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<XML>
  <JOURNAL>   
    <YEAR>2022</YEAR>
    <VOL>23</VOL>
    <NO>1</NO>
    <MOSALSAL>90</MOSALSAL>
    <PAGE_NO>70</PAGE_NO>  
    <ARTICLES>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Polycystic Ovarian Syndrome and Endometriosis as Two Evil Extremes of Health Continuum</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Endometriosis is a common, benign, inflammatory, and generally reproductive tract disorder that significantly aggravates the quality of life in affected women; moreover, evidence shows that endometriosis has a heritable component as a result of its high familial incidence and roughly 10% of women at reproductive age are suffering from the disease. The hallmark of endometriosis is proliferation of the endometrial tissue outside the uterus, typically on the ovaries, pelvic cavity, fallopian tubes, or rectovaginal area. Such &quot;ectopic&quot; tissue drives estradiol-induced growth and destructive changes similar to the &quot;entopic&quot; inner lining of the uterus during menstrual cycles. The estrogen-induced changes during menstrual cycle cause severe pelvic pain and chronic inflammation that culminate in reduced fertility and infertility. In fact, there is no cure and effective treatment for endometriosis prior to the decline in estrogen levels at menopause. Currently, the gold standard treatment is surgical exicion of endometrial lesions, or hysterectomy (1).&lt;br /&gt;
Menstrual blood and tissue discharge during menstruation is a rare physiological phenomenon in mammals that is restricted to humans and few other mammals. From the past to present, two main hypotheses are propounded for the etiopathogenesis of endometriosis. The first attributes the development of endometriosis to non-M&#252;llerian stem cells, the Sampson’s theory, due to retrograde flow of menstrual blood and the second is related to M&#252;llerian stem cells, caused by altered differentiation and movement of M&#252;llerian remnants over the early development of the uterus. However, current evidence approves the multifactorial nature of endometriosis as a result of combined contribution of anatomical, hormonal, immunological, estrogenic, genetic, epigenetic, and environmental factors in women; yet, other pieces of evidence confirm that endometriosis occurs due to changes in intrauterine conditions during prenatal development (1, 2).&lt;br /&gt;
Polycystic ovary syndrome (PCOS) is another common gynecologic disorder, affecting up to 20% of women during their reproductive age. PCOS is accompanied with anovulation, polycystic ovaries, hyperandrogenism, hirsutism, abdominal obesity, insulin resistance, and increased body mass index (BMI) and waist to hip ratio (WHR). The exact etiopathogenesis of PCOS symptoms is still quite unclear. As of today, genetic, environmental, nutritional, and metabolic factors have been identified as the main causes of this syndrome. However, similar to endometriosis, new evidence supports the association of PCOS with changes in intrauterine environment during prenatal development (3, 4).&lt;br /&gt;
The endocrinopathy is a general risk factor for endometriosis and PCOS, but the pattern of hormonal changes is quite opposite. In endometriosis, the levels of LH, testosterone, and anti-M&#252;llerian hormone (AMH) decrease whereas the levels of follicle-stimulating hormone (FSH), sex hormone-binding globulin (SHBG), and oxytocin increase. On the other side, women with PCOS have increased levels of LH, AMH and androgens while decreased levels of FSH, SHBG and oxytocin are detected among them. By evaluating these patterns of hormonal changes, it seems that the causes of two disorders may be the same; therefore, endometriosis and PCOS appear to be typical instances of diametric diseases such as osteoporosis and osteoarthritis, preeclampsia and postpartum hemorrhage, and cancer and neurodegeneration (2, 4, 5).&lt;br /&gt;
Anogenital distance (AGD) is defined as the distance between the anus and external genitalia which is measured in men from the base of the scrotum to the anus and in women from the end of the vagina to the anus. AGD in men is longer than women. Another difference between men and women is the ratio of the 2nd to the 4th finger length (2D:4D) that is lower in men than women. The difference in AGD and 2D:4D indices in men and women are the result of the exposure of embryos of each sex to different levels of testosterone during prenatal development. The pattern of these two indices is completely different and opposite in PCOS and endometriosis. In PCOS, these two parameters show values close to the male pattern while in endometriosis, the lowest values of female pattern indicate the role of testosterone levels in development of reproductive organs during intrauterine growth of the female fetus and the probability of occurrence of these two diseases after puberty (3, 4).&lt;br /&gt;
Recent evidence confirms that occurrence of PCOS and endometriosis during reproductive age is related to disruption of utero development of hypothalamic–pituitary–ovarian (HPO) axis in female fetus. The HPO axis organizes the neural and hormonal network of reproductive system throughout the life before the fetus is born and subsequently after puberty, in particular secretion of GnRH, FSH, and LH to control ovarian and uterine functions. Thus, PCOS is a developmental disorder of the HPO axis that results from relatively high levels of prenatal testosterone, while endometriosis is caused by relatively low levels of prenatal testosterone (2, 3, 5).&lt;br /&gt;
In the experimental model of rodents, the symptoms of PCOS can be established through administration of testosterone at an initial stage of prenatal development in these animals (2-4). In addition, epidemiological studies show that the prevalence rates of endometriosis are higher in Asian and European women in comparison with African populations. In contrast, the incidence of PCOS among Asian and European is lower than African women. Measurement of serum testosterone during pregnancy in these three populations of women confirmed the above hypothesis; accordingly, higher level of testosterone in African pregnant women increases the risk of PCOS and reduces the risk of endometriosis in their daughters and lower level of testosterone in Asian and European women increases the risk of endometriosis and reduces the risk of PCOS in their daughters (4).&lt;br /&gt;
Despite the above evidence, there are conflicting findings for which further research should be conducted, such as coexistence of PCOS and endometriosis in one woman which is probably an exception to the finding on the effect of prenatal testosterone on female fetus or the discrepancies are due to inaccuracy of previous studies (6).&lt;br /&gt;
All in all, these findings can be regarded as valuable milestones in prevention and treatment of these two diseases. The occurrence of the diseases is connected to changes in testosterone levels in the prenatal period. However, the actions for modifying or reducing the serum levels of testosterone in pregnant mothers to prevent the diseases are extremely risky and unsafe. Each hormone has a variety of roles and functions in a complex network with other hormones and growth factors that their imbalance may have tremendous consequences for the fetus and mother. Though the above cited valuable approach has provided a brilliant opportunity for preventing polycystic ovary syndrome and endometriosis, extensive research should be conducted to validate these findings and use the outcomes for clinical application.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>01</FPAGE>
            <TPAGE>3</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>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR</Organization>
</Organizations>
<Universities>
<University>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>sadeghi@ari.ir</Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>No Keyword</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120145.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Lagan&#224; AS, Garzon S, G&#246;tte M, Vigan&#242; P, Franchi M, Ghezzi F, et al. The pathogenesis of endometriosis: molecular and cell biology insights. Int J Mol Sci. 2019;20(22):5615.##Dinsdale N, Nepomnaschy P, Crespi B. The evolutionary biology of endometriosis. Evol Med Public Health. 2021; 9(1):174-91.##Pan Z, Zhu F, Zhou K. A systematic review of anogenital distance and gynecological disorders: endometriosis and polycystic ovary syndrome. Front Endocrinol (Lausanne). 2021;12:696879.##Crespi B. Variation among human populations in endometriosis and PCOS A test of the inverse comorbidity model. Evol Med Public Health. 2021;9(1):295-310.##Dinsdale NL, Crespi BJ. Endometriosis and polycystic ovary syndrome are diametric disorders. Evol Appl. 2021;14(7):1693-715.##Holoch KJ, Savaris RF, Forstein DA, Miller PB, Higdon Iii HL, Likes CE, et al. Coexistence of polycystic ovary syndrome and endometriosis in women with infertility. J Endomet Pelvic Pain Disord. 2014;6(2):79-83.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Dual Trigger with Gonadotropin Releasing Hormone Agonist and Human Chorionic Gonadotropin of Fresh Autologous Cycles in High Responders: A Systematic Review</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: The purpose of the current study was to investigate the effect of coadministration of human chorionic gonadotropin (hCG) with gonadotropin releasing hormone agonist (GnRH-a) trigger (dual trigger) in high responders for fresh autologous cycles in order to investigate the pregnancy outcomes and rates of ovarian hyperstimulation syndrome (OHSS) in comparison to GnRH-a trigger alone.&lt;br /&gt;
Methods: A systematic search was performed in PubMed and Ovid MEDLINE from inception through February 2020. The included materials were case-control, cohort and, cross-sectional studies as well as clinical trials in which the outcomes of dual trigger with GnRH-a were compared for final oocyte maturation in high responders undergoing GnRH-ant cycles.&lt;br /&gt;
Results: Five retrospective studies were included for this review. Three of the studies showed that the use of dual trigger versus GnRH-a trigger resulted in no statistically significant difference in rates of OHSS while achieving a statistically significant difference in favor of the dual trigger group in ongoing pregnancy rates, early pregnancy loss, and fertilization rates.&lt;br /&gt;
Conclusion: Currently, there is insufficient evidence to support improved clinical pregnancy rate, fertilization rate, live birth rate, and early pregnancy loss rate by the use of dual trigger versus GnRH-a trigger. Larger double-blind clinical studies are required to properly evaluate the efficacy of this protocol for use in high responders.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>03</FPAGE>
            <TPAGE>18</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Andreas A</Name>
<MidName>AA</MidName>
<Family>Vyrides</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Barts and The London School of Medicine and Dentistry, Queen Mary University of London</Organization>
</Organizations>
<Universities>
<University>Barts and The London School of Medicine and Dentistry, Queen Mary University of London</University>
</Universities>
<Countries>
<Country>United Kingdom</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Essam El</Name>
<MidName>EE</MidName>
<Family>Mahdi</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynaecology, Newham University Hospital NHS Trust</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynaecology, Newham University Hospital NHS Trust</University>
</Universities>
<Countries>
<Country>United Kingdom</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Demetris</Name>
<MidName>D</MidName>
<Family>Lamnisos</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Health Sciences, School of Sciences, European University of Cyprus</Organization>
</Organizations>
<Universities>
<University>Department of Health Sciences, School of Sciences, European University of Cyprus</University>
</Universities>
<Countries>
<Country>Cyprus</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Konstantinos</Name>
<MidName>K</MidName>
<Family>Giannakou</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Health Sciences, School of Sciences, European University of Cyprus</Organization>
</Organizations>
<Universities>
<University>Department of Health Sciences, School of Sciences, European University of Cyprus</University>
</Universities>
<Countries>
<Country>Cyprus</Country>
</Countries>
<EMAILS>
