120 results on '"Filippi, Sandra"'
Search Results
102. Blockade of adenosine receptors unmasks a stimulatory effect of ATP on cardiac contractility
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Mantelli, Laura, primary, Amerini, Sandra, additional, Filippi, Sandra, additional, and Ledda, Fabrizio, additional
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- 1993
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103. The inhibitory effect of opioid and α2-adrenoceptor agonists on cardiac sensory neurones is pertussis toxin-insensitive
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Amerini, Sandra, primary, Rubino, Annalisa, additional, Mantelli, Laura, additional, Filippi, Sandra, additional, and Ledda, Fabrizio, additional
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- 1992
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- View/download PDF
104. Testosterone protects from metabolic syndrome-associated prostate inflammation: an experimental study in rabbit.
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Vignozzi, Linda, Morelli, Annamaria, Sarchielli, Erica, Comeglio, Paolo, Filippi, Sandra, Cellai, Ilaria, Maneschi, Elena, Serni, Sergio, Gacci, Mauro, Carini, Marco, Piccinni, Marie-Pierre, Saad, Farid, Adorini, Luciano, Vannelli, Gabriella B., and Maggi, Mario
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TESTOSTERONE ,METABOLIC syndrome ,INFLAMMATION ,BENIGN prostatic hyperplasia ,LABORATORY rabbits ,URINARY tract infections ,HYPOGONADISM - Abstract
Metabolic syndrome (MetS) and benign prostatic hyperplasia (BPH)/lower urinary tract symptoms (LUTS) are often associated. One of their common denominators is hypogonadism. However, testosterone supplementation is limited by concerns for potential prostatic side effects. The objective was to determine whether MetS-associated prostate alterations are prevented by testosterone supplementation. We used a previously described animal model of MetS, obtained by feeding male rabbits a high-fat diet (HFD) for 12 weeks. Subsets of HFD rabbits were treated with testosterone or with the farnesoid X receptor agonist INT-747. Rabbits fed a standard diet were used as controls. HFD-animals develop hypogonadism and all the MetS features: hyperglycemia, glucose intolerance, dyslipidemia, hypertension, and visceral obesity. In addition, HFD-animals show a prostate inflammation. Immunohistochemical analysis demonstrated that HFD-induced prostate fibrosis, hypoxia, and inflammation. The mRNA expression of several proinflammatory (IL8, IL6, IL1b, and TNFa), T lymphocyte (CD4, CD8, Tbet, Gata3, and ROR gt), macrophage (TLR2, TLR4, and STAMP2), neutrophil (lactoferrin), inflammation (COX2 and RAGE), and fibrosis/myofibroblast activation (TGFb, SM22a, aSMA, RhoA, and ROCK1/ROCK2) markers was significantly increased in HFD prostate. Testosterone, as well as INT-747, treatment prevented some MetS features, although only testosterone normalized all the HFD-induced prostate alterations. Interestingly, the ratio between testosterone and estradiol plasma level retains a significant, negative, association with all the fibrosis and the majority of inflammatory markers analyzed. These data highlight that testosterone protects rabbit prostate from MetS-induced prostatic hypoxia, fibrosis, and inflammation, which can play a role toward the development/progression of BPH/LUTS. [ABSTRACT FROM AUTHOR]
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- 2012
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105. Characterization of metabolic syndrome-related morpho-functional changes in the lung and the role of testosterone treatment in an animal model.
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Guarnieri, Giulia, Filippi, Sandra, Pini, Alessandro, Comeglio, Paolo, Cellai, Ilaria, Maggi, Mario, Vignozzi, Linda, and Morelli, Annamaria
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LUNGS , *ANIMAL models in research , *TESTOSTERONE , *MEDICAL sciences , *HIGH-fat diet , *EMBRYOLOGY - Abstract
The article presents a study which explores the characterization of metabolic syndrome-related morpho-functional changes in the lung and the role of testosterone treatment in an animal model. It mentions that metabolic syndrome (MetS), a cluster of metabolic and cardiovascular risk factors strictly linked to unhealthy lifestyle, dietary habit and physical inactivity.
