<?xml version="1.0" encoding="utf-8" ?>

<XML>
  <JOURNAL>   
    <YEAR>2013</YEAR>
    <VOL>14</VOL>
    <NO>4</NO>
    <MOSALSAL>57</MOSALSAL>
    <PAGE_NO>60</PAGE_NO>  
    <ARTICLES>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Advanced Reproductive Technologies and Postponement of Parenthood</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>580</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Industrialization of developed and developing countries during recent and the end of the 20th century was accompanied with fundamental changes in habits and life style of communities. The change in family planning and childbirth is greatly emphasized due to its numerous effects on mothers, newborns, families and societies. Postponing parenthood is a very common aspect of revolution in family planning during past decades. Postponement of parenthood is generally related to socio-demographic reasons including tremendous tendency in higher levels of education, increased rate of women employment and imbalance of financial status to support a child immediately after the marriage.&lt;br&gt;Increased age of men and women results in a decrease in fecundity. There is no consensus on the descrip-tion of reproductive age of women but the age of 35 is accepted as cutoff age. The reserve of ovary and quality of oocyte remnants decrease in women older than 35 years. In addition, the rate of other obstetric and gynecological diseases including gynecological cancers, endometriosis, myomas, endometrial polyps and other malignant diseases would increase in aging women. The same situation is predictable in aging of men. In addition to the increased risk of malignant diseases particularly testis cancer, sperm counts, sperm quality (especially chromatin integrity), sex hormones and sex drive decrease during aging of men and all of them lead to a decline in fecundity in older men (1). &#160;&lt;br&gt;Recently, most of young couples are wrongly informed that there is no problem to delay their pregnancy and parenthood to the age of 35 or above and it is worse that they are mistakenly advised that development&#160; in advanced reproductive technologies can help them for recovery of age-related consequences of infecundity. Therefore, in some European countries, about 5% of children are born following ART treatment. Application of IUI, IVF, ICSI and other advanced techniques can eliminate some failure related to male and female infertility but they cannot recover the age-related decrease in quality of sperm, oocyte and uterus. Couples should be aware that assisted reproduction technology (ART) cannot compensate for the age-related reduction in male and female fecundity (2).&lt;br&gt;Recent findings show that postponing pregnancy and childbearing potentially increases the prevalence of multiple pregnancies, spontaneous abortions, ectopic pregnancy, intrauterine growth restriction, intrauterine fetal death and stillbirths, diabetes and chronic hypertension, preterm labor, peripartum complications, maternal morbidity and mortality and genetic and congenital birth defects such as cerebral palsy, neurocognitive and psychiatric disorders (3). &lt;br&gt;Despite the use of donated oocytes and embryos for aged women after 40, the risk of gamete and embryo related complications such as genetic and congenital birth defects has been reduced somewhat, but these options are more expensive and are not available for all aged women and also raises some legal, psychological and social issues (1). &lt;br&gt;Therefore, it is necessary to inform policy makers, health care providers and community about the potential risks and complications related to postponing marriage, pregnancy and childbirth. Counseling and increasing the young couples’ knowledge culminate in their awareness about reproductive aging and their lower chance of childbirth with their own biological gametes. Increased knowledge of the issue will help them to change their wrong assumption and thinking and there upon they make mindful decisions for starting their parenthood. In addition, more governmental and public support is necessary for young couples in order to motivate them for planning to have their childbirths at an earlier age. &lt;br&gt;&lt;br&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>157</FPAGE>
            <TPAGE>158</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Mohammad Reza</Name>
<MidName>MR</MidName>
<Family>Sadeghi</Family>
<NameE> محمدرضا</NameE>
<MidNameE></MidNameE>
<FamilyE>صادقی</FamilyE>
<Organizations>
<Organization>Editor-in-chief</Organization>
</Organizations>
<Universities>
<University>Editor-in-chief</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>No Keyword</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>580.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Schmidt L, Sobotka T, Bentzen JG, Nyboe Andersen A; ESHRE Reproduction and Society Task Force. Demographic and medical consequences of the postponement of parenthood. Hum Reprod Update. 2012;18(1):29-43.##Mintziori G, Lambrinoudaki I, Kolibianakis EM, Ceausu I, Depypere H, Erel CT, et al. EMAS position statement: Late parenthood. Maturitas. 2013;76(2):200-4.##Balasch J, Gratacos E. Delayed childbearing: effects on fertility and the outcome of pregnancy. Curr Opin Obstet Gynecol. 2012;24(3):187-93.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Pharmacology of Free Radicals and the Impact of Reactive Oxygen Species on the Testis</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>540</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>The role of free radicals in normal cellular functions and different pathological conditions has been a focus of pharmacological studies in the recent past. Reactive oxygen species (ROS) and free radicals in general are essential for cell signaling and other vital physiological functions; however, excessive amounts can cause alteration in cellular reduction-oxidation (redox) balance, and disrupt normal biological functions. When there is an imbalance between activities of ROS and antioxidant/scavenging defense systems, oxidative stress (OS) occurs. A good number of studies have shown OS is involved in the development of several disease conditions, including male infertility. In the present article, generation of free radicals and their effects, as well as the mechanisms of antioxidant/scavenging defense systems are discussed, with particular focus on the testis. The review also discusses the contribution of OS on testicular dysfunction and briefly focuses on some OS-induced conditions that will alter testicular function.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>158</FPAGE>
            <TPAGE>173</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Jonah</Name>
<MidName>JS</MidName>
<Family>Aprioku</Family>
<NameE>Jonah</NameE>
<MidNameE></MidNameE>
<FamilyE>Aprioku</FamilyE>
<Organizations>
<Organization>Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt</Organization>
</Organizations>
<Universities>
<University>Department of Pharmacology, Faculty of Basic Medical Sciences, University of Port Harcourt</University>
</Universities>
<Countries>
<Country>Nigeria</Country>
</Countries>
<EMAILS>
<Email>sydaprio@yahoo.com</Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Antioxidant</KeyText></KEYWORD><KEYWORD><KeyText>ROS</KeyText></KEYWORD><KEYWORD><KeyText>Scavenging</KeyText></KEYWORD><KEYWORD><KeyText>Superoxide anion</KeyText></KEYWORD><KEYWORD><KeyText>Testis</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>540.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Halliwell B, Gutteridge JMC. Free radicals in biology and medicine. New York: Oxford University Press; 1999.##Halliwell B. Role of free radicals in the neurodegenerative diseases: therapeutic implications for antioxidant treatment. Drugs Aging. 2001;18(9):685-716.##Anas AA, Wiersinga WJ, de Vos AF, van der Poll T. Recent insights into the pathogenesis of bacterial sepsis. Neth J Med. 2010;68(4):147-52.##Aviram M. Review of human studies on oxidative damage and antioxidant protection related to cardiovascular diseases. Free Radic Res. 2000;33 Suppl:S85-97.##Klaunig JE, Kamendulis LM. The role of oxidative stress in carcinogenesis. Annu Rev Pharmacol Toxicol. 2004;44:239-67.##Santos FW, Graca DL, Zeni G, Rocha JB, Weis SN, Favero AM, et al. Sub-chronic administration of diphenyl diselenide potentiates cadmium induced testicular damage in mice. Reprod Toxicol. 2006;22:546-50.##Schoneich C. Mass spectrometry in aging research. Mass Spectrom Rev. 2005;24:701-18.##Allen JA. Diemer T, Janus P, Hales KH, Hales DB. Bacterial endotoxin lipopolysaccharide and reactive oxygen species inhibit Leydig cell steroidogenesis via perturbation of mitochondria. Endocrine. 2004;25(3):265-75.##Khan MA, Tania M, Zhang D, Chen H. Antioxidant enzymes and cancer. Chin J Cancer Res. 2010;22:87-92.##Sohal R, Mockett R, Orr W. Mechanisms of aging: an appraisal of the oxidative stress hypothesis. Free Radic Biol Med. 2002;33:575–86.##Victor VM, Rocha M, De la Fuente M. Immune cells: free radicals and antioxidants in sepsis. Int Immunopharmacol. 2004;4:327-47.##Aprioku JS, Obianime AW. Comparative interactive studies of aqueous leaf extracts of Ocimum gratissimum Linn. (Lamiaeceae), vitamins C. and E on the basal serum phosphatase levels of male guinea-pigs. West Afr J Pharmacol Drug Res. 2008;24:48-55.##Obianime AW, Ahiwe NJ, Aprioku JS. Effects of vitamins C and E pretreatments on cadmium-induced serum levels of some biochemical and hormonal parameters in the female guinea pig. Afr J Biotech. 2010;9(39):6582-7.##Rattan SI. Theories of biological aging: genes, proteins, and free radicals. Free Radic Res. 2006;40:1230-8.##Stocker R, Keaney JF Jr. Role of oxidative modifications in atherosclerosis. Physiol Rev. 2004;84(4):1381-478.##Szabo C. Role of nitrosative stress in the athogenesis of diabetic vascular dysfunction. Br J Pharmacol. 2009;156:713-27.##Hitchon CA, El-Gabalawy HS. Oxidation in rheumatoid arthritis. Arthritis Res Ther. 2004;6(6):265-78.##Nunomura A, Castellani RJ, Zhu X, Moreira PI, Perry G, Smith MA. Involvement of oxidative stress in Alzheimer disease. J Neuropathol Exp Neurol. 2006;65(7):631-41.##Wood-Kaczmar A, Gandhi S, Wood NW. Understanding the molecular causes of Parkinson&#39;s disease. Trends Mol Med. 2006;12(11):521-8.##Kohen R, Nyska A. Oxidation of biological systems: oxidative stress phenomena, antioxidants, redox reactions, and methods for their quantification. Toxicol Pathol. 2002;30(6):620-50.##Pryor WA, Houk KN, Foote CS, Fukuto JM, Ignarro LJ, Squadrito GL, et al. Free radical biology and medicine: it&#39;s a gas, man! Am J Physiol Regul Integr Comp Physiol. 2006;291(3):R491-511.##Slater TF. Free-radical mechanisms in tissue injury. Biochem J. 1984;222(1):1-15.##Valko M, Izakovic M, Mazur M, Rhodes CJ, Telser J. Role of oxygen radicals in DNA damage and cancer incidence. Mol Cell Biochem. 2004;266(1-2):37-56.##Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem. 2005;12(10):1161-208.##Aruoma OI, Halliwell B, Gajewski E, Dizdaroglu M. Copper-ion-dependent damage to the bases in DNA in the presence of hydrogen peroxide. Biochem J. 1991;273 ( Pt 3):601-4.##Webster NR, Nunn JF. Molecular structure of free radicals and their importance in biological reactions. Br J Anaesth. 1988;60(1):98-108.##Cadenas E. Mitochondrial free radical production and cell signaling. Mol Aspects Med. 2004;25(1-2):17-26.##Pacher P, Beckman JS, Liaudet L. Nitric oxide and peroxynitrite in health and disease. Physiol Rev. 2007;87(1):315-424.##Lenaz G. The mitochondrial production of reactive oxygen species: mechanisms and implications in human pathology. IUBMB Life. 2001;52(3-5):159-64.##Matesanz N, Lafuente N, Azcutia V, Martin D, Cuadrado A, Nevado J, et al. Xanthine oxidase-derived extracellular superoxide anions stimulate activator protein 1 activity and hypertrophy in human vascular smooth muscle via c-Jun N-terminal kinase and p38 mitogen-activated protein kinases. J Hypertens. 2007;25(3):609-18.##Zangar RC, Davydov DR, Verma S. Mechanisms that regulate production of reactive oxygen species by cytochrome P450. Toxicol Appl Pharmacol. 2004;199(3):316-31.##Schrader M, Fahimi HD. Mammalian peroxisomes and reactive oxygen species. Histochem Cell Biol. 2004;122(4):383-93.##Li WG, Miller FJ Jr, Zhang HJ, Spitz DR, Oberley LW, Weintraub NL. H(2)O(2)-induced O(2) production by a non-phagocytic NAD(P)H oxidase causes oxidant injury. J Biol Chem. 2001;276(31):29251-6.##D&#39;Autreaux B, Toledano MB. ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis. Nat Rev Mol Cell Biol. 2007;8(10):813-24.