34 results on '"Gianfriddo, M."'
Search Results
2. The adenosine A2A receptor antagonist ZM241385 enhances neuronal survival after oxygen-glucose deprivation in rat CA1 hippocampal slices
- Author
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Pugliese, A M, Traini, C, Cipriani, S, Gianfriddo, M, Mello, T, Giovannini, M G, Galli, A, and Pedata, F
- Published
- 2009
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3. Expression of neuronal and inducible nitric oxide synthase in neuronal and glial cells after transient occlusion of the middle cerebral artery
- Author
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Vannucchi, M.G., Corsani, L., Gianfriddo, M., Pedata, F., and Faussone-Pellegrini, M.S.
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- 2005
- Full Text
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4. Adenosine A2A receptor antagonism increases nNOS-immunoreactive neurons in the striatum of Huntington transgenic mice
- Author
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Cipriani, S., Bizzoco, E., Gianfriddo, M., Melani, A., Vannucchi, M. G., and Pedata, F.
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- 2008
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5. Adenosine and glutamate extracellular concentrations and mitogen-activated protein kinases in the striatum of Huntington transgenic mice. Selective antagonism of adenosine A 2A receptors reduces transmitter outflow
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Gianfriddo, M., Melani, A., Turchi, D., Giovannini, M.G., and Pedata, F.
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- 2004
- Full Text
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6. Valsartan for prevention of recurrent atrial fibrillation
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GISSI AF Investigators, Disertori M, Latini R, Barlera S, Franzosi MG, Staszewsky L, Maggioni AP, Lucci D, Di Pasquale G, Tognoni G, Delise P, Bertocchi F, Maiocchi G, Geraci E, Correale E, Lombardi F, Mugelli A, Urso R, Scardi S, Fabbri G, Bartolomei B, Barbato G, Carbonieri E, Ciricugno S, Cosmi F, Pratola C, Rossi MG, Sciarra L, Zeni P, Ceseri M, Atzori A, Bambi F, Baviera M, Bianchini F, Fenicia E, Gianfriddo M, Lonardo G, Luise A, Nota R, Orlando ME, Petrolo R, Pierattini C, Pierota V, Ragno A, Serio C, Tafi A, Tellaroli E, Masson S, Vago T, Gramenzi S, Orso F, Suliman I, Nicolis E, Casola C, Dall'Osso D, Gorini M, Bianchini E, Cabiddu S, Cangioli I, Carnaghi A, Cipressa ML, Cipressa L, Galbiati L, Lorimer A, Priami P, Moccetti T, Vaghi F, Capello AF, Rossetti G, Viada E, Morena L, Delucchi M, Reynaud SG, Allemano P, Massobrio N, Gavazzi A, Taddei F, Mor DA, Bortolini F, Lorini M, Inama G, Durin O, Pirelli S, Spotti A, Procopio R, Cuzzucrea D, Gentile G, Margonato A, Bassanelli G, Tavazzi L, Buzzi MP, Rordorf R, Gualco A, Opasich C, Gronda E, Genovese L, Mattioli R, Donatelli F, Uriarte JA, Rauhe W, Bertagnolli C, Canestrini S, Stefenelli C, Cioffi G, Giovanelli C, Rigatelli G, Boni S, Pasini A, Sitta N, Sacchetta A, Borgese L, Sciascia R, Targa L, Raviele A, Madalosso M, Bertaglia E, Zoppo FC, Capanna M, Fiorencis R, Baracca E, Rossi R, Rossi I, Trappolin R, Morgera T, Barducci E, Baldin MG, Gobbo G, Zardo F, Hrovatin E, Mos L, Vriz O, Sinagra G, Aleksova A, Mazzone C, Fresco C, Rubartelli P, Moroni LA, Camerieri A, Piana M, Mureddu R, Bertoli D, Petacchi R, Pancaldi LG, Gabrieli L, Urbinati S, Pedone C, Di Niro M, Brunelli A, Bosi S, Censi S, Moruzzi P, Pastori P, Modena MG, Malavasi V, Mezzetti M, Melandri F, Zuppiroli A, Fazi A, Testa R, Venturini E, Mazzinghi F, Cosmi D, Santoro GM, Minneci C, Galli M, Paperini L, Bovenzi FM, Cortigiani L, Cocchieri M, Severini D, Arcuri GM, Bagliani G, Bernardinangeli M, Proietti G, Bocconcelli P, Pierantozzi A, Monti F, Giamundo L, Tancredi P, Rossini E, Bianchi C, Bettiol F, Giovannini E, Fera MS, Santini M, Bianconi L, Boccanelli A, Morosetti P, Volpe M, Facciolo C, Vacri A, Romanazzi F, Napoletano C, Piccioni LL, Candelmo F, De Marco G, Arnese MR, Vetrano A, Prinzi D, De Rosa P, Capuano V, Torre S, D'Onofrio A, Ammendola E, Battista R, De Fusco A, Molero U, Iervoglini A, Stefanelli S, Fattore L, Bosco B, Liguori A, Padula G, De Luca I, Sorino M, Colonna P, D'Agostino C, Pierfelice O, Pettinati G, Muscella A, De Lorenzi E, Falco M, Giannattasio C, Baldi N, Clemente MA, D'Alessandro B, Truncellito L, Arabia F, Ciconte VA, Perticone F, Ruberto C, Buffon A, Tomaselli C, De Rosa F, Mazza S, Zampaglione G, Pirozzi AM, Butera A, Levato M, Musacchio D, Polimeni RM, Lacquaniti V, Pulitanò G, Ruggeri A, Provenzano A, Cuccurullo O, Musolino M, Marrari A, Anastasio L, Schiavello M, Comito MG, Gulizia MM, Francese GM, Vasquez L, Coppolino C, Casale A, D'Urso G, Oliva G, Giordano U, Andolina S, Sanfilippo N, Ingrillì F, Accardo S, Grasso S, Buffa L, Serra E., CHIARIELLO, MASSIMO, PERRONE FILARDI, PASQUALE, Delise, P., Bertocchi, F., Maiocchi, G., Geraci, E., Correale, E., Lombardi, F., Mugelli, A., Urso, R., Scardi, S., Fabbri, G., Bartolomei, B., Barbato, G., Carbonieri, E., Ciricugno, S., Cosmi, F., Pratola, C., Rossi, M. G., Sciarra, L., Zeni, P., Ceseri, M., Atzori, A., Bambi, F., Baviera, M., Bianchini, F., Fenicia, E., Gianfriddo, M., Lonardo, G., Luise, A., Nota, R., Orlando, M. E., Petrolo, R., Pierattini, C., Pierota, V., Ragno, A., Serio, C., Tafi, A., Tellaroli, E., Masson, S., Vago, T., Gramenzi, S., Orso, F., Suliman, I., Nicolis, E., Casola, C., Dall'Osso, D., Gorini, M., Bianchini, E., Cabiddu, S., Cangioli, I., Carnaghi, A., Cipressa, M. L., Cipressa, L., Galbiati, L., Lorimer, A., Priami, P., Moccetti, T., Vaghi, F., Capello, A. F., Rossetti, G., Viada, E., Morena, L., Delucchi, M., Reynaud, S. G., Allemano, P., Massobrio, N., Gavazzi, A., Taddei, F., Mor, D. A., Bortolini, F., Lorini, M., Inama, G., Durin, O., Pirelli, S., Spotti, A., Procopio, R., Cuzzucrea, D., Gentile, G., Margonato, A., Bassanelli, G., Tavazzi, L., Buzzi, M. P., Rordorf, R., Gualco, A., Opasich, C., Gronda, E., Genovese, L., Mattioli, R., Donatelli, F., Uriarte, J. A., Rauhe, W., Bertagnolli, C., Canestrini, S., Stefenelli, C., Cioffi, G., Giovanelli, C., Rigatelli, G., Boni, S., Pasini, A., Sitta, N., Sacchetta, A., Borgese, L., Sciascia, R., Targa, L., Raviele, A., Madalosso, M., Bertaglia, E., Zoppo, F. C., Capanna, M., Fiorencis, R., Baracca, E., Rossi, R., Rossi, I., Trappolin, R., Morgera, T., Barducci, E., Baldin, M. G., Gobbo, G., Zardo, F., Hrovatin, E., Mos, L., Vriz, O., Sinagra, G., Aleksova, A., Mazzone, C., Fresco, C., Rubartelli, P., Moroni, L. A., Camerieri, A., Piana, M., Mureddu, R., Bertoli, D., Petacchi, R., Pancaldi, L. G., Gabrieli, L., Urbinati, S., Pedone, C., Di Niro, M., Brunelli, A., Bosi, S., Censi, S., Moruzzi, P., Pastori, P., Modena, M. G., Malavasi, V., Mezzetti, M., Melandri, F., Zuppiroli, A., Fazi, A., Testa, R., Venturini, E., Mazzinghi, F., Cosmi, D., Santoro, G. M., Minneci, C., Galli, M., Paperini, L., Bovenzi, F. M., Cortigiani, L., Cocchieri, M., Severini, D., Arcuri, G. M., Bagliani, G., Bernardinangeli, M., Proietti, G., Bocconcelli, P., Pierantozzi, A., Monti, F., Giamundo, L., Tancredi, P., Rossini, E., Bianchi, C., Bettiol, F., Giovannini, E., Fera, M. S., Santini, M., Bianconi, L., Boccanelli, A., Morosetti, P., Volpe, M., Facciolo, C., Vacri, A., Romanazzi, F., Napoletano, C., Piccioni, L. L., Candelmo, F., De Marco, G., Arnese, M. R., Vetrano, A., Prinzi, D., De Rosa, P., Capuano, V., Torre, S., D'Onofrio, A., Ammendola, E., Chiariello, M., Filardi, Pp., Battista, R., De Fusco, A., Molero, U., Iervoglini, A., Stefanelli, S., Fattore, L., Bosco, B., Liguori, A., Padula, G., De Luca, I., Sorino, M., Colonna, P., D'Agostino, C., Pierfelice, O., Pettinati, G., Muscella, A., De Lorenzi, E., Falco, M., Giannattasio, C., Baldi, N., Clemente, M. A., D'Alessandro, B., Truncellito, L., Arabia, F., Ciconte, V. A., Perticone, F., Ruberto, C., Buffon, A., Tomaselli, C., De Rosa, F., Mazza, S., Zampaglione, G., Pirozzi, A. M., Butera, A., Levato, M., Musacchio, D., Polimeni, R. M., Lacquaniti, V., Pulitano, G., Ruggeri, A., Provenzano, A., Cuccurullo, O., Musolino, M., Marrari, A., Anastasio, L., Schiavello, M., Comito, M. G., Gulizia, M. M., Francese, G. M., Vasquez, L., Coppolino, C., Casale, A., D'Urso, G., Oliva, G., Giordano, U., Andolina, S., Sanfilippo, N., Ingrilli, F., Accardo, S., Grasso, S., Buffa, L., Serra, E., Disertori, Marcello, Latini, Roberto, Barlera, Simona, Franzosi, Maria Grazia, Staszewsky, Lidia, Maggioni, Aldo Pietro, Lucci, Donata, Di Pasquale, Giuseppe, Tognoni, Gianni, GISSI AF, Investigator, Disertori, M, Latini, R, Barlera, S, Franzosi, Mg, Staszewsky, L, Maggioni, Ap, Lucci, D, Di