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- 2022
106. Trophic effects induced by α1D-adrenoceptors on endothelial cells are potentiated by hypoxia.
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Vinci, Maria Cristina, Bellik, Lydia, Filippi, Sandra, Ledda, Fabrizio, and Parenti, Astrid
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CATECHOLAMINES ,BETA adrenoceptors ,NEOVASCULARIZATION ,HYPOXEMIA ,ADRENERGIC receptors ,CELL proliferation - Abstract
Catecholamines have been shown to be involved in vascular remodeling through the stimulation of α-adrenoceptors (α
1 -ARs). Recently, it has been demonstrated that catecholamines can stimulate angiogenesis in pathological conditions, even if the mechanisms and the AR subtypes involved still remain unclear. We investigated the influence of hypoxia (3% O2 ) on the ability of picomolar concentrations of phenylephrine (PHE), which are unable to induce any vascular contraction, to induce atrophic effect in human endothelial cells through stimulation of the α1D -subtype ARs. PHE, at picomolar concentrations, significantly promoted pseudocapillary formation from fragments of human mature vessels in vitro. Exposure to hypoxia significantly potentiated this effect, which was inhibited by the selective α1D -AR antagonist BMY-7378 and by the nitric oxide synthase inhibitor L-NAME, suggesting that α1D -ARs were involved in this effect through activation of the nitric oxide pathway. Proliferation and migration of HUVEC were also affected by picomolar PHE concentrations. Again, these effects were significantly potentiated in cells exposed to hypoxia and were inhibited by BMY-7378 and by NG -nitro-L-arginine methyl ester. Conversely, the α1A -AR-selective antagonist (S)-(+)-niguldipine hydrochloride and the α1B -AR antagonist chloroethylclonidine dihydrochloride did not modify endothelial cell migration and proliferation in response to PHE. These results demonstrate that the stimulation of α1D -ARs, triggered by picomolar PHE concentrations devoid of any contractile vascular effects, induces a proangiogenic phenotype in human endothelial cells that is enhanced in a hypoxic environment. The role of α1D -ARs may become more prominent in the adaptive responses to hypoxic vasculature injury. [ABSTRACT FROM AUTHOR]- Published
- 2007
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107. Testosterone Restores Diabetes-Induced Erectile Dysfunction and Sildenafil Responsiveness in Two Distinct Animal Models of Chemical Diabetes.
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Xin-Hua Zhang, Filippi, Sandra, Morelli, Annamaria, Vignozzi, Linda, Luconi, Michaela, Donati, Silvia, Forti, Gianni, and Maggi, Mario
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HYPOGONADISM , *DIABETES complications , *IMPOTENCE , *PHOSPHODIESTERASES , *SILDENAFIL - Abstract
Introduction. Hypogonadism is often associated with diabetes and both conditions represent major risk factors for erectile dysfunction (ED). Aim. To investigate the role of hypogonadism on phosphodiesterase type 5 (PDE5) expression and sildenafil responsiveness in diabetes. Methods. Two different models of experimental diabetes were used: (i) alloxan-induced diabetic rabbit; and (ii) streptozotocin (STZ)-induced diabetic rat. In both experimental models, animals were separated into three groups: control, diabetic, diabetic supplemented with testosterone (T) enanthate. Rabbits were used for “in vitro” experiments. Conversely, each rats group was further subdivided: no further treatment or acute sildenafil dosing (25 mg/kg, 1 hour before “in vivo” electrical stimulation [ES]). Main Outcome Measure. Erectile capacity was evaluated either by “in vitro” contractility study (alloxan-induced diabetic rabbit) and “in vivo” evaluation of erectile response elicited by ES of cavernous nerve (STZ-induced diabetic