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Search Results: 1 - 10 of 9230 matches for " Silvia Bini "
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Hyperreflective Intraretinal Spots in Diabetics without and with Nonproliferative Diabetic Retinopathy: An In Vivo Study Using Spectral Domain OCT
Stela Vujosevic,Silvia Bini,Giulia Midena,Marianna Berton,Elisabetta Pilotto,Edoardo Midena
Journal of Diabetes Research , 2013, DOI: 10.1155/2013/491835
Abstract: Purpose. To evaluate the presence of hyperreflective spots (HRS) in diabetic patients without clinically detectable retinopathy (no DR) or with nonproliferative mild to moderate retinopathy (DR) without macular edema, and compare the results to controls. Methods. 36 subjects were enrolled: 12 with no DR, 12 with DR, and 12 normal subjects who served as controls. All studied subjects underwent full ophthalmologic examination and spectral domain optical coherence tomography (SD-OCT). SD-OCT images were analyzed to measure and localize HRS. Each image was analyzed by two independent, masked examiners. Results. The number of HRS was significantly higher in both diabetics without and with retinopathy versus controls ( ) and in diabetics with retinopathy versus diabetics without retinopathy ( ). The HRS were mainly located in the inner retina layers (inner limiting membrane, ganglion cell layer, and inner nuclear layer). The intraobserver and interobserver agreement was almost perfect ( ). Conclusions. SD-OCT hyperreflective spots are present in diabetic eyes even when clinical retinopathy is undetectable. Their number increases with progressing retinopathy. Initially, HRS are mainly located in the inner retina, where the resident microglia is present. With progressing retinopathy, HRS reach the outer retinal layer. HRS may represent a surrogate of microglial activation in diabetic retina. 1. Introduction An increasing body of evidence suggests that retinal neurodegeneration and inflammation occur in human diabetes even before the development of clinical signs of diabetic retinopathy (DR) [1]. Retinal neural cell loss (neurodegeneration) has already been demonstrated in vivo (as thinning of retinal nerve fiber and ganglion cell layers), both in type 1 and 2 diabetes [2–7]. Retinal microglia activation has been recognized as the main responsible for the initial inflammatory response, even though the exact mechanism through which inflammatory cytokines are released remains poorly known [8]. Some experimental studies have shown that retinal inflammation occurring during the course of diabetes mellitus is a relatively early event and that it precedes both vascular dysfunction and neuronal degeneration [1, 8]. Joussen at al. demonstrated in animal models of diabetes mellitus that ICAM-1- and CD18-mediated leukocyte adhesion is increased in the retinal vasculature and accounts for many of the signature lesions of DR [1]. Ibrahim et al. demonstrated in rats that the accumulation of Amadori-glycated albumin (AGA) within the 8-week diabetic retina elicits microglial
Servizi Sociali Territoriali e Università: Esempi di Sinergie Possibili per un Percorso di Qualità
Bini, Laura
Social Work and Society , 2007,
Abstract: Although – or because – social work education in Italy has for some 15 years now been exclusively in the domain of the university the relationship between the academic world and that of practice has been highly tenuous. Research is indeed being conducted by universities, but rarely on issues that are of immediate practice relevance. This means that forms of practice develop and become established habitually which are not checked against rigorous standards of research and that the creation of knowledge at academic level pays scant attention to the practice implications of social changes. This situation has been made even worse by the dwindling resources both in social services and at the level of the universities which means that bureaucratic procedures or imports of specialisations from other disciplines frequently dominate the development of practice instead of a theory-based approach to methodology. This development does not do justice to the actual requirements of Italian society faced with ever increasing post-modern complexity which is reflected also in the nature of social problems because it implies a continuation of a faith in modernity with its idea of technical, clear-cut solutions while social relations have decidedly moved beyond that belief. This discrepancy puts even greater strain on the personnel of welfare agencies and does ultimately not satisfy the ever increasing demands for quality and accountability of services on the part of users and the general public. Social workers badly lack fundamental theoretical reference points which could guide them in their difficult work to arrive at autonomous, situation-specific methodological answers not based on procedures but on analytical knowledge. Thirty years ago, in 1977, a Presidential Decree created the legal basis for the establishment of social service departments at the level of municipalities which created opportunities for the direct involvement of the community in the fight against exclusion. For this potential to be fully utilized it would have required the bringing together of three dimensions, the organizational structure, the opportunities for learning and research in the territory and the contribution by the professional community. As this did not occur social services in Italy still often retain the character of charity which does not concern itself with the actual causes of poverty and exclusion. This in turn affects the relationship with citizens in general who cannot develop trust in those services. Through uncritical processes of interaction Edgar Morin’s dictum manifests its
Sismondi "astronomo d'uomini, non di stelle" e l'inedito giornale "Il Cannocchiale" (1796)
Alessio Bini
Scienza & Politica : per una Storia delle Dottrine , 2001, DOI: 10.6092/issn.1825-9618/2883
Abstract: Sismondi "astronomo d'uomini, non di stelle" e l'inedito giornale "Il Cannocchiale" (1796)
Recent Results on Light Meson Physics
C. Bini
Physics , 2003,
Abstract: Some recent results on light meson physics are reviewed. The new evidence of low mass scalar mesons together with an improved measurement of the phi radiative decays in scalar mesons, give new insight into the nature and the structure of the scalar spectrum. The evidence of new states with a mass close to twice the proton mass, and a new analysis of the gluonium content of the eta' are discussed.
