S A. 2007;104(42):16558-63.##Han IS, Sylvester SR, Kim KH, Schelling ME, Venkateswaran S, Blanckaert VD, et al. Basic fibroblast growth factor is a testicular germ cell product which may regulate Sertoli cell function. Mol Endocrinol. 1993;7(7):889-97.##Deng CX, Wynshaw-Boris A, Shen MM, Daugherty C, Ornitz DM, Leder P. Murine FGFR-1 is required for early postimplantation growth and axial organization. Genes Dev. 1994;8(24):3045-57.##Arman E, Haffner-Krausz R, Chen Y, Heath JK, Lonai P. Targeted disruption of fibroblast growth factor (FGF) receptor 2 suggests a role for FGF signaling in pregastrulation mammalian development. Proc Natl Acad Sci U S A. 1998;95(9):5082-7.##Deng C, Wynshaw-Boris A, Zhou F, Kuo A, Leder P. Fibroblast growth factor receptor 3 is a negative regulator of bone growth. Cell. 1996;84(6):911-21.##Weinstein M, Xu X, Ohyama K, Deng CX. FGFR-3 and FGFR-4 function cooperatively to direct alveogenesis in the murine lung. Development. 1998;125(18):3615-23.##Yu C, Wang F, Kan M, Jin C, Jones RB, Weinstein M, et al. Elevated cholesterol metabolism and bile acid synthesis in mice lacking membrane tyrosine kinase receptor FGFR4. J Biol Chem. 2000;275(20):15482-9.##Trokovic N, Trokovic R, Mai P, Partanen J. Fgfr1 regulates patterning of the pharyngeal region. Genes Dev. 2003;17(1):141-53.##Trokovic R, Trokovic N, Hernesniemi S, Pirvola U, Vogt Weisenhorn DM, Rossant J, et al. FGFR1 is independently required in both developing mid- and hindbrain for sustained response to isthmic signals. EMBO J. 2003;22(8):1811-23.##Yu K, Xu J, Liu Z, Sosic D, Shao J, Olson EN, et al. Conditional inactivation of FGF receptor 2 reveals an essential role for FGF signaling in the regulation of osteoblast function and bone growth. Development. 2003;130(13):3063-74.##Blak AA, Naserke T, Saarimäki-Vire J, Peltopuro P, Giraldo-Velasquez M, Vogt Weisenhorn DM, et al. 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The Protective Effect of Vitamin E on Morphological and Biochemical Alteration Induced by Pre and Postnatal Ethanol Administration in the Testis of Male Rat Offspring: A Three Months Follow-up Study 2 1 587 2 Background: Dysmorphology and dysfunction caused by prenatal ethanol consumption in different organs of the offspring are wellknown phenomena. The objective of the present study was to explore the antioxidant effect of vitamin E supplementation on testis damage induced by maternal ethanol consumption during pregnancy and early postnatal days. Methods: Pregnant Wistar rats on gestation day 7 were assigned to 3 groups, namely, control, ethanol and ethanol-vitamin E groups. Ethanol-treated rats received 4.5 g/kg BW ethanol once per day from day 7 and the procedure continued through postnatal day 21. Vitamin E group received 300 mg of vitamin E and the same amount of ethanol. The male offspring from each group were anesthetized by 10% chloral hydrate (0.5 ml/kg body weight) on day 21 and 90 (n=8 offspring form each group on day 21 and day 90). The results were analyzed by one-way ANOVA. A p<0.05 was considered significant. Results: The results revealed significant (p<0.05) changes in oxidative stress parameters, luteinizing hormone and follicle-stimulating hormone, as well as testis structural alteration in offspring of ethanol group after 21 and 90 days of birth as compared to the control. Significant amelioration of changes in testis structure, along with restoration of the elevated level of oxidative stress parameters were found in vitamin E-treated animals. Conclusion: The findings revealed that prenatal and postnatal ethanol-induced toxicity in testis was exerted through oxidative stress and implied that these effects could be alleviated by vitamin E as an antioxidant. 134 142 Alireza AR Shirpoor Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences Iran ashirpoor@yahoo.com Leila L Norouzi Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences Iran Mohammad-Hasan MH Khadem-Ansari Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences Iran Behrouz B Ilkhanizadeh Department of Pathology, Faculty of Medicine, Urmia University of Medical Sciences Department of Pathology, Faculty of Medicine, Urmia University of Medical Sciences Iran Mojtaba M Karimipour Department of Anatomy, Faculty of Medicine, Urmia University of Medical Sciences Department of Anatomy, Faculty of Medicine, Urmia University of Medical Sciences Iran EthanolOxidative stressRatTestisVitamin E 587.pdf Barr HM, Streissguth AP. Identifying maternal self-reported alcohol use associated with fetal alcohol spectrum disorders. Alcohol Clin Exp Res. 2001;25(2):283-7.##Olson HC, Morse BA, Huffine C. Development and Psychopathology: Fetal Alcohol Syndrome and Related Conditions. Semin Clin Neuropsychiatry. 1998;3(4):262-84.##Roebuck TM, Mattson SN, Riley EP. A review of the neuroanatomical findings in children with fetal alcohol syndrome or prenatal exposure to alcohol. Alcohol Clin Exp Res. 1998;22(2):339-44.##Estrada G, Krasinski SD, Rings EH, Buller HA, Grand RJ, Lopez-Tejero MD. Prenatal ethanol exposure alters the expression of intestinal hydrolase mRNAs in newborn rats. Alcohol Clin Exp Res. 1996;20(9):1662-8.##Turcotte LA, Aberle NS, Norby FL, Wang GJ, Ren J. Influence of prenatal ethanol exposure on vascular contractile response in rat thoracic aorta. Alcohol. 2002;26(2):75-81.