rats). Also endothelial nitric oxide synthase, neural nitric oxide synthase (nNOS), and PDE5 protein (Western blot) and mRNA (quantitative real-time reverse transcriptase polymerase chain reaction [RT-PCR]) expression were measured in rat penile samples of each group. Results. In both models, hypogonadism was observed, characterized by reduced T and atrophy of androgen-dependent accessory glands. T substitution completely reverted hypogonadism and diabetes-induced penile hyposensitivity to “in vitro” (acetylcholine, rabbit) or “in vivo” (ES, rat) relaxant stimuli, along with nNOS expression, which was reduced ( P < 0.05) in STZ rats. In diabetic animals, T substitution reinstated sildenafil-induced enhancement of both “in vitro” nitric oxide donor (NCX 4040) relaxant effect (rabbit) and “in vivo” ES-induced erection (rat). PDE5 was reduced in diabetic STZ rats ( P < 0.05) and normalized by T. In STZ rats, sodium nitroprusside (SNP) intracavernous injection induced a more sustained erection than in control rats, which was no further enhanced by sildenafil. T substitution normalized both hyper-responsiveness to SNP and sildenafil efficacy. Conclusion. In two models of diabetes T deficiency underlies biochemical alterations leading to ED. Normalizing T in diabetes restores nNOS and PDE5, and reinstates sensitivity to relaxant stimuli and responsiveness to sildenafil. Zhang X-H, Filippi S, Morelli A, Vignozzi L, Luconi M, Donati S, Forti G, and Maggi M. Testosterone restores diabetes-induced erectile dysfunction and sildenafil responsiveness in two distinct animal models of chemical diabetes. J Sex Med 2006;3:253–266. [ABSTRACT FROM AUTHOR]
- Published
- 2006
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108. Effect of hypoxia and endothelial loss on vascular smooth muscle cell responsiveness to VEGF-A: role of flt-1/VEGF-receptor-1
- Author
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Parenti, Astrid, Brogelli, Laura, Filippi, Sandra, Donnini, Sandra, and Ledda, Fabrizio
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HYPOXEMIA ,VASCULAR smooth muscle ,GROWTH factors - Abstract
Objective: The influence of hypoxia and endothelial loss on the responsiveness of vascular smooth muscle cells (VSMCs) to vascular endothelial growth factor (VEGF-A) was tested. Methods and results: Exposure to hypoxia induced a potentiation of cultured cell proliferation in response to either the agonist for the VEGF receptor 1 (flt-1) placental growth factor (PlGF-1) or to VEGF-A. This effect was mediated by the mitogen activated protein kinase (MAPK) cascade, since it was inhibited by the MAPK kinase inhibitor PD98059 and by the farnesyl transferase inhibitor II. Accordingly, PlGF-1 activated extracellular signal-regulated kinase
1/2 . In rat aortic rings deprived of endothelium and cultured in three-dimensional fibrin gels, an increased sprouting of tubular structures in response to VEGF-A was observed only under hypoxia. Studies on rat aorta preparations revealed an endothelium-dependent vasorelaxation in response to either VEGF-A or PlGF1, which was reversed to a contractile response in endothelium-deprived preparations exposed to hypoxia. Western blot and immunohistochemistry of endothelium-deprived preparations exposed to hypoxia showed flt-1 receptor expression in all medial cells. Conversely, flt-1 mRNA, of endothelium-deprived aortic preparations and of tubular structures, was unchanged by hypoxia. Conclusion: These findings demonstrate that experimental conditions mimicking pathological vascular injury can make VSMCs responsive to VEGF-A through the induction of functional flt-1 receptors. [Copyright &y& Elsevier]- Published
- 2002
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109. Effects of physical exercise on metabolic syndrome-associated hypothalamic and testis alterations in the rabbit.