Pasquale, G, Tognoni, G, Delise, P, Bertocchi, F, Maiocchi, G, Geraci, E, Correale, E, Lombardi, F, Mugelli, A, Urso, R, Scardi, S, Fabbri, G, Bartolomei, B, Barbato, G, Carbonieri, E, Ciricugno, S, Cosmi, F, Pratola, C, Rossi, Mg, Sciarra, L, Zeni, P, Ceseri, M, Atzori, A, Bambi, F, Baviera, M, Bianchini, F, Fenicia, E, Gianfriddo, M, Lonardo, G, Luise, A, Nota, R, Orlando, Me, Petrolo, R, Pierattini, C, Pierota, V, Ragno, A, Serio, C, Tafi, A, Tellaroli, E, Masson, S, Vago, T, Gramenzi, S, Orso, F, Suliman, I, Nicolis, E, Casola, C, Dall'Osso, D, Gorini, M, Bianchini, E, Cabiddu, S, Cangioli, I, Carnaghi, A, Cipressa, Ml, Cipressa, L, Galbiati, L, Lorimer, A, Priami, P, Moccetti, T, Vaghi, F, Capello, Af, Rossetti, G, Viada, E, Morena, L, Delucchi, M, Reynaud, Sg, Allemano, P, Massobrio, N, Gavazzi, A, Taddei, F, Mor, Da, Bortolini, F, Lorini, M, Inama, G, Durin, O, Pirelli, S, Spotti, A, Procopio, R, Cuzzucrea, D, Gentile, G, Margonato, A, Bassanelli, G, Tavazzi, L, Buzzi, Mp, Rordorf, R, Gualco, A, Opasich, C, Gronda, E, Genovese, L, Mattioli, R, Donatelli, F, Uriarte, Ja, Rauhe, W, Bertagnolli, C, Canestrini, S, Stefenelli, C, Cioffi, G, Giovanelli, C, Rigatelli, G, Boni, S, Pasini, A, Sitta, N, Sacchetta, A, Borgese, L, Sciascia, R, Targa, L, Raviele, A, Madalosso, M, Bertaglia, E, Zoppo, Fc, Capanna, M, Fiorencis, R, Baracca, E, Rossi, R, Rossi, I, Trappolin, R, Morgera, T, Barducci, E, Baldin, Mg, Gobbo, G, Zardo, F, Hrovatin, E, Mos, L, Vriz, O, Sinagra, G, Aleksova, A, Mazzone, C, Fresco, C, Rubartelli, P, Moroni, La, Camerieri, A, Piana, M, Mureddu, R, Bertoli, D, Petacchi, R, Pancaldi, Lg, Gabrieli, L, Urbinati, S, Pedone, C, Di Niro, M, Brunelli, A, Bosi, S, Censi, S, Moruzzi, P, Pastori, P, Modena, Mg, Malavasi, V, Mezzetti, M, Melandri, F, Zuppiroli, A, Fazi, A, Testa, R, Venturini, E, Mazzinghi, F, Cosmi, D, Santoro, Gm, Minneci, C, Galli, M, Paperini, L, Bovenzi, Fm, Cortigiani, L, Cocchieri, M, Severini, D, Arcuri, Gm, Bagliani, G, Bernardinangeli, M, Proietti, G, Bocconcelli, P, Pierantozzi, A, Monti, F, Giamundo, L, Tancredi, P, Rossini, E, Bianchi, C, Bettiol, F, Giovannini, E, Fera, M, Santini, M, Bianconi, L, Boccanelli, A, Morosetti, P, Volpe, M, Facciolo, C, Vacri, A, Romanazzi, F, Napoletano, C, Piccioni, Ll, Candelmo, F, De Marco, G, Arnese, Mr, Vetrano, A, Prinzi, D, De Rosa, P, Capuano, V, Torre, S, D'Onofrio, A, Ammendola, E, Chiariello, Massimo, PERRONE FILARDI, Pasquale, Battista, R, De Fusco, A, Molero, U, Iervoglini, A, Stefanelli, S, Fattore, L, Bosco, B, Liguori, A, Padula, G, De Luca, I, Sorino, M, Colonna, P, D'Agostino, C, Pierfelice, O, Pettinati, G, Muscella, A, De Lorenzi, E, Falco, M, Giannattasio, C, Baldi, N, Clemente, Ma, D'Alessandro, B, Truncellito, L, Arabia, F, Ciconte, Va, Perticone, F, Ruberto, C, Buffon, A, Tomaselli, C, De Rosa, F, Mazza, S, Zampaglione, G, Pirozzi, Am, Butera, A, Levato, M, Musacchio, D, Polimeni, Rm, Lacquaniti, V, Pulitanò, G, Ruggeri, A, Provenzano, A, Cuccurullo, O, Musolino, M, Marrari, A, Anastasio, L, Schiavello, M, Comito, Mg, Gulizia, Mm, Francese, Gm, Vasquez, L, Coppolino, C, Casale, A, D'Urso, G, Oliva, G, Giordano, U, Andolina, S, Sanfilippo, N, Ingrillì, F, Accardo, S, Grasso, S, and Buffa, L
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Male ,medicine.medical_specialty ,medicine.medical_treatment ,Tetrazoles ,Cardiomegaly ,Comorbidity ,Placebo ,Cardioversion ,Double-Blind Method ,Recurrence ,Multicenter trial ,Internal medicine ,Angiotensin II Type 1 Receptor Blocker ,Cardiovascular Disease ,Atrial Fibrillation ,medicine ,Left atrial enlargement ,Diabetes Mellitus ,Humans ,Sinus rhythm ,cardiovascular diseases ,Prospective Studies ,Tetrazole ,Proportional Hazards Models ,Aged ,business.industry ,Medicine (all) ,Hazard ratio ,Atrial fibrillation ,Diabetes Mellitu ,Valine ,General Medicine ,Middle Aged ,medicine.disease ,valsartan ,atrial fibrillation ,Prospective Studie ,Valsartan ,Cardiovascular Diseases ,cardiovascular system ,Cardiology ,Proportional Hazards Model ,Female ,business ,Angiotensin II Type 1 Receptor Blockers ,medicine.drug ,Human - Abstract
BACKGROUND: Atrial fibrillation is the most common cardiac arrhythmia, and no current therapy is ideal for control of this condition. Experimental studies suggest that angiotensin II-receptor blockers (ARBs) can influence atrial remodeling, and some clinical studies suggest that they may prevent atrial fibrillation. METHODS: We conducted a large, randomized, prospective, placebo-controlled, multicenter trial to test whether the ARB valsartan could reduce the recurrence of atrial fibrillation. We enrolled patients who were in sinus rhythm but had had either two or more documented episodes of atrial fibrillation in the previous 6 months or successful cardioversion for atrial fibrillation in the previous 2 weeks. To be eligible, patients also had to have underlying cardiovascular disease, diabetes, or left atrial enlargement. Patients were randomly assigned to receive valsartan or placebo. The two primary end points were the time to a first recurrence of atrial fibrillation and the proportion of patients who had more than one recurrence of atrial fibrillation over the course of 1 year. RESULTS: A total of 1442 patients were enrolled in the study. Atrial fibrillation recurred in 371 of the 722 patients (51.4%) in the valsartan group, as compared with 375 of 720 (52.1%) in the placebo group (adjusted hazard ratio, 0.97; 96% confidence interval [CI], 0.83 to 1.14; P = 0.73). More than one episode of atrial fibrillation occurred in 194 of 722 patients (26.9%) in the valsartan group and in 201 of 720 (27.9%) in the placebo group (adjusted odds ratio, 0.89; 99% CI, 0.64 to 1.23; P = 0.34). The results were similar in all predefined subgroups of patients, including those who were not receiving angiotensin-converting-enzyme inhibitors. CONCLUSIONS: Treatment with valsartan was not associated with a reduction in the incidence of recurrent atrial fibrillation. (ClinicalTrials.gov number, NCT00376272.) Copyright © 2009 Massachusetts Medical Society.
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- 2009
7. Regular Wine Consumption in Chronic Heart Failure: Impact on Outcomes, Quality of Life, and Circulating Biomarkers
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Cosmi, Franco, Di Giulio, Paola, Masson, Serge, Finzi, Andrea, Marfisi, Rosa Maria, Cosmi, Deborah, Scarano, Marco, Tognoni, Gianni, Maggioni, Aldo P., Porcu, Maurizio, Boni, Silvana, Cutrupi, Giovanni, Tavazzi, Luigi, Latini, Roberto Tavazzi, L, Tognoni, G, Barlera, S, Franzosi, Mg, Latini, R, Lucci, D, Maggioni, Ap, Marchioli, R, Nicolosi, Gl, Porcu, M, Yusuf, S, Camerini, F, Cohn, Jn, Decarli, A, Pitt, B, Sleight, P, Poole-Wilson, Pa, Geraci, E, Scherillo, M, Fabbri, G, Bartolomei, B, Bertoli, D, Cobelli, F, Fresco, C, Ledda, A, Levantesi, G, Opasich, C, Rusconi, F, Sinagra, G, Turazza, F, Volpi, A, Ceseri, M, Alongi, G, Atzori, A, Bambi, F, Bastarolo, D, Bianchini, F, Cangioli, I, Canu, V, Caporusso, C, Cenni, G, Cintelli, L, Cocchio, M, Confente, A, Fenicia, E, Friso, G, Gianfriddo, M, Grilli, G, Lazzaro, B, Lonardo, G, Luise, A, Nota, R, Orlando, M, Petrolo, R, Pierattini, C, Pierota, V, Provenzani, A, Quartuccio, V, Ragno, A, Serio, C, Spolaor, A, Tafi, A, Tellaroli, E, Ghio, S, Ghizzardi, E, Masson, S, Crociati, L, Rovere, Mt, Corra, U, Di Giulio, P, Finzi, A, Gorini, M, Gonzini, L, Milani, V, Orsini, G, Bianchini, E, Cabiddu, S, Cipressa, L, Cipressa, Ml, Di Bitetto, G, Ferri, B, Galbiati, L, Lorimer, A, Pera, C, Priami, P, Rossi, Mg, Pasotti, E, Vaghi, F, Roncarolo, P, Zunino, Mt, Matta, F, Actis, E, Gaita, F, Azzaro, G, Zanetta, M, Paino, Am, Parravicini, U, Vegis, D, Conte, R, Ferraro, P, De Bernardi, A, Morelloni, S, Fagnani, M, Lucchina, Pg, Montagna, L, Bellone, E, Sappe, D, Ferraro, F, Delucchi, M, Reynaud, Sg, Dore, M, La, A, Massobrio, N, Bo, L, Trinchero, R, Imazio, M, Brocchi, G, Nejrotti, A, Rissone, L, Gabasio, S, Zocchi, C, Randazzo, S, Crenna, A, Giannuzzi, P, Bonanomi, E, Mezzani, A, De Marchi, M, Begliuomini, G, Gianonatti, Ca, Gavazzi, A, Grosu, A, Cas, Ld, Nodari, S, Garyfallidis, P, Bertoletti, A, Bonifazi, C, Arisi, S, Mascaro, F, Fraccarollo, M, Dell, S, Sfolcini, M, Bortolini, F, Raccagni, D, Turelli, A, Santarone, M, Miglierina, E, Sormani, L, Jemoli, R, Tettamanti, F, Pirelli, S, Bianchi, C, Verde, S, Mariani, M, Ziacchi, V, Ferrazza, A, Russo, A, Bortolotti, M, Pasini, Gf, Jones, Kn, Cuzzucrea, D, Gullace, G, Carbone, C, Granata, A, De, S, Del Rosso, G, Inserra, C, Renaldini, E, Zappa, C, Moretti, M, Zanini, R, Ferrari, M, Cei, A, Lissi, C, Dovico, E, Fiorentini, C, Palermo, P, Brusoni, B, Negrini, M, Heyman, J, Danzi, Gb, Frigerio, M, Beretta, L, Sachero, A, Casazza, F, Squadroni, L, Lombardi, F, Marano, L, Margonato, A, Fragasso, G, Febo, Oc, Aiolfi, E, Olmetti, F, Grieco, A, Antonazzo, V, Specchia, G, Mortara, A, Robustelli, F, Songini, Mg, Schweiger, C, Frisinghelli, A, Palvarini, M, Campana, C, Scelsi, L, Marsan, Na, Gualco, A, De Feo, S, Iannone, Ma, Diaco, T, Zaniboni, D, Milanesi, G, Nassiacos, D, Meloni, S, Giani, P, Nicoli, T, Malinverni, C, Gusmini, A, Pozzoni, L, Bisiani, G, Margaroli, P, Schizzarotto, A, Daverio, A, Morelli, E, Occhi, G, Partesana, N, Bandini, P, Rosella, Mg, Giustiniani, S, Cucchi, G, Pedretti, R, Raimondo, R, Vaninetti, R, Fedele, A, Ghezzi, I, Rezzonico, E, Salerno, Ja, Morandi, F, Salvucci, F, Valenti, C, Graziano, G, Romano, M, Cimminiello, C, Mangone, I, Lombardo, M, Quorso, P, Marinoni, G, Breghi, M, Erckert, M, Dienstl, A, Mirante, G, Stefenelli, C, Cioffi, G, Buczkowska, E, Bonanome, A, Bazzanini, F, Parissenti, L, Serafini, C, Catania, G, Tarantini, L, Rigatelli, G, Boni, S, Pasini, A, Masini, E, Zampiero, Aa, Zanchetta, M, Franceschetto, L, Delise, P, Marcon, C, Sacchetta, A, Borgese, L, Artusi, L, Casolino, P, Corbara, F, Banzato, A, Barbiero, M, Aldegheri, Mp, Bazzucco, R, Crivellenti, G, Raviele, A, Zanella, C, Pascotto, P, Sarto, P, Milan, S, Barbieri, E, Girardi, P, Dalla, W, Mule, Jd, Di Sipio