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<XML>
  <JOURNAL>   
    <YEAR>2011</YEAR>
    <VOL>12</VOL>
    <NO>3</NO>
    <MOSALSAL>48</MOSALSAL>
    <PAGE_NO>57</PAGE_NO>  
    <ARTICLES>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Post-thaw Embryo Transfer Cycles as the Future Hope for Boosting IVF Success Rates</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT>570</CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>The history of IVF is synonymous with several millstones and each of these have led to a revolution in our understanding of human fertility or causes of male and female infertility, as well as introducing new treatment protocols for infertility. It can undoubtedly be claimed that one of the&#160; best of these was the introduction of ultra-rapid glass-like solidification of a solution without ice-crystal formation or vitrification method for cryo-preservation of human embryos and gametes in 1990 (1).&lt;br&gt;Vitrification has brought about fundamental changes in cryopreservation and human fertility preservation. Vitrification of embryos at cleavage or belastocyst stage seems to be a promising procedure for improving implantation and pregnancy rate in IVF cycles. It improves cryosurvival rate of embryos close to 100% which is comparable to slow freezing through prevention of ice-crystal formation. Simplicity and speed and no need for expensive freezing machines are reasons for its rapid expansion. Vitrification has been improved and standardized for human gametes and embryos through large numbers of studies since 1990 (2).&lt;br&gt;However, two decades past the first live-birth from vitrified embryos, there are still some doubts on the safety of these methods and its probable deleterious effects on the health of children born from vitrified embryos or oocytes. There is concern that application of high concentrations of cryoprotectants may lead to genetic or epigenetic abnormalities with subsequent inborn malformations. Therefore, there is no consensus or scientific recommendations for the substitution of slow freezing method with vitrification worldwide. In spite of concerns about the toxic effects of high concentrations of cryoprotectants, most studies indicate that the survival rate, implantation and clinical pregnancy of post-thaw vitrified embryos is far better than those from slow freezing method, as substitution of slow rate freezing by vitrification increased pregnancy rate per cycle from 7% to 64% and delivery and live birth rate per cycle from 7% to 50%.&#160; But still slow freezing method is the only acceptable method for embryo and gametes cryopreservation in large numbers of IVF centers in Australia and European countries (2). &lt;br&gt;According to current practice, 3-4 cleavage embryos or 1-2 blastocyst embryos are frozen on loading devices such as Cryotop&#174;. Following artificial endometrial preparation in none-stimulated cycles, the post-thaw survived embryos are transferred to uterus; however post-thaw survival alone is not enough to support their implantation, therefore, embryo culture is necessary to confirm resumed embryo cleavage. Embryo culture increases pregnancy rate following freezing/thawing cycles by preventing transfer of embryos with post-thaw cleavage arrest (3). &lt;br&gt;Several studies have revealed that controlled ovarian stimulation severely decreases endometrial receptivity for embryo, therefore, more attention and research on implantation is needed regarding synchronization of endometrium and embryo development to increase endometrial receptivity. Embryo transfer during implantation window is a critical factor in the success of IVF cycles but it is usually missed in most fresh cycles; although it is achievable through post-thaw embryo transfer cycles (3).&lt;br&gt;Later, several studies proposed freeze-all cycles in which all embryos are frozen in stimulation cycle and transferred at blastocyst stage following artificial preparation of endometrium. This method seems to increase embryo and endometrial synchronicity and decrease the number of transferred embryos and subsequent multiple pregnancies. &lt;br&gt;Moreover, some studies suggested transferring higher numbers of low quality embryos in fresh cycles and keeping high quality embryos which are later developed to blastocyst stage and are subsequently vitrified for future transfer without stimulation (4).&lt;br&gt;Although the present data supports the efficiency and potential safety of vitrification, but more profound studies on its details are still needed, including embryonic stage, loading devices, the media and practice protocols for its worldwide application.&#160; Finally, it could be claimed that future improvements in IVF success rates will depend on the role played by embryology field, especially control of in vitro conditions of embryo culture and cryo-preservation of embryos and gametes, specifically vitrification method that would be the most important part of this scenario. &lt;br&gt;&lt;br&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>179</FPAGE>
            <TPAGE>181</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Mohammad Reza</Name>
<MidName>MR</MidName>
<Family>Sadeghi</Family>
<NameE> محمدرضا</NameE>
<MidNameE></MidNameE>
<FamilyE>صادقی</FamilyE>
<Organizations>
<Organization>Editor-in-chief</Organization>
</Organizations>
<Universities>
<University>Editor-in-chief</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>No Keyword</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>570.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Gordts S, Roziers P, Campo R, Noto V. Survival and pregnancy outcome after ultrarapid freezing of human embryos. Fertil Steril. 1990;53(3):469-72.##Kader AA, Choi A, Orief Y, Agarwal A. Factors affecting the outcome of human blastocyst vitrification. Reprod Biol Endocrinol. 2009;7:99.##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 transfer in normal responders. Fertil Steril. 2011;96(2):344-8.##Aflatoonian A, Oskouian H, Ahmadi S, Oskouian L. Can fresh embryo transfers be replaced by cryopreserved-thawed embryo transfers in assisted reproductive cycles? A randomized controlled trial. J Assist Reprod Genet. 2010;27(7):357-63.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>The Genetic Bases of Uterine Fibroids; A Review</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Uterine leiomyomas/fibroids are the most common pelvic tumors of the female genital tract. The initiators remaining unknown, estrogens and progesterone are considered as promoters of fibroid growth. Fibroids are monoclonal tumors showing 40-50% karyo-typically detectable chromosomal abnormalities. Cytogenetic aberrations involving chromosomes 6, 7, 12 and 14 constitute the major chromosome abnormalities seen in leiomyomata. This has led to the discovery that disruptions or dysregulations of HMGIC and HMGIY genes contribute to the development of these tumors. Genes such as RAD51L1 act as translocation partners to HMGIC and lead to disruption of gene structure leading to the pathogenesis of uterine fibroids. The mechanism underlying this disease is yet to be identified. The occurrence of PCOLCE amid a cluster of at least eight Alu sequences is potentially relevant to the possible involvement of PCOLCE in the 7q22 rearrangements that occur in many leiomyomata. PCOLCE is implicated in cell growth processes. Involvement of Alu sequences in rearrangements can lead to the disruption of this gene and, hence, loss of control for gene expression leading to uncontrolled cell growth. This can also lead to the formation of fibroids. Though, cytogenetics provides a broad perspective on uterine fibroid formation, further molecular analysis is required to understand the etiopathogenesis of uterine fibroids.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>181</FPAGE>
            <TPAGE>192</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Veronica</Name>
<MidName>V</MidName>
<Family>Medikare</Family>
<NameE>Veronica</NameE>
<MidNameE></MidNameE>
<FamilyE>Medikare</FamilyE>
<Organizations>
<Organization>Department of Genetics, Osmania University</Organization>
</Organizations>
<Universities>
<University>Department of Genetics, Osmania University</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Lakshmi</Name>
<MidName>L</MidName>
<Family>Rao Kandukuri</Family>
<NameE>Lakshmi</NameE>
<MidNameE></MidNameE>
<FamilyE>Rao Kandukuri</FamilyE>
<Organizations>
<Organization>Center for Cellular and Molecular Biology, Habsiguda</Organization>
</Organizations>
<Universities>
<University>Center for Cellular and Molecular Biology, Habsiguda</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Ananthapur</Name>
<MidName>A</MidName>
<Family>Venkateshwari</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Institute of Genetics and Hospital for Genetic Diseases, Begumpet</Organization>
</Organizations>
<Universities>
<University>Institute of Genetics and Hospital for Genetic Diseases, Begumpet</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Mamata</Name>
<MidName>M</MidName>
<Family>Deenadayal</Family>
<NameE>Mamata</NameE>
<MidNameE></MidNameE>
<FamilyE>Deenadayal</FamilyE>
<Organizations>
<Organization>Infertility Institute and research Center</Organization>
</Organizations>
<Universities>
<University>Infertility Institute and research Center</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Pratibha</Name>
<MidName>P</MidName>
<Family>Nallari</Family>
<NameE>Pratibha</NameE>
<MidNameE></MidNameE>
<FamilyE>Nallari</FamilyE>
<Organizations>
<Organization>Department of Genetics, Osmania University</Organization>
</Organizations>
<Universities>
