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Search Results: 1 - 10 of 14049 matches for " Andrea Duranti "
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The long-term preservation of the digital heritage: the case of universities institutional repositories La conservazione a lungo termine del patrimonio digitale: il caso degli archivi istituzionali delle università
Luciana Duranti
JLIS.it , 2010, DOI: 10.4403/jlis.it-12
Abstract: L'articolo affronta le tematiche legate ai problemi della conservazione a lungo termine del contenuto degli archivi digitali. Il materiale d'archivio richiede un'attenzione speciale ad aspetti quali la credibilità, il valore giuridico, i diritti morali e legali e la privacy. La necessità di assicurare accessibilità e integrità ai dati informatici è tuttavia una problematica che attraversa tutti i campi dell'informatizzazione ed è strettamente legata a fattori come la frequente duplicazione e la corretta scelta dei metadadi. Attraverso l'analisi del caso di studio rappresentato da cIRcle, l'istitutional digital repository della University of British Columbia (UBC), il contributo mostra problemi, rischi e soluzioni utili nella gestione di un archivio digitale, mostrando che l'esperienza degli archivisti può essere utile per sviluppare sistemi legati a depositi di informazione non prettamente archivistici. The article faces the problems related to long-term preservation of the digital archives content. Archival material requires a special attentio due to credibility, juridical value, moral and legal rights, and privacy. The need to ensure accessibility and integrity of informatic data is a problem that involves all aspects and fields of informatization, and it is closely related to metadata choice and duplication. Through the analysis of the case-study represented by cIrcle, the istitutional digital repository della University of British Columbia (UBC), the article shows problems, risks, and solutions in managing a digital archive, showing that the professional experience of archivists can be useful in order to develop technological systems for non-archivistic contents.
Induction of Endoplasmic Reticulum Stress Response by the Indole-3-Carbinol Cyclic Tetrameric Derivative CTet in Human Breast Cancer Cell Lines
Luca Galluzzi, Mauro De Santi, Rita Crinelli, Cinzia De Marco, Nadia Zaffaroni, Andrea Duranti, Giorgio Brandi, Mauro Magnani
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043249
Abstract: Background Indole-3-carbinol and its metabolic products are considered promising chemopreventive and anticancer agents. Previously we have shown that the indole-3-carbinol cyclic tetrameric derivative CTet induces autophagy and inhibits cell proliferation via inhibition of Akt activity and overexpression of p21/CDKN1A and GADD45A, in both estrogen receptor-positive (MCF-7) and triple negative (MDA-MB-231) breast cancer cell lines. In the present study, we further characterize the autophagic response and investigate the mechanism through which CTet regulates these events. Methodology/Principal Findings Analysis of gene expression microarray data and subsequent confirmation by quantitative real-time PCR, showed that CTet is able to induce up-regulation of key signaling molecules involved in endoplasmic reticulum (ER) stress response (e.g. DDIT3/CHOP, CHAC1, ATF3, HSPA5/BiP/GRP78, CEBPB, ASNS) and autophagy (e.g. MAP1LC3B), in both MCF-7 and MDA-MB-231 cell lines. Moreover, the monitoring of Xbp-1 splicing confirmed the activation of IRE1/Xbp-1 ER stress response branch after CTet treatment. The role of autophagic processes (known to be induced by ER stress) was investigated further through ATG5 gene silencing and pharmacological inhibition of AVOs formation. CTet was shown to induce an autophagy-related cell death. Moreover, CTet-treated cells stained with Hoechst/PI revealed the presence of necrotic processes without evidence of apoptosis. Conclusions/Significance The ER stress response was identified as the main upstream molecular mechanism through which CTet acts in both hormone-responsive and triple-negative breast cancer cells. Because of its important role in cancer development, ER stress is a potential target in cancer therapy. The abiltiy of CTet to induce ER stress response and subsequently activate a death program in tumor cells confirms this molecule as a promising anticancer agent.
