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1. Inflammasome, T Lymphocytes and Innate-Adaptive Immunity Crosstalk: Role in Cardiovascular Disease and Therapeutic Perspectives

Author

Pedicino, Daniela, Giglio, Ada Francesca, Ruggio, Aureliano, Massaro, G, D'Aiello, Alessia, Trotta, Francesco, Lucci, Claudia, Graziani, Francesca, Biasucci, Luigi Marzio, Crea, Filippo, Liuzzo, Giovanna, Pedicino D, Giglio AF, Ruggio A, Trotta F, Lucci C, Graziani F (ORCID:0000-0002-4520-5689), Biasucci LM (ORCID:0000-0002-6921-6497), Crea F (ORCID:0000-0001-9404-8846), Liuzzo G (ORCID:0000-0002-5714-0907), Pedicino, Daniela, Giglio, Ada Francesca, Ruggio, Aureliano, Massaro, G, D'Aiello, Alessia, Trotta, Francesco, Lucci, Claudia, Graziani, Francesca, Biasucci, Luigi Marzio, Crea, Filippo, Liuzzo, Giovanna, Pedicino D, Giglio AF, Ruggio A, Trotta F, Lucci C, Graziani F (ORCID:0000-0002-4520-5689), Biasucci LM (ORCID:0000-0002-6921-6497), Crea F (ORCID:0000-0001-9404-8846), and Liuzzo G (ORCID:0000-0002-5714-0907)

Abstract

Over the past few decades, lot of evidences have shown atherosclerosis as a chronic progressive disease with an exquisite inflammatory feature. More recently, the role of innate immune response in the onset and progression of coronary artery disease (CAD) and an adaptive immunity imbalance, mostly involving T cell sub-sets, have been documented. Therefore, like in many other inflammatory and autoimmune disorders, an altered innate-adaptive immunity crosstalk could represent the key of the inflammatory burden leading to atherosclerotic plaque formation and progression and to the breakdown of plaque stability. In this review, we will address the role of inflammasome in innate immunity and in the imbalance of adaptive immunity. We will discuss how this altered immune crosstalk is related to CAD onset and progression. We will also discuss how unravelling the key molecular mechanisms is of paramount importance in the development of therapeutic tools to delay the chronic progression and prevent the acute destabilization of atherosclerotic plaque.

Published
2018

2. Centrality dependence of the pseudorapidity density distribution for charged particles in Pb-Pb collisions at √sNN = 2.76 TeV

Author