<Email>K.Giannakou@euc.ac.cy</Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Dual trigger</KeyText></KEYWORD><KEYWORD><KeyText>Fresh autologous cycles</KeyText></KEYWORD><KEYWORD><KeyText>Gonadotropin releasing hormone (GnRH)</KeyText></KEYWORD><KEYWORD><KeyText>Ovarian hyperstimulation syndrome (OHSS)</KeyText></KEYWORD><KEYWORD><KeyText>Systematic review</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120139.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Tobler KJ, Zhao Y, Weissman A, Majumdar A, Leong M, Shoham Z. Worldwide survey of IVF practices: trigger, retrieval and embryo transfer techniques. Arch Gynecol Obstet. 2014;290(3):561-8.##Albano C, Riethm&#252;ller-Winzen H, Smitz J, Van Steirteghem A, Camus M, Devroey P. Comparison of different doses of gonadotropin-releasing hormone antagonist Cetrorelix during controlled ovarian hyperstimulation. Fertil Steril. 1997;67(5):917-22.##Borm G, Mannaerts B. Treatment with the gonadotrophin-releasing hormone antagonist ganirelix in women undergoing ovarian stimulation with recombinant follicle stimulating hormone is effective, safe and convenient: results of a controlled, randomized, multicentre trial. Hum Reprod. 2000;15(7):1490-8.##Itskovitz-Eldor J, Kol S, Mannaerts B, Bennink HC. First established pregnancy after controlled ovarian hyperstimulation with recombinant follicle stimulating hormone and the gonadotrophin-releasing hormone antagonist ganirelix (Org 37462). Hum Reprod. 1998;13(2):294-5.##Navot D, Bergh PA, Laufer N. Ovarian hyperstimulation syndrome in novel reproductive technologies: Prevention and treatment. Fertil Steril. 1992;58(2):249-61.##Mathur RS, Akande AV, Keay SD, Hunt LP, Jenkins JM. Distinction between early and late ovarian hyperstimulation syndrome. Fertil Steril. 2000;73(5):901-7.##Dourron NE, Williams DB. Prevention and treatment of ovarian hyperstimulation syndrome. Semin Reprod Endocrinol. 1996;14(4):355-65.##Papanikolaou EG, Pozzobon C, Kolibianakis EM, Camus M, Tournaye H, Fatemi HM, et al. Incidence and prediction of ovarian hyperstimulation syndrome in women undergoing gonadotropin-releasing hormone antagonist in vitro fertilization cycles. Fertil Steril. 2006;85(1):112-20.##Golan A, Weissman A. Symposium: update on prediction and management of OHSS-A modern classification of OHSS. Reprod Biomed Online. 2009;19(1):28-32.##Humaidan P, Nelson SM, Devroey P, Coddington CC, Schwartz LB, Gordon K, et al. Ovarian hyperstimulation syndrome: Reviewand new classification criteria for reporting in clinical trials. Hum Reprod. 2016;31(9):1997-2004.##Delvigne A, Kostyla K, Murillo D, Van Hoeck J, Rozenberg S. Oocyte quality and IVF outcome after coasting to prevent ovarian hyperstimulation syndrome. Int J Fertil Womens Med. 2003;48(1):25-31.##De Geyter C, Calhaz-Jorge C, Kupka MS, Wyns C, Mocanu E, Motrenko T, et al. ART in Europe, 2014: results generated from European registries by ESHRE: the European IVF-monitoring Consortium (EIM) for the European society of human reproduction and embryology (ESHRE). Hum Reprod. 2018;33(9):1586-601.##De Geyter C, Calhaz-Jorge C, Kupka MS, Wyns C, Mocanu E, Motrenko T, et al. ART in Europe, 2015: results generated from European registries by ESHRE. Hum Reprod Open. 2020;2020(1):hoz038.##Wyns C, Bergh C, Calhaz-Jorge C, De Geyter Ch, Kupka MS, Motrenko T, et al. ART in Europe, 2016: results generated from European registries by ESHRE. Hum Reprod Open. 2020;2020(3):hoaa032.##Shanbhag S, Bhattacharya S. Current management of ovarian hyperstimulation syndrome. Hosp Med. 2002;63(9):528-32.##Kol S. Luteolysis induced by a gonadotropin-releasing hormone agonist is the key to prevention of ovarian hyperstimulation syndrome. Fertil Steril. 2004;81(1):1-5.##Kol S, Itskovitz-Eldor J. Severe OHSS: yes, there is a strategy to prevent it! Hum Reprod. 2000;15(11):2266-7.##Orvieto R. Can we eliminate severe ovarian hyperstimulation syndrome? Hum Reprod. 2005;20(2):320-2.##Humaidan P, Bredkj&#230;r HE, Bungum L, Bungum M, Gr&#248;ndahl ML, Westergaard L, et al. GnRH agonist (buserelin) or hCG for ovulation induction in GnRH antagonist IVF/ICSI cycles: a prospective randomized study. Hum Reprod. 2005;20(5):1213-20.##Kolibianakis EM, Schultze-Mosgau A, Schroer A, van Steirteghem A, Devroey P, Diedrich K, et al. A lower ongoing pregnancy rate can be expected when GnRH agonist is used for triggering final oocyte maturation instead of HCG in patients undergoing IVF with GnRH antagonists. Hum Reprod. 2005;20(10):2887-92.##Vlaisavljević V, Kovačič B, Knez J. Cumulative live birth rate after GnRH agonist trigger and elective cryopreservation of all embryos in high responders. Reprod Biomed Online. 2017;35(1):42-8.##Lin MH, Wu FS, Lee RK, Li SH, Lin SY, Hwu YM. Dual trigger with combination of gonadotropin-releasing hormone agonist and human chorionic gonadotropin significantly improves the live-birth rate for normal responders in GnRH-antagonist cycles. Fertil Steril. 2013;100(5):1296-302.##Haas J, Bassil R, Samara N, Zilberberg E, Mehta C, Orvieto R, et al. GnRH agonist and hCG (dual trigger) versus hCG trigger for final follicular maturation: a double-blinded, randomized controlled study. Hum Reprod. 2020;35(7):1648-54.##Moher D, Liberati A, Tetzlaff J, Altman DG, PRISMA Group. 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Dual trigger of oocyte maturation with gonadotropin-releasing hormone agonist and low-dose human chorionic gonadotropin to optimize live birth rates in high responders. Fertil Steril. 2012;97(6):1316-20.##Huang CY, Shieh ML, Li HY. The benefit of individualized low-dose hCG support for high responders in GnRHa-triggered IVF/ICSI cycles. J Chin Med Assoc. 2016;79(7):387-93.##Shapiro BS, Daneshmand ST, Garner FC, Aguirre M, Hudson C. Comparison of &quot;triggers&quot; using leuprolide acetate alone or in combination with low-dose human chorionic gonadotropin. Fertil Steril. 2011;95(8):2715-7.##National institute for health and clinical excellence. Ectopic pregnancy and miscarriage: diagnosis and initial management. NICE Guideline NG126. 2019 [cited 2021 Jun 17]; (April 2019):1–34. Available from: www.nice.org.uk/guidance/ng126##Banker M, Patel J, Patel A, Banker J, Gupte-Shah A. Miscarriage: biochemical and clinical. In: Skinner M, editor. Encyclopedia of reproduction. US: Academic Press; 2018. p. 317-23.##Golan A, Ron-el R, Herman A, Soffer Y, Weinraub Z, Caspi E. Ovarian hyperstimulation syndrome: an update review. Obstet Gynecol Surv. 1989;44(6):430-40.##Gonen Y, Balakier H, Powell W, Casper RF. Use of gonadotropin-releasing hormone agonist to trigger follicular maturation for in vitro fertilization. J Clin Endocrinol Metab. 1990;71(4):918-22.##Itskovitz J, Boldes R, Levron J, Erlik Y, Kahana L, Brandes JM. Induction of preovulatory luteinizing hormone surge and prevention of ovarian hyperstimulation syndrome by gonadotropin-releasing hormone agonist. Fertil Steril. 1991;56(2):213-20.##Kolibianakis EM, Bourgain C, Platteau P, Albano C, Van Steirteghem AC, Devroey P. Abnormal endometrial development occurs during the luteal phase of nonsupplemented donor cycles treated with recombinant follicle-stimulating hormone and gonadotropin-releasing hormone antagonists. 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Luteal phase support in infertility treatment: A meta-analysis of the randomized trials. Hum Reprod. 2002;17(9):2287-99.##Kolibianakis E, Bourgain C, Albano C, Osmanagaoglu K, Smitz J, Van Steirteghem A, et al. Effect of ovarian stimulation with recombinant follicle-stimulating hormone, gonadotropin releasing hormone antagonists, and human chorionic gonadotropin on endometrial maturation on the day of oocyte pick-up. Fertil Steril. 2002;78(5):1025-9.##Daya S, Gunby JL. Luteal phase support in assisted reproduction cycles. Cochrane Database Syst Rev. 2004;3:CD004830.##Hoff JD, Quigley ME, Yen SSC. Hormonal dynamics at midcycle: A reevaluation. J Clin Endocrinol Metab. 1983;57(4):792-6.##Filicori M, Santoro N, Merriam GR, Crowley WF. Characterization of the physiological pattern of episodic gonadotropin secretion throughout the human menstrual Cycle. J Clin Endocrinol Metab. 1986;62(6):1136-44.##Casper RF, Yen SS. Induction of luteolysis in the human with a long-acting analog of luteinizing hormone-releasing factor. Science. 1979;205(4404):408-10.##Rao C V. Multiple novel roles of luteinizing hormone. Fertil Steril. 2001;76(6):1097-100.##Sugino N, Kashida S, Takiguchi S, Karube A, Kato H. Expression of vascular endothelial growth factor and its receptors in the human corpus luteum during the menstrual cycle and in early pregnancy. J Clin Endocrinol Metab. 2000;85(10):3919-24.##Tesarik J, Hazout A, Mendoza C. Luteinizing hormone affects uterine receptivity independently of ovarian function. Reprod Biomed Online. 2003;7(1):59-64.##Licht P, Russu V, Lehmeyer S, Wildt L. Molecular aspects of direct LH/hCG effects on human endometrium--lessons from intrauterine microdialysis in the human female in vivo. Reprod Biol. 2001;1(1):10-9.##Licht P, Russu V, Wildt L. On the role of human chorionic gonadotropin (hCG) in the embryo-endometrial microenvironment: Implications for differentiation and implantation. Semin Reprod Med. 2001;19(1):37-47.##Fatemi HM. The luteal phase after 3 decades of IVF: what do we know? Reprod Biomed Online. 2009;19 Suppl 4:4331.##Fauser BCJM, Devroey P. Reproductive biology and IVF: Ovarian stimulation and luteal phase consequences. Trends Endocrinol Metab. 2003;14(5):236-42.##Tavaniotou A, Devroey P. Effect of human chorionic gonadotropin on luteal luteinizing hormone concentrations in natural cycles. Fertil Steril. 2003;80(3):654-5.##Tavaniotou A, Albano C, Smitz J, Devroey P. Comparison of LH concentrations in the early and mid-luteal phase in IVF cycles after treatment with HMG alone or in association with the GnRH antagonist Cetrorelix. Hum Reprod. 2001;16(4):663-7.##Engmann LL, Maslow BS, Kaye LA, Griffin DW, Diluigi AJ, Schmidt DW, et al. Low dose human chorionic gonadotropin administration at the time of gonadotropin releasing-hormone agonist trigger versus 35 h later in women at high risk of developing ovarian hyperstimulation syndrome - a prospective randomized double-blind clinical tri. J Ovarian Res. 2019;12(1):8.##Martazanova B, Mishieva N, Vtorushina V, Vedikhina I, Levkov L, Korneeva I, et al. Angiogenic cytokine and interleukin 8 levels in early luteal phase after triggering ovulation with gonadotropin-releasing hormone agonist in high-responder patients. Am J Reprod Immunol. 2021;85(6):e13381.##Chen SU, Chou CH, Lin CW, Lee H, Wu JC, Lu HF, et al. Signal mechanisms of vascular endothelial growth factor and interleukin-8 in ovarian hyperstimulation syndrome: Dopamine targets their common pathways. Hum Reprod. 2010;25(3):757-67.##Kaye L, Griffin D, Thorne J, Neuber E, Nulsen J, Benadiva C, et al. Independent serum markers of corpora lutea function after gonadotropin-releasing hormone agonist trigger and adjuvant low dose human chorionic gonadotropin in in vitro fertilization. Fertil Steril. 2019;112(3):534-44.##Shapiro BS, Daneshmand ST, Garner FC, Aguirre M, Hudson C, Thomas S. Evidence of impaired endometrial receptivity after ovarian stimulation for in vitro fertilization: a prospective randomized trial comparing fresh and frozen-thawed embryo transfers in high responders. Fertil Steril. 2011;96(2):516-8.##Kummer N, Benadiva C, Feinn R, Mann J, Nulsen J, Engmann L. Factors that predict the probability of a successful clinical outcome after induction of oocyte maturation with a gonadotropin-releasing hormone agonist. Fertil Steril. 2011;96(1):63-8.##Delvinge A, Rozenberg S. Epidemiology and prevention of ovarian hyperstimulation syndrome (OHSS): A review. Hum Reprod Update. 2002;8(6):559-77.##Tarlatzis BC, Bosdou J, Kolibianakis S. Elimination of OHSS by GnRH agonist and freezing embryos. In: Rizk J, editor. Complications and outcomes of assisted reproduction. Cambridge: Cambridge University Press; 2017. p. 149-63. ##Bosdou JK, Venetis CA, Tarlatzis BC, Grimbizis GF, Kolibianakis EM. Higher probability of live-birth in high, but not normal, responders after first frozen-embryo transfer in a freeze-only cycle strategy compared to fresh-embryo transfer: a meta-analysis. Hum Reprod. 2019;34(3):491-505.##Giannakou K. Perinatal epidemiology: issues, challenges, and potential solutions. Obstet Med. 2021;14(2):77-82.##de Geyter C, Wyns C, Calhaz-Jorge C, de Mouzon J, Ferraretti AP, Kupka M, et al. 20 years of the European IVF-monitoring Consortium registry: what have we learned? A comparison with registries from two other regions. Hum Reprod. 2020;35(12):2832-49.##Royal College of Obstetricians &amp; Gynaecologists. The management of ovarian hyperstimulation syndrome. Green-top Guidline No. 5. 2016. 22 p.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Investigating the Effect of Crocus sativus (Saffron) Petal Hydro-alcoholic Extract on Ovarian Follicle, Inflammatory Markers, and Antioxidant Enzymes in Mice Model of Polycystic Ovary Syndrome</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: Saffron petals have traditionally been used to treat a variety of diseases, such as gynecological diseases, primary dysmenorrhea, and premenstrual syndrome. Polycystic ovary syndrome (PCOS) is a kind of gynecological disease that causes infertility, menopausal and urogenital disorders and saffron petals seem to be an efficient treatment for such disorders.&lt;br /&gt;
