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1. Gender-differences in disease distribution and outcome in hospitalized elderly: Data from the REPOSI study

Author

Corrao, S, Santalucia, P, Argano, C, Djade, C, Barone, E, Tettamanti, M, Pasina, L, Franchi, C, Kamal Eldin, T, Marengoni, A, Salerno, F, Marcucci, M, Mannucci, P, Nobili, A, Mannucci, M, Sparacio, E, Alborghetti, S, Di Costanzo, R, Djignefa Djade, C, Prisco, D, Silvestri, E, Cenci, C, Barnini, T, Delitala, G, Carta, S, Atzori, S, Guarnieri, G, Zanetti, M, Spalluti, A, Serra, M, Bleve, M, Vanoli, M, Grignani, G, Casella, G, Gasbarrone, L, Maniscalco, G, Gunelli, M, Tirotta, D, Brucato, A, Ghidoni, S, Bernardi, M, Bassi, S, Santi, L, Agnelli, G, Iorio, A, Marchesini, E, Mannarino, E, Lupattelli, G, Rondelli, P, Paciullo, F, Fabris, F, Carlon, M, Turatto, F, Baroni, M, Zardo, M, Manfredini, R, Molino, C, Pala, M, Fabbian, F, Nuti, R, Valenti, R, Ruvio, M, Cappelli, S, Paolisso, G, Rizzo, M, Laieta, M, Salvatore, T, Sasso, F, Utili, R, Durante Mangoni, E, Pinto, D, Olivieri, O, Stanzial, A, Fellin, R, Volpato, S, Fotini, S, Barbagallo, M, Dominguez, L, Plances, L, D'Angelo, D, Rini, G, Mansueto, P, Pepe, I, Licata, G, Calvo, L, Valenti, M, Borghi, C, Strocchi, E, Rinaldi, E, Zoli, M, Fabbri, E, Magalotti, D, Auteri, A, Pasqui, A, Puccetti, L, Laghi Pasini, F, Capecchi, P, Bicchi, M, Sabbà, C, Vella, F, Marseglia, A, Luglio, C, Palasciano, G, Modeo, M, Aquilino, A, Raffaele, P, Pugliese, S, Capobianco, C, Postiglione, A, Barbella, M, De Stefano, F, Fenoglio, L, Brignone, C, Bracco, C, Giraudo, A, Musca, G, Cuccurullo, O, Cricco, L, Fiorentini, A, Cappellini, M, Fabio, G, Seghezzi, S, De Amicis, M, Fargion, S, Bonara, P, Bulgheroni, M, Lombardi, R, Magrini, F, Massari, F, Tonella, T, Peyvandi, F, Tedeschi, A, Rossio, R, Moreo, G, Ferrari, B, Roncari, L, Monzani, V, Savojardo, V, Folli, C, Magnini, M, Mari, D, Rossi, P, Damanti, S, Prolo, S, Lilleri, M, Micale, G, Podda, M, Selmi, C, Meda, F, Accordino, S, Conca, A, Monti, V, Corazza, G, Miceli, E, Lenti, M, Padula, D, Balduini, C, Bertolino, G, Provini, S, Quaglia, F, Murialdo, G, Bovio, M, Dallegri, F, Ottonello, L, Quercioli, A, Barreca, A, Secchi, M, Ghelfi, D, Chin, W, Carassale, L, Caporotundo, S, Anastasio, L, Carbone, M, Traisci, G, De Feudis, L, Davì, G, Guagnano, M, Sestili, S, Bergami, E, Rizzioli, E, Cagnoni, C, Bertone, L, Manucra, A, Buratti, A, Tognin, T, Liberato, N, Bernasconi, G, Nardo, B, Bianchi, G, Benetti, G, Quagliolo, M, Centenaro, G, Purrello, F, Di Pino, A, Piro, S, Mancuso, G, Calipari, D, Bartone, M, Gullo, F, Cortellaro, M, Magenta, M, Perego, F, Meroni, M, Cicardi, M, Magenta, A, Sacco, A, Bonelli, A, Dentamaro, G, Rozzini, R, Falanga, L, Giordano, A, Perin, P, Lorenzati, B, Gruden, G, Bruno, G, Montrucchio, G, Greco, E, Tizzani, P, Fera, G, Di Luca, M, Renna, D, Perciccante, A, Coralli, A, Tassara, R, Melis, D, Rebella, L, Menardo, G, Bottone, S, Sferrazzo, E, Ferri, C, Striuli, R, Scipioni, R, Salmi, R, Gaudenzi, P, Gamberini, S, Ricci, F, Morabito, C, Fava, R, Semplicini, A, Gottardo, L, Vendemiale, G, Serviddio, G, Forlano, R, Bolondi, L, Rasciti, L, Serio, I, Masala, C, Mammarella, A, Raparelli, V, Rossi Fanelli, F, Delfino, M, Amoroso, A, Violi, F, Basili, S, Perri, L, Serra, P, Fontana, V, Falcone, M, Landolfi, R, Grieco, A, Gallo, A, Zuccalà, G, Franceschi, F, De Marco, G, Chiara, C, Marta, S, Bellusci, M, Setti, D, Pedrazzoli, F, Romanelli, G, Pirali, C, Amolini, C, Rosei, E, Rizzoni, D, Castoldi, L, Picardi, A, Gentilucci, U, Mazzarelli, C, Gallo, P, Guasti, L, Castiglioni, L, Maresca, A, Squizzato, A, Contini, S, Molaro, M, Annoni, G, Corsi, M, Zazzetta, S, Bertolotti, M, Mussi, C, Scotto, R, Ferri, M, Veltri, F, Arturi, F, Succurro, E, Sesti, G, Gualtieri, U, Perticone, F, Sciacqua, A, Quero, M, Bagnato, C, Loria, P, Becchi, M, Martucci, G, Fantuzzi, A, Maurantonio, M, Corinaldesi, R, De Giorgio, R, Grasso, V, Ruggeri, E, Carozza, L, Pignatti, F, Mannucci M, Nobili A, Tettamanti M, Pasina L, Franchi C, Salerno F, Corrao S, Marengoni A, Marcucci M, Sparacio E, Alborghetti S, Di Costanzo R, Djignefa Djade C, Prisco D, Silvestri E, Cenci C, Barnini T, Delitala G, Carta S, Atzori S, Guarnieri G, Zanetti M, Spalluti A, Serra MG, Bleve MA, Vanoli M, Grignani G, Casella G, Gasbarrone L, Maniscalco G, Gunelli M, Tirotta D, Brucato A, Ghidoni S, Bernardi M, Bassi SL, Santi L, Agnelli G, Iorio A, Marchesini E, Mannarino E, Lupattelli G, Rondelli P, Paciullo F, Fabris F, Carlon M, Turatto F, Baroni MC, Zardo M, Manfredini R, Molino C, Pala M, Fabbian F, Nuti R, Valenti R, Ruvio M, Cappelli S, Paolisso G, Rizzo MR, Laieta MT, Salvatore T, Sasso FC, Utili R, Durante Mangoni E, Pinto D, Olivieri O, Stanzial AM, Fellin R, Volpato S, Fotini S, Barbagallo M, Dominguez L, Plances L, D'Angelo D, Rini G, Mansueto P, Pepe I, Licata G, Calvo L, Valenti M, Borghi C, Strocchi E, Rinaldi