ML, Cazzin, R, Milan, D, Zonzin, P, Carraro, M, Rossi, R, Carbonieri, E, Rossi, I, Stritoni, P, Meneghetti, P, Risica, G, Tenderini, Pl, Vassanelli, C, Zanolla, L, Perini, G, Brighetti, G, Chiozza, R, Giuliano, G, Baldin, Mg, Gortan, R, Cesanelli, R, Piazza, R, Mos, L, Vriz, O, Pavan, D, Pascottini, G, Alberti, E, Werren, M, Solinas, L, Longaro, F, Fioretti, P, Albanese, Mc, Miani, D, Gianrossi, R, Pende, A, Rubartelli, P, Magaia, O, Caruso, D, Faraguti, As, Magliani, L, Miccoli, F, Guglielmino, G, Cantarelli, A, Orlandi, S, Vallebona, A, Pozzati, A, Brega, G, Pancaldi, Lg, Vandelli, R, Urbinati, S, Poci, Mg, Zoli, M, Costa, Gm, Guiducci, U, Zobbi, G, Tartagni, F, Tisselli, A, Gentili, A, Pieri, P, Cagnetta, E, Bendinelli, S, Barbieri, A, Conti, R, Ferrari, R, Merlini, F, Fucili, A, Moruzzi, P, Buia, E, Galvani, M, Ferrini, D, Baggioni, G, Yiannacopulu, P, Canè, G, Bonfiglioli, A, Zandomeneghi, R, Brugioni, L, Giannini, A, Di, R, Giuliani, M, Rusconi, L, Del Corso, P, Piovaccari, G, Bologna, F, Venturi, P, Melandri, F, Bagni, E, Bolognese, L, Perticucci, R, Zuppiroli, A, Nannini, M, Consoli, N, Petrone, P, Pipitò, C, Colombi, L, Bernardi, D, Mariani, Pr, Testa, R, Mazzinghi, F, Cosmi, F, Cosmi, D, Zipoli, A, Cecchi, A, Castelli, G, Ciaccheri, M, Mori, F, Pieri, F, Valoti, P, Chiarantini, D, Santoro, Gm, Minneci, C, Marchi, F, Milli, M, Zambaldi, G, Geri, Aa, Cipriani, M, Alessandri, M, Severi, S, Stefanelli, S, Comella, A, Poddighe, R, Digiorgio, A, Carluccio, M, Berti, S, Rizza, A, Bonatti, V, Molendi, V, Brancato, A, D'Aprile, N, Giappichini, G, Del Vecchio, S, Mantini, G, De Tommasi, F, Meucci, G, Cordoni, M, Bechi, S, Barsotti, L, Baldini, P, Romei, M, Scopelliti, G, Lauri, G, Pestelli, F, Furiozzi, F, Cocchieri, M, Severini, D, Patriarchi, F, Chiocchi, P, Buccolieri, M, Martinelli, S, Wee, A, Angelici, F, Bernardinangeli, M, Proietti, G, Biscottini, B, Panciarola, R, Marinacci, L, Perna, Gp, Gabrielli, D, Moraca, A, Moretti, L, Partemi, L, Gregori, G, Amici, R, Patteri, G, Capone, P, Savini, E, Morgagni, Gl, Paccaloni, L, Pezzuoli, F, Carincola, S, Papi, S, De Crescentini, S, Gerardi, P, Midi, P, Gallenzi, E, Pajes, G, Mancone, C, Di, V, Di Gennaro, M, Calcagno, S, Toscano, S, Antonicoli, S, Carta, F, Giorgi, G, Comito, F, Daniele, E, Goretti, Sm, Ciarla, O, Gelfo, Pg, Acquaviva, A, Testa, D, Testa, G, Pagliaro, Fa, Russo, F, Vetta, F, Marchese, I, Di, G, D'Ambrosio, A, Leggio, F, Del Sindaco, D, Lacchè, A, Avallone, A, Risa, Mp, Azzolini, P, Baldo, E, Giovannini, E, Pulignano, G, Tondo, C, Picchio, E, Biffani, E, Tanzi, P, Pozzar, F, Farnetti, F, Azzarito, M, Santini, M, Varveri, A, Ferraiuolo, G, Valtorta, C, Gaspardone, A, Barbato, G, Ceci, V, Aspromonte, N, Bellocci, F, Colizzi, C, Fedele, F, Perez, Fi, Galati, A, Rossetti, A, Mainella, A, Ciuffetta, D, Matteucci, C, Busi, G, De, A, Farina, G, Granatelli, A, Leone, F, Frasca, F, Castellani, G, Massaro, G, Mastrogiuseppe, G, Vacri, A, De Sanctis, F, Cioli, M, Di Luzio, S, Napoletano, C, Piccioni, Ll, De Simone, G, Ottaviano, A, Mazza, V, Spedaliere, C, Staniscia, Td, Calgione, E, De Marco, G, Chiacchio, T, Di, T, Romanzi, S, Salvatore, G, Golino, P, Palermo, A, Mascia, F, Vetrano, A, Vinciguerra, A, Caliendo, L, Longobardi, R, De Caro, G, Di Nola, R, Piemonte, F, Prinzi, D, De Rosa, P, De, V, Riello, F, Capuano, V, Vecchio, G, Landi, M, Amato, S, Garofalo, M, D'Avino, M, Sensale, P, Maiolica, O, Santoro, R, Caso, P, Miceli, D, Maurea, N, Bianchi, U, Crispo, C, Chiariello, M, Filardi, Pp, Russo, L, Capuano, N, Ungaro, G, Vergara, G, Scafuro, F, D'Angelo, G, Campaniello, C, Bottiglieri, P, Volpe, A, Battista, R, De Risi, L, Cardillo, G, Sibilio, G, Marino, Ap, Silvestri, F, Predotti, P, Iervoglini, A, De Matteis, C, Sarnicola, P, Matarazzo, Mm, Baldi, S, Iuliano, V, Astarita, C, Cuccaro, P, Liguori, A, Liguori, G, Gregorio, G, Petraglia, L, Antonelli, G, Amodio, G, De Luca, I, Franchini, G, Lenti, Ml, Cavallari, D, D'Agostino, C, Scalera, G, Altamura, Cm, Russo, M, Mascolo, Ar, Pettinati, G, Ciricugno, Sa, Scrutinio, D, Passantino, A, Mastrangelo, D, Di Masi, A, De, R, Cannone, M, Dibiase, F, Pensato, M, Loliva, F, Trapani, F, Panettieri, I, Leone, L, Di, M, Carrone, M, Gallone, V, Cocco, F, Costantini, M, Tritto, C, Cavalieri, F, Stella, L, Magliari, F, Callerame, M, De Giorgi, A, Pellegrino, L, Correra, M, Portulano, V, Nisi, Gl, Grassi, G, Cristallo, E, De Laura, D, Salerno, C, Fanelli, R, Villella, M, Pede, S, Renna, A, De Lorenzi, E, Urso, L, Lenti, V, Peluso, A, Baldi, N, Polimeni, G, Palma, P, Lauletta, R, Tagliamonte, E, Cirillo, T, Centonze, G, D'Alessandro, B, Truncellito, L, Mecca, D, Petruzzi, Ma, Coviello, Ro, Lopizzo, A, Chiaffitelli, M, Barbuzzi, S, Gubelli, S, Germinario, G, Cosentino, N, Mingrone, A, Vico, R, Borrello, G, Mazza, Ml, Cimino, R, Galasso, D, Cassadonte, F, Talarico, U, Perticone, F, Cassano, S, Catapano, F, Calemme, S, Feraco, E, Cloro, C, Misuraca, G, Caporale, R, Vigna, L, Spagnuolo, V, De Rosa, F, Spadafora, G, Zampaglione, G, Russo, R, Schipani, Fa, Ferragina, Af, Stranieri, D, Musca, G, Carpino, C, Bencardino, P, Raimondo, F, Musacchio, D, Pulitano, G, Ruggeri, A, Provenzano, A, Salituri, S, Musolino, M, Calandruccio, S, Marrari, A, Tripodi, E, Scali, R, Anastasio, L, Arone, A, Aragona, P, Donnangelo, L, Comito, Mg, Bilotta, F, Vaccaro, I, Rametta, R, Ventura, V, Bonvegna, A, Alì, A, Cinnirella, C, Raineri, M, Pompeo, F, Ingurgio, Nc, Carini, V, Coco, R, Giunta, G, Leonardi, G, Randazzo, V, Di Blasi, V, Tamburino, C, Russo, G, Mangiameli, S, Cardillo, R, Castelli, D, Inserra, V, Arena, A, Gulizia, Mm, Raciti, S, Rapisarda, G, Romano, R, Prestifilippo, P, Braschi, Gb, Ledda, G, Terrazzino, R, De Caro, M, Scilabra, G, Graffagnino, B, Grassi, R, Scimone, Gf, Vasquez, L, Coppolino, C, Casale, A, Castelli, M, D'Urso, G, D'Antonio, E, Presti, Ll, Badalamenti, E, Conti, P, Sanfilippo, N, Cirrincione, V, Cinà, Mt, Cusimano, G, Taormina, A, Giuliano, P, Bajardi, A, Mandala, V, Canonico, A, Geraci, G, Sabella, Fp, Enia, F, Floresta, Am, Cascio, Il, Gumina, D, Cavallaro, A, Piccione, G, Ferrante, R, Blandino, M, Iudicello, Ms, Mossuti, E, Romano, G, Lombardo, L, Monastra, P, Di Vincenzo, D, Orru, P, Muscas, F, Giardina, G, Corda, M, Locci, G, Podda, A, Ledda, M, Siddi, P, Lai, C, Pili, G, Mercuro, G, Mureddu, G, Ganau, A, Meloni, G, Poddighe, G, Sanna, G., Cosmi, Franco, Di Giulio, Paola, Masson, Serge, Finzi, Andrea, Marfisi, Rosa Maria, Cosmi, Deborah, Scarano, Marco, Tognoni, Gianni, Maggioni, Aldo P, Porcu, Maurizio, Boni, Silvana, Cutrupi, Giovanni, Tavazzi, Luigi, Latini, Roberto, on behalf of the GISSI-HF, Investigator, Margonato, Alberto, DI GIULIO, Paola, Maggioni, Aldo P., GISSI HF, Investigator, and Sinagra, Gianfranco
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Male ,Health Status ,Left ,Wine ,Comorbidity ,Ventricular Function, Left ,Health Statu ,Quality of life ,Risk Factors ,Surveys and Questionnaires ,Prevalence ,Ventricular Function ,Surveys and Questionnaire ,Depression (differential diagnoses) ,Depression ,Medicine (all) ,Middle Aged ,Prognosis ,biological marker ,Italy ,Female ,Risk assessment ,Cardiology and Cardiovascular Medicine ,biological markers ,Human ,Cardiac function curve ,Vasculitis ,medicine.medical_specialty ,Vasculiti ,Alcohol Drinking ,Prognosi ,Lower risk ,Risk Assessment ,Internal medicine ,medicine ,Humans ,Protective Factor ,Aged ,Heart Failure ,business.industry ,Risk Factor ,Stroke Volume ,Biomarker ,quality of life ,wine ,aged ,alcohol drinking ,biomarkers ,chronic disease ,comorbidity ,depression ,female ,heart failure ,humans ,italy ,male ,middle aged ,prevalence ,prognosis ,protective factors ,risk assessment ,risk factors ,stroke volume ,surveys and questionnaires ,vasculitis ,ventricular function, left ,health status ,cardiology and cardiovascular medicine ,Biomarkers ,Chronic Disease ,Protective Factors ,Quality of Life ,medicine.disease ,Clinical trial ,Heart failure ,Physical therapy ,business - Abstract
Background— Moderate, regular alcohol consumption is generally associated with a lower risk of cardiovascular events but data in patients with chronic heart failure are scarce. We evaluated the relations between wine consumption, health status, circulating biomarkers, and clinical outcomes in a large Italian population of patients with chronic heart failure enrolled in a multicenter clinical trial. Methods and Results— A brief questionnaire on dietary habits was administered at baseline to 6973 patients enrolled in the Gruppo Italiano per lo Studio della Sopravvivenza nell’Insufficienza Cardiaca-Heart Failure (GISSI-HF) trial. The relations between wine consumption, fatal and nonfatal clinical end points, quality of life, symptoms of depression, and circulating biomarkers of cardiac function and inflammation (in subsets of patients) were evaluated with simple and multivariable-adjusted statistical models. Almost 56% of the patients reported drinking at least 1 glass of wine per day. After adjustment, clinical outcomes were not significantly different in the predefined 4 groups of wine consumption. However, patients with more frequent wine consumption had a significantly better perception of health status (Kansas City Cardiomyopathy Questionnaire score, adjusted P P =0.01), and lower plasma levels of biomarkers of vascular inflammation (osteoprotegerin and C-terminal proendothelin-1, adjusted P P =0.01) after adjusting for possible confounders. Conclusions— We show for the first time in a large cohort of patients with chronic heart failure that moderate wine consumption is associated with a better perceived and objective health status, lower prevalence of depression, and less vascular inflammation, but does not translate into more favorable clinical 4-year outcomes. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT0033633.