Methods: NMRI mice (total=60, each group n=12) were divided into control, PCOS, and the treatment groups. PCOS and treatment groups were injected with testosterone enanthate (TE=1 &lt;em&gt;mg/kg&lt;/em&gt;). After 4 weeks, the treatment group was treated with Saffron Petal Extract (SPE) for 14 days. Ovary and blood samples were collected for histological and serological analyses, and expression of NF-κB, NF-κB p65, and IκB genes was analyzed. Finally, data were analyzed using one-way ANOVA (p&lt;0.05).&lt;br /&gt;
Results: In this study, the number of corpus luteum decreased in PCOS mice (p&lt;0.001) but increased with SPE treatment (p&lt;0.05, p&lt;0.01, p&lt;0.001). The number of cystic follicles increased in PCOS mice (p&lt;0.001), but decreased with SPE treatment (p&lt;0.05, p&lt;0.001). TNFα, IL1&#223;, IL6, IL18, and CRP levels increased in PCOS mice (p&lt;0.001), but decreased following SPE treatment (p&lt;0.05, p&lt;0.001). Glutathione (GSH) and glutathione S-transferase (GST) serum levels decreased in PCOS mice (p&lt;0.001), but increased with SPE treatment (p&lt;0.05, p&lt;0.001). The transcriptional level (s) of NF-κB, NF-κB p65, IκB genes changed in PCOS condition (p&lt;0.001), and were regulated by SPE treatment (p&lt;0.05, p&lt;0.01 and p&lt;0.001).&lt;br /&gt;
Conclusion: The present study shows that SPE improved the PCOS symptoms in mice via increasing antioxidant factors and reducing inflammatory markers in serum.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>18</FPAGE>
            <TPAGE>26</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Fazeleh</Name>
<MidName>F</MidName>
<Family>Moshfegh</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Biology, Faculty of Basic Sciences, Mashhad Branch, Islamic Azad University</Organization>
</Organizations>
<Universities>
<University>Department of Biology, Faculty of Basic Sciences, Mashhad Branch, Islamic Azad University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Saeedeh</Name>
<MidName>S</MidName>
<Family>Zafar Balanejad</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Biology, Faculty of Basic Sciences, Mashhad Branch, Islamic Azad University</Organization>
</Organizations>
<Universities>
<University>Department of Biology, Faculty of Basic Sciences, Mashhad Branch, Islamic Azad University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>mojgan_zafar@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Khadige</Name>
<MidName>Kh</MidName>
<Family>Shahrokhabady</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Biology, Faculty of Basic Sciences, Mashhad Branch, Islamic Azad University</Organization>
</Organizations>
<Universities>
<University>Department of Biology, Faculty of Basic Sciences, Mashhad Branch, Islamic Azad University</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Armin</Name>
<MidName>A</MidName>
<Family>Attaranzadeh</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Milad IVF, Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Department of Milad IVF, Imam Reza Hospital, Faculty of Medicine, Mashhad University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Antioxidant enzymes</KeyText></KEYWORD><KEYWORD><KeyText>Crocus sativus (saffron) petals</KeyText></KEYWORD><KEYWORD><KeyText>Infertility</KeyText></KEYWORD><KEYWORD><KeyText>Inflammatory markers</KeyText></KEYWORD><KEYWORD><KeyText>Ovarian follicle</KeyText></KEYWORD><KEYWORD><KeyText>Polycystic ovarian syndrome</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120136.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Demir I, Guler A, Alarslan P, Isil AM, Ucman O, Aslanipour B, et al. Fractalkine: an inflammatory chemokine elevated in subjects with polycystic ovary syndrome. Endocrine. 2019;65(1):175-83.##Hussein Al Musawy SH, Al Saimary E, Sherif Flaifil M. Levels of cytokines profile in polycystic ovary syndrome. Med J Babylon. 2018;15(2):124-8.##Fu Xiafei, He Yuanli, Wang Xuefeng, Peng Dongxian, Chen Xiaoying, Li Xinran, et al. MicroRNA-16 promotes ovarian granulosa cell proliferation and suppresses apoptosis through targeting PDCD4 in polycystic ovarian syndrome. Cell Physiol Biochem. 2018;48(2):670-82.##Osuka S, Nakanishi N, Murase T, Nakamura T, Goto M, Iwase A, et al. Animal models of polycystic ovary syndrome: a review of hormone‐induced rodent models focused on hypothalamuspituitary‐ovary axis and neuropeptides. Reprod Med Biol. 2018;18(2):151-60.##Lee YH, Yang H, Lee SR, Kwon S, Hong E, Lee HW. Welsh onion root (Allium fistulosum) restores ovarian functions from letrozole induced-polycystic ovary syndrome. Nutrients. 2018;10(10):1430.##Shao Y, Chang Z, Cheng Y, Wang X, Zhang J, Feng X, et al. Shaoyao-Gancao Decoction alleviated hyperandrogenism in a letrozole-induced rat model of polycystic ovary syndrome by inhibition of NF-κB activation. Biosci Rep. 2019;39(1):BSR20181877.##Abbasian N, Momtazb S, Baeeric M, Navaei-Nigjeh M, Hosseini R, Abdollahi M. Molecular and biochemical evidence on the role of zearalenone in rat polycystic ovary. Toxicon. 2018;154:7-14.##Mohammadi Sh, Kayedpoor P, Karimzadeh-Bardei L, Nabiuni M. The effect of curcumin on TNF-α, IL-6 and CRP expression in a model of polycystic ovary syndrome as an inflammation state. J Reprod Infertil. 2017;18(4):352-60.##Tahmasebi F, Movahedin M, Mazaheri Z. Antioxidant effects of calligonum extract on ovarian tissue of PCO model: an experimental study. Int J Reprod Biomed. 2018;16(10):641-8.##Christiane Ndeingang E, Brice Defo Deeh P, Watcho P, Kamanyi A. Phyllanthus muellerianus (Euphorbiaceae) restores ovarian functions in letrozole-induced polycystic ovarian syndrome in rats. Evid Based Complement Alternat Med. 2019;2019:2965821.##Jelodar G, Masoomi S, Rahmanifar F. Hydroalcoholic extract of flaxseed improves polycystic ovary syndrome in a rat model. Iran J Basic Med Sci. 2018;21(6):645-50.##Darabia P, Khazalia H, Mehrabani Natanzi M. Therapeutic potentials of the natural plant flavonoid apigenin in polycystic ovary syndrome in rat model: via modulation of pro-inflammatory cytokines and antioxidant activity. Gynecol Endocrinol. 2019;36(7):582-7.##Mohammadi Sh, Karimzadeh Bardei L, Hojati V, Ghorbani A, Nabiuni M. Anti-inflammatory effects of curcumin on insulin resistance index, levels of Interleukin-6, C-Reactive protein, and liver histology in polycystic ovary syndrome-induced rats. Cell J. 2017;19(3):425-33.##Ardalan T, Ardalan P, Heravi M. Kinetic study of free radicals scavenging by saffron petal extracts. J Chem Health Risks. 2012;2(4):29-36.##Tavana S, Eimani H, Azarnia M, Shahverdi A, Eftekhari P. Effects of saffron (Crocus sativus L.) aqueous extract on in vitro maturation, fertilization and embryo development of mouse oocytes. Cell J. 2012;13(4):259-64.##Bagherzade G, Manzari Tavakoli M, Namaei M. Green synthesis of silver nanoparticles using aqueous extract of saffron (Crocus sativus L.) wastages and its antibacterial activity against six bacteria. Asian Pac J Trop Biomed. 2017;7(3):227-33.##Zeka K, Ruparelia K, Continenza M, Stagos D, Vegli&#242; F, Arroo R. Petals of Crocus sativus L. as a potential source of the antioxidants crocin and kaempferol. Fitoterapia. 2015;107:128-34.##Hosseini A, Razavi BM, Hosseinzadeh H. Saffron (Crocus sativus) petal as a new pharmacological target: a review. Iran J Basic Med Sci. 2018;21(11):1091-9.##Babaei A, Arshami J, Haghparast A, Danesh Mesgaran M. Effects of saffron (Crocus sativus) petal ethanolic extract on hematology, antibody response, and spleen histology in rats. Avicenna J Phytomed. 2014;4(2):103-9.##Babaei A, Arshami J, Haghparast AR, Danesh Mesgaran M. Effects of Crocus sativus petals extract on biochemical blood parameters in male rats. J Arak Univ Med Sci. 2014;16(6):14-21.##Jafari A, Pashazadeh M. Antibacterial effect of methanolic extract of saffron petal (Crocus sativus L.) on some standard gram positive and gram-ngative pathogenic bacteria in vitro. Curr Pers Med Arom. 2020;3(1):1-7.##Boskabady MH, Farkhondeh T. Antiinflammatory, antioxidant, and immunomodulatory effects of Crocus sativus L. and its main constituents. Phytother Res. 2016;30(7):1072-94.##Kalhori Z, Azadbakht M, Bazdar A, Zeinali H. Polycystic ovary induction in mouse by testosterone enanthate. J Fasa Univ Med Sci. 2013;3(4):387-91.##Kalhori Z, Soleimani Mehranjani M, Azadbakht M, Shariaatzadeh M. Ovary stereological features and serum biochemical factors following induction of polycystic ovary syndrome with testosterone enanthate in mice: an experimental study. Int J Reprod Biomed. 2018;16(4):267-74.##Hu Q, Jin J, Zhou H, Yu D, Qian W, Zhong Y, et al. Crocetin attenuates DHT-induced polycystic ovary syndrome in mice via revising kisspeptin neurons. Biomed Pharmacother. 2018;107:1363-9.##Kang B, Wang X, Xu Q, Wu Y, Si X, Jiang D. Effect of 3- nitropropionic acid inducing oxidative stress and apoptosis of granulosa cells in geese. Biosci Rep. 2018;38(5):BSR20180274.##Hong Y, Yin Y, Tan Y, Hong K, Zhou H. The flavanone, naringenin, modifies antioxidant and steroidogenic enzyme activity in a rat model of letrozole-induced polycystic ovarysyndrome. Med Sci Monit. 2019;25:395-401.##Jadouali SM, Atifi H, Mamouni R, Majourhat A, Bouzouba&#226; Z, Laknifli A, et al. Chemical characterization and antioxidant compounds of flower parts of Moroccan crocus sativus L. J Saudi Soci Agricult Sci. 2018;18(4):476-480. ##Ahmadi Shadmehri A, Namvar F, Miri H, Yaghmaei P, Nakhaei Moghaddam M. Cytotoxicity, antioxidant and antibacterial activities of Crocus sativus petal extract. Int J Res Appl Basic Med Sci. 2019;5(1):69-76. ##Hosseinzadeh H, Younesi H. Antinociceptive and anti-inflammatory effects of Crocus sativus L. Stigma and petal extracts in mice. BMC Pharmacol. 2002;2:7.##Ghowsi M, Khazali H, Sisakhtnezhad S. Evaluation of TNFα and IL-6 mRNAs expression in visceral and subcutaneous adipose tissues of polycystic ovary rats and effects of resveratrol. Iran J Basic Med Sci. 2018;21(2):165-74.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Seminal L-Carnitine In Infertile Oligoasthenoteratozoospermic Men with Varicocele</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: Few studies have investigated the relationship of seminal L-Carnitine (LC) with male infertility associated with varicocele. The purpose of this prospective cross-sectional study was to assess seminal plasma LC levels in infertile oligoathenoteratozoospermic (OAT) men with varicocele.&lt;br /&gt;
Methods: Overall, 86 men were investigated. They were divided into infertile OAT men with varicocele (n=45), infertile OAT men without varicocele (n=21), and fertile men (n=20) as a control group. According to WHO guidelines, these men were subjected to history taking, clinical examination, and semen analysis. Seminal LC levels were evaluated by the colorimetric method. Statistical comparisons were done using Kruskal-Wallis and Mann-Whitney U tests and correlations were verified by the Pearson test. P-value&lt;0.05 was set to be statistically significant.&lt;br /&gt;
Results: The mean seminal plasma LC levels were significantly lower in infertile OAT men with varicocele (216.3&#177;57.1 &lt;em&gt;ng/ml&lt;/em&gt;) compared to infertile OAT men without varicocele (252.9&#177;62.9 &lt;em&gt;ng/ml&lt;/em&gt;, p=0.01), or fertile men (382.8&#177;63.6 &lt;em&gt;ng/ml&lt;/em&gt;, p=0.001). Besides, the mean seminal plasma LC level exhibited statistically significant decreases in infertile OAT men of varicocele grade III compared to varicocele grade II cases, and in infertile OAT men with bilateral varicocele compared with unilateral varicocele cases. Collectively, there was a statistically significant positive correlation between seminal LC levels with sperm concentration, motility, and normal morphology.&lt;br /&gt;
Conclusion: Seminal LC levels are expressively reduced in infertile OAT men with varicocele and are influenced by an increase in varicocele grade and laterality.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>26</FPAGE>
            <TPAGE>33</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Taymour</Name>
<MidName>T</MidName>