<University>Department of Genetics, Osmania University</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email>prathinallari@yahoo.com</Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Chromosomal translocation</KeyText></KEYWORD><KEYWORD><KeyText>Chromosomal</KeyText></KEYWORD><KEYWORD><KeyText>Estrogen</KeyText></KEYWORD><KEYWORD><KeyText>Gene rearrangement</KeyText></KEYWORD><KEYWORD><KeyText>Progesterone</KeyText></KEYWORD><KEYWORD><KeyText>Uterine fibroids</KeyText></KEYWORD><KEYWORD><KeyText>Uterine Leiomyomas</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>467.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Center for Uterine Fibroids [Internet]. Boston: Brigham and Women’s Hospital; 2011. What are fibroids?; 2006 Sept 19 [cited 2011 Mar 13]; [about 3 screens]. Available from: http://www.fibroids. net/aboutfibroids.html##Nivethithai P, Nikhat SR, Rajesh BV. Uterine Fibroids: A Review. Indian J Pharm Pract. 2010;3 (1):6-11.##Blake RE. Leiomyomata uteri: hormonal and molecular determinants of growth. J Natl Med Assoc. 2007;99(10):1170-84.##Luo X, Chegini N. The expression and potential regulatory function of microRNAs in the pathogenesis of leiomyoma. Semin Reprod Med. 2008;26 (6):500-14.##Zavadil J, Ye H, Liu Z, Wu J, Lee P, Hernando E, et al. Profiling and functional analyses of microRNAs and their target gene products in human uterine leiomyomas. PLoS One. 2010;5(8):e12362.##Sandberg AA. Updates on the cytogenetics and molecular genetics of bone and soft tissue tumors: leiomyoma. Cancer Genet Cytogenet. 2005;158(1): 1-26.##Cramer SF, Horiszny JA, Leppert P. Epidemiology of uterine leiomyomas. With an etiologic hypothesis. J Reprod Med. 1995;40(8):595-600.##Parazzini F, La Vecchia C, Negri E, Cecchetti G, Fedele L. Epidemiologic characteristics of women with uterine fibroids: a case-control study. Obstet Gynecol. 1988;72(6):853-7.##Samadi AR, Lee NC, Flanders WD, Boring JR 3rd, Parris EB. Risk factors for self-reported uterine fibroids: a case-control study. Am J Public Health. 1996;86(6):858-62.##Marshall LM, Spiegelman D, Goldman MB, Manson JE, Colditz GA, Barbieri RL, et al. A prospective study of reproductive factors and oral contraceptive use in relation to the risk of uterine leiomyomata. Fertil Steril. 1998;70(3):432-9.##Zaitseva M, Vollenhoven BJ, Rogers PA. In vitro culture significantly alters gene expression profiles and reduces differences between myometrial and fibroid smooth muscle cells. Mol Hum Reprod. 2006;12(3):187-207.##Marshall LM, Spiegelman D, Barbieri RL, Goldman MB, Manson JE, Colditz GA, et al. Variation in the incidence of uterine leiomyoma among premenopausal women by age and race. Obstet Gynecol. 1997;90(6):967-73.##Flake GP, Andersen J, Dixon D. Etiology and pathogenesis of uterine leiomyomas: a review. Environ Health Perspect. 2003;111(8):1037-54.##Faerstein E, Szklo M, Rosenshein NB. Risk factors for uterine leiomyoma: a practice-based casecontrol study. II. Atherogenic risk factors and potential sources of uterine irritation. Am J Epidemiol. 2001;153(1):11-9.##Rein MS. Advances in uterine leiomyoma research: the progesterone hypothesis. Environ Health Perspect. 2000;108 Suppl 5:791-3.##Parker WH. Etiology, symptomatology, and diagnosis of uterine myomas. Fertil Steril. 2007;87 (4):725-36.##Romieu I, Walker AM, Jick S. Determinants of uterine fibroids. Post Marketing Surveill. 1991;5: 119-33.##Ross RK, Pike MC, Vessey MP, Bull D, Yeates D, Casagrande JT. Risk factors for uterine fibroids: reduced risk associated with oral contraceptives. Br Med J (Clin Res Ed). 1986;293(6543):359-62.##Friedman AJ, Harrison-Atlas D, Barbieri RL, Benacerraf B, Gleason R, Schiff I. A randomized, placebo-controlled, double-blind study evaluating the efficacy of leuprolide acetate depot in the treatment of uterine leiomyomata. Fertil Steril. 1989;51(2):251-6.##Mashal RD, Fejzo ML, Friedman AJ, Mitchner N, Nowak RA, Rein MS, et al. Analysis of androgen receptor DNA reveals the independent clonal origins of uterine leiomyomata and the secondary nature of cytogenetic aberrations in the development of leiomyomata. Genes Chromosomes Cancer. 1994;11(1):1-6.##GLOWM: The Global Library of Women’s Medicine [Internet]. London: The Foundation for The Global Library of Women’s Medicine; 2010. Genetics of uterine leiomyomas; 2009 May [cited 2011 Mar 13]. Available from: http://www.glowm. com/?p=glowm.cml/section_view&amp;articleid=363##Levy B, Mukherjee T, Hirschhorn K. Molecular cytogenetic analysis of uterine leiomyoma and leiomyosarcoma by comparative genomic hybridization. Cancer Genet Cytogenet. 2000;121(1):1-8.##Packenham JP, du Manoir S, Schrock E, Risinger JI, Dixon D, Denz DN, et al. Analysis of genetic alterations in uterine leiomyomas and leiomyosarcomas by comparative genomic hybridization. Mol Carcinog. 1997;19(4):273-9.##Hodge JC, Morton CC. Genetic heterogeneity among uterine leiomyomata: insights into malignant progression. Hum Mol Genet. 2007;16 Spec No 1:R7-13.##Nibert M, Heim S. Uterine leiomyoma cytogenetics. Genes Chromosomes Cancer. 1990;2(1):3-13.##El-Gharib MN, Elsobky ES. Cytogenetic aberrations and the development of uterine leiomyomata. J Obstet Gynaecol Res. 2010;36(1):101-7.##Fusco A, Fedele M. Roles of HMGA proteins in cancer. Nat Rev Cancer. 2007;7(12):899-910.##Kazmierczak B, Pohnke Y, Bullerdiek J. Fusion transcripts between the HMGIC gene and RTVLH-related sequences in mesenchymal tumors without cytogenetic aberrations. Genomics. 1996; 38(2):223-6.##Ashar HR, Fejzo MS, Tkachenko A, Zhou X, Fletcher JA, Weremowicz S, et al. Disruption of the architectural factor HMGI-C: DNA-binding AT hook motifs fused in lipomas to distinct transcriptional regulatory domains. Cell. 1995;82(1):57-65.##Schoenmakers EF, Van de Ven WJ. From chromosome aberrations to the high mobility group protein gene family: evidence for a common genetic denominator in benign solid tumor development. Cancer Genet Cytogenet. 1997;95(1):51-8.##Tallini G, Vanni R, Manfioletti G, Kazmierczak B, Faa G, Pauwels P, et al. HMGI-C and HMGI(Y) immunoreactivity correlates with cytogenetic abnormalities in lipomas, pulmonary chondroid hamartomas, endometrial polyps, and uterine leiomyomas and is compatible with rearrangement of the HMGI-C and HMGI(Y) genes. Lab Invest. 2000;80(3):359-69.##Gross KL, Neskey DM, Manchanda N, Weremowicz S, Kleinman MS, Nowak RA, et al. HMGA2 expression in uterine leiomyomata and myometrium: quantitative analysis and tissue culture studies. Genes Chromosomes Cancer. 2003;38(1): 68-79.##Quade BJ, Weremowicz S, Neskey DM, Vanni R, Ladd C, Dal Cin P, et al. Fusion transcripts involving HMGA2 are not a common molecular mechanism in uterine leiomyomata with rearrangements in 12q15. Cancer Res. 2003;63(6):1351-8.##Peng Y, Laser J, Shi G, Mittal K, Melamed J, Lee P, et al. Antiproliferative effects by Let-7 repression of high-mobility group A2 in uterine leiomyoma. Mol Cancer Res. 2008;6(4):663-73.##Wang T, Zhang X, Obijuru L, Laser J, Aris V, Lee P, et al. A micro-RNA signature associated with race, tumor size, and target gene activity in human uterine leiomyomas. Genes Chromosomes Cancer. 2007;46(4):336-47.##Kazmierczak B, Bol S, Wanschura S, Bartnitzke S, Bullerdiek J. PAC clone containing the HMGI(Y) gene spans the breakpoint of a 6p21 translocation in a uterine leiomyoma cell line. Genes Chromosomes Cancer. 1996;17(3):191-3.##Dal Cin P, Wanschura S, Christiaens MR, Van den Berghe I, Moerman P, Polito P, et al. Hamartoma of the breast with involvement of 6p21 and rearrangement of HMGIY. Genes Chromosomes Cancer. 1997;20(1):90-2.##Williams AJ, Powell WL, Collins T, Morton CC. HMGI(Y) expression in human uterine leiomyomata. Involvement of another high-mobility group architectural factor in a benign neoplasm. Am J Pathol. 1997;150(3):911-8.##Xiao S, Lux ML, Reeves R, Hudson TJ, Fletcher JA. HMGI(Y) activation by chromosome 6p21 rearrangements in multilineage mesenchymal cells from pulmonary hamartoma. Am J Pathol. 1997; 150(3):901-10.##Schoenmakers EF, Huysmans C, Van de Ven WJ. Allelic knockout of novel splice variants of human recombination repair gene RAD51B in t(12;14) uterine leiomyomas. Cancer Res. 1999;59(1):19-23.##Ingraham SE, Lynch RA, Kathiresan S, Buckler AJ, Menon AG. hREC2, a RAD51-like gene, is disrupted by t(12;14) (q15;q24.1) in a uterine leiomyoma. Cancer Genet Cytogenet. 1999;115(1): 56-61.##Takahara K, Kessler E, Biniaminov L, Brusel M, Eddy RL, Jani-Sait S, et al. Type I procollagen COOH-terminal proteinase enhancer protein: identification, primary structure, and chromosomal localization of the cognate human gene (PCOL CE). J Biol Chem. 1994;269(42):26280-5.##Xing YP, Powell WL, Morton CC. The del(7q) subgroup in uterine leiomyomata: genetic and biologic characteristics. Further evidence for the secondary nature of cytogenetic abnormalities in the pathobiology of uterine leiomyomata. Cancer Genet Cytogenet. 1997;98(1):69-74.##Scott IC, Clark TG, Takahara K, Hoffman GG, Greenspan DS. Structural organization and expression patterns of the human and mouse genes for the type I procollagen COOH-terminal proteinase enhancer protein. Genomics. 1999;55(2):229-34.##Stewart EA, Nowak RA. Leiomyoma-related bleeding: a classic hypothesis updated for the molecular era. Hum Reprod Update. 1996;2(4): 295-306.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>The Profile of Human Sperm Proteome; A Mini-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;New advances in mass spectrometry-based proteomics technology are having amajor impact on our understanding of how human spermatozoa acquire their capacity for fertilization. A complete analysis of the proteins found in the human spermatozoa is essential for understanding the events leading up to, and including, fertilization and early embryo development. In this short review, we have collected the human sperm proteome from the literature and analyzed it by the Database for Annotation, Visualization and Integrated Discovery (DAVID) software. Bioinformatics analysis demonstrated that the collected 1,300 proteins were involved in various metabolic pathways including catabolic processes. Additionally, the majority of the collected human sperm proteome belonged to cytoplasm. Application of the multi-dimensional protein identification technology (MudPIT) for obtaining a better coverage of the hydrophobic and basic proteins of the human sperm proteome is recommended.&lt;/p&gt;</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>193</FPAGE>
            <TPAGE>200</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Kambiz</Name>
<MidName>K</MidName>
<Family>Gilany</Family>
<NameE>کامبیز</NameE>
<MidNameE></MidNameE>
<FamilyE>گیلانی</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>k.gilany@avicenna.ac.ir</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Niknam</Name>
<MidName>N</MidName>
<Family>Lakpour</Family>
<NameE>نیکنام</NameE>
<MidNameE></MidNameE>
<FamilyE>لک‌پور</FamilyE>
<Organizations>
<Organization>Nanobiotechnology Research Center, Avicenna Research Institute (ACECR)</Organization>
</Organizations>
<Universities>
<University>Nanobiotechnology Research Center, Avicenna Research Institute (ACECR)</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Mohtaram</Name>
<MidName>M</MidName>
<Family>Vafakhah</Family>
<NameE>محترم</NameE>
<MidNameE></MidNameE>
<FamilyE>وفاخواه</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></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Mohammad Reza</Name>
<MidName>MR</MidName>
<Family>Sadeghi</Family>
<NameE> محمدرضا</NameE>
<MidNameE></MidNameE>
<FamilyE>صادقی</FamilyE>
<Organizations>
<Organization>Monoclonal Antibody Research Center, Avicenna Research Institute (ACECR)</Organization>
</Organizations>
<Universities>