##Szabo C, Ischiropoulos H, Radi R. Peroxynitrite: biochemistry, pathophysiology and development of therapeutics.  Nat Rev Drug Discov. 2007;6(8):662-80.##Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med. 1995;18(2):321-36.##Yu BP. Cellular defenses against damage from reactive oxygen species. Physiol Rev. 1994;74(1):139-62.##Mates JM, Sanchez-Jimenez F. Antioxidant enzymes and their implications in pathophysiologic processes. Front Biosci. 1999;4:D339-45.##Ishikawa T, Kondo Y, Goda K, Fujisawa M. Overexpression of endothelial nitric oxide synthase in transgenic mice accelerates testicular germ cell apoptosis induced by experimental cryptorchidism. J Androl. 2005;26(2):281-8.##Zhang J, Jin B, Li L, Block ER, Patel JM. Nitric oxide-induced persistent inhibition and nitrosylation of active site cysteine residues of mitochondrial cytochrome-c oxidase in lung endothelial cells. Am J Physiol Cell Physiol. 2005;288(4):C840-9.##Sandoo A, van Zanten JJ, Metsios GS, Carroll D, Kitas GD. The endothelium and its role in regulating vascular tone. Open Cardiovasc Med J. 2010;4:302-12.##Szabo C. Role of nitric oxide in endotoxic shock. An overview of recent advances. Ann N Y Acad Sci. 1998;851:422-5.##Stadtman ER, Moskovitz J, Levine RL. Oxidation of methionine residues of proteins: biological consequences. Antioxid Redox Signal. 2003;5(5):577-82.##Catala A. An overview of lipid peroxidation with emphasis in outer segments of photoreceptors and the chemiluminescence assay. Int J Biochem Cell Biol. 2006;38(9):1482-95.##Esterbauer H, Schaur RJ, Zollner H. Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes. Free Radic Biol Med. 1991;11(1):81-128.##Dalle-Donne I, Rossi R, Colombo R, Giustarini D, Milzani A. Biomarkers of oxidative damage in human disease. Clin Chem. 2006;52(4):601-23.##Vertuani S, Angusti A, Manfredini S. The antioxidants and pro-antioxidants network: an overview. Curr Pharm Des. 2004;10(14):1677-94.##Zelko IN, Mariani TJ, Folz RJ. Superoxide dismutase multigene family: a comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and expression. Free Radic Biol Med. 2002;33(3):337-49.##Nozik-Grayck E, Suliman HB, Piantadosi CA. Extracellular superoxide dismutase. Int J Biochem Cell Biol. 2005;37(12):2466-71.##Mannervik B. The enzymes of glutathione metabolism: an overview. Biochem Soc Trans. 1987;15 (4):717-8.##McDermott JH. Antioxidant nutrients: current dietary recommendations and research update. J Am Pharm Assoc (Wash). 2000;40(6):785-99.##Pastore A, Federici G, Bertini E, Piemonte F. Analysis of glutathione: implication in redox and detoxification. Clin Chim Acta. 2003;333(1):19-39.##Meister A. Glutathione metabolism and its selective modification. J Biol Chem. 1988;263(33):17205-8.##Herrera E, Barbas C. Vitamin E: action, metabolism and perspectives. J Physiol Biochem. 2001;57(2):43-56.##Traber MG, Atkinson J. Vitamin E, antioxidant and nothing more. Free Radic Biol Med. 2007;43(1):4-15.##Niki E, Noguchi N, Tsuchihashi H, Gotoh N. Interaction among vitamin C, vitamin E, and beta-carotene. Am J Clin Nutr. 1995;62(6 Suppl):1322S-1326S.##Padayatty SJ, Katz A, Wang Y, Eck P, Kwon O, Lee JH, et al. Vitamin C as an antioxidant: evaluation of its role in disease prevention. J Am Coll Nutr. 2003;22(1):18-35.##Meister A. Glutathione-ascorbic acid antioxidant system in animals. J Biol Chem. 1994;269(13):9397-400.##Tanaka K, Hashimoto T, Tokumaru S, Iguchi H, Kojo S. Interactions between vitamin C and vitamin E are observed in tissues of inherently scorbutic rats. J Nutr. 1997;127(10):2060-4.##Glantzounis GK, Tsimoyiannis EC, Kappas AM, Galaris DA. Uric acid and oxidative stress. Curr Pharm Des. 2005;11(32):4145-51.##Strazzullo P, Puig JG. Uric acid and oxidative stress: relative impact on cardiovascular risk? Nutr Metab Cardiovasc Dis. 2007;17(6):409-14.##Dimitroula HV, Hatzitolios AI, Karvounis HI. The role of uric acid in stroke: the issue remains unresolved.  Neurologist. 2008;14(4):238-42.##Jansen T, Hortmann M, Oelze M, Opitz B, Steven S, Schell R, et al. Conversion of biliverdin to bilirubin by biliverdin reductase contributes to endothelial cell protection by heme oxygenase-1 evidence for direct and indirect antioxidant actions of bilirubin. J Mol Cell Cardiol. 2010;49(2):186-95.##Reiter R, Tang L, Garcia JJ, Munoz-Hoyos A. Pharmacological actions of melatonin in oxygen radical pathophysiology. Life Sci. 1997;60(25):2255-71.##Pablos MI, Agapito MT, Gutierrez R, Recio JM, Reiter RJ, Barlow-Walden L, et al. Melatonin stimulates the activity of the detoxifying enzyme glutathione peroxidase in several tissues of chicks. J Pineal Res. 1995;19(3):111-5.##Tan DX, Manchester LC, Reiter RJ, Qi WB, Karbownik M, Calvo JR. Significance of melatonin in antioxidative defense system: reactions and products. Biol Signals Recept. 2000;9(3-4):137-59.##Armstrong JS, Rajasekaran M, Hellstrom WJ, Sikka SC. Antioxidant potential of human serum albumin: role in the recovery of high quality human spermatozoa for assisted reproductive technology. J Androl. 1998;19(4):412-9.##Keys SA, Zimmerman WF. Antioxidant activity of retinol, glutathione, and taurine in bovine photoreceptor cell membranes. Exp Eye Res. 1999;68(6):693-702.##Merati G, Pasquali P, Vergani C, Landi L. Antioxidant activity of ubiquinone-3 in human low density lipoprotein. Free Radic Res Commun. 1992;16(1):11-7.##Shenkin A. The key role of micronutrients. Clin Nutr. 2006;25(1):1-13.##Arner ES, Holmgren A. Physiological functions of thioredoxin and thioredoxin reductase. Eur J Biochem. 2000;267(20):6102-9.##Clermont Y. Kinetics of spermatogenesis in mammals: seminiferous epithelium cycle and spermatogonial renewal. Physiol Rev. 1972;52(1):198-236.##de Kretser DM, Kerr JB, editors. The cytology of the testis. New York: Raven Press; 1988. p. 837-932. (Knobil E, Neill JB, Ewing LL, Greenwald GS, Markert CL, Pfaff DW, editors. The physiology of reproduction).##Walker WH. Non-classical actions of testosterone and spermatogenesis. Philos Trans R Soc Lond B Biol Sci. 2010;365(1546):1557-69.##Payne AH, Hales DB. Overview of steroidogenic enzymes in the pathway from cholesterol to active steroid hormones. Endocr Rev. 2004;25(6):947-70.##Guyton AC, Hall JE. Text book of medical physiology. 11th ed. Philadelphia: Elsevier Saunders; 2006.##Neill JD, Herbison AE, editor. Physiology of the gonadotropin-releasing hormone neuronal network. Amsterdam: Elsevier; 2006. p. 1415-82. (Neill JD, editor. Knobil and Neill&#39;s physiology of reproduction).##Skinner MK, McLachlan RI, Bremner WJ. Stimulation of Sertoli cell inhibin secretion by the testicular paracrine factor PModS. Mol Cell Endocrinol. 1989;66(2):239-49.##Hull MG, Glazener CM, Kelly NJ, Conway DI, Foster PA, Hinton RA, et al. Population study of causes, treatment, and outcome of infertility. Br Med J (Clin Res Ed). 1985;291(6510):1693-7.##Brugh VM 3rd, Matschke HM, Lipshultz LI. Male factor infertility. Endocrinol Metab Clin North Am. 2003;32(3):689-707.##Agarwal A, Prabakaran SA, Said TM. Prevention of oxidative stress injury to sperm. J Androl. 2005;26(6):654-60.##Reddy MM, Mahipal SV, Subhashini J, Reddy MC, Roy KR, Reddy GV, et al. Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats. Reprod Toxicol. 2006;22(3):493-500.##Turner TT, Lysiak JJ. Oxidative stress: a common factor in testicular dysfunction. J Androl. 2008;29(5):488-98.##Sikka SC. Relative impact of oxidative stress on male reproductive function. Curr Med Chem. 2001;8(7):851-62.##Agarwal A, Saleh RA. Role of oxidants in male infertility: rationale, significance, and treatment. Urol Clin North Am. 2002;29(4):817-27.##Agarwal A, Sharma RK, Nallella KP, Thomas AJ Jr, Alvarez JG, Sikka SC. Reactive oxygen species as an independent marker of male factor infertility. Fertil Steril. 2006;86(4):878-85.##Aitken RJ. Molecular mechanisms regulating human sperm function. Mol Hum Reprod. 1997;3(3):169-73.##Gil-Guzman E, Ollero M, Lopez MC, Sharma RK, Alvarez JG, Thomas AJ Jr, et al. Differential production of reactive oxygen species by subsets of human spermatozoa at different stages of maturation. Hum Reprod. 2001;16(9):1922-30.##Aitken RJ, Buckingham DW, West KM. Reactive oxygen species and human spermatozoa: analysis of the cellular mechanisms involved in luminol- and lucigenin-dependent chemiluminescence. J Cell Physiol. 1992;151(3):466-77.##Gavella M, Lipovac V. NADH-dependent oxidoreductase (diaphorase) activity and isozyme pattern of sperm in infertile men. Arch Androl. 1992;28(2):135-41.##Plante M, de Lamirande E, Gagnon C. Reactive oxygen species released by activated neutrophils, but not by deficient spermatozoa, are sufficient to affect normal sperm motility. Fertil Steril. 1994;62(2):387-93.##Ollero M, Gil-Guzman E, Lopez MC, Sharma RK, Agarwal A, Larson K, et al. Characterization of subsets of human spermatozoa at different stages of maturation: implications in the diagnosis and treatment of male infertility. Hum Reprod. 2001;16(9):1912-21.##Aitken RJ, West K, Buckingham D. Leukocytic infiltration into the human ejaculate and its association with semen quality, oxidative stress, and sperm function. J Androl. 1994;15(4):343-52.##Sharma RK, Pasqualotto AE, Nelson DR, Thomas AJ Jr, Agarwal A. Relationship between seminal white blood cell counts and oxidative stress in men treated at an infertility clinic. J Androl. 2001;22(4):575-83.##Sikka SC. Role of oxidative stress and antioxidants in andrology and assisted reproductive technology. J Androl. 2004;25(1):5-18.##Colagar AH, Marzony ET. Ascorbic Acid in human seminal plasma: determination and its relationship to sperm quality. J Clin Biochem Nutr. 2009;45(2):144-9.##Pasqualotto FF, Sharma RK, Nelson DR, Thomas AJ, Agarwal A. Relationship between oxidative stress, semen characteristics, and clinical diagnosis in men undergoing infertility investigation. Fertil Steril. 2000;73(3):459-64.##Blake DR, Allen RE, Lunec J. Free radicals in biological systems--a review orientated to inflammatory processes. Br Med Bull. 1987;43(2):371-85.##Alvarez JG, Touchstone JC, Blasco L, Storey BT. Spontaneous lipid peroxidation and production of hydrogen peroxide and superoxide in human spermatozoa. Superoxide dismutase as major enzyme protectant against oxygen toxicity. J Androl. 1987;8(5):338-48.##Ishii T, Matsuki S, Iuchi Y, Okada F, Toyosaki S, Tomita Y, et al. Accelerated impairment of spermatogenic cells in SOD1-knockout mice under heat stress. Free Radic Res. 2005;39(7):697-705.##Pons E, Sipila P, Britan A, Vernet P, Poutaneri M, Huhtaniemi I, et al, editors. Epididymal expression of mouse GPX proteins: analysis of the mechanisms of GPX5 tissue and region-specific expression through in vitro and in vivo approaches. Charlottesville, Va: The Van Doren Company; 2003. p. 74-93. (Hinton BT, Turner TT, editors. Third international conference on the epididymis).##Thiele JJ, Friesleben HJ, Fuchs J, Ochsendorf FR. Ascorbic acid and urate in human seminal plasma: determination and interrelationships with chemiluminescence in washed semen. Hum Reprod. 1995;10(1):110-5.##Colagar AH, Marzony ET. Ascorbic Acid in human seminal plasma: determination and its relationship to sperm quality. J Clin Biochem Nutr. 2009;45(2):144-9.##Kutlubay R, Oguz EO, Can B, Guven MC, Sinik Z, Tuncay OL. Vitamin E protection from testicular damage caused by intraperitoneal aluminium. Int J Toxicol. 2007;26(4):297-306.##Xu K, Shang X, Chen Y, Zhao F, Zhu P, Huang Y. [Measurement of uric acid of seminal plasma in fertile and infertile males]. Zhonghua Nan Ke Xue. 2004;10(12):900-1, 906. Chinese.##Zhang HY, Lu JC, Zhang RS, Xia YX, Huang YF. [Determination of uric acid in seminal plasma and correlation between seminal uric acid and semen parameters]. Zhonghua Nan Ke Xue. 2007;13(11):1016-9. Chinese.##Webb GW,Affiliations Arns MJ. Effect of pyruvate and lactate on motility of cold stored stallion spermatozoa challenged by hydrogen peroxide. J Equine Vet Sci. 2006;26:406-11.##Lenzi A, Culasso F, Gandini L, Lombardo F, Dondero F. Placebo-controlled, double-blind, cross-over trial of glutathione therapy in male infertility. Hum Reprod. 1993;8(10):1657-62.##Giannattasio A, De Rosa M, Smeraglia R, Zarrilli S, Cimmino A, Di Rosario B, et al. Glutathione peroxidase (GPX) activity in seminal plasma of healthy and infertile males. J Endocrinol Invest. 2002;25(11):983-6.##Alvarez JG, Storey BT. Taurine, hypotaurine, epinephrine and albumin inhibit lipid peroxidation in rabbit spermatozoa and protect against loss of motility. Biol Reprod. 1983;29(3):548-55.##Khosrowbeygi A, Zarghami N, Deldar Y. Correlation between sperm quality parameters and seminal plasma antioxidants status. Iran J Reprod Med. 2004;2:58-64.