##Blanchard BA, Hannigan JH. Prenatal ethanol exposure: effects on androgen and nonandrogen dependent behaviors and on gonadal development in male rats. Neurotoxicol Teratol. 1994;16(1):31-9.##Dahlgren IL, Eriksson CJ, Gustafsson B, Harthon C, Hard E, Larsson K. Effects of chronic and acute ethanol treatment during prenatal and early postnatal ages on testosterone levels and sexual behaviors in rats. Pharmacol Biochem Behav. 1989;33(4):867-73.##Hard E, Dahlgren IL, Engel J, Larsson K, Liljequist S, Lindh AS, Musi B. Development of sexual behavior in prenatally ethanol-exposed rats. Drug Alcohol Depend. 1984;14(1):51-61.##Anderson RA Jr, Willis BR, Phillips JF, Oswald C, Zaneveld LJ. Delayed pubertal development of the male reproductive tract associated with chronic ethanol ingestion. Biochem Pharmacol. 1987;36(13):2157-67.##Fermoso J, Esquifino AI, Mateos A, Agrasal C, Martin I. Possible role of prolactin in the induction of hypogonadism by chronic alcohol treatment in the male rat. 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The Effects of Nitric Oxide Donors on Uterine Artery and Sub-endometrial Blood Flow in Patients with Unexplained Recurrent Abortion 2 1 588 2 Background: Nitric oxide plays a major role in increasing uterine blood flow during the luteal phase and early pregnancy. This study was done to compare uterine artery and sub-endometrial blood flow indices during the luteal phase between patients with unexplained recurrent abortion and fertile women and also to evaluate the effects of nitric oxide donors on blood flow indices in the abortion group. Methods: The study included a control group of 30 primiparae who had normal vaginal delivery and no history of abortion and an abortion group of 30 nulliparous women with history of two or more unexplained recurrent abortions. Transvaginal three-dimensional pulsed color Doppler ultrasound was done on days 21-23 of the cycle to measure uterine artery resistance and pulsation indices and the subendometrial vascular, flow and vascular-flow indices. Isosorbide mononitrate 20 mg tablet was administered vaginally in the abortion group and blood flow indices were measured again after two hours. The Student t-test and the paired t-test were used for analysis of results and a p-value of ≤0.05 was considered significant. Results: Patients with unexplained recurrent abortion had significantly higher uterine artery resistance and pulsation indices and lower sub-endometrial vascular, flow and vascular-flow index (p<0.01-0.0001). Isosorbide mononitrite significantly decreased uterine artery and increased sub-endometrial blood flow indices (p<0.001). Conclusion: Uterine artery and sub-endometrial blood flow decreased during the luteal phase in patients with unexplained recurrent abortion. Nitric oxide donors increased blood flow and may be of a therapeutic value. 142 147 Mohamed M Abdel-Razik Department of Obstetrics and Gynecology, Benha Faculty of Medicine, Benha Department of Obstetrics and Gynecology, Benha Faculty of Medicine, Benha Egypt mohamedabdelrazik@hotmail.com Seham S El-Berry Department of Obstetrics and Gynecology, Benha Faculty of Medicine, Benha Department of Obstetrics and Gynecology, Benha Faculty of Medicine, Benha Egypt Ahmed A Mostafa Department of Obstetrics and Gynecology, Benha Faculty of Medicine, Benha Department of Obstetrics and Gynecology, Benha Faculty of Medicine, Benha Egypt AbortionHabitualNitric oxide donors 588.pdf Jauniaux E, Farquharson RG, Christiansen OB, Exalto N. Evidence-based guidelines for the investigation and medical treatment of recurrent miscarriage. Hum Reprod. 2006;21(9):2216-22.##Practice Committee of the American Society for Reproductive Medicine. Definitions of infertility and recurrent pregnancy loss. 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Reprod Domest Anim. 2009;44 Suppl 2:174-81.##Alexander BT, Llinas MT, Kruckeberg WC, Granger JP. L-arginine attenuates hypertension in pregnant rats with reduced uterine perfusion pressure. Hypertension. 2004;43(4):832-6.##Valdes G, Kaufmann P, Corthorn J, Erices R, Brosnihan KB, Joyner-Grantham J. Vasodilator factors in the systemic and local adaptations to pregnancy. Reprod Biol Endocrinol. 2009;7:79.##El-Far M, El-Motwally Ael-G, Hashem IA, Bakry N. Biochemical role of intravaginal sildenafil citrate as a novel antiabortive agent in unexplained recurrent spontaneous miscarriage: first clinical study of four case reports from Egypt. Clin Chem Lab Med. 2009;47(11):1433-8.##Amin AF, Shaaban OM, Bediawy MA. N-acetyl cysteine for treatment of recurrent unexplained pregnancy loss. Reprod Biomed Online. 2008;17(5):722-6.##Amit A, Thaler I, Paz Y, Itskovitz-Eldor J. The effect of a nitric oxide donor on Doppler flow velocity waveforms in the uterine artery during the first trimester of pregnancy. Ultrasound Obstet Gynecol. 1998;11(2):94-8.##Jirous J, Diejomaoh ME, Al-Abdulhadi F, Boland MH, Nazar M. A comparison of the uterine and intraovarian arterial flows in nonpregnant women having a history of recurrent spontaneous miscarriage associated with antiphospholipid syndrome. Arch Gynecol Obstet. 2004;270(2):74-8.##Habara T, Nakatsuka M, Konishi H, Asagiri K, Noguchi S, Kudo T. Elevated blood flow resistance in uterine arteries of women with unexplained recurrent pregnancy loss. Hum Reprod. 2002;17(1):190-4.##Ferreira AM, Pires CR, Moron AF, Araujo Júnior E, Traina E, Mattar R. Doppler assessment of uterine blood flow in recurrent pregnancy loss. Int J Gynaecol Obstet. 