E. Abbas a, B. Abelev bt, J. Adam al, D. Adamová ca, A. M. Adare dz, M. M. Aggarwal ce, G. Aglieri Rinella ah, M. Agnello cv, A. G. Agocs dy, A. Agostinelli ab, Z. Ahammed dt, A. Ahmad Masoodi r, N. Ahmad r, S. U. Ahn bm, S. A. Ahn bm, I. Aimo y, cv, ck, M. Ajaz p, A. Akindinov ay, D. Aleksandrov cq, B. Alessandro cv, A. Alici cx, m, A. Alkin d, E. Almaráz Aviña bi, J. Alme aj, T. Alt an, V. Altini af, S. Altinpinar s, I. Altsybeev dv, C. Andrei bw, A. Andronic cn, V. Anguelov cj, J. Anielski bg, C. Anson t, T. Anticˇic ́ co, F. Antinori cw, P. Antonioli cx, L. Aphecetche dd, H. Appelshäuser be, N. Arbor bp, S. Arcelli ab, A. Arend be, N. Armesto q, R. Arnaldi cv, T. Aronsson dz, I. C. Arsene cn, M. Arslandok be, A. Asryan dv, A. Augustinus ah, R. Averbeck cn, T. C. Awes cb, J. Äystö aq, M. D. Azmi r, M. Bach an, A. Badalà cu, Y. W. Baek bo, R. Bailhache be, R. Bala ch, A. Baldisseri o, F. Baltasar Dos Santos Pedrosa ah, J. Bán az, R. C. Baral ba, R. Barbera aa, F. Barile af, G. G. Barnaföldi dy, L. S. Barnby cs, V. Barret bo, J. Bartke dh, M. Basile ab, N. Bastid bo, S. Basu dt, B. Bathen bg, G. Batigne dd, B. Batyunya bk, P. C. Batzing v, C. Baumann be, I. G. Bearden by, H. Beck be, N. K. Behera as, I. Belikov bj, F. Bellini ab, R. Bellwied dn, E. Belmont Moreno bi, G. Bencedi dy, S. Beole y, I. Berceanu bw, A. Bercuci bw, Y. Berdnikov cc, D. Berenyi dy, A. A. E. Bergognon dd, R. A. Bertens ax, D. Berzano y, L. Betev ah, A. Bhasin ch, A. K. Bhati ce, J. Bhom dr, N. Bianchi bq, L. Bianchi y, C. Bianchin ax, J. Bielcˇík al, J. Bielcˇíková ca, A. Bilandzic by, S. Bjelogrlic ax, F. Blanco k, F. Blanco dn, D. Blau cq, C. Blume be, M. Boccioli ah, S. Böttger bd, A. Bogdanov bu, H. Bøggild by, M. Bogolyubsky av, L. Boldizsár dy, M. Bombara am, J. Book be, H. Borel o, A. Borissov dx, F. Bossú cg, M. Botje bz, E. Botta y, E. Braidot bs, P. Braun Munzinger cn, M. Bregant dd, T. Breitner bd, T. A. Broker be, T. A. Browning cl, M. Broz ak, R. Brun ah, E. Bruna y, G. E. Bruno af, D. Budnikov cp, H. Buesching be, S. Bufalino y, P. Buncic ah, O. Busch cj, Z. Buthelezi cg, D. Caffarri ac, X. Cai h, H. Caines dz, E. Calvo Villar ct, V. Canoa Roman l, G. Cara Romeo cx, F. Carena ah, W. Carena ah, N. Carlin Filho dk, F. Carminati ah, A. Casanova Díaz bq, J. Castillo Castellanos o, J. F. Castillo Hernandez cn, E. A. R. Casula x, V. Catanescu bw, C. Cavicchioli ah, C. Ceballos Sanchez j, J. Cepila al, P. Cerello cv, B. Chang aq, S. Chapeland ah, J. L. Charvet o, S. Chattopadhyay dt, S. Chattopadhyay cr, M. Cherney cd, C. Cheshkov ah, B. Cheynis dm, V. Chibante Barroso ah, D. D. Chinellato dn, P. Chochula ah, M. Chojnacki by, S. Choudhury dt, P. Christakoglou bz, C. H. Christensen by, P. Christiansen ag, T. Chujo dr, S. U. Chung cm, C. Cicalo cy, L. Cifarelli ab, F. Cindolo cx, J. Cleymans cg, F. Colamaria af, D. Colella af, A. Collu x, G. Conesa Balbastre bp, Z. Conesa del Valle