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- 2015
8. Valsartan for prevention of recurrent atrial fibrillation (New England Journal of Medicine (2009) 360, (1606-1617))
- Author
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Delise, P., Bertocchi, F., Maiocchi, G., Geraci, E., Correale, E., Lombardi, F., Mugelli, A., Urso, R., Scardi, S., Fabbri, G., Bartolomei, B., Barbato, G., Carbonieri, E., Ciricugno, S., Cosmi, F., Pratola, C., Rossi, M. G., Sciarra, L., Zeni, P., Ceseri, M., Atzori, A., Bambi, F., Baviera, M., Bianchini, F., Fenicia, E., Gianfriddo, M., Lonardo, G., Luise, A., Nota, R., Orlando, M. E., Petrolo, R., Pierattini, C., Pierota, V., Ragno, A., Serio, C., Tafi, A., Tellaroli, E., Masson, S., Vago, T., Gramenzi, S., Orso, F., Suliman, I., Nicolis, E., Casola, C., Dall Osso, D., Gorini, M., Bianchini, E., Cabiddu, S., Cangioli, I., Carnaghi, A., Cipressa, M. L., Cipressa, L., Galbiati, L., Lorimer, A., Priami, P., Moccetti, T., Vaghi, F., Capello, A. F., Rossetti, G., Viada, E., Morena, L., Delucchi, M., Reynaud, S. G., Allemano, P., Massobrio, N., Gavazzi, A., Taddei, F., Mor, D. A., Bortolini, F., Lorini, M., Inama, G., Durin, O., Pirelli, S., Spotti, A., Procopio, R., Cuzzucrea, D., Gentile, G., Margonato, A., Bassanelli, G., Tavazzi, L., Buzzi, M. P., Rordorf, R., Gualco, A., Opasich, C., Gronda, E., Genovese, L., Mattioli, R., Donatelli, F., Uriarte, J. A., Rauhe, W., Bertagnolli, C., Canestrini, S., Stefenelli, C., Cioffi, G., Giovanelli, C., Rigatelli, G., Boni, S., Pasini, A., Sitta, N., Sacchetta, A., Borgese, L., Sciascia, R., Targa, L., Raviele, A., Madalosso, M., Bertaglia, E., Franco Zoppo, Capanna, M., Fiorencis, R., Baracca, E., Rossi, R., Rossi, I., Trappolin, R., Morgera, T., Barducci, E., Baldin, M. G., Gobbo, G., Zardo, F., Hrovatin, E., Mos, L., Vriz, O., Sinagra, G., Aleksova, A., Mazzone, C., Fresco, C., Rubartelli, P., Moroni, L. A., Camerieri, A., Piana, M., Mureddu, R., Bertoli, D., Petacchi, R., Pancaldi, L. G., Gabrieli, L., Urbinati, S., Pedone, C., Di Niro, M., Brunelli, A., Bosi, S., Censi, S., Moruzzi, P., Pastori, P., Modena, M. G., Malavasi, V., Mezzetti, M., Melandri, F., Zuppiroli, A., Fazi, A., Testa, R., Venturini, E., Mazzinghi, F., Cosmi, D., Santoro, G. M., Minneci, C., Galli, M., Paperini, L., Bovenzi, F. M., Cortigiani, L., Cocchieri, M., Severini, D., Arcuri, G. M., Bagliani, G., Bernardinangeli, M., Proietti, G., Bocconcelli, P., Pierantozzi, A., Monti, F., Giamundo, L., Tancredi, P., Rossini, E., Bianchi, C., Bettiol, F., Giovannini, E., Fera, M. S., Santini, M., Bianconi, L., Boccanelli, A., Morosetti, P., Volpe, M., Facciolo, C., Vacri, A., Romanazzi, F., Napoletano, C., Piccioni, L. L., Candelmo, F., Marco, G., Arnese, M. R., Vetrano, A., Prinzi, D., Rosa, P., Capuano, V., Torre, S., D Onofrio, A., Ammendola, E., Chiariello, M., Filardi, Pp, Battista, R., Fusco, A., Molero, U., Iervoglini, A., Stefanelli, S., Fattore, L., Bosco, B., Liguori, A., Padula, G., Luca, I., Sorino, M., Colonna, P., D Agostino, C., Pierfelice, O., Pettinati, G., Muscella, A., Lorenzi, E., Falco, M., Giannattasio, C., Baldi, N., Clemente, M. A., D Alessandro, B., Truncellito, L., Arabia, F., Ciconte, V. A., Perticone, F., Ruberto, C., Buffon, A., Tomaselli, C., Rosa, F., Mazza, S., Zampaglione, G., Pirozzi, A. M., Butera, A., Levato, M., Musacchio, D., Polimeni, R. M., Lacquaniti, V., Pulitano, G., Ruggeri, A., Provenzano, A., Cuccurullo, O., Musolino, M., Marrari, A., Anastasio, L., Schiavello, M., Comito, M. G., Gulizia, M. M., Francese, G. M., Vasquez, L., Coppolino, C., Casale, A., D Urso, G., Oliva, G., Giordano, U., Andolina, S., Sanfilippo, N., Ingrilli, F., Accardo, S., Grasso, S., Buffa, L., Serra, E., Disertori, M., Latini, R., Barlera, S., Franzosi, M. G., Staszewsky, L., Maggioni, A. P., Lucci, D., Di Pasquale, G., Tognoni, G., Delise, P., Bertocchi, F., Maiocchi, G., Geraci, E., Correale, E., Lombardi, F., Mugelli, A., Urso, R., Scardi, S., Fabbri, G., Bartolomei, B., Barbato, G., Carbonieri, E., Ciricugno, S., Cosmi, F., Pratola, C., Rossi, M. G., Sciarra, L., Zeni, P., Ceseri, M., Atzori, A., Bambi, F., Baviera, M., Bianchini, F., Fenicia, E., Gianfriddo, M., Lonardo, G., Luise, A., Nota, R., Orlando, M. E., Petrolo, R., Pierattini, C., Pierota, V., Ragno, A., Serio, C., Tafi, A., Tellaroli, E., Masson, S., Vago, T., Gramenzi, S., Orso, F., Suliman, I., Nicolis, E., Casola, C., Dall'Osso, D., Gorini, M., Bianchini, E., Cabiddu, S., Cangioli, I., Carnaghi, A., Cipressa, M. L., Cipressa, L., Galbiati, L., Lorimer, A., Priami, P., Moccetti, T., Vaghi, F., Capello, A. F., Rossetti, G., Viada, E., Morena, L., Delucchi, M., Reynaud, S. G., Allemano, P., Massobrio, N., Gavazzi, A., Taddei, F., Mor, D. A., Bortolini, F., Lorini, M., Inama, G., Durin, O., Pirelli, S., Spotti, A., Procopio, R., Cuzzucrea, D., Gentile, G., Margonato, A., Bassanelli, G., Tavazzi, L., Buzzi, M. P., Rordorf, R., Gualco, A., Opasich, C., Gronda, E., Genovese, L., Mattioli, R., Donatelli, F., Uriarte, J. A., Rauhe, W., Bertagnolli, C., Canestrini, S., Stefenelli, C., Cioffi, G., Giovanelli, C., Rigatelli, G., Boni, S., Pasini, A., Sitta, N., Sacchetta, A., Borgese, L., Sciascia, R., Targa, L., Raviele, A., Madalosso, M., Bertaglia, E., Zoppo, F. C., Capanna, M., Fiorencis, R., Baracca, E., Rossi, R., Rossi, I., Trappolin, R., Morgera, T., Barducci, E., Baldin, M. G., Gobbo, G., Zardo, F., Hrovatin, E., Mos, L., Vriz, O., Sinagra, G., Aleksova, A., Mazzone, C., Fresco, C., Rubartelli, P., Moroni, L. A., Camerieri, A., Piana, M., Mureddu, R., Bertoli, D., Petacchi, R., Pancaldi, L. G., Gabrieli, L., Urbinati, S., Pedone, C., Di Niro, M., Brunelli, A., Bosi, S., Censi, S., Moruzzi, P., Pastori, P., Modena, M. G., Malavasi, V., Mezzetti, M., Melandri, F., Zuppiroli, A., Fazi, A., Testa, R., Venturini, E., Mazzinghi, F., Cosmi, D., Santoro, G. M., Minneci, C., Galli, M., Paperini, L., Bovenzi, F. M., Cortigiani, L., Cocchieri, M., Severini, D., Arcuri, G. M., Bagliani, G., Bernardinangeli, M., Proietti, G., Bocconcelli, P., Pierantozzi, A., Monti, F., Giamundo, L., Tancredi, P., Rossini, E., Bianchi, C., Bettiol, F., Giovannini, E., Fera, M. S., Santini, M., Bianconi, L., Boccanelli, A., Morosetti, P., Volpe, M., Facciolo, C., Vacri, A., Romanazzi, F., Napoletano, C., Piccioni, L. L., Candelmo, F., De Marco, G., Arnese, M. R., Vetrano, A., Prinzi, D., De Rosa, P., Capuano, V., Torre, S., D'Onofrio, A., Ammendola, E., Chiariello, M., Filardi, Pp., Battista, R., De Fusco, A., Molero, U., Iervoglini, A., Stefanelli, S., Fattore, L., Bosco, B., Liguori, A., Padula, G., De Luca, I., Sorino, M., Colonna, P., D'Agostino, C., Pierfelice, O., Pettinati, G., Muscella, A., De Lorenzi, E., Falco, M., Giannattasio, C., Baldi, N., Clemente, M. A., D'Alessandro, B., Truncellito, L., Arabia, F., Ciconte, V. A., Perticone, F., Ruberto, C., Buffon, A., Tomaselli, C., De Rosa, F., Mazza, S., Zampaglione, G., Pirozzi, A. M., Butera, A., Levato, M., Musacchio, D., Polimeni, R. M., Lacquaniti, V., Pulitano, G., Ruggeri, A., Provenzano, A., Cuccurullo, O., Musolino, M., Marrari, A., Anastasio, L., Schiavello, M., Comito, M. G., Gulizia, M. M., Francese, G. M., Vasquez, L., Coppolino, C., Casale, A., D'Urso, G., Oliva, G., Giordano, U., Andolina, S., Sanfilippo, N., Ingrilli, F., Accardo, S., Grasso, S., Buffa, L., Serra, E., Disertori, Marcello, Latini, Roberto, Barlera, Simona, Franzosi, Maria Grazia, Staszewsky, Lidia, Maggioni, Aldo Pietro, Lucci, Donata, Di Pasquale, Giuseppe, and Tognoni, Gianni
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Medicine (all) - Published
- 2009
9. Valsartan for prevention of recurrent atrial
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Disertori, M, Latini, R, Maggioni, Ap, Barlera, S, Di Pasquale, G, Franzosi, Mg, Lucci, D, Staszewsky, L, Tognoni, G, Delise, P, Bertocchi, F, Maiocchi, G, Geraci, E, Correale, E, Lombardi, F, Mugelli, A, Urso, R, Scardi, S, Fabbri, G, Bartolomei, B, Barbato, G, Carbonieri, E, Ciricugno, S, Cosmi, F, Pratola, C, Rossi, Mg, Sciarra, L, Zeni, P, Ceseri, M, Atzori, A, Bambi, F, Baviera, M, Bianchini, F, Cfenicia, E, Gianfriddo, M, Lonardo, G, Luise, A, Nota, R, Orlando, Me, Petrolo, R, Pierattini, C, Pierota, V, Ragno, A, Serio, C, Tafi, A, Tellaroli, E, Masson, S, Vago, T, Gramenzi, S, Orso, F, Suliman, I, Nicolis, E, Casola, C, Dall'Osso, D, Gorini, M, Bianchini, E, Cabiddu, S, Cangioli, I, Carnaghi, A, Cipressa, Ml, Cipressa, L, Galbiati, L, Lorimer, A, Priami, P, Moccetti, T, Vaghi, F, Capello, Af, Rossetti, G, Viada, E, Morena, L, Delucchi, M, Reynaud SG, Allemano, P, Massobrio, N, Gavazzi, A, Taddei, F, Mor, Da, Bortolini, F, Lorini, M, Inama, G, Durin, O, Pirelli, S, Spotti, A, Procopio, R, Cuzzucrea, D, Gentile, G, Margonato, A, Bassanelli, G, Tavazzi, L, Buzzi, Mp, Rordorf, R, Gualco, A, Opasich, C, Gronda, E, Genovese, L, Mattioli, R, Donatelli, F, Uriarte, Ja, Rauhe, W, Bertagnolli, C, Canestrini, S, Stefenelli, C, Cioffi, G, Giovanelli, C, Rigatelli, G, Boni, S, Pasini, A, Sitta, N, Sacchetta, A, Borgese, L, Sciascia, R, Targa L, Raviele, A, Madalosso, M, Bertaglia, E, Zoppo, Fc, Capanna, M, Fiorencis, R, Baracca, E, Rossi, R, Rossi, I, Trappolin, R, Morgera, T, Barducci, E, Baldin, Mg, Gobbo, G, Zardo, F, Hrovatin, E, Mos, L, Vriz, O, Sinagra, G, Aleksova, A, Mazzone, C, Fresco, C, Rubartelli, P, Moroni, La, Camerieri, A, Piana, M, Mureddu, R, Bertoli, D, Petacchi, R, Pancaldi, Lg, Gabrieli, L, Urbinati, S, Pedone, C, Di Niro, M, Brunelli, A, Bosi, S, Censi, S, Moruzzi, P, Pastori, P, Modena, Mg, Malavasi, V, Mezzetti, M, Melandri, F, Zuppiroli, A, Fazi, A, Testa, R, Venturini, E, Mazzinghi, F, Cosmi, D, Santoro, Gm, Minneci, C, Galli, M, Paperini, L, Bovenzi, Fm, Cortigiani, L, Cocchieri, M, Severini, D, Arcuri, Gm, Bagliani, G, Bernardinangeli, M, Proietti, G, Bocconcelli, P, Pierantozzi, A, Monti, F, Giamundo, L, Tancredi, P, Rossini, E, Bianchi, C, Bettiol, F, Giovannini, E, Fera, Ms, Santini, M, Bianconi, L, Boccanelli, A, Morosetti, P, Volpe, M, Facciolo, C, Vacri, A, Romanazzi, F, Napoletano, C, Piccioni, Ll, Candelmo, F, De Marco, G, Arnese, Mr, Vetrano, A, Prinzi, D, De Rosa, P, Capuano, V, Torre, S, D'Onofrio, A, Ammendola, E, Chiariello, M, Filardi, Pp, Battista, R, De Fusco, A, Molero, U, Iervoglini, A, Stefanelli, S, Fattore, L, Bosco, B, Liguori, A, Padula, G, De Luca, I, Sorino, M, Colonna, P, D'Agostino, C, Pierfelice, O, Pettinati, G, Muscella, A, De Lorenzi, E, Falco, M, Giannattasio, C, Baldi, N, Clemente, Ma, D'Alessandro, B, Truncellito, L, Arabia, F, Ciconte, Va, Perticone, F, Ruberto, C, Buffon, A, Tomaselli, C, De Rosa, F, Mazza, S, Zampaglione, G, Pirozzi, Am, Butera, A, Levato, M, Musacchio, D, Polimeni, Rm, Lacquaniti, V, Pulitanò, G, Ruggeri, A, Provenzano, A, Cuccurullo, O, Musolino, M, Marrari, A, Anastasio, L, Schiavello, M, Comito, Mg, Gulizia, Mm, Francese GM, Vasquez, L, Coppolino, C, Casale, A, D'Urso, G, Oliva, G, Giordano, U, Andolina, S, Sanfilippo, N, Ingrillì, F, Accardo, S, Grasso, S, Buffa, L, Bambi, Serra E., Baviera, M., Bianchini, F., Fenicia, E., Gianfriddo, M., Lonardo, G., Luise, A., Nota, R., Orlando, M. E., Petrolo, R., Pierattini, C., Pierota, V., Ragno, A., Serio, C., Tafi, A., Tellaroli, E., Masson, Core