2007;98(2):115-9.##Vaquero E, Lazzarine N, Exacoustos C, Romanini E, Bertonotti E. Recurrent miscarriage: three dimentional power Doppler evaluation of endometrial and subendometrial volume and vascularity and correlation to uterine arteries blood flow. Ultrasound Obstet Gynecol. 2008;32:262-6.##Ng EH, Chan CC, Tang OS, Yeung WS, Ho PC. Endometrial and subendometrial vascularity is higher in pregnant patients with livebirth following ART than in those who suffer a miscarriage. Hum Reprod. 2007;22(4):1134-41.##Zaidi J, Campbell S, Pittrof R, Tan SL. Endometrial thickness, morphology, vascular penetration and velocimetry in predicting implantation in an in vitro fertilization program. Ultrasound Obstet Gynecol. 1995;6(3):191-8.##Chien LW, Au HK, Chen PL, Xiao J, Tzeng CR. Assessment of uterine receptivity by the endometrial-subendometrial blood flow distribution pattern in women undergoing in vitro fertilization-embryo transfer. Fertil Steril. 2002;78(2):245-51.##El-mashad AI, Mohamed MA, Farag MA, Ahmad MK, Ismail Y. Role of uterine artery Doppler velocimetry indices and plasma adrenomedullin level in women with unexplained recurrent pregnancy loss. J Obstet Gynaecol Res. 2011;37(1):51-7.##Yildiz G, Yavuzcan A, Yildiz P, Goynumer G, Yucel N. Effect of uterine artery blood flow on recurrent pregnancy loss. Clin Exp Obstet Gynecol. 2012;39(3):326-9.##Hale SA, Jones CW, Osol G, Schonberg A, Badger GJ, Bernstein IM. Sildenafil increases uterine blood flow in nonpregnant nulliparous women. Reprod Sci. 2010;17(4):358-65.##Kublickiene KR, Nisell H, Poston L, Kruger K, Lindblom B. Modulation of vascular tone by nitric oxide and endothelin 1 in myometrial resistance arteries from pregnant women at term. Am J Obstet Gynecol. 2000;182(1 Pt 1):87-93.##Storment JM, Meyer M, Osol G. Estrogen augments the vasodilatory effects of vascular endothelial growth factor in the uterine circulation of the rat. Am J Obstet Gynecol. 2000;183(2):449-53.##Moncada S. The 1991 Ulf von Euler Lecture. The L-arginine: nitric oxide pathway. Acta Physiol Scand. 1992;145(3):201-27.##Albina JE, Cui S, Mateo RB, Reichner JS. Nitric oxide-mediated apoptosis in murine peritoneal macrophages. J Immunol. 1993;150(11):5080-5.##Longo M, Jain V, Vedernikov YP, Saade GR, Goodrum L, Facchinetti F, et al. Effect of nitric oxide and carbon monoxide on uterine contractility during human and rat pregnancy. Am J Obstet Gynecol. 1999;181(4):981-8.##

The Effect of Progesterone Suppositories on Threatened Abortion: A Randomized Clinical Trial 2 1 589 2 Background: Threatened abortion is a common complication of pregnancy. In order to prevent miscarriage in the cases with threatened abortion, this study was conducted to determine whether progesterone suppository is effective in allowing pregnancy to proceed beyond week 20 in women with threatened abortion. Methods: This single-blind clinical trial study was done on 60 pregnant women with threatened abortion. Pregnant women, who had vaginal bleeding until 20 weeks of their pregnancy, were assessed for inclusion. Participants were divided into two groups by random allocation; the control group, which did not undergo any treatment and the case group. The case group was given 400 mg of vaginal progesterone suppository (Cyclogest) each day until their bleeding stopped in less than one week. Participants were followed up until the end of their pregnancy. The treatment was considered successful if pregnancy continued beyond 20 weeks of gestation. Qualitative and quantitative variables were analyzed statistically by Chi Square and T- test respectively. The p-values of less than 0.05 were considered significant. Results: There was no statistically significant difference between the case and the control groups in terms of background variables. The number of abortions in the case group (6 cases, 20%) was lower than the control group which had 10 abortions (33.3%). Conclusion: The study demonstrated that the rate of abortion was reduced in women treated with progesterone suppositories. However, the difference was not statistically significant. 147 152 Fakhrolmolouk F Yassaee Fakhrolmolouk Yassaee Genomic Research Center, Taleghani Hospital, Shahid Beheshti University of Medical Sciences Genomic Research Center, Taleghani Hospital, Shahid Beheshti University of Medical Sciences Iran Reza R Shekarriz-Foumani Community Medicine Department, Faculty of Medicine, Shahid Beheshti University of Medical Sciences Community Medicine Department, Faculty of Medicine, Shahid Beheshti University of Medical Sciences Iran Shabnam Sh Afsari Infertility and Reproductive Health Research center, Taleghani Hospital, Department of Obstetrics and Gynecology, Shahid Beheshti University of Medical Sciences Infertility and Reproductive Health Research center, Taleghani Hospital, Department of Obstetrics and Gynecology, Shahid Beheshti University of Medical Sciences Iran Masoumeh M Fallahian معصومه فلاحیان Infertility and Reproductive Health Research center, Taleghani Hospital, Department of Obstetrics and Gynecology, Shahid Beheshti University of Medical Sciences Infertility and Reproductive Health Research center, Taleghani Hospital, Department of Obstetrics and Gynecology, Shahid Beheshti University of Medical Sciences Iran M_fallahian@yahoo.com Progesterone suppositoryThreatened abortion 589.pdf Lok IH, Neugebauer R. Psychological morbidity following miscarriage. Best Pract Res Clin Obstet Gynaecol. 