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        <title>Reproductive Biology and Endocrinology - Most accessed articles</title>
        <link>http://www.rbej.com</link>
        <description>The most accessed research articles published by Reproductive Biology and Endocrinology</description>
        <dc:date>2010-03-06T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.rbej.com/content/1/1/110" />
                                <rdf:li rdf:resource="http://www.rbej.com/content/4/1/59" />
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        <item rdf:about="http://www.rbej.com/content/1/1/110">
        <title>Assessment of fetal intracranial pathologies first demonstrated late in pregnancy: cell proliferation disorders</title>
        <description>A considerable number of central nervous system pathologies remain undiagnosed during the first two trimesters of pregnancy. This group of disorders includes anomalies of brain proliferation, migration and cortical organization. Due to the fact that a detailed ultrasound examination of the fetal brain is usually not performed during the third trimester the diagnosis of these disorders is usually only made in families with a previously affected child or in many cases be mere chance. In this article we review the feasibility of prenatal diagnosis of disorders of brain proliferation: microcephaly, macrocephaly, hemimegalencephaly and neoplastic and non-neoplastic abnormal cell types. We discuss the differential diagnosis and offer a stepwise approach to the diagnosis of the more common disorders.</description>
        <link>http://www.rbej.com/content/1/1/110</link>
                <dc:creator>Gustavo Malinger</dc:creator>
                <dc:creator>Dorit Lev</dc:creator>
                <dc:creator>Tally Lerman-Sagie</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2003, 1:110</dc:source>
        <dc:date>2003-11-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-1-110</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>1</prism:volume>
        <prism:startingPage>110</prism:startingPage>
        <prism:publicationDate>2003-11-14T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.rbej.com/content/4/1/59">
        <title>Molecular patterns of sex determination in the animal kingdom: a comparative study of the biology of reproduction</title>
        <description>Determining sexual fate is an integral part of reproduction, used as a means to enrich the genome. A variety of such regulatory mechanisms have been described so far and some of the more extensively studied ones are being discussed.For the insect order of Hymenoptera, the choice lies between uniparental haploid males and biparental diploid females, originating from unfertilized and fertilized eggs accordingly. This mechanism is also known as single-locus complementary sex determination (slCSD). On the other hand, for Dipterans and Drosophila melanogaster, sex is determined by the ratio of X chromosomes to autosomes and the sex switching gene, sxl. Another model organism whose sex depends on the X:A ratio, Caenorhabditis elegans, has furthermore to provide for the brief period of spermatogenesis in hermaphrodites (XX) without the benefit of the &quot;male&quot; genes of the sex determination pathway.Many reptiles have no discernible sex determining genes. Their sexual fate is determined by the temperature of the environment during the thermosensitive period (TSP) of incubation, which regulates aromatase activity. Variable patterns of sex determination apply in fish and amphibians. In birds, while sex chromosomes do exist, females are the heterogametic (ZW) and males the homogametic sex (ZZ). However, we have yet to decipher which of the two (Z or W) is responsible for the choice between males and females.In mammals, sex determination is based on the presence of two identical (XX) or distinct (XY) gonosomes. This is believed to be the result of a lengthy evolutionary process, emerging from a common ancestral autosomal pair. Indeed, X and Y present different levels of homology in various mammals, supporting the argument of a gradual structural differentiation starting around the SRY region. The latter initiates a gene cascade that results in the formation of a male. Regulation of sex steroid production is also a major result of these genetic interactions. Similar observations have been described not only in mammals, but also in other vertebrates, emphasizing the need for further study of both normal hormonal regulators of sexual phenotype and patterns of epigenetic/environmental disruption.</description>
        <link>http://www.rbej.com/content/4/1/59</link>
                <dc:creator>Panagiota Manolakou</dc:creator>
                <dc:creator>Giagkos Lavranos</dc:creator>
                <dc:creator>Roxani Angelopoulou</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2006, 4:59</dc:source>
        <dc:date>2006-11-13T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-4-59</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>4</prism:volume>
        <prism:startingPage>59</prism:startingPage>
        <prism:publicationDate>2006-11-13T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.rbej.com/content/8/1/21">
        <title>Management of the infertile couple: an evidence-based protocol </title>
        <description>Background:
Infertility is defined as inability of a couple to conceive naturally after one year of regular unprotected sexual intercourse. It remains a major clinical and social problem, affecting perhaps one couple in six. Evaluation usually starts after 12 months; however it may be indicated earlier. The most common causes of infertility are: male factor such as sperm abnormalities, female factor such as ovulation dysfunction and tubal pathology, combined male and female factors and unexplained infertility.Objectives: The aim of this study is to provide the healthcare professionals an evidence-based management protocol for infertile couples away from medical information overload.