ah, M. E. Connors dz, G. Contin w, J. G. Contreras l, T. M. Cormier dx, Y. Corrales Morales y, P. Cortese ae, I. Cortés Maldonado c, M. R. Cosentino bs, F. Costa ah, M. E. Cotallo k, E. Crescio l, P. Crochet bo, E. Cruz Alaniz bi, R. Cruz Albino l, E. Cuautle bh, L. Cunqueiro bq, A. Dainese ac, H. H. Dalsgaard by, R. Dangh, A. Danubc, K. Dascr, I. Dasau, S. Dase, D. Dascr, A. Dashdl, S. Dashas, S. Dedt, G. O. V. de Barros dk, A. De Caro ad, G. de Cataldo da, J. de Cuveland an, A. De Falco x, D. De Gruttola ad, H. Delagrange dd, A. Deloff bv, N. De Marco cv, E. Dénes dy, S. De Pasquale ad, A. Deppman dk, G. D. Erasmo af, R. de Rooij ax, M. A. Diaz Corchero k, D. Di Bari af, T. Dietel bg, C. Di Giglio af, S. Di Liberto db, A. Di Mauro ah, P. Di Nezza bq, R. Divià ah, Ø. Djuvsland s, A. Dobrin dx, ag, ax, T. Dobrowolski bv, B. Dönigus cn, O. Dordic v, O. Driga dd, A. K. Dubey dt, A. Dubla ax, L. Ducroux dm, P. Dupieux bo, A. K. Dutta Majumdar cr, D. Elia da, D. Emschermann bg, H. Engel bd, B. Erazmus ah, H. A. Erdal aj, D. Eschweiler an, B. Espagnon au, M. Estienne dd, S. Esumi dr, D. Evans cs, S. Evdokimov av, G. Eyyubova v, D. Fabris ac, J. Faivre bp, D. Falchieri ab, A. Fantoni bq, M. Fasel cj, D. Fehlker s, L. Feldkamp bg, D. Felea bc, A. Feliciello cv, B. Fenton Olsen bs, G. Feofilov dv, A. Fernández Téllez c, A. Ferretti y, A. Festanti ac, J. Figiel dh, M. A. S. Figueredo dk, S. Filchagin cp, D. Finogeev aw, F. M. Fionda af, E. M. Fiore af, E. Floratos cf, M. Floris ah, S. Foertsch cg, P. Foka cn, S. Fokin cq, A. Francescon ah, U. Frankenfeld cn, U. Fuchs ah, C. Furget bp, M. Fusco Girard ad, J. J. Gaardhøje by, M. Gagliardi y, A. Gago ct, M. Gallio y, D. R. Gangadharan t, P. Ganoti cb, C. Garabatos cn, E. Garcia Solis n, C. Gargiulo ah, I. Garishvili bt, J. Gerhard an, M. Germain dd, C. Geuna o, A. Gheata ah, M. Gheata bc, B. Ghidini af, P. Ghosh dt, P. Gianotti bq, M. R. Girard dw, P. Giubellino ah, E. Gladysz Dziadus dh, P. Glässel cj, R. Gomez dj, l, E. G. Ferreiro q, L. H. González Trueba bi, P. González Zamora k, S. Gorbunov an, A. Goswami ci, S. Gotovac df, L. K. Graczykowski dw, R. Grajcarek cj, A. Grelli ax, A. Grigoras ah, C. Grigoras ah, V. Grigoriev bu, A. Grigoryan b, S. Grigoryan bk, B. Grinyov d, N. Grion cz, P. Gros ag, J. F. Grosse Oetringhaus ah, J. Y. Grossiord dm, R. Grosso ah, F. Guber aw, R. Guernane bp, B. Guerzoni ab, M. Guilbaud dm, K. Gulbrandsen by, H. Gulkanyan b, T. Gunji dq, R. Gupta ch, A. Gupta ch, R. Haake bg, Ø. Haaland s, C. Hadjidakis au, M. Haiduc bc, H. Hamagaki dq, G. Hamar dy, B. H. Han