<University>Monoclonal Antibody Research Center, Avicenna Research Institute (ACECR)</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>DAVID bioinformatics</KeyText></KEYWORD><KEYWORD><KeyText>Gene Ontology</KeyText></KEYWORD><KEYWORD><KeyText>Mass spectrometry-based proteomics</KeyText></KEYWORD><KEYWORD><KeyText>Proteome</KeyText></KEYWORD><KEYWORD><KeyText>Sperm</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>466.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Baccetti B, Afzelius BA. The biology of the sperm cell. Monogr Dev Biol. 1976;(10):1-254.##Mezquita C. Chromatin composition, structure and function in spermatogenesis. Revis Biol Celular. 1985;5:V-XIV, 1-124.##Oliva R, Dixon GH. Vertebrate protamine genes and the histone-to-protamine replacement reaction. Prog Nucleic Acid Res Mol Biol. 1991;40:25-94.##Dadoune JP. Expression of mammalian spermatozoal nucleoproteins. Microsc Res Tech. 2003;61(1):56-75.##Ainsworth C. Cell biology: the secret life of sperm. Nature. 2005;436(7052):770-1.##Aebersold R, Mann M. Mass spectrometry-based proteomics. Nature. 2003;422(6928):198-207.##Conner SJ, Lefi&#232;vre L, Kirkman-Brown J, Michelangeli F, Jimenez-Gonzalez C, Machado-Oliveira GS, et al. Understanding the physiology of prefertilisation events in the human spermatozoa--a necessary prerequisite to developing rational therapy.  Soc Reprod Fertil Suppl. 2007;63:237-55.##Domon B, Aebersold R. Mass spectrometry and protein analysis. Science. 2006;312(5771):212-7.##Bailey JL, Tardif S, Dub&#233; C, Beaulieu M, Reyes Moreno C, Lefi&#232;vre L, et al. Use of phosphorproteomics to study tyrosine kinase activity in capacitating boar sperm. Kinase activity and capacitation. Theriogenology. 2005;63(2):599-614.##Bohring C, Krause W. The characterization of human spermatozoa membrane proteins--surface antigens and immunological infertility. Electrophoresis. 1999;20(4-5):971-6.##Miller MA. Sperm and oocyte isolation methods for biochemical and proteomic analysis. Methods Mol Biol. 2006;351:193-201.##Wang Y, Zhou ZM. [Update of the researches on sperm proteome]. Zhonghua Nan Ke Xue. 2007;13 (3):250-4. Chinese.##Huang da W, Sherman BT, Lempicki RA. Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nat Protoc. 2009;4(1):44-57.##Wasinger VC, Cordwell SJ, Cerpa-Poljak A, Yan JX, Gooley AA, Wilkins MR, et al. Progress with gene-product mapping of the Mollicutes: Mycoplasma genitalium. Electrophoresis. 1995;16(7): 1090-4.##Jungblut PR, Holzh&#252;tter HG, Apweiler R, Schl&#252;ter H. The speciation of the proteome. Chem Cent J. 2008;2:16.##de Mateo S, Mart&#237;nez-Heredia J, Estanyol JM, Dom&#237;nguez-Fandos D, Vidal-Taboada JM, Ballesc&#224; JL, et al. Marked correlations in protein expression identified by proteomic analysis of human spermatozoa. Proteomics. 2007;7(23):4264-77.##Shetty J, Diekman AB, Jayes FC, Sherman NE, Naaby-Hansen S, Flickinger CJ, et al. Differential extraction and enrichment of human sperm surface proteins in a proteome: identification of immunocontraceptive candidates. Electrophoresis. 2001;22 (14):3053-66.##Pixton KL, Deeks ED, Flesch FM, Moseley FL, Bj&#246;rndahl L, Ashton PR, et al. Sperm proteome mapping of a patient who experienced failed fertilization at IVF reveals altered expression of at least 20 proteins compared with fertile donors: case report. Hum Reprod. 2004;19(6):1438-47.##Baker MA, Witherdin R, Hetherington L, Cunningham-Smith K, Aitken RJ. Identification of post-translational modifications that occur during sperm maturation using difference in two-dimensional gel electrophoresis. Proteomics. 2005; 5(4):1003-12.##Li LW, Fan LQ, Zhu WB, Nien HC, Sun BL, Luo KL, et al. Establishment of a high-resolution 2-D reference map of human spermatozoal proteins from 12 fertile sperm-bank donors. Asian J Androl. 2007;9(3):321-9.##Mart&#237;nez-Heredia J, Estanyol JM, Ballesc&#224; JL, Oliva R. Proteomic identification of human sperm proteins. Proteomics. 2006;6(15):4356-69.##Zhao C, Huo R, Wang FQ, Lin M, Zhou ZM, Sha JH. Identification of several proteins involved in regulation of sperm motility by proteomic analysis. Fertil Steril. 2007;87(2):436-8.##Liao TT, Xiang Z, Zhu WB, Fan LQ. Proteome analysis of round-headed and normal spermatozoa by 2-D fluorescence difference gel electrophoresis and mass spectrometry. Asian J Androl. 2009;11 (6):683-93.##Johnston DS, Wooters J, Kopf GS, Qiu Y, Roberts KP. Analysis of the human sperm proteome. Ann N Y Acad Sci. 2005;1061:190-202.##Baker MA, Reeves G, Hetherington L, M&#252;ller J, Baur I, Aitken RJ. Identification of gene products present in Triton X-100 soluble and insoluble fractions of human spermatozoa lysates using LC-MS/MS analysis. Proteomics Clin Appl. 2007;1(5): 524-32.##Gilany K, Van Elzen R, Mous K, Coen E, Van Dongen W, Vandamme S, et al. The proteome of the human neuroblastoma cell line SH-SY5Y: an enlarged proteome. Biochim Biophys Acta. 2008; 1784(7-8):983-5.##Harrison PM, Kumar A, Lang N, Snyder M, Gerstein M. A question of size: the eukaryotic proteome and the problems in defining it. Nucleic Acids Res. 2002;30(5):1083-90.##Lander ES, Linton LM, Birren B, Nusbaum C, Zody MC, Baldwin J, et al. Initial sequencing and analysis of the human genome. Nature. 2001;409 (6822):860-921.##Jensen ON. Modification-specific proteomics: characterization of post-translational modifications by mass spectrometry. Curr Opin Chem Biol. 2004;8(1):33-41.##Baker MA, Aitken RJ. Proteomic insights into spermatozoa: critiques, comments and concerns. Expert Rev Proteomics. 2009;6(6):691-705.##Fago A, Hundahl C, Dewilde S, Gilany K, Moens L, Weber RE. Allosteric regulation and temperature dependence of oxygen binding in human neuroglobin and cytoglobin. Molecular mechan-isms and physiological significance. J Biol Chem. 2004;279(43):44417-26.##Maes MB, Lambeir AM, Gilany K, Senten K, Van der Veken P, Leiting B, et al. Kinetic investigation of human dipeptidyl peptidase II (DPPII)-mediated hydrolysis of dipeptide derivatives and its identification as quiescent cell proline dipeptidase (QPP)/dipeptidyl peptidase 7 (DPP7). Biochem J. 2005;386(Pt 2):315-24.##de Godoy LM, Olsen JV, Cox J, Nielsen ML, Hubner NC, Fr&#246;hlich F, et al. Comprehensive mass-spectrometry-based proteome quantification of haploid versus diploid yeast. Nature. 2008;455 (7217):1251-4.##Peddinti D, Nanduri B, Kaya A, Feugang JM, Burgess SC, Memili E. Comprehensive proteomic analysis of bovine spermatozoa of varying fertility rates and identification of biomarkers associated with fertility. BMC Syst Biol. 2008;2:19.##Dennis G Jr, Sherman BT, Hosack DA, Yang J, Gao W, Lane HC, et al. DAVID: Database for Annotation, Visualization, and Integrated Discovery. Genome Biol. 2003;4(5):P3.##Hosack DA, Dennis G Jr, Sherman BT, Lane HC, Lempicki RA. Identifying biological themes within lists of genes with EASE. Genome Biol. 2003;4 (10):R70.##Ashburner M, Ball CA, Blake JA, Botstein D, Butler H, Cherry JM, et al. Gene ontology: tool for the unification of biology. The Gene Ontology Consortium. Nat Genet. 2000;25(1):25-9.##Wu CC, MacCoss MJ, Howell KE, Yates JR 3rd. A method for the comprehensive proteomic analysis of membrane proteins. Nat Biotechnol. 2003; 21(5):532-8.##Lohaus C, Nolte A, Bl&#252;ggel M, Scheer C, Klose J, Gobom J, et al. Multidimensional chromatography: a powerful tool for the analysis of membrane proteins in mouse brain. J Proteome Res. 2007;6 (1):105-13.##Schirle M, Heurtier MA, Kuster B. Profiling core proteomes of human cell lines by one-dimensional PAGE and liquid chromatography-tandem mass spectrometry. Mol Cell Proteomics. 2003;2(12): 1297-305.##Oliva R, de Mateo S, Estanyol JM. Sperm cell proteomics. Proteomics. 2009;9(4):1004-17.##Wang H, Qian WJ, Chin MH, Petyuk VA, Barry RC, Liu T, et al. Characterization of the mouse brain proteome using global proteomic analysis complemented with cysteinyl-peptide enrichment. J Proteome Res. 2006;5(2):361-9.##Birkeland E, Nygaard G, Oveland E, Mjaavatten O, Ljones M, Doskeland SO, et al. Epac-induced Alterations in the Proteome of Human SH-SY5Y Neuroblastoma Cells. J Proteomics Bioinform. 2009;2:244-54.##Gevaert K, Goethals M, Martens L, Van Damme J, Staes A, Thomas GR, et al. Exploring proteomes and analyzing protein processing by mass spectrometric identification of sorted N-terminal peptides. Nat Biotechnol. 2003;21(5):566-9.##Washburn MP, Wolters D, Yates JR 3rd. Largescale analysis of the yeast proteome by multi-dimensional protein identification technology. Nat Biotechnol. 2001;19(3):242-7.##Chen EI, Hewel J, Felding-Habermann B, Yates JR 3rd. Large scale protein profiling by combination of protein fractionation and multidimensional protein identification technology (MudPIT). Mol Cell Proteomics. 2006;5(1):53-6.##Staes A, Van Damme P, Helsens K, Demol H, Vandekerckhove J, Gevaert K. Improved recovery of proteome-informative, protein N-terminal peptides by combined fractional diagonal chromatography (COFRADIC). Proteomics. 2008;8(7):1362-70.##Chu DS, Liu H, Nix P, Wu TF, Ralston EJ, Yates JR 3rd, et al. Sperm chromatin proteomics identifies evolutionarily conserved fertility factors. Nature. 2006;443(7107):101-5.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Effects of Nicotine on Sperm Characteristics and Fertility Profile in Adult Male Rats: A Possible</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Infertility is common among couples of child-bearing age and ap-proximately half of known causes of primary infertility are attributable to male factor. It is still unclear whether the injurious effects of cigarette smoking on sperm characteristics and infertility are due to nicotine. Therefore, the present study investigated the effects of orally administered of nicotine on sperm characteristics and libido in adult male albino rats. The study also sought nicotine effects on fertility rate, litter size and weight in female animals cohabited with nicotine treated male rats.
Methods: Forty male and twenty-five female rats were used for the study. The male rats were divided into five groups and were treated for a period of 30 days with nicotine 0.5 mg/kg (low dose) and 1.0 mg/kg (high dose) per body weight while the control rats received 0.2 ml/kg normal saline. The fourth and fifth groups were gavaged with 0.5 mg/kg and 1.0 mg/kg body weight of nicotine but were left untreated for another 30 days. These groups served as the recovery groups.  At the end of each experimental period, sperm analysis, fertility study, litter weight and size were determined. 
Results: Sperm motility and count significantly decreased (P&lt;0.05) while the percentage of abnormality significantly increased (P&lt;0.05) in both treatment groups. However, there was an insignificant decrease (P&gt;0.05) in the viability and semen volume of the treated groups. Fertility studies revealed that nicotine reduced libido in male rats, litter weight and number delivered by the untreated female during the experiments.