##Morte MI, Rodrigues AM, Soares D, Rodrigues AS, Gamboa S, Ramalho-Santos J. The quantification of lipid and protein oxidation in stallion spermatozoa and seminal plasma: seasonal distinctions and correlations with DNA strand breaks, classical seminal parameters and stallion fertility. Anim Reprod Sci. 2008;106(1-2):36-47.##Yeni D, Gundogan M, Cigerci IH, Avdatek F, Fidan AF. Seasonal variation of oxidative stress parameters in ram seminal plasma. J Anim Vet Adv. 2010;9:49-55.##Aitken RJ, Clarkson JS. Cellular basis of defective sperm function and its association with the genesis of reactive oxygen species by human spermatozoa. J Reprod Fertil. 1987;81(2):459-69.##Ernster L, editor. Lipid peroxidation in biological membranes: mechanisms and implications. Boca Raton, FL: CRC Press; 1993. p. 1-38. (Yagi K, editor. Active oxygen, lipid peroxides and antioxidants).##Aaberg RA, Sauer MV, Sikka S, Rajfer J. Effects of extracellular ionized calcium, diltiazem and cAMP on motility of human spermatozoa. J Urol. 1989;141(5):1221-4.##Alvarez JG, Storey BT. Role of glutathione peroxidase in protecting mammalian spermatozoa from loss of motility caused by spontaneous lipid peroxidation. Gamete Res. 1989;23(1):77-90.##Thomas JA, Poland B, Honzatko R. Protein sulfhydryls and their role in the antioxidant function of protein S-thiolation. Arch Biochem Biophys. 1995;319(1):1-9.##Aitken RJ, Fisher HM, Fulton N, Gomez E, Knox W, Lewis B, et al. Reactive oxygen species generation by human spermatozoa is induced by exogenous NADPH and inhibited by the flavoprotein inhibitors diphenylene iodonium and quinacrine. Mol Reprod Dev. 1997;47(4):468-82.##Griveau JF, Dumont E, Renard P, Callegari JP, Le Lannou D. Reactive oxygen species, lipid peroxidation and enzymatic defence systems in human spermatozoa. J Reprod Fertil. 1995;103(1):17-26.##Evenson DP, Larson KL, Jost LK. Sperm chromatin structure assay: its clinical use for detecting sperm DNA fragmentation in male infertility and comparisons with other techniques. J Androl. 2002;23(1):25-43.##Agarwal A, Said TM. Role of sperm chromatin abnormalities and DNA damage in male infertility. Hum Reprod Update. 2003;9(4):331-45.##Sakkas D, Moffatt O, Manicardi GC, Mariethoz E, Tarozzi N, Bizzaro D. Nature of DNA damage in ejaculated human spermatozoa and the possible involvement of apoptosis. Biol Reprod. 2002;66(4):1061-7.##Zini A, San Gabriel M, Baazeem A. Antioxidants and sperm DNA damage: a clinical perspective. J Assist Reprod Genet. 2009;26(8):427-32.##Duran EH, Morshedi M, Taylor S, Oehninger S. Sperm DNA quality predicts intrauterine insemination outcome: a prospective cohort study. Hum Reprod. 2002;17(12):3122-8.##Meseguer M, Martinez-Conejero JA, O&#39;Connor JE, Pellicer A, Remohi J, Garrido N. The significance of sperm DNA oxidation in embryo development and reproductive outcome in an oocyte donation program: a new model to study a male infertility prognostic factor. Fertil Steril. 2008;89(5):1191-9.##Kao SH, Chao HT, Wei YH. Multiple deletions of mitochondrial DNA are associated with the decline of motility and fertility of human spermatozoa. Mol Hum Reprod. 1998;4(7):657-66.##Lysiak JJ, Turner SD, Nguyen QA, Singbartl K, Ley K, Turner TT. Essential role of neutrophils in germ cell-specific apoptosis following ischemia/reperfusion injury of the mouse testis. Biol Reprod. 2001;65(3):718-25.##Matsui Y. Regulation of germ cell death in mammalian gonads. APMIS. 1998;106(1):142-8.##Brinkworth MH, Weinbauer GF, Schlatt S, Nieschlag E. Identification of male germ cells undergoing apoptosis in adult rats. J Reprod Fertil. 1995;105(1):25-33.##Turner TT, Bang HJ, Lysiak JL. The molecular pathology of experimental testicular torsion suggests adjunct therapy to surgical repair. J Urol. 2004;172(6 Pt 2):2574-8.##Cudicini C, Lejeune H, Gomez E, Bosmans E, Ballet F, Saez J, et al. Human Leydig cells and Sertoli cells are producers of interleukins-1 and -6. J Clin Endocrinol Metab. 1997;82(5):1426-33.##Lysiak JJ, Bang HJ, Nguyen QA, Turner TT. Activation of the nuclear factor kappa B pathway following ischemia-reperfusion of the murine testis. J Androl. 2005;26(1):129-35.##Collin O, Bergh A, Damber JE, Widmark A. Control of testicular vasomotion by testosterone and tubular factors in rats. J Reprod Fertil. 1993;97(1):115-21.##Nilsson H, Aalkjaer C. Vasomotion: mechanisms and physiological importance. Mol Interv. 2003;3(2):79-89, 51.##Lysiak JJ, Nguyen QA, Turner TT. Fluctuations in rat testicular interstitial oxygen tensions are linked to testicular vasomotion: persistence after repair of torsion. Biol Reprod. 2000;63(5):1383-9.##Shiraishi K, Naito K, Yoshida K. Nitric oxide promotes germ cell necrosis in the delayed phase after experimental testicular torsion of rat. Biol Reprod. 2001;65(2):514-21.##Ozturk H, Buyukbayram H, Ozdemir E, Ketani A, Gurel A, Onen A, et al. The effects of nitric oxide on the expression of cell adhesion molecules (ICAM-1, UEA-1, and tenascin) in rats with unilateral testicular torsion. J Pediatr Surg. 2003;38(11):1621-7.##Laroux FS, Lefer DJ, Kawachi S, Scalia R, Cockrell AS, Gray L, et al. Role of nitric oxide in the regulation of acute and chronic inflammation. Antioxid Redox Signal. 2000;2(3):391-6.##Pasqualotto FF, Sharma RK, Nelson DR, Thomas AJ, Agarwal A. Relationship between oxidative stress, semen characteristics, and clinical diagnosis in men undergoing infertility investigation. Fertil Steril. 2000;73(3):459-64.##Ishikawa T, Kondo Y, Goda K, Fujisawa M. Overexpression of endothelial nitric oxide synthase in transgenic mice accelerates testicular germ cell apoptosis induced by experimental cryptorchidism. J Androl. 2005;26(2):281-8.##Zirkin BR, Chen H. Regulation of Leydig cell steroidogenic function during aging. Biol Reprod. 2000;63(4):977-81.##Turner TT, Bang HJ, Lysiak JJ. Experimental testicular torsion: reperfusion blood flow and subsequent testicular venous plasma testosterone concentrations. Urology. 2005;65(2):390-4.##Hanukoglu I. Antioxidant protective mechanisms against reactive oxygen species (ROS) generated by mitochondrial P450 systems in steroidogenic cells. Drug Metab Rev. 2006;38(1-2):171-96.##Luo L, Chen H, Trush MA, Show MD, Anway MD, Zirkin BR. Aging and the brown Norway rat leydig cell antioxidant defense system. J Androl. 2006;27(2):240-7.##Kostic T, Andric S, Kovacevic R, Maric D. The involvement of nitric oxide in stress-impaired testicular steroidogenesis. Eur J Pharmacol. 1998; 346(2-3):267-73.##Cao L, Leers-Sucheta S, Azhar S. Aging alters the functional expression of enzymatic and non-enzymatic anti-oxidant defense systems in testicular rat Leydig cells. J Steroid Biochem Mol Biol. 2004;88(1):61-7.##Spiess AN, Feig C, Schulze W, Chalmel F, Cappallo-Obermann H, Primig M, et al. Cross-platform gene expression signature of human spermatogenic failure reveals inflammatory-like response. Hum Reprod. 2007;22(11):2936-46.##Rodriguez MG, Rival C, Theas MS, Lustig L. Immunohistopathology of the contralateral testis of rats undergoing experimental torsion of the spermatic cord. Asian J Androl. 2006;8(5):576-83.##Romeo C, Ientile R, Impellizzeri P, Turiaco N, Teletta M, Antonuccio P, et al. Preliminary report on nitric oxide-mediated oxidative damage in adolescent varicocele. Hum Reprod. 2003;18(1):26-9.##Ishikawa T, Kondo Y, Goda K, Fujisawa M. Overexpression of endothelial nitric oxide synthase in transgenic mice accelerates testicular germ cell apoptosis induced by experimental cryptorchidism. J Androl. 2005;26(2):281-8.##Misro MM, Chaki SP, Gautam DK. Germ cell death and their removal during initial stages of testicular ischemia and cryptorchidism: a comparative analysis. Indian J Exp Biol. 2005;43(11):1080-7.##Samanta L, Chainy GB. Comparison of hexa-chlorocyclohexane-induced oxidative stress in the testis of immature and adult rats. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1997;118(3):319-27.##Homma-Takeda S, Hiraku Y, Ohkuma Y, Oikawa S, Murata M, Ogawa K, et al. 2,4,6-trinitrotoluene-induced reproductive toxicity via oxidative DNA damage by its metabolite. Free Radic Res. 2002;36(5):555-66.##Meng Z, Bai W. Oxidation damage of sulfur dioxide on testicles of mice. Environ Res. 2004;96(3):298-304.##Wellejus A, Poulsen HE, Loft S. Iron-induced oxidative DNA damage in rat sperm cells in vivo and in vitro. Free Radic Res. 2000;32(1):75-83.##Siu ER, Mruk DD, Porto CS, Cheng CY. Cadmium-induced testicular injury. Toxicol Appl Pharmacol. 2009;238(3):240-9.##Hsu PC, Liu MY, Hsu CC, Chen LY, Guo YL. Lead exposure causes generation of reactive oxygen species and functional impairment in rat sperm. Toxicology. 1997;122(1-2):133-43.##Wolf MB, Baynes JW. The anti-cancer drug, doxorubicin, causes oxidant stress-induced endothelial dysfunction. Biochim Biophys Acta. 2006;1760(2):267-71.##Santos NA, Bezerra CS, Martins NM, Curti C, Bianchi ML, Santos AC. Hydroxyl radical scavenger ameliorates cisplatin-induced nephrotoxicity by preventing oxidative stress, redox state unbalance, impairment of energetic metabolism and apoptosis in rat kidney mitochondria. Cancer Chemother Pharmacol. 2008;61(1):145-55.##William P Jr, Adamec C. The Encyclopedia of endocrine diseases and disorders. New York: Facts on File Inc; 2005.##Orisakwe OE, Obi E, Udemezue OO. Effect of halofantrin on testicular architecture and testosterone level in guinea pigs. Eur Bull Drug Res. 2003;11:105-9.##Obianime AW, Aprioku JS. Comparative study of artesunate, ACTs and their combinants on the spermatic parameters of the male guinea pig. Niger J Physiol Sci. 2009;24(1):1-6.##Obianime AW, Aprioku JS. Mechanism of action of artemisinins on biochemical, hematological and reproductive parameters in male guinea pigs. Int J Pharmacol. 2011;7(1):84-95.##Aprioku JS, Obianime AW. Evaluation of biochemical indices following administration of artemether, halofantrine and a combination of artemether and lumefantrine in guinea pigs. J Appl Pharma Sci. 2012;2(10):054-2.##Morakinyo AO, Iranloye BO, Adegoke OA. Antireproductive effect of calcium channel blockers on male rats. Reprod Med Biol. 2009;8:97-102.##Afify M, Abd Elmaksoud MDE, Mosa T, Elshaer M, Kotb N. Differential effects of amitriptyline treatment on testicular and liver functions in adult male rats. New York: Science Journal; 2010. p. 10-8.##Tilgada E. Chemotherapy: induction of stress responses. Endocr Rel Cancer. 2006;13(Suppl 1):S115-24.##Wu D, Cederbaum AI. Alcohol, oxidative stress, and free radical damage. Alcohol Res Health. 2003;27(4):277-84.##Peltola V, Mantyla E, Huhtaniemi I, Ahotupa M. Lipid peroxidation and antioxidant enzyme activities in the rat testis after cigarette smoke inhalation or administration of polychlorinated biphenyls or polychlorinated naphthalenes. J Androl. 1994;15(4):353-61.##Mostafa T, Tawadrous G, Roaia MM, Amer MK, Kader RA, Aziz A. Effect of smoking on seminal plasma ascorbic acid in infertile and fertile males. Andrologia. 2006;38(6):221-4.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>The Effects of cAMP-elevating Agents and Alpha Lipoic Acid on In Vitro Maturation of Mouse Germinal Vesicle Oocytes</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>541</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: In spite of extensive efforts to improve in vitro oocyte maturation, the obtained results are not very efficient. This study was conducted to assess impacts of cAMP elevating agents and alpha lipoic acid (ALA) on in vitro oocyte maturation and fertilization.
Methods: Mouse germinal vesicle (GV) oocytes were categorized into cumulus denuded oocytes (DOs; n=896) and cumulus oocyte complexes (COCs; n=1077) groups. GV oocytes were matured in vitro with or without ALA; (I) without the meiotic inhibitors; (II) supplemented with cilostamide; (III) supplemented with forskolin and (IV) supplemented with Forskolin plus cilostamide. The obtained metaphase II (MII) oocytes were subjected to in vitro fertilization. Independent-samples t-testand ANOVA were used for data analysis. A p-value less than 0.05 was considered to be statistically significant.
Results: The COCs maturation, fertilization and two cell embryo rates were higher than those of DOs in the control group, while no significant difference was observed between relevant COCs and DOs when they were cultured with cilostamide meiotic inhibitors in two step manner. Combined treatment of cilostamide and forskolin significantly elevated the developmental rates in both COCs and DOs as compared to other groups. The developmental rates of COCs and DOs in the presence of ALA were similar to their respective groups without ALA.