2007;21(2):229-47.##Siriwachirachai T, Piriyasupong T. Effect of Dydro-gesterone on Treatment of Threatened Miscarriage: A Systematic Review and Meta-Analyses. Thai J Obstet Gynaecol. 2011;19:97-104.##Pandian RU. Dydrogesterone in threatened miscarriage: a Malaysian experience. Maturitas. 2009;65 Suppl 1:S47-50.##Weiss JL, Malone FD, Vidaver J, Ball RH, Nyberg DA, Comstock CH, et al. Threatened abortion: A risk factor for poor pregnancy outcome, a population-based screening study. Am J Obstet Gynecol. 2004;190(3):745-50.##Qureshi NS. Treatment options for threatened miscarriage. Maturitas. 2009;65 Suppl 1:S35-41.##Daya S. Luteal support: progestogens for pregnancy protection. Maturitas. 2009;65 Suppl 1:S29-34.##Duan L, Yan D, Zeng W, Yang X, Wei Q. Effect of progesterone treatment due to threatened abortion in early pregnan-cy for obstetric and perinatal outcomes. Early Hum Dev. 2010;86(1):41-3.##Palagiano A, Bulletti C, Pace MC, DE Ziegler D, Cicinelli E, Izzo A. Effects of vaginal progesterone on pain and uterine contractility in patients with threatened abortion before twelve weeks of pregnancy. Ann N Y Acad Sci. 2004;1034:200-10.##Sotiriadis A, Papatheodorou S, Makrydimas G. Threatened miscarriage: evaluation and management. BMJ. 2004;329(7458):152-5.##Tien JC, Tan TY. Non-surgical interventions for threatened and recurrent miscarriages. Singapore Med J. 2007;48(12):1074-90.##Yassaee F, Mostafaee L. The role of cervical cerclage in pregnancy outcome in women with uterine anomaly. J Reprod Infertil. 2011;12(4):277-9.##Kalinka J, Szekeres-Bartho J. The impact of dydro-gesterone supplementation on hormonal profile and progesterone-induced blocking factor concentrations in women with threatened abortion. Am J Reprod Immunol. 2005;53(4):166-71.##Potdar N, Konje JC. The endocrinological basis of recurrent miscarriages. Curr Opin Obstet Gynecol. 2005;17(4):424-8.##Miranda S, Litwin S, Barrientos G, Szereday L, Chuluyan E, Bartho JS, et al. Dendritic cells therapy confers a protective microenvironment in murine pregnancy. Scand J Immunol. 2006;64(5):493-9.##Wahabi HA, Abed Althagafi NF, Elawad M. Pro-gestogen for treating threatened miscarriage. Cochrane Database Syst Rev. 2007;(3):CD005943.##El-Zibdeh MY, Yousef LT. Dydrogesterone support in threatened miscarriage. Maturitas. 2009;65 Suppl 1:S43-6.##Ahmed SR, El-Sammani Mel-K, Al-Sheeha MA, Aitallah AS, Jabin Khan F, Ahmed SR. Pregnancy outcome in women with threatened miscarriage: a year study. Mater Sociomed. 2012;24(1):26-8.##Tita AT, Rouse DJ. Progesterone for preterm birth prevention: an evolving intervention. Am J Obstet Gynecol. 2009;200(3):219-24.##Rai P, Rajaram S, Goel N, Ayalur Gopalakrishnan R, Agarwal R, Mehta S. Oral micronized progesterone for prevention of preterm birth. Int J Gynaecol Obstet. 2009;104(1):40-3.##Hansen PJ. Regulation of uterine immune function by progesterone--lessons from the sheep. J Reprod Immunol. 1998;40(1):63-79.##Omar MH, Mashita MK, Lim PS, Jamil MA. Dy- drogesterone in threatened abortion: pregnancy outcome. J Steroid Biochem Mol Biol. 2005;97 (5):421-5.##Raghupathy R, Al-Mutawa E, Al-Azemi M, Makh-seed M, Azizieh F, Szekeres-Bartho J. Progesterone-induced blocking factor (PIBF) modulates cytokine production by lymphocytes from women with recurrent miscarriage or preterm delivery. J Reprod Immunol. 2009;80(1-2):91-9.##

The Use of Single Versus Double Dose of Intra-vaginal Prostaglandin E2 "Misoprostol" prior to Abdominal Myomectomy: A Randomized Controlled Clinical Trial 2 1 590 2 Background: The study aimed to investigate the effectiveness of a single versus double dose of prostaglandin E2 "misoprostol, 400 microgram" prior to myomectomy for multiple uterine fibroids. Methods: This was a prospective randomized controlled trial comprised of 69 patients with multiple myomas undergoing myomectomy. Patients received either an intra-vaginal single dose of 400 microgram misoprostol 1 hr pre-operatively (group A, 34 cases) or 2 doses, 3 and 1 hr prior to surgery (group B, 35 cases). Operation time, intra and post-operative blood loss, hemoglobin concentration, blood pressure and body's temperature were estimated and compared in both groups. The data were statistically analyzed using chi-square test. The p<0.05 was considered significant. Results: In group B, the mean operative time was significantly (p<0.001) shorter than in group A (25.8±4.14 vs. 35.4±5.6 min respectively). The mean value for operative blood loss was significantly (p<0.001) smaller in group B (101.4±25.5 vs. 200.16±18.8 ml). There was a significant (p<0.01) rise of the body temperature in group B (38.5±0.7 vs. 37.18±0.84 C). There were no differences between the two groups regarding hemoglobin levels, post-operative febrile morbidity or length of hospital stay. Conclusion: In this study, two doses of pre-operative intra-vaginal misoprostol were more effective than one dose in reducing intra and post-operative blood loss and shortening of operation time during abdominal myomectomy. 152 157 Ahmed A Ragab Department of Obstetrics and Gynecology, Mansoura University Department of Obstetrics and Gynecology, Mansoura University Egypt Moustafa M Khaiary Department of Obstetrics and Gynecology, Mansoura University Department of Obstetrics and Gynecology, Mansoura University Egypt Ahmed A Badawy Ahmed Badawy Department of Obstetrics and Gynecology, Mansoura University Department of Obstetrics and Gynecology, Mansoura University Egypt ambadawy@yahoo.com Abdominal myomectomyDouble doseMisoprostol 590.pdf Buttram VC Jr, Reiter RC. Uterine leiomyomata: etiology, symptomatology, and management. Fertil Steril. 