Conclusion: The present study showed that nicotine has a dose-dependent deleterious effect on the sperm characteristics and that fertility is ameliorated by nicotine cessation in male rats.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>201</FPAGE>
            <TPAGE>208</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Ibukun Peter</Name>
<MidName>IP</MidName>
<Family>Oyeyipo</Family>
<NameE></NameE>
<MidNameE></MidNameE>
<FamilyE></FamilyE>
<Organizations>
<Organization>Department of Physiology, College of Health Sciences, Osun State University</Organization>
</Organizations>
<Universities>
<University>Department of Physiology, College of Health Sciences, Osun State University</University>
</Universities>
<Countries>
<Country>Nigeria</Country>
</Countries>
<EMAILS>
<Email>greatibuks@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Raji</Name>
<MidName>R</MidName>
<Family>Yinusa</Family>
<NameE>Raji</NameE>
<MidNameE></MidNameE>
<FamilyE>Yinusa</FamilyE>
<Organizations>
<Organization>Department of Physiology, College of Medicine, University of Ibadan</Organization>
</Organizations>
<Universities>
<University>Department of Physiology, College of Medicine, University of Ibadan</University>
</Universities>
<Countries>
<Country>Nigeria</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Benjamin</Name>
<MidName>B</MidName>
<Family>Obukowho Emikpe</Family>
<NameE>Benjamin</NameE>
<MidNameE></MidNameE>
<FamilyE>Obukowho Emikpe</FamilyE>
<Organizations>
<Organization>Department of Veterinary Pathology, Faculty of Veterinary Medicine, University of Ibadan</Organization>
</Organizations>
<Universities>
<University>Department of Veterinary Pathology, Faculty of Veterinary Medicine, University of Ibadan</University>
</Universities>
<Countries>
<Country>Nigeria</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Adeyombo</Name>
<MidName>A</MidName>
<Family>Folashade Bolarinwa</Family>
<NameE>Adeyombo</NameE>
<MidNameE></MidNameE>
<FamilyE>Folashade Bolarinwa</FamilyE>
<Organizations>
<Organization>Department of Physiology, College of Medicine, University of Ibadan</Organization>
</Organizations>
<Universities>
<University>Department of Physiology, College of Medicine, University of Ibadan</University>
</Universities>
<Countries>
<Country>Nigeria</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Hypertension</KeyText></KEYWORD><KEYWORD><KeyText>Pregnancy</KeyText></KEYWORD><KEYWORD><KeyText>Risk factor</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>469.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Yales CA, Thomas C, Kovacs GT, De Krester DM. Androgen, male factor, infertility and IVF. In: Wood C, Trouson A, editors. Clinical in vitro fertilization. USA: Springer-Verlag; 1989. pp. 95-111.##Yeşilli C, Mungan G, Se&#231;kiner I, Akduman B, A&#231;ikg&#246;z S, Altan K, et al. Effect of varicocelectomy on sperm creatine kinase, HspA2 chaperone protein (creatine kinase-M type), LDH, LDH-X, and lipid peroxidation product levels in infertile men with varicocele. Urology. 2005;66(3):610-5.##Reijo R, Alagappan RK, Patrizio P, Page DC. Severe oligozoospermia resulting from deletions of azoospermia factor gene on Y chromosome. Lancet. 1996;347(9011):1290-3.##Bonde JP. Male fertility. In: Comhaire FM, editor. Chapman and Hall Medicals. New York: Chapman and Hall; 1996. p. 266-84.##Kapoor D, Jones TH. Smoking and hormones in health and endocrine disorders. Eur J Endocrinol. 2005;152(4):491-9.##Russell MA, Jarvis MJ, Devitt G, Feyerabend C. Nicotine intake by snuff users. Br Med J (Clin Res Ed). 1981;283(6295):814-7.##Armitage AK, Dollery CT, George CF, Houseman TH, Lewis PJ, Turner DM. Absorption and metabolism of nicotine from cigarettes. Br Med J. 1975;4 (5992):313-6.##Weisberg E. Smoking and reproductive health. Clin Reprod Fertil. 1985;3(3):175-86.##Aydos K, G&#252;ven MC, Can B, Erg&#252;n A. Nicotine toxicity to the ultrastructure of the testis in rats. BJU Int. 2001;88(6):622-6.##Mlynarcikova A, Fickova M, Scsukova S. Ovarian intrafollicular processes as a target for cigarette smoke components and selected environmental reproductive disruptors. Endocr Regul. 2005;39(1): 21-32.##Tank&#243; LB, Christiansen C. An update on the antiestrogenic effect of smoking: a literature review with implications for researchers and practitioners. Menopause. 2004;11(1):104-9.##Jones TH, Jones RD, Channer KS. Testosterone and its beneficial actions on cardiovascular disorders. In: Plotsky PM, Hunzicke-Dunne M, Rose JC, Brenner RM, editors. Recent research developments in endocrinology &amp; metabolism, Volume 1. USA: Transworld research network; 2003. p. 143-68.##Carmines EL, Gaworski CL, Faqi AS, Rajendran N. In utero exposure to 1R4F reference cigarette smoke: evaluation of developmental toxicity. Toxicol Sci. 2003;75(1):134-47.##Gaworski CL, Carmines EL, Faqi AS, Rajendran N. In utero and lactation exposure of rats to 1R4F reference cigarette mainstream smoke: effect on prenatal and postnatal development. Toxicol Sci. 2004;79(1):157-69.##Oyeyipo IP, Raji Y, Emikpe BO, Bolarinwa AF. Effects of oral administration of nicotine on organ weight, serum testosterone level and testicular pathology in adult male rats. Niger J Psychol Sci. 2010;25(1):81-86.##Iranloye BO, Bolarinwa AF. Effect of nicotine administration on weight and histology of some vital visceral organs in female albino rats. Niger J Physiol Sci. 2009;24(1):7-12.##Dhawan K, Sharma A. Prevention of chronic alcohol and nicotine-induced azospermia, sterility and decreased libido, by a novel tri-substituted benzo-flavone moiety from Passiflora incarnata Linneaus in healthy male rats. Life Sci. 2002;71(26):3059-69.##Bolarinwa Y. Gastric acid secretion in pregnant and lactating rat. Trop Vet.1993;11:35-38.##Raji Y, Oloyo AK, Morakinyo AO. Effect of methanol extract of Ricinus communis seed on reproduction of male rats. Asian J Androl. 2006;8 (1):115-21.##Raji Y, Udoh US, Mewoyeka OO, Ononye FC, Bolarinwa AF. Implication of reproductive endocrine malfunction in male antifertility efficacy of Azadirachta indica extract in rats. Afr J Med Med Sci. 2003;32(2):159-65.##Morrissey RE, Schwetz BA, Lamb JC 4th, Ross MD, Teague JL, Morris RW. Evaluation of rodent sperm, vaginal cytology, and reproductive organ weight data from National Toxicology Program 13-week studies. Fundam Appl Toxicol. 1988;11 (2):343-58.##Wyrobek AJ, Bruce WR. The induction of sperm shape abnormalities in mice and humans. In:  Hollaender A, De Serres FJ. Chemical mutagens Vol. 5.  New York: Plenum Press; 1980. p. 257-85.##Freund M, Carol B. Factors affecting haemocytometer count of sperm concentration in human semen. J Reprod Fertil. 1964;8:149-55.##Andrzej B, Hahn DW, Foldsey RG, Megure JL. Experimental studies in the development of male contraceptives. In: Zatuchni G, Goldsmith A, Spieller JM, Saara JJ, editors. Male contraception, advances and future prospects. New York: Harper and Row; 1985. p. 158-82.##Pacifici R, Altieri I, Gandini L, Lenzi A, Passa AR, Pichini S, et al. Environmental tobacco smoke: nicotine and cotinine concentration in semen. Environ Res. 1995;68(1):69-72.##Sharpe RM, Maddocks S, Millar M, Kerr JB, Saunders PT, McKinnell C. Testosterone and spermatogenesis. Identification of stage-specific, androgen-regulated proteins secreted by adult rat seminiferous tubules. J Androl. 1992;13(2):172-84.##Tulsiani DR, Orgebin-Crist MC, Skudlarek MD. Role of luminal fluid glycosyltransferases and glycosidases in the modification of rat sperm plasma membrane glycoproteins during epididymal maturation. J Reprod Fertil Suppl. 1998;53:85-97.##Mooradian AD, Morley JE, Korenman SG. Biological actions of androgens. Endocr Rev. 1987;8 (1):1-28.##Yamamoto Y, Isoyama E, Sofikitis N, Miyagawa I. Effects of smoking on testicular function and fertilizing potential in rats. Urol Res. 1998;26(1):45-8.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Protective Effects of Rutin and Naringin in Testicular Ischemia-Reperfusion Induced Oxidative Stress in Rats</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Testicular torsion and detorsion causes reperfusion injury which damages the testicular tissue and affects the quality of sperm. Deterioration in the quality of sperm worldwide is the recent scenario and one of its reasons is testicular ischemic/ reperfusion (IR) injury. Therefore the present study aims at producing new drugs for the treatment of testicular IR injury. 
Methods: 42 animals were selected for the study and divided into 7 groups, each containing 6 rats. Bioflavonoids were tested for their efficacy in reversing the damage done to the testicular tissue by causing testicular torsion and detorsion in rats. As oxidative stress produced in the above condition causes tissue damage, MDA level was measured and antioxidant enzymes SOD and catalse were evaluated. Histolo-gical examination was conducted to find the extent of damage and the protective effect of rutin and naringin. One-way ANOVA and Tukey’s post-hoc test were used for data analysis. A p-value&lt;0.001 was considered statistically significant.
Results: MDA levels increased and antioxidant enzymes were reduced drastically in the group of rats with testicular torsion and detorsion which clearly indicates rise in oxidative stress (68% rise in the case of MDA and 20% and 16% decrease in the levels of SOD and Catalase respectively).  Rutin and naringin-treated groups showed the beneficial effects of the medicinal drugs, particularly in higher doses. Rutin 
10 mg/kg was effective when compared to naringin in providing protection. In Rutin 10 mg/kg treated group there was 30% reduction in MDA levels and 20% increment in SOD levels and fivefold increase in Catalse when compared with control group animals. Histological examination supported the above claims.