u, L. D. Hanratty cs, A. Hansen by, Z. Harmanová Tóthová am, J. W. Harris dz, M. Hartig be, A. Harton n, D. Hatzifotiadou cx, S. Hayashi dq, A. Hayrapetyan ah, b, S. T. Heckel be, M. Heide bg, H. Helstrup aj, A. Herghelegiu bw, G. Herrera Corral l, N. Herrmann cj, B. A. Hess ds, K. F. Hetland aj, B. Hicks dz, B. Hippolyte bj, Y. Hori dq, P. Hristov ah, I. Hrˇivnácˇová au, M. Huang s, T. J. Humanic t, D. S. Hwang u, R. Ichou bo, R. Ilkaev cp, I. Ilkiv bv, M. Inaba dr, E. Incani x, P. G. Innocenti ah, G. M. Innocenti y, M. Ippolitov cq, M. Irfan r, C. Ivan cn, V. Ivanov cc, A. Ivanov dv, M. Ivanov cn, O. Ivanytskyi d, A. Jachołkowski aa, P. M. Jacobs bs, C. Jahnke dk, H. J. Jang bm, M. A. Janik dw, P. H. S. Y. Jayarathna dn, S. Jena as, D. M. Jha dx, R. T. Jimenez Bustamante bh, P. G. Jones cs, H. Jung ao, A. Jusko cs, A. B. Kaidalov ay, S. Kalcher an, P. Kalinˇák az, T. Kalliokoski aq, A. Kalweit ah, J. H. Kang eb, V. Kaplin bu, S. Kar dt, A. Karasu Uysal ah, ea, bn, O. Karavichev aw, T. Karavicheva aw, E. Karpechev aw, A. Kazantsev cq, U. Kebschull bd, R. Keidel ec, B. Ketzer be, K. H. Khan p, M. M. Khan r, P. Khan cr, S. A. Khan dt, A. Khanzadeev cc, Y. Kharlov av, B. Kileng aj, M. Kim eb, S. Kim u, B. Kim eb, T. Kim eb, D. J. Kim aq, D. W. Kim ao, J. H. Kim u, J. S. Kim ao, M. Kim ao, S. Kirsch an, I. Kisel an, S. Kiselev ay, A. Kisiel dw, J. L. Klay g, J. Klein cj, C. Klein Bösing bg, M. Kliemant be, A. Kluge ah, M. L. Knichel cn, A. G. Knospe di, M. K. Köhler cn, T. Kollegger an, A. Kolojvari dv, M. Kompaniets dv, V. Kondratiev dv, N. Kondratyeva bu, A. Konevskikh aw, V. Kovalenko dv, M. Kowalski dh, S. Kox bp, G. Koyithatta Meethaleveedu as, J. Kral aq, I. Králik az, F. Kramer be, A. Kravcˇáková am, M. Krelina al, M. Kretz an, M. Krivda cs, F. Krizek aq, M. Krus al, E. Kryshen cc, M. Krzewicki cn, V. Kucera ca, Y. Kucheriaev cq, T. Kugathasan ah, C. Kuhn bj, P. G. Kuijer bz, I. Kulakov be, J. Kumar as, P. Kurashvili bv, A. Kurepin aw, A. B. Kurepin aw, A. Kuryakin cp, S. Kushpil ca, V. Kushpil ca, H. Kvaerno v, M. J. Kweon cj, Y. Kwon eb, P. Ladrón de Guevara bh, I. Lakomov au, R. Langoy s, S. L. La Pointe ax, C. Lara bd, A. Lardeux dd, P. La Rocca aa, M. Lechman ah, S. C. Lee ao, G. R. Lee cs, I. Legrand ah, J. Lehnert be, R. C. Lemmon dc, M. Lenhardt cn, V. Lenti da, H. León bi, M. Leoncino y, I. León Monzón dj, P. Lévai dy, S. Li bo, h, J. Lien s, R. Lietava cs, S. Lindal v, V. Lindenstruth an, C. Lippmann cn, M. A. Lisa t, H. M. Ljunggren ag, D. F. Lodato ax, P. I. Loenne s, V. R. Loggins dx, V. Loginov bu, D. Lohner