Laboratories — S., Latini, R., Vago (Biomarkers), T., Staszewsky, L., Gramenzi (Echocardiography), S., Orso, F., Suliman (Electrocardiography), I., Nicolis, Database Management and Statistics — E., Casola, C., Barlera, S., Dall'Osso, D., Gorini, M., Lucci, D., Regulatory, Administrative, Bianchini, and Secretariat — E., Cabiddu, S., Cangioli, I., Carnaghi, A., Cipressa, M. L., Cipressa, L., Galbiati, L., Lorimer, A., Priami, P., Moccetti, Participating Centers and Investigators — Switzerland: Lugano (T., Rossi, M. G., Vaghi), F., Capello), Italy: Piemonte: Asti (A. F. L., Rossetti, Cuneo (G., Viada, E., Morena), L., Delucchi, Saluzzo (M., Reynaud, S. G., Allemano), P., Massobrio), Torino Valdese (N., Gavazzi, Lombardia: Bergamo (A., Taddei), F., Mor), Brescia (D. A., Bortolini, Chiari (F., Lorini), M., Inama, Crema (G., Durin), O., Pirelli, Cremona (S., Spotti, A., Procopio), R., Cuzzucrea, Giussano (D., Gentile), G., Margonato, Milano San Raffaele (A., Bassanelli), G., Tavazzi, Pavia San Matteo (L., Buzzi, M. P., Rordorf), R., Gualco, Pavia Fondazione Salvatore Maugeri (A., Opasich), C., Gronda, Rozzano (E., Genovese), L., Mattioli, Sesto San Giovanni (R., Donatelli), F., Salerno Uriarte), Varese (J. A., Rauhe), P. A. Bolzano: Bolzano (W., Bertagnolli, P. A. Trento: Cles (C., Canestrini), S., Stefenelli, Trento Villa Bianca (C., Cioffi), G., Disertori, Trento Santa Chiara (M., Zeni, P., Giovanelli), C., Rigatelli, Veneto: Bovolone (G., Boni, S., Pasini), A., Sitta), Conegliano Santa Maria dei Battuti (N., Sacchetta, Conegliano Veneto De Gironcoli (A., Borgese, L., Sciascia), R., Targa), Este (L., Raviele, Mestre (A., Madalosso), M., Bertaglia, Mirano (E., Zoppo), F. C., Capanna, Porto Viro (M., Fiorencis), R., Baracca), Rovigo (E., Rossi, San Bonifacio (R., Carbonieri, E., Rossi), I., Trappolin), Villafranca di Verona (R., Morgera, Friuli Venezia Giulia: Monfalcone (T., Barducci), E., Baldin, Palmanova (M. G., Gobbo), G., Zardo, Pordenone (F., Hrovatin), E., Mos, San Daniele del Friuli (L., Vriz), O., Sinagra, Trieste Az. Ospedaliera-Universitaria Ospedali Riuniti (G., Aleksova), A., Scardi, Trieste Az. Servizi Sanitari n. 1 Triestina (S., Mazzone), C., Fresco), Udine (C., Rubartelli, Liguria: Genova-Sampierdarena (P., Moroni), L. A., Camerieri), Genova-Voltri (A., Piana), Imperia (M., Mureddu), Pietra Ligure (R., Bertoli, Sarzana-Loc. S. Caterina (D., Petacchi), R., Pancaldi, Emilia Romagna: Bentivoglio (L. G., Gabrieli), L., Urbinati, Bologna Bellaria (S., Pedone), C., Di Pasquale, Bologna Maggiore (G., Di Niro, M., Brunelli), A., Bosi, Cotignola (S., Censi), S., Pratola), Ferrara (C., Moruzzi, Fidenza (P., Pastori), P., Modena, Modena (M. G., Malavasi), V., Mezzetti), Rimini (M., Melandri), Sassuolo (F., Zuppiroli, Toscana: Bagno a Ripoli (A., Fazi), A., Testa, Cecina (R., Venturini, E., Mazzinghi), F., Cosmi, Cortona (F., Cosmi), D., Santoro, Firenze Nuovo Osp. S Giovanni di Dio (G. M., Minneci), C., Galli, Livorno (M., Paperini), L., Bovenzi, Lucca (F. M., Cortigiani), L., Cocchieri, Umbria: Città di Castello (M., Severini, D., Arcuri), G. M., Bagliani), Foligno (G., Bernardinangeli, Terni (M., Proietti, G., Proietti), G., Bocconcelli, Marche: Pesaro (P., Pierantozzi), A., Monti, Lazio: Albano Laziale (F., Giamundo), L., Tancredi, Formia (P., Rossini), E., Bianchi), Roma Centro Traumatologico Ortopedico (C., Roma San Camillo, Bettiol), Cardiologia Riabilitativa e Preventiva (F., Giovannini, Cardiologia I (E., Fera), M. S., Santini, Roma San Filippo Neri (M., Bianconi), L., Boccanelli, Roma San Giovanni (A., Morosetti), P., Volpe, Roma Sant'Andrea (M., Facciolo), C., Vacri, Abruzzo: Penne (A., Romanazzi), F., Napoletano, Teramo (C., Piccioni), L. L., Candelmo), Campania: Avellino (F., De Marco, Aversa (G., Arnese), M. R., Vetrano), Caserta (A., Prinzi, Giugliano in Campania (D., De Rosa), P., Capuano, Mercato San Severino (V., Torre), S., D'Onofrio, Napoli Azienda Ospedaliera Monaldi (A., Ammendola), E., Chiariello, Napoli Policlinico Universitario Federico II (M., Perrone Filardi), P., Battista, Piedimonte Matese (R., De Fusco), A., Molero), Pozzuoli (U., Iervoglini, San Felice a Cancello (A., Stefanelli), S., Fattore, Santa Maria Capua Vetere (L., Bosco), B., Liguori, Vallo della Lucania (A., Padula), G., De Luca, Puglia: Bari Ospedale Consorziale Policlinico (I., Sorino, M., Colonna), P., D'Agostino, Bari-Carbonara (C., Pierfelice), O., Pettinati, Casarano (G., Muscella), A., De Lorenzi, Scorrano (E., Falco), M., Giannattasio), Taranto Villa Verde (C., Baldi), Taranto Santissima Annunziata (N., Clemente), Basilicata: Matera (M. A., D'Alessandro, Policoro (B., Truncellito), L., Arabia, Calabria: Catanzaro Pugliese (F., Ciconte), V. A., Perticone, Catanzaro Germaneto (F., Ruberto), C., Buffon, Cosenza Santissima Annunziata (A., Tomaselli), C., De Rosa, Cosenza Mariano Santo (F., Mazza), S., Zampaglione, Crotone (G., Pirozzi), A. M., Butera, Lamezia Terme (A., Levato), M., Musacchio), Paola (D., Polimeni, Polistena (R. M., Lacquaniti), V., Pulitanò, Reggio Calabria (G., Ruggeri), A., Provenzano), Rogliano (A., Cuccurullo), San Marco Argentano (O., Musolino, Scilla (M., Marrari), A., Anastasio, Soriano Calabro (L., Schiavello), M., Comito), Vibo Valentia (M. G. A., Gulizia, Sicilia: Catania (M. M., Francese), G. M., Vasquez, Milazzo (L., Coppolino), C., Casale, Nicosia (A., D'Urso), G., Oliva, Palermo Civico e Benfratelli (G., Giordano, U., Andolina), S., Sanfilippo, Palermo Villa Sofia (N., Ingrillì), F., Accardo), Palermo Buccheri La Ferla (S., Grasso, Palermo Cervello (S., Buffa), L., and Sardegna: Cagliari Brotzu, (E. Serra).
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- 2009
10. The Wnt inhibitor DKK1 is neurotoxic in cultured neurons and in vivo
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Scali, C., Diodato, E., Gianfriddo, M., Roncarati, R., Copani, A., Caraci, Filippo, Nicoletti, F., Pollio, G., Gaviraghi, G., and Caricasole, G. TERSTAPPEN AND A.
- Published
- 2005
11. The adenosine A2Areceptor antagonist ZM241385 enhances neuronal survival after oxygen-glucose deprivation in rat CA1 hippocampal slices
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Pugliese, AM, primary, Traini, C, additional, Cipriani, S, additional, Gianfriddo, M, additional, Mello, T, additional, Giovannini, MG, additional, Galli, A, additional, and Pedata, F, additional
- Published
- 2009
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12. The protective effect of adenosine A2Areceptor antagonism in cerebral ischemia
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Pedata, F., primary, Gianfriddo, M., additional, Turchi, D., additional, and Melani, A., additional
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- 2005
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13. Adenosine and glutamate extracellular concentrations and mitogen-activated protein kinases in the striatum of Huntington transgenic mice. Selective antagonism of adenosine A2A receptors reduces transmitter outflow
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Gianfriddo, M., primary, Melani, A., additional, Turchi, D., additional, Giovannini, M.G., additional, and Pedata, F., additional
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- 2004
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14. Effects of dietary extra-virgin olive oil on behaviour and brain biochemical parameters in ageing rats.
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Pitozzi V, Jacomelli M, Zaid M, Luceri C, Bigagli E, Lodovici M, Ghelardini C, Vivoli E, Norcini M, Gianfriddo M, Esposto S, Servili M, Morozzi G, Baldi E, Bucherelli C, Dolara P, and Giovannelli L
- Published
- 2010
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15. The protective effect of adenosine A2A receptor antagonism in cerebral ischemia.
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Pedata, F., Gianfriddo, M., Turchi, D., and Melani, A.
- Subjects
ADENOSINES ,RECEPTOR antibodies ,CEREBRAL ischemia ,NEUROLOGY ,AMINO acids ,LATHES - Abstract
Objectives: We reviewed our most recent work on the protective effect of adenosine A
2A antagonism in cerebral ischemia. Methods: Focal ischemia was produced in rats by introducing a nylon monofilament pre-coated with silicone through the external carotid artery to occlude the right MCA at its origin. Results: A2A antagonism was found protective in the model of permanent focal ischemia induced by the monofilament technique. This methodology provides the possibility of evaluating the protection against the outflow of excitatory amino acids and against an acute motor disturbance, i.e.contralateral turning to the ischemic side in the first hours after ischemia in awake rats. Hours later, a definite neurological deficit and necrotic neuronal damage can be evaluated. Discussion: Our results suggest that A2A antagonism may be protective from the earliest up to several hours after the ischemic event. [ABSTRACT FROM AUTHOR]- Published
- 2005
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16. Adenosine and glutamate extracellular concentrations and mitogen-activated protein kinases in the striatum of Huntington transgenic mice. Selective antagonism of adenosine A2A receptors reduces transmitter outflow
- Author
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Gianfriddo, M., Melani, A., Turchi, D., Giovannini, M.G., and Pedata, F.
- Subjects
- *
HUNTINGTON disease , *BRAIN , *GABA , *AMINO acids - Abstract
The basal ganglia and deep layers of cerebral cortex neurodegeneration typically characterize the postmortem brain of Huntington disease (HD) patients. In this study, we employed 10- to 11-week-old transgenic HD mice (R6/2 line), in which the striatal adenosine extracellular levels, measured using the microdialysis technique, are significantly increased in comparison to wild-type mice. An increase in striatal adenosine is probably a precocious index of mitochondrial dysfunction that is described in both the postmortem brain of HD patients and transgenic mice striatal cells. The adenosine increase is matched by activation of the p38 mitogen-activated protein kinase (MAPK) in the striatal neurons of R6/2 mouse but not in the cortex. This result indicates that p38 MAPK is a correlate of striatal damage and suggests a role for p38 in the striatal neuron suffering and apoptosis described in this disease. The selective adenosine A2A receptor antagonist SCH 58261, administered through microdialysis fiber into the striatum, significantly decreases the outflow of glutamate in R6/2 mice. Antagonism of adenosine A2A receptors might be regarded as potentially useful in the treatment of this disease to control striatal excitotoxicity. [Copyright &y& Elsevier]
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- 2004
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17. Adenosine A2A receptor antagonism increases nNOS-immunoreactive neurons in the striatum of Huntington transgenic mice
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Cipriani, S., Bizzoco, E., Gianfriddo, M., Melani, A., Vannucchi, M.G., and Pedata, F.