1981;36(4):433-45.##Verkauf BS. Changing trends in treatment of leiomyomata uteri. Curr Opin Obstet Gynecol. 1993;5(3):301-10.##Garcia CR. Management of the symptomatic fibroid in women older than 40 years of age. Hysterectomy or myomectomy? Obstet Gynecol Clin North Am. 1993;20(2):337-48.##Lethaby A, Vollenhoven B, Sowter M. Pre-operative GnRH analogue therapy before hysterectomy or myomectomy for uterine fibroids. Cochrane Database Syst Rev. 2001;(2):CD000547.##LaMorte AI, Lalwani S, Diamond MP. Morbidity associated with abdominal myomectomy. Obstet Gynecol. 1993;82(6):897-900.##Liu WM, Tzeng CR, Yi-Jen C, Wang PH. Combining the uterine depletion procedure and myomectomy may be useful for treating symptomatic fibroids. Fertil Steril. 2004;82(1):205-10.##Morita M, Asakawa Y, Uchiide I, Nakakuma M, Kubo H. Surgery results using different uterine wall incision directions in laparoscopic myomectomy of the intramural myoma. Reprod Med Biol. 2004;3:33-7.##Ngeh N, Belli AM, Morgan R, Manyonda I. Pre-myomectomy uterine artery embolisation minimises operative blood loss. BJOG. 2004;111(10):1139-40.##Rossetti A, Paccosi M, Sizzi O, Zulli S, Mancuso S, Lanzone A. Dilute ornitin vasopressin and a myoma drill for laparoscopic myomectomy. J Am Assoc Gynecol Laparosc. 1999;6(2):189-93.##Burkert H. Clinical overview of mesna. Cancer Treat Rev. 1983;10 Suppl A:175-81.##Kongnyuy EJ, van den Broek N, Wiysonge CS. A systematic review of randomized controlled trials to reduce hemorrhage during myomectomy for uterine fibroids. Int J Gynaecol Obstet. 2008;100(1):4-9.##Okin CR, Guido RS, Meyn LA, Ramanathan S. Vasopressin during abdominal hysterectomy: a randomized controlled trial. Obstet Gynecol. 2001;97(6):867-72.##Tulandi T, Beique F, Kimia M. Pulmonary edema: a complication of local injection of vasopressin at laparoscopy. Fertil Steril. 1996;66(3):478-80.##Zullo F, Palomba S, Corea D, Pellicano M, Russo T, Falbo A, et al. Bupivacaine plus epinephrine for laparoscopic myomectomy: a randomized placebo-controlled trial. Obstet Gynecol. 2004;104(2):243-9.##Fuchs AR, Fuchs F, Husslein P, Soloff MS. Oxytocin receptors in the human uterus during pregnancy and parturition. Am J Obstet Gynecol. 1984;150(6):734-41.##Verkauf BS. Changing trends in treatment of leiomyomata uteri. Curr Opin Obstet Gynecol. 1993;5(3):301-10.##Farquhar C, Brown PM, Furness S. Cost effectiveness of pre-operative gonadotrophin releasing analogues for women with uterine fibroids undergoing hysterectomy or myomectomy. BJOG. 2002;109(11):1273-80.##Wray S. Uterine contraction and physiological mechanisms of modulation. Am J Physiol. 1993;264(1 Pt 1):C1-18.##Baxter GS, Clayton JK, Coleman RA, Marshall K, Sangha R, Senior J. Characterization of the prostanoid receptors mediating constriction and relaxation of human isolated uterine artery. Br J Pharmacol. 1995;116(1):1692-6.##Celik H, Sapmaz E. Use of a single preoperative dose of misoprostol is efficacious for patients who undergo abdominal myomectomy. Fertil Steril. 2003;79(5):1207-10.##Zieman M, Fong SK, Benowitz NL, Banskter D, Darney PD. Absorption kinetics of misoprostol with oral or vaginal administration. Obstet Gynecol. 1997;90(1):88-92.##Elsheikh A, Antsaklis A, Mesogitis S, Papantoniou N, Rodolakis A, Vogas E, et al. Use of misoprostol for the termination of second trimester pregnancies. Arch Gynecol Obstet. 2001;265(4):204-6.##

Frequency of Molar Pregnancies in Health Care Centers of Tehran, Iran 2 1 591 2 Background: Hydatidiform mole is an important obstetric problem which can result in harmful and serious outcomes. In this study, an attempt was made to determine the proportion of hydatidiform mole in prenatal clinics of Iran University of Medical Sciences (IUMS) to find the precise frequency of this disease. Methods: Between January 2012 and January 2013, all women who immediately after positive pregnancy test or after retarded menstruation came to prenatal clinics in health care centers of IUMS were included in the study. The women were followed until 8-10 weeks of pregnancy and at this time abdominal sonography was used for confirmation or exclusion of molar pregnancy. Results: In this descriptive study between January 2012 and January 2013, 8614 pregnant women with mentioned criteria were included and 61 cases of hydatidiform mole were diagnosed (0.7% or 7 per 1000 pregnancy). Ten cases (16.4%) were patients with partial moles. There was no significant difference in blood types in molar and non-molar pregnancies, but molar group differed significantly from non-molar group in terms of history of molar pregnancy, abortion, OCP use and ovulation induction. Discussion: Proportion of hydatidiform mole in this study was more than the reported European and American statistics. 157 161 Alireza AR Almasi Department of Radiology, Faculty of Medicine, Iran University of Medical Sciences (IUMS) Department of Radiology, Faculty of Medicine, Iran University of Medical Sciences (IUMS) Iran Fariba F Almassinokiani Department of Obstetrics and Gynecology, Rasoul-e-Akram Hospital, Iran University of Medical Sciences (IUMS) Department of Obstetrics and Gynecology, Rasoul-e-Akram Hospital, Iran University of Medical Sciences (IUMS) Iran dralmassi@yahoo.com Peyman P Akbari Tehran University of Medical Sciences (TUMS) Tehran University of Medical Sciences (TUMS) Iran Gestational trophoblastic diseaseHydatidiform moleProportion 591.pdf Drake RD, Rao GG, McIntire DD, Miller DS, Schorge JO. Gestational trophoblastic disease among Hispanic women: a 21-year hospital-based study. Gynecol Oncol. 