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1.
Fertil Steril ; 95(2): 621-4, 2011 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-21093858

RESUMO

OBJECTIVE: To evaluate a potential association among the hormonal profile, PROGINS polymorphism, and erectile dysfunction (ED) complaints in a large population-based sample in Sao Paulo, Brazil. DESIGN: Population-based questionnaire study. SETTING: Interviews, sleep recording, and blood sample were conducted in a sleep institute. PATIENT(S): The total study participants included 467 men. INTERVENTION(S): General information was obtained through interviews, and a blood sample was collected for hormone levels, DNA extraction, and PROGINS genotyping. MAIN OUTCOME MEASURE(S): The effect of progesterone and the PROGINS polymorphism on the risk of developing ED were measured by questionnaire and blood sample. RESULT(S): Progesterone, prolactin, testosterone, and estradiol levels did not differ between the genotype groups (T1/T1 and T1/T2+T2/T2). No significant genotypic or allelic differences were found between individuals with ED complaints and controls. Multivariate logistic regression analyses including age, body mass index, hypertension, diabetes, apnea-hypopnea index, and genetic ancestry estimation, as well as the PROGINS polymorphism, confirmed the lack of association between the T2 allele carriers and the risk of ED (odds ratio = 0.80; 95% confidence interval = 0.40-1.62). CONCLUSION(S): This is the first study to demonstrate the genotypic and allelic frequencies of the PROGINS polymorphism in a large population-based sample of men. The results do not support a direct role for the PROGINS polymorphism in the risk of developing ED; however, further examination of other variants within PR gene will be necessary to completely rule out an effect.


Assuntos
Disfunção Erétil/genética , Hormônios/sangue , Receptores de Progesterona/genética , Adulto , Idoso , Alelos , Coleta de Dados , Disfunção Erétil/diagnóstico , Disfunção Erétil/epidemiologia , Frequência do Gene , Predisposição Genética para Doença , Genética Populacional , Genótipo , Hormônios/metabolismo , Humanos , Masculino , Metaboloma , Pessoa de Meia-Idade , Isoformas de Proteínas/genética
2.
Fertil Steril ; 95(4): 1379-84, 2011 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-20605140

RESUMO

OBJECTIVE: To evaluate the effect of melatonin both on the ovaries of pinealectomized female rats through histomorphometric analysis and on steroid receptors, proliferating cell nuclear antigen (PCNA), and vascular endothelial growth factor (VEGF) expression. DESIGN: Experimental study. SETTING: Federal University of São Paulo, Brazil. ANIMAL(S): Forty female rats. INTERVENTION(S): Forty rats were divided equally into four groups: GI-vehicle without surgery; GII--surgery without removal of the pineal gland (sham); GIII--pinealectomized with vehicle; and GIV--pinealectomized with melatonin treatment. After treatment for 3 consecutive months, the animals were killed and their ovaries removed for analysis. MAIN OUTCOME MEASURE(S): Estrogen and progesterone receptors, histologic and immunohistochemical analysis. RESULT(S): The GIII samples presented signals of proliferation on ovarian surface epithelium and interstitial cells as well as high expressions of PCNA and VEGF in those structures compared with GI, GII, and GIV. Also, the levels of progesterone receptor (fmol/g) in ovaries of GIII (250.6 ± 32.4) were significantly lower than in those of GI (429.0 ± 23,8), GII (442.3 ± 30.2), and GIV (564.1 ± 78.7). The levels of progesterone in GIII were superior to those in GI, GII, and GIV. CONCLUSION(S): Our findings suggest that melatonin may attenuate proliferation in ovarian structures and increase the number of luteal bodies as well as the levels of progesterone receptor.


Assuntos
Melatonina/fisiologia , Ovário/metabolismo , Glândula Pineal/cirurgia , Antígeno Nuclear de Célula em Proliferação/biossíntese , Receptores de Esteroides/biossíntese , Fator A de Crescimento do Endotélio Vascular/biossíntese , Animais , Células Epiteliais/citologia , Células Epiteliais/metabolismo , Feminino , Regulação da Expressão Gênica , Ovário/citologia , Glândula Pineal/metabolismo , Ligação Proteica/genética , Ratos , Ratos Wistar , Receptores de Esteroides/genética , Transdução de Sinais/genética , Fator A de Crescimento do Endotélio Vascular/genética
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