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Sarchielli, Erica, Guarnieri, Giulia, Comeglio, Paolo, Filippi, Sandra, Vannelli, Gabriella Barbara, and Morelli, Annamaria
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EXERCISE ,METABOLIC syndrome ,LABORATORY rabbits - Abstract
Metabolic Syndrome (MetS) is a cluster of clinical conditions, associated to an increased cardiovascular (CV) and metabolic risk along with hypogonadism (HG). Lifestyle modifications (including physical exercise, PhyEx) are well-known treatments for this condition [1]. We previously established a rabbit model of MetS that recapitulates the human phenotype, including HG [2]. We now report studies on the effects of PhyEx on hypothalamus-pituitary-testis (HPT) axis. MetS was induced in adult male rabbits fed a high-fat diet (HFD). Rabbits fed a regular diet were used as controls (RD). RD and HFD rabbits were exercise-trained to run on a treadmill for 12 weeks (RD + PhyEx and HFD+ PhyEx). HFD rabbits showed typical metabolic and CV features of MetS along with hypogonadotropic HG (reduced testosterone and LH plasma levels). Within the hypothalamus (preoptic region) a significant reduction of GnRH- and KISS1R-positive neurons, along with the increase of genes related to inflammation (COX2, IL6, CD68), glucose metabolism (GLUT1, GLUT4, IRS-1) and estrogen action (ERb, GPR30) was detected in HFD rabbit, as compared to RD group. Immunohistochemistry analysis confirmed the HFD-induced hypothalamic inflammation. Interestingly, genes encoding for inhibitory factors for GnRH, such as NPY, were also increased in HFD hypothalamus. Within the testis, HFD down-regulated LH receptor and all the steroidogenic enzymes leading to T synthesis. PhyEx completely restored T and LH plasma levels and GnRH/KISS1R immunostaining. All the aforementioned HDF-induced increase of inflammatory markers were significantly reduced in HFD+ PhyEx, with the exception of IL6. Moreover, at hypothalamic level, PhyEx decreased orexigenic and GnRH-inhibiting factors (dinorphin and its receptors OPRD1 and OPRK1), whereas increased anorexigenic ones (POMC). Within the testis, genes related to T formation (17ßHSD3) and metabolism (5a-reductase 1) were increased by PhyEx. In conclusion, in this experimental model, endurance training (PhyEx) completely reverted MetS-induced hypogonadotropic hypogonadism, exerting beneficial effects on the HPT axis. Particularly, in the hypothalamus PhysEX reduced HFD-induced inflammation. Hence, aerobic exercise training can be regarded an interesting strategy to combat MetS-associated alterations of the HPT axis. [ABSTRACT FROM AUTHOR]
- Published
- 2018
110. Differential Effects of Testosterone and Estradiol on Clitoral Function: An Experimental Study in Rats.
- Author
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Comeglio, Paolo, Cellai, Ilaria, Filippi, Sandra, Corno, Chiara, Corcetto, Francesca, Morelli, Annamaria, Maneschi, Elena, Maseroli, Elisa, Mannucci, Edoardo, Fambrini, Massimiliano, Maggi, Mario, and Vignozzi, Linda
- Subjects
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CLITORIS , *PHYSIOLOGICAL effects of estradiol , *THERAPEUTIC use of sex hormones , *WOMEN'S sexual behavior , *PHYSIOLOGICAL effects of testosterone , *OVARIECTOMY , *DISEASES - Abstract
Introduction Female sexual response is a complex phenomenon in which psychological, neurologic, and vascular mechanisms and hormonal factors interact. During the arousal phase, they cooperate to increase genital blood flow, thus inducing engorgement of the clitoris and lubrication of the vagina. Regulation of vascular and non-vascular smooth muscle tone is the crucial event in the erectile process. Preclinical studies have suggested that nitric oxide (NO) is the main vasodilator neurotransmitter modulating, through the second messenger cyclic guanosine monophosphate (cGMP), clitoral flow vessels. Aim To investigate the effects of sexual steroid hormones on pro-erectile and relaxant (mediated by NO and cGMP) and anti-erectile and contractile (mediated by ras homolog gene family member A [RhoA] and Rho-associated protein kinase [ROCK]) mechanisms in the clitoris using a validated animal model of female ovariectomized Sprague-Dawley rats. Methods Subgroups of ovariectomized rats were treated with 17β-estradiol, progesterone, testosterone, or testosterone and letrozole for 6 weeks. The experimental groups were compared with a control group of intact rats. Main Outcome Measures Sex steroids plasma levels were assessed and in vitro contractility studies were carried out in order to investigate the effect of ovariectomy and in vivo treatments on clitoris smooth muscle activity. Smooth muscle cells (SMCs) from rat clitoral biopsies were isolated and characterized. RhoA activity was determined in SMCs cell cultures. RNA from tissues and cells was analyzed by quantitative real-time RT-PCR. Results Using real-time polymerase chain reaction, testosterone treatment upregulated the expression of NO-mediated pathway genes (endothelial and neuronal NO synthase, guanylate cyclase soluble subunit-α 3 , guanylate cyclase soluble subunit-β 3 , cGMP-dependent protein kinase 1, and phosphodiesterase type 5). Conversely, estrogen replacement upregulated the expression of calcium-sensitizing RhoA-ROCK pathway genes. In vitro contractility studies were performed on phenylephrine pre-contracted clitoris strips. Ovariectomy resulted in a decreased responsiveness to Y-27632, a ROCK inhibitor, which was fully restored by 17β-estradiol supplementation. To further examine the effect of 17β-estradiol on the RhoA-ROCK pathway, smooth muscle cells were isolated from rat clitoris and their migration capacity was evaluated. Conclusion Collectively, these data demonstrate that testosterone improves the relaxation of vascular smooth muscle cells through the NO-cGMP pathway, and that testosterone and 17β-estradiol are necessary to maintain a functional contractile and relaxant machinery in the clitoris. This new concept might provide support for the concomitant use of estrogen and testosterone during the treatment of sexual arousal disorders related to hormonal imbalance or insufficiency. [ABSTRACT FROM AUTHOR]
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- 2016
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111. Effects of Aging and Hypertension on Vasorelaxant Activity of Calcitonin GeneRelated Peptide
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Amerini, Sandra, Mantelli, Laura, Filippi, Sandra, and Ledda, Fabrizio
- Abstract
We investigated the influence of aging and hypertension on the vasorelaxant effect of calcitonin generelated peptide CGRP, examining the responses to stimulation of perivascular vasodilatory nerves and to administration of the peptide in isolated mesenteric vascular bed preparations of young aged 23 months and old aged 18 months normotensive WistarKyoto WKY rats and spontaneously hypertensive rats SHR. We used preparations preconstricted by perfusion with 100 Mmethoxamine with addition of 5 Mguanethidine. The stimulationinduced vasorelaxation in the preparations of young SHR animals was significantly lower than that in those of agematched WKY rats. Moreover, the vasodilator response to stimulation displayed an agedependent decline in vascular beds of normotensive animals. The degree of the relaxant response to CGRP 0.011 Mdid not differ significantly between vascular preparations of normotensive and hypertensive rats but was significantly reduced in preparations of both SHR and WKY rats aged 18 months as compared with those of young animals. An agedependent decrement in the vascular reactivity, qualitatively similar to that observed with CGRP, was also detected with two other vasodilators, i.e., the endotheliumdependent vasodilator acetylcholine ACh 0.1100 Mand the directly acting nitrovasodilator sodium nitroprusside SNP, 110 M. We conclude that the vascular sensitivity to CGRP, as well as that to other vasodilator agents acting by different mechanisms, decreases with age in both normotensive and genetically hypertensive rats.
- Published
- 1994
112. Distal vagina smooth muscle contractility mechanisms: effects of in vivo sex steroids treatment in an animal experimental model of ovariectomy.