Conclusion: cAMP elevating agents were more effective on DOs than COCs with regard to rates of maturation and fertilization. However, ALA did not affect the developmental rates of both COCs and DOs in in vitro maturation in one or two step manner.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>173</FPAGE>
            <TPAGE>184</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Ali</Name>
<MidName>A</MidName>
<Family>Rahnama</Family>
<NameE>Ali</NameE>
<MidNameE></MidNameE>
<FamilyE>Rahnama</FamilyE>
<Organizations>
<Organization>School of Biology, Damghan University</Organization>
</Organizations>
<Universities>
<University>School of Biology, Damghan University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Saeed</Name>
<MidName>S</MidName>
<Family>Zavareh</Family>
<NameE>Saeed</NameE>
<MidNameE></MidNameE>
<FamilyE>Zavareh</FamilyE>
<Organizations>
<Organization>School of Biology, Damghan University</Organization>
</Organizations>
<Universities>
<University>School of Biology, Damghan University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>Zavareh.S@gmail.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Mohammad Taghi</Name>
<MidName>MT</MidName>
<Family>Ghorbanian</Family>
<NameE>Mohammad Taghi</NameE>
<MidNameE></MidNameE>
<FamilyE>Ghorbanian</FamilyE>
<Organizations>
<Organization>School of Biology, Damghan University</Organization>
</Organizations>
<Universities>
<University>School of Biology, Damghan University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Isaac</Name>
<MidName>I</MidName>
<Family>Karimi</Family>
<NameE>Isaac</NameE>
<MidNameE></MidNameE>
<FamilyE>Karimi</FamilyE>
<Organizations>
<Organization>Laboratory of Molecular and Cellular Biology, Department of Basic Veterinary Sciences, School of Veterinary Medicine, Razi University,</Organization>
</Organizations>
<Universities>
<University>Laboratory of Molecular and Cellular Biology, Department of Basic Veterinary Sciences, School of Veterinary Medicine, Razi University,</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>ALA</KeyText></KEYWORD><KEYWORD><KeyText>cAMP-elevating agents</KeyText></KEYWORD><KEYWORD><KeyText>Cumulus cell</KeyText></KEYWORD><KEYWORD><KeyText>In vitro maturation</KeyText></KEYWORD><KEYWORD><KeyText>Mouse</KeyText></KEYWORD><KEYWORD><KeyText>Oocyte</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>541.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Canipari R. Oocyte--granulosa cell interactions. Hum Reprod Update. 2000;6(3):279-89.##Tanghe S, Van Soom A, Nauwynck H, Coryn M, de Kruif A. Minireview: Functions of the cumulus oophorus during oocyte maturation, ovulation, and fertilization. Mol Reprod Dev. 2002;61(3):414-24.##Combelles CM, Carabatsos MJ, Kumar TR, Matzuk MM, Albertini DF. Hormonal control of somatic cell oocyte interactions during ovarian follicle development. Mol Reprod Dev. 2004;69(3):347-55.##Gilchrist RB, Ritter LJ, Armstrong DT. Oocyte-somatic cell interactions during follicle development in mammals. Anim Reprod Sci. 2004;82-83:431-46.##Smith GD. In vitro maturation of oocytes. Curr Womens Health Rep. 2001;1(2):143-51.##Trounson A, Anderiesz C, Jones G. Maturation of human oocytes in vitro and their developmental competence. Reproduction. 2001;121(1):51-75.##Ali A, Benkhalifa M, Miron P. In-vitro maturation of oocytes: biological aspects. Reprod Biomed Online. 2006;13(3):437-46.##Salamone DF, Damiani P, Fissore RA, Robl JM, Duby RT. Biochemical and developmental evidence that ooplasmic maturation of prepubertal bovine oocytes is compromised. Biol Reprod. 2001;64(6):1761-8.##Schramm RD, Paprocki AM, VandeVoort CA. Causes of developmental failure of in-vitro matured rhesus monkey oocytes: impairments in embryonic genome activation. Hum Reprod. 2003;18(4):826-33.##Jimenez-Macedo AR, Izquierdo D, Urdaneta A, Anguita B, Paramio MT. Effect of roscovitine on nuclear maturation, MPF and MAP kinase activity and embryo development of prepubertal goat oocytes. Theriogenology. 2006;65(9):1769-82.##Combelles CM, Cekleniak NA, Racowsky C, Albertini DF. Assessment of nuclear and cytoplasmic maturation in in-vitro matured human oocytes. Hum Reprod. 2002;17(4):1006-16.##Eppig JJ, Schultz RM, O&#39;Brien M, Chesnel F. Relationship between the developmental programs controlling nuclear and cytoplasmic maturation of mouse oocytes. Dev Biol. 1994;164(1):1-9.##Anderiesz C, Fong CY, Bongso A, Trounson AO. Regulation of human and mouse oocyte maturation in vitro with 6-dimethylaminopurine. Hum Reprod. 2000;15(2):379-88.##Nogueira D, Cortvrindt R, De Matos DG, Vanhoutte L, Smitz J. Effect of phosphodiesterase type 3 inhibitor on developmental competence of immature mouse oocytes in vitro. Biol Reprod. 2003;69(6):2045-52.##Nogueira D, Cortvrindt R, Everaerdt B, Smitz J. Effects of long-term in vitro exposure to phosphodiesterase type-3 inhibitors on follicle and oocyte development. Reproduction. 2005;130(2):177-86.##Dieleman SJ, Hendriksen PJ, Viuff D, Thomsen PD, Hyttel P, Knijn HM, et al. Effects of in vivo prematuration and in vivo final maturation on developmental capacity and quality of pre-implantation embryos. Theriogenology. 2002;57(1):5-20.##Sela-Abramovich S, Edry I, Galiani D, Nevo N, Dekel N. Disruption of gap junctional communication within the ovarian follicle induces oocyte maturation. Endocrinology. 2006;147(5):2280-6.##Bilodeau-Goeseels S. Effects of phosphodiesterase inhibitors on spontaneous nuclear maturation and cAMP concentrations in bovine oocytes. Theriogenology. 2003;60(9):1679-90.##Masciarelli S, Horner K, Liu C, Park SH, Hinckley M, Hockman S, et al. Cyclic nucleotide phosphodiesterase 3A-deficient mice as a model of female infertility. J Clin Invest. 2004;114(2):196-205.##Conti M, Andersen CB, Richard F, Mehats C, Chun SY, Horner K, et al. Role of cyclic nucleotide signaling in oocyte maturation. Mol Cell Endocrinol. 2002;187(1-2):153-9.##Horner K, Livera G, Hinckley M, Trinh K, Storm D, Conti M. Rodent oocytes express an active adenylyl cyclase required for meiotic arrest. Dev Biol. 2003;258(2):385-96.##Soderling SH, Beavo JA. Regulation of cAMP and cGMP signaling: new phosphodiesterases and new functions. Curr Opin Cell Biol. 2000;12(2):174-9.##Sasseville M, Cote N, Guillemette C, Richard FJ. New insight into the role of phosphodiesterase 3A in porcine oocyte maturation. BMC Dev Biol. 2006;6:47.##Nogueira D, Albano C, Adriaenssens T, Cortvrindt R, Bourgain C, Devroey P, et al. Human oocytes reversibly arrested in prophase I by phosphodiesterase type 3 inhibitor in vitro. Biol Reprod. 2003;69(3):1042-52.##Nogueira D, Ron-El R, Friedler S, Schachter M, Raziel A, Cortvrindt R, et al. Meiotic arrest in vitro by phosphodiesterase 3-inhibitor enhances maturation capacity of human oocytes and allows subsequent embryonic development. Biol Reprod. 2006;74(1):177-84.##Bagg MA, Nottle MB, Grupen CG, Armstrong DT. Effect of dibutyryl cAMP on the cAMP content, meiotic progression, and developmental potential of in vitro matured pre-pubertal and adult pig oocytes. Mol Reprod Dev. 2006;73(10):1326-32.##Vanhoutte L, De Sutter P, Nogueira D, Gerris J, Dhont M, Van der Elst J. Nuclear and cytoplasmic maturation of in vitro matured human oocytes after temporary nuclear arrest by phosphodiesterase 3-inhibitor. Hum Reprod. 2007;22(5):1239-46.##Shu YM, Zeng HT, Ren Z, Zhuang GL, Liang XY, Shen HW, et al. Effects of cilostamide and forskolin on the meiotic resumption and embryonic development of immature human oocytes. Hum Reprod. 2008;23(3):504-13.##Luciano AM, Modina S, Vassena R, Milanesi E, Lauria A, Gandolfi F. Role of intracellular cyclic adenosine 3&#39;,5&#39;-monophosphate concentration and oocyte-cumulus cells communications on the acquisition of the developmental competence during in vitro maturation of bovine oocyte. Biol Reprod. 2004;70(2):465-72.##Zavareh S, Saberivand A, Salehnia M. The effect of progesterone on the in vitro maturation and developmental competence of mouse germinal vesicle oocytes. Int J Fertil Steril. 2009;3(1):21-8.##Zavareh S, Salehnia M, Saberivand A. Comparison of different vitrification procedures on developmental competence of mouse germinal vesicle oocytes in the presence or absence of cumulus cells. Int J Fertil Steril. 2009;3(3):111-8.##Gilchrist RB, Thompson JG. Oocyte maturation: emerging concepts and technologies to improve developmental potential in vitro. Theriogenology. 2007;67(1):6-15.##Jamnongjit M, Hammes SR. Oocyte maturation: the coming of age of a germ cell. Semin Reprod Med. 2005;23(3):234-41.##Norris RP, Ratzan WJ, Freudzon M, Mehlmann LM, Krall J, Movsesian MA, et al. Cyclic GMP from the surrounding somatic cells regulates cyclic AMP and meiosis in the mouse oocyte. Development. 2009;136(11):1869-78.##Norris RP, Freudzon M, Mehlmann LM, Cowan AE, Simon AM, Paul DL, et al. Luteinizing hormone causes MAP kinase-dependent phosphorylation and closure of connexin 43 gap junctions in mouse ovarian follicles: one of two paths to meiotic resumption. Development. 2008;135(19):3229-38.##Combelles CM, Gupta S, Agarwal A. Could oxidative stress influence the in-vitro maturation of oocytes? Reprod Biomed Online. 2009;18(6):864-80.##Agarwal A, Gupta S, Sikka S. The role of free radicals and antioxidants in reproduction. Curr Opin Obstet Gynecol. 2006;18(3):325-32.##Talebi A, Zavareh S, Kashani MH, Lashgarbluki T, Karimi I. The effect of alpha lipoic acid on the developmental competence of mouse isolated preantral follicles. J Assist Reprod Genet. 2012;29(2):175-83.##Yamasaki M, Kawabe A, Nishimoto K, Madhyastha H, Sakakibara Y, Suiko M, et al. Dihydro-alpha-lipoic acid has more potent cytotoxicity than alpha-lipoic acid. In Vitro Cell Dev Biol Anim. 2009;45(5-6):275-80.##Packer L, Witt EH, Tritschler HJ. alpha-Lipoic acid as a biological antioxidant. Free Radic Biol Med. 1995;19(2):227-50.##Azadbakht M, Valojerdi MR. Development of vitrified-warmed mouse embryos co-cultured with polarized or non-polarized uterine epithelial cells using sequential culture media. J Assist Reprod Genet. 2008;25(6):251-61.##Summers MC, McGinnis LK, Lawitts JA, Raffin M, Biggers JD. IVF of mouse ova in a simplex optimized medium supplemented with amino acids. Hum Reprod. 2000;15(8):1791-801.##Richard FJ, Tsafriri A, Conti M. Role of phosphodiesterase type 3A in rat oocyte maturation. Biol Reprod. 2001;65(5):1444-51.##Gilchrist RB, Lane M, Thompson JG. Oocyte-secreted factors: regulators of cumulus cell function and oocyte quality. Hum Reprod Update. 2008;14(2):159-77.##Son WY, Lee SY, Lim JH. Fertilization, cleavage and blastocyst development according to the maturation timing of oocytes in in vitro maturation cycles. Hum Reprod. 2005;20(11):3204-7.##Thomas RE, Thompson JG, Armstrong DT, Gilchrist RB. Effect of specific phosphodiesterase isoenzyme inhibitors during in vitro maturation of bovine oocytes on meiotic and developmental capacity. Biol Reprod. 2004;71(4):1142-9.##Luvoni GC, Keskintepe L, Brackett BG. Improvement in bovine embryo production in vitro by glutathione-containing culture media. Mol Reprod Dev. 1996;43(4):437-43.##Ali AA, Bilodeau JF, Sirard MA. Antioxidant requirements for bovine oocytes varies during in vitro maturation, fertilization and development. Theriogenology. 2003;59(3-4):939-49.##Takami M, Preston SL, Toyloy VA, Behrman HR. Antioxidants reversibly inhibit the spontaneous resumption of meiosis. Am J Physiol. 1999;276(4 Pt 1):E684-8.##Tamura H, Takasaki A, Miwa I, Taniguchi K, Maekawa R, Asada H, et al. Oxidative stress impairs oocyte quality and melatonin protects oocytes from free radical damage and improves fertilization rate. J Pineal Res. 2008;44(3):280-7.##Tarin JJ. Potential effects of age-associated oxidative stress on mammalian oocytes/embryos. Mol Hum Reprod. 1996;2(10):717-24.##de Matos DG, Furnus CC, Moses DF, Baldassarre H. Effect of cysteamine on glutathione level and developmental capacity of bovine oocyte matured in vitro. Mol Reprod Dev. 1995;42(4):432-6.##de Matos DG, Furnus CC, Moses DF, Martinez AG, Matkovic M. Stimulation of glutathione synthesis of in vitro matured bovine oocytes and its effect on embryo development and freezability. Mol Reprod Dev. 1996;45(4):451-7.##Blondin P, Coenen K, Sirard MA. The impact of reactive oxygen species on bovine sperm fertilizing ability and oocyte maturation. J Androl. 1997;18(4):454-60.##Abedelahi A, Salehnia M, Allameh AA, Davoodi D. Sodium selenite improves the in vitro follicular development by reducing the reactive oxygen species level and increasing the total antioxidant capacity and glutathione peroxide activity. Hum Reprod. 2010;25(4):977-85.##Cetica PD, Pintos LN, Dalvit GC, Beconi MT. Antioxidant enzyme activity and oxidative stress in bovine oocyte in vitro maturation. IUBMB Life. 2001;51(1):57-64.##El Mouatassim S, Guerin P, Menezo Y. Expression of genes encoding antioxidant enzymes in human and mouse oocytes during the final stages of maturation. Mol Hum Reprod. 1999;5(8):720-5.##Harvey MB, Arcellana-Panlilio MY, Zhang X, Schultz GA, Watson AJ. Expression of genes encoding antioxidant enzymes in preimplantation mouse and cow embryos and primary bovine oviduct cultures employed for embryo coculture. Biol Reprod. 1995;53(3):532-40.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Endothelial Nitric Oxide Synthase (eNOS) 4a/b and G894T Polymorphisms and Susceptibility to Preeclampsia</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>542</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Preeclampsia is a pregnancy complication with unknown etiology and its incidence is associated with genetic and environmental factors. There are inconsistent reports related to the role of endothelial nitric oxide synthase (eNOS) 4a/b polymorphism on the risk of preeclampsia development. The aim of the present study was to investigate the possible influence of eNOS 4a/b and its synergism with eNOS G894T polymorphism on the risk of preeclampsia.