Conclusion: Oxidative stress in testicular injury affects the quality of sperm. Rutin and naringin in higher doses protected testicular tissue effectively. Further studies in this direction may prove beneficial.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>209</FPAGE>
            <TPAGE>215</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Butchi Raju</Name>
<MidName>BR</MidName>
<Family>Akondi</Family>
<NameE>Butchi Raju</NameE>
<MidNameE></MidNameE>
<FamilyE>Akondi</FamilyE>
<Organizations>
<Organization>Division of Pharmacology, Andhra University College of Pharmaceutical Sciences, Andhra University, Visakhapatnam</Organization>
</Organizations>
<Universities>
<University>Division of Pharmacology, Andhra University College of Pharmaceutical Sciences, Andhra University, Visakhapatnam</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email>drraju2020@gmail.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Siva Reddy</Name>
<MidName>SR</MidName>
<Family>Challa</Family>
<NameE>Siva Reddy</NameE>
<MidNameE></MidNameE>
<FamilyE>Challa</FamilyE>
<Organizations>
<Organization>Division of Pharmacology, Andhra University College of Pharmaceutical Sciences, Andhra University, Visakhapatnam</Organization>
</Organizations>
<Universities>
<University>Division of Pharmacology, Andhra University College of Pharmaceutical Sciences, Andhra University, Visakhapatnam</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Annapurna</Name>
<MidName>A</MidName>
<Family>Akula</Family>
<NameE>Annapurna</NameE>
<MidNameE></MidNameE>
<FamilyE>Akula</FamilyE>
<Organizations>
<Organization>Division of Pharmacology, Andhra University College of Pharmaceutical Sciences, Andhra University, Visakhapatnam</Organization>
</Organizations>
<Universities>
<University>Division of Pharmacology, Andhra University College of Pharmaceutical Sciences, Andhra University, Visakhapatnam</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Ischemic reperfusion injury</KeyText></KEYWORD><KEYWORD><KeyText>Ischemia</KeyText></KEYWORD><KEYWORD><KeyText>Male infertility</KeyText></KEYWORD><KEYWORD><KeyText>Naringin</KeyText></KEYWORD><KEYWORD><KeyText>Reperfusion</KeyText></KEYWORD><KEYWORD><KeyText>Rutin</KeyText></KEYWORD><KEYWORD><KeyText>Testicular torsion</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>470.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Wei SM, Yan ZZ, Zhou J. Beneficial effect of taurine on testicular ischemia-reperfusion injury in rats. Urology. 2007;70(6):1237-42.##Koc A, Narci A, Duru M, Gergerlioglu HS, Akaydin Y, Sogut S. The protective role of erdosteine on testicular tissue after testicular torsion and detorsion. Mol Cell Biochem. 2005;280(1-2):193-9.##Salmasi AH, Beheshtian A, Payabvash S, Demehri S, Ebrahimkhani MR, Karimzadegan M, et al. Effect of morphine on ischemia-reperfusion injury: experimental study in testicular torsion rat model. Urology. 2005;66(6):1338-42.##Ozkan KU, K&#252;&#231;&#252;kaydin M, Muhtaroğlu S, Kontaş O. Evaluation of contralateral testicular damage after unilateral testicular torsion by serum inhibin B levels. J Pediatr Surg. 2001;36(7):1050-3.##Ozkan KU, Boran C, Kilin&#231; M, Garipardi&#231; M, Kurutaş EB. The effect of zinc aspartate pretreatment on ischemia-reperfusion injury and early changes of blood and tissue antioxidant enzyme activities after unilateral testicular torsion-detorsion. J Pediatr Surg. 2004;39(1):91-5.##Can C, T&#246;re F, Tun&#231;el N, Uysal O, G&#252;rer F, Ak D, et al. Protective effect of vasoactive intestinal peptide on testicular torsion-detorsion injury: association with heparin-containing mast cells. Urology. 2004;63(1):195-200.##Turrens JF, Boveris A. Generation of superoxide anion by the NADH dehydrogenase of bovine heart mitochondria. Biochem J. 1980;191(2):421-7.##Anderson JB, Williamson RC. Testicular torsion in Bristol: a 25-year review. Br J Surg. 1988;75(10): 988-92.##Turrens JF. Superoxide production by the mitochondrial respiratory chain. Biosci Rep. 1997;17(1):3-8.##Lysiak JJ, Turner SD, Nguyen QA, Singbartl K, Ley K, Turner TT. Essential role of neutrophils in germ cell-specific apoptosis following ischemia/ reperfusion injury of the mouse testis. Biol Reprod. 2001;65(3):718-25.##Rabani R, Sadeghipour-Roodsari HR, Sepehri H, Hassanzadeh-Salmasi AA, Dehpour AR. Effect of cannabinoids on testicular Ischemia-reperfusion injury in rat. 2006;44(6):365-370.##Wei SM, Yan ZZ, Zhou J. Curcumin attenuates ischemia-reperfusion injury in rat testis. Fertil Steril. 2009;91(1):271-7.##Mogilner JG, Elenberg Y, Lurie M, Shiloni E, Coran AG, Sukhotnik I. Effect of dexamethasone on germ cell apoptosis in the contralateral testis after testicular ischemia-reperfusion injury in the rat. Fertil Steril. 2006;85 Suppl 1:1111-7.##Annapurna A, Reddy CS, Akondi RB, Rao SR. Cardioprotective actions of two bioflavonoids, quercetin and rutin, in experimental myocardial infarction in both normal and streptozotocin-induced type I diabetic rats. J Pharm Pharmacol. 2009;61 (10):1365-74.##Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem. 1979;95(2):351-8.##Beauchamp C, Fridovich I. Superoxide dismutase: improved assays and an assay applicable to acrylamide gels. Anal Biochem. 1971;44(1):276-87.##Aebi H. Catalase in vitro. Methods Enzymol. 1984; 105:121-6.##Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem. 1951;193(1):265-75.##Cosentino MJ, Nishida M, Rabinowitz R, Cockett AT. Histopathology of prepubertal rat testes subjected to various durations of spermatic cord torsion. J Androl. 1986;7(1):23-31.##Turrens JF. Superoxide production by the mitochondrial respiratory chain. Biosci Rep. 1997;17 (1):3-8.##Turner TT, Bang HJ, Lysiak JL. The molecular pathology of experimental testicular torsion suggests adjunct therapy to surgical repair.  J Urol. 2004;172(6 Pt 2):2574-8.##Hanasaki Y, Ogawa S, Fukui S. The correlation between active oxygens scavenging and antioxidative effects of flavonoids. Free Radic Biol Med. 1994;16(6):845-50.##Shoskes DA. Effect of bioflavonoids quercetin and curcumin on ischemic renal injury: a new class of renoprotective agents. Transplantation. 1998;66(2): 147-52.##Chang WS, Lee YJ, Lu FJ, Chiang HC. Inhibitory effects of flavonoids on xanthine oxidase. Anticancer Res. 1993;13(6A):2165-70.##Iio M, Ono Y, Kai S, Fukumoto M. Effects of flavonoids on xanthine oxidation as well as on cytochrome c reduction by milk xanthine oxidase. J Nutr Sci Vitaminol (Tokyo). 1986;32(6):635-42.##Bennett JP, Gomperts BD, Wollenweber E. Inhibitory effects of natural flavonoids on secretion from mast cells and neutrophils. Arzneimittelforschung. 1981;31(3):433-7.##Ferr&#225;ndiz ML, Alcaraz MJ. Anti-inflammatory activity and inhibition of arachidonic acid metabolism by flavonoids. Agents Actions. 1991;32(3-4): 283-8.##N&#232;gre-Salvayre A, Affany A, Hariton C, Salvayre R. Additional antilipoperoxidant activities of alpha tocopherol and ascorbic acid on membrane-like systems are potentiated by rutin. Pharmacology. 1991;42(5):262-72.##Ali MM, El Kader MA. The influence of naringin on the oxidative state of rats with streptozotocin-induced acute hyperglycaemia. Z Naturforsch C. 2004;59(9-10):726-33.##Russo A, Acquaviva R, Campisi A, Sorrenti V, Di Giacomo C, Virgata G, et al. Bioflavonoids as antiradicals, antioxidants and DNA cleavage protectors. Cell Biol Toxicol. 2000;16(2):91-8.##Dokmeci D, Kanter M, Inan M, Aydogdu N, Basaran UN, Yalcin O, et al. Protective effects of ibuprofen on testicular torsion/detorsion-induced ischemia/reperfusion injury in rats. Arch Toxicol. 2007;81(9):655-63.##Payabvash S, Salmasi AH, Kiumehr S, Tavangar SM, Nourbakhsh B, Faghihi SH, et al. Salutary effects of N-acetylcysteine on apoptotic damage in a rat model of testicular torsion. Urol Int. 2007;79 (3):248-54.##Payabvash S, Salmasi AH, Kiumehr S, Tavangar SM, Nourbakhsh B, Faghihi SH, et al. Salutary effects of N-acetylcysteine on apoptotic damage in a rat model of testicular torsion. Urol Int. 2007;79 (3):248-54.##Avlan D, Erdouğan K, Cimen B, D&#252;şmez Apa D, Cinel I, Aks&#246;yek S. The protective effect of selenium on ipsilateral and contralateral testes in testicular reperfusion injury. Pediatr Surg Int. 2005;21(4): 274-8.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Down-regulation of HLA-G Attenuates Cleavage Rate in Human Triploid Embryos</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: HLA-G is a major histocompatibility complex (MHC), class Ib molecule that is selectively expressed at the fetal–maternal interface. It is thought to play a role in protecting the fetus from the maternal immune response. Interestingly, the preimplantation embryo development (Ped) gene product Qa-2 is also a mouse MHC class Ib protein that affects cleavage and division of preimplantation mouse embryos and subsequent embryonic survival. Data from many human in vitro fertilization (IVF) clinics suggest that the mouse Ped phenomenon also exists in human because embryos fertilized at the same time have different cleavage rates and consequently different IVF outcomes. As HLA-G is expressed in human early embryos, it is highly regarded as the functional homologue of Qa-2. Whether HLA-G expression is correlated with the cleavage rate of human embryos has great potential clinical value. 
Methods: In this study, 45 human early abnormal fertilized embryos (3 PN) from patients undergoing in vitro fertilization were used to test the effects of HLA-G knock-down via infection with adenovirus carrying its specific siRNA on the cleavage rate in a 2-day culture period. One- way ANOVA, Post hoc and Chi-square were used to compare groups. A p-value smaller than 0.05 was considered statistically significant.
Results: Knocking-down HLA-G in human preimplantation stage embryos resulted in a higher cell arrest rate and a slower cleavage rate.
