13 research outputs found
Adenomyotic Cyst in a 25-Year-Old Woman: Case Report
Adenomyotic cysts are uncommon findings, usually in the context of diffuse adenomyosis and <5 mm in diameter. Herein we report a 4.5-cm adenomyotic cyst in a 25-year-old nulliparous woman with severe dysmenorrhea and pelvic pain. Transvaginal ultrasonography and magnetic resonance imaging revealed a well-circumscribed hypoechogenic mass in the posterior uterine wall, well separated from the uterine cavity. Pathologic analysis demonstrated that the cyst was lined with endometrial epithelium and stroma and was surrounded by smooth muscle hyperplasia. In the literature, we found 30 reports of cysts with similar characteristics. Because this cyst has not been clearly defined, it has been called by various names including adenomyotic cyst, cystic adenomyosis, and cystic adenomyoma. We believe this lesion should not be called an adenomyoma, but is more correctly called an adenomyotic cyst or, depending on age at onset, a juvenile adenomyotic cyst
Effects of Nandrolone Stimulation on Testosterone Biosynthesis in Leydig Cells
Anabolic androgenic steroids (AAS) are among the drugs most used by athletes for improving physical performance, as well as for aesthetic purposes. A number of papers have showed the side effects of AAS in different organs and tissues. For example, AAS are known to suppress gonadotropin-releasing hormone, luteinizing hormone, and follicle-stimulating hormone. This study investigates the effects of nandrolone on testosterone biosynthesis in Leydig cells using various methods, including mass spectrometry, western blotting, confocal microscopy and quantitative real-time PCR. The results obtained show that testosterone levels increase at a 3.9μM concentration of nandrolone and return to the basal level a 15.6μM dose of nandrolone. Nandrolone-induced testosterone increment was associated with upregulation of the steroidogenic acute regulatory protein (StAR) and downregulation of 17a-hydroxylase/17, 20 lyase (CYP17A1). Instead, a 15.6μM dose of nandrolone induced a down-regulation of CYP17A1. Further in vivo studies based on these data are needed to better understand the relationship between disturbed testosterone homeostasis and reproductive system impairment in male subjects
Nandrolone decanoate interferes on testosterone biosynthesis and alters blood-testis barrier.
Nandrolone decanoate (ND) is a synthetic testosterone analogue considered one of the most commonly abused anabolic androgenic steroids by adolescents and athletes. ND is alleged to promote an increase in muscle mass and improves both physical appearance and sporting performance, but ND abuse is often associated with serious adverse effects, interfering with the endocrine system and the reproductive system. In a previous study, we demonstrated that ND treatment of Leydig cells interferes with the biosynthesis of testosterone in a dose increase-dependent fashion (1). As a consequence of the results obtained in vitro, in this study an animal model was utilized to better understand the side effects of ND administration in sedentary and trained mice. A group of mice underwent endurance training while another set led a sedentary lifestyle. All experimental groups were treated with either ND or peanut oil at different doses for 6 weeks. Testosterone serum levels were measured via liquid chromatography–mass spectrometry. Western blot analysis and quantitative real-time PCR were utilized to determine gene and protein expression levels of the primary enzymes implicated in testosterone biosynthesis and gene expression levels of the blood–testis barrier (BTB) components. Immunohistochemistry and immunofluorescence were conducted for testicular morphological evaluation. The study demonstrated that moderate to high doses of ND induced a diminished serum testosterone level and altered the expression level of the key steroidogenic enzymes involved in testosterone biosynthesis. At the morphological level, ND induced degradation of the BTB by targeting the tight junction protein-1 (TJP1). ND stimulation deregulated metalloproteinase-9, metalloproteinase-2 (MMP-2) and the tissue inhibitor of MMP-2. Moreover, ND administration resulted in a mislocalization of mucin-1. In conclusion, ND abuse induces a decline in testosterone production that is unable to regulate the internalization and redistribution of TJP1 and may induce the deregulation of other BTB constituents via the inhibition of MMP-2. ND may well be considered as both a potential inducer of male infertility and a potential risk factor to a low endogenous bioavailable testosterone
ASSOCIAZIONE TRA ATEROSCLEROSI CAROTIDEA, DISFUNZIONE ENDOTELIALE E STEATOSI EPATICA IN UNA POPOLAZIONE CON SINDROME METABOLICA.
Significato clinico e prognostico dell'aterosclerosi carotidea nella valutazione del rischio cardiovascolare globale
Effects of mild aerobic exercise training on the diaphragm in mdx mice
Mild endurance exercise training positively affects limb skeletal muscle in the mdx mice model of Duchenne Muscular Dystrophy (DMD). However, few and controversial data are available on the effects of mild exercise training on the diaphragm of mdx mice. The diaphragm was examined in mdx and wild type mice either under sedentary conditions (mdx-SD, WT-SD) or during mild exercise training (mdx-EX, WT-EX). At baseline and after 30 and 45 days of training (5 d/wk for 6 weeks), diaphragm muscle morphology and Cx39 protein were assessed. In addition, tissue levels of the chaperonin Hsp60 were measured at the same time points in gastrocnemius, quadriceps and diaphragm in each experimental group. Although morphological analysis showed unchanged total area of necrosis/regeneration in the diaphragm after training, there was a trend for regeneration areas to be larger than necrosis areas. However, the levels of Cx39 protein, a marker associated with active degeneration-regeneration process in damaged muscle were similar in the diaphragm of mdx-EX and mdx-SD mice. The diaphragm, but not limb muscles, of both trained and sedentary mdx mice showed decreased Hsp60 expression at 45 days, suggesting exhaustion of potentially protective mechanisms in the diaphragm similar to previous findings in lung epithelium. Compared to the positive effects of exercise training previously observed in limb skeletal muscles, the diaphragm showed little change after training