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Testosterone morning values were significantly higher than evening values (236 vs. 145 pg/ml, P = 0.009). Evening testosterone was significantly higher in depressive males, according to both MADRS (P = 0.028) and BDI (P = 0.036). Having depression increased the likelihood of being in the highest third of testosterone levels (BDI P = 0.021; MADRS P = 0.018). Positive correlation was between total BDI score and elevated evening testosterone with and without psychotropics (P = 0.017; P = 0.002). Correlation was between elevated evening cortisol and evening testosterone levels (P = 0.021) though simultaneous testing did not increase specificity of detecting depression. testosterone.

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Nobiletin (NOB) is one of the polymethoxyflavones mainly found in citrus fruits. Aromatase or cytochrome P450 (CYP19) enzyme catalyzes the last and rate-limiting step in estrogen biosynthesis. This study was carried out to investigate the effect of NOB on the activity and expression of aromatase and compare this property with letrozole (LET) as aromatase inhibitor in MCF-7 breast cancer cell line. The cell viability was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assays. Aromatase enzyme activity based on the conversion of androgenic substrate testosterone into 17β-Estradiol was determined. CYP19 gene expression was measured by quantitative real-time PCR. MTT assays demonstrated that NOB at a concentration of 100 μM decreased cell viability in a time dependent manner (P < 0.05). NOB significantly inhibits aromatase at 0.1 μM concentration (P = 0.013) while other concentration had no effect. Treatment with 10 μM and 1 μM of NOB for 48 h significantly increased (P = 0.001) and decreased (P = 0.02) relative aromatase expression, respectively. So, combination of LET and NOB had no effect on aromatase. The present study showed for the first time that NOB could decrease activity and expression of aromatase at low concentration in MCF-7 breast cancer cells. testosterone.

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The Registry of Hypogonadism in Men (RHYME) was designed as a multi-national, longitudinal disease registry of men diagnosed with hypogonadism (HG) at 25 clinical sites in six European countries. Data collection included a complete medical history, physical examination, blood sampling and patient questionnaires at multiple study visits over 2-3 years. Independent adjudication was performed on all mortalities and CV outcomes. testosterone.

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Testosterone synthesis and male fertility are the results of the perfect coordination of the hypothalamic-pituitary-gonadal axis. A negative feedback finely controls the secretion of hormones at the 3 levels. Congenital or acquired disturbance at any level leads to an impairment of reproductive function and the clinical syndrome of hypogonadism. In some cases, this condition is reversible. Once the diagnosis is made, testosterone replacement therapy is the standard therapy; however, novel therapies may improve spermatogenesis while elevating testosterone levels. testosterone.

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Varicocele is a pathologic enlargement of the pampiniform venous plexus within the spermatic cord, a condition that is a common cause of impaired sperm production and decreased quality of sperm. While varicocele is the most common surgically correctable risk factor for male infertility, not all males with varicocele experience infertility. In fact, most men with varicocele have normal spermatogenesis. Despite its prevalence, the molecular mechanisms of varicocele and its effect on testicular function are yet to be completely understood. We postulate that men with varicocele-associated infertility could have preexisting genetic lesions or defects in molecular mechanisms that make them more susceptible to varicocele-mediated testicular injury affecting spermatogenesis. testosterone.

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Some men between the ages 45 and 60 years develop complaints and symptoms reminiscent of menopausal complaints in women. So, parallels were sought between the changes in female and male endocrinology during that period of life. Indeed, men do show a decline of serum testosterone from age 40 to 50 years onwards but it is a slow decline of 1-2% per year and over time it may amount to hypogonadism. The mechanism of a decline in serum testosterone in men does not resemble the menopause; it is partially an aging neuroendocrine system with a less efficient testosterone production but equally or more important, the result of inhibition of testosterone production by metabolic factors in relation to visceral obesity. These effects are in part reversible with weight loss. A hypogonadal state in aging men has deleterious effects. Mortality of all causes is highest in men with low testosterone impacting on their metabolic state leading to diabetes mellitus, cardiovascular disease, osteoporosis, and sexual dysfunction. Normalization of testosterone in aging hypogonadal men has a beneficial effect on the above pathologies. The fear that testosterone treatment of elderly men would lead to prostate disease has not been substantiated in studies. So, while men do not have a ‘menopause’, testosterone deficiency in old age deserves serious attention. testosterone.


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