Conclusion: The results from the present study suggested that HLA-G might play an important role in early human embryo development.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>215</FPAGE>
            <TPAGE>222</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Li Li</Name>
<MidName>LL</MidName>
<Family>Sun</Family>
<NameE>Li Li</NameE>
<MidNameE></MidNameE>
<FamilyE>Sun</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynecology, Navy General Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynecology, Navy General Hospital</University>
</Universities>
<Countries>
<Country>China</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Ai</Name>
<MidName>A</MidName>
<Family>Ming Wang</Family>
<NameE>Ai</NameE>
<MidNameE></MidNameE>
<FamilyE>Ming Wang</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynecology, Navy General Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynecology, Navy General Hospital</University>
</Universities>
<Countries>
<Country>China</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Christopher</Name>
<MidName>Ch</MidName>
<Family>J Haines</Family>
<NameE>Christopher</NameE>
<MidNameE></MidNameE>
<FamilyE>J Haines</FamilyE>
<Organizations>
<Organization>Shanghai First Maternity and Infants Hospital, Tongji University</Organization>
</Organizations>
<Universities>
<University>Shanghai First Maternity and Infants Hospital, Tongji University</University>
</Universities>
<Countries>
<Country>China</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Yibing</Name>
<MidName>Y</MidName>
<Family>Han</Family>
<NameE>Yibing</NameE>
<MidNameE></MidNameE>
<FamilyE>Han</FamilyE>
<Organizations>
<Organization>Shanghai First Maternity and Infants Hospital, Tongji University</Organization>
</Organizations>
<Universities>
<University>Shanghai First Maternity and Infants Hospital, Tongji University</University>
</Universities>
<Countries>
<Country>China</Country>
</Countries>
<EMAILS>
<Email>ybhan@cuhk.edu.hk</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Yuan</Name>
<MidName>Y</MidName>
<Family>Qing Yao</Family>
<NameE>Yuan</NameE>
<MidNameE></MidNameE>
<FamilyE>Qing Yao</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynecology, General Hospital of Chinese PLA</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynecology, General Hospital of Chinese PLA</University>
</Universities>
<Countries>
<Country>China</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Adenovirus</KeyText></KEYWORD><KEYWORD><KeyText>Cleavage</KeyText></KEYWORD><KEYWORD><KeyText>HLA-G</KeyText></KEYWORD><KEYWORD><KeyText>&lt;i&gt;In Vitro&lt;/i&gt; fertilization</KeyText></KEYWORD><KEYWORD><KeyText>Mouse Qa-2 antigen</KeyText></KEYWORD><KEYWORD><KeyText>Preimplantation embryo</KeyText></KEYWORD><KEYWORD><KeyText>RNAi</KeyText></KEYWORD><KEYWORD><KeyText>Adenovirus vector</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>471.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Yao YQ, Barlow DH, Sargent IL. Differential expression of alternatively spliced transcripts of HLA-G in human preimplantation embryos and inner cell masses. J Immunol. 2005;175(12):8379-85.##Jurisicova A, Casper RF, MacLusky NJ, Mills GB, Librach CL. HLA-G expression during preimplantation human embryo development. Proc Natl Acad Sci U S A. 1996;93(1):161-5.##Cao W, Brenner CA, Alikani M, Cohen J, Warner CM. Search for a human homologue of the mouse Ped gene. Mol Hum Reprod. 1999;5(6):541-7.##Jurisicova A, Antenos M, Kapasi K, Meriano J, Casper RF. Variability in the expression of trophectodermal markers beta-human chorionic gonadotrophin, human leukocyte antigen-G and pregnancy specific beta-1 glycoprotein by the human blastocyst. Hum Reprod. 1999;14(7):1852-8.##Noci I, Fuzzi B, Rizzo R, Melchiorri L, Criscuoli L, Dabizzi S, et al. Embryonic soluble HLA-G as a marker of developmental potential in embryos. Hum Reprod. 2005;20(1):138-46.##Yie SM, Balakier H, Motamedi G, Librach CL. Secretion of human leukocyte antigen-G by human embryos is associated with a higher in vitro fertilization pregnancy rate. Fertil Steril. 2005;83(1):30-6.##Fisch JD, Keskintepe L, Ginsburg M, Adamowicz M, Sher G. Graduated Embryo Score and soluble human leukocyte antigen-G expression improve assisted reproductive technology outcomes and suggest a basis for elective single-embryo transfer. Fertil Steril. 2007;87(4):757-63.##Geraghty DE, Koller BH, Orr HT. A human major histocompatibility complex class I gene that encodes a protein with a shortened cytoplasmic segment. Proc Natl Acad Sci U S A. 1987;84(24):9145-9.##Comiskey M, Goldstein CY, De Fazio SR, Mammolenti M, Newmark JA, Warner CM. Evidence that HLA-G is the functional homolog of mouse Qa2, the Ped gene product. Hum Immunol. 2003;64 (11):999-1004.##Comiskey M, Warner CM, Schust DJ. MHC molecules of the preimplantation embryo and trophoblast. In: Markert UR. Immunology of pregnancy. Switzerland: Karger Publishers; 2005. p. 72-80.##Comiskey M, Domino KE, Warner CM. HLA-G is found in lipid rafts and can act as a signaling molecule. Hum Immunol. 2007;68(1):1-11.##Clements CS, Kjer-Nielsen L, Kostenko L, Hoare HL, Dunstone MA, Moses E, et al. Crystal structure of HLA-G: a nonclassical MHC class I molecule expressed at the fetal-maternal interface. Proc Natl Acad Sci U S A. 2005;102(9):3360-5.##Warner CM, Gollnick SO, Flaherty L, Goldbard SB. Analysis of Qa-2 antigen expression by preimplantation mouse embryos: possible relationship to the preimplantation-embryo-development (Ped) gene product. Biol Reprod. 1987;36(3):611-6.##McElhinny AS, Warner CM. Detection of major histocompatibility complex class I antigens on the surface of a single murine blastocyst by immuno-PCR. Biotechniques. 1997;23(4):660-2.##McElhinny AS, Kadow N, Warner CM. The expression pattern of the Qa-2 antigen in mouse preimplantation embryos and its correlation with the Ped gene phenotype. Mol Hum Reprod. 1998;4 (10):966-71.##Goldbard SB, Verbanac KM, Warner CM. Role of the H-2 complex in preimplantation mouse embryo development. Biol Reprod. 1982;26(4):591-6.##Magli MC, Gianaroli L, Munn&#233; S, Ferraretti AP. Incidence of chromosomal abnormalities from a morphologically normal cohort of embryos in poor-prognosis patients. J Assist Reprod Genet. 1998;15(5):297-301.##Biezinov&#225; J, Svobodov&#225; M, Oborn&#225; I, Fingerov&#225; H, Dost&#225; J, Krskov&#225; M. [Embryo quality evaluation according to the speed of the first cleavage after conventional IVF]. Ceska Gynekol. 2006;71 (2):105-10. Czech.##Xu Y, Jin P, Mellor AL, Warner CM. Identification of the Ped gene at the molecular level: the Q9 MHC class I transgene converts the Ped slow to the Ped fast phenotype. Biol Reprod. 1994;51(4):695-9.##Sun LL, Han Y, Chen JH, Yao YQ. Down-regulation of HLA-G boosted natural killer cell-mediated cytolysis in JEG-3 cells cultured in vitro. Fertil Steril. 2008;90(6):2398-405.##Barbash-Hazan S, Frumkin T, Malcov M, Yaron Y, Cohen T, Azem F, et al. Preimplantation aneuploid embryos undergo self-correction in correlation with their developmental potential. Fertil Steril. 2009;92(3):890-6.##Brownell MS, Warner CM. Ped gene expression by embryos cultured in vitro. Biol Reprod. 1988;39 (4):806-11.##Tian Z, Xu Y, Warner CM. Removal of Qa-2 antigen alters the Ped gene phenotype of preimplantation mouse embryos. Biol Reprod. 1992;47(2): 271-6.##Xu Y, Jin P, Warner CM. Modulation of preimplantation embryonic development by antisense oligonucleotides to major histocompatibility complex genes. Biol Reprod. 1993;48(5):1042-6.##Wu L, Feng H, Warner CM. Identification of two major histocompatibility complex class Ib genes, Q7 and Q9, as the Ped gene in the mouse. Biol Reprod. 1999;60(5):1114-9.##McElhinny AS, Exley GE, Warner CM. Painting Qa-2 onto Ped slow preimplantation embryos increases the rate of cleavage. Am J Reprod Immunol. 2000;44(1):52-8.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Comparing the Effects of Echinophora-platyloba, Fennel and Placebo on Pre-menstrual Syndrome</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: Premenstrual syndrome (PMS) is a condition characterized by a number of behavioral, psychological and physical symptoms recurring cyclically during the luteal phase of the menstrual cycle. The uncertainty in the pathogenesis of PMS has led to many treatment protocols being suggested as possible therapies. The present study was carried out to compare the effects of echinophora-platyloba and fennel extracts on the PMS against placebo in students of Shahrekord University of Medical Sciences in 2008.
Methods: In this single-blind randomized clinical trial, 90 students with moderate to severe PMS enrolled in the study and were randomely divided into three equal groups. The first group received echinophora-platyloba extract, the second group received fennel extracts and the third group received placebo. The severity of PMS was measured by Daily Record of Severity of Problems (DRSP) questionnaire at the end of the first and second menstrual cycles before the intervention and the results were compared with them after the intervention. Data was analyzed using Dunn, Kruskal Wallis, and Pearson correlation tests by SPSS (v. 11.5) and P&lt;0.05 was considered statistically significant. 
Results: There were not any significant differences in the means of premenstrual syndrome scores before the intervention among the three groups (100.8&#177;22.1 in echinophora-platyloba group, 101.3&#177;27.1 in fennel group and 104.3&#177;19.5 in placebo group, P&gt;0.05), but the differences were significant after the intervention (49.7&#177;23.2 in echinophora-platyloba group, 64.4&#177;27.5 in fennel group and 79.1&#177;28.1 in placebo group, respectively, P&lt;0.001). No significant differences were seen between the echinophora-platyloba and fennel groups.
Conclusion: The echinophora-platyloba and fennel extracts could reduce the severity of PMS. The effects of echinophora-platyloba and fennel were similar and greater than the placebo. Administration of the extracts of these herbs is suggested for relieving the signs and symptoms of PMS.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>221</FPAGE>
            <TPAGE>227</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Masoumeh</Name>
<MidName>M</MidName>
<Family>Delaram</Family>
<NameE>معصومه </NameE>
<MidNameE></MidNameE>
<FamilyE>دل‌آرام </FamilyE>
<Organizations>
<Organization>Department of Midwifery, Faculty of Nursing &amp;amp; Midwifery, Shahrekord University of Medical Science &amp;amp; Health Services</Organization>
</Organizations>
<Universities>
<University>Department of Midwifery, Faculty of Nursing &amp; Midwifery, Shahrekord University of Medical Science &amp; Health Services</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email>masoumehdelaram@yahoo.com</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Soleiman</Name>
<MidName>S</MidName>
<Family>Kheiri</Family>
<NameE>سلیمان</NameE>
<MidNameE></MidNameE>
<FamilyE>خیری</FamilyE>
<Organizations>
<Organization>Department of Statistic&amp;amp; Epidemiology, Faculty of Medicine, Shahrekord University of Medical Science</Organization>
</Organizations>
<Universities>