- Subjects
- *
HUNTINGTON disease , *INTERNEURONS , *SOMATOSTATIN , *ADENOSINES - Abstract
Abstract: Medium spiny GABAergic projection neurons are progressively lost in Huntington''s disease (HD), whereas there is preferential sparing of the few interneurons co-expressing NPY, somatostatin and neuronal nitric oxide synthase. We investigated the effect of the selective adenosine A2A receptor antagonist SCH58261 (0.01 mg/kg, acutely and chronically administered i.p.) on nNOS striatal expression and motor impairment in R6/2 transgenic mice in clearly symptomatic phase (10–11-week old). SCH58261 chronically administered increased the number of nNOS-immunoreactive neurons (nNOS-IR) in the striatum of R6/2 mice. No glial activation was detected in the striatum or cortex. SCH58261 also improved walking in the inclined plane test but not motor capability evaluated by the rotarod test. These findings demonstrate for the first time a role of adenosine A2A receptors in regulating nNOS expression in the striatum. We suggest that the protective effect of A2A antagonism in HD is related to the increase in striatal nNOS-IR neurons. [Copyright &y& Elsevier]
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- 2008
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18. Expression of neuronal and inducible nitric oxide synthase in neuronal and glial cells after transient occlusion of the middle cerebral artery
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Vannucchi, M.G., Corsani, L., Gianfriddo, M., Pedata, F., and Faussone-Pellegrini, M.S.
- Subjects
- *
NITRIC oxide , *PREOPERATIVE care , *IMMUNOHISTOCHEMISTRY , *BLOOD vessels - Abstract
Abstract: We presently investigated the time-course of neuronal nitric oxide synthase and inducible nitric oxide synthase expression and content in the rat striatum up to 6 days after ischemia induced by transient middle cerebral artery occlusion, a condition that potentially allows functional recovery, with the aim to identify the cell types expressing these two enzymes and to correlate neuronal nitric oxide synthase and inducible nitric oxide synthase changes in order to verify whether and how these changes are related to tissue damage, motor-sensory performances and survival. Before and after surgery, the animals underwent neurological evaluation. The results demonstrated that the rats with a score ≥12 at the neurological evaluation 24 h after ischemia showed a significant increase in neuronal nitric oxide synthase-immunoreactive neurones and absence of inducible nitric oxide synthase-immunoreactive cells and survived up to the sixth day; conversely, the rats with a score <12 at the neurological evaluation 24 h after ischemia showed a progressive significant decrease in neuronal nitric oxide synthase-immunoreactive neurones and appearance of inducible nitric oxide synthase-immunoreactive cells and none of the rats survived up to the sixth day. Microglia cells were activated in both groups but only in the latter did these cells express inducible nitric oxide synthase. Measurement of the infarct area demonstrated that it occupied a similar territory in both groups of rats but in those with a score <12 the edema was more extended. In conclusion, we demonstrated that a neurotoxic insult such as ischemia can induce neuronal nitric oxide synthase expression in the neurones and that when neuronal nitric oxide synthase-immunoreactive neurones increase in number, microglia activation is less extended, inducible nitric oxide synthase-immunoreactive cells are absent, tissue damage reduced and the rats survive longer. Conversely, when there is a significant decrease of neuronal nitric oxide synthase-immunoreactive neurones, microglia cells are intensely activated, inducible nitric oxide synthase-immunoreactive cells appear and the animal survival is shortened. [Copyright &y& Elsevier]
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- 2006
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19. A potent and selective Sirtuin 1 inhibitor alleviates pathology in multiple animal and cell models of Huntington's disease.
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Smith MR, Syed A, Lukacsovich T, Purcell J, Barbaro BA, Worthge SA, Wei SR, Pollio G, Magnoni L, Scali C, Massai L, Franceschini D, Camarri M, Gianfriddo M, Diodato E, Thomas R, Gokce O, Tabrizi SJ, Caricasole A, Landwehrmeyer B, Menalled L, Murphy C, Ramboz S, Luthi-Carter R, Westerberg G, and Marsh JL
- Subjects
- Animals, Disease Models, Animal, Drosophila Proteins genetics, Drosophila Proteins metabolism, Drosophila melanogaster drug effects, Drosophila melanogaster genetics, Drosophila melanogaster metabolism, Female, Histone Deacetylases genetics, Histone Deacetylases metabolism, Humans, Huntington Disease genetics, Huntington Disease pathology, Male, Mice, Mice, Inbred C57BL, PC12 Cells, Rats, Rats, Sprague-Dawley, Sirtuin 1 genetics, Sirtuin 1 metabolism, Sirtuins genetics, Sirtuins metabolism, Carbazoles administration & dosage, Drosophila Proteins antagonists & inhibitors, Enzyme Inhibitors administration & dosage, Huntington Disease drug therapy, Huntington Disease enzymology, Sirtuin 1 antagonists & inhibitors, Sirtuins antagonists & inhibitors
- Abstract
Protein acetylation, which is central to transcriptional control as well as other cellular processes, is disrupted in Huntington's disease (HD). Treatments that restore global acetylation levels, such as inhibiting histone deacetylases (HDACs), are effective in suppressing HD pathology in model organisms. However, agents that selectively target the disease-relevant HDACs have not been available. SirT1 (Sir2 in Drosophila melanogaster) deacetylates histones and other proteins including transcription factors. Genetically reducing, but not eliminating, Sir2 has been shown to suppress HD pathology in model organisms. To date, small molecule inhibitors of sirtuins have exhibited low potency and unattractive pharmacological and biopharmaceutical properties. Here, we show that highly selective pharmacological inhibition of Drosophila Sir2 and mammalian SirT1 using the novel inhibitor selisistat (selisistat; 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide) can suppress HD pathology caused by mutant huntingtin exon 1 fragments in Drosophila, mammalian cells and mice. We have validated Sir2 as the in vivo target of selisistat by showing that genetic elimination of Sir2 eradicates the effect of this inhibitor in Drosophila. The specificity of selisistat is shown by its effect on recombinant sirtuins in mammalian cells. Reduction of HD pathology by selisistat in Drosophila, mammalian cells and mouse models of HD suggests that this inhibitor has potential as an effective therapeutic treatment for human disease and may also serve as a tool to better understand the downstream pathways of SirT1/Sir2 that may be critical for HD.
- Published
- 2014
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20. VSTM2L is a novel secreted antagonist of the neuroprotective peptide Humanin.
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Rossini L, Hashimoto Y, Suzuki H, Kurita M, Gianfriddo M, Scali C, Roncarati R, Franceschini D, Pollio G, Trabalzini L, Terstappen GC, Matsuoka M, and Caricasole A
- Subjects
- Amino Acid Sequence, Animals, Base Sequence, Brain cytology, Brain metabolism, Cell Line, Cloning, Molecular, Female, Humans, Intracellular Signaling Peptides and Proteins genetics, Male, Molecular Sequence Data, Nerve Tissue Proteins genetics, Neurons cytology, Neurons metabolism, Rats, Rats, Wistar, Saccharomyces cerevisiae, Spinal Cord metabolism, Two-Hybrid System Techniques, Gene Expression Regulation physiology, Intracellular Signaling Peptides and Proteins antagonists & inhibitors, Intracellular Signaling Peptides and Proteins metabolism, Nerve Tissue Proteins metabolism
- Abstract
Humanin (HN) is a 24-residue peptide displaying a protective activity in vitro against a range of cytotoxic and neurotoxic insults, as well as mediating in vivo amelioration of Alzheimer disease (AD)-related memory impairment in experimental models. Published evidence suggests that the mechanisms through which HN exerts its cyto- and neuroprotective activity may include its secretion and binding to membrane-associated receptors. Here, we describe the identification of a new modulator of HN neuroprotective activity, V-set and transmembrane domain containing 2 like (VSTM2L), previously known as C20orf102. VSTM2L interacts with HN in both yeast and mammalian cells, is secreted in cultured cells, is present in serum, and is selectively expressed in the central nervous system. VSTM2L colocalizes with HN in distinct brain areas as well as in primary cultured neurons, where it plays a role in the modulation of neuronal viability. When tested in HN neuroprotection bioassays, VSTM2L acts as a strong antagonist of HN neuroprotective activity. In summary, VSTM2L is the first example of a secreted antagonist of HN and may play a role in the modulation of HN biological functions.
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- 2011
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21. Increased Dickkopf-1 expression in transgenic mouse models of neurodegenerative disease.
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Rosi MC, Luccarini I, Grossi C, Fiorentini A, Spillantini MG, Prisco A, Scali C, Gianfriddo M, Caricasole A, Terstappen GC, and Casamenti F
- Subjects
- Age Factors, Amyloid beta-Peptides metabolism, Amyloid beta-Protein Precursor genetics, Analysis of Variance, Animals, Antibodies, Monoclonal metabolism, Brain cytology, Brain metabolism, Choline O-Acetyltransferase metabolism, Disease Models, Animal, Gene Expression Regulation genetics, Glycogen Synthase Kinase 3 metabolism, Humans, Intercellular Signaling Peptides and Proteins genetics, LDL-Receptor Related Proteins genetics, LDL-Receptor Related Proteins metabolism, Low Density Lipoprotein Receptor-Related Protein-5, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mutation genetics, Neurodegenerative Diseases genetics, Neurodegenerative Diseases pathology, Neurons metabolism, Peptide Fragments metabolism, Phosphopyruvate Hydratase metabolism, Presenilin-1 genetics, beta Catenin metabolism, tau Proteins metabolism, Gene Expression Regulation physiology, Intercellular Signaling Peptides and Proteins metabolism, Neurodegenerative Diseases metabolism
- Abstract
To investigate the role of the Wnt inhibitor Dickkopf-1 (DKK-1) in the pathophysiology of neurodegenerative diseases, we analysed DKK-1 expression and localization in transgenic mouse models expressing familial Alzheimer's disease mutations and a frontotemporal dementia mutation. A significant increase of DKK-1 expression was found in the diseased brain areas of all transgenic lines, where it co-localized with hyperphosphorylated tau-bearing neurons. In TgCRND8 mice, DKK-1 immunoreactivity was detected in neurons surrounding amyloid deposits and within the choline acetyltransferase-positive neurons of the basal forebrain. Active glycogen synthase kinase-3 (GSK-3) was found to co-localize with DKK-1 and phospho-tau staining. Downstream to GSK-3, a significant reduction in beta-catenin translocation to the nucleus, indicative of impaired Wnt signaling functions, was found as well. Cumulatively, our findings indicate that DKK-1 expression is associated with events that lead to neuronal death in neurodegenerative diseases and support a role for DKK-1 as a key mediator of neurodegeneration with therapeutic potential.
- Published
- 2010
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22. Small molecule drug discovery for Huntington's Disease.
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Fecke W, Gianfriddo M, Gaviraghi G, Terstappen GC, and Heitz F
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- Animals, Cell Aggregation drug effects, Cell Death drug effects, Disease Models, Animal, Drug Delivery Systems methods, Drug Evaluation, Preclinical methods, Humans, Huntingtin Protein, Huntington Disease etiology, Huntington Disease genetics, Models, Biological, Nerve Tissue Proteins genetics, Nuclear Proteins genetics, Protein Array Analysis, Transcription, Genetic drug effects, Drug Discovery methods, Huntington Disease drug therapy, Small Molecule Libraries
- Abstract
Huntington's Disease (HD) is a rare neurodegenerative disease caused by mutation of the huntingtin gene that results in a protein with an expanded stretch of glutamine repeats (polyQ). Knowledge of validated targets is in its infancy, and thus, traditional target-based drug discovery strategies are of limited use. Alternative approaches are needed, and early attempts were aimed at identifying molecules that inhibited the aggregation of polyQ huntingtin fragments. More recently, phenotypic assays were used to find molecules able to reverse some of the pathogenic mechanisms of HD. Such discovery strategies have an impact on the configuration of screening cascades for effective translation of drug candidates toward clinical trials.
- Published
- 2009
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23. Procognitive and neuroprotective activity of a novel alpha7 nicotinic acetylcholine receptor agonist for treatment of neurodegenerative and cognitive disorders.