Methods: The present case-control study consisted of 179 unrelated women with preeclampsia including 118 with mild and 61 with severe preeclampsia and 96 unrelated women with normal pregnancy as controls. All studied women were from Kermanshah Province of Iran. eNOS 4a/b and G894T genotypes were detected using polymerase chain reaction (PCR), and PCR-restriction fragment length polymorphism (RFLP) methods, respectively. The categorical variables between groups were compared using χ2 test and the Odds ratios (OR) were obtained by SPSS logistic regression. Statistical significance was assumed at p&lt;0.05 level.
Results: The frequency of eNOS a allele was slightly higher in both mild (16.5%) and severe (17.2%) preeclamptic women than controls (15.1%). Also, no significant difference was found between early- and late-onset preeclamptic women regarding the distribution of eNOS 4a/b genotypes. The presence of each allele of eNOS a or T was not associated with the risk of preeclampsia. However, the concomitant presence of both eNOS a and T alleles was associated with a non significant increased risk of severe preeclampsia by 1.77-fold (p=0.35). 
Conclusion: The present study indicates the lack of association between eNOS a and T alleles with the risk of mild preeclampsia and a non significant increased risk of severe preeclampsia in the presence of both alleles which needs to be investigated in a study with larger samples.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>184</FPAGE>
            <TPAGE>190</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Zohreh</Name>
<MidName>Z</MidName>
<Family>Rahimi</Family>
<NameE>Zohreh</NameE>
<MidNameE></MidNameE>
<FamilyE>Rahimi</FamilyE>
<Organizations>
<Organization>Medical Biology Research Center, Kermanshah University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Medical Biology Research Center, Kermanshah University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>rahimizus@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Amir</Name>
<MidName>A</MidName>
<Family>Aghaei</Family>
<NameE>Amir</NameE>
<MidNameE></MidNameE>
<FamilyE>Aghaei</FamilyE>
<Organizations>
<Organization>Department of Biochemistry, Medical School, Kermanshah University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Department of Biochemistry, Medical School, Kermanshah University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Ziba</Name>
<MidName>Z</MidName>
<Family>Rahimi</Family>
<NameE>Ziba</NameE>
<MidNameE></MidNameE>
<FamilyE>Rahimi</FamilyE>
<Organizations>
<Organization>Medical Biology Research Center, Kermanshah University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Medical Biology Research Center, Kermanshah University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Asad</Name>
<MidName>A</MidName>
<Family>Vaisi-Raygani</Family>
<NameE>Asad</NameE>
<MidNameE></MidNameE>
<FamilyE>Vaisi-Raygani</FamilyE>
<Organizations>
<Organization>Department of Biochemistry, Medical School, Kermanshah University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Department of Biochemistry, Medical School, Kermanshah University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>eNOS 4a/b</KeyText></KEYWORD><KEYWORD><KeyText>eNOS G894T</KeyText></KEYWORD><KEYWORD><KeyText>Mild preeclampsia</KeyText></KEYWORD><KEYWORD><KeyText>Polymorphism</KeyText></KEYWORD><KEYWORD><KeyText>Severe preeclampsia</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>542.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Rahimi Z, Rahimi Z, Shahsavandi MO, Bidoki K, Rezaei M. MMP-9 (-1562 C:T) polymorphism as a biomarker of susceptibility to severe pre-eclampsia. Biomark Med. 2013;7(1):93-8.##Rahimi Z, Malek-Khosravi S, Rahimi Z, Jalilvand F, Parsian A. MTHFR C677T and eNOS G894T variants in preeclamptic women: Contribution to lipid peroxidation and oxidative stress. Clin Biochem. 2013;46(1-2):143-7.##Malek-Khosravi S, Rahimi Z, Rahimi Z, Jalilvand F, Parsian A. Thrombophilic mutations and susceptibility to preeclampsia in Western Iran. J Thromb Thrombolysis. 2012;33(1):109-15.##Ahluwalia TS, Ahuja M, Rai TS, Kohli HS, Sud K, Bhansali A, et al. Endothelial nitric oxide synthase gene haplotypes and diabetic nephropathy among Asian Indians. Mol Cell Biochem. 2008;314(1-2):9-17.##He Y, Fan Z, Zhang J, Zhang Q, Zheng M, Li Y, et al.Polymorphisms of eNOS gene are associated with diabetic nephropathy: a meta-analysis. Mutagenesis. 2011;26(2):339-49.##Rahimi Z, Rahimi Z, Shahvaisi-Zadeh F, Sadeghei S, Vessal M, Yavari N. eNOS 4a/b polymorphism and its interaction with eNOS G894T variants in type 2 diabetes mellitus: modifying the risk of diabetic nephropathy. Dis Markers. 2013;34(6):437-43.##Sandrim VC, Palei AC, Cavalli RC, Araujo FM, Ramos ES, Duarte G, et al. eNOS haplotypes associated with gestational hypertension or preeclampsia. Pharmacogenomics. 2008;9(10):1467-73.##Chen H, Zhao G, Sun M, Wang H, Liu J, Gao W, et al. Endothelial nitric oxide synthase gene polymorphisms (G894T, 4b/a and T-786C) and preeclampsia: meta-analysis of 18 case-control studies. DNA Cell Biol. 2012;31(6):1136-45.##Chen LK, Huang CH, Yeh HM, Lee CN, Shyu MK, Hsieh FJ, et al. Polymorphisms in the endothelial nitric oxide synthase gene may be protective against preeclampsia in a Chinese population. Reprod Sci. 2007;14(2):175-81.##Salimi S, Naghavi A, Mokhtari M, Noora M, Yaghmaei M. Lack of relationship between endothelial nitric oxide synthase gene 4b/a and T-786C polymorphisms with preeclampsia in southeast of Iran. Arch Gynecol Obstet. 2012;285(2):405-9.##Aggarwal PK, Jain V, Jha V. Endothelial nitric oxide synthase, angiotensin-converting enzyme and angiotensinogen gene polymorphisms in hypertensive disorders of pregnancy. Hypertens Res. 2010;33(5):473-7.##Publications Committee, Society for Maternal-Fetal Medicine, Sibai BM. Evaluation and management of severe preeclampsia before 34 weeks&#39; gestation. Am J Obstet Gynecol. 2011;205(3):191-8.##Sowmya S, Ramaiah A, Sunitha T, Nallari P, Jyothy A, Venkateshwari A. Evaluation of Interleukin-10 (G-1082A) Promoter Polymorphism in Preeclampsia. J Reprod Infertil. 2013;14(2):62-6.##Landau R, Xie HG, Dishy V, Wood AJ, Stein CM, Smiley RM. No association of the Asp298 variant of the endothelial nitric oxide synthase gene with preeclampsia. Am J Hypertens. 2004;17(5 Pt 1):391-4.##Dai B, Liu T, Zhang B, Zhang X, Wang Z. The polymorphism for endothelial nitric oxide synthase gene, the level of nitric oxide and the risk for pre-eclampsia: a meta-analysis. Gene. 2013;519 (1):187-93.##Qi HP, Fraser WD, Luo ZC, Julien P, Audibert F, Wei SQ. Endothelial nitric oxide synthase gene polymorphisms and risk of preeclampsia. Am J Perinatol. 2013;30(10):795-804.##Sandrim VC, Palei AC, Luizon MR, Izidoro-Toledo TC, Cavalli RC, Tanus-Santos JE. eNOS haplotypes affect the responsiveness to antihypertensive therapy in preeclampsia but not in gestational hypertension. Pharmacogenomics J. 2010;10(1):40-5.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Protective Effect of Ethyl Pyruvate on Epididymal Sperm Characteristics, Oxidative Stress and Testosterone Level in Methotrexate Treated Mice</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>543</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Methotrexate (MTX) is an anti-metabolite drug widely used in treatment of neoplastic disorders, rheumatoid arthritis and psoriasis. The ester derivative, ethyl pyruvate (EP) is stable in solution and should function as an antioxidant and energy precursor. This study was conducted to evaluate the protective role of EP on sperm parameters, testosterone level and malondialdehyde (MDA) production in mice treated with MTX.
Methods: 32 adult male NMRI mice weighing 26&#177;2 g were divided into 4 groups. Group 1 received 0.1 ml/mice/day of distilled water intraperitoneally for 30 days (ip). Group 2 was treated with methotrexate at a dose of 20 mg/kg once a week (ip) for 30 days. Group 3 was treated with ethyl pyruvate at a dose of 40 mg/kg/daily (ip) for 30 days. Group 4 was treated with methotrexate (20 mg/kg) once a week simultaneously with ethyl pyruvate 40 mg/kg for 30 days. The results were analyzed by one-way ANOVA. A p&lt;0.05 was considered to be significant.
Results: The results showed significant (p&lt;0.05) decrease in sperm count and sperm motility as well as testosterone concentration while sperm with damaged DNA and MDA concentration in mice treated with MTX in comparison with control and MX+EP groups increased significantly (p&lt;0.05). Instead, MTX+EP group caused partial amelioration in all parameters mentioned above.