ER, Zoli M, Fabbri E, Magalotti D, Auteri A, Pasqui AL, Puccetti L, Laghi Pasini F, Capecchi PL, Bicchi M, Sabbà C, Vella FS, Marseglia A, Luglio CV, Palasciano G, Modeo ME, Aquilino A, Raffaele P, Pugliese S, Capobianco C, Postiglione A, Barbella MR, De Stefano F, Fenoglio L, Brignone C, Bracco C, Giraudo A, Musca G, Cuccurullo O, Cricco L, Fiorentini A, Cappellini MD, Fabio G, Seghezzi S, De Amicis MM, Fargion S, Bonara P, Bulgheroni M, Lombardi R, Magrini F, Massari F, Tonella T, Peyvandi F, Tedeschi A, Rossio R, Moreo G, Ferrari B, Roncari L, Monzani V, Savojardo V, Folli C, Magnini M, Mari D, Rossi PD, Damanti S, Prolo S, Lilleri MS, Micale G, Podda M, Selmi C, Meda F, Accordino S, Conca A, Monti V, Corazza GR, Miceli E, Lenti MV, Padula D, Balduini CL, Bertolino G, Provini S, Quaglia F, Murialdo G, Bovio M, Dallegri F, Ottonello L, Quercioli A, Barreca A, Secchi MB, Ghelfi D, Chin WS, Carassale L, Caporotundo S, Anastasio L, Carbone M, Traisci G, De Feudis L, Davì G, Guagnano MT, Sestili S, Bergami E, Rizzioli E, Cagnoni C, Bertone L, Manucra A, Buratti A, Tognin T, Liberato NL, Bernasconi G, Nardo B, Bianchi GB, Benetti G, Quagliolo M, Centenaro GR, Purrello F, Di Pino A, Piro S, Mancuso G, Calipari D, Bartone M, Gullo F, Cortellaro M, Magenta M, Perego F, Meroni MR, Cicardi M, Magenta AG, Sacco A, Bonelli A, Dentamaro G, Rozzini R, Falanga L, Giordano A, Perin PC, Lorenzati B, Gruden G, Bruno G, Montrucchio G, Greco E, Tizzani P, Fera G, Di Luca ML, Renna D, Perciccante A, Coralli A, Tassara R, Melis D, Rebella L, Menardo G, Bottone S, Sferrazzo E, Ferri C, Striuli R, Scipioni R, Salmi R, Gaudenzi P, Gamberini S, Ricci F, Morabito C, Fava R, Semplicini A, Gottardo L, Vendemiale G, Serviddio G, Forlano R, Bolondi L, Rasciti L, Serio I, Masala C, Mammarella A, Raparelli V, Rossi Fanelli F, Delfino M, Amoroso A, Violi F, Basili S, Perri L, Serra P, Fontana V, Falcone M, Landolfi R, Grieco A, Gallo A, Zuccalà G, Franceschi F, De Marco G, Chiara C, Marta S, Bellusci M, Setti D, Pedrazzoli F, Romanelli G, Pirali C, Amolini C, Rosei EA, Rizzoni D, Castoldi L, Picardi A, Gentilucci UV, Mazzarelli C, Gallo P, Guasti L, Castiglioni L, Maresca A, Squizzato A, Contini S, Molaro M, Corsi M, Bertolotti M, Mussi C, Scotto R, Ferri MA, Veltri F, Arturi F, Succurro E, Sesti G, Gualtieri U, Perticone F, Sciacqua A, Quero M, Bagnato C, Loria P, Becchi MA, Martucci G, Fantuzzi A, Maurantonio M, Corinaldesi R, De Giorgio R, Serra M, Grasso V, Ruggeri E, Carozza LM, Pignatti F., ANNONI, GIORGIO, ZAZZETTA, SARA, Corrao, S, Santalucia, P, Argano, C, Djade, C, Barone, E, Tettamanti, M, Pasina, L, Franchi, C, Kamal Eldin, T, Marengoni, A, Salerno, F, Marcucci, M, Mannucci, P, Nobili, A, Mannucci, M, Sparacio, E, Alborghetti, S, Di Costanzo, R, Djignefa Djade, C, Prisco, D, Silvestri, E, Cenci, C, Barnini, T, Delitala, G, Carta, S, Atzori, S, Guarnieri, G, Zanetti, M, Spalluti, A, Serra, M, Bleve, M, Vanoli, M, Grignani, G, Casella, G, Gasbarrone, L, Maniscalco, G, Gunelli, M, Tirotta, D, Brucato, A, Ghidoni, S, Bernardi, M, Bassi, S, Santi, L, Agnelli, G, Iorio, A, Marchesini, E, Mannarino, E, Lupattelli, G, Rondelli, P, Paciullo, F, Fabris, F, Carlon, M, Turatto, F, Baroni, M, Zardo, M, Manfredini, R, Molino, C, Pala, M, Fabbian, F, Nuti, R, Valenti, R, Ruvio, M, Cappelli, S, Paolisso, G, Rizzo, M, Laieta, M, Salvatore, T, Sasso, F, Utili, R, Durante Mangoni, E, Pinto, D, Olivieri, O, Stanzial, A, Fellin, R, Volpato, S, Fotini, S, Barbagallo, M, Dominguez, L, Plances, L, D'Angelo, D, Rini, G, Mansueto, P, Pepe, I, Licata, G, Calvo, L, Valenti, M, Borghi, C, Strocchi, E, Rinaldi, E, Zoli, M, Fabbri, E, Magalotti, D, Auteri, A, Pasqui, A, Puccetti, L, Laghi Pasini, F, Capecchi, P, Bicchi, M, Sabbà, C, Vella, F, Marseglia, A, Luglio, C, Palasciano, G, Modeo, M, Aquilino, A, Raffaele, P, Pugliese, S, Capobianco, C, Postiglione, A, Barbella, M, De Stefano, F, Fenoglio, L, Brignone, C, Bracco, C, Giraudo, A, Musca, G, Cuccurullo, O, Cricco, L, Fiorentini, A, Cappellini, M, Fabio, G, Seghezzi, S, De Amicis, M, Fargion, S, Bonara, P, Bulgheroni, M, Lombardi, R, Magrini, F, Massari, F, Tonella, T, Peyvandi, F, Tedeschi, A, Rossio, R, Moreo, G, Ferrari, B, Roncari, L, Monzani, V, Savojardo, V, Folli, C, Magnini, M, Mari, D, Rossi, P, Damanti, S, Prolo, S, Lilleri, M, Micale, G, Podda, M, Selmi, C, Meda, F, Accordino, S, Conca, A, Monti, V, Corazza, G, Miceli, E, Lenti, M, Padula, D, Balduini, C, Bertolino, G, Provini, S, Quaglia, F, Murialdo, G, Bovio, M, Dallegri, F, Ottonello, L, Quercioli, A, Barreca, A, Secchi, M, Ghelfi, D, Chin, W, Carassale, L, Caporotundo, S, Anastasio, L, Carbone, M, Traisci, G, De Feudis, L, Davì, G, Guagnano, M, Sestili, S, Bergami, E, Rizzioli, E, Cagnoni, C, Bertone, L, Manucra, A, Buratti, A, Tognin, T, Liberato, N, Bernasconi, G, Nardo, B, Bianchi, G, Benetti, G, Quagliolo, M, Centenaro, G, Purrello, F, Di