Endocannabinoid Regulation of Acute and Protracted Nicotine Withdrawal: Effect of FAAH Inhibition
Andrea Cippitelli, Giuseppe Astarita, Andrea Duranti, Giovanni Caprioli, Massimo Ubaldi, Serena Stopponi, Marsida Kallupi, Gianni Sagratini, Fernando Rodrìguez de Fonseca, Daniele Piomelli, Roberto Ciccocioppo
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0028142
Abstract: Evidence shows that the endocannabinoid system modulates the addictive properties of nicotine. In the present study, we hypothesized that spontaneous withdrawal resulting from removal of chronically implanted transdermal nicotine patches is regulated by the endocannabinoid system. A 7-day nicotine dependence procedure (5.2 mg/rat/day) elicited occurrence of reliable nicotine abstinence symptoms in Wistar rats. Somatic and affective withdrawal signs were observed at 16 and 34 hours following removal of nicotine patches, respectively. Further behavioral manifestations including decrease in locomotor activity and increased weight gain also occurred during withdrawal. Expression of spontaneous nicotine withdrawal was accompanied by fluctuation in levels of the endocannabinoid anandamide (AEA) in several brain structures including the amygdala, the hippocampus, the hypothalamus and the prefrontal cortex. Conversely, levels of 2-arachidonoyl-sn-glycerol were not significantly altered. Pharmacological inhibition of fatty acid amide hydrolase (FAAH), the enzyme responsible for the intracellular degradation of AEA, by URB597 (0.1 and 0.3 mg/kg, i.p.), reduced withdrawal-induced anxiety as assessed by the elevated plus maze test and the shock-probe defensive burying paradigm, but did not prevent the occurrence of somatic signs. Together, the results indicate that pharmacological strategies aimed at enhancing endocannabinoid signaling may offer therapeutic advantages to treat the negative affective state produced by nicotine withdrawal, which is critical for the maintenance of tobacco use.
Synthesis and Biological Evaluation of a γ-Cyclodextrin-based Formulation of the Anticancer Agent 5,6,11,12,17,18,23,24- Octahydrocyclododeca[1,2-b:4,5-b’:7,8-b’’:10,11-b’’’]tetraindole (CTet)
Simone Lucarini,Mauro De Santi,Francesca Antonietti,Giorgio Brandi,Giuseppe Diamantini,Alessandra Fraternale,Maria Filomena Paoletti,Andrea Tontini,Mauro Magnani,Andrea Duranti
Molecules , 2010, DOI: 10.3390/molecules15064085
Abstract: 5,6,11,12,17,18,23,24-octahydrocyclododeca[1,2-b:4,5-b’:7,8-b’’:10,11- b’’’]tetrai ndole (CTet), an indole-3-carbinol (I3C) metabolite endowed with anticancer properties, is poorly soluble in the solvents most frequently used in biological tests. This study indicates that the use of γ-cyclodextrin (γ-CD) avoids this problem. Formulated with γ-CD CTet is a potent inhibitor of DNA synthesis in both estrogen receptor positive (MCF-7) and estrogen receptor negative (MDA-MB-231) human breast cell lines (IC50 = 1.20 ± 0.04 μM and 1.0 ± 0.1 μM, respectively).
The indole-3-carbinol cyclic tetrameric derivative CTet inhibits cell proliferation via overexpression of p21/CDKN1A in both estrogen receptor-positive and triple-negative breast cancer cell lines
Mauro De Santi, Luca Galluzzi, Simone Lucarini, Maria Filomena Paoletti, Alessandra Fraternale, Andrea Duranti, Cinzia De Marco, Mirco Fanelli, Nadia Zaffaroni, Giorgio Brandi, Mauro Magnani
Breast Cancer Research , 2011, DOI: 10.1186/bcr2855
Abstract: Estrogen receptor-positive MCF-7 and triple-negative MDA-MB-231 breast cancer cell lines were exposed to CTet to evaluate cell cycle perturbation (propidium iodide staining and cytofluorimetric acquisition), induction of autophagic morphological features (co-localization of LC3b autophagosome marker and LAMP2a lysosome marker by immunofluorescence) and changes in protein expression (immunoblot and microarray-based gene expression analyses). To test the in vivo efficacy of CTet, female athymic nude mice inoculated with MCF-7 cells were i.p. treated with 5 mg/kg/day of CTet for five days/week for two weeks and the tumor mass was externally monitored.CTet induced accumulation in G2/M phase without evidence of apoptotic response induction in both cell lines tested. In triple-negative MDA-MB-231 the autophagic lysosomal activity was significantly up-regulated after exposure to 4 μM of CTet for 8 hours, while the highest CTet concentration was necessary to observe autophagic features in MCF-7 cells. The inhibition of Akt activity and p53-independent p21/CDKN1A and GADD45A overexpression were identified as the main molecular events responsible for CTet activity in MCF-7 and p53-mutant MDA-MB-231 cells. In vivo, CTet administration was able to significantly inhibit the growth of