Conclusion: Based on the present study, it can be concluded that MTX induced toxicity in sperm parameters and serum level of testosterone and increased MDA level. EP with its antioxidant properties could be administrated during treatment with MTX due to its protective effects on sperm parameters, plasma testosterone levels and lipid peroxidation.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>190</FPAGE>
            <TPAGE>197</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Elham</Name>
<MidName>E</MidName>
<Family>Atashfaraz</Family>
<NameE>Elham</NameE>
<MidNameE></MidNameE>
<FamilyE>Atashfaraz</FamilyE>
<Organizations>
<Organization>Faculty of Science, Urmia University</Organization>
</Organizations>
<Universities>
<University>Faculty of Science, Urmia University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>a.farazelham@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Farah</Name>
<MidName>F</MidName>
<Family>Farokhi</Family>
<NameE>Farah</NameE>
<MidNameE></MidNameE>
<FamilyE>Farokhi</FamilyE>
<Organizations>
<Organization>Department of Histology and Embryology, Faculty of Science, Urmia University</Organization>
</Organizations>
<Universities>
<University>Department of Histology and Embryology, Faculty of Science, Urmia University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Gholamreza</Name>
<MidName>Gh</MidName>
<Family>Najafi</Family>
<NameE>Gholamreza</NameE>
<MidNameE></MidNameE>
<FamilyE>Najafi</FamilyE>
<Organizations>
<Organization>Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Urmia University</Organization>
</Organizations>
<Universities>
<University>Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Urmia University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Ethyl pyruvate</KeyText></KEYWORD><KEYWORD><KeyText>Malondialdehyde</KeyText></KEYWORD><KEYWORD><KeyText>Methotrexate</KeyText></KEYWORD><KEYWORD><KeyText>Mice</KeyText></KEYWORD><KEYWORD><KeyText>Spermatozoa</KeyText></KEYWORD><KEYWORD><KeyText>Testosterone</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>543.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Frei B, Higdon JV. Antioxidant activity of tea polyphenols in vivo: evidence from animal studies. J Nutr. 2003;133(10):3275S-84S.##Havsteen BH. The biochemistry and medical significance of the flavonoids. Pharmacol Ther. 2002;96(2-3):67-202.##Varma SD, Hegde KR, Kovtun S. Oxidative damage to lens in culture: reversibility by pyruvate and ethyl pyruvate. Ophthalmologica. 2006;220(1):52-7.##O&#39;Donnell-Tormey J, Nathan CF, Lanks K, DeBoer CJ, de la Harpe J. Secretion of pyruvate. An antioxidant defense of mammalian cells. J Exp Med. 1987;165(2):500-14.##Varma SD, Devamanoharan PS, Ali AH. Prevention of intracellular oxidative stress to lens by pyruvate and its ester. Free Radic Res. 1998;28(2):131-5.##Olek RA, Antosiewicz J, Popinigis J, Gabbianelli R, Fedeli D, Falcioni G. Pyruvate but not lactate prevents NADH-induced myoglobin oxidation. Free Radic Biol Med. 2005;38(11):1484-90.##Constantopoulos G, Barranger JA. Nonenzymatic decarboxylation of pyruvate. Anal Biochem. 1984;139(2):353-8.##Sims CA, Wattanasirichaigoon S, Menconi MJ, Ajami AM, Fink MP. Ringer&#39;s ethyl pyruvate solution ameliorates ischemia/reperfusion-induced intestinal mucosal injury in rats. Crit Care Med. 2001;29(8):1513-8.##Devamanoharan PS, Henein M, Ali AH, Varma SD. Attenuation of sugar cataract by ethyl pyruvate. Mol Cell Biochem. 1999;200(1-2):103-9.##Arnon J, Meirow D, Lewis-Roness H, Ornoy A. Genetic and teratogenic effects of cancer treatments on gametes and embryos. Hum Reprod Update. 2001;7(4):394-403.##Peters GJ, van der Wilt CL, van Moorsel CJ, Kroep JR, Bergman AM, Ackland SP. Basis for effective combination cancer chemotherapy with antimetabolites. Pharmacol Ther. 2000;87(2-3):227-53.##Choudhury RC, Ghosh SK, Palo AK. Cytogenetic toxicity of methotrexate in mouse bone marrow. Environ Toxicol Pharmacol. 2000;8(3):191-196.##Jensen SB, Mouridsen HT, Reibel J, Brunner N, Nauntofte B. Adjuvant chemotherapy in breast cancer patients induces temporary salivary gland hypofunction. Oral Oncol. 2008;44(2):162-73.##Chow M, Koo J, Ng P, Rubin H. Random population-wide genetic damage induced in replicating cells treated with methotrexate. Mutat Res. 1998;413(3):251-64.##Gisondi P, Girolomoni G. Biologic therapies in psoriasis: a new therapeutic approach. Autoimmun Rev. 2007;6(8):515-9.##Novakovic T, Dordevic OM, Grujicic D, Marinkovic D, Jankovic S, Arsenijevic S. Effect of intratumoral application of methotrexate in vivo on frequency of micronuclei in peripheral blood lymphocytes. Arch Oncol. 2003;11:1-4.##Tian H, Cronstein BN. Understanding the mechanisms of action of methotrexate: implications for the treatment of rheumatoid arthritis. Bull NYU Hosp Jt Dis. 2007;65(3):168-73.##Padmanabhan S, Tripathi DN, Vikram A, Ramarao P, Jena GB. Methotrexate-induced cytotoxicity and genotoxicity in germ cells of mice: intervention of folic and folinic acid. Mutat Res. 2009;673(1):43-52.##Saxena AK, Dhungel S, Bhattacharya S, Jha CB, Srivastava AK. Effect of chronic low dose of methotrexate on cellular proliferation during spermatogenesis in rats. Arch Androl. 2004;50(1):33-5.##Shrestha S, Dhungel S, Saxena AK, Bhattacharya S, Maskey D. Effect of methotrexate (MTX) administration on spermatogenesis: an experimental on animal model. Nepal Med Coll J. 2007;9(4):230-3.##Padmanabhan S, Tripathi DN, Vikram A, Ramarao P, Jena GB. Cytotoxic and genotoxic effects of methotrexate in germ cells of male Swiss mice. Mutat Res. 2008;655(1-2):59-67.##Wyrobek AJ, Gordon LA, Burkhart JG, Francis MW, Kapp RW Jr, Letz G, et al. An evaluation of the mouse sperm morphology test and other sperm tests in nonhuman mammals. A report of the U.S. Environmental Protection Agency Gene-Tox Program. Mutat Res. 1983;115(1):1-72.##World Health Organization. WHO Laboratory manual for the examination of human semen and sperm – cervical mucus interaction. 3rd ed. Cambridge: Cambridge University press; 1992.##Carrell DT, Emery BR, Hammoud S. Altered protamine expression and diminished spermatogenesis: what is the link? Hum Reprod Update. 2007;13(3):313-27.##Bungum M, Humaidan P, Spano M, Jepson K, Bungum L, Giwercman A. The predictive value of sperm chromatin structure assay (SCSA) parameters for the outcome of intrauterine insemination, IVF and ICSI. Hum Reprod. 2004;19(6):1401-8.##Rezvanfar M, Sadrkhanlou R, Ahmadi A, Shojaei-Sadee H, Rezvanfar M, Mohammadirad A, et al. Protection of cyclophosphamide-induced toxicity in reproductive tract histology, sperm characteristics, and DNA damage by an herbal source; evidence for role of free-radical toxic stress. Hum Exp Toxicol. 2008;27(12):901-10.##Erenpreiss J, Bars J, Lipatnikova V, Erenpreisa J, Zalkalns J. Comparative study of cytochemical tests for sperm chromatin integrity. J Androl. 2001;22(1):45-53.##Meistrich ML, Brock WA, Grimes SR, Platz RD, Hnilica LS. Nuclear protein transitions during spermatogenesis. Fed Proc. 1978;37(11):2522-5.##Talebi AR, Moein MR, Tabibnejad N, Ghasemzadeh J. Effect of varicocele on chromatin condensation and DNA integrity of ejaculated spermatozoa using cytochemical tests. Andrologia. 2008;40(4):245-51.##Hosseinzadeh H, Sadeghnia HR. Safranal, a constituent of Crocus sativus (saffron), attenuated cerebral ischemia induced oxidative damage in rat hippocampus. J Pharm Pharm Sci. 2005;8(3):394-9.##Anders MW, Bull RJ, Cantor KP, Chakraborti D, Chen CJ, DeAngelo AB, et al. Monographs on the evaluation of carcinogenic risks to humans: pharmaceutical drugs. Lyon, France: IARC Scientific Publication; 1990. p. 415.##Choudhury RC, Ghosh SK, Palo AK. Cytogenetic toxicity of methotrexate in mouse bone marrow. Environ Toxicol Pharmacol. 2000;8(3):191-196.##Padmanabhan S, Tripathi DN, Vikram A, Ramarao P, Jena GB. Cytotoxic and genotoxic effects of methotrexate in germ cells of male Swiss mice. Mutat Res. 2008;655(1-2):59-67.##Abdel Aziz AH, Shouman SA, Attia AS, Saad SF. A study on the reproductive toxicity of erythrosine in male mice. Pharmacol Res. 1997;35(5):457-62.##Schimenti KJ, Hanneman WH, Schimenti JC. Evidence for cyclophosphamide-induced gene conversion and mutation in mouse germ cells. Toxicol Appl Pharmacol. 1997;147(2):343-50.##Tabassum H, Parvez S, Rehman H, Dev Banerjee B, Siemen D, Raisuddin S. Nephrotoxicity and its prevention by taurine in tamoxifen induced oxidative stress in mice. Hum Exp Toxicol. 2007;26(6):509-18.##Jahovic N, Cevik H, Sehirli AO, Yegen BC, Sener G. Melatonin prevents methotrexate-induced hepatorenal oxidative injury in rats. J Pineal Res. 2003;34(4):282-7.##Jahovic N, Sener G, Cevik H, Ersoy Y, Arbak S, Yegen BC. Amelioration of methotrexate-induced enteritis by melatonin in rats. Cell Biochem Funct. 2004;22(3):169-78.##Sener G, Ekşioglu-Demiralp E, Cetiner M, Ercan F, Sirvanci S, Gedik N, et al. L-Carnitine ameliorates methotrexate-induced oxidative organ injury and inhibits leukocyte death. Cell Biol Toxicol. 2006;22(1):47-60.##Song M, Kellum JA, Kaldas H, Fink MP. Evidence that glutathione depletion is a mechanism responsible for the anti-inflammatory effects of ethyl pyruvate in cultured lipopolysaccharide-stimulated RAW 264.7 cells. J Pharmacol Exp Ther. 2004;308(1):307-16.##Tawadrous ZS, Delude RL, Fink MP. Resuscitation from hemorrhagic shock with Ringer&#39;s ethyl pyruvate solution improves survival and ameliorates intestinal mucosal hyperpermeability in rats. Shock. 2002;17(6):473-7.##Tsung A, Kaizu T, Nakao A, Shao L, Bucher B, Fink MP, et al. Ethyl pyruvate ameliorates liver ischemia-reperfusion injury by decreasing hepatic necrosis and apoptosis. Transplantation. 2005;79(2):196-204.##Vardi N, Parlakpinar H, Cetin A, Erdogan A, Cetin Ozturk I. Protective effect of beta-carotene on methotrexate-induced oxidative liver damage. Toxicol Pathol. 2010;38(4):592-7.##Babiak RM, Campello AP, Carnieri EG, Oliveira MB. Methotrexate: pentose cycle and oxidative stress. Cell Biochem Funct. 1998;16(4):283-93.##Tabassum H, Rehman H, Banerjee BD, Raisuddin S, Parvez S. Attenuation of tamoxifen-induced hepatotoxicity by taurine in mice. Clin Chim Acta. 2006;370(1-2):129-36.##Ajami AM, Sims CA, Fink MP, investors. Pyruvate ester composition and method of use for resuscitation after events of ischemia and reperfusion. United States patent US 10:116-707. 2004.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Assessment of C-reactive Protein and C3 as Inflammatory Markers of Insulin Resistance in Women with Polycystic Ovary Syndrome: A Case-Control Study</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>544</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Polycystic ovary syndrome (PCOS), a common endocrine disorder, is associated with infertility, menstrual dysfunction, hirsutism and frequent miscarriages. Insulin resistance, as a major cause of PCOS, represents a disorder with increase in inflammatory markers and risk of type 2 diabetes.  We aimed to investigate whether inflammatory markers, including C-reactive protein and C3 (Complement), are related and altered in polycystic ovary syndrome.
Methods: A case-control study including forty-two women diagnosed with PCOS, according to Rotterdam criteria, and forty-two healthy controls, matched for body mass index (BMI) and age, was conducted in 2012. C-Reactive protein (CRP) and C3 were assessed as possible determinants of the homeostasis model assessment (HOMA) index. Independent-sample t-test was used to compare the means of the groups in age, BMI, C3, FBS and BS 2hpp (2 hr postprandial glucose) and for CRP, Fasting Insulin and 2 hr Plasma Insulin and HOMA index. Mann-Whitney test and Pearson correlation were used for analyzing the data. The p&lt;0.05 was considered as statistically significant.
Results: Levels of plasma CRP (p=0.039), 2 hr pp (p=0.045), Fasting Insulin (p=0.002), 2 hr Plasma Insulin (p=0.002) and HOMA index (p=0.002) were significantly higher in PCOS patients. But C3 was not significantly higher in cases (p=0.885). There was no significant correlation between C3 and CRP with HOMA index.
Conclusion: CRP increased significantly in patients with PCOS and was associated with insulin resistance, the most probable cause of PCOS. However, such an association was not found in C3.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>197</FPAGE>
            <TPAGE>202</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Setareh</Name>
<MidName>S</MidName>
<Family>Dehdashtihaghighat</Family>
<NameE>Setareh</NameE>
<MidNameE></MidNameE>
<FamilyE>Dehdashtihaghighat </FamilyE>
<Organizations>
<Organization>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Abolfazl</Name>
<MidName>A</MidName>
<Family>Mehdizadehkashi</Family>
<NameE>Abolfazl</NameE>
<MidNameE></MidNameE>
<FamilyE>Mehdizadehkashi</FamilyE>
<Organizations>
<Organization>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>amehdizadehkashi@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Amirmohsen</Name>
<MidName>A</MidName>
<Family>Arbabi</Family>
<NameE>Amirmohsen</NameE>
<MidNameE></MidNameE>
<FamilyE>Arbabi</FamilyE>
<Organizations>
<Organization>Iran University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Iran University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Mohadeseh</Name>
<MidName>M</MidName>
<Family>Pishgahroudsari</Family>
<NameE>Mohadeseh</NameE>
<MidNameE></MidNameE>
<FamilyE>Pishgahroudsari</FamilyE>
<Organizations>
<Organization>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Shahla</Name>
<MidName>Sh</MidName>
<Family>Chaichian</Family>
<NameE>Shahla</NameE>
<MidNameE></MidNameE>
<FamilyE>Chaichian</FamilyE>
<Organizations>
<Organization>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Minimally Invasive Surgery Research Center, Iran University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>C3</KeyText></KEYWORD><KEYWORD><KeyText>C-reactive protein</KeyText></KEYWORD><KEYWORD><KeyText>Insulin resistance</KeyText></KEYWORD><KEYWORD><KeyText>Polycystic ovary syndrome</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>544.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Evian Annual Reproduction (EVAR) Workshop Group 2010, Fauser BC, Diedrich K, Bouchard P, Dom&#237;nguez F, Matzuk M, et al. Contemporary genetic technologies and female reproduction. Hum Reprod Update. 2011;17(6):829-47.##Goodarzi MO, Korenman SG. The importance of insulin resistance in polycystic ovary syndrome. Fertil Steril. 2003;80(2):255-8.##Oktenli C, Ozgurtas T, Dede M, Sanisoglu YS, Yenen MC, Yesilova Z, et al. Metformin decreases circulating acylation-stimulating protein levels in polycystic ovary syndrome. Gynecol Endocrinol. 2007;23(12):710-5.##Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, Yildiz BO. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab. 2004;89(6):2745-9.##Diamanti-Kandarakis E, Paterakis T, Alexandraki K, Piperi C, Aessopos A, Katsikis I, et al. Indices of low-grade chronic inflammation in polycystic ovary syndrome and the beneficial effect of metformin. Hum Reprod. 2006;21(6):1426-31.##Ehrmann DA, Barnes RB, Rosenfield RL, Cavaghan MK, Imperial J. Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care. 1999;22(1):141-6.##Muscari A, Antonelli S, Bianchi G, Cavrini G, Dapporto S, Ligabue A, et al. Serum C3 is a stronger inflammatory marker of insulin resistance than C-reactive protein, leukocyte count, and erythrocyte sedimentation rate: comparison study in an elderly population. Diabetes Care. 2007;30(9):2362-8.##Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol. 1999;19(4):972-8.##Florez H, Castillo-Florez S, Mendez A, Casanova-Romero P, Larreal-Urdaneta C, Lee D, et al. C-reactive protein is elevated in obese patients with the metabolic syndrome. Diabetes Res Clin Pract. 2006;71(1):92-100.##Ford ES. Body mass index, diabetes, and C-reactive protein among U.S. adults. Diabetes Care. 1999;22(12):1971-7.##Frohlich M, Imhof A, Berg G, Hutchinson WL, Pepys MB, Boeing H, et al. Association between C-reactive protein and features of the metabolic syndrome: a population-based study. Diabetes Care. 2000;23(12):1835-9.##Ridker PM, Buring JE, Cook NR, Rifai N. C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: an 8-year follow-up of 14 719 initially healthy American women. Circulation. 2003;107(3):391-7.##Wannamethee SG, Lowe GD, Shaper AG, Rumley A, Lennon L, Whincup PH. The metabolic syndrome and insulin resistance: relationship to haemostatic and inflammatory markers in older non-diabetic men. Atherosclerosis. 2005;181(1):101-8.##Yang S, Li Q, Song Y, Tian B, Cheng Q, Qing H, et al. Serum complement C3 has a stronger association with insulin resistance than high-sensitivity C-reactive protein in women with polycystic ovary syndrome. Fertil Steril. 2011;95(5):1749-53.##Ravn P, Haugen AG, Glintborg D. Overweight in polycystic ovary syndrome. An update on evidence based advice on diet, exercise and metformin use for weight loss. Minerva Endocrinol. 2013;38(1):59-76.##Tosi F, Dorizzi R, Castello R, Maffeis C, Spiazzi G, Zoppini G, et al. Body fat and insulin resistance independently predict increased serum C-reactive protein in hyperandrogenic women with polycystic ovary syndrome. Eur J Endocrinol. 2009;161(5):737-45.##Adams J, Polson DW, Franks S. Prevalence of polycystic ovaries in women with anovulation and idiopathic hirsutism. Br Med J (Clin Res Ed). 1986;293(6543):355-9.##Robinson S, Henderson AD, Gelding SV, Kiddy D, Niththyananthan R, Bush A, et al. Dyslipidaemia is associated with insulin resistance in women with polycystic ovaries. Clin Endocrinol (Oxf). 1996;44(3):277-84.##Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000;342(12):836-43.##Marette A. Mediators of cytokine-induced insulin resistance in obesity and other inflammatory settings. Curr Opin Clin Nutr Metab Care. 2002;5(4):377-83.##Forouhi NG, Sattar N, McKeigue PM. Relation of C-reactive protein to body fat distribution and features of the metabolic syndrome in Europeans and South Asians. Int J Obes Relat Metab Disord. 2001;25(9):1327-31.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Association between Coping Strategies and Infertility Stress among a Group of Women with Fertility Problem in Shiraz, Iran</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>545</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Studies have shown that individuals with fertility problems experience psychosocial problems. The use of various coping strategies seems to have different impacts on women with infertility stress. The aim of this study was to examine the role of coping strategies (active-avoidance, passive-avoidance, active-confronting and meaning based) in predicting infertility stress among a group of women seeking infertility treatment in Shiraz. 