Pino, A, Piro, S, Mancuso, G, Calipari, D, Bartone, M, Gullo, F, Cortellaro, M, Magenta, M, Perego, F, Meroni, M, Cicardi, M, Magenta, A, Sacco, A, Bonelli, A, Dentamaro, G, Rozzini, R, Falanga, L, Giordano, A, Perin, P, Lorenzati, B, Gruden, G, Bruno, G, Montrucchio, G, Greco, E, Tizzani, P, Fera, G, Di Luca, M, Renna, D, Perciccante, A, Coralli, A, Tassara, R, Melis, D, Rebella, L, Menardo, G, Bottone, S, Sferrazzo, E, Ferri, C, Striuli, R, Scipioni, R, Salmi, R, Gaudenzi, P, Gamberini, S, Ricci, F, Morabito, C, Fava, R, Semplicini, A, Gottardo, L, Vendemiale, G, Serviddio, G, Forlano, R, Bolondi, L, Rasciti, L, Serio, I, Masala, C, Mammarella, A, Raparelli, V, Rossi Fanelli, F, Delfino, M, Amoroso, A, Violi, F, Basili, S, Perri, L, Serra, P, Fontana, V, Falcone, M, Landolfi, R, Grieco, A, Gallo, A, Zuccalà, G, Franceschi, F, De Marco, G, Chiara, C, Marta, S, Bellusci, M, Setti, D, Pedrazzoli, F, Romanelli, G, Pirali, C, Amolini, C, Rosei, E, Rizzoni, D, Castoldi, L, Picardi, A, Gentilucci, U, Mazzarelli, C, Gallo, P, Guasti, L, Castiglioni, L, Maresca, A, Squizzato, A, Contini, S, Molaro, M, Annoni, G, Corsi, M, Zazzetta, S, Bertolotti, M, Mussi, C, Scotto, R, Ferri, M, Veltri, F, Arturi, F, Succurro, E, Sesti, G, Gualtieri, U, Perticone, F, Sciacqua, A, Quero, M, Bagnato, C, Loria, P, Becchi, M, Martucci, G, Fantuzzi, A, Maurantonio, M, Corinaldesi, R, De Giorgio, R, Grasso, V, Ruggeri, E, Carozza, L, Pignatti, F, Mannucci M, Nobili A, Tettamanti M, Pasina L, Franchi C, Salerno F, Corrao S, Marengoni A, Marcucci M, Sparacio E, Alborghetti S, Di Costanzo R, Djignefa Djade C, Prisco D, Silvestri E, Cenci C, Barnini T, Delitala G, Carta S, Atzori S, Guarnieri G, Zanetti M, Spalluti A, Serra MG, Bleve MA, Vanoli M, Grignani G, Casella G, Gasbarrone L, Maniscalco G, Gunelli M, Tirotta D, Brucato A, Ghidoni S, Bernardi M, Bassi SL, Santi L, Agnelli G, Iorio A, Marchesini E, Mannarino E, Lupattelli G, Rondelli P, Paciullo F, Fabris F, Carlon M, Turatto F, Baroni MC, Zardo M, Manfredini R, Molino C, Pala M, Fabbian F, Nuti R, Valenti R, Ruvio M, Cappelli S, Paolisso G, Rizzo MR, Laieta MT, Salvatore T, Sasso FC, Utili R, Durante Mangoni E, Pinto D, Olivieri O, Stanzial AM, Fellin R, Volpato S, Fotini S, Barbagallo M, Dominguez L, Plances L, D'Angelo D, Rini G, Mansueto P, Pepe I, Licata G, Calvo L, Valenti M, Borghi C, Strocchi E, Rinaldi ER, Zoli M, Fabbri E, Magalotti D, Auteri A, Pasqui AL, Puccetti L, Laghi Pasini F, Capecchi PL, Bicchi M, Sabbà C, Vella FS, Marseglia A, Luglio CV, Palasciano G, Modeo ME, Aquilino A, Raffaele P, Pugliese S, Capobianco C, Postiglione A, Barbella MR, De Stefano F, Fenoglio L, Brignone C, Bracco C, Giraudo A, Musca G, Cuccurullo O, Cricco L, Fiorentini A, Cappellini MD, Fabio G, Seghezzi S, De Amicis MM, Fargion S, Bonara P, Bulgheroni M, Lombardi R, Magrini F, Massari F, Tonella T, Peyvandi F, Tedeschi A, Rossio R, Moreo G, Ferrari B, Roncari L, Monzani V, Savojardo V, Folli C, Magnini M, Mari D, Rossi PD, Damanti S, Prolo S, Lilleri MS, Micale G, Podda M, Selmi C, Meda F, Accordino S, Conca A, Monti V, Corazza GR, Miceli E, Lenti MV, Padula D, Balduini CL, Bertolino G, Provini S, Quaglia F, Murialdo G, Bovio M, Dallegri F, Ottonello L, Quercioli A, Barreca A, Secchi MB, Ghelfi D, Chin WS, Carassale L, Caporotundo S, Anastasio L, Carbone M, Traisci G, De Feudis L, Davì G, Guagnano MT, Sestili S, Bergami E, Rizzioli E, Cagnoni C, Bertone L, Manucra A, Buratti A, Tognin T, Liberato NL, Bernasconi G, Nardo B, Bianchi GB, Benetti G, Quagliolo M, Centenaro GR, Purrello F, Di Pino A, Piro S, Mancuso G, Calipari D, Bartone M, Gullo F, Cortellaro M, Magenta M, Perego F, Meroni MR, Cicardi M, Magenta AG, Sacco A, Bonelli A, Dentamaro G, Rozzini R, Falanga L, Giordano A, Perin PC, Lorenzati B, Gruden G, Bruno G, Montrucchio G, Greco E, Tizzani P, Fera G, Di Luca ML, Renna D, Perciccante A, Coralli A, Tassara R, Melis D, Rebella L, Menardo G, Bottone S, Sferrazzo E, Ferri C, Striuli R, Scipioni R, Salmi R, Gaudenzi P, Gamberini S, Ricci F, Morabito C, Fava R, Semplicini A, Gottardo L, Vendemiale G, Serviddio G, Forlano R, Bolondi L, Rasciti L, Serio I, Masala C, Mammarella A, Raparelli V, Rossi Fanelli F, Delfino M, Amoroso A, Violi F, Basili S, Perri L, Serra P, Fontana V, Falcone M, Landolfi R, Grieco A, Gallo A, Zuccalà G, Franceschi F, De Marco G, Chiara C, Marta S, Bellusci M, Setti D, Pedrazzoli F, Romanelli G, Pirali C, Amolini C, Rosei EA, Rizzoni D, Castoldi L, Picardi A, Gentilucci UV, Mazzarelli C, Gallo P, Guasti L, Castiglioni L, Maresca A, Squizzato A, Contini S, Molaro M, Corsi M, Bertolotti M, Mussi C, Scotto R, Ferri MA, Veltri F, Arturi F, Succurro E, Sesti G, Gualtieri U, Perticone F, Sciacqua A, Quero M, Bagnato C, Loria P, Becchi MA, Martucci G, Fantuzzi A, Maurantonio M, Corinaldesi R, De Giorgio R, Serra M, Grasso V, Ruggeri E, Carozza LM, Pignatti F., ANNONI, GIORGIO, and ZAZZETTA, SARA