<Family>Mostafa</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Andrology, Sexology &amp;amp; STIs, Faculty of Medicine, Cairo University</Organization>
</Organizations>
<Universities>
<University>Department of Andrology, Sexology &amp; STIs, Faculty of Medicine, Cairo University</University>
</Universities>
<Countries>
<Country>Egypt</Country>
</Countries>
<EMAILS>
<Email>taymour.mostafa@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Khadiga M</Name>
<MidName>KM</MidName>
<Family>Abougabal</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Clinical and Chemical Pathology, Faculty of Medicine, Beni-Suef University</Organization>
</Organizations>
<Universities>
<University>Department of Clinical and Chemical Pathology, Faculty of Medicine, Beni-Suef University</University>
</Universities>
<Countries>
<Country>Egypt</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Gesthimani</Name>
<MidName>G</MidName>
<Family>Mintziori</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Unit of Reproductive Endocrinology, Department of Obstetrics &amp;amp; Gynecology, Medical School, Aristotle University of  Thessaloniki</Organization>
</Organizations>
<Universities>
<University>Unit of Reproductive Endocrinology, Department of Obstetrics &amp; Gynecology, Medical School, Aristotle University of  Thessaloniki</University>
</Universities>
<Countries>
<Country>Egypt</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Nashaat</Name>
<MidName>N</MidName>
<Family>Nabil</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Andrology, Sexology &amp;amp; STIs, Faculty of Medicine, Beni-Suef University</Organization>
</Organizations>
<Universities>
<University>Department of Andrology, Sexology &amp; STIs, Faculty of Medicine, Beni-Suef University</University>
</Universities>
<Countries>
<Country>Egypt</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Mohamed</Name>
<MidName>M</MidName>
<Family>Adel</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Andrology, Sexology &amp;amp; STIs, Faculty of Medicine, Beni-Suef University</Organization>
</Organizations>
<Universities>
<University>Department of Andrology, Sexology &amp; STIs, Faculty of Medicine, Beni-Suef University</University>
</Universities>
<Countries>
<Country>Egypt</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Ahmed F</Name>
<MidName>AF</MidName>
<Family>AboSief</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Andrology, Sexology &amp;amp; STIs, Faculty of Medicine, Beni-Suef University</Organization>
</Organizations>
<Universities>
<University>Department of Andrology, Sexology &amp; STIs, Faculty of Medicine, Beni-Suef University</University>
</Universities>
<Countries>
<Country>Egypt</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Oligoasthenoteratozoospermic</KeyText></KEYWORD><KEYWORD><KeyText>Infertility</KeyText></KEYWORD><KEYWORD><KeyText>L-Carnitine</KeyText></KEYWORD><KEYWORD><KeyText>Men</KeyText></KEYWORD><KEYWORD><KeyText>Semen</KeyText></KEYWORD><KEYWORD><KeyText>Sperm</KeyText></KEYWORD><KEYWORD><KeyText>Varicocele</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120132.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Punab M, Poolamets O, Paju P, Vihljajev V, Pomm K, Ladva R, et al. Causes of male infertility: a 9-year prospective monocentre study on 1737 patients with reduced total sperm counts. Hum Reprod. 2017;32(1):18-31.##Mintziori G, Nigdelis MP, Mathew H, Mousiolis A, Goulis DG, Mantzoros CS. The effect of excess body fat on female and male reproduction. Metabolism. 2020;107(6):154193.##Henkel R, Offor U, Fisher D. The role of infections and leukocytes in male infertility. Andrologia. 2021;53(1):e13743.##Mintziori G, Kita M, Duntas L, Goulis DG. Consequences of hyperthyroidism in male and female fertility: pathophysiology and current management. J Endocrinol Invest. 2016;39(8):849-53.##Vander-Borght M, Wyns C. Fertility and infertility: definition and epidemiology. Clin Biochem. 2018;62:2-10.##Roque M, Esteves SC. Effect of varicocele repair on sperm DNA fragmentation: a review. Int Urol Nephrol. 2018;50(4):583-603.‏##D&#39;Andrea S, Micillo A, Barbonetti A, Giordano AV, Carducci S, Mancini A, et al. Determination of spermatic vein reflux after varicocele repair helps to define the efficacy of treatment in improving sperm parameters of subfertile men. J Endocrinol Invest. 2017;40(10):1145-53.##Pallotti F, Paoli D, Carlini T, Vestri AR, Martino G, Lenzi A, et al. Varicocele and semen quality: a retrospective case-control study of 4230 patients from a single centre. J Endocrinol Invest. 2018;41(2):185-92.##Mostafa T, Nabil N, Rashed L, Abo-Sief AF, Eissa HH. Seminal SIRT1-oxidative stress relationship in infertile oligoasthenoteratozoospermic men with varicocele after its surgical repair. Andrologia. 2020;52(1):e13456.##Mostafa T, Rashed LA, Nabil NI, Osman I, Mostafa R, Farag M. Seminal miRNA relationship with apoptotic markers and oxidative stress in infertile men with varicocele. Biomed Res Int. 2016;2016:4302754.##Jensen CFS, &#216;stergren P, Dupree JM, Ohl DA, S&#248;nksen J, Fode M. Varicocele and male infertility. Nat Rev Urol. 2017;14(9):523-33.##Ringseis R, Keller J, Eder K. Role of carnitine in the regulation of glucose homeostasis and insulin sensitivity: evidence from in vivo and in vitro studies with carnitine supplementation and carnitine deficiency. Eur J Nutr. 2012;51(1):1-18.##Ribas GS, Vargas CR, Wajner M. L-carnitine supplementation as a potential antioxidant therapy for inherited neurometabolic disorders. Gene. 2014;533(2):469-76.##Bene J, Hadzsiev K, Melegh B. Role of carnitine and its derivatives in the development and management of type 2 diabetes. Nutr Diabetes. 2018;8(1):8.##Potts RJ, Jeﬀeries TM, Notarianni LJ. Antioxidant capacity of the epididymis. Hum Reprod. 1999;14(10):2513-6.##Agarwal A, Said TM. Carnitines and male infertility. Reprod Biomed Online. 2004;8(4):376-84.##Sigman M, Glass S, Campagnone J, Pryor JL. Carnitine for the treatment of idiopathic asthenozoospermia: a randomized, double-blind, placebo-controlled trial. Fertil Steril. 2006;85(5):1409-14.##Lenzi A, Sgr&#242; P, Salacone P, Paoli D, Gilio B, Lombardo F, et al. Placebo controlled double blind randomized trial on the use of L-carnitine and L-acetyl-carnitine combined treatment in asthenozoospermia. Fertil Steril. 2004;81(6):1578-84.##Mongioi L, Calogero AE, Vicari E, Condorelli RA, Russo GI, Privitera S, et al. The role of carnitine in male infertility. Andrology. 2016;4(5):800-7.‏##Hasson MA. The relationship between the use of L-Carnitine supplements and the male sub-infertility. Int J Pharm Qual Assur. 2019;10(4):735-40.‏##Steiner AZ, Hansen KR, Barnhart KT, Cedars MI, Legro RS, Diamond MP, et al. The effect of antioxidants on male factor infertility: the males, antioxidants, and infertility (MOXI) randomized clinical trial. Fertil Steril. 2020;113(3):552-60.e3.##Zhang X, Cui Y, Dong L, Sun M, Zhang Y. The efficacy of combined l-carnitine and l-acetyl carnitine in men with idiopathic oligoasthenoteratozoospermia: a systematic review and meta-analysis. Andrologia. 2020;52(2):e13470.##Tsampoukas G, Khan MF, Katsouri A, Akhter W, Moussa M, Deliveliotis K, et al. L-carnitine as primary or adjuvant treatment in infertile patients with varicocele. a systematic review. Arch Ital Urol Androl. 2020;92(3).##Abbaticchio G, Giagulli VA, Defini M, Micale FM, Giorgino R. Free l-carnitine in human semen. Arch Androl. 1985;15(2-3):137-42.##And&#243; S, Carpino A, Buffone M, Maggiolini M, Sisci D. The evaluation of free-L-carnitine, zinc and fructose in the seminal plasma of patients with varicocele and normozoospermia. Andrologia. 1989;21(2):155-60.##Pajovic B, Dimitrovski A, Radojevic N, Vukovic M. A correlation between selenium and carnitine levels with hypo-osmotic swelling test for sperm membrane in low- grade varicocele patients. Eur Rev Med Pharmacol Sci. 2016;20(4):598-604.##Dawson B, Trapp R. Basic and clinical biostatistics. 4th ed. USA: McGraw-Hill; 2004. 416 p.##World Health Organization. WHO laboratory manual for the examination and processing of human semen. 5th ed. Switzerland: Geneva: WHO Press; 2010. 271 p.##Lotti F, Maggi M. Ultrasound of the male genital tract in relation to male reproductive health. Hum Reprod Update. 2015;21(1):56-83.##Kim YS, Kim SK, Cho IC, Min SK. Efficacy of scrotal Doppler ultrasonography with the Valsalva maneuver, standing position, and resting-Valsalva ratio for varicocele diagnosis. Korean J Urol. 2015;56(2):144-9.##Chen YW, Niu YH, Wang DQ, Li H, Pokhrel G, Xu H, et al. Effect of adjuvant drug therapy after varicocelectomy on fertility outcome in males with varicocele-associated infertility: systematic review and meta-analysis. Andrologia. 2018;50(8):e13070.##Majzoub A, ElBardisi H, Covarrubias S, Mak N, Agarwal A, Henkel R, et al. Effect of microsurgical varicocelectomy on fertility outcome and treatment plans of patients with severe oligozoospermia: an original report and meta-analysis. Andrologia. 2021;53(6):e14059.##Matalliotakis I, Koumantaki Y, Evageliou A, Matalliotakis G, Goumenou A, Koumantakis E. L-carnitine levels in the seminal plasma of fertile and infertile men: correlation with sperm quality. Int J Fertil Womens Med. 2000;45(3):236-40.##G&#252;rb&#252;z B, Yalti S, Fi&#231;icioğlu C, Zehir K. Relationship between semen quality and seminal plasma total carnitine in infertile men. J Obstet Gynaecol. 2003;23(6):653-6.##De Rosa M, Boggia B, Amalfi B, Zarrilli S, Vita A, Colao A, et al. Correlation between seminal carnitine and functional spermatozoal characteristics in men with semen dysfunction of various origins. Drugs R D. 2005;6(1):1-9.##Sheikh N, Goodarzi M, Bab Al-Havaejee H, Safari M, Amiri I, Najafi R, et al. L-carnitine level in seminal plasma of fertile and infertile men. J Res Health Sci. 2007;7(1):43-8.##Tang LF, Jiang H, Shang XJ, Zhao LM, Bai Q, Hong K, et al. [Seminal plasma levocarnitine significantly correlated with semen quality]. Zhonghua Nan Ke Xue. 2008;14(8):704-8. Chninese.##Haseen Ahmed SD, Ahsan S, Iqbal T, Ahmed Burney SI. Relationship of seminal free L-Carnitine with functional spermatozoal characteristics: results from an observational study conducted in a tertiary care hospital of Karachi, Pakistan. J Pak Med Assoc. 2017;67(2):280-4.##Xu Y, Lu H, Wang Y, Zhang Z, Wu Q. Comprehensive metabolic profiles of seminal plasma with different forms of male infertility and their correlation with sperm parameters. J Pharm Biomed Anal. 2020;177:112888.‏##Roaiah MM, Mostafa T, Salem D, El-Nashar AR, Kamel II, El-Kashlan MS. alpha-1,4-Glucosidase activity in infertile oligoasthenozoospermic men with and without varicocele. Andrologia. 2007;39(1):28-32.##Vivas-Acevedo G, Lozano-Hern&#225;ndez R, Camejo MI. Varicocele decreases epididymal neutral α-glucosidase and is associated with alteration of nuclear DNA and plasma membrane in spermatozoa. BJU Int. 2014;113(4):642-9.##Zhu B, Zheng YF, Zhang YY, Cao YS, Zhang L, Li XG, et al. Protective effect of L-carnitine in cyclophosphamide-induced germ cell apoptosis. J Zhejiang Univ Sci B. 2015;16(9):780-7.##Modanloo M, Shokrzadeh M. Analyzing mitochondrial dysfunction, oxidative stress, and apoptosis: potential role of L-carnitine. Iran J Kidney Dis. 2019;13(2):74-86.‏##Naderi Noreini S, Malmir M, Ghafarizadeh A, Faraji T, Bayat R. Protective effect of L-carnitine on apoptosis, DNA fragmentation, membrane integrity and lipid peroxidation of spermatozoa in the asthenoteratospermic men. Andrologia. 2021;53(2):e13932.##Mostafa T, Anis T, Imam H, El-Nashar AR, Osman IA. Seminal reactive oxygen species-antioxidant relationship in fertile males with and without varicocele. Andrologia. 2009;41(2):125-9.##Mostafa T, Rashed L, Nabil N, Amin R. Seminal BAX and BCL2 gene and protein expressions in infertile men with varicocele. Urology. 2014;84(3):590-5.##Lehtihet M, Arver S, Kalin B, Kvist U, Pousette A. Left-sided grade 3 varicocele may affect the biological function of the epididymis. Scand J Urol. 2014;48(3):284-9.##Sofimajidpour H, Ghaderi E, Ganji O. Comparison of the effects of varicocelectomy and oral L-carnitine on sperm parameters in infertile men with varicocele. J Clin Diagn Res. 2016;10(4):PC07-10.##Mostafa T, Rashed L, Taymour M. Seminal cyclooxygenase relationship with oxidative stress in infertile oligoasthenoteratozoospermic men with varicocele. Andrologia. 2016;48(2):137-42.##Alkan İ, Y&#252;ksel M, Canat H, Atalay HA, Can O, &#214;zveri H, et al. Superoxide anion production by the spermatozoa of men with varicocele: relationship with Varicocele grade and semen parameters. World J Mens Health. 2018;36(3):255-62.‏##Ashrafzade A, Sadighi-Gilani M, Topraggaleh T, Khojasteh M, Sepidarkish M, Borjian Boroujeni P, et al. Oxidative stress-related miRNAs in spermatozoa may reveal the severity of damage in grade III varicocele. Andrologia. 2020;52(9):e13598.‏##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Luteal Phase Support in Intrauterine Insemination Cycles: A Randomized Clinical Trial of Vaginal Versus Intramuscular Progesterone Administration</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: Different progesterone doses and routes are used for luteal phase support in stimulated intrauterine insemination (IUI) cycles, but the optimal supplementation scheme has not yet been determined. Therefore, our aim was to compare the administration of two different doses of vaginal progesterone with two doses of intramuscular (IM) progesterone for luteal phase support in patients undergoing IUI cycles.&lt;br /&gt;