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Roncarati R, Scali C, Comery TA, Grauer SM, Aschmi S, Bothmann H, Jow B, Kowal D, Gianfriddo M, Kelley C, Zanelli U, Ghiron C, Haydar S, Dunlop J, and Terstappen GC
- Subjects
- Animals, Behavior, Animal drug effects, Calcium metabolism, Cell Line, Cognition drug effects, Cognition Disorders metabolism, Humans, Male, Membrane Potentials drug effects, Molecular Structure, Morpholines chemistry, Morpholines pharmacokinetics, Morpholines pharmacology, Motor Activity drug effects, Neurodegenerative Diseases metabolism, Neuroprotective Agents chemistry, Neuroprotective Agents pharmacokinetics, Neuroprotective Agents pharmacology, Nicotinic Agonists chemistry, Nicotinic Agonists pharmacokinetics, Nicotinic Agonists pharmacology, Patch-Clamp Techniques, Protein Binding, Pyridines chemistry, Pyridines pharmacokinetics, Pyridines pharmacology, Radioligand Assay, Rats, Rats, Long-Evans, Rats, Wistar, alpha7 Nicotinic Acetylcholine Receptor, Cognition Disorders drug therapy, Morpholines therapeutic use, Neurodegenerative Diseases drug therapy, Neuroprotective Agents therapeutic use, Nicotinic Agonists therapeutic use, Pyridines therapeutic use, Receptors, Nicotinic metabolism
- Abstract
The alpha7 nicotinic acetylcholine receptor (nAChR) is a promising target for treatment of cognitive dysfunction associated with Alzheimer's disease and schizophrenia. Here, we report the pharmacological properties of 5-morpholin-4-yl-pentanoic acid (4-pyridin-3-yl-phenyl)-amide [SEN12333 (WAY-317538)], a novel selective agonist of alpha7 nAChR. SEN12333 shows high affinity for the rat alpha7 receptor expressed in GH4C1 cells (K(i) = 260 nM) and acts as full agonist in functional Ca(2+) flux studies (EC(50) = 1.6 microM). In whole-cell patch-clamp recordings, SEN12333 activated peak currents and maximal total charges similar to acetylcholine (EC(50) = 12 microM). The compound did not show agonist activity at other nicotinic receptors tested and acted as a weak antagonist at alpha3-containing receptors. SEN12333 treatment (3 mg/kg i.p.) improved episodic memory in a novel object recognition task in rats in conditions of spontaneous forgetting as well as cognitive disruptions induced via glutamatergic [5H-dibenzo[a,d]cyclohepten-5,10-imine (dizocilpine maleate); MK-801] or cholinergic (scopolamine) mechanisms. This improvement was blocked by the alpha7-selective antagonist methyllycaconitine, indicating that it is mediated by alpha7 activation. SEN12333 also prevented a scopolamine-induced deficit in a passive avoidance task. In models targeting other cognitive domains, including attention and perceptual processing, SEN12333 normalized the apomorphine-induced deficit of prepulse inhibition. Neuroprotection of SEN12333 was demonstrated in quisqualate-lesioned animals in which treatment with SEN12333 (3 mg/kg/day i.p.) resulted in a significant protection of choline acetyltransferase-positive neurons in the lesioned hemisphere. Cumulatively, our results demonstrate that the novel alpha7 nAChR agonist SEN12333 has procognitive and neuroprotective properties, further demonstrating utility of alpha7 agonists for treatment of neurodegenerative and cognitive disorders.
- Published
- 2009
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24. Inducible nitric oxide synthase appears and is co-expressed with the neuronal isoform in interneurons of the rat hippocampus after transient ischemia induced by middle cerebral artery occlusion.
- Author
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Corsani L, Bizzoco E, Pedata F, Gianfriddo M, Faussone-Pellegrini MS, and Vannucchi MG
- Subjects
- Animals, Gene Expression Regulation, Enzymologic physiology, Hippocampus pathology, Infarction, Middle Cerebral Artery pathology, Interneurons pathology, Ischemic Attack, Transient pathology, Male, Nitric Oxide Synthase Type I genetics, Nitric Oxide Synthase Type II genetics, Rats, Rats, Wistar, Hippocampus enzymology, Infarction, Middle Cerebral Artery enzymology, Interneurons enzymology, Ischemic Attack, Transient enzymology, Nitric Oxide Synthase Type I biosynthesis, Nitric Oxide Synthase Type II biosynthesis
- Abstract
The hippocampus (dentate gyrus DG plus Cornu Ammonis, CA) is vulnerable to neuropathological events such as ischemia. The DG is a region where neurogenesis takes place and it has been demonstrated that ischemia stimulates neurogenesis. Nitric oxide (NO) plays a major role in ischemic damage evolution and increases in rat hippocampus after ischemia. No information is available on the presence of nNOS-immunoreactive (IR) neurons in the hippocampus of ischemic animals; whereas, the presence of the iNOS protein has been reported in the DG after focal ischemia. We evaluated, immunohistochemically, the cell types expressing nNOS and iNOS in the rat hippocampus by 24 up to 144 h after transient middle cerebral artery occlusion to ascertain whether ischemia induces changes in nNOS or iNOS expression and whether a relationship exists between these changes and the animal survival. nNOS-IR interneurons were detected in control and ischemic rats; in the latter, their number was significantly decreased at all time points. iNOS-IR interneurons appeared in the hippocampus of ischemic rats at 24 h; their number was significantly higher in the animals with longer survival and did not change at later time points. More than 50% of the nNOS-IR interneurons co-expressed iNOS-IR. All these changes were seen both in the ipsilateral and contralateral hippocampus. In conclusion, the focal ischemia affects the hippocampus which responds bilaterally to the injury. We hypothesize that the decrease in the nNOS-IR neurons is likely due to either a neuronal loss or a switching towards the iNOS production which, by inducing neurogenesis, might compensate the neuronal loss.
- Published
- 2008
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25. Relationships between neurons expressing neuronal nitric oxide synthase, degree of microglia activation and animal survival. A study in the rat cortex after transient ischemia.
- Author
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Vannucchi MG, Bizzoco E, Corsani L, Gianfriddo M, Pedata F, and Faussone-Pellegrini MS
- Subjects
- Animals, Cell Count, Cerebral Infarction pathology, Cerebral Infarction physiopathology, Disease Models, Animal, Gliosis pathology, Gliosis physiopathology, Immunohistochemistry, Infarction, Middle Cerebral Artery metabolism, Infarction, Middle Cerebral Artery pathology, Infarction, Middle Cerebral Artery physiopathology, Ischemic Attack, Transient pathology, Ischemic Attack, Transient physiopathology, Male, Nitrergic Neurons metabolism, Nitric Oxide metabolism, Nitric Oxide Synthase Type I metabolism, Nitric Oxide Synthase Type II metabolism, Rats, Rats, Wistar, Recovery of Function physiology, Survival Rate, Telencephalon metabolism, Telencephalon pathology, Telencephalon physiopathology, Up-Regulation physiology, Cerebral Infarction metabolism, Gliosis metabolism, Ischemic Attack, Transient metabolism, Microglia metabolism, Neurons metabolism, Nitric Oxide Synthase metabolism
- Abstract
The focal ischemia obtained in an animal model of middle cerebral artery occlusion (MCAo) causes the "core" of damage in the striatum and the "penumbra" of damage in the fronto-parietal cortex. The latter is mainly functionally affected and shows changes in nNOS and iNOS expression during the acute phase of ischemia. With the aim to study possible relationships between these changes and the affection entity during the animal recovery, we investigated from 24 up to 144 h after reperfusion the expression and content of these two NOS isoforms in the neurons and microglia and the degree of microglia reactivity in the fronto-parietal cortices of rats undertaken to transient MCAo. Evaluation of motor-sensory performances and survival allowed dividing the animals into two groups. Immunohistochemistry, western blot and quantitative analysis demonstrated, both in the ischemic and contralateral cortex of the rats with longer survival, wellness and significantly increased number of the nNOS-IR neurons at 24 h and moderately activated microglia up to 144 h. In the rats not recovering, injured and significantly decreased nNOS-IR neurons, intensely activated microglia and appearance of iNOS-IR were seen at all time points. In conclusion, since the recovery occurs when nNOS-IR neurons are greatly increased, we presume nNOS protect the tissue likely controlling the passage from the state of reactive to that of activated microglia. Moreover, the morphological signs of wellness and the two-fold increase in number of the nNOS-IR neurons appear to be characteristic of the "penumbra" area and could explain why this region is mainly functionally affected.
- Published
- 2007
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26. Inhibition of Wnt signaling, modulation of Tau phosphorylation and induction of neuronal cell death by DKK1.
- Author
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Scali C, Caraci F, Gianfriddo M, Diodato E, Roncarati R, Pollio G, Gaviraghi G, Copani A, Nicoletti F, Terstappen GC, and Caricasole A
- Subjects
- Animals, Basal Nucleus of Meynert drug effects, Basal Nucleus of Meynert metabolism, Basal Nucleus of Meynert physiopathology, Brain pathology, Brain physiopathology, Cell Death drug effects, Cell Death physiology, Cells, Cultured, Enzyme Inhibitors pharmacology, Gliosis chemically induced, Gliosis metabolism, Gliosis physiopathology, Glycogen Synthase Kinase 3 antagonists & inhibitors, Glycogen Synthase Kinase 3 metabolism, Glycogen Synthase Kinase 3 beta, Hippocampus drug effects, Hippocampus metabolism, Hippocampus physiopathology, Humans, Intercellular Signaling Peptides and Proteins genetics, Intercellular Signaling Peptides and Proteins pharmacology, Lithium pharmacology, Male, Nerve Degeneration genetics, Nerve Degeneration physiopathology, Neurons pathology, Phosphorylation, Proto-Oncogene Proteins c-bcl-2 genetics, Proto-Oncogene Proteins c-bcl-2 metabolism, Rats, Rats, Sprague-Dawley, Rats, Wistar, Signal Transduction physiology, bcl-2-Associated X Protein genetics, bcl-2-Associated X Protein metabolism, beta Catenin metabolism, Brain metabolism, Intercellular Signaling Peptides and Proteins metabolism, Nerve Degeneration metabolism, Neurons metabolism, Wnt Proteins metabolism, tau Proteins metabolism
- Abstract
Expression of the Wnt antagonist Dickkopf-1 (DKK1) is induced during neurodegenerative processes associated with Alzheimer's Disease and brain ischemia. However, little is known about DKK1-mediated effects on neurons. We now describe that, in cultured neurons, DKK1 is able to inhibit canonical Wnt signaling, as assessed by TCF reporter assay and analysis of beta-catenin levels, and to elicit cell death associated with loss of BCL-2 expression, induction of BAX, and TAU hyperphosphorylation. Local infusion of DKK1 in rats caused neuronal cell death and astrocytosis in the CA1 region of the hippocampus and death of cholinergic neurons in the nucleus basalis magnocellularis. Both effects were reversed by systemic administration of lithium ions, which rescue the Wnt pathway by inhibiting glycogen synthase kinase-3beta. The demonstration that DKK1 inhibits Wnt signaling in neurons and causes neuronal death supports the hypothesis that inhibition of the canonical Wnt pathway contributes to the pathophysiology of neurodegenerative disorders.
- Published
- 2006
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27. P2X7 receptor modulation on microglial cells and reduction of brain infarct caused by middle cerebral artery occlusion in rat.
- Author
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Melani A, Amadio S, Gianfriddo M, Vannucchi MG, Volontè C, Bernardi G, Pedata F, and Sancesario G
- Subjects
- Animals, Brain Ischemia etiology, Brain Ischemia physiopathology, Cerebral Infarction etiology, Cerebral Infarction metabolism, Disease Models, Animal, Dose-Response Relationship, Drug, Infarction, Middle Cerebral Artery complications, Infarction, Middle Cerebral Artery metabolism, Male, Microglia cytology, Purinergic P2 Receptor Antagonists, Rats, Rats, Wistar, Receptors, Purinergic P2 biosynthesis, Receptors, Purinergic P2X7, Triazines pharmacology, Brain Ischemia prevention & control, Cerebral Infarction prevention & control, Infarction, Middle Cerebral Artery physiopathology, Microglia metabolism, Receptors, Purinergic P2 metabolism
- Abstract
Adenosine 5'-triphosphate outflow increases after an ischemic insult in the brain and may induce the expression of P2X7 receptors in resting microglia, determining its modification into an activated state. To assess the effects of P2X7 receptor blockade in preventing microglia activation and ameliorating brain damage and neurological impairment, we delivered the P2 unselective antagonist Reactive Blue 2 to rats after middle cerebral artery occlusion. In sham-operated animals, devoid of brain damage, double immunofluorescence verified the absence of P2X7 immunoreactivity on resting microglia, astrocytes, and neurons, identified, respectively, by OX-42, glial fibrillary acid protein, and neuronal nuclei (NeuN) immunoreactivity. After ischemia, vehicle-treated rats showed monolateral sensorimotor deficit and tissue damage in striatum and frontoparietal cortex. Moreover, P2X7 immunoreactivity was de novo expressed on activated microglia in infarcted and surrounding areas, as well as on a reactive form of microglia, resting in shape but P2X7 immunoreactive, present in ipsi- and contralateral cingulate and medial frontal cortex. Reactive Blue 2 improved sensorimotor deficit and restricted the volume of infarction, without preventing the expression of P2X7, but inducing it in the microglia of contralateral frontal and parietal cortex and striatum, which had lost reciprocal connections with the remote infarct area. De novo expression of P2X7 occurred in both activated and reactive microglia, suggesting their differentiated roles in the area of infarct and in remote regions. Reactive Blue 2 reduced ischemic brain damage, likely blocking the function of activated microglia in the infarct area, but in the remote brain regions promoted the expression of P2X7 on reactive microglia, developing defense and reparative processes.