Abstract

Background and purpose Women live longer and outnumber men. On the other hand, older women develop more chronic diseases and conditions such as arthritis, osteoporosis and depression, leading to a greater number of years of living with disabilities. The aim of this study was to describe whether or not there are gender differences in the demographic profile, disease distribution and outcome in a population of hospitalized elderly people. Methods Retrospective observational study including all patients recruited for the REPOSI study in the year 2010. Analyses are referred to the whole group and gender categorization was applied. Results A total of 1380 hospitalized elderly subjects, 50.5% women and 49.5% men, were considered. Women were older than men, more often widow and living alone or in nursing homes. Disease distribution showed that malignancy, diabetes, coronary artery disease, chronic kidney disease and chronic obstructive pulmonary disease were more frequent in men, but hypertension, osteoarthritis, anemia and depression were more frequent in women. Severity and comorbidity indexes according to the Cumulative Illness Rating Scale (CIRS-s and CIRS-c) were higher in men, while cognitive impairment evaluated by the Short Blessed Test (SBT), mood disorders by the Geriatric Depression Scale (GDS) and disability in daily life measured by Barthel Index (BI) were worse in women. In-hospital and 3-month mortality rates were higher in men. Conclusions Our study showed a gender dimorphism in the demographic and morbidity profiles of hospitalized elderly people, emphasizing once more the need for a personalized process of healthcare. © 2014 European Federation of Internal Medicine.

Published
2014

2. Statins discontinuation in compliant chronic users induces atherothrombotic profile despite baseline clinical setting and treatments.

Author

Puccetti L, Pasqui AL, Scarpini F, Cappellone R, Ghezzi A, Ceccatelli L, and Auteri A

Subjects
Atherosclerosis etiology, Female, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors adverse effects, Male, Substance Withdrawal Syndrome etiology, Thrombosis etiology, Treatment Outcome, Atherosclerosis blood, Hydroxymethylglutaryl-CoA Reductase Inhibitors administration & dosage, Medication Adherence, Substance Withdrawal Syndrome blood, Thrombosis blood
Published
2011
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3. Levosimendan improves pro/anti-inflammatory cytokines imbalance in male patients with advanced heart failure. A randomized, double-blind, placebo-controlled study.

Author

Pasqui AL, Maffei S, Di Renzo M, Pompella G, Auteri A, and Puccetti L

Subjects
Double-Blind Method, Humans, Male, Placebos, Simendan, Treatment Outcome, Cytokines blood, Heart Failure drug therapy, Heart Failure immunology, Hydrazones therapeutic use, Pyridazines therapeutic use, Vasodilator Agents therapeutic use
Published
2011
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4. Effects of atorvastatin and rosuvastatin on thromboxane-dependent platelet activation and oxidative stress in hypercholesterolemia.

Author

Puccetti L, Santilli F, Pasqui AL, Lattanzio S, Liani R, Ciani F, Ferrante E, Ciabattoni G, Scarpini F, Ghezzi A, Auteri A, and Davì G

Subjects
3' Untranslated Regions, Anticholesteremic Agents pharmacology, Atorvastatin, Double-Blind Method, Female, Humans, Lipids chemistry, Male, Middle Aged, Oxidative Stress, Platelet Activation, Polymorphism, Genetic, Prospective Studies, Prostaglandins A metabolism, Regression Analysis, Rosuvastatin Calcium, Blood Platelets drug effects, Fluorobenzenes pharmacology, Heptanoic Acids pharmacology, Hypercholesterolemia metabolism, Pyrimidines pharmacology, Pyrroles pharmacology, Sulfonamides pharmacology, Thromboxane B2 metabolism
Abstract