MCF-7 xenotransplanted into nude mice, without adverse effect on body weight or on haematological parameters.Our data support CTet formulated with γ-CD as a promising and injectable anticancer agent for both hormone-responsive and triple-negative breast tumors.Breast cancer is one of the most common malignancies in industrialized countries and is characterized by distinct classes of tumors that respond differently to targeted therapies such as selective estrogen receptor modulator (SERM) treatments (for example, tamoxifen) in estrogen receptor (ER)-positive breast cancer or monoclonal antibodies (for example, trastuzumab) in HER2/Neu-positive breast cancer. However, about 10% to 15% of breast cancer
Assessing the Fecal Microbiota: An Optimized Ion Torrent 16S rRNA Gene-Based Analysis Protocol
Christian Milani, Arancha Hevia, Elena Foroni, Sabrina Duranti, Francesca Turroni, Gabriele Andrea Lugli, Borja Sanchez, Rebeca Martín, Miguel Gueimonde, Douwe van Sinderen, Abelardo Margolles, Marco Ventura
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068739
Abstract: Assessing the distribution of 16S rRNA gene sequences within a biological sample represents the current state-of-the-art for determination of human gut microbiota composition. Advances in dissecting the microbial biodiversity of this ecosystem have very much been dependent on the development of novel high-throughput DNA sequencing technologies, like the Ion Torrent. However, the precise representation of this bacterial community may be affected by the protocols used for DNA extraction as well as by the PCR primers employed in the amplification reaction. Here, we describe an optimized protocol for 16S rRNA gene-based profiling of the fecal microbiota.
Oxidative Stress and Vascular Damage in Hypertension: Role of Angiotensin II
Agostino Virdis,Emiliano Duranti,Stefano Taddei
International Journal of Hypertension , 2011, DOI: 10.4061/2011/916310
Abstract: Reactive oxygen species are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. In healthy conditions, ROS are produced in a controlled manner at low concentrations and function as signaling molecules regulating vascular contraction-relaxation and cell growth. Physiologically, the rate of ROS generation is counterbalanced by the rate of elimination. In hypertension, an enhanced ROS generation occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. In the present paper, major angiotensin II-induced vascular ROS generation within the vasculature, and relative sources, will be discussed. Recent development of signalling pathways whereby angiotensin II-driven vascular ROS induce and accelerate functional and structural vascular injury will be also considered.
Oxidative Stress and Vascular Damage in Hypertension: Role of Angiotensin II
Agostino Virdis,Emiliano Duranti,Stefano Taddei
International Journal of Hypertension , 2011, DOI: 10.4061/2011/916310
Abstract: Reactive oxygen species are oxygen derivates and play an active role in vascular biology. These compounds are generated within the vascular wall, at the level of endothelial and vascular smooth muscle cells, as well as by adventitial fibroblasts. In healthy conditions, ROS are produced in a controlled manner at low concentrations and function as signaling molecules regulating vascular contraction-relaxation and cell growth. Physiologically, the rate of ROS generation is counterbalanced by the rate of elimination. In hypertension, an enhanced ROS generation occurs, which is not counterbalanced by the endogenous antioxidant mechanisms, leading to a state of oxidative stress. In the present paper, major angiotensin II-induced vascular ROS generation within the vasculature, and relative sources, will be discussed. Recent development of signalling pathways whereby angiotensin II-driven vascular ROS induce and accelerate functional and structural vascular injury will be also considered. 1. Introduction Hypertension is associated with increased peripheral resistance, resulting predominantly from functional, structural, and mechanical alterations at the level of small-resistance arteries. Functional alterations, which include an impaired endothelial function, are mainly assessed as an impaired acetylcholine-induced, endothelium-dependent relaxation. Vascular structural changes include vascular remodeling, secondary to an increased cell growth, cell migration, and low-grade vascular inflammation [1, 2]. In particular, an increased media-to-lumen ratio (M/L) may result from a reduced outer diameter that narrows the lumen without net growth (eutrophic remodeling) or from a thicker media encroaching on the lumen (hypertrophic remodeling) [1, 2]. Another hallmark of hypertension-induced