Methods:
A comprehensive review where the literature was searched for &quot;Management of infertility and/or infertile couples&quot; at library website of University of Bristol (MetaLib) by using a cross-search of different medical databases besides the relevant printed medical journals and periodicals. Guidelines and recommendations were retrieved from the best evidence reviews such as that from the American College of Obstetricians and Gynaecologists (ACOG), American Society for Reproductive Medicine (ASRM), Canadian Fertility and Andrology Society (CFAS), and Royal College of Obstetricians and Gynaecologists (RCOG).
Results:
A simple guide for the clinicians to manage the infertile couples.
Conclusions:
The study deploys a new strategy to translate the research findings and evidence-base recommendations into a simplified focused guide to be applied on routine daily practice. It is an approach to disseminate the recommended medical care for infertile couple to the practicing clinicians.</description>
        <link>http://www.rbej.com/content/8/1/21</link>
                <dc:creator>Remah Kamel</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2010, 8:21</dc:source>
        <dc:date>2010-03-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-8-21</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>21</prism:startingPage>
        <prism:publicationDate>2010-03-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.rbej.com/content/8/1/18">
        <title>Improved pregnancy rate with administration of hCG after intrauterine insemination: a pilot study</title>
        <description>Background:
In natural cycles, women conceive when intercourse takes place during a six-day period ending on the day of ovulation. The current practice in intrauterine insemination (IUI) cycles is to perform the IUI 24-36 hours after the hCG administration, when the ovulation is already imminent. In this study hCG was administered after the IUI, which more closely resembles the fertilisation process in natural cycles.
Methods:
All the IUIs performed since the beginning of 2007 were analysed retrospectively. Our standard protocol has been to perform the IUI 24-32 hours after hCG administration. From the end of 2008, we started to inject hCG after the IUI at random. The main outcome measure was the result of a urinary pregnancy test. Generalized Estimating Equations (GEE) was used to identify independent factors affecting the cycle outcome.
Results:
The analysis included 228 cycles with hCG administered before and 104 cycles hCG administered after the IUI. The pregnancy rates were 10.9% and 19.6% (P = 0.040), respectively. Independent factors (OR, 95% CI) affecting the cycle outcome were sperm count (2.65, 1.20-5.81), number of follicles &gt; 16 mm at IUI (2.01, 1.07-3.81) and the time of hCG administration (2.21, 1.16-4.19).
Conclusion:
Improved pregnancy rate was observed with administration of hCG after IUI.</description>
        <link>http://www.rbej.com/content/8/1/18</link>
                <dc:creator>Ilkka Jarvela</dc:creator>
                <dc:creator>Juha Tapanainen</dc:creator>
                <dc:creator>Hannu Martikainen</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2010, 8:18</dc:source>
        <dc:date>2010-02-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-8-18</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>18</prism:startingPage>
        <prism:publicationDate>2010-02-23T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.rbej.com/content/8/1/20">
        <title>Doxorubicin-induced ovarian toxicity</title>
        <description>Background:
Young cancer patients may occasionally face infertility and premature gonadal failure. Apart from its direct effect on follicles and oocytes, chemotherapy may induce ovarian toxicity via an impact on the entire ovary. The role of doxorubicin in potential ovarian failure remains obscure. Our intention was to elucidate doxorubicin-related toxicity within ovaries.
Methods:
Female mice were injected intraperitoneally with 7.5 or 10 mg/kg doxorubicin and their ovaries were visualized in vivo by high resolution MRI, one day and one month following treatment. Ovaries of other treated mice were excised and weighed at the same post-treatment intervals. Ovarian histological sections were stained for TUNEL or active caspase-3 and follicles were counted and categorized. Ovulation rates were evaluated in superovulated female mice treated with doxorubicin.
Results:
A single injection of doxorubicin resulted in a major reduction in both ovarian size and weight that lasted even one month post treatment. A dramatic reduction in ovulation rate was observed one week after treatment, followed by a partial recovery at one month. Histological examination revealed positive staining of TUNEL and active caspase-3. We observed a significant reduction in the population of secondary and primordial follicles one month following treatment.