<University>Department of Statistic&amp; Epidemiology, Faculty of Medicine, Shahrekord University of Medical Science</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Mohammad Reza</Name>
<MidName>MR</MidName>
<Family>Hodjati</Family>
<NameE>محمدرضا</NameE>
<MidNameE></MidNameE>
<FamilyE>حجتی</FamilyE>
<Organizations>
<Organization>Department of Physiology, Shahrekord University of Medical Sciences</Organization>
</Organizations>
<Universities>
<University>Department of Physiology, Shahrekord University of Medical Sciences</University>
</Universities>
<Countries>
<Country>Iran</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Echinophora-platyloba</KeyText></KEYWORD><KEYWORD><KeyText>Fennel</KeyText></KEYWORD><KEYWORD><KeyText>Placebo</KeyText></KEYWORD><KEYWORD><KeyText>Premenstrual syndrome</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>472.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Tschudin S, Bertea PC, Zemp E. Prevalence and predictors of premenstrual syndrome and premenstrual dysphoric disorder in a population-based sample. Arch Womens Ment Health. 2010;13(6): 485-94.##Nisar N, Zehra N, Haider G, Munir AA, Sohoo NA. Frequency, intensity and impact of premenstrual syndrome in medical students. J Coll Physicians Surg Pak. 2008;18(8):481-4.##Silva CM, Gigante DP, Carret ML, Fassa AG. [Population study of premenstrual syndrome]. Rev Saude Publica. 2006;40(1):47-56. Portuguese.##Wittchen HU, Becker E, Lieb R, Krause P. Prevalence, incidence and stability of premenstrual dysphoric disorder in the community. Psychol Med. 2002;32(1):119-32.##Potter J, Bouyer J, Trussell J, Moreau C. Premenstrual syndrome prevalence and fluctuation over time: results from a French population-based survey. J Womens Health (Larchmt). 2009;18(1):31-9.##Freeman MP. Screening and treatment for women with mood disorders associated with reproductive events. J Clin Psychiatry. 2007;68(12):1946.##Fujii H, Sakai R, Masatsugu A, Ohta M, Matsumoto T, Doi T, et al. Case of premenstrual syndrome inducing monthly episodes of vesiculobullous eruptions on the face. J Dermatol. 2008;35(4):246-7.##Pakgohar M, Ahmadi M, Salehi surmaghi MH, Mehran A, Akhondzadeh Sh. [Effect of Hypericum perforatum L. for treatment of premenstrual syndrome]. J Med Plants. 2005;4(3):33-42. Persian.##Bertone-Johnson ER. Vitamin D and the occurrence of depression: causal association or circumstantial evidence? Nutr Rev. 2009;67(8):481-92.##Land&#233;n M, Erlandsson H, Bengtsson F, Andersch B, Eriksson E. Short onset of action of a serotonin reuptake inhibitor when used to reduce premenstrual irritability. Neuropsychopharmacology. 2009;34(3):585-92.##Salehi L, Salehi F. [The effect of pyridoxine (vit B6) on premenstrual syndrome]. J kordestan Univ Med Sci. 2007;2(3):32-9. Persian.##Studd J, Panay N. Are oestrogens useful for the treatment of depression in women? Best Pract Res Clin Obstet Gynaecol. 2009;23(1):63-71.##peroff L,  Fritz MA. Clinical gynecologic endocrinology and infertility. 7th ed.  Philadelphia: Lippincott Williams &amp; Wilkins; c2005. Chapter 14, Menstrual Disorders; p. 531-571 .##Jarvis CI, Lynch AM, Morin AK. Management strategies for premenstrual syndrome/premenstrual dysphoric disorder. Ann Pharmacother. 2008;42 (7):967-78.##Segebladh B, Borgstr&#246;m A, Nyberg S, Bixo M, Sundstr&#246;m-Poromaa I. Evaluation of different addback estradiol and progesterone treatments to gonadotropin-releasing hormone agonist treatment in patients with premenstrual dysphoric disorder. Am J Obstet Gynecol. 2009;201(2):139.e1-8.##Yazdani M, Shahriyary M, Hamedi B. [Comparison of fennel  versus placebo on dysmenorrhea and PMS]. J Hormozgan Univ Med Sci. 2004;8(1):57-61. Persian.##D&#246;ll M. [The premenstrual syndrome: effectiveness of Vitex agnus castus]. Med Monatsschr Pharm. 2009;32(5):186-91.German.##Jing Z, Yang X, Ismail KM, Chen X, Wu T. Chinese herbal medicine for premenstrual syn-drome. Cochrane Database Syst Rev. 2009;(1): CD006414.##He Z, Chen R, Zhou Y, Geng L, Zhang Z, Chen S, et al. Treatment for premenstrual syndrome with Vitex agnus castus: A prospective, randomized, multi-center placebo controlled study in China. Maturitas. 2009;63(1):99-103.##Sadraei H, Asghari Gh, Yaghoubi Kh. [Study of the effect of hydro-Alcoholic and essential  oil of Echinophora Platyloba on rat isolated ileum contractions in vitro]. J Res Med Sci. 2003;7(Suppl 2):150-5. Persian.##Avijgan M, Saadat M, Nilforooshzadeh MA, Hafi-zi M. [Anti fungal effect of Echinophora platyloba extract on some common dermathophytes]. J Med Plants. 2006;5(18):10-6. Persian.##Avijgan M, Mahboubi M, Darabi M, Kasaiyan N. [Anti candidal activity of Echinophora platyloba against candida albicans and comparison with Amphotricin]. J Med Plants. 2009;8(30):36-43. Persian.##Moura LS, Carvalho JR, Stefanini MB, Ming LC, Meireles MAA. Supercritical fluid extraction from fennel (Foeniculum vulgare): global yield, composition and kinetic data. J Supercrit Fluids. 2005; 35(3):212-9.##Birdane FM, Cemek M, Birdane YO, G&#252;l&#231;in I, B&#252;y&#252;kokuroğlu ME. Beneficial effects of Foeniculum vulgare on ethanol-induced acute gastric mucosal injury in rats. World J Gastroenterol. 2007;13(4):607-11.##Shams Ardekani MR, Haji Akhoondi A, Jamshidi AH, Abdi Kh. [The study of volatile oil of Foeniculum Vulgare Miller in their tissue culture and comparison with the whole plant]. J Med Plants. 2005;4(15): 80-73. Persian.##Torkzahrani Sh, Akhavan-Amjadi M, Mojab F, Alavi Majd H. Clinical effects of Foeniculum vulgare extract on primary dysmenorrhea. J Reprod Infertil. 2007;8(1):45-51.##Modaress Nejad V, Motamedi B,  Asadi pour M. [Comparison between the Pain-Relief Effect of Fennel and Mefenamic Acid on Primary Dysmenorrhea]. J Rafsanjan Univ Med Sci. 2006;5(1):1-6. Persian.##Ostad SN, Soodi M, Shariffzadeh M, Khorshidi N, Marzban H. The effect of fennel essential oil on uterine contraction as a model for dysmenorrhea, pharmacology and toxicology study. J Ethnopharmacol. 2001;76(3):299-304.##Borenstein JE, Dean BB, Yonkers KA, Endicott J. Using the daily record of severity of problems as a screening instrument for premenstrual syndrome. Obstet Gynecol. 2007;109(5):1068-75.##Entezari M, Hashemi M, Ashki M, Ebrahimian S, Bayat M, Azizi Saraji AR, et al. Studying the Effect Echinophora Platyloba Extract on Bactira (Staphilococus aureus and Pseudomonas aeroginosa) and Fungi (Candidia albicans, Aspergilus flavus and Aspergilus niger) In Vitro. World J Med Sci. 2009;4(2):89-92.##Shahhosseini Z, Amin Qh, Salehi sormaghi MH, Danesh MM. [Double blind study of anti primary dysmenorrhea effects of Vitagnus]. J Mazandaran Univ Med Sci. 2005;15(50):15-21. Persian.##Agajani Delavar M, Nasiri F, Hoseini SH. [A double-blind placebo-controlled evaluation of Vitex agnus castus in premenstrual syndrome]. J Med Plants.2002;1(2):15-21. Persian.##Ozgoli G, Selselei EA, Mojab F, Majd HA. A randomized, placebo-controlled trial of Ginkgo biloba L. in treatment of premenstrual syndrome. J Altern Complement Med. 2009;15(8):845-51.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>Risk Factors for Hypertensive Disorders in Pregnancy: A Report from the Maroua Regional Hospital, Cameroon</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: A recent study at the Maroua Provincial Hospital revealed that hypertension in pregnancy was the first cause of maternal death, representing 17.5% of the 63 maternal deaths recorded between 2003 and 2005. Knowing little about the causes, this study was to identify the possible risk factors for hypertensive disorders in pregnancy. 
Methods: This case-control study was-done at the Maroua Regional Hospital, Cameroon between June 2005 and May 2007. All the 152 deliveries complicated with hypertension were compared and analyzed with 414 pregnancies that were not complicated with the disease. Data analysis was performed using EPI Info 3.5.1. The differences were considered to be significant if the p-values were less than 0.05. 
Results: Using univariate analysis, several factors linked to hypertensive disorder in pregnancy were identified. They included early adolescence, nulliparity, illiteracy, lack of occupation and family history of hypertension. At multivariate analysis, the risk of having hypertension during pregnancy remained greater for illiterate women (OR: 1.6; 95%CI: 1.0-2.3), housewives (OR: 2.8; 95%CI: 1.1-6.9), nulliparae (OR: 2.8; 95%CI: 1.5-3.6), women with family histories  of  hypertension (OR: 3.6; 95%CI: 1.6-8.5) and women with histories of  hypertension during  pregnancy  (OR: 7.0; 95%CI: 3.0-16.4). 
Conclusion: Risk factors for hypertensive diseases in pregnancy in Maroua, Cameroon seem to include early teenage status, illiteracy, housewife status, nulliparity and family or personal histories of hypertension. The knowledge about the aforesaid factors seems to lay the tracks for its prevention in Cameroon.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>227</FPAGE>
            <TPAGE>235</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Pierre Marie</Name>
<MidName>PM</MidName>
<Family>Tebeu</Family>
<NameE>Pierre Marie</NameE>
<MidNameE></MidNameE>
<FamilyE>Tebeu</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynaecology, University Hospitals</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynaecology, University Hospitals</University>
</Universities>
<Countries>
<Country>Cameroon</Country>
</Countries>
<EMAILS>
<Email>pmtebeu@yahoo.fr</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Pascal</Name>
<MidName>P</MidName>
<Family>Foumane</Family>
<NameE>Pascal</NameE>
<MidNameE></MidNameE>
<FamilyE>Foumane</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynaecology, University Hospitals</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynaecology, University Hospitals</University>
</Universities>
<Countries>
<Country>Cameroon</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Robinson</Name>
<MidName>R</MidName>
<Family>Mbu</Family>
<NameE>Robinson</NameE>
<MidNameE></MidNameE>
<FamilyE>Mbu</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynaecology, University Hospitals</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynaecology, University Hospitals</University>
</Universities>
<Countries>
<Country>Cameroon</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Gis&#232;le</Name>
<MidName>G</MidName>
<Family>Fosso</Family>
<NameE>Gis&#232;le</NameE>
<MidNameE></MidNameE>
<FamilyE>Fosso</FamilyE>
<Organizations>
<Organization>Ligue d’Initiative et de Recherche Active pour la Sant&amp;#233; et l’Education de la Femme (LIRASEF)</Organization>
</Organizations>
<Universities>
<University>Ligue d’Initiative et de Recherche Active pour la Sant&#233; et l’Education de la Femme (LIRASEF)</University>
</Universities>
<Countries>
<Country>Cameroon</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Paul</Name>
<MidName>P</MidName>
<Family>Tjek Biyaga</Family>
<NameE>Paul</NameE>
<MidNameE></MidNameE>
<FamilyE>Tjek Biyaga</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynaecology, Regional Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynaecology, Regional Hospital</University>
</Universities>
<Countries>