Objectives: We examined the time-dependent effects of atorvastatin and rosuvastatin on in vivo oxidative stress and platelet activation, to assess whether these phenomena are related to any pleiotropic effect of any statin or to their LDL-lowering effect. We also asked whether the presence of specific allele frequencies in carriers of the 3'UTR/lectin-like oxidized LDL receptor-1 (LOX-1) polymorphism may influence the effect of either statin., Methods: We included 60 hypercholesterolemic subjects, previously screened for LOX-1 3'UTR polymorphism, randomized, according to genetic profile (15 T and 15 C carriers for each arm), to atorvastatin 20mg/day or rosuvastatin 10mg/day., Results: After 8 weeks, atorvastatin and rosuvastatin were associated with comparable, significant reductions in LDL cholesterol (40.8% and 43.6%, respectively), plasma hs-CRP (9.5% vs. 13.8%), urinary 11-dehydro-thromboxane (TX) B(2) (38.9% vs. 27.1%) and 8-iso-prostaglandin (PG) F(2α) (39.4% vs. 19.4%). The impact of rosuvastatin or atorvastatin on CRP, 8-iso-PGF(2α), and 11-dehydro-TXB(2) did not differ according to the LOX-1 haplotype. On multiple regression analyses, only CRP and LDL were independent predictors of 11-dehydro-TXB(2), and only LDL was a significant predictor of 8-iso-PGF(2α)., Conclusions: Both atorvastatin and rosuvastatin cause comparable reductions of thromboxane-dependent platelet activation, lipid peroxidation and inflammation. The presence of 3'UTR/LOX-1 polymorphism does not affect the changes induced by either statin., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Published
2011
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5. Cardiac dysautonomia and arterial distensibility in essential hypertensives.

Author

Acampa M, Franchi M, Guideri F, Lamberti I, Bruni F, Pastorelli M, Bova G, Pasqui AL, Puccetti L, and Auteri A

Subjects
Adult, Aged, Electrocardiography, Female, Humans, Male, Middle Aged, Tilt-Table Test, Vagus Nerve physiopathology, Arrhythmias, Cardiac physiopathology, Arteries physiopathology, Heart Conduction System physiopathology, Heart Rate physiology, Hypertension physiopathology, Sympathetic Nervous System physiopathology, Vascular Resistance physiology
Abstract

Introduction: The central nervous system plays an important role in the regulation of blood pressure: the sympathetic nervous system may be a primary contributor to the development of some forms of essential hypertension. Hypertension is also associated with reduced distensibility of large arteries. The aim of our study is the evaluation of a correlation between cardiac dysautonomia (evaluated by means of heart rate variability [HRV]) and altered artery distensibility (evaluated by means of measurement of the time interval from the onset of the QRS wave and the detection of the last Korotkoff sound [QKD interval])., Materials and Methods: HRV and QKD interval were evaluated in 23 patients (60.9+/-8.7 years) with untreated hypertension and in 20 control subjects (53.2+/-16.8 years). QKD interval and QKD(100-60) (that is QKD for a 100 mm Hg systolic blood pressure and 60 bpm heart rate) were measured during a 24-hours blood pressure monitoring. HRV was evaluated by means of a spectral method. Three main spectral components were distinguished: very low frequency (VLF), low frequency (LF) and high frequency (HF) component., Results: Patients with reduced QKD(100-60) interval show reduced total power and spectral components values, with higher LF/HF ratio in basal conditions in comparison with control group. In patients with hypertension, QKD(100-60) values correlated significantly with LF/HF ratio (Spearman r=-0.551; p=0.006), HF spectral component (Spearman r=0.630; p=0.001) and total power (Spearman r=0.426; p=0.004)., Conclusions: Our results suggest that sympathetic overactivity may be the contributor of reduced arterial distensibility observed in patients with essential hypertension.

Published
2009
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6. Lectin-like oxidized-LDL receptor-1 (LOX-1) polymorphisms influence cardiovascular events rate during statin treatment.

Author

Puccetti L, Pasqui AL, Bruni F, Pastorelli M, Ciani F, Palazzuoli A, Pontani A, Ghezzi A, and Auteri A

Subjects
Aged, Atorvastatin, C-Reactive Protein metabolism, Cholesterol, LDL blood, Coronary Artery Disease epidemiology, Drug Resistance genetics, Female, Heterozygote, Humans, Hypercholesterolemia drug therapy, Hypercholesterolemia epidemiology, Hypercholesterolemia genetics, Male, Middle Aged, Polymorphism, Genetic, Retrospective Studies, Risk Factors, Simvastatin administration & dosage, Thrombosis drug therapy, Thrombosis epidemiology, Thrombosis genetics, Anticholesteremic Agents administration & dosage, Coronary Artery Disease drug therapy, Coronary Artery Disease genetics, Heptanoic Acids administration & dosage, Pyrroles administration & dosage, Scavenger Receptors, Class E genetics
Abstract

Background: Oxidized-LDL (ox-LDL) are involved in atherothrombosis by induction of endothelial dysfunction and thrombosis. The specific receptor lectin-like oxidized-LDL receptor-1 (LOX-1) is expressed in endothelial cells, monocytes and platelets. LOX-1 gene allelic variants (3'UTR/T) have been related with cardiovascular events and reduced anti-platelet activity induced by statins., Objectives: To detect whether LOX-1 polymorphisms could affect statins effectiveness in cardiovascular prevention., Patients/methods: The present was a retrospective study performed in 751 white hypercholesterolemic subjects treated with increasing doses of atorvastatin (n=382, 247 male, 135 female) or simvastatin (n=369, 244 male, 125 female) up to 4 years, whose LDL target was 3.36 mmol/L according to the National Cholesterol Education Program, Adult Treatment Panel III (NCEP-ATPIII). Single nucleotide polymorphism were evaluated by allelic discrimination assays (PCR), lipid profile by enzymatic-colorimetric methods and C-reactive protein (CRP) by a nephelometric technique., Results: Twenty-three non-ST elevation (NSTEMI) and eleven ST-elevation myocardial infarction (STEMI) were encountered in the observational period without differences between treatments (p=0.175) and sex (p=0.139). Each symptomatic subject (10 reaching the appropriate LDL target and 24 with still undesirable LDL) had the 3'UTR/T allelic variant (adjusted O.R. 4.63, 95% C.I. 3.46-6.70, p<0.0001). Among patients not reaching LDL target the C allele resulted protective with respect to T carriers (p<0.00001). Also, similar changes of CRP resulted in different event rate between T and C carriers (p<0.001) in the whole cohort., Conclusions: In the studied population LOX-1 genetic variants influence cardiovascular risk reduction induced by statins also in patients not reaching the LDL target. The previously described LOX-1-related antithrombotic actions of both statins employed could have a specific role in what observed, suggesting a genetic influence in statins LDL-lowering partially related actions.