Conclusions:
Our results may imply a mechanism of chemotherapy-induced ovarian toxicity, manifested by reduced ovulation and accompanied by a reduction in ovarian size, caused probably by an acute insult to the ovary.</description>
        <link>http://www.rbej.com/content/8/1/20</link>
                <dc:creator>Irit Ben-Aharon</dc:creator>
                <dc:creator>Hadas Bar-Joseph</dc:creator>
                <dc:creator>Galia Tzarfaty</dc:creator>
                <dc:creator>Lital Kuchinsky</dc:creator>
                <dc:creator>Shulamith Rizel</dc:creator>
                <dc:creator>Salomon Stemmer</dc:creator>
                <dc:creator>Ruth Shalgi</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2010, 8:20</dc:source>
        <dc:date>2010-03-04T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-8-20</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>20</prism:startingPage>
        <prism:publicationDate>2010-03-04T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.rbej.com/content/8/1/14">
        <title>Short term hypothyroidism affects ovarian function in the cycling rat</title>
        <description>Background:
Rats made hypothyroid with propilthyouracil start showing abnormal cycling on the second cycle after the start of the treatment, with a high proportion of spontaneous pseudopregnancies and reduced fertility.
Methods:
To investigate some of the mechanisms involved in these reproductive abnormalities, hypothyroidism was induced in virgin rats by propilthyouracil (0.1 g/L in the drinking water) and we determined circulating hormones by radioimmunoassay and whole ovary expression of ovarian hormone receptors, growth factors and steroidogenic enzymes using semi-quantitative RT-PCR.The study was performed on days 6 to 9 of treatment, corresponding to diestrus I (at 20.00-22.00 h), diestrus II (at 20.00-22.00 h), proestrus and estrus (both at 8.00-10.00 h and 20.00-22.00 h) of the second estrous cycle after beginning propilthyouracil treatment. Another group of rats was mated on day 8 and the treatment continued through the entire pregnancy to evaluate reproductive performance.
Results:
Hypothyroidism increased circulating prolactin and estradiol on estrus 5 to 7-fold and 1.2 to 1.4-fold respectively. Growth hormone and insulin-like growth factor 1 diminished 60 and 20% respectively on proestrus morning. Hypothyroidism doubled the ovarian mRNA contents of estrogen receptor-beta on proestrus and estrus evenings, cyp19A1 aromatase mRNA on estrus evening and of growth hormone receptor on proestrus evening. Hypothyroidism did not influence ovulation rate or the number of corpora lutea at term, but a diminished number of implantation sites and pups per litter were observed (Hypothyroid: 11.7 +/- 0.8 vs. Control: 13.9 +/- 0.7).
Conclusions:
Short term hypothyroidism alters normal hormone profile in the cycling rat increasing the expression of estrogen receptor-beta and cyp19A1 aromatase on estrus, which in turn may stimulate estradiol and prolactin secretion, favouring corpus luteum survival and the subsequent instauration of pseudopregnancy.</description>
        <link>http://www.rbej.com/content/8/1/14</link>
                <dc:creator>Maria Hapon</dc:creator>
                <dc:creator>Carlos Gamarra-Luques</dc:creator>
                <dc:creator>Graciela Jahn</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2010, 8:14</dc:source>
        <dc:date>2010-02-11T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-8-14</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>14</prism:startingPage>
        <prism:publicationDate>2010-02-11T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.rbej.com/content/2/1/14">
        <title>Fundulus heteroclitusgonadotropins.5: Small scale chromatographic fractionation of pituitary extracts into components with different steroidogenic activities using homologous bioassays</title>
        <description>Fractionation and characterization of gonadotropins (GtH) from Fundulus heteroclitus pituitary extracts were carried out using a biocompatible liquid chromatographic procedure (Pharmacia FPLC system). Chromatographic fractions were monitored for gonadotropic activities (induction of oocyte maturation and steroid production) using homologous follicle bioassays in vitro. Size-exclusion chromatography eluted gonadotropic activity in one major protein peak (Mr ~ 30,000). Anion-exchange and hydrophobic-interaction chromatography (HIC) yielded two distinct peaks of 17beta-estradiol (E2)- and 17alpha-hydroxy,20beta-dihydroprogesterone (DHP)-promoting activity with associated oocyte maturation. Two-dimensional chromatography (chromatofocusing followed by HIC) resolved pituitary extracts into two active fractions; both induced E2 synthesis, but one was relatively poor in eliciting DHP and testosterone production. Thus, using homologous bioassays, at least two quantitatively different gonadotropic (steroidogenic) activities: an E2-promoting gonadotropin (GtH I-like) and a DHP-promoting gonadotropin (GtH II-like), which has a lower isoelectric point but greater hydrophobicity than the former, can be distinguished from F. heteroclitus pituitaries by a variety of chromatographic procedures. This study complements previous biochemical and molecular data in F. heteroclitus and substantiates the duality of GtH function in a multiple-spawning teleost.</description>
        <link>http://www.rbej.com/content/2/1/14</link>
                <dc:creator>Yu-Wai Lin</dc:creator>