cj, C. Loizides bs, K. K. Loo aq, X. Lopez bo, E. López Torres j, G. Løvhøiden v, X. G. Lu cj, P. Luettig be, M. Lunardon ac, J. Luo h, C. Luzzi ah, K. Ma h, R. Ma dz, D. M. Madagodahettige Don dn, A. Maevskaya aw, M. Mager bf, D. P. Mahapatra ba, A. Maire cj, M. Malaev cc, I. Maldonado Cervantes bh, Ludmila Malinina bk, 1, D. Mal’Kevich ay, P. Malzacher cn, A. Mamonov cp, L. Manceau cv, L. Mangotra ch, V. Manko cq, F. Manso bo, V. Manzari da, Y. Mao h, M. Marchisone bo, y, J. Mareš bb, A. Margotti cx, A. Marín cn, C. Markert di, M. Marquard be, I. Martashvili dp, N. A. Martin cn, P. Martinengo ah, M. I. Martínez c, G. Martínez García dd, Y. Martynov d, A. Mas dd, S. Masciocchi cn, M. Masera y, A. Masoni cy, L. Massacrier dd, A. Mastroserio af, A. Matyja dh, C. Mayer dh, J. Mazer dp, M. A. Mazzoni db, F. Meddi z, A. Menchaca Rocha bi, J. Mercado Pérez cj, M. Meres ak, Y. Miake dr, K. Mikhaylov bk, L. Milano ah, Jovan Milosevic v, 2, A. Mischke ax, A. N. Mishra ci, D. Mis ́kowiec cn, C. Mitu bc, S. Mizuno dr, J. Mlynarz dx, B. Mohanty dt, L. Molnar dy, L. Montaño Zetina l, M. Monteno cv, E. Montes k, T. Moon eb, M. Morando ac, D. A. Moreira De Godoy dk, S. Moretto ac, A. Morreale aq, A. Morsch ah, V. Muccifora bq, E. Mudnic df, S. Muhuri dt, M. Mukherjee dt, H. Müller ah, M. G. Munhoz dk, S. Murray cg, L. Musa ah, J. Musinsky az, B. K. Nandi as, R. Nania cx, E. Nappi da, C. Nattrass dp, T. K. Nayak dt, S. Nazarenko cp, A. Nedosekin ay, M. Nicassio af, M. Niculescu bc, B. S. Nielsen by, T. Niida dr, S. Nikolaev cq, V. Nikolic co, S. Nikulin cq, V. Nikulin cc, B. S. Nilsen cd, M. S. Nilsson v, F. Noferini cx, P. Nomokonov bk, G. Nooren ax, A. Nyanin cq, A. Nyatha as, C. Nygaard by, J. Nystrand s, A. Ochirov dv, H. Oeschler bf, ah, cj, S. Oh dz, S. K. Oh ao, J. Oleniacz dw, A. C. Oliveira Da Silva dk, C. Oppedisano cv, A. Ortiz Velasquez ag, A. Oskarsson ag, P. Ostrowski dw, J. Otwinowski cn, K. Oyama cj, K. Ozawa dq, Y. Pachmayer cj, M. Pachr al, F. Padilla y, P. Pagano ad, G. Paic ́ bh, F. Painke an, C. Pajares q, S. K. Pal dt, A. Palaha cs, A. Palmeri cu, V. Papikyan b, G. S. Pappalardo cu, W. J. Park cn, A. Passfeld bg, D. I. Patalakha av, V. Paticchio da, B. Paul cr, A. Pavlinov dx, T. Pawlak dw, T. Peitzmann ax, H. Pereira Da Costa o, E. Pereira De Oliveira Filho dk, D. Peresunko cq, C. E. Pérez Lara bz, D. Perrino af, W. Peryt dw, A. Pesci cx, Y. Pestov f, V. Petrácˇek al, M. Petran al, M. Petris bw, P. Petrov cs, M. Petrovici bw, C. Petta aa, M. Pikna ak, P. Pillot dd, O. Pinazza ah, L. Pinsky dn, N. Pitz be, D. B. Piyarathna