Published
2007
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7. Cytokines in acute coronary syndromes.

Author

Pasqui AL, Di Renzo M, Auteri A, and Puccetti L

Subjects
Acute Disease, Humans, Angina, Unstable immunology, Interferon-gamma biosynthesis, Interleukin-10 biosynthesis, Monocytes immunology, Myocardial Infarction immunology, Tumor Necrosis Factor-alpha biosynthesis
Abstract

The aim of this study was to show the presence of an imbalance between pro-inflammatory and anti-inflammatory mediators in patients affected by acute coronary syndromes (ACS). We evaluated the production in cultured and stimulated lymphomonocytes of interferon (IFN)gamma and tumor necrosis factor (TNF)alpha, which are well known to possess pro-inflammatory effects, and of interleukin (IL)10, which has been shown to have a protective anti-inflammatory activity, in two groups of 30 patients affected by acute myocardial infarction (AMI) and unstable angina (UA), compared with two equivalent groups of patients with stable angina (SA) and of healthy volunteers. We found a significant increase of IFNgamma and TNFalpha production (p<0.01) and a significant decrease of IL-10 production (p<0.01) in cultures of lymphomonocytes taken from patients with AMI and UA compared with SA patients and controls. No significant changes were found between AMI and UA patients and SA patients and controls. We conclude that a relevant imbalance in cytokine release is present in ACS, markedly favoring pro-inflammatory effects.

Published
2005
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8. 3'UTR/T polymorphism of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is associated with modified anti-platelet activity of atorvastatin in hypercholesterolemic subjects.

Author

Puccetti L, Pasqui AL, Pastorelli M, Ciani F, Palazzuoli A, Gioffrè W, Auteri A, and Bruni F

Subjects
Adult, Alleles, Atorvastatin, Blood Platelets metabolism, Chromatography, High Pressure Liquid, Citrulline metabolism, Female, Genotype, Humans, Hypercholesterolemia drug therapy, Hypercholesterolemia genetics, Intracellular Fluid metabolism, Male, Middle Aged, Nitric Oxide Synthase metabolism, P-Selectin metabolism, Polymerase Chain Reaction, Scavenger Receptors, Class E antagonists & inhibitors, Scavenger Receptors, Class E blood, Anticholesteremic Agents therapeutic use, DNA genetics, Heptanoic Acids therapeutic use, Hypercholesterolemia blood, Platelet Activation drug effects, Polymorphism, Genetic, Pyrroles therapeutic use, Scavenger Receptors, Class E genetics
Abstract

Oxidized-low density lipoproteins (ox-LDL) and the specific receptor LOX-1 are involved in atherogenesis and atherothrombosis. LOX-1 downregulation is associated with the anti-platelet action of atorvastatin. 3'UTR/T LOX-1 polymorphism has been associated with increased risk of coronary artery disease. This study was planned to determine whether LOX-1 genetic variations could affect anti-platelet action of atorvastatin. We studied by platelet P-selectin (P-sel), CD36 and LOX-1 expression (cytofluorimetric detection) whether differences in cellular activation could be suitable in 109 3'UTR/T carriers out of 201 hypercholesterolemic subjects treated with atorvastatin 20mg/day. Hyperactivated platelets (P-sel in resting cells and % variation upon thrombin activation, p<0.001) were detected at baseline in patients without significant differences between T or C carriers. P-sel and platelet-associated ox-LDL, were significantly decreased (all p<0.001) in C carriers after one week of treatment before LDL reduction. In 3'UTR/T carriers P-sel was reduced (p<0.01) after 6 weeks of treatment according to LDL and ox-LDL reduction. In 3'UTR/T carriers atorvastatin reduced platelet activity by LDL and ox-LDL lowering and not by rapid CD36 and LOX-1 downregulation as in C carriers. Such data suggest that in T carriers LDL lowering is needed to achieve anti-platelet action.

Published
2005
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9. Structural and functional abnormality of systemic microvessels in cardiac syndrome X.

Author

Pasqui AL, Puccetti L, Di Renzo M, Bruni F, Camarri A, Palazzuoli A, Biagi F, Servi M, Bischeri D, Auteri A, and Pastorelli M

Subjects
Angina Pectoris, Variant physiopathology, Case-Control Studies, Female, Humans, Male, Microscopic Angioscopy, Microscopy, Video, Middle Aged, Syndrome, Angina Pectoris physiopathology, Coronary Circulation physiology, Coronary Vessels pathology, Microcirculation physiopathology
Abstract

Background and Aim: Microvascular damage of coronary bed has been considered the main pathogenetic factor of cardiac syndrome X (chest pain, exercise-induced ischemic ST-segment changes and angiographically normal coronary arteries). Previous studies have demonstrated that vascular abnormalities are not confined to the heart, suggesting a peripheral vascular dysfunction. On the hypothesis of a generalized microvascular disturbance in cardiac syndrome X, we performed a morphologic and functional study of systemic microcirculation in patients with syndrome X compared to normal subjects., Methods and Results: Microvessels were evaluated with intravital videocapillaroscopy (VCP) executed in peripheral and conjunctival observation sites which explore micro and paramicrocirculation; biohumoral study included markers of inflammation and of endothelial function, coagulative-fibrinolytic system and lipid metabolism. Videocapillaroscopy showed several morphologic changes (present in high percent of patients with syndrome X and not in controls) and significant quantitative alterations (capillary density, granular flow score, alterations of vessel profile, length of capillary loop branches and of arteriole/venule diameter) which indicated a severe alteration of whole vessel structure and an important rearrangement of microvascular disposition. In a similar way, the humoral study showed some significant changes of endothelial (vWF, ICAM-1, E-sel, PAI-1), inflammatory (C-reactive protein (CRP), fibrinogen) and metabolic factors (HDL-chol) which are commonly associated with inflammatory response., Conclusions: We conclude that patients with cardiac syndrome X exhibited some structural and functional alterations of systemic microvasculature; the pattern is similar to that detected in systemic inflammatory diseases and suggests a vascular lesion of inflammatory type. The same changes could be operating also in coronary microvessels of patients with syndrome X.

Published
2005
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10. Effect of atorvastatin on different fibrinolyis mechanisms in hypercholesterolemic subjects.