Methods: In this randomized clinical trial, 312 women with unexplained or male-factor infertility intending to start IUI cycles between April 2015 and January 2018 were included. They were randomized into four groups (n=78/each) including group 1 who received IM progesterone in oil (25 &lt;em&gt;mg&lt;/em&gt; daily), group 2 who received IM progesterone in oil (50 &lt;em&gt;mg&lt;/em&gt; daily), group 3 who received progesterone suppository (400 &lt;em&gt;mg&lt;/em&gt; daily), and group 4 who received progesterone suppository (800 &lt;em&gt;mg&lt;/em&gt; daily; 400 &lt;em&gt;mg&lt;/em&gt; twice daily). The primary outcome was the clinical pregnancy rate. The ongoing pregnancy rate, abortion rate, and patients’ satisfaction, and convenience the secondary outcomes.&lt;br /&gt;
Results: In our study, the overall clinical and ongoing pregnancy rates per cycle with COS and IUI were 16.02% and 12.8%, respectively. There were no significant differences in clinical pregnancy, ongoing pregnancy, and abortion rates among groups (p=0.84). The overall patients’ satisfaction and convenience was significantly higher in the vaginal progesterone suppository groups than the IM progesterone groups (p=0.001).&lt;br /&gt;
Conclusion: The results of this study showed that vaginal progesterone administration provides a more easy-to-use and convenient method than IM progesterone administration for luteal phase support in IUI cycles with comparable pregnancy rates.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>33</FPAGE>
            <TPAGE>39</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Azam</Name>
<MidName>A</MidName>
<Family>Azargoon</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Abnormal Uterine Bleeding Research Center, Semnan University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Abnormal Uterine Bleeding Research Center, Semnan University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>azarmona2003@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Gohar</Name>
<MidName>G</MidName>
<Family>Joorabloo</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Abnormal Uterine Bleeding Research Center, Semnan University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Abnormal Uterine Bleeding Research Center, Semnan University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Majid</Name>
<MidName>M</MidName>
<Family>Mirmohammadkhani</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Social Determinants of Health Research Center, Semnan University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Social Determinants of Health Research Center, Semnan University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Gonadotropins</KeyText></KEYWORD><KEYWORD><KeyText>Infertility</KeyText></KEYWORD><KEYWORD><KeyText>Injections</KeyText></KEYWORD><KEYWORD><KeyText>Intramuscular administration</KeyText></KEYWORD><KEYWORD><KeyText>Luteal phase</KeyText></KEYWORD><KEYWORD><KeyText>Male</KeyText></KEYWORD><KEYWORD><KeyText>Progestins</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120146.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Honda T, Tsutsumi M, Komoda F, Tatsumi K. Acceptable pregnancy rate of unstimulated intrauterine insemination: a retrospective analysis of 17,830 cycles. Reprod Med Biol. 2015;14(1):27-32.##Cohlen BJ. Should luteal phase support be introduced in ovarian stimulation/IUI programmes? an evidence-based review. Reprod Biomed Online. 2009;19 Suppl 4:31-8.##van der Linden M, Buckingham K, Farquhar C, Kremer JAM, Metwally M. Luteal phase support for assisted reproduction cycles. Cochrane Database Syst Rev. 2015;2015(7):CD009154.##Fauser BCJM, Devroey P. Reproductive biology and IVF: ovarian stimulation and luteal phase consequences. Trends Endocrinol Metab. 2003;14(5):236-42.##Erdem A, Erdem M, Atmaca S, Guler I. Impact of luteal phase support on pregnancy rates in intrauterine insemination cycles: a prospective randomized study. Fertil Steril. 2009;91(6):2508-13.##Seckin B, Turkcapar F, Yildiz Y, Senturk B, Yilmaz N, Gulerman C. Effect of luteal phase support with vaginal progesterone in intrauterine insemination cycles with regard to follicular response: a prospective randomized study. J Reprod Med. 2014;59(5-6):260-6.##Peeraer K, D’Hooghe T, Laurent P, Pelckmans S, Delvigne A, Laenen A, et al. Impact of luteal phase support with vaginal progesterone on the clinical pregnancy rate in intrauterine insemination cycles stimulated with gonadotropins: a randomized multicenter study. Fertil Steril. 2016;106(6):1490-5.##Keskin M, Ayta&#231; R. Does luteal phase support effect pregnancy rates in intrauterine insemination cycles? a prospective randomised controlled study in a tertiary center. Obstet Gynecol Int. 2020;2020:6234070.##Green KA, Zolton JR, Schermerhorn SMV, Lewis TD, Healy MW, Terry N, et al. Progesterone luteal support after ovulation induction and intrauterine insemination: an updated systematic review and meta-analysis. Fertil Steril. 2017;107(4):924-33.##Miralpeix E, Gonz&#225;lez-Comadran M, Sol&#224; I, Manau D, Carreras R, Checa MA. Efficacy of luteal phase support with vaginal progesterone in intrauterine insemination: a systematic review and meta-analysis. J Assist Reprod Genet. 2014;31(1):89-100.##G&#252;n İ, &#214;zdamar &#214;, Yılmaz A. Luteal phase support in intrauterine insemination cycles. Turk J Obstet Gynecol. 2016;13(2):90-4.##Tavaniotou A, Smitz J, Bourgain C, Devroey P. Comparison between different routes of progesterone administration as luteal phase support in infertility treatments. Hum Reprod Update. 2000;6(2):139-48.##Zarutskie PW, Phillips JA. A meta-analysis of the route of administration of luteal phase support in assisted reproductive technology: vaginal versus intramuscular progesterone. Fertil Steril. 2009;92(1):163-9.##Cicinelli E, de Ziegler D, Bulletti C, Matteo MG, Schonauer LM, Galantino P. Direct transport of progesterone from vagina to uterus. Obstet Gynecol. 2000;95(3):403-6.##Khadem N, Looii MA. Comparing 17-α-hydroxyprogesterone caproate and progesterone in oil for luteal phase support in IUI cycles. J Reprod Infertil. 2007;8(3):230-7.##Khosravi D, Taheripanah R, Taheripanah A, Monfared VT, Hosseini-Zijoud SM. Comparison of oral dydrogesterone with vaginal progesteronefor luteal support in IUI cycles: a randomized clinical trial. Iran J Reprod Med. 2015;13(7):433-8.##Biberoglu EH, Tanrıkulu F, Erdem M, Erdem A, Biberoglu KO. Luteal phase support in intrauterine insemination cycles: a prospective randomized study of 300 mg versus 600 mg intravaginal progesterone tablet. Gynecol Endocrinol. 2016;32(1):55-7.##Beltsos AN, Sanchez MD, Doody KJ, Bush MR, Domar AD, Collins MG. Patients’ administration preferences: progesterone vaginal insert (endometrin&#174;) compared to intramuscular progesterone for luteal phase support. Reprod Health. 2014;11:78.##Doody K, Bush M, Collins M. Progesterone supplementation for luteal support: efficacy and patient experiences with vaginal inserts (endometrin&#174;) versus intramuscular injection. Fertil Steril. 2012;97(3):S18.##Zaman AY, Coskun S, Alsanie AA, Awartani KA. Intramuscular progesterone (Gestone) versus vaginal progesterone suppository (Cyclogest) for luteal phase support in cycles of in vitro fertilization–embryo transfer: patient preference and drug efficacy. Fertil Res Pract. 2017;3:17.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Genetic Factors of Idiopathic Recurrent Miscarriage in Kazakh Population</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: It seems that 50% of the possible causes of recurrent miscarriage do not have any explainable etiology and they require in-depth etiopathogenesis analysis. The purpose of this research was to study polymorphisms relationship of the immune response genes including Val249Ile CX3CR1 (rs3732379), CT60 G/A CTLA4 (rs3087243), and HLA DQA1, DQB1, DRB1 (major histocompatibility complex, class II) with development of idiopathic form of recurrent miscarriage (iRM) in Kazakh population.&lt;br /&gt;
Methods: TagMan genotyping for 302 patients with iRM and 300 women with normal reproduction was performed. Molecular genetic studies were carried out by the TaqMan method of unified site-specific amplification and real-time genotyping using test systems. Statistical tests and Chi Square were carried out using PLINK, STATA13 software and p˂0.05 was considered statistically significant.&lt;br /&gt;
Results: It has been shown that carriage of unfavorable genotypes (Val/Ile, Val/Val) by the Val249Ile polymorphism of CX3CR1 gene increases the risk of developing iRM by 1.43 times. Search for associations of genes allelic variants of HLA class 2 complex with iRM revealed 501 allele in DQA1 locus, 0301 in DQB1 locus, 10, 12, 15, 16 alleles in DRB1 locus, which increase the risk of developing iRM in Kazakh population.&lt;br /&gt;
Conclusion: The highly significant associations of immune response genes with development of iRM in Kazakh population indicate the possible involvement of the immune system interaction of mother cells with syncytiotrophoblast, which is realized by vascular defects and defective embryo implantation, causing termination of pregnancy.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>39</FPAGE>
            <TPAGE>46</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Gulnara S</Name>
<MidName>GS</MidName>
<Family>Svyatova</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Scientific Center of Obstetrics, Gynecology and Perinatology</Organization>
</Organizations>
<Universities>
<University>Scientific Center of Obstetrics, Gynecology and Perinatology</University>
</Universities>
<Countries>
<Country>Republic of Kazakhstan</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Dinara D</Name>
<MidName>DD</MidName>
<Family>Mirzakhmetova</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Scientific Center of Obstetrics, Gynecology and Perinatology</Organization>
</Organizations>
<Universities>
<University>Scientific Center of Obstetrics, Gynecology and Perinatology</University>
</Universities>
<Countries>
<Country>Republic of Kazakhstan</Country>
</Countries>
<EMAILS>
<Email>mirzakhmetova6947-1@uoel.uk</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Galina M</Name>
<MidName>GM</MidName>
<Family>Berezina</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Scientific Center of Obstetrics, Gynecology and Perinatology</Organization>
</Organizations>
<Universities>
<University>Scientific Center of Obstetrics, Gynecology and Perinatology</University>
</Universities>
<Countries>
<Country>Republic of Kazakhstan</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Alexandra V</Name>
<MidName>AV</MidName>
<Family>Murtazaliyeva</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Scientific Center of Obstetrics, Gynecology and Perinatology</Organization>
</Organizations>
<Universities>
<University>Scientific Center of Obstetrics, Gynecology and Perinatology</University>
</Universities>
<Countries>