- Author
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Cipriani, Sarah, Cellai, Ilaria, Comeglio, Paolo, Filippi, Sandra, Martinelli, Serena, Rapizzi, Elena, Maseroli, Elisa, Sarchielli, Erica, Guarnieri, Giulia, Morelli, Prof. Annamaria, Rastrelli, Prof. Giulia, Maggi, Prof. Mario, and Vignozzi, Prof. Linda
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SMOOTH muscle , *ANIMAL welfare , *LABORATORY animals , *VAGINA , *WESTERN immunoblotting , *SMOOTH muscle contraction - Abstract
The female sexual response is a complex phenomenon where multiple psychophysiological factors are involved. Sex steroids play a pivotal role in female health and sexuality. The aim of this study was to investigate the effects of sex hormones on the smooth muscle contractile mechanism in the distal vagina using a validated animal model of ovariectomized (OVX) Sprague-Dawley rats. Subgroups of OVX rats were treated with 17β-oestradiol (E2), testosterone (T), or testosterone and letrozole (T+L) for 6 weeks and compared with a group of intact female rats. In vitro contractility studies were carried out on noradrenaline (NA) pre-contracted distal vaginal strips to investigate the effect of OVX and in vivo treatments on vaginal smooth muscle activity. The mRNA from vagina tissue samples was analysed by semi-quantitative RT-PCR, and membrane translocation of RhoA was evaluated by Western blot analysis. The dose dependent relaxion induced on NA pre-contracted vaginal strips by Y-27632, a selective ROCK inhibitor (1 nM-100 μM), was significantly decreased by OVX and restored by oestrogen, but not by T or T+L administration. The pre-incubation with NO synthase inhibitor L-NAME significantly increased the response to Y-27632 in CTRL and OVX+T groups, but not in OVX. Interestingly, OVX significantly reduced the mRNA expression of NO signalling gene PKG1, an effect counteracted by T±L but not by E2 administration, and the RhoA/ROCK pathway genes, normalized by the treatment with T±L and E2. Finally, Western blot analysis showed how, compared to controls, OVX increased the membrane translocated active form of RhoA and T treatment reverted this effect by increasing the inactive cytosolic form. E2 administration normalized the expression of the active protein. This study confirms the beneficial effects of androgens on the well-being of the vagina supporting their therapeutic role in the treatment of genitourinary syndrome of menopause (GSM) symptoms associated to hormonal decrease. The authors declare that they have no conflict of interest. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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113. Estrogen Mediates Metabolic Syndrome-Induced Erectile Dysfunction: A Study in the Rabbit.
- Author
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Vignozzi, Linda, Comeglio, Paolo, Cellai, Ilaria, Marchetta, Matilde, Maggi, Mario, Filippi, Sandra, and Morelli, Annamaria
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TREATMENT of sexual dysfunction , *IMPOTENCE , *METABOLIC syndrome , *ESTROGEN receptors , *ESTROGEN regulation , *TAMOXIFEN - Abstract
Introduction Estrogen receptor ( ER) α is critical in mediating the harmful effects of hyperestrogenism in fetal or neonatal life on the developing penis. In contrast, little is known on the impact of an excess of estrogens on penile function in adulthood. Aim To investigate the effect of estrogens on metabolic syndrome ( MetS)-associated erectile dysfunction ( ED). Methods We employed a recently established animal model of high fat diet ( HFD)-induced MetS. Subgroups of MetS rabbits were dosed with either testosterone ( T) or tamoxifen. We evaluated penile responsiveness to acetylcholine (Ach) as well as the expression of genes related to penile smooth muscle relaxation and contractility. Main Outcome Measure Associations between MetS-induced penile alterations and sex steroids were investigated in an animal model of HFD-induced MetS. To understand the role of either androgen deficiency or estrogen excess on ED, we treated subgroups of MetS rabbits with either T or tamoxifen, a classical ER antagonist. Results Feeding an HFD-induced MetS was associated to elevated estradiol ( E2) and low T levels. E2, but not T, was independently and negatively associated with genes able to affect penile erection. Smooth muscle-related markers decreased as a function of E2 and were positively associated with all the variables investigated. Increasing concentrations of circulating E2 were negatively associated with Ach-induced relaxation. In HFD rabbits, in vivo T dosing significantly improved MetS and completely normalized circulating E2. Conversely, in vivo tamoxifen dosing reduced visceral adiposity and partially restored T level. Ach-induced relaxation was severely impaired by HFD and significantly restored, up to the control level, by both tamoxifen and T dosing. In rabbit smooth muscle cells cultures 17β- E2 (1 nM) significantly reduced the expression of α-smooth muscle actin, transgelin, and phosphodiesterase type 5. The effects of 17β- E2 were completely reverted by tamoxifen (100 nM). Conclusions This study demonstrates, for the first time, that HFD-induced ED is more associated with a high E2, rather than to a low T, milieu. HFD-induced ED is partially restored by in vivo treatment not only with T but also with the nonsteroidal ER antagonist, tamoxifen. Vignozzi L, Filippi S, Comeglio P, Cellai I, Morelli A, Marchetta M, and Maggi M. Estrogen mediates metabolic syndrome-induced erectile dysfunction: A study in the rabbit. J Sex Med 2014;11:2890-2902. [ABSTRACT FROM AUTHOR]
- Published
- 2014
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114. 3rd European Meeting on Vascular Biology and Medicine: pp II/80–II/139.