Author

Bruni F, Pasqui AL, Pastorelli M, Bova G, Di Renzo M, Cercigani M, Leo A, Auteri A, and Puccetti L

Subjects
Adult, Analysis of Variance, Atorvastatin, Female, Humans, Male, Middle Aged, Statistics, Nonparametric, Fibrinolysis drug effects, Heptanoic Acids pharmacology, Hydroxymethylglutaryl-CoA Reductase Inhibitors pharmacology, Hypercholesterolemia drug therapy, Pyrroles pharmacology
Abstract

Background: Hydroxymethyl-glutaryl-CoA-reductase inhibitors (statins) reduce cardiovascular events by cholesterol lowering as well as non-lipid related actions. Among them, the modulation of fibrinolysis could play a relevant role in vascular protection. Atorvastatin is able of reducing platelet activity and thrombin generation before low-density lipoprotein cholesterol (LDL-C) decrease in hypercholesterolemic subjects in which coagulation and fibrinolysis are linked by the activation of thrombin activable fibrinolysis inhibitor (TAFI). The aim of our study was to evaluate whether atorvastatin could modulate fibrinolysis by interactions with endothelial mechanisms and thrombin generation., Methods: Forty-four pure hypercholesterolemic subjects (26 M, 18 F, mean age 52.7+/-13.7, LDL-C 194.8+/-9.3t mg/dl) were evaluated for plasmin-antiplasmin complexes (PAP), tissue-plasminogen acivator (t-PA) and its inhibitor (PAI-1) (ELISA), TAFI activity (HPLC), platelet P-selectin (P-sel) (cytofluorymetric detection), platelet-dependent thrombin generation (PDTG, coagulative-chromogenic method) and lipid profile at baseline and after 7, 14, 28 and 90 days of atorvastatin (10 mg/die) treatment., Results: PAP were significantly reduced at baseline in hypercholesterolemic versus control subjects (P<0.05) and were related to P-sel (P<0.01), PDTG (P<0.01) and its inhibitor (PAI-1) after venous occlusion (VO) (P<0.05). Atorvastatin induced a significant increase of PAP at T(2) related to modifications of P-sel (P<0.01) and PDTG (P<0.01) before significant LDL-C reduction (P=0.132). PAI-1 was significantly changed at T(3) with relation to LDL-C (P<0.01), Von Willebrand factor (VWF) (P<0.01) and sE-sel (P<0.05)., Conclusions: The profibrinolytic activity of atorvastatin in hypercholesterolemic subjects is related, initially, to the positive effects exerted on platelet function and thrombin generation which can modulate fibrinolysis by TAFI activity.

Published
2004
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11. Enhanced apoptosis of peripheral blood mononuclear cells in cardiac transplanted patients undergoing chronic immunosuppressive treatment.

Author

Di Renzo M, Capecchi PL, Camurri A, Di Ciolla F, Maccherini M, Lisi G, Pompella G, Pasqui AL, Auteri A, Abbracchio MP, and Pasini FL

Subjects
Adult, Aged, Cell Survival, Fas Ligand Protein, Humans, Interleukin-2 biosynthesis, Leukocytes, Mononuclear physiology, Membrane Glycoproteins physiology, Middle Aged, RNA, Messenger analysis, fas Receptor physiology, Apoptosis drug effects, Heart Transplantation, Immunosuppressive Agents pharmacology, Leukocytes, Mononuclear drug effects
Abstract

Apoptosis plays a major role in tissue transplantation because intact T-cell-apoptosis pathways are required for the induction of tolerance to allografts. Moreover, immunosuppressive agents commonly used in clinical transplantation medicine promote lymphocyte apoptosis inhibiting the expression and production of cytokines involved in lymphocyte survival. The aim of our study was to evaluate peripheral blood mononuclear cells (PBMC) spontaneous apoptosis in patients undergoing chronic immunosuppressive treatment after cardiac transplantation. PBMC obtained from patients (n = 31) and controls matched for age and sex (n = 25) were cultured for 72 h and apoptosis was evaluated by quantification of fragmented DNA, staining with Hoechst 33258 dye and annexin V binding. We also investigated Fas expression and FasL mRNA expression as well as the ability of an IgM anti-Fas antibody to induce apoptosis. Finally, we evaluated IL2 production induced by PHA and the ability of IL2 to prevent apoptosis. In patients, PBMC underwent enhanced spontaneous apoptosis in comparison with controls. However, we could not find any difference between patients and normals as regards the expression of Fas and of FasL mRNA, even if the cross-linking of the Fas molecule induced apoptosis in PBMC from patients, whereas it failed to induce cell death in normals. We also found that IL2 production was significantly decreased in patients and that the addition of IL2 to the culture medium reduced PBMC spontaneous apoptosis. Our findings suggest that in cardiac transplanted patients PBMC undergo enhanced spontaneous apoptosis, which may contribute to prevent allograft rejection.

Published
2002
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12. Transmitral and pulmonary venous flow study in elite male runners and young adults.

Author

Palazzuoli A, Puccetti L, Pastorelli M, Pasqui AL, Auteri A, and Bruni F

Subjects
Adaptation, Physiological physiology, Adult, Blood Flow Velocity physiology, Diastole physiology, Echocardiography, Doppler, Humans, Male, Coronary Circulation physiology, Hypertrophy, Left Ventricular physiopathology, Pulmonary Veins physiology, Running physiology
Abstract

Background: Even if diastolic function has been assessed in athletes by analysis of transmitral Doppler flow, no one has studied pulmonary venous flow in this population. The aim of this study was to establish if the physiological adaptations following a prolonged physical training could influence the diastolic function in a professional Olympic male runner group., Methods: From February to December 1999 we studied 25 athletes (Group I) during the period of maximal training compared with 18 age- and sex-matched healthy sedentary subjects (Group II). We used mono- and bidimensional Echocardiography to assess left ventricular structure and systolic function. The diastolic function was evaluated by Doppler method assessing transmitral and venous pulmonary flow., Results: From the comparison between the two groups, we found great differences in the interventricular septum and the posterior wall thickness; the analysis of the systolic function demonstrated a significant increase in ejection fraction, stroke volume, left ventricular mass, and end diastolic volume in the athletes' population. Fluximetric study showed that ventricular diastolic function is not influenced by hypertrophy: indeed, Doppler evaluation of the transmitral flow showed a bigger velocity of the E wave, similarly, when we assessed pulmonary venous flow, we found faster retrograde Ar wave in group I., Conclusions: Our data indicate that diastolic function remains normal or improves in some cases after physical training; left ventricular hypertrophy and concentric remodeling do not involve diastolic changes like hypertrophic and hypertensive heart diseases.