<Country>Republic of Kazakhstan</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Gene polymorphism</KeyText></KEYWORD><KEYWORD><KeyText>Genotypes</KeyText></KEYWORD><KEYWORD><KeyText>Implantation</KeyText></KEYWORD><KEYWORD><KeyText>Pregnancy</KeyText></KEYWORD><KEYWORD><KeyText>Reproductive medicine</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120147.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Practice Committee of the American Society for Reproductive Medicine. Definitions of infertility and recurrent pregnancy loss: a committee opinion. Fertil Steril. 2020;113(3):533-5.##Wan X, Li L, Liu Z, Fan Z, Yu L. Recurrent spontaneous abortion related to balanced translocation of chromosomes: two case reports. J Med Case Rep. 2021;15(1):270.##Xiang H, Yan H, Sun B, Feng F, Chen P. Decreased expression of long non-coding RNA SNHG7 cause recurrent spontaneous abortion through suppression proliferation and invasion of trophoblast cells via miR-34a. Am J Transl Res. 2019;11(1):463-72.##Wysocka U, Sakowicz A, Jakubowski L, Pinkier I, Rybak-Krzyszkowska M, Alaszewski W, et al. Association between idiopathic recurrent pregnancy loss and genetic polymorphisms in cytokine and matrix metalloproteinase genes. Ginekol Pol. 2021. In press.##Rasti Z, Nasiri M. Association of the 49 A/G polymorphism of CTLA4 gene with idiopathic recurrent spontaneous abortion in women in southwest of Iran. J Reprod Infertil. 2016;17(3):151-6.##Mojarrad M, Hassanzadeh-Nazarabadi M, Tafazoli N. Polymorphism of genes and implantation failure. Int J Mol Cell Med. 2013;2(1):1-8.##Homer HA. Modern management of recurrent miscarriage. Aust N Z J Obstet Gynaecol. 2019;59(1):36-44.##Svyatova GS, Berezina GM. Analysis of GWAS and meta-studies of habitual miscarriage according to world information databases. Obstet Gynecol Perinat. 2018;1(2):140-4.##Svyatova GS, Berezina GM, Murtazaliyeva AV. Association of polymorphisms of cardiovascular system genes with idiopathic recurrent pregnancy loss of Kazakh populations. Rev Latinoamer de Hiperten. 2019;14(4):319-25.##Ahmadi S, Rostamzadeh J, Khosravi D, Shariati P, Shakiba N. Association of CTLA-4 gene 49 A/G polymorphism with the incidence of type 1 diabetes mellitus in the Iranian Kurdish population. Pak J Biol Sci. 2013;16(24):1929-35.##Misra MK, Mishra A, Phadke SR, Agrawal S. Association of functional genetic variants of CTLA4 with reduced serum CTLA4 protein levels and increased risk of idiopathic recurrent miscarriages. Fertil Steril. 2016;106(5):1115-23.e6.##Tutchenko TM, Burka OA, Samilyk VS, Trokhymovych OV, Krotik OI, Gromova OL. Time to reduce the rate of idiopathic recurrent pregnancy losses. Reprod Endocrin. 2021;55:21-8.##Colley E, Hamilton S, Smith P, Morgan NV, Coomarasamy A, Allen S. Potential genetic causes of miscarriage in euploid pregnancies: A systematic review. Hum Reprod Update. 2019;25(4):452-72.##Atia TA. Overview of genetic causes of recurrent miscarriage and the diagnostic approach. Biocell. 2019;43(4):253-62.##Grimstad F, Krieg S. Immunogenetic contributions to recurrent pregnancy loss. J Assist Reprod Genet. 2016;33(7):833-47.##Meuleman T, Lashley LE, Dekkers OM, van Lith JM, Claas FH, Bloemenkamp KW. HLA associations and HLA sharing in recurrent miscarriage: a systematic review and meta-analysis. Hum Immunol. 2015;76(5):362-73.##Lowe M, Payton A, Verma A, Worthington J, Gemmell I, Hamilton P, et al. Associations between human leukocyte antigens and renal function. Sci Rep. 2021;11(1):3158.##Ali S, Majid S, Niamat Ali M, Taing S, El-Serehy H, Al-Misned FA. Evaluation of etiology and pregnancy outcome in recurrent miscarriage patients. Saudi J Biol Sci. 2020;27(10):2809-17.##Aruna M, Nagaraja T, Andal Bhaskar S, Tarakeswari S, Reddy К, Thangaraj L. Novel alleles of HLA-DQ and – DR loci show association with recurrent miscarriages among South Indian women. Hum Reprod. 2011;26(4):765-74.##El Hachem H, Crepaux V, May-Panloup P, Descamps P, Legendre G, Bouet PE. Recurrent pregnancy loss: current perspectives. Int J Womens Health. 2017;9:331-45.##Arias-Sosa LA, Acosta ID, Lucena-Quevedo E, Moreno-Ortiz H, Esteban-P&#233;rez C, Forero-Castro M. Genetic and epigenetic variations associated with idiopathic recurrent pregnancy loss. J Assist Reprod Gen. 2018;35(3):355-66.##Purcell S, Neale B, Todd-Brown K, Thomas L, Ferreira MA, Bender D, et al. PLINK: a tool set for whole-genome association and population-based linkage analyses. Am J Hum Gen. 2007;81(3):559-75.##Wang XP, Li QD, Ma ZW, Hong Y, Zhao AM, Di W, et al. [A/G polymorphism at position 49 in exon 1 of CTLA-4 gene in Chinese women with unexplained recurrent spontaneous abortion]. Zhonghua Fu Chan Ke Za Zhi. 2006;41(3):155-8. Chinese.##Parveen F, Faridi RM, Singh BS. Analysis of CCR5 and CX3CR1 gene polymorphisms in association with unexplained recurrent miscarriages among north Indian women. Cytokine. 2011;56(2):239-44.##Larsen CE, Alper CA. The genetics of HLA-associated disease. Curr Opin Immunol. 2004;16(5):660-7.##Segal S, Hill AV. Genetic susceptibility to infectious disease. Trends Microbiol. 2003;11(9):445-8.##Gordeeva LA, Shabaldin AV, Glushkov AN, Glushkova OA, Makarchenko OS. Association HLA-DRB1 with reproductive pathology in women. Med Immunol. 2007;9(6):643-8.##Tkach IR, Sosnina KO, Huleyuk NL, Terpylyak OI. Contribution of chromosomal abnormalities and genes of the major histocompatibility complex to early pregnancy losses. Biopolym Cell. 2015;31(1):38-45.##Iskhakov AT, Asatova MM, Rasulova MI. HLA profiles for miscarriage. Immunology. 1996;1:27-28.##Boldyreva MN, Bartseva OB, Kurilo LF, Tkachenko ER, Alekseev LP, Adamyan LV. Connection of the HLA-DRB1 genotype with reproductive failures. Reprod Issues. 2010;6:59-63.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>A Comparative Analysis of Outcomes Between Two Different Intramuscular Progesterone Preparations in Women Undergoing Frozen Embryo Transfer Cycles</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: The purpose of the current study was to assess if luteal support with intramuscular (IM) 17 alpha-hydroxyprogesterone caproate (17-OHPC) (Lentogest, IBSA, Italy) improves the pregnancy outcome in comparison to natural intramuscu-lar progesterone (Prontogest, AMSA, Italy) when administered to recipients in a frozen embryo transfer cycle.&lt;br /&gt;
Methods: A retrospective comparative study was performed to evaluate outcomes between two different intramuscular regimens used for luteal support in frozen embryo transfer cycles in patients underwent autologous in vitro fertilization (IVF) cycles (896 IVF cycles) and intracytoplasmic sperm injection (ICSI) who had a blastocyst transfer from February 2014 to March 2017 at the Centre for Reproductive and Genetic Health (CRGH) in London.&lt;br /&gt;
Results: The live birth rates were significantly lower for the IM natural progesterone group when compared to 17-OHPC group (41.8% &lt;em&gt;vs.&lt;/em&gt; 50.9%, adjusted OR of 0.63 (0.31-0.91)). The miscarriage rates were significantly lower in the 17-OHPC group compared to the IM natural progesterone group (14.5% &lt;em&gt;vs.&lt;/em&gt; 19.2%, OR of 1.5, 95% CI of 1.13-2.11). The gestational age at birth and birth weight were similar in both groups (p=0.297 and p=0.966, respectively).&lt;br /&gt;
Conclusion: It is known that both intramuscular and vaginal progesterone preparations are the standard of care for luteal phase support in women having frozen embryo transfer cycles. However, there is no clear scientific consensus regarding the optimal luteal support. In this study, it was revealed that live birth rates are significantly higher in women who received artificial progesterone compared to women who received natural progesterone in frozen embryo transfer cycles.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>46</FPAGE>
            <TPAGE>54</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Srividya</Name>
<MidName>S</MidName>
<Family>Seshadri</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email>v9dya@hotmail.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Rabi</Name>
<MidName>R</MidName>
<Family>Odia</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Ozkan</Name>
<MidName>O</MidName>
<Family>Ozturk</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Saab</Name>
<MidName>S</MidName>
<Family>Wiam</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Gilbert and Rose-Marie Chagoury Health Sciences Center, The Lebanese American University</Organization>
</Organizations>
<Universities>
<University>Gilbert and Rose-Marie Chagoury Health Sciences Center, The Lebanese American University</University>
</Universities>
<Countries>
<Country>Lebanon</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Ali</Name>
<MidName>A</MidName>
<Family>AlChami</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Xavier</Name>
<MidName>XV</MidName>
<Family>Gonzalez</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Saba</Name>
<MidName>S</MidName>
<Family>Salim</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Wael</Name>
<MidName>W</MidName>
<Family>Saab</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Paul</Name>
<MidName>P</MidName>
<Family>Serha</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>The Centre for Reproductive and Genetic Health</Organization>
</Organizations>
<Universities>
<University>The Centre for Reproductive and Genetic Health</University>
</Universities>
<Countries>
<Country>UK</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Frozen embryo transfer cycles</KeyText></KEYWORD><KEYWORD><KeyText>Luteal support</KeyText></KEYWORD><KEYWORD><KeyText>Progesterone</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120135.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Trouson A, Moher L. Human pregnancy following cryopreservation, thawing and transfer of an eight-cell embryo. Nature. 1983;305(5936):707-9.##Loutradi KE, Kolibianakis EM, Venetis CA, Papanikolaou EG, Pados G, Bontis I, et al. Cryopreservation of human embryos by vitrifaication or slow freezing: a systematic review and meta-analysis. Fertil Steril. 2008;90(1):186-93.##Roque M, Lattes K, Serra S, Sol&#224; I, Geber S, Carreras R, et al. Fresh embryo transfer versus frozen embryo transfer in in vitro fertilization cycles: a systematic review and meta-analysis.  Fertil Steril. 2013;99(1):156-62.##Li Z, Wang YA, Ledger W, Edgar DH, Sullivan EA. Clinical outcomes following cryopreservation of blastocysts by vitrification or slow freezing: a population-based cohort study. Hum Reprod. 2014;29(12):2794-801.##&#214;zg&#252;r K, Berkkanoğlu M, Bulut H, Isikli A, Coetzee K. Higher clinical pregnancy rates from frozen-thawed blastocyst transfers compared to fresh blastocyst transfers: a retrospective matched-cohort study. J Assist Reprod Genet. 2015;32(10):1483-90.##Gerris J, De Neubourg D, De Sutter P, Van Royen E, Mangelschots K, Vercruyssen M. Cryopreservation as a tool to reduce multiple birth. Reprod Biomed Online. 2003;7(3):286-94.##Devine K, Connell MT, Richter KS, Ramirez CI, Levens ED, DeCherney AH, et al. Single vitrified blastocyst transfer maximizes liveborn children per embryo while minimizing preterm birth. Fertil Steril. 2015;103(6):1454-60.e1.##Ishihara O, Araki R, Kuwahara A, Itakura A, Saito H, Adamson GD. Impact of frozen-thawed single-blastocyst transfer on maternal and neonatal outcome: an analysis of 277,042 single-embryo transfer cycles from 2008 to 2010 in Japan. Fertil Steril. 2014;101(1):128-33.##Maheshwari A, Pandey S, Shetty A, Hamilton M, Bhattacharya S. Obstetric and perinatal outcomes in singleton pregnancies resulting from the transfer of frozen thawed versus fresh embryos generated through in vitro fertilization treatment: a systematic review and meta-analysis. Fertil Steril. 2012;98(2):368-77.e1-9.##Roque M, Valle M, Guimar&#227;es F, Sampaio M, Geber S. Freeze-all policy: fresh vs. frozen-thawed embryo transfer. Fertil Steril. 2015;103(5):1190-3.##Maheshwari A, Bhattacharya S. Elective frozen replacement cycles for all: ready for prime time? Hum Reprod. 2013;28(1):6-9.##Casper RF, Yanushpolsky EH. Optimal endometrial preparation for frozen embryo transfer cycles: window of implantation and progesterone support. Fertil Steril. 2016;105(4):867-72.##DiLuigi AJ, Nulsen JC. Effects of gonadotropin-releasing hormone agonists and antagonists on luteal function. Curr Opin Obstet Gynecol. 2007;19(3):258-65.##Frydman R, Testart J, Giacomini P, Imbert MC, Martin E, Nahoul K. Hormonal and histological study of the luteal phase in women following aspiration of the preovulatory follicle. Fertil Steril. 1982;38(3):312-7.##Boynukalin FK, Gultomruk M, Turgut E, Demir B, Findikli N, Serdarogullari M, et al. Measuring the serum progesterone level on the day of transfer can be an additional tool to maximize ongoing pregnancies in single euploid frozen blastocyst transfers. Reprod Biol Endocrinol. 2019;17(1):102.##Beltsos AN, Sanchez MD, Doody KJ, Bush MR, Domar AD, Collins MG. Patients&#39; administration preferences: progesterone vaginal insert (Endometrin&#174;) compared to intramuscular progesterone for Luteal phase support. Reprod Health. 2014;11:78.##Shapiro DB, Pappadakis JA, Ellsworth NM, Hait HI, Nagy ZP. Progesterone replacement with vaginal gel versus i.m. injection: cycle and pregnancy outcomes in IVF patients receiving vitrified blastocysts. Hum Reprod. 2014;29(8):1706-11.##Leonard PH, Hokenstad AN, Khan Z, Jensen JR, Stewart EA, Coddington CC. Progesterone support for frozen embryo transfer: intramuscular versus vaginal suppository demonstrates no difference in a cohort. J Reprod Med. 2015;60(3-4):103-8.##Kaser DJ, Ginsburg ES, Missmer SA, Correia KF, Racowsky C. Intramuscular progesterone versus 8% Crinone vaginal gel for luteal phase support for day 3 cryopreserved embryo transfer. Fertil Steril. 