2006;103(1):81-6.##Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Rouse DJ, Spong CY, editors. Williams Obstetrics. 23rd ed. Gestational Trophoblastic Disease. USA: McGraw-Hill; 2010. 257 p.##Schorge JO, Goldstein DP, Bernstein MR, Berkowitz RS. Recent advances in gestational trophoblastic disease. J Reprod Med. 2000;45(9):692-700.##Berkowitz RS, Goldstein DP, editors. Gestational Trophoblastic Disease. New Delhi: Wolters Kluwer Health-Lippincott Williams and Wilkins; 2012. 1458 p. (Jonathan S. Berek, editor. Berek and Novak’s Gynaecology).##Nizam K, Haider G, Memon N, Haider A. Gestational trophoblastic disease: experience at Nawabshah Hospital. J Ayub Med Coll Abbottabad. 2009;21(1):94-7.##Mourali M, Fkih C, Essoussi-Chikhaoui J, Ben Haj Hassine A, Binous N, Ben Zineb N, et al. Gestational trophoblastic disease in Tunisia. Tunis Med. 2008;86(7):665-9.##Audu BM, Takai IU, Chama CM, Bukar M, Kyari O. Hydatidiform mole as seen in a university teaching hospital: a 10-year review. J Obstet Gynaecol. 2009;29(4):322-5.##Boufettal H, Coullin P, Mahdaoui S, Noun M, Hermas S, Samouh N. [Complete hydatiforme mole in Morocco: epidemiological and clinical study]. J Gynecol Obstet Biol Reprod (Paris). 2011;40(5):419-29. French.##Thapa K, Shrestha M, Sharma S, Pandey S. Trend of complete hydatidiform mole. JNMA J Nepal Med Assoc. 2010;49(177):10-3.##Soares PD, Maestá I, Costa OL, Charry RC, Dias A, Rudge MV. Geographical distribution and demographic characteristics of gestational trophoblastic disease. J Reprod Med. 2010;55(7-8):305-10.##Loukovaara M, Pukkala E, Lehtovirta P, Leminen A. Epidemiology of hydatidiform mole in Finland, 1975 to 2001. Eur J Gynaecol Oncol. 2005;26(2):207-8.##Salehi S, Eloranta S, Johansson AL, Bergström M, Lambe M. Reporting and incidence trends of hydatidiform mole in Sweden 1973-2004. Acta Oncol. 2011;50(3):367-72.##Savage P, Williams J, Wong SL, Short D, Casalboni S, Catalano K, et al. The demographics of molar pregnancies in England and Wales from 2000-2009. J Reprod Med. 2010;55(7-8):341-5.##Matsui H, Iitsuka Y, Yamazawa K, Tanaka N, Seki K, Sekiya S. Changes in the incidence of molar pregnancies. A population-based study in Chiba Prefecture and Japan between 1974 and 2000. Hum Reprod. 2003;18(1):172-5.##Matsui H, Kihara M, Yamazawa K, Mitsuhashi A, Seki K, Sekiya S. Recent changes of the incidence of complete and partial mole in Chiba prefecture. Gynecol Obstet Invest. 2007;63(1):7-10.##Altieri A, Franceschi S, Ferlay J, Smith J, La Vecchia C. Epidemiology and aetiology of gestational trophoblastic diseases. Lancet Oncol. 2003;4(11):670-8.##Li AJ, editor. Gestational trophoblastic neoplasms. USA: Lippincott Williams and Wilkins; 2008. 1073 p. (Gibbs RS, Karlan BY, Haney A, Nygaard I, editors. Danforth's Obstetrics and Gynecology; vol. 63.).##Kim SJ, Lee C, Kwon SY, Na YJ, Oh YK, Kim CJ. Studying changes in the incidence, diagnosis and management of GTD: the South Korean model. J Reprod Med. 2004;49(8):643-54.##Shi YF, Li JQ, Zheng W, Chen XJ, Qiao YH, Hao M, et al. [Survey of gestational trophoblastic disease incidence among 3.6 million pregnancies in China]. Zhonghua Fu Chan Ke Za Zhi. 2005;40(2):76-8. Chinese.##Chechia A, Koubaa A, Makhlouf T, Anis B, Terras K, Hamouda B, et al. [Molar pregnancy. Retrospective study of 60 cases in Tunisia]. Tunis Med. 2001;79(8-9):441-6. French.##Harma M, Harma M, Yurtseven S, Gungen N. Gestational trophoblastic disease in Sanliurfa, southeast Anatolia, Turkey. Eur J Gynaecol Oncol. 2005;26(3):306-8.##Soper JT. Gestational trophoblastic disease. Obstet Gynecol. 2006;108(1):176-87.##Osamor JO, Oluwasola AO, Adewole IF. A clinico-pathological study of complete and partial hydatidiform moles in a Nigerian population. J Obstet Gynaecol. 2002;22(4):423-5.##

A Study of Adenylate Kinase Locus 1 (AK1) Genetic Polymorphism in Diabetic Pregnancy 2 1 592 2 Background: Previous studies suggest that adenylate kinase locus 1 (AK1) has an important role in the control of blood glucose level and in the glycation of structural and functional proteins in type 2 diabetes and in the balanced development of feto-placental unit in healthy puerperae (HP). In this study, an attempt was made to investigate the relationship of AK1 with maternal and neonatal parameters in puerperae with gestational diabetes (GDP) and with preexisting type 1 diabetes (T1DP). Methods: This study was carried on 402 HP, 347 consecutive healthy newborns, 102 GDP and 111 T1DP with their newborn infants. AK1 phenotype was determined by starch gel electrophoresis. Chi-square test of independence was carried out by SPSS program. The analysis of three way contingency table was carried out by a loglinear model. Significant level was 0.05. Results: In T1DP, the frequency of AK1*2 allele was higher than in GDP and in HP. Serum glucose level was higher in T1DP than in GDP with higher values in carriers of AK1*2 allele. Neonatal hypoglycemia was more frequent in T1DP than in GDP with a positive association with AK1*2 allele. The correlation