Published
2002
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13. Effect of diet and treatment with statins on platelet-dependent thrombin generation in hypercholesterolemic subjects.

Author

Puccetti L, Bruni F, Bova G, Cercignani M, Palazzuoli A, Console E, Auteri A, and Pasqui AL

Subjects
Adult, Anticholesteremic Agents therapeutic use, Atorvastatin, Blood Platelets metabolism, Dose-Response Relationship, Drug, Fatty Acids, Monounsaturated pharmacology, Fatty Acids, Monounsaturated therapeutic use, Female, Fluvastatin, Heptanoic Acids pharmacology, Heptanoic Acids therapeutic use, Humans, Hypercholesterolemia blood, Hypercholesterolemia diet therapy, Hypercholesterolemia drug therapy, Indoles pharmacology, Indoles therapeutic use, Male, Middle Aged, Pravastatin pharmacology, Pravastatin therapeutic use, Pyridines pharmacology, Pyridines therapeutic use, Pyrroles pharmacology, Pyrroles therapeutic use, Simvastatin pharmacology, Simvastatin therapeutic use, Treatment Outcome, Anticholesteremic Agents pharmacology, Blood Platelets drug effects, Cholesterol blood, Hypercholesterolemia therapy, Thrombin biosynthesis
Abstract

Background and Aim: Platelets are strictly involved in arterial thrombosis and their hyperactivity has been shown in hypercholesterolemia. It has been reported that drugs affecting cholesterol metabolism (statins) decrease cardiovascular events by lowering lipid levels or by means of non-lipidic actions such as the direct inhibition of platelet function. The aim of this study was to detect the effect on platelet-dependent thrombin generation (PDTG) of a reduction in cholesterol obtained by means of a lipid-lowering diet or treatment with statins., Methods and Results: We compared PDTG (T0) in 144 hypercholesterolemic subjects (94 males and 50 females of child-bearing age, mean age 48.2 +/- 13.8, plasma total cholesterol 6.93 +/- 0.64, high density lipoprotein cholesterol 1.25 +/- 0.14, triglycerides 1.15 +/- 0.19 mmol/L) and 70 normolipidemic controls (37 males and 33 females, mean age 43.1 +/- 12.6. After six weeks on an appropriate diet, the patients were randomised to receive different statin therapies if there was no reduction in their lipid profile and/or PDTG (T1). They were re-evaluated six weeks later, and the drug doses were maintained or increased on the basis of the variables (T2). A final evaluation was made after a further six weeks (T3). All of the data were evaluated using ANOVA and Spearman's correlation coefficent. The results showed increased PDTG in hypercholesterolemic subjects (418.2 +/- 29.2 mIU/mL, p < 0.001 vs controls). Diet alone did not reduce PDTG (380.2 +/- 28.5 mIU/mL, p = 0.226 vs controls). At T2, simvastatin and atorvastatin significantly decreased PDTG (P < 0.001 vs T0-1) and low-density lipoprotein cholesterol (LDL-C). No correlation was found between the two variables in the simvastatin group (r = 0.16). Cerivastatin reduced PDTG without significantly decreasing LDL-C (p < 0.001 and p = 0.476, r = 0.14). Pravastatin and fluvastatin significantly reduced thrombin generation only at T3 (40 mg/day); pravastatin was also associated with a decrease in LDL-C (p < 0.01, r = 0.66)., Conclusions: Our results confirm an increased PDTG in patients with type IIa hyperlipoproteinemia, which is not reduced by diet. Statins at different doses significantly decrease PDTG but do not correlate with a reduction in LDL-C.

Published
2001

14. Complement activation in hypercholesterolemia.

Author

Pasqui AL, Bova G, Puccetti L, Bruni F, Pompella G, and Auteri A

Subjects
Adult, Aged, Arteriosclerosis immunology, Arteriosclerosis physiopathology, Cholesterol blood, Female, Humans, Hypercholesterolemia immunology, Hypercholesterolemia physiopathology, Male, Middle Aged, Arteriosclerosis blood, Complement Activation, Hypercholesterolemia blood
Abstract

Background and Aim: Inflammatory and lipid factors share an important role in atherosclerosis. This study evaluates their relations in dyslipidemic subjects., Methods and Results: We compared the complement system (serum hemolytic activity CH50, C3 and C4 fractions and terminal complex sC5b-9) in 30 hypercholesterolemic patients with elevated cholesterol and decreased HDL-cholesterol levels, 30 normolipemic patients with clinical atherosclerosis and 30 matched normal subjects. In addition we evaluated the circulating immune complexes containing cholesterol (chol-CIC) on the assumption that they might be important in complement activation, and the circulating levels of the adhesion molecule ICAM-1 (sICAM-1) as a sign of endhotelial dysfunction. We found a significant increase of sC5b-9 (but not of CH50 and C3, C4) in the hypercholesterolemics compared with the other groups. The plasma sC5b-9 level was inversely and significantly related to HDL-chol (regression analysis), whereas no direct significant relation was found between sC5b-9 and cholesterol. Chol-CIC were also significantly increased in this group. The atherosclerosis patients also presented a significant increase of sC5b-9. Lastly, both patient groups displayed a significant increase of sICAM-1., Conclusions: We suggest that complement activation in dyslipidemics may be induced by their increased immune complexes. However, the decrease of complement regulatory proteins carried by HDL is another important factor, while complement changes may be related to variations of other humoral and cell systems (endothelium, coagulative/fibrinolytic system), whose involvement is suggested in our study by the changes of sICAM-1.

Published
2000

15. Effect of Pidotimod, a new immunostimulating agent, on some aspects of immune response. In vitro study.

Author

Auteri A, Pasqui AL, Bruni F, Saletti M, Di Renzo M, and Bova G

Subjects
Complement System Proteins biosynthesis, Humans, Lymphocyte Activation drug effects, Lymphocytes drug effects, Neutrophils drug effects, Neutrophils metabolism, Phagocytosis drug effects, Pyrrolidonecarboxylic Acid pharmacology, Thiazolidines, Adjuvants, Immunologic pharmacology, Immunity, Cellular drug effects, Pyrrolidonecarboxylic Acid analogs & derivatives, Thiazoles pharmacology
Published
1992
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