2012;98(6):1464-9.##Casper RF. Luteal phase support for frozen embryo transfer cycles: intramuscular or vaginal progesterone. Fertil Steril. 2014;101(3):627-8.##Society for Maternal-Fetal Medicine Publications Committee, with assistance of Vincenzo Berghella. Progesterone and preterm birth prevention: translating clinical trials data into clinical practice. Am J Obstet Gynecol. 2012;206(5):376-86.##Costabile L, Gerli S, Manna C, Rossetti D, Di Renzo GC, Unfer V. A prospective randomized study comparing intramuscular progesterone and 17alpha-hydroxyprogesterone caproate in patients undergoing in vitro fertilization-embryo transfer cycles. Fertil Steril. 2001;76(2):394-6.##Gibbons WE, Toner JP, Hamacher P, Kolm P. Experience with a novel vaginal progesterone preparation in a donor oocyte program. Fertil Steril. 1998;69(1):96-101.##Jobanputra K, Toner JP, Denoncourt R, Gibbons WE. Crinone 8% (90 mg) given once daily for progesterone support therapy in donor egg cycles. Fertil Steril. 1999;72(6):980-4.##Devine K, Richter KS, Widra EA, McKeeby JL. Vitrified blastocyst transfer cycles with the use of only vaginal progesterone replacement with Endometrin have inferior ongoing pregnancy rates: results from the planned interim analysis of a three-arm randomized controlled noninferiority trial. Fertil Steril. 2018;109(2):266-75.##Zaman AY, Coskun S, Alsanie AA, Awartani KA. Intramuscular progesterone (Gestone) versus vaginal progesterone suppository (Cyclogest) for luteal phase support in cycles of in vitro fertilization–embryo transfer: patient preference and drug efficacy. Fertil Res Pract. 2017;3:17.##Travanty MN, Calawa B, Shalaby WS, Jozwiakowski MJ, Haraldsen KB. Development and usability of a new subcutaneous auto-injector device to administer hydroxyprogesterone caproate to reduce the risk of recurrent preterm birth. Med Devices (Auckl). 2018;11:241-52.##Northen AT, Norman GS, Anderson K, Moseley L, DiVito M, Cotroneo M, et al. Follow-up of children exposed in utero to 17 α-hydroxyprogesterone caproate compared with placebo. Obstet Gynecol. 2007;110(4):865-72.##Attardi BJ, Zeleznik A, Simhan H, Chiao JP, Mattison DR, Caritis SN, et al. Comparison of progesterone and glucocorticoid receptor binding and stimulation of gene expression by progesterone, 17-alpha hydroxyprogesterone caproate, and related progestins. Am J Obstet Gynecol. 2007;197(6):599.e1-7.##Feinberg EC, Beltsos AN, Nicolaou E, Marut EL, Uhler ML. Endometrin as luteal phase support in assisted reproduction. Fertil Steril. 2013;99(1):174-8.e1.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Association Between AMH Levels and Fertility/Reproductive Outcomes Among Women Undergoing IVF: A Retrospective Study</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: Anti-mullerian hormone (AMH) is a marker for predicting ovarian response to gonadotropin stimulation. It plays an important role in ovarian primordial follicle recruitment and dominant follicle selection. Therefore, the present study evaluated the AMH levels and their association with fertility/reproductive outcomes among women undergoing IVF.&lt;br /&gt;
Methods: A retrospective study was conducted on 665 women in GarbhaGudi Institute of Reproductive Health and Research in India from October 2018 to 2019. Subjects were divided into &lt;span style=&quot;font-size:11.0pt&quot;&gt;&lt;span style=&quot;font-family:&quot;Times New Roman&quot;,serif&quot;&gt;≥&lt;/span&gt;&lt;/span&gt;1.1 and &lt;span style=&quot;font-size:11.0pt&quot;&gt;&lt;span style=&quot;font-family:&quot;Times New Roman&quot;,serif&quot;&gt;≤&lt;/span&gt;&lt;/span&gt;1.1 AMH level groups. Data on age, luteinizing hormone; LH (&lt;em&gt;mIU/L&lt;/em&gt;), follicle-stimulating hormone values; FSH (&lt;em&gt;mIU/ml&lt;/em&gt;), LH value, oocytes retrieved, and oocytes fertilization were collected. AMH category was considered as the primary explanatory variable. Independent sample t-test and chisquare tests were performed. The p&lt;0.05 was considered statistically significant.&lt;br /&gt;
Results: Couple’s age, FSH values (&lt;em&gt;mIU/ml&lt;/em&gt;), number of large follicles, matured oocytes, fertilized oocytes, and cleaved embryos were statistically significant (p&lt;0.001) among subjects with &lt;span style=&quot;font-size:11.0pt&quot;&gt;&lt;span style=&quot;font-family:&quot;Times New Roman&quot;,serif&quot;&gt;≥&lt;/span&gt;&lt;/span&gt;1.1 AMH values. Percentage of women with successful embryo transfer was slightly higher among AMH category 1.1 (p=0.09). Fertilization rate (86.67&#177;20.08 &lt;em&gt;vs. &lt;/em&gt;83.64&#177;21.39, p=0.18) and clinical pregnancy rate (43.38% &lt;em&gt;vs.&lt;/em&gt; 36.36%, p=0.19) were slightly higher among women with AMH level of &lt;span style=&quot;font-size:11.0pt&quot;&gt;&lt;span style=&quot;font-family:&quot;Times New Roman&quot;,serif&quot;&gt;≥&lt;/span&gt;&lt;/span&gt;1.1 as compared to AMH of &lt;1.1. Live birth rate was slightly higher among women with AMH level of 1.1 (25.85% &lt;em&gt;vs. &lt;/em&gt;22.22%, p=0.45). Also, the number of fertilized oocytes was associated with clinical pregnancy rate (aOR=1.20, 95%CI 1.09-1.33).&lt;br /&gt;
Conclusion: Women with &lt;span style=&quot;font-size:11.0pt&quot;&gt;&lt;span style=&quot;font-family:&quot;Times New Roman&quot;,serif&quot;&gt;≥&lt;/span&gt;&lt;/span&gt;1.10 serum AMH levels had more number of retrieved oocytes, good oocyte quality, increased embryo transfer, and fertilization rates.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>54</FPAGE>
            <TPAGE>61</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Asha</Name>
<MidName>AS</MidName>
<Family>Vijay</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Scientific Director and Dean, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</Organization>
</Organizations>
<Universities>
<University>Scientific Director and Dean, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email>ashasvijay@gmail.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Murali Mohan</Name>
<MidName>MM</MidName>
<Family>Reddy Gopireddy</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Evidence Generation, Evidencian Research Associates</Organization>
</Organizations>
<Universities>
<University>Evidence Generation, Evidencian Research Associates</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Syed</Name>
<MidName>S</MidName>
<Family>Fyzullah</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Embryology, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</Organization>
</Organizations>
<Universities>
<University>Department of Embryology, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Gollapalli</Name>
<MidName>G</MidName>
<Family>Priyanka</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Evidence Generation, Evidencian Research Associates</Organization>
</Organizations>
<Universities>
<University>Evidence Generation, Evidencian Research Associates</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Maheswari</Name>
<MidName>M</MidName>
<Family>M</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Reproductive Medicine, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</Organization>
</Organizations>
<Universities>
<University>Department of Reproductive Medicine, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Usha</Name>
<MidName>U</MidName>
<Family>Rani</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Embryology, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</Organization>
</Organizations>
<Universities>
<University>Department of Embryology, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Swathi</Name>
<MidName>S</MidName>
<Family>Rajesh</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Embryology, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</Organization>
</Organizations>
<Universities>
<University>Department of Embryology, GarbhaGudi Institute of Reproductive Health and Research (GGIRHR), Hanumanthnagar</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Anti- mullerian hormone</KeyText></KEYWORD><KEYWORD><KeyText>Fertilization</KeyText></KEYWORD><KEYWORD><KeyText>Pregnancy rate</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120134.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Chen C, Kattera S. Comparison of pronuclear zygote morphology and early cleavage status of zygotes as additional criteria in the selection of day 3 embryos: a randomized study. Fertil Steril. 2006;85(2):347-52.##La Marca A, Sighinolfi G, Radi D, Argento C, Baraldi E, Artenisio AC, et al. Anti-M&#252;llerian hormone (AMH) as a predictive marker in assisted reproductive technology (ART). Hum Reprod Update. 2010;16(2):113-30.##Josso N. Anti-mullerian hormone: hormone or growth factor? Prog Growth Factor Res. 1990;2(3):169-79.##Weenen C, Laven JS, Von Bergh AR, Cranfield M, Groome NP, Visser JA, et al. Anti-Mullerian hormone expression pattern in the human ovary: potential implications for initial and cyclic follicle recruitment. Mol Hum Reprod. 2004;10(2):77-83.##de Vet A, Laven JS, de Jong FH, Themmen AP, Fauser BC. Antimullerian hormone serum levels: a putative marker for ovarian aging. Fertil Steril. 2002;77(2):357-62.##Tremellen KP, Kolo M, Gilmore A, Lekamge DN. Anti‐m&#252;llerian hormone as a marker of ovarian reserve. Aust N Z J Obstet Gynaecol. 2005;45(1):20-4.##Penarrubia J, F&#225;bregues F, Manau D, Creus M, Casals G, Casamitjana R, et al. Basal and stimulation day 5 anti-M&#252;llerian hormone serum concentrations as predictors of ovarian response and pregnancy in assisted reproductive technology cycles stimulated with gonadotropin-releasing hormone agonist–gonadotropin treatment. Hum Reprod Update. 2005;20(4):915-22.##Irez T, Ocal P, Guralp O, Cetin M, Aydogan B, Sahmay S. Different serum anti-Mullerian hormone concentrations are associated with oocyte quality, embryo development parameters and IVF-ICSI outcomes. Arch Gynecol Obstet. 2011;284(5):1295-301.##Lekamge DN, Barry M, Kolo M, Lane M, Gilchrist RB, Tremellen KP. Anti-M&#252;llerian hormone as a predictor of IVF outcome. Reprod Biomed Online. 2007;14(5):602-10.##Nardo LG, Gelbaya TA, Wilkinson H, Roberts SA, Yates A, Pemberton P, et al. Circulating basal anti-M&#252;llerian hormone levels as predictor of ovarian response in women undergoing ovarian stimulation for in vitro fertilization. Fertil Steril. 2009;92(5):1586-93.##Ebner T, Sommergruber M, Moser M, Shebl O, Schreier-Lechner E, Tews G. Basal level of anti-M&#252;llerian hormone is associated with oocyte quality in stimulated cycles. Hum Reprod. 2006;21(8):2022-6.##Sowers M, McConnell D, Gast K, Zheng H, Nan B, McCarthy JD, et al. Anti-M&#252;llerian hormone and inhibin B variability during normal menstrual cycles. Fertil Steril. 2010;94(4):1482-6.##Revelli A, Biasoni V, Gennarelli G, Canosa S, Dalmasso P, Benedetto C. IVF results in patients with very low serum AMH are significantly affected by chronological age. J Assist Reprod Genet. 2016;33(5):603-9.##Van Rooij I, Broekmans F, Te Velde E, Fauser B, Bancsi L, De Jong F, et al. Serum anti-M&#252;llerian hormone levels: a novel measure of ovarian reserve. Hum Reprod. 2002;17(12):3065-71.##Seifer DB, Baker VL, Leader B. Age-specific serum anti-M&#252;llerian hormone values for 17,120 women presenting to fertility centers within the United States. Fertil Steril. 2011;95(2):747-50.##Majumder K, Gelbaya TA, Laing I, Nardo LG. The use of anti-M&#252;llerian hormone and antral follicle count to predict the potential of oocytes and embryos. Eur J Obstet Gynecol Reprod Biol. 2010;150(2):166-70.##Takahashi C, Fujito A, Kazuka M, Sugiyama R, Ito H, Isaka K. Anti-M&#252;llerian hormone substance from follicular fluid is positively associated with success in oocyte fertilization during in vitro fertilization. Fertil Steril. 2008;89(3):586-91.##Lundin K, Bergh C, Hardarson T. Early embryo cleavage is a strong indicator of embryo quality in human IVF. Hum Reprod. 2001;16(12):2652-7.##Hazout A, Bouchard P, Seifer DB, Aussage P, Junca AM, Cohen-Bacrie P. Serum antim&#252;llerian hormone/m&#252;llerian-inhibiting substance appears to be a more discriminatory marker of assisted reproductive technology outcome than follicle-stimulating hormone, inhibin B, or estradiol. Fertil Steril. 2004;82(5):1323-9.##Cupisti S, Dittrich R, Mueller A, Strick R, Stiegler E, Binder H, et al. Correlations between anti-m&#252;llerian hormone, inhibin B, and activin A in follicular fluid in IVF/ICSI patients for assessing the maturation and developmental potential of oocytes. Eur J Med Res. 2007;12(12):604-8.##Van den Bergh MJ, Fahy-Deshe M, Hohl MK. Pronuclear zygote score following intracytoplasmic injection of hyaluronan-bound spermatozoa: a prospective randomized study. Reprod Biomed Online. 2009;19(6):796-801.##Honnma H, Baba T, Sasaki M, Hashiba Y, Oguri H, Fukunaga T, et al. Serum anti-Mullerian hormone levels affect the rate of ongoing pregnancy after in vitro fertilization. Reprod Sci. 2013;20(1):51-9.##Kissin DM, Schieve LA, Reynolds MA. Multiple-birth risk associated with IVF and extended embryo culture: USA, 2001. Hum Reprod. 2005;20(8):2215-23.##Tal R, Seifer DB, Khanimov M, Schwartz E, Grazi RV, Malter HE. Anti-M&#252;llerian hormone as an independent predictor of twin versus singleton pregnancy in fresh cycles. Reprod Biomed Online. 2013;26(4):360-7.##Singer T, Barad DH, Weghofer A, Gleicher N. Correlation of antimullerian hormone and baseline follicle-stimulating hormone levels. Fertil Steril. 2009;91(6):2616-9.##Dumesic DA, Lesnick TG, Stassart JP, Ball GD, Wong A, Abbott DH. Intrafollicular antimullerian hormone levels predict follicle responsiveness to follicle-stimulating hormone (FSH) in normoandrogenic ovulatory women undergoing gonadotropin releasing-hormone analog/recombinant human FSH therapy for in vitro fertilization and embryo transfer. Fertil Steril. 2009;92(1):217-21.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Assisted Reproductive Technologies in the Republic of Kazakhstan: A 6-Year Trend Analysis from Efficacy to Availability </TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: The first child after in vitro fertilization (IVF) in the country was born in 1996. However, registering and recording data on assisted reproductive technologies (ARTs) in Kazakhstan is not mandatory. The purpose of the current study was to assess the treatment outcomes, availability, regulations, and ART cycles trends between 2011 and 2016.&lt;br /&gt;