Chern Classes of the Moduli Stack of Curves
Gilberto Bini
Mathematics , 2005,
Abstract: Here we calculate the Chern classes of ${\bar {\mathcal M}}_{g,n}$, the moduli stack of stable n-pointed curves. In particular, we prove that such classes lie in the tautological ring.
Quotients of Hypersurfaces in Weighted Projective Space
Gilberto Bini
Mathematics , 2009,
Abstract: In [1] some quotients of one-parameter families of Calabi-Yau varieties are related to the family of Mirror Quintics by using a construction due to Shioda. In this paper, we generalize this construction to a wider class of varieties. More specifically, let $A$ be an invertible matrix with non-negative integer entries. We introduce varieties $X_A$ and $\overline{M}_A$ in weighted projective space and in ${\mathbb P}^n$, respectively. The variety $\overline{M}_A$ turns out to be a quotient of a Fermat variety by a finite group. As a by-product, $X_A$ is a quotient of a Fermat variety and $\overline{M}_A$ is a quotient of $X_A$ by a finite group. We apply this construction to some families of Calabi-Yau manifolds in order to show their birationality.
Novel Targets of Sulforaphane in Primary Cardiomyocytes Identified by Proteomic Analysis
Cristina Angeloni, Silvia Turroni, Laura Bianchi, Daniele Fabbri, Elisa Motori, Marco Malaguti, Emanuela Leoncini, Tullia Maraldi, Luca Bini, Patrizia Brigidi, Silvana Hrelia
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0083283
Abstract: Cardiovascular diseases represent the main cause of mortality in the industrialized world and the identification of effective preventive strategies is of fundamental importance. Sulforaphane, an isothiocyanate from cruciferous vegetables, has been shown to up-regulate phase II enzymes in cardiomyocytes and counteract oxidative stress-induced apoptosis. Aim of the present study was the identification and characterization of novel sulforaphane targets in cardiomyocytes applying a proteomic approach. Two-dimensional gel electrophoresis and mass spectrometry were used to generate protein profiles of primary neonatal rat cardiomyocytes treated and untreated with 5 μM sulforaphane for 1-48 h. According to image analysis, 64 protein spots were found as differentially expressed and their functional correlations were investigated using the MetaCore program. We mainly focused on 3 proteins: macrophage migration inhibitory factor (MIF), CLP36 or Elfin, and glyoxalase 1, due to their possible involvement in cardioprotection. Validation of the time-dependent differential expression of these proteins was performed by western blotting. In particular, to gain insight into the cardioprotective role of the modulation of glyoxalase 1 by sulforaphane, further experiments were performed using methylglyoxal to mimic glycative stress. Sulforaphane was able to counteract methylglyoxal-induced apoptosis, ROS production, and glycative stress, likely through glyoxalase 1 up-regulation. In this study, we reported for the first time new molecular targets of sulforaphane, such as MIF, CLP36 and glyoxalase 1. In particular, we gave new insights into the anti-glycative role of sulforaphane in cardiomyocytes, confirming its pleiotropic behavior in counteracting cardiovascular diseases.
