1,721,206 research outputs found

    Prevention of Male Infertility: From Childhood to Adulthood

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    Many andrological pathologies seen in adults, including infertility, actually arise at a younger age, due to the strong susceptibility and vulnerability of the male gonad to external insults, starting from age of gestation and during all growth phases. Although three main phases are particularly susceptible for subsequent normal testis development and function (the intrauterine phase, the neonatal phase comprising the so-called “minipuberty”, and puberty), even during infancy, when the testes are apparently “sleeping”, damaging causes with permanent effects on testicular function can occur. Since a great number of risk factors for future male fertility might already be present at young ages, the possibility for early diagnosis and prevention of negative sequelae is unfortunately low if systematic health and information programmes are lacking. Indeed, interventions focused on childhood and adolescence could have a profound effect on sexual and reproductive health later in life. To do this, multiple level interventions are necessary

    Testicular Function and Skeletal Alterations

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    Although testosterone is the major testicular factor that acts on the bone and allows for skeletal growth and bone mass accrual during development and puberty and maintain bone metabolism during adulthood, other functions of the Leydig cells are important in the testis-bone crosstalk. These cells in fact contribute to bone homeostasis also by producing the peptide hormone INSL3, which has an anabolic role acting on osteoblasts and osteocytes, and by expressing CYP2R1, an enzyme that converts the inactive cholecalciferol to 25-hydroxy vitamin D. All these functions are under the control of the pituitary LH hormone. Disturbed Leydig cell function, as observed in the primary, secondary, and subclinical hypogonadism, is associated with reduction of INSL3, 25-hydroxy vitamin D, and testosterone, therefore increasing the risk of osteoporosis. Leydig cell function is also regulated by the skeleton, as osteocalcin produced by osteoblasts acts in parallel to LH to stimulate testosterone and 25-hydroxy vitamin D production

    The INSL3-LGR8 hormonal system in humans: Testicular descent, cryptorchidism and testicular functions

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    INSL3 is a member of the relaxin-insulin family, and it is expressed in pre- and postnatal Leydig cells of the testis in a variety of mammalian species, including humans. This peptide affects testicular descent during embryonic development by acting on gubernaculum via its specific receptor LGR8. From initial animal data showing the cryptorchid phenotype of Insl3/Lgr8 mutants, an extensive search for mutations in the INSL3 and LGR8 genes was undertaken in human patients with cryptorchidism. Six mutations in INSL3 and one in LGR8 genes have been detected exclusively in men with undescended testes, with an overall frequency of mutation in cryptorchid or ex-cryptorchid men of 4-5%. Definitive proofs of a causative role for many of these mutations are still lacking. However, the specific association with cryptorchidism actually suggests that they might be responsible for the phenotype. Apart from the role in testicular descent and cryptorchidism, more recent data suggest additional yet unidentified endocrine and paracrine actions in adults. INSL3 is produced constitutively, but in a differentiation-dependent manner by the adult Leydig cells, and its production and secretion is dependent on LH. INSL3 circulates at high concentrations in serum of adult males and it is increasingly used as a specific marker of Leydig cell differentiation and function. Research is needed to clarify the possible paracrine role of the INSL3/LGR8 system in the testis and ovary, and endocrine effects in many tissues where LGR8 expression has been identified. © 2005 Bentham Science Publishers Ltd

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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