                <dc:creator>Teresa Petrino</dc:creator>
                <dc:creator>Robin Wallace</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2004, 2:14</dc:source>
        <dc:date>2004-03-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-2-14</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>14</prism:startingPage>
        <prism:publicationDate>2004-03-24T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.rbej.com/content/3/1/28">
        <title>Role of oxidative stress in female reproduction</title>
        <description>In a healthy body, ROS (reactive oxygen species) and antioxidants remain in balance. When the balance is disrupted towards an overabundance of ROS, oxidative stress (OS) occurs. OS influences the entire reproductive lifespan of a woman and even thereafter (i.e. menopause). OS results from an imbalance between prooxidants (free radical species) and the body&apos;s scavenging ability (antioxidants). ROS are a double-edged sword &#8211; they serve as key signal molecules in physiological processes but also have a role in pathological processes involving the female reproductive tract. ROS affect multiple physiological processes from oocyte maturation to fertilization, embryo development and pregnancy. It has been suggested that OS modulates the age-related decline in fertility. It plays a role during pregnancy and normal parturition and in initiation of preterm labor. Most ovarian cancers appear in the surface epithelium, and repetitive ovulation has been thought to be a causative factor. Ovulation-induced oxidative base damage and damage to DNA of the ovarian epithelium can be prevented by antioxidants. There is growing literature on the effects of OS in female reproduction with involvement in the pathophsiology of preeclampsia, hydatidiform mole, free radical-induced birth defects and other situations such as abortions. Numerous studies have shown that OS plays a role in the pathoysiology of infertility and assisted fertility. There is some evidence of its role in endometriosis, tubal and peritoneal factor infertility and unexplained infertility. This article reviews the role OS plays in normal cycling ovaries, follicular development and cyclical endometrial changes. It also discusses OS-related female infertility and how it influences the outcomes of assisted reproductive techniques. The review comprehensively explores the literature for evidence of the role of oxidative stress in conditions such as abortions, preeclampsia, hydatidiform mole, fetal embryopathies, preterm labour and preeclampsia and gestational diabetes. The review also addresses the growing literature on the role of nitric oxide species in female reproduction. The involvement of nitric oxide species in regulation of endometrial and ovarian function, etiopathogenesis of endometriosis, and maintenance of uterine quiescence, initiation of labour and ripening of cervix at parturition is discussed. Complex interplay between cytokines and oxidative stress in the etiology of female reproductive disorders is discussed. Oxidant status of the cell modulates angiogenesis, which is critical for follicular growth, corpus luteum formation endometrial differentiation and embryonic growth is also highlighted in the review. Strategies to overcome oxidative stress and enhance fertility, both natural and assisted are delineated. Early interventions being investigated for prevention of preeclampsia are enumerated. Trials investigating combination intervention strategy of vitamin E and vitamin C supplementation in preventing preeclampsia are highlighted. Antioxidants are powerful and there are few trials investigating antioxidant supplementation in female reproduction. However, before clinicians recommend antioxidants, randomized controlled trials with sufficient power are necessary to prove the efficacy of antioxidant supplementation in disorders of female reproduction. Serial measurement of oxidative stress biomarkers in longitudinal studies may help delineate the etiology of some of the diosorders in female reproduction such as preeclampsia.</description>
        <link>http://www.rbej.com/content/3/1/28</link>
                <dc:creator>Ashok Agarwal</dc:creator>
                <dc:creator>Sajal Gupta</dc:creator>
                <dc:creator>Rakesh Sharma</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2005, 3:28</dc:source>
        <dc:date>2005-07-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-3-28</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>3</prism:volume>
        <prism:startingPage>28</prism:startingPage>
        <prism:publicationDate>2005-07-14T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.rbej.com/content/8/1/19">
        <title>Effects of luteectomy in early pregnancy on the maintenance of gestation and plasma progesterone concentrations in the viviparous temperate lizard Barisia imbricata imbricata</title>
        <description>Background:
Several studies have shown that the corpus luteum is the principal source of progesterone during the gravidity period in reptiles; however, its participation in the maintenance of gestation in the viviparous squamata is in dispute. The effects of ovariectomy or luteectomy vary according to the species and the time at which the procedure is performed. In this paper, we describe the effects of luteectomy during early pregnancy on the maintenance of gestation and progesterone concentrations in the temperate Mexican viviparous lizard Barisia imbricata imbricata.