- Published
- 2006
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28. The selective A2A receptor antagonist SCH 58261 protects from neurological deficit, brain damage and activation of p38 MAPK in rat focal cerebral ischemia.
- Author
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Melani A, Gianfriddo M, Vannucchi MG, Cipriani S, Baraldi PG, Giovannini MG, and Pedata F
- Subjects
- Analysis of Variance, Animals, Blotting, Western methods, Brain drug effects, Brain metabolism, Brain pathology, Brain Injuries etiology, Brain Injuries pathology, Brain Ischemia complications, Brain Ischemia drug therapy, Disease Models, Animal, Enzyme Activation drug effects, Functional Laterality physiology, Immunohistochemistry methods, Male, Microscopy, Confocal methods, Motor Activity drug effects, Motor Activity physiology, Nervous System Diseases etiology, Neurologic Examination methods, Rats, Rats, Wistar, Brain Injuries prevention & control, Nervous System Diseases prevention & control, Neuroprotective Agents administration & dosage, Pyrimidines administration & dosage, Triazoles administration & dosage, p38 Mitogen-Activated Protein Kinases metabolism
- Abstract
We investigated the protective effect of subchronic treatment of the A2A receptor antagonist, SCH 58261 (0.01 mg/kg, i.p.), administered 5 min, 6 h and 15 h after permanent right middle cerebral artery occlusion (MCAo). Twenty-four hours after ischemia, an extensive pallid area, evaluated by cresyl violet staining, is evident in the vascular territories supplied by the MCA, the striatum and the sensory motor cortex. The pallid area reflects the extent of necrotic neurons. Soon after waking, rats showed a definite contralateral turning behavior which was significantly reduced by SCH 58261 treatment. Twenty-four hours after MCAo, SCH 58261 significantly improved the neurological deficit and reduced ischemic damage in the striatum and cortex. Phospho-p38 mitogen-activated protein kinase (MAPK), evaluated by Western Blot, increased by 500% in the ischemic striatum 24 h after MCAo. SCH 58261 treatment significantly reduced phospho-p38 MAPK by 70%. Microglia was immunostained using the OX-42 antibody. Phospho-p38 MAPK and OX-42-immunoreactive cells are localized in the ventral striatum and frontoparietal cortex. Furthermore, both OX-42 and phospho-p38 MAPK-immunoreactive cells have overlapping morphological features, typical of reactive microglia. SCH 58261 reduced phospho-p38 MAPK immunoreactivity in the striatum and in the cortex without changing the microglial cell morphology. These results indicate that the protective effect of the adenosine antagonist SCH 58261 during ischemia is not due to reduced microglial activation but involves inhibition of phospho-p38 MAPK and suggest that treatment with the A2A antagonist from the first hour to several hours after ischemia may be a useful therapeutic approach in cerebral ischemia.
- Published
- 2006
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29. ATP extracellular concentrations are increased in the rat striatum during in vivo ischemia.
- Author
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Melani A, Turchi D, Vannucchi MG, Cipriani S, Gianfriddo M, and Pedata F
- Subjects
- 5'-Nucleotidase antagonists & inhibitors, 5'-Nucleotidase metabolism, Adenosine metabolism, Animals, Brain Infarction etiology, Brain Infarction metabolism, Brain Infarction physiopathology, Brain Ischemia physiopathology, Corpus Striatum physiopathology, Disease Models, Animal, Enzyme Inhibitors pharmacology, Infarction, Middle Cerebral Artery metabolism, Infarction, Middle Cerebral Artery physiopathology, Male, Microdialysis, Movement Disorders etiology, Movement Disorders metabolism, Movement Disorders physiopathology, Rats, Rats, Wistar, Receptors, Purinergic P2 metabolism, Up-Regulation drug effects, Adenosine Triphosphate metabolism, Brain Ischemia metabolism, Corpus Striatum metabolism, Extracellular Fluid metabolism, Up-Regulation physiology
- Abstract
Interest is growing in the role of adenosine triphosphate (ATP) on P2 receptors during hypoxic/ischemic events in the brain. However, there is no direct evidence of an increase in extracellular ATP levels during cerebral ischemia in vivo. The aim of the present study was to evaluate ATP outflow from the rat striatum by the microdialysis technique associated with focal cerebral ischemia in vivo by intraluminal occlusion of the right middle cerebral artery (MCA). Between 1 and 4h after ischemia, rats showed a clear turning behavior contralateral to the ischemic side. Twenty-four hour after MCA occlusion, ischemic rats had definite neurological deficit and striatal and cortical damage. The ATP concentration (mean+/-S.E.M.) in the striatum of normoxic rats (n = 8) was 3.10+/-0.34 nM. During 220 min after MCA occlusion, the extracellular ATP levels significantly increased two-fold, being 5.90+/-0.61 nM (p < 0.01 versus normoxic level). ATP outflow showed a tendency to increase over time during the 220 min of ischemia. Since extracellular ATP is rapidly metabolized to adenosine, we also assessed ATP outflow in the presence of the ecto-5'-nucleotidase inhibitor, alpha,beta-methylene-adenosine diphosphate (AOPCP, 1 mM) directly perfused into the striatum. The ATP concentration in normoxic rats (n = 8) was increased three-fold in the presence of the ecto-5'-nucleotidase inhibitor (9.57+/-0.26 nM). During 220 min of ischemia, extracellular ATP levels significantly increased 1.3-fold in AOPCP-treated rats (12.62+/-0.65 nM, p < 0.01 versus normoxic level). The present study confirms that ATP is continuously released in the brain and demonstrates for the first time that ATP outflow increases during ischemia in vivo. These results confirm that ATP may be an important mediator in brain ischemia.
- Published
- 2005
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30. The protective effect of adenosine A2A receptor antagonism in cerebral ischemia.
- Author
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Pedata F, Gianfriddo M, Turchi D, and Melani A
- Subjects
- Animals, Aspartic Acid metabolism, Brain Ischemia complications, Disease Models, Animal, Glutamic Acid metabolism, Hypoxia, Brain etiology, Hypoxia, Brain pathology, Receptor, Adenosine A2A physiology, Time Factors, Adenosine A2 Receptor Antagonists, Brain Ischemia prevention & control, Hypoxia, Brain prevention & control, Neuroprotective Agents therapeutic use
- Abstract
Objectives: We reviewed our most recent work on the protective effect of adenosine A(2A)antagonism in cerebral ischemia., Methods: Focal ischemia was produced in rats by introducing a nylon monofilament pre-coated with silicone through the external carotid artery to occlude the right MCA at its origin., Results: A(2A) antagonism was found protective in the model of permanent focal ischemia induced by the monofilament technique. This methodology provides the possibility of evaluating the protection against the outflow of excitatory amino acids and against an acute motor disturbance, i.e.contralateral turning to the ischemic side in the first hours after ischemia in awake rats. Hours later, a definite neurological deficit and necrotic neuronal damage can be evaluated., Discussion: Our results suggest that A(2A) antagonism may be protective from the earliest up to several hours after the ischemic event.
- Published
- 2005
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31. A2A receptors in neuroprotection of dopaminergic neurons.
- Author
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Pedata F, Pugliese AM, Melani A, and Gianfriddo M
- Subjects
- Adenosine A2 Receptor Antagonists, Animals, Caffeine therapeutic use, Disease Models, Animal, Dose-Response Relationship, Drug, Enzyme Inhibitors therapeutic use, Female, Humans, Male, Neurons drug effects, Parkinson Disease drug therapy, Purines therapeutic use, Pyrimidines therapeutic use, Sex Factors, Triazoles therapeutic use, Dopamine metabolism, Neurons metabolism, Neuroprotective Agents therapeutic use, Parkinson Disease metabolism, Receptor, Adenosine A2A metabolism
- Published
- 2003
- Full Text
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32. Adenosine A(2A) antagonism increases striatal glutamate outflow in the quinolinic acid rat model of Huntington's disease.
- Author
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Gianfriddo M, Corsi C, Melani A, Pèzzola A, Reggio R, Popoli P, and Pedata F
- Subjects
- Adenosine analysis, Animals, Chromatography, High Pressure Liquid, Corpus Striatum drug effects, Corpus Striatum metabolism, Extracellular Space chemistry, Glutamic Acid analysis, Glutamic Acid drug effects, Huntington Disease chemically induced, Male, Microdialysis, Models, Animal, Neuroprotective Agents pharmacology, Pyrimidines pharmacology, Quinolinic Acid pharmacology, Rats, Rats, Wistar, Receptor, Adenosine A2A, Time Factors, Triazoles pharmacology, Corpus Striatum chemistry, Glutamic Acid metabolism, Huntington Disease physiopathology, Purinergic P1 Receptor Antagonists
- Abstract
In the quinolinic acid (QA)-rat model of Huntington's disease (HD), 15 days after QA injection, striatal glutamate, measured by in vivo microdialysis, was unchanged while a significant decrease in adenosine occurred. The decrease in adenosine may depend on QA-induced striatal cell loss. Probe perfusion of the adenosine A(2A) receptor antagonist SCH 58261 significantly increased striatal glutamate outflow, suggesting a potential detrimental effect of A(2A) antagonism at later stages of the neurodegenerative process induced by QA.
- Published
- 2003
- Full Text
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33. Adenosine A2A receptor antagonism increases striatal glutamate outflow in dopamine-denervated rats.
- Author
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Corsi C, Pinna A, Gianfriddo M, Melani A, Morelli M, and Pedata F
- Subjects
- Animals, Corpus Striatum metabolism, Denervation, Dopamine physiology, Male, Microdialysis, Oxidopamine pharmacology, Rats, Rats, Sprague-Dawley, Receptor, Adenosine A2A, Receptors, Purinergic P1 physiology, Time Factors, Corpus Striatum drug effects, Glutamic Acid metabolism, Purinergic P1 Receptor Antagonists, Pyrimidines pharmacology, Triazoles pharmacology
- Abstract
The objective of the work was to study, by in vivo microdialysis, the effect of the adenosine A(2A) receptor antagonist 7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH 58261) on glutamate outflow in the striata of unilateral 6-hydroxydopamine-infused rats. Two vertical microdialysis probes were implanted bilaterally in both the denervated striatum and in the intact striatum. Glutamate concentrations in the dialysate were determined by high-performance liquid chromatography (HPLC). Infusion of the adenosine A(2A) receptor antagonist SCH 58261 (50 nM), through the microdialysis fiber, significantly increased glutamate outflow from the denervated striatum while it decreased glutamate outflow from the intact striatum. The opposite effects of SCH 58261 on glutamate outflow in the intact and 6-hydroxydopamine-lesioned striatum might be attributed to blockade of striatal adenosine A(2A) receptors located on either striatal indirect output pathways or glutamatergic terminals. These results may be relevant to our understanding of the mechanism of action of adenosine A(2A) receptor antagonists in Parkinson's disease.
- Published
- 2003
- Full Text
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34. The selective A2A receptor antagonist SCH 58261 reduces striatal transmitter outflow, turning behavior and ischemic brain damage induced by permanent focal ischemia in the rat.
- Author
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Melani A, Pantoni L, Bordoni F, Gianfriddo M, Bianchi L, Vannucchi MG, Bertorelli R, Monopoli A, and Pedata F
- Subjects
- Animals, Brain Ischemia drug therapy, Brain Ischemia pathology, Corpus Striatum metabolism, Male, Pyrimidines therapeutic use, Rats, Rats, Wistar, Receptor, Adenosine A2A, Receptors, Purinergic P1 metabolism, Triazoles therapeutic use, Brain Ischemia metabolism, Corpus Striatum drug effects, Motor Activity drug effects, Neurotransmitter Agents metabolism, Purinergic P1 Receptor Antagonists, Pyrimidines pharmacology, Triazoles pharmacology
- Abstract
Adenosine A(2A) receptor antagonists have been proved protective in different ischemia models. In this study we verified if the protective effect of the selective A(2A) antagonist, SCH 58261, could be attributed to the reduction of the excitatory amino acid outflow induced by cerebral focal ischemia. A vertical microdialysis probe was inserted into the striatum of male Wistar rats and, after 24 h, permanent right intraluminal middle cerebral artery occlusion (MCAo) was induced. Soon after waking, rats showed a definite contralateral turning behavior, which persisted up to 7 h after MCAo. During 4 h after MCAo, glutamate, aspartate, GABA, adenosine and taurine outflow increased. SCH 58261 (0.01 mg/kg, i.p.), administered 5 min after MCAo, suppressed turning behavior and significantly reduced the outflow of glutamate, aspartate, GABA and adenosine. At 24 h after MCAo, the rats showed severe sensorimotor deficit and damage in both the striatum and cortex. SCH 58261 significantly reduced cortical damage but did not protect against the sensorimotor deficit. The protective effect of SCH 58261 against turning behavior and increased outflow of excitatory amino acids in the first hours after MCAo suggests the potential utility of selective adenosine A(2A) antagonists when administered in the first hours after ischemia. Furthermore, this study, for the first time, proposes that turning behavior after permanent intraluminal MCAo, be used as a precocious index of neurological deficit and neuronal damage.
- Published
- 2003
- Full Text
- View/download PDF
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