between birth weight (BW) and placental weight (PW) was lower in infants from T1DP than HP. In healthy puerperae the correlation is higher in AK1 2-1 than in AK11 phenotype while in diabetic puerperae the pattern is reversed with lower values in AK12-1 than in AK11 phenotype. The lowest value of correlation is observed in infants from T1D mothers carrying the AK1*2 allele. Conclusion: The data confirmed the involvement of AK1 in glucose metabolism and showed a disturbance of the balance between placental and fetal growth which was more marked in T1DP. 161 165 Fulvia F Gloria-Bottini Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Italy gloria@med.uniroma2.it Adalgisa A Pietropolli Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Italy Anna A Neri Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Italy Luca L Coppeta Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Italy Andrea A Magrini Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Italy Egidio E Bottini Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Department of Biomedicine and Prevention, School of Medicine, University of Rome Tor Vergata Italy Adenylate kinaseBW-PW correlationGestational diabetesNeonatal hypoglycemiaPreexisting T1D 592.pdf Gloria-Bottini F, Antonacci E, Cozzoli E, De Acetis C, Bottini E. The effect of genetic variability on the correlation between blood glucose and glycated hemoglobin levels. Metabolism. 2011;60(2):250-5.##Gloria-Bottini F, Antonacci E, Cozzoli E, De Acetis C, Bottini E. Adenylate kinase locus 1 genetic polymorphism and type 2 diabetes. Health. 2011;3(2):77-81.##Gloria-Bottini F, Pietroiusti A, Neri A, Saccucci P, Amante A, Bottini E, et al. Adenylate kinase locus 1 polymorphism and feto-placental development. Eur J Obstet Gynecol Reprod Biol. 2011;159(2):273-5.##Gloria-Bottini F, Magrini A, Pietropolli A, Bergamaschi A, Bottini E. Smoking and human reproduction: the effect of adenylate kinase genetic polymorphism. Am J Perinatol. 2009;26(2):117-21.##Khakh BS, Burnstock G. The double life of ATP. Sci Am. 2009;301(6):84-90, 92.##Dzeja P, Terzic A. Adenylate kinase and AMP signaling networks: metabolic monitoring, signal communication and body energy sensing. Int J Mol Sci. 2009;10(4):1729-72.##Fildes RA, Harris H. Genetically determined variation of adenylate kinase in man. Nature. 1966;209(5020):261-3.##Sokal RR, Rohlf JF. Biometry. 2nd ed. New York: WH Freeman; 1981. 959 p.##Barker DJ, Bull AR, Osmond C, Simmonds SJ. Fetal and placental size and risk of hypertension in adult life. BMJ. 1990;301(6746):259-62.##Edwards A, Megens A, Peek M, Wallace EM. Sexual origins of placental dysfunction. Lancet. 2000;355(9199):203-4.##Hales CN, Barker DJ. The thrifty phenotype hypothesis. Br Med Bull. 2001;60:5-20.##Zeltser LM, Leibel RL. Roles of the placenta in fetal brain development. Proc Natl Acad Sci U S A. 2011;108(38):15667-8.##Nelson KB, Blair E. The placenta and neurologic and psychiatric outcomes in the child: study design matters. Placenta. 2011 Sep;32(9):623-5.##

Cellular Angiofibroma of Vagina Presenting with Secondary Infertility 2 1 593 2 Background: Cellular angiofibroma, first described in 1997, is known to occur in both genders with equal predilection occurring in middle aged females and older males. Case Presentation: In this study, a case of vaginal cellular angiofibroma was reported in a 30 year old female presenting with secondary infertility. The case was diagnosed based on morphology and immunohistochemistry and was treated surgically. The interesting feature of the case was the rarity of its incidence at the vagina and its resemblance to other benign and more aggressive tumours in the same site. Conclusion: Cellular angiofibromas are benign tumours, which rarely occur in vagina. Although middle aged females are affected more, cellular angiofibromas can affect females of reproductive age group and can cause secondary infertility. These tumours need to be distinguished from other benign tumours and aggressive tumours occurring in the same site. 165 168 Jyotsna JN Bharti Department of Pathology, Maulana Azad Medical College Department of Pathology, Maulana Azad Medical College India Biswajit B Dey Department of Pathology, Maulana Azad Medical College Department of Pathology, Maulana Azad Medical College India drbish25@rediffmail.com Vikram V Raj Department of Pathology, Maulana Azad Medical College Department of Pathology, Maulana Azad Medical College India Prerna P Arora Department of Pathology, Maulana Azad Medical College Department of Pathology, Maulana Azad Medical College India AngiofibromaImmunohistochemistrySecondary infertilityVagina 593.pdf Nucci MR, Granter SR, Fletcher CD. Cellular angiofibroma: a benign neoplasm distinct from angiomyofibroblastoma and spindle cell lipoma. Am J Surg Pathol. 1997;21(6):636-44.##Flucke U, van Krieken JH, Mentzel T. Cellular angiofibroma: analysis of 25 cases emphasizing its relationship to spindle cell lipoma and mammary-type myofibroblastoma. Mod Pathol. 2011;24(1):82-9.##Sujatha VV, Veeragandham S. Angiofibroma of vagina during pregnancy presenting as antepartum hemorrhage: a case report. J Clin Gynecol Obstet. 2012;1(1):28-9.##Iwasa Y, Fletcher CD. Cellular angiofibroma: clinicopathologic and immunohistochemical analysis of 51 cases. Am J Surg Pathol. 2004;28(11):1426-35.##Nucci MR, Fletcher CD. Vulvovaginal soft tissue tumours: update and review. Histopathology. 2000;36(2):97-108.##McCluggage WG, Perenyei M, Irwin ST. Recurrent cellular angiofibroma of the vulva. J Clin Pathol. 2002;55(6):477-9.##Sutton BJ, Laudadio J. Aggressive angiomyxoma. Arch Pathol Lab Med. 2012;136(2):217-21.##