Severely Obese Adolescents and Adults Exhibit a Different Association of Circulating Levels of Adipokines and Leukocyte Expression of the Related Receptors with Insulin Resistance
Antonello E. Rigamonti,Fiorenza Agosti,Alessandra De Col,Giancarlo Silvestri,Nicoletta Marazzi,Silvia Bini,Sara Bonomo,Marialuisa Giunta,Silvano G. Cella,Alessandro Sartorio
International Journal of Endocrinology , 2013, DOI: 10.1155/2013/565967
Abstract: Obese adults frequently exhibit a low-grade inflammation and insulin resistance, which have been hypothesized to be established early in childhood. Aim of this study was to evaluate the age-dependent relationships between inflammatory state and insulin resistance in obese adolescents and adults. Clinical and metabolic parameters, circulating adipokines (TNF-α, adiponectin, and leptin), ghrelin, their leukocyte receptors (TNFR1, ADIPOR2, OBRL and GHSR1a), and acute phase reactants (CRP and white blood cells) were assessed in lean and obese adolescents compared with the adult counterparts. Only obese adults had higher HOMA-IR, insulin, and triglycerides compared to the lean group. An inflammatory state was present in obese adolescents and adults, as demonstrated by the higher values of CRP and neutrophils. There were no group differences in circulating levels of TNF-α and leukocyte expression of TNFR1. Adiponectin concentrations and leukocyte expression of ADIPOR2 were higher in the lean groups than in the corresponding obese counterparts. For leptin and leukocyte expression of OBRL, the results were opposed. Circulating levels of ghrelin were higher in lean adolescents and adults than the related lean groups, while there was a higher leukocyte expression of GHSR1a in (only) lean adults than obese adults. When the analysis was performed in (lean or obese) adults, TNF-α, neutrophils, leptin, and GHSR1a were predictors of HOMA-IR. None of the considered independent variables accounted for the degree of insulin resistance in the adolescent group. In conclusion, a dissociation between the low-grade inflammation and insulin resistance is supposed to exist in the early phases of obesity. 1. Introduction Obesity is considered a low-grade chronic inflammatory disease that may contribute to the development of insulin resistance [1]. Obese adolescents and adults are at higher risk for developing type 2 diabetes (T2D), cardiovascular disease, nonalcoholic fatty liver disease (NAFLD), osteoarticular diseases, and several forms of cancer [2]. Recent clinical studies have suggested that mediators of low-grade chronic inflammation, such as adipokines, cytokines, ghrelin, and acute phase reactants, are involved in the development of these comorbid conditions [3, 4]. Tumor necrosis factor-α (TNF-α) is one of the main mediators of the inflammatory response in obesity and is expressed by infiltrating macrophages and adipocytes in the hypertrophic adipose tissue [5]. TNF-α receptors 1 (TNFR1) and 2 (TNFR2) are the two main transducers of the TNF-α signals in most cells and
Subclinical Inflammatory Status in Rett Syndrome
Alessio Cortelazzo,Claudio De Felice,Roberto Guerranti,Cinzia Signorini,Silvia Leoncini,Alessandra Pecorelli,Gloria Zollo,Claudia Landi,Giuseppe Valacchi,Lucia Ciccoli,Luca Bini,Joussef Hayek
Mediators of Inflammation , 2014, DOI: 10.1155/2014/480980
Abstract: Inflammation has been advocated as a possible common central mechanism for developmental cognitive impairment. Rett syndrome (RTT) is a devastating neurodevelopmental disorder, mainly caused by de novo loss-of-function mutations in the gene encoding MeCP2. Here, we investigated plasma acute phase response (APR) in stage II (i.e., “pseudo-autistic”) RTT patients by routine haematology/clinical chemistry and proteomic 2-DE/MALDI-TOF analyses as a function of four major MECP2 gene mutation types (R306C, T158M, R168X, and large deletions). Elevated erythrocyte sedimentation rate values (median 33.0?mm/h versus 8.0?mm/h, ) were detectable in RTT, whereas C-reactive protein levels were unchanged ( ). The 2-DE analysis identified significant changes for a total of 17 proteins, the majority of which were categorized as APR proteins, either positive ( spots) or negative ( spots), and to a lesser extent as proteins involved in the immune system ( spots), with some proteins having overlapping functions on metabolism ( spots). The number of protein changes was proportional to the severity of the mutation. Our findings reveal for the first time the presence of a subclinical chronic inflammatory status related to the “pseudo-autistic” phase of RTT, which is related to the severity carried by the MECP2 gene mutation. 