Objectives:The aim of the present study was to explore the effects of three different types of alpha-1 adrenoceptor blockers (a1-blocker) on lower urinary tract symptoms (LUTS), erectile dysfunction (ED) and ejaculatory dysfunction (EjD) in patients with benign prostatic hyperplasia. Methods: A total of 136 male LUTS patients aged 50-80 years with International Prostate Symptom Score (IPSS) Ն8 were enrolled. They were divided into three groups. Group S received silodosin at 4 mg twice a day; group T received tamsulosin at 0.2 mg once a day; and group N received naftopidil at 50 mg once a day. Assessment included IPSS, quality of life indexes (QOL), International Index of Erectile Function (IIEF-5), an ejaculation questionnaire, Qmax and post-void residual urine volume (PVR). These parameters were recorded at baseline, and at 1 and 3 months after treatment had ended. Results: Mean IPSS and Qmax significantly improved after treatment in all groups without any significant difference among them. As for the IIEF-5 score, only group N significantly improved at 1 and 3 months. After treatment, 2.6 and 2.4% of patients complained of a de novo reduced volume of ejaculation in both groups T and N, respectively. Ten out of 41 patients (24.4%) complained of a total absence of antegrade ejaculation in group S after treatment. Conclusions: All three types of a1-blockers provided an objective and subjective improvement of LUTS in the present study population. However, erectile function only improved in patients treated with naftopidil and a higher rate of EjD was observed in those receiving silodosin. Because of their variable effects, we should consider the sexual dimension when prescribing a1-blockers for LUTS.
Glucocorticoids, the most downstream effectors of the hypothalamus-pituitary-adrenal axis, are one of main mediators of the stress reaction. Indeed, exposure to high levels of stresstriggered glucocorticoids is detrimental to brain development associated with abnormal behaviors in experimental animals and the risk of psychiatric disorders in humans. Despite the wealth of this knowledge, the cellular and molecular mechanisms underlying the detrimental effects of glucocorticoids on brain development remain unclear. Here, we show that excess glucocorticoids retard the radial migration of post-mitotic neurons during the development of the cerebral cortex, and identify an actin regulatory protein, caldesmon, as the glucocorticoids' main target. The upregulation of caldesmon expression is mediated by glucocorticoid receptor-dependent transcription of the CALD1 gene encoding caldesmon. This upregulated caldesmon negatively controls the function of myosin II, leading to changes in cell shape and migration. The depletion of caldesmon in vivo impairs radial migration. The overexpression of caldesmon also causes delayed radial migration during cortical development, mimicking the excessive glucocorticoid-induced retardation of radial migration. We conclude that an appropriate range of caldesmon expression is critical for radial migration, and that its overexpression induced by excess glucocorticoid retards radial migration during cortical development. Thus, this study provides a novel insight into the underlying mechanism of glucocorticoid-related neurodevelopmental disorders.
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