structural abnormalities is represented by changes in the mechanical properties of arteries, with particular regard for increased stiffness [3]. Vascular fibrosis is critically important in the determinism of vascular structural modifications, and it involves changes in extracellular matrix (ECM) components, including collagen type I and III, elastin, and fibronectin. An increase in collagen and fibronectin and a decrease in elastin contents have been shown in the media of small arteries from hypertensive animals [3–5]. It is widely accepted that angiotensin (Ang) II, traditionally involved in modulating blood pressure and electrolyte homeostasis, is also greatly implicated in the pathogenesis of endothelial dysfunction and vascular remodeling [6–8]. This concept is strengthened by
Problems concerning ovine milk clotting aptitude
E. Duranti,P. Bolla,A. Caroli,L. Chiofalo
Italian Journal of Animal Science , 2003,
Abstract: A comparative study of the lactodynamographic parameters was carried out on ovine milk. Besides evaluating the repeatability and reproducibility of the analytical method, the influence of some variables such as the genetic type (three breeds), the kind of milk (whole or skimmed), and its concentration after reconstitution (12g or 20g /100 ml) was evaluated. The working plan involved 6 laboratories for the final statistic analyses, by the use of freeze-dried milk samples (adequately reconstituted on the basis of established methods) from Sardinia, Comisana, and Massese ewes. All the considered variability factors showed a highly significant effect (P<0.001) on the lactodynamographic parameters considered. In particular, Massese ewe milk showed the shortest curd speed (k20) and the best coagulum strength (a30 and a45), although clotting time (CT) was the highest one. The same trend was registered for skimmed milk and for the most concentrated one (20g). Repeatability values within laboratories were 96% and 97% for CT and k20, lowering for a30 e a45, (respectively 87% and 85%). Much lower coefficients were found for the among laboratories reproducibility, ranging from a maximum of 58% for CT to a minimum of 18% for k20. The wide variability observed indicates that lactodynamographic parameters are comparable only within the same lab. Further investigation is needed to compare different labs in order to obtain more homogeneous results.
Adipocytokine levels mark endothelial function in normotensive individuals
Anna Solini, Francesco Stea, Eleonora Santini, Rosa Bruno, Emiliano Duranti, Stefano Taddei, Lorenzo Ghiadoni
Cardiovascular Diabetology , 2012, DOI: 10.1186/1475-2840-11-103
Abstract: In 92 newly diagnosed, drug-na?ve essential hypertensive patients (HT, mean age 49 yrs) without organ damage and 66 normotensive subjects (NT, mean age 47 yrs), by an automated system, we measured endothelium-dependent and -independent vasodilation as brachial artery flow-mediated dilation before and after administration of glyceryl-trinitrate. Retinol binding protein-4 (RBP4) and resistin levels were determined by ELISA and RIA, respectively. Oxidative stress was evaluated by measuring serum malondyaldehyde (MDA).Flow-mediated dilation was significantly (p?=?0.03) lower in HT (5.3?±?2.6%) than NT (6.1?±?3.1%), while response to glyceryl-trinitrate (7.5?±?3.7% vs 7.9?±?3.4%) was similar. RBP4 (60.6?±?25.1 vs 61.3?±?25.9 μg/ml), resistin (18.8?±?5.3 vs 19.9?±?6.1 ng/ml) and MDA levels (2.39?±?1.26 vs 2.08?±?1.17 nmol/ml) were not different in HT and NT.RBP4 (r?=??0.25; p?=?0.04) and resistin levels (r?=??0.29; p?=?0.03) were related to flow-mediated dilation in NT, but not in HT (r?=??0.03 and r?=??0.10, respectively). In NT, multivariate analysis including RBP4 and confounders showed that only BMI or waist circumference remained related to flow- mediated dilation. In the multivariate model including resistin and confounders, BMI, age and resistin were significantly related to flow-mediated dilation, while only age significant correlated with this parameter when BMI was replaced by waist circumference.Adipocytokine levels may be independent predictors of endothelial dysfunction in the peripheral circulation of healthy subjects, providing a pathophysiological link between inflammation from adipose tissue and early vascular alterations.Endothelium integrity is essential in the maintenance of vascular homeostasis, and its dysfunction, identified as a reduced vasodilatory response to endothelium-dependent stimuli, predisposes to the development of early atherosclerotic lesions [1]. Therefore, endothelial dysfunction is recognized as at least a marker, if not an independe
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