Methods: Cycle-based data were collected from voluntarily participating ART centers and then descriptive analysis was performed. The study included 10470 ART cycles using different ART methods during 2011-2016. The availability rate of ART in the country was calculated by dividing the number of treatment cycles per million of the population.&lt;br /&gt;
Results: The availability of ART per million inhabitants increased by 53.6%, from 236.9/million in 2011, to 364.0/million in 2016. In IVF cycles, clinical pregnancy rates (PRs) per aspiration remained stable, on average 37.1%. After ICSI, the average PR was 42.5%. In frozen embryo replacement cycles, there was an increase in the PR per transfer from 37.0% in 2011, to 42.5% in 2016, on average 39.2%.&lt;br /&gt;
Conclusion: Assisted reproductive technologies are developing rapidly in Kazakhstan; therefore, ART monitoring should be improved and become mandatory. Although the data is not yet representative, the most compelling evidence points to low access to ART. Since the use of ART in Central Asian countries is infrequent in comparison to European countries, there is a need to combine IVF data across different nations. This will allow for a deeper assessment of the scientific evidence and reduction of infertility burden through joint efforts.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>61</FPAGE>
            <TPAGE>67</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Lokshin</Name>
<MidName>L</MidName>
<Family>Vyacheslav</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Reproductive Health Department, International Clinical Centre of Reproduction &amp;quot;PERSONA&amp;quot;</Organization>
</Organizations>
<Universities>
<University>Reproductive Health Department, International Clinical Centre of Reproduction &quot;PERSONA&quot;</University>
</Universities>
<Countries>
<Country>Kazakhstan</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Omar</Name>
<MidName>O</MidName>
<Family>Meruyert</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Population Health and Social Sciences, Kazakhstan&amp;#39;s Medical University School of Public Health</Organization>
</Organizations>
<Universities>
<University>Department of Population Health and Social Sciences, Kazakhstan&#39;s Medical University School of Public Health</University>
</Universities>
<Countries>
<Country>Kazakhstan</Country>
</Countries>
<EMAILS>
<Email>meruyert.omar.md@gmail.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Karibaeva</Name>
<MidName>K</MidName>
<Family>Sholpan</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Reproductive Health Department, International Clinical Centre of Reproduction &amp;quot;PERSONA&amp;quot;</Organization>
</Organizations>
<Universities>
<University>Reproductive Health Department, International Clinical Centre of Reproduction &quot;PERSONA&quot;</University>
</Universities>
<Countries>
<Country>Kazakhstan</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Assisted reproductive techniques</KeyText></KEYWORD><KEYWORD><KeyText>Availability</KeyText></KEYWORD><KEYWORD><KeyText>Infertility</KeyText></KEYWORD><KEYWORD><KeyText>IVF</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120131.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Lokshin V, Irina K. Personified approach to genetic screening of infertility couples in art programs. Medicine. 2018;1(317):37-41.##Lokshin V, Dhusubalieva. Assisted reproductive technologies in the Republic of Kazakhstan according to the 2011 register. Reprod uktivnaya Med. 2013;275:5-10.##Nygren KG, Sullivan E, Zegers-Hochschild F, Mansour R, Ishihara O, Adamson GD, et al. International committee for monitoring assisted Reproductive technology (ICMART) world report: assisted reproductive technology 2003. Fertil Steril. 2011;95(7):2209-2222.e1-e17.##Lokshin V, Dhusubalieva T. Clinical Practice in Reproductive Medicine. 1st ed. Almaty: MedMedia. 2015. 566 p.##Agadjanian V, Dommaraju P, Nedoluzhko L. Economic fortunes, ethnic divides, and marriage and fertility in Central Asia: Kazakhstan and Kyrgyzstan compared. J Popul Res. 2013;30(3):197-211.##Ferraretti AP, Goossens V, Kupka M, Bhattacharya S, De Mouzon J, Castilla JA, et al. Assisted reproductive technology in Europe, 2009: results generated from European registers by ESHRE. Hum Reprod. 2013;28(9):2318-31.##Zegers-Hochschild F, Adamson GD, De Mouzon J, Ishihara O, Mansour R, Nygren K, et al. The international committee for monitoring assisted reproductive technology (ICMART) and the World Health Organization (WHO) revised glossary on ART terminology, 2009. Hum Reprod. 2009;24(11):2683-7.##Ministry of Justice of the Republic of Kazakhstan. On approval of the rules on the procedure and conditions for the use of assisted reproductive methods and technologies. 2009 No. KR DSM-295/2020. Available from: https://adilet.zan.kz/##Ministry of Health. The Code of the Republic of Kazakhstan ‘On people’s health and the health care system’. 2011 No-360-VI ЗРК. Available from: https://adilet.zan.kz/##De Geyter C, Calhaz-Jorge C, Kupka MS, Wyns C, Mocanu E, Motrenko T, et al. ART in Europe, 2015: results generated from European registries by ESHRE. Hum Reprod Open. 2020;2020(1):hoz038.##Zegers-Hochschild F, Crosby JA, Musri C, de Souza M do CB, Martinez AG, Silva AA, et al. Assisted reproductive technology in Latin America: the Latin American Registry, 2017. Reprod Biomed Online. 2020;41(1):44-54.##Order of Ministry of Health. About the health of the people and the health system. 2009 No. KR DSM-295/2020.Available from: https://adilet.zan.kz/##Ministry of Health. On approval of the Rules and conditions for the storage of germ cells (gametes). 2009No. KR DSM-295/2020. Available from: https://adilet.zan.kz/##Dyer S, Archary P, Potgieter L, Smit I, Ashiru O, Bell EG. Assisted reproductive technology in Africa: a 5-year trend analysis from the African Network and Registry for ART. Reprod Biomed Online. 2020;41(4):604-15.##Ministry of health of the Republic of Kazakhstan ‘RCHD’ National health accounts of the Republic of Kazakhstan review of health expenditures for 2010-2016. Astana - 2017. 67 p.##OECD.Stat. Health expenditure and financing.2020 [Internet]. Available from: https://stats.oecd.org/##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Luteoma of Pregnancy with Uterine Leiomyoma as a Diagnostic Challenge and Mimicker of Ovarian Malignancy: A Rare Case From Rural India</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>&lt;p&gt;Background: Luteoma of pregnancy is a rare, non-neoplastic lesion of the ovary which mimics ovarian tumor. It develops hirsutism or virilization during pregnancy and regresses in postpartum phase spontaneously. A few number of cases are described in literature. The synchronization of ovarian luteoma with uterine leiomyomas is a rare condition; to the best of my knowledge, the association of both conditions is not reported till date.&lt;br /&gt;
Case Presentation: A 35 year old multiparous woman presented with mass and pain in abdomen came to the gynecology department of Uttar Pradesh University of Medical Sciences in India. On examination, a hard mass in uterus was diagnosed. Ultrasonography revealed a highly vascular uterine adnexal mass possibly arising from ovary with malignant features. Hysterectomy with bilateral salpingo-oophorectomy was done and this specimen with separate mass was sent for histopathology. Right sided ovary was measured 3x3 cm, well demarcated with solid brown areas. CA -125 (cancer antigen -125) level was raised. A separate tumor was measured 15x12x8 &lt;em&gt;cm &lt;/em&gt;and it was smooth while cut surface was grey/white with whirling and hemorrhagic foci.&lt;br /&gt;
Results: The section from ovary revealed luteoma of pregnancy. Endometrium microscopy confirmed pregnancy. Section from another mass/ tumor showed leiomyoma with degenerations.&lt;br /&gt;
Conclusion: Pregnancy luteoma is a pregnancy induced lesion which mimics malignancy so, it is clinically misinterpreted and over diagnosed. Histopathological investigation is mandatory to diagnose and prevent unnecessary surgeries. The synchronous ovarian luteoma with uterine leiomyoma is a rare condition which represents unusual response to altered hormonal effect in pregnancy; therefore, more studies should be done to understand its pathogenesis.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>67</FPAGE>
            <TPAGE>71</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Seema</Name>
<MidName>S</MidName>
<Family>Dayal</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Pathology, Uttar Pradesh University of Medical Sciences, Saifai</Organization>
</Organizations>
<Universities>
<University>Department of Pathology, Uttar Pradesh University of Medical Sciences, Saifai</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email>seemadayal77@rediffmail.com</Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Histopathology</KeyText></KEYWORD><KEYWORD><KeyText>Leiomyoma</KeyText></KEYWORD><KEYWORD><KeyText>Luteoma of pregnancy</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>120130.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Limaiem F, Bouraoui S, Bouslama S, Lahmar A, Mzabi S. A puzzling ovarian tumor pregnancy luteoma with diffuse endometriosis. Pathologica. 2016;108(3):144-7.##Spitzer RF, Wherrett D, Chitayat D, Colgan T, Dodge JE, Salle JL et al. Maternal luteoma of pregnancy presenting with virilization of the female infant. J Obstet Gynaecol Can. 2007;29(10):835-40.##Chiang G, Levine D. Imaging of adnexal masses in pregnancy. J Ultrasound Med. 2004;23(6):805-19.##Mohan H. Textbook of pathology. 6th ed. New Delhi: Jaypee brothers medical publishers; 2010. Chapter 24, The female genital tract; p. 721-53.##Nelson MJ, Cavalieri R, Graham D, Sanders RC. Cyst in pregnancy discovered by sonography. J Clin Ultrasound. 1986;14(7):509-12.##Kao HW, Wu CJ, Chung KT, Wang SR, Chen CY. MR imaging of pregnancy luteoma: a case report and correlation with the clinical features. Korean J Radiol. 2005;6(1):44-6.##Phelan N, Conway GS. Management of ovarian disease in pregnancy. Best Pract Res Clin Endocrinol Metab. 2011;25(6):985-92.##Zander J, Mickan H, Holzmann K, Lohe KJ. Androluteoma syndrome of pregnancy. Am J Obstet Gynecol. 1978;130(2):170-7.##Rodriguez M, Harrison TA, Nowacki MR. Leutoma of pregnancy presenting with massive ascitis and markedly elevated CA125. Obstet Gynecol. 1999;94(5 Pt 2):854.##Verma V, Paul S, Chahal KS, Singh J. Pregnancy leutoma: a rare case report. Int J Appl Basic Med Res. 2016;6(4):282-3.##Rosai J. Text book surgical pathology. 9th ed. New Delhi: Elsevier; 2004. chapter 19, Leomyoma; p. 1603-8.##Dayal S, Kumar A, Verma A. Clinico pathologic correlation of Leiomyoma with clinical findings and secondary changes in a rural population of North India. Am J Clin Pathol. 2014;141(2):275-9.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

    </ARTICLES>
  </JOURNAL>
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