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1.
Asian Journal of Andrology ; (6): 929-936, 2008.
Artigo em Inglês | WPRIM | ID: wpr-284726

RESUMO

<p><b>AIM</b>To study the effect and mechanism of gonadotrophin-releasing hormone (GnRH) on murine Leydig cell steroidogenesis.</p><p><b>METHODS</b>Purified murine Leydig cells were treated with GnRH-I and -II agonists, and testosterone production and steroidogenic enzyme expressions were determined.</p><p><b>RESULTS</b>GnRH-I and -II agonists significantly stimulated murine Leydig cell steroidogenesis 60%-80% in a dose- and time-dependent manner (P < 0.05). The mRNA expressions of steroidogenic acute regulatory (StAR) protein, P450scc, 3beta-hydroxysteroid dehydrogenase (HSD), but not 17alpha-hydroxylase or 17beta-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase (P < 0.05). However, only 3beta-HSD protein expression was induced by both GnRH agonists, with a 1.6- to 2-fold increase (P < 0.05).</p><p><b>CONCLUSION</b>GnRH directly stimulated murine Leydig cell steroidogenesis by activating 3b-HSD enzyme expression.</p>


Assuntos
Animais , Masculino , Camundongos , 3-Hidroxiesteroide Desidrogenases , Genética , Western Blotting , Separação Celular , Células Cultivadas , Enzima de Clivagem da Cadeia Lateral do Colesterol , Relação Dose-Resposta a Droga , Hormônio Liberador de Gonadotropina , Farmacologia , Células Intersticiais do Testículo , Metabolismo , Camundongos Endogâmicos C57BL , Fosfoproteínas , Genética , RNA , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Maturidade Sexual , Fisiologia , Esteroides , Testosterona
2.
Asian Journal of Andrology ; (6): 856-858, 2007.
Artigo em Inglês | WPRIM | ID: wpr-310441

RESUMO

<p><b>AIM</b>To describe an unusual symptom of benign prostatic hyperplasia (BPH).</p><p><b>METHODS</b>A patient presented to our urology clinic having experienced post-coital gross hematuria for 2 years. He had not experienced lower urinary tract symptoms (LUTS). A series of examinations were performed to determine the source of bleeding.</p><p><b>RESULTS</b>The prostate was defined as the active bleeding source responsible for the patient's post-coital hematuria. Endoscopic fulguration did not alleviate the symptom. The use of dutasteride, a dual inhibitor of 5alpha-reductase, solved the problem.</p><p><b>CONCLUSION</b>This study reports for the first time that post-coital gross hematuria is one of the clinical presentations of BPH, which can be successfully treated with 5alpha-reductase inhibitor.</p>


Assuntos
Humanos , Masculino , Pessoa de Meia-Idade , Inibidores de 5-alfa Redutase , Azasteroides , Usos Terapêuticos , Coito , Fisiologia , Dutasterida , Inibidores Enzimáticos , Usos Terapêuticos , Hematúria , Tratamento Farmacológico , Hiperplasia Prostática , Diagnóstico , Sistema Urinário
3.
Asian Journal of Andrology ; (6): 379-381, 2006.
Artigo em Inglês | WPRIM | ID: wpr-253832

RESUMO

We describe an unusual complication of coital trauma in a 29-year-old man who presented with a 3-year history of hematospermia and post-coital gross hematuria. Using urethroscopy under a semi-tumescent penis, an isolated urethral injury with active bleeding was detected at the prostatic urethra. The patient was successfully treated with transurethral fulguration. We suggest that isolated posterior urethral injury is one of the causes of male coital trauma, which might be asymptomatic when the penis is flaccid but show symptomatic bleeding when the penis is erect.


Assuntos
Adulto , Feminino , Humanos , Masculino , Coito , Ejaculação , Hematúria , Uretra , Ferimentos e Lesões , Doenças Uretrais
4.
Asian Journal of Andrology ; (6): 205-211, 2006.
Artigo em Inglês | WPRIM | ID: wpr-253856

RESUMO

<p><b>AIM</b>To determine the deletion junctions of infertile men in Taiwan with azoospermia factor region c (AZFc) deletions and to evaluate the genotype/phenotype correlation.</p><p><b>METHODS</b>Genomic DNAs from 460 infertile men were examined. Bacterial artificial chromosome clones were used to verify the accuracy of polymerase chain reaction. Deletion junctions of the AZFc region were determined by analysis of sequence-tagged sites and gene-specific markers.</p><p><b>RESULTS</b>Complete AZFc deletions, including BPY2, CDY1 and DAZ genes, were identified in 24 men. The proximal breakpoints were clustered between sY1197 and sY1192, and the distal breakpoints were clustered between sY1054 and sY1125 in all but one of the 24 men. The testicular phenotypes of men with complete AZFc deletion varied from oligozoospermia, to hypospermatogenesis, to maturation arrest.</p><p><b>CONCLUSION</b>We identified a group of infertile men with uniform deletion junctions of AZFc in the Taiwan population. Despite this homogeneous genetic defect in the AZFc region, no clear genotype/phenotype correlation could be demonstrated.</p>


Assuntos
Humanos , Masculino , Povo Asiático , Genética , Sequência de Bases , Cromossomos Humanos Y , Genética , Primers do DNA , Proteína 1 Suprimida em Azoospermia , Deleção de Genes , Loci Gênicos , Infertilidade Masculina , Genética , Proteínas Nucleares , Genética , Oligospermia , Genética , Fenótipo , Reação em Cadeia da Polimerase , Proteínas , Genética , Proteínas de Ligação a RNA , Genética , Proteínas de Plasma Seminal , Genética , Taiwan , Testículo
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