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MEDICINE ,VASCULAR diseases ,CONFERENCES & conventions ,CARDIOVASCULAR system ,ATHEROSCLEROSIS ,BIOLOGY ,APOLIPOPROTEIN E ,IMMUNOGLOBULINS - Abstract
This article presents abstracts of papers presented at the 3rd European meeting on vascular biology and medicine. The aim of the study titled "Antibody Conjugated Near Infrared Dye Detects Focal Atherosclerotic Lesions in ApoE Deficient Mice," by M. Roser and colleagues, was to examine the expression of ED-B fibronectin in a murine model of moderate atherosclerosis to investigate its relevance for imaging of early atherosclerotic lesions. In order to better characterize the role of the B7/CD28 pathway in atherosclerosis, the study titled "Protective Role of B7 and CD28 Co-Stimulatory Molecules in the Development of Atherosclerosis," by S. Potteaux and colleagues, generated chimeric mice.
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- 2005
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115. Age-dependent changes in the modulatory role of prostanoids on cardiac adrenergic neurotransmission in normal and hypertensive rats
- Author
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Ledda, Fabrizio, Filippi, Sandra, Mantelli, Laura, and Amerini, Sandra
- Published
- 1992
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116. Interference of prostanoids on adrenergic and peptidergic neurotransmission in resistance vessels
- Author
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Mantelli, Laura, Amerini, Sandra, Filippi, Sandra, and Ledda, Fabrizio
- Published
- 1992
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117. Responses to endothelium-dependent and independent vasodilator agents in resistance vessels of rats of different age
- Author
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Amerini, Sandra, Mantelli, Laura, Filippi, Sandra, and Ledda, Fabrizio
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- 1992
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118. Co-carcinogenic effects of vitamin E in prostate.
- Author
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Vivarelli, Fabio, Canistro, Donatella, Cirillo, Silvia, Papi, Alessio, Spisni, Enzo, Vornoli, Andrea, Croce, Clara M. Della, Longo, Vincenzo, Franchi, Paola, Filippi, Sandra, Lucarini, Marco, Zanzi, Cristina, Rotondo, Francesca, Lorenzini, Antonello, Marchionni, Silvia, and Paolini, Moreno
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THERAPEUTIC use of vitamin E , *PROSTATE cancer risk factors , *DIETARY supplements , *DNA damage , *POLYCYCLIC aromatic hydrocarbons - Abstract
A large number of basic researches and observational studies suggested the cancer preventive activity of vitamin E, but large-scale human intervention trials have yielded disappointing results and actually showed a higher incidence of prostate cancer although the mechanisms underlying the increased risk remain largely unknown. Here we show through in vitro and in vivo studies that vitamin E produces a marked inductive effect on carcinogen-bioactivating enzymes and a pro-oxidant status promoting both DNA damage and cell transformation frequency. First, we found that vitamin E in the human prostate epithelial RWPE-1 cell line has the remarkable ability to upregulate the expression of various phase-I activating cytochrome P450 (CYP) enzymes, including activators of polycyclic aromatic hydrocarbons (PAHs), giving rise to supraphysiological levels of reactive oxygen species. Furthermore, our rat model confirmed that vitamin E in the prostate has a powerful booster effect on CYP enzymes associated with the generation of oxidative stress, thereby favoring lipid-derived electrophile spread that covalently modifies proteins. We show that vitamin E not only causes DNA damage but also promotes cell transformation frequency induced by the PAH-prototype benzo[a]pyrene. Our findings might explain why dietary supplementation with vitamin E increases the prostate cancer risk among healthy men. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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119. Vardenafil can Improve Continence Recovery after Bilateral Nerve Sparing Prostatectomy: Results of a Randomized, Double Blind, Placebo-Controlled Pilot Study