Methods: One hundred twenty infertile women were recruited from several infertility clinics in Shiraz using convenience sampling method. The participants completed research measures including the Infertility Problem Stress Inventory and the Ways of Coping Scale (passive-avoidance, active-avoidance, active-confronting, meaning-based). Multiple regression analysis was used for data analysis. A p-value less than 0.05 was considered as statistically significant.
Results: The findings showed that participants had the highest scores on passive-avoidance coping strategies followed by meaning-based coping, active-confronting coping and active-avoidance coping. The findings also indicated that women who utilized more active-avoidance coping strategies reported less infertility stress. Furthermore, the results of regression analysis demonstrated that two coping strategies including active-avoidance (β=0.35, p&lt;0.001) and meaning-based coping (β=-0.50, p&lt;0.001) predicted infertility stress significantly. Moreover, meaning-based coping strategy was the strongest predictor of low infertility stress.
Conclusions: The present study showed that the majority of infertile women used passive-avoidance coping strategy. Furthermore, those who perceived their infertility problem as meaningful had a low infertility stress, while those who used active-avoidance coping strategies had high infertility stress.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>202</FPAGE>
            <TPAGE>207</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Abdulaziz</Name>
<MidName>A</MidName>
<Family>Aflakseir</Family>
<NameE>Abdulaziz</NameE>
<MidNameE></MidNameE>
<FamilyE>Aflakseir</FamilyE>
<Organizations>
<Organization>Department of Clinical Psychology, School of Education &amp;amp; Psychology, Shiraz University</Organization>
</Organizations>
<Universities>
<University>Department of Clinical Psychology, School of Education &amp; Psychology, Shiraz University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>aaflakseir@shirazu.ac.ir</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Masoumeh</Name>
<MidName>M</MidName>
<Family>Zarei</Family>
<NameE>Masoumeh</NameE>
<MidNameE></MidNameE>
<FamilyE>Zarei</FamilyE>
<Organizations>
<Organization>Department of Clinical Psychology, School of Education &amp;amp; Psychology, Shiraz University</Organization>
</Organizations>
<Universities>
<University>Department of Clinical Psychology, School of Education &amp; Psychology, Shiraz University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Coping skills</KeyText></KEYWORD><KEYWORD><KeyText>Female</KeyText></KEYWORD><KEYWORD><KeyText>Fertility</KeyText></KEYWORD><KEYWORD><KeyText>Infertility</KeyText></KEYWORD><KEYWORD><KeyText>Psychological</KeyText></KEYWORD><KEYWORD><KeyText>Stress</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>545.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Kazem M, Ardelan A. An overview of the epidemiology of primary infertility in Iran. J Reprod Infertil. 2009;10(3):213-6.##Tarlatzis I, Tarlatzis BC, Diakogiannis I, Bontis J, Lagos S, Gavriilidou D, et al. Psychosocial impacts of infertility on Greek couples. Hum Reprod. 1993;8(3):396-401.##Fido A, Zahid MA. Coping with infertility among Kuwaiti women: cultural perspectives. Int J Soc Psychiatry. 2004;50(4):294-300.##Greil AL, Slauson-Blevins K, McQuillan J. The experience of infertility: a review of recent literature. Sociol Health Illn. 2010;32(1):140-62.##Kavlak O, Saruhan A. A study on determination the loneliness level in infertile women and to assess the factors that effects of the loneliness level. Ege J Med. 2002; 41:229-32.##Fode M, Krogh-Jespersen S, Brackett NL, Ohl DA, Lynne CM, Sonksen J. Male sexual dysfunction and infertility associated with neurological disorders. Asian J Androl. 2012;14(1):61-8.##Wirtberg I, Moller A, Hogstrom L, Tronstad SE, Lalos A. Life 20 years after unsuccessful infertility treatment. Hum Reprod. 2007;22(2):598-604.##Greil AL, McQuillan J, Lowry M, Shreffler KM. Infertility treatment and fertility-specific distress: A longitudinal analysis of a population-based sample of U.S. women. Soc Sci Med. 2011;73(1):87-94.##Redshaw M, Hockley C, Davidson LL. A qualitative study of the experience of treatment for infertility among women who successfully became pregnant. Hum Reprod. 2007;22(1):295-304.##Karlsen B, Bru E. Coping styles among adults with type 1 and type 2 diabetes. Psychol Health Med. 2002;7:245-259.##Bento SP, Goodin BR, Fabian LA, Page GG, Quinn NB, McGuire L. Perceived control moderates the influence of active coping on salivary cortisol response to acute pain among women but not men. Psychoneuroendocrinology. 2010;35(6):944-8.##Peterson BD, Newton CR, Rosen KH, Skaggs GE. Gender differences in how men and women who are referred for IVF cope with infertility stress. Hum Reprod. 2006;21(9):2443-9.##Shahnooshi M, Karimi Z. [Sociological impact of infertility upon family in Isfahan province]. J Soc Sci. 2010;11(4):171-198. Persian.##O&#39;Donnell E. Infertile in Iran [Internet]. Paris: Le Monde Diplomatique; 2008 Apr [cited 2013 Aug 12]. Available from: http://mondediplo.com/2008/04/15iran##Schmidt L, Holstein BE, Christensen U, Boivin J. Communication and coping as predictors of fertility problem stress: cohort study of 816 participants who did not achieve a delivery after 12 months of fertility treatment. Hum Reprod. 2005;20(11):3248-56.##Lazarus RS, Folkman S. Stress, appraisal, and coping. New York: Springer; 1984. 256 p.##Folkman S. Positive psychological states and coping with severe stress. Soc Sci Med. 1997;45(8):1207-21.##Younesi SJ, Akbari-Zardkhaneh S, Behjati Ardekani Z. [Evaluating stigma among infertile men and women in Iran]. J Reprod Infertil. 2006;6(5):531-545. Persian.##Rouchou B. Consequences of infertility in developing countries. Perspect Public Health. 2013;133(3):174-9.##Schmidt L, Christensen U, Holstein BE. The social epidemiology of coping with infertility. Hum Reprod. 2005;20(4):1044-52.##Lykeridou K, Gourounti K, Sarantaki A, Loutradis D, Vaslamatzis G, Deltsidou A. Occupational social class, coping responses and infertility-related stress of women undergoing infertility treatment. J Clin Nurs. 2011;20(13-14):1971-80.##Peterson BD, Newton CR, Rosen KH, Skaggs GE. The relationship between coping and depression in men and women referred for in vitro fertilization. Fertil Steril. 2006;85(3):802-4.##Berghuis JP, Stanton AL. Adjustment to a dyadic stressor: a longitudinal study of coping and depressive symptoms in infertile couples over an insemination attempt. J Consult Clin Psychol. 2002;70(2):433-8.##Gibson DM. The relationship of infertility and death: using the relational/cultural model of counseling in making meaning. J Humanist Psychol. 2007;35(3):275-289.##Peterson BD, Pirritano U, Christensen U, Schmidt L. The impact of partner coping in couples experiencing infertility. Hum Reprod. 2008;23(5):1128-1137.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Efficacy of Combined Contraceptive Vaginal Ring Versus Oral Contraceptive Pills in Achieving Hypothalamic-Pituitary-Ovarian Axis Suppression in Egg Donor In Vitro Fertilization Cycles</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>546</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Our study compares the efficacy of the combined contraceptive vaginal ring to oral contraceptive pills (OCPs) for hypothalamic-pituitary-ovarian (HPO) axis suppression in egg donor in vitro fertilization (IVF) cycles.
Methods: Our retrospective cohort study includes patients from the Center for Assisted Reproduction (CARE) in Bedford, Texas undergoing IVF cycles as egg donors from January 2003 through December 2009. Twenty-five and thirty-nine women were treated with OCPs and the combined contraceptive vaginal ring, respectively. Statistical analyses were performed using the SigmaStat Software package (Systat, Chicago, IL). Data were analyzed by t or Mann-whitney test and Chi-square of Fisher exact test. Statistical significance was set at p&lt;0.05.
Results: Prior to gonadotropin initiation, endometrial thickness and serum estradiol were 5.6&#177;2.6 mm and 33.6&#177;19.9 pg/ml in the OCP group and 6.0&#177;2.4 mm and 36.6&#177;24.3 pg/ml in the combined contraceptive vaginal ring group, respectively (p=0.49 and p=0.33). Average serum FSH and LH were 1.7&#177;1.9 and 1.7&#177;2.5 mIU/ml in the OCP group and 1.7&#177;1.6 and 1.2&#177;1.4 mIU/ml in the combined contraceptive vaginal ring group, respectively (p=0.45 and p=0.95). No significant differences were found for gonadotropin requirement, peak estradiol, maximal endometrial thickness, number of oocytes retrieved, number of normally fertilized embryos, number of cryopreserved embryos, or live birth rates.