1. Introduction RTT (OMIM ID: 312750) occurs with a frequency of up to 1?:?10,000 live female births. Causative mutations in the X linked methyl-CpG binding protein 2 gene (MECP2) are detectable in up to 95% of cases, although a wide genetical and phenotypical heterogeneity is well established [1]. Approximately 80% of RTT clinical cases show the so-called “typical” clinical picture; after an apparently normal development for 6–18 months, RTT girls lose their acquired cognitive, social, and motor skills in a typical 4-stage neurological regression [2]. It has become apparent that there is a spectrum of severity in RTT, as some patients may present with atypical features, sometimes overlapping with those suggestive of autism spectrum disorders (ASDs) [3–5]. Autistic features are typically transient in RTT, although this condition has long been considered as a genetic/epigenetic model of ASDs [6, 7], RTT has been recently distinct from the ASDs group [8, 9]. Recently, the gene sequence analysis indicates that several hundreds of gene mutations appear to be associated with the MECP2 gene mutation and, therefore, are to be considered as potential disease modifiers [10], although the genetic mechanisms of RTT have been explored to an extraordinary extent, to
A Plasma Proteomic Approach in Rett Syndrome: Classical versus Preserved Speech Variant
Alessio Cortelazzo,Roberto Guerranti,Claudio De Felice,Cinzia Signorini,Silvia Leoncini,Alessandra Pecorelli,Claudia Landi,Luca Bini,Barbara Montomoli,Claudia Sticozzi,Lucia Ciccoli,Giuseppe Valacchi,Joussef Hayek
Mediators of Inflammation , 2013, DOI: 10.1155/2013/438653
Abstract: Rett syndrome (RTT) is a progressive neurodevelopmental disorder mainly caused by mutations in the gene encoding the methyl-CpG-binding protein 2 (MeCP2). Although over 200 mutations types have been identified so far, nine of which the most frequent ones. A wide phenotypical heterogeneity is a well-known feature of the disease, with different clinical presentations, including the classical form and the preserved speech variant (PSV). Aim of the study was to unveil possible relationships between plasma proteome and phenotypic expression in two cases of familial RTT represented by two pairs of sisters, harbor the same MECP2 gene mutation while being dramatically discrepant in phenotype, that is, classical RTT versus PSV. Plasma proteome was analysed by 2-DE/MALDI-TOF MS. A significant overexpression of six proteins in the classical sisters was detected as compared to the PSV siblings. A total of five out of six (i.e., 83.3%) of the overexpressed proteins were well-known acute phase response (APR) proteins, including alpha-1-microglobulin, haptoglobin, fibrinogen beta chain, alpha-1-antitrypsin, and complement C3. Therefore, the examined RTT siblings pairs proved to be an important benchmark model to test the molecular basis of phenotypical expression variability and to identify potential therapeutic targets of the disease. 1. Introduction Rett syndrome (RTT; OMIM no. 312750), with a frequency of ~1?:?10000–1?:?15000 females, is a severe and complex neurodevelopmental disorder, as well as the second most common cause of severe mental retardation in the female gender [1]. RTT presents in about 74% of cases in a classical form (typical presentation); after 6–18 months of an apparently normal development girls lose their acquired cognitive, social, and motor skills in a typical 4-stage neurological regression. A wide phenotypical heterogeneity is a well-known feature of the disease, which includes at least four major different clinical presentations, that is, classical, preserved speech (PSV), early seizure (ESV), and congenital variants [2]. Studies have implicated de novo mutations of the X-linked methyl-CpG-binding protein 2 (MECP2) gene (OMIM*300005) in the majority of the RTT cases, while mutations in cyclin-dependent kinase-like 5 (CDKL5) and forkhead box G1 (FOXG1) have been more rarely reported [3–5]. Typical RTT has been described worldwide, whereas PSV is more rarely reported. Girls affected by PSV have been often misreported with various diagnoses ranging from autism to mental retardation [6, 7]. While the available RTT literature is mainly
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