Methods:
Twenty-four lizards were subjected to three different treatments: luteectomy, sham luteectomy or non-surgical treatment, and blood samples were obtained before and after surgical treatment at different stages of gestation to determine the effects of luteectomy on the maintenance of gestation and progesterone concentrations.
Results:
Spontaneous abortion was not observed in any of the females. However, luteectomy provoked abnormal parturition and a significant reduction in the number of young born alive. Parturition was normal in untreated females as well as those submitted to sham luteectomy. The surgical treatment also caused a significant reduction in progesterone concentrations in luteectomised females during early and middle gestation. However, no significant differences in hormone concentrations were observed among the three groups during late gestation or immediately post-parturition.
Conclusions:
Our observations indicate that the presence of the corpus luteum is not necesary for the maintenance of gestation, but that it does participate in parturition control. Moreover, the corpus luteum of the viviparous lizard B. i. imbricata produces progesterone, at least during the first half of pregnancy, and that an extra-ovarian source of progesterone must maintain gestation in the absence of luteal tissue.</description>
        <link>http://www.rbej.com/content/8/1/19</link>
                <dc:creator>Martin Martinez-Torres</dc:creator>
                <dc:creator>Marta Hernandez-Caballero</dc:creator>
                <dc:creator>Juana Alba Luis-Diaz</dc:creator>
                <dc:creator>Guadalupe Ortiz-Lopez</dc:creator>
                <dc:creator>Mario Cardenas-Leon</dc:creator>
                <dc:creator>Leticia Moreno-Fierros</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2010, 8:19</dc:source>
        <dc:date>2010-02-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-8-19</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>19</prism:startingPage>
        <prism:publicationDate>2010-02-25T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.rbej.com/content/8/1/17">
        <title>Evaluation of the leptin receptor in human spermatozoa</title>
        <description>Background:
Leptin, a 167 amino acid peptide hormone, profoundly effects reproduction exerting its biological effects via interaction with the leptin receptor (ObR) which is widely expressed on peripheral tissues. In this study, we have attempted to assess leptin receptor expression in the spermatozoa of fertile males and those diagnosed with male factor infertility; both at the mRNA or protein levels.
Methods:
Semen samples were collected from fertile males and individuals with male factor infertility. In order to evaluate leptin receptor expression several techniques were utilized, including: reverse transcriptase-polymerase chain reaction (RT-PCR), immunostaining, flow cytometry, and western blotting. Mononuclear cells isolated from volunteers&apos; peripheral blood were used as positive controls for leptin receptor expression.
Results:
leptin receptor was noted on mononuclear cells but we were unable to detect this receptor on spermatozoa at the protein level. Leptin receptor expression was detected on peripheral blood mononuclear cells (PBMCs) as positive controls; however it was not detectable on the spermatozoa of both groups by immunofluorescence microscopy or flow cytometry. Furthermore, positive expression of the ObR long isoform as assessed by RT-PCR was observed in the sperm of only four cases, whereas expression of beta-Actin, a house keeping gene, and HspA2, a testis specific gene, was present in all cases.
Conclusion:
The long isoform of leptin receptor may not be present on human sperm. Species difference may be accounted for diverse reproductive physiology which depends on metabolic requirement. Leptin receptor expression at the mRNA level in some individuals may be related to contamination by other cells in semen.</description>
        <link>http://www.rbej.com/content/8/1/17</link>
                <dc:creator>Leila Hatami-Baroogh</dc:creator>
                <dc:creator>Shahnaz Razavi</dc:creator>
                <dc:creator>Hamid Zarkesh-Esfahani</dc:creator>
                <dc:creator>Marziyeh Tavalaee</dc:creator>
                <dc:creator>Somayeh Tanhaei</dc:creator>
                <dc:creator>Kamran Ghaedi</dc:creator>
                <dc:creator>Mohammad Reza Deemeh</dc:creator>
                <dc:creator>Farzaneh Rabiee</dc:creator>
                <dc:creator>Mohammad Hossein Nasr-Esfahani</dc:creator>
                <dc:source>Reproductive Biology and Endocrinology 2010, 8:17</dc:source>
        <dc:date>2010-02-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1477-7827-8-17</dc:identifier>
        <prism:publicationName>Reproductive Biology and Endocrinology</prism:publicationName>
        <prism:issn>1477-7827</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>17</prism:startingPage>
        <prism:publicationDate>2010-02-23T00:00:00Z</prism:publicationDate>
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