Sildenafil Citrate in Fetal Growth Restriction 2 1 594 2 Background: Pregnancies with early onset fetal growth restriction have poor perinatal outcome. Sildenafil citrate (PDE -5 inhibitor) as a vasodilator increases uteroplacental blood flow and potentiates fetal growth. Case Presentation: In this study, a case was examined and Sildenafil was administered for her. It was found that Sildenafil improved the uterine blood flow with a favorable fetal outcome at delivery. Conclusion: Sildenafil, as a vasodilator has emerged as a potential management option in the treatment of Intra Uterine Growth Retardation (IUGR) and preeclampsia by later normalization in velocimetric profile. 168 170 Subrat S Panda سوبرت پاندا Department of Obstetrics & Gynecology, North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences (NEIGRIHMS) Department of Obstetrics & Gynecology, North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences (NEIGRIHMS) India Ananya A Das آنانیا داس Department of Obstetrics & Gynecology, North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences (NEIGRIHMS) Department of Obstetrics & Gynecology, North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences (NEIGRIHMS) India mailmedrananyadas@rediffmail.com Hossain HM Nowroz Department of Obstetrics & Gynecology, North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences (NEIGRIHMS) Department of Obstetrics & Gynecology, North Eastern Indira Gandhi Regional Institute of Health & Medical Sciences (NEIGRIHMS) India Fetal growth restrictionPregnancySildenafil citrate 594.pdf Soregaroli M, Valcamonico A, Scalvi L, Danti L, Frusca T. Late normalisation of uterine artery velocimetry in high risk pregnancy. Eur J Obstet Gynecol Reprod Biol. 2001;95(1):42-5.##Zoma WD, Baker RS, Clark KE. Effects of combined use of sildenafil citrate (Viagra) and 17beta-estradiol on ovine coronary and uterine hemodynamics. Am J Obstet Gynecol. 2004;190(5):1291-7.##Wareing M, Myers JE, O'Hara M, Kenny LC, Taggart MJ, Skillern L, et al. Phosphodiesterase-5 inhibitors and omental and placental small artery function in normal pregnancy and pre-eclampsia. Eur J Obstet Gynecol Reprod Biol. 2006;127(1):41-9.##Wareing M, Myers JE, O'Hara M, Baker PN. Sildenafil citrate (Viagra) enhances vasodilatation in fetal growth restriction. J Clin Endocrinol Metab. 2005;90(5):2550-5.##Ballard SA, Gingell CJ, Tang K, Turner LA, Price ME, Naylor AM. Effects of sildenafil on the relaxation of human corpus cavernosum tissue in vitro and on the activities of cyclic nucleotide phosphodiesterase isozymes. J Urol. 1998;159(6):2164-71.##von Dadelszen P, Dwinnell S, Magee LA, Carleton BC, Gruslin A, Lee B, et al. Sildenafil citrate therapy for severe early-onset intrauterine growth restriction. BJOG. 2011;118(5):624-8.##Samangaya RA, Mires G, Shennan A, Skillern L, Howe D, McLeod A, et al. A randomised, double-blinded, placebo-controlled study of the phosphodiesterase type 5 inhibitor sildenafil for the treatment of preeclampsia. Hypertens Pregnancy. 2009;28(4):369-82.##

Letter to Editor on "Correlation of the Day 3 FSH/LH Ratio and LH Cocentration in Predicting IVF Outcome" 2 1 595 2 We read with interest the study by Prasad et al. (1), on Correlation of Day 3 FSH/LH Ratio and LH Concentration in Predicting IVF Outcome. In this study, they demonstrated that elevated day 3 FSH/LH ratio is associated with inferior outcome in IVF treatment cycles and it could be used as an additional predictor of decreased ovarian reserve. Surprisingly, two of our clinically relevant studies went unnoticed. While studying patients undergoing COH for IVF, with a favorable prognosis a priori, day 3 FSH: LH ratio, but not LH level, was found to predict IVF treatment outcome. Moreover, the FSH/LH ratio cutoff levels differ between those using the GnRH-agonist or GnRH-anta-gonist COH protocols. We demonstrated that patients undergoing ovarian stimulation using the GnRH antagonist with FSH/LH ratios >2, or using agonist protocols with FSH/LH ratios >3, achieved significantly lower pregnancy rates (2). Furthermore, in a subsequent study, we observed significantly higher number of top-quality embryos, and higher implantation and clinical pregnancy rates in patients undergoing COH for IVF, using HMG compared with rFSH (3). Conflict of Interest The authors declare no conflict of interest. 170 171 Giuseppe G Morgante Department of Obstetrics and Gynecology, University of Siena, Policlinico Santa Maria Le Scotte Department of Obstetrics and Gynecology, University of Siena, Policlinico Santa Maria Le Scotte Italy morgante@unisi.it No Keyword 595.pdf Prasad S, Gupta T, Divya A. Correlation of the day 3 FSH/LH ratio and LH concentration in predicting IVF outcome. J Reprod Infertil. 2013;14(1):23-28.##Orvieto R, Meltzer S, Rabinson J, Gemer O, Anteby EY, Nahum R. Does day 3 luteinizing-hormone level predict IVF success in patients undergoing controlled ovarian stimulation with GnRH analogues? Fertil Steril. 2008;90(4):1297-300.##Orvieto R, Homburg R, Meltcer S, Rabinson J, An-teby EY, Nahum R. HMG improves IVF outcome in patients with high basal FSH/LH ratio: a preliminary study. Reprod Biomed Online. 2009;18(2):205-8.##