<Country>Cameroon</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Joseph</Name>
<MidName>J</MidName>
<Family>Nelson Fomulu</Family>
<NameE>Joseph</NameE>
<MidNameE></MidNameE>
<FamilyE>Nelson Fomulu</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynaecology, Regional Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynaecology, Regional Hospital</University>
</Universities>
<Countries>
<Country>Cameroon</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Hypertension</KeyText></KEYWORD><KEYWORD><KeyText>Pregnancy</KeyText></KEYWORD><KEYWORD><KeyText>Risk factor</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>468.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>ACOG. ACOG technical bulletin. Hypertension in pregnancy. Number 219--January 1996 (replaces no. 91, February 1986). Committee on Technical Bulletins of the American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet. 1996;53(2): 175-83.##Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Gilstrap III LC, Wenstrom KD. Williams Obstetrics. 22th ed. USA: McGraw-Hill Companies Inc; 2005. Chapter 34, Hypertensive disorders in pregnancy; p. 426-50.##McCaw Binns AM, MacGillivray I, Hawkins N, Golding J, Ashley DEC. International variation in the incidence of hypertension in pregnancy among primiparae: the Jamaican experience. West Indian Med J. 1997;46(Suppl 2):29.##Schroeder BM; American College of Obstetricians and Gynecologists. ACOG practice bulletin on diagnosing and managing preeclampsia and eclampsia. American College of Obstetricians and Gynecologists. Am Fam Physician. 2002;66(2):330-1.##Working Group on High Blood Pressure . Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol. 2000;183(1):S1-S22.##Roberts CL, Algert CS, Morris JM, Ford JB, Henderson-Smart DJ. Hypertensive disorders in pregnancy: a population-based study. Med J Aust. 2005;182(7):332-5.##Golding J. A randomised trial of low dose aspirin for primiparae in pregnancy. The Jamaica Low Dose Aspirin Study Group. Br J Obstet Gynaecol. 1998; 105(3):293-9.##Levine RJ, Hauth JC, Curet LB, Sibai BM, Catalano PM, Morris CD, et al. Trial of calcium to prevent preeclampsia. N Engl J Med. 1997;337(2):69-76.##Conde-Agudelo A, Beliz&#225;n JM. Risk factors for preeclampsia in a large cohort of Latin American and Caribbean women. BJOG. 2000;107(1):75-83.##Trogstad LI, Eskild A, Magnus P, Samuelsen SO, Nesheim BI. Changing paternity and time since last pregnancy; the impact on pre-eclampsia risk. A study of 547 238 women with and without previous pre-eclampsia. Int J Epidemiol. 2001;30 (6):1317-22.##Shey Wiysonge CU, Ngu Blackett K, Mbuagbaw JN. Risk factors and complications of hypertension in Yaounde, Cameroon. Cardiovasc J S Afr. 2004; 15(5):215-9.##Pridjian G, Puschett JB. Preeclampsia. Part 1: clinical and pathophysiologic considerations. Obstet Gynecol Surv. 2002;57(9):598-618.##Leeners B, Rath W, Kuse S, Irawan C, Imthurn B, Neumaier-Wagner P. BMI: new aspects of a classical risk factor for hypertensive disorders in pregnancy. Clin Sci (Lond). 2006;111(1):81-6.##Tebeu PM, Ngassa P, Kouam L, Major AL, Fomulu JN. Maternal mortality in Maroua Provincial Hospital, Cameroon (2003-2005). West Indian Med J. 2007;56(6):502-7.##Chesley LC. History and epidemiology of preeclampsia-eclampsia. Clin Obstet Gynecol. 1984; 27(4):801-20.##Saftlas AF, Olson DR, Franks AL, Atrash HK, Pokras R. Epidemiology of preeclampsia and eclampsia in the United States, 1979-1986. Am J Obstet Gynecol. 1990;163(2):460-5.##Adeyinka DA, Oladimeji O, Adekanbi TI, Adeyinka FE, Falope Y, Aimakhu C. Outcome of adolescent pregnancies in southwestern Nigeria: a case control study. J Matern Fetal Neonatal Med. 2010; 23(8):785-9.##Usta IM, Zoorob D, Abu-Musa A, Naassan G, Nassar AH. Obstetric outcome of teenage pregnancies compared with adult pregnancies. Acta Obstet Gynecol Scand. 2008;87(2):178-83.##Suzuki S, Igarashi M. Risk factors for preeclampsia in Japanese twin pregnancies: comparison with those in singleton pregnancies. Arch Gynecol Obstet. 2009;280(3):389-93.##Assis TR, Viana FP, Rassi S. Study on the major maternal risk factors in hypertensive syndromes. Arq Bras Cardiol. 2008;91(1):11-7.##Poon LC, Kametas NA, Chelemen T, Leal A, Nicolaides KH. Maternal risk factors for hypertensive disorders in pregnancy: a multivariate approach. J Hum Hypertens. 2010;24(2):104-10.##Jacobs DJ, Vreeburg SA, Dekker GA, Heard AR, Priest KR, Chan A. Risk factors for hypertension during pregnancy in South Australia. Aust N Z J Obstet Gynaecol. 2003;43(6):421-8.##Kimbally KG, Barassoumbi H, Buambo SF, Gombet T, Kibeke P, Monabeka HG, et al. [Arterial hypertension: epidemiological aspects and risk factors on pregnant and delivered woman]. Dakar Med. 2007;52(2):148-52. French.##Li DK, Wi S. Changing paternity and the risk of preeclampsia/eclampsia in the subsequent pregnancy. Am J Epidemiol. 2000;151(1):57-62.##Trupin LS, Simon LP, Eskenazi B. Change in paternity: a risk factor for preeclampsia in multiparas. Epidemiology. 1996;7(3):240-4.##Silva LM, Coolman M, Steegers EA, Jaddoe VW, Moll HA, Hofman A, et al. Low socioeconomic status is a risk factor for preeclampsia: the Generation R Study. J Hypertens. 2008;26(6): 1200-8.##Silva L, Coolman M, Steegers E, Jaddoe V, Moll H, Hofman A, et al. Maternal educational level and risk of gestational hypertension: the Generation R Study. J Hum Hypertens. 2008;22(7):483-92.##Mittendorf R, Lain KY, Williams MA, Walker CK. Preeclampsia. A nested, case-control study of risk factors and their interactions. J Reprod Med. 1996; 41(7):491-6.##Najman JM, Morrison J, Williams GM, Andersen MJ, Keeping JD. The employment of mothers and the outcomes of their pregnancies: an Australian study. Public Health. 1989;103(3):189-98.##Jansen PW, Tiemeier H, Verhulst FC, Burdorf A, Jaddoe VW, Hofman A, et al. Employment status and the risk of pregnancy complications: the Generation R Study. Occup Environ Med. 2010;67(6): 387-94.##El-Gilany AH, El-Wehady A, El-Hawary A. Maternal employment and maternity care in Al-Hassa, Saudi Arabia. Eur J Contracept Reprod Health Care. 2008;13(3):304-12.##Bao Y, Hu Y, Fu S, Zhang J, Zhang F, Wang X. [Studies on relationship between occupation and pregnancy outcome]. Zhonghua Yu Fang Yi Xue Za Zhi. 1999;33(1):30-3. Chinese.##Craici I, Wagner S, Garovic VD. Preeclampsia and future cardiovascular risk: formal risk factor or failed stress test? Ther Adv Cardiovasc Dis. 2008; 2(4):249-59.##Luealon P, Phupong V. Risk factors of preeclampsia in Thai women. J Med Assoc Thai. 2010;93(6): 661-6.##Hjartardottir S, Leifsson BG, Geirsson RT, Steinthorsdottir V. Paternity change and the recurrence risk in familial hypertensive disorder in pregnancy. Hypertens Pregnancy. 2004;23(2):219-25.##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

<ARTICLE>
    <TitleF></TitleF>
    <TitleE>An Unusual Etiology of Spontaneous Pyometra Perforation; A Case Report</TitleE>
    <TitleLang_ID>2</TitleLang_ID>
    <ABSTRACTS>
        <ABSTRACT>
            <Language_ID>1</Language_ID>
            <CONTENT></CONTENT>
        </ABSTRACT>
        <ABSTRACT>
            <Language_ID>2</Language_ID>
            <CONTENT>Background: By presenting this case we aimed to describe an uncommon complication of generalized peritonitis following spontaneous pyometra perforation in untreated cervical carcinoma.
Case Presentation: This report describes a 60-year-old postmenopausal woman presenting with clinical features mimicking intestinal perforation who was later diagnosed as cervical carcinoma with pyometra perforation at exploratory laparotomy. The patient had good post-operative recovery following drainage and peritoneal lavage. 
Conclusion: Spontaneous pyometra perforation in a case of untreated carcinoma of cervix is a rare condition, yet it should be suspected and kept in the differential diagnosis of acute abdomen in elderly women.</CONTENT>
        </ABSTRACT>
    </ABSTRACTS>
    <PAGES>
        <PAGE>
            <FPAGE>235</FPAGE>
            <TPAGE>239</TPAGE>
        </PAGE>
    </PAGES>
    <AUTHORS>
        <AUTHOR>
<Name>Rachna</Name>
<MidName>R</MidName>
<Family>Agarwal</Family>
<NameE>Rachna</NameE>
<MidNameE></MidNameE>
<FamilyE>Agarwal</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email>Rachna_anila@yahoo.co.in</Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Amita</Name>
<MidName>A</MidName>
<Family>Suneja</Family>
<NameE>Amita</NameE>
<MidNameE></MidNameE>
<FamilyE>Suneja</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Abha</Name>
<MidName>A</MidName>
<Family>Sharma</Family>
<NameE>Abha</NameE>
<MidNameE></MidNameE>
<FamilyE>Sharma</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR><AUTHOR>
<Name>Neelam</Name>
<MidName>N</MidName>
<Family>Bala Vaid</Family>
<NameE>Neelam</NameE>
<MidNameE></MidNameE>
<FamilyE>Bala Vaid</FamilyE>
<Organizations>
<Organization>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</Organization>
</Organizations>
<Universities>
<University>Department of Obstetrics and Gynecology, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital</University>
</Universities>
<Countries>
<Country>India</Country>
</Countries>
<EMAILS>
<Email></Email>
</EMAILS>
</AUTHOR>
    </AUTHORS>
    <KEYWORDS>
        <KEYWORD><KeyText>Acute abdomen</KeyText></KEYWORD><KEYWORD><KeyText>Cervical cancer</KeyText></KEYWORD><KEYWORD><KeyText>Perforation</KeyText></KEYWORD><KEYWORD><KeyText>Pyometra</KeyText></KEYWORD>
    </KEYWORDS>
    <PDFFileName>473.pdf</PDFFileName>
    <REFRENCES>
        <REFRENCE>
            <REF>Yildizhan B, Uyar E, Sişmanoğlu A, G&#252;ll&#252;oğlu G, Kavak ZN. Spontaneous perforation of pyometra. Infect Dis Obstet Gynecol. 2006;2006:26786.##Chan LY, Lau TK, Wong SF, Yuen PM. Pyometra. What is its clinical significance? J Reprod Med. 2001;46(11):952-6.##Iwase F, Shimizu H, Koike H, Yasutomi T. Spontaneously perforated pyometra presenting as diffuse peritonitis in older females at nursing homes. J Am Geriatr Soc. 2001;49(1):95-6.##Shahid N, Khan H, Onon TS. Perforation of pyometra leading to diffuse peritonitis is not necessarily iatrogenic. J Obstet Gynaecol. 2006;26(1):76-7.##Saha PK, Gupta P, Mehra R, Goel P, Huria A. Spontaneous perforation of pyometra presented as an acute abdomen: a case report. Medscape J Med. 2008;10(1):15.##Geranpayeh L, Fadaei-Araghi M, Shakiba B. Spontaneous uterine perforation due to pyometra presenting as acute abdomen. Infect Dis Obstet Gynecol. 2006;2006:60276.##Babarinsa IA, Campbell OB, Adewole IF. Pyometra complicating cancer of the cervix. Int J Gynaecol Obstet. 1999;64(1):75-6.##Vyas S, Kumar A, Prakash M, Kapoor R, Kumar P, Khandelwal N. Spontaneous perforation of pyome-tra in a cervical cancer patient: a case report and literature review. Cancer Imaging. 2009;9:12-4.##National Comprehensive Cancer Network: your best resource in fight of cancer [Internet]. Washington PA: National Comprehensive Cancer Network; 2011. NCCN Clinical Practice Guidelines in Oncology: Cervical Cancer vol.1; 2011 [cited 2011 Jul 20]. Available from: http://www.nccn.org/profes sionals/physician_gls/PDF/cervical.pdf##</REF>
        </REFRENCE>
    </REFRENCES>
</ARTICLE>

    </ARTICLES>
  </JOURNAL>
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