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Alessandro Ierardi, Mauro Gacci, Stefano Tazzioli, E. Scapaticci, Augusto Delle Rose, Marco Carini, Giulio Nicita, Francesco Montorsi, Sandra Filippi, Mario Maggi, Gacci, Mauro, Ierardi, Alessandro, Delle Rose, Augusto, Tazzioli, Stefano, Scapaticci, Emanuele, Filippi, Sandra, Maggi, Mario, Nicita, Giulio, Carini, Marco, and Montorsi, Francesco
- Subjects
medicine.medical_specialty ,business.industry ,Urology ,Endocrinology, Diabetes and Metabolism ,Urinary system ,medicine.disease ,Placebo ,Urinary function ,Psychiatry and Mental health ,Prostate cancer ,Endocrinology ,Erectile dysfunction ,Reproductive Medicine ,Lower urinary tract symptoms ,Vardenafil ,medicine ,Analysis of variance ,business ,medicine.drug - Abstract
Introduction Phosphodiesterase type 5 inhibitors (PDE5-I) have acquired an established role in the treatment of post-prostatectomy erectile dysfunction (ED). Several trials in men with ED and lower urinary tract symptoms associated with benign prostatic hyperplasia suggest that PDE5-I could improve both erectile function and urinary symptoms. Aim To assess the role of vardenafil in continence recovery after bilateral nerve sparing radical prostatectomy (BNS-RP). Methods Thirty-nine patients with prostate cancer were recruited. After BNS-RP, patients were double-blinded assigned to three arms: a) vardenafil on demand; b) vardenafil nightly; and c) placebo. Main Outcomes Measures Urinary function (UF) and urinary bother (UB) of University of California–Los Angeles Prostate Cancer Index questionnaire were assessed preoperatively and at 1, 3, 6, 9, 10, and 12 months. Twelve-month outcomes were compared to 1 month with a t -test. The differences in UF and UB (at 3, 6, 9, 10, and 12 months) between the three treatment arms were calculated by an analysis of variance. With ALLFIT we estimated half-maximal recovery times (ER50) and maximal recovery ( R max ) in three groups. Results The improvement of UF and UB between 1 and 12 months was significant in all arms except for placebo (UF: P = 0.125; UB: P = 0.089). Nightly resulted in greater UF at 3, 6, and 9 months and greater UB at 6 months compared with placebo ( P = 0.042, P = 0.044 and P = 0.039); after nightly administration, patients presented higher UB than after on-demand use, 3 and 6 months postoperatively ( P = 0.036 and P = 0.017). ALLFIT demonstrated a similar ER50 in all groups (2.6 months for both UF and UB) and indicated that nightly administration induced significant improvements in R max compared with placebo (both Conclusions Vardenafil can improve continence recovery after BNS-RP compared with placebo. The daily use of vardenafil seems to provide better continence rate, although it does not seem to influence the timing needed to achieve full continence. Gacci M, Ierardi A, Delle Rose A, Tazzioli S, Scapaticci E, Filippi S, Maggi M, Nicita G, Carini M, and Montorsi F. Vardenafil can improve continence recovery after bilateral nerve sparing prostatectomy: Results of a randomized, double blind, placebo-controlled pilot study.
- Published
- 2010
120. The Origins of the Love Song: Sexual Selection or Sexual Frustration?
- Author
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Nino Tsitsishvili, Author and Nino Tsitsishvili, Author
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- Sexual selection in animals, Sex in popular culture, Sex--History, Human evolution
- Abstract
The book offers a radically new perspective on the origins of the love song and human sexuality in an evolutionary context. By comparing different human societies and animal species, past and present, it reveals that love songs, romantic love and exclusive pair-bonds are not the original evolutionary features of Homo sapiens. One of the key findings of the book is that early humans practiced multiple-partner sexual relations, similar to our closest relatives bonobos and chimpanzees, but, with the emergence of culture and sexual taboo, their behaviour had to adjust. It contends that, since the exodus from Africa and the rise of culture, humans started to distance themselves from the rest of the animal kingdom, drastically restraining their innate sexual nature. The book will appeal to both scholars and laypeople with an interest in evolutionary theory, socio-biology, anthropology, and the origins of culture.
- Published
- 2023
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