Conclusion: The combined contraceptive vaginal ring is effective for HPO axis suppression in egg donor IVF cycles and associated with cycle characteristics similar to those observed with OCP treatment. The combined contraceptive vaginal ring may provide an important advantage over OCPs due to improved patient compliance.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>207</FPAGE>
            <TPAGE>214</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Robin</Name>
<MidName>RL</MidName>
<Family>Thomas</Family>
<NameE>Robin</NameE>
<MidNameE></MidNameE>
<FamilyE>Thomas</FamilyE>
<Organizations>
<Organization>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</Organization>
</Organizations>
<Universities>
<University>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</University>
</Universities>
<Countries>
<Country>USA</Country>
</Countries>
<EMAILS>
<Email>robin.thomas@utsouthwestern.edu</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Lisa</Name>
<MidName>LM</MidName>
<Family>Halvorson</Family>
<NameE>Lisa</NameE>
<MidNameE></MidNameE>
<FamilyE>Halvorson</FamilyE>
<Organizations>
<Organization>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</Organization>
</Organizations>
<Universities>
<University>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</University>
</Universities>
<Countries>
<Country>USA</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Bruce</Name>
<MidName>BR</MidName>
<Family>Carr</Family>
<NameE>Bruce</NameE>
<MidNameE></MidNameE>
<FamilyE>Carr</FamilyE>
<Organizations>
<Organization>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</Organization>
</Organizations>
<Universities>
<University>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</University>
</Universities>
<Countries>
<Country>USA</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Kathleen</Name>
<MidName>KM</MidName>
<Family>Doody</Family>
<NameE>Kathleen</NameE>
<MidNameE></MidNameE>
<FamilyE>Doody</FamilyE>
<Organizations>
<Organization>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</Organization>
</Organizations>
<Universities>
<University>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</University>
</Universities>
<Countries>
<Country>USA</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Kevin</Name>
<MidName>KJ</MidName>
<Family>Doody</Family>
<NameE>Kevin</NameE>
<MidNameE></MidNameE>
<FamilyE>Doody</FamilyE>
<Organizations>
<Organization>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</Organization>
</Organizations>
<Universities>
<University>Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas</University>
</Universities>
<Countries>
<Country>USA</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Contraception</KeyText></KEYWORD><KEYWORD><KeyText>Egg donor</KeyText></KEYWORD><KEYWORD><KeyText>HPO axis suppression</KeyText></KEYWORD><KEYWORD><KeyText>&lt;i&gt;In Vitro&lt;/i&gt; fertilization</KeyText></KEYWORD><KEYWORD><KeyText>Serum hormone levels</KeyText></KEYWORD><KEYWORD><KeyText>Vaginal ring</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>546.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Frydman R, Forman R, Rainhorn JD, Belaisch-Allart J, Hazout A, Testart J. A new approach to follicular stimulation for in vitro fertilization: programed oocyte retrieval. Fertil Steril. 1986;46(4):657-62.##Patton PE, Burry KA, Wolf DP, Kiessling AA, Craemer MJ. The use of oral contraceptives to regulate oocyte retrieval. Fertil Steril. 1988;49(4):716-8.##Finer LB, Henshaw SK. Disparities in rates of unintended pregnancy in the United States, 1994 and 2001. Perspect Sex Reprod Health. 2006;38(2):90-6.##Rosenberg MJ, Waugh MS, Long S. Unintended pregnancies and use, misuse and discontinuation of oral contraceptives. J Reprod Med. 1995;40(5):355-60.##Roumen FJ, Apter D, Mulders TM, Dieben TO. Efficacy, tolerability and acceptability of a novel contraceptive vaginal ring releasing etonogestrel and ethinyl oestradiol. Hum Reprod. 2001;16(3):469-75.##Oddsson K, Leifels-Fischer B, de Melo NR, Wiel-Masson D, Benedetto C, Verhoeven CH, et al. Efficacy and safety of a contraceptive vaginal ring (NuvaRing) compared with a combined oral contraceptive: a 1-year randomized trial. Contraception. 2005;71(3):176-82.##Dieben TO, Roumen FJ, Apter D. Efficacy, cycle control, and user acceptability of a novel combined contraceptive vaginal ring. Obstet Gynecol. 2002;100(3):585-93.##Bruni V, Pontello V, Luisi S, Petraglia F. An open-label, multicentre trial to evaluate the vaginal bleeding pattern of the combined contraceptive vaginal ring NuvaRing. Eur J Obstet Gynecol Reprod Biol. 2008;139(1):65-71.##Ahrendt HJ, Nisand I, Bastianelli C, G&#243;mez MA, Gemzell-Danielsson K, Urdl W, et al. Efficacy, acceptability and tolerability of the combined contraceptive ring, NuvaRing, compared with an oral contraceptive containing 30 microg of ethinyl estradiol and 3 mg of drospirenone. Contraception. 2006;74(6):451-7.##Bjarnad&#243;ttir RI, Tuppurainen M, Killick SR. Comparison of cycle control with a combined contraceptive vaginal ring and oral levonorgestrel/ethinyl estradiol. Am J Obstet Gynecol. 2002;186(3):389-95.##Oddsson K, Leifels-Fischer B, Wiel-Masson D, de Melo NR, Benedetto C, Verhoeven CH, et al. Superior cycle control with a contraceptive vaginal ring compared with an oral contraceptive containing 30 microg ethinylestradiol and 150 microg levonorgestrel: a randomized trial. Hum Reprod. 2005;20(2):557-62.##Milsom I, Lete I, Bjertnaes A, Rokstad K, Lindh I, Gruber CJ, et al. Effects on cycle control and bodyweight of the combined contraceptive ring, NuvaRing, versus an oral contraceptive containing 30 microg ethinyl estradiol and 3 mg drospirenone. Hum Reprod. 2006;21(9):2304-11.##Timmer CJ, Mulders TM. Pharmacokinetics of etonogestrel and ethinylestradiol released from a combined contraceptive vaginal ring. Clin Pharmacokinet. 2000;39(3):233-42.##van den Heuvel MW, van Bragt AJ, Alnabawy AK, Kaptein MC. Comparison of ethinylestradiol pharmacokinetics in three hormonal contraceptive formulations: the vaginal ring, the transdermal patch and an oral contraceptive. Contraception. 2005;72(3):168-74.##Abrams LS, Skee DM, Natarajan J, Wong FA, Lasseter KC. Multiple-dose pharmacokinetics of a contraceptive patch in healthy women participants. Contraception. 2001;64(5):287-94.##Kuhnz W, al-Yacoub G, Fuhrmeister A. Pharmacokinetics of levonorgestrel and ethinylestradiol in 9 women who received a low-dose oral contraceptive over a treatment period of 3 months and, after a wash-out phase, a single oral administration of the same contraceptive formulation. Contraception. 1992;46(5):455-69.##Roumen FJ, Dieben TO. Comparison of uterine concentrations of ethinyl estradiol and etonogestrel after use of a contraceptive vaginal ring and an oral contraceptive. Fertil Steril. 2006;85(1):57-62.##Cycle control, safety and efficacy of a 24-day regimen of gestodene 60 microg/ ethinylestradiol 15 microg and a 21-day regimen of desogestrel 150 microg/ethinylestradiol 20 microg. Eur J Contracept Reprod Health Care. 1999;4 Suppl 2:17-25.##The safety and contraceptive efficacy of a 24-day low-dose oral contraceptive regimen containing gestodene 60 microg and ethinylestradiol 15 microg. Eur J Contracept Reprod Health Care. 1999;4 Suppl 2:9-15.##Sulak PJ, Smith V, Coffee A, Witt I, Kuehl AL, Kuehl TJ. Frequency and management of breakthrough bleeding with continuous use of the transvaginal contraceptive ring: a randomized controlled trial. Obstet Gynecol. 2008;112(3):563-71.##Mulders TM, Dieben TO. Use of the novel combined contraceptive vaginal ring NuvaRing for ovulation inhibition. Fertil Steril. 2001;75(5):865-70.##Mulders TM, Dieben TO, Bennink HJ. Ovarian function with a novel combined contraceptive vaginal ring. Hum Reprod. 2002;17(10):2594-9.##Korver T, Goorissen E, Guillebaud J. The combined oral contraceptive pill: what advice should we give when tablets are missed? Br J Obstet Gynaecol. 1995;102(8):601-7.##Duijkers IJ, Klipping C, Verhoeven CH, Dieben TO. Ovarian function with the contraceptive vaginal ring or an oral contraceptive: a randomized study. Hum Reprod. 2004;19(11):2668-73.##Duijkers IJ, Verhoeven CH, Dieben TO, Klipping C. Follicular growth during contraceptive pill or vaginal ring treatment depends on the day of ovulation in the pretreatment cycle. Hum Reprod. 2004;19(11):2674-9.##Endrikat J, D&#252;sterberg B, Ruebig A, Gerlinger C, Strowitzki T. Comparison of efficacy, cycle control, and tolerability of two low-dose oral contraceptives in a multicenter clinical study. Contraception. 1999;60(5):269-74.##Rosenberg MJ, Meyers A, Roy V. Efficacy, cycle control, and side effects of low- and lower-dose oral contraceptives: a randomized trial of 20 micrograms and 35 micrograms estrogen preparations. Contraception. 1999;60(6):321-9.##Creinin MD, Meyn LA, Borgatta L, Barnhart K, Jensen J, Burke AE, et al. Multicenter comparison of the contraceptive ring and patch: a randomized controlled trial. Obstet Gynecol. 2008;111(2 Pt 1):267-77.##Novak A, de la Loge C, Abetz L, van der Meulen EA. The combined contraceptive vaginal ring, NuvaRing: an international study of user acceptability. Contraception. 2003;67(3):187-94.##Gilliam ML, Neustadt A, Kozloski M, Mistretta S, Tilmon S, Godfrey E. Adherence and acceptability of the contraceptive ring compared with the pill among students: a randomized controlled trial. Obstet Gynecol. 2010;115(3):503-10.##Brucker C, Karck U, Merkle E. Cycle control, tolerability, efficacy and acceptability of the vaginal contraceptive ring, NuvaRing: results of clinical experience in Germany. Eur J Contracept Reprod Health Care. 2008;13(1):31-8.##Merki-Feld GS, Hund M. Clinical experience with NuvaRing in daily practice in Switzerland: cycle control and acceptability among women of all reproductive ages. Eur J Contracept Reprod Health Care. 2007;12(3):240-7.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Prevalence of Tubal Obstruction in the Hysterosalpingogram of Women with Primary and Secondary Infertility</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>547</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: The purpose of this study was to evaluate the fallopian tube of women with infertility and to observe whether there are any significant differences in the Hysterosalpingogram findings with regard to prevalence of tubal block in women with primary and secondary infertility.
Methods: A retrospective study of unilateral and bilateral tubal obstruction in Hysterosalpingogram of women with primary and secondary infertility was carried out. 
Results: The frequencies of tubal obstruction were about 19% in women with primary infertility and 29% in secondary infertility. Chlamydia antigen positivity rate was similar in both groups. Ectopic pregnancy (p&lt;0.01) and previous pelvic surgery (p&lt;0.001) were higher in women with secondary infertility.
Conclusion: Tubal obstruction is a cause of female infertility according to this study. Bilateral tubal obstruction was similar in primary and secondary infertility groups and previous pelvic surgery may be the cause of tubal obstruction in the secondary infertility group.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>214</FPAGE>
            <TPAGE>217</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Taimoora</Name>
<MidName>T</MidName>
<Family>Al Subhi</Family>
<NameE>Taimoora</NameE>
<MidNameE></MidNameE>
<FamilyE>Al Subhi</FamilyE>
<Organizations>
<Organization>Sultan Qaboos University Hospital</Organization>
</Organizations>
<Universities>
<University>Sultan Qaboos University Hospital</University>
</Universities>
<Countries>
<Country>Oman</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Ruqaiya</Name>
<MidName>RN</MidName>
<Family>Al Jashnmi</Family>
<NameE>Ruqaiya</NameE>
<MidNameE></MidNameE>
<FamilyE>Al Jashnmi</FamilyE>
<Organizations>
<Organization>Sultan Qaboos University Hospital</Organization>
</Organizations>
<Universities>
<University>Sultan Qaboos University Hospital</University>
</Universities>
<Countries>
<Country>Oman</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Maha</Name>
<MidName>M</MidName>
<Family>Al Khaduri</Family>
<NameE>Maha</NameE>
<MidNameE></MidNameE>
<FamilyE>Al Khaduri</FamilyE>
<Organizations>
<Organization>Sultan Qaboos University Hospital</Organization>
</Organizations>
<Universities>
<University>Sultan Qaboos University Hospital</University>
</Universities>
<Countries>
<Country>Oman</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Vaidyanathan</Name>
<MidName>V</MidName>
<Family>Gowri</Family>
<NameE>Vaidyanathan</NameE>
<MidNameE></MidNameE>
<FamilyE>Gowri</FamilyE>
<Organizations>
<Organization></Organization>
</Organizations>
<Universities>
<University></University>
</Universities>
<Countries>
<Country></Country>
</Countries>
<EMAILS>
<Email>gowrie61@hotmail.com</Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Chlamydia</KeyText></KEYWORD><KEYWORD><KeyText>Fallopian tube blockage</KeyText></KEYWORD><KEYWORD><KeyText>Hysterosalpingography</KeyText></KEYWORD><KEYWORD><KeyText>Infertility</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>547.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Lash MM, Yaghamee A, Strohsnitter W, Lalwani S. Association between secondary infertility and fallopian tube obstruction on hysterosalpingography. J Reprod Med. 2008;53(9):677-80.##Bello TO. Tubal abnormalities on ysterosalpingography in primary and secondary infertility. West Afr J Med. 2006;25(2):130-3.##Romero Ramos R, Romero Guti&#233;rrez G, Abortes Monroy I, Medina S&#225;nchez HG. [Risk factors associated to female infertility]. Ginecol Obstet Mex. 2008;76(12):717-21. Spanish.##Malik A, Jain S, Rizvi M, Shukla I, Hakim S. Chlamydia trachomatis infection in women with secondary infertility. Fertil Steril. 2009;91(1):91-5.##Brunham RC, Peeling RW. Chlamydia trachomatis antigens: role in immunity and pathogenesis. Infect Agents Dis. 1994;3(5):218-33.##Mardh PA. Tubal factor infertility, with special regard to chlamydial salpingitis. Curr Opin Infect Dis. 2004;17(1):49-52.##Land JA, Van Bergen JE, Morr&#233; SA, Postma MJ. Epidemiology of Chlamydia trachomatis infection in women and the cost-effectiveness of screening. Hum Reprod Update. 2010;16(2):189-204.##Meldrum DR, editor. Infertility and assisted reproductive technologies.  Philadelphia: Saunders/ Elsevier; 2010. 375 p. (Hacker NF, Gambone JC, Hobel CJ, editors. Essentials of Obstetrics and Gynecology; vol. 34).##Ghazal-Aswad S, Badrinath P, Osman N, Abdul-Khaliq S, Mc Ilvenny S, Sidky I. Prevalence of Chlamydia trachomatis infection among women in a Middle Eastern community. BMC Womens Health. 2004;4(1):3.##Luttjeboer FY, Verhoeve HR, van Dessel HJ, van der Veen F, Mol BW, Coppus SF. The value of medical history taking as risk indicator for tuboperitoneal pathology: a systematic review. BJOG. 2009;116(5):612-25.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

    </ARTICLES>
  </JOURNAL>
</XML>