dn, M. Planinic co, M. Płoskon ́ bs, J. Pluta dw, T. Pocheptsov bk, S. Pochybova dy, P. L. M. Podesta Lerma dj, M. G. Poghosyan ah, K. Polák bb, B. Polichtchouk av, N. Poljak ax, A. Pop bw, S. Porteboeuf Houssais bo, V. Pospíšil al, B. Potukuchi ch, S. K. Prasad dx, R. Preghenella cx, F. Prino cv, C. A. Pruneau dx, I. Pshenichnov aw, G. Puddu x, V. Punin cp, M. Putiš am, J. Putschke dx, H. Qvigstad v, A. Rachevski cz, A. Rademakers ah, T. S. Räihä aq, J. Rak aq, A. Rakotozafindrabe o, L. Ramello ae, S. Raniwala ci, R. Raniwala ci, S. S. Räsänen aq, B. T. Rascanu be, D. Rathee ce, W. Rauch ah, K. F. Read dp, J. S. Real bp, K. Redlich bv, 3, R. J. Reed dz, A. Rehman s, P. Reichelt be, M. Reicher ax, R. Renfordt be, A. R. Reolon bq, A. Reshetin aw, F. Rettig an, J. P. Revol ah, K. Reygers cj, L. Riccati cv, R. A. Ricci br, T. Richert ag, M. Richter v, P. Riedler ah, W. Riegler ah, F. Riggi aa, M. Rodríguez Cahuantzi c, A. Rodriguez Manso bz, K. Røed s, v, E. Rogochaya bk, D. Rohr an, D. Röhrich s, R. Romita cn, F. Ronchetti bq, P. Rosnet bo, S. Rossegger ah, A. Rossi ah, P. Roy cr, C. Roy bj, A. J. Rubio Montero k, R. Russo y, E. Ryabinkin cq, A. Rybicki dh, S. Sadovsky av, K. Šafarˇík ah, R. Sahoo at, P. K. Sahu ba, J. Saini dt, H. Sakaguchi ar, S. Sakai bs, D. Sakata dr, C. A. Salgado q, J. Salzwedel t, S. Sambyal ch, V. Samsonov cc, X. Sanchez Castro bj, L. Šándor az, A. Sandoval bi, M. Sano dr, G. Santagati aa, R. Santoro ah, J. Sarkamo aq, D. Sarkar dt, E. Scapparone cx, F. Scarlassara ac, R. P. Scharenberg cl, C. Schiaua bw, R. Schicker cj, H. R. Schmidt ds, C. Schmidt cn, S. Schuchmann be, J. Schukraft ah, T. Schuster dz, Y. Schutz ah, K. Schwarz cn, K. Schweda cn, G. Scioli ab, E. Scomparin cv, R. Scott dp, P. A. Scott cs, G. Segato ac, I. Selyuzhenkov cn, S. Senyukov bj, J. Seo cm, S. Serci x, E. Serradilla k, A. Sevcenco bc, A. Shabetai dd, G. Shabratova bk, R. Shahoyan ah, N. Sharma dp, S. Sharma ch, S. Rohni ch, K. Shigaki ar, K. Shtejer j, Y. Sibiriak cq, E. Sicking bg, S. Siddhanta cy, T. Siemiarczuk bv, D. Silvermyr cb, C. Silvestre bp, G. Simatovic bh, G. Simonetti ah, R. Singaraju dt, R. Singh ch, S. Singha dt, V. Singhal dt, B. C. Sinha dt, T. Sinha cr, B. Sitar ak, M. Sitta ae, T. B. Skaali v, K. Skjerdal s, R. Smakal al, N. Smirnov dz, R. J. M. Snellings ax, C. Søgaard ag, R. Soltz bt, M. Song eb, J. Song cm, C. Soos ah, F. Soramel ac, I. Sputowska dh, M. Spyropoulou Stassinaki cf, B. K. Srivastava cl, J. Stachel cj, I. Stan bc, G. Stefanek bv, M. Steinpreis t, E. Stenlund ag, G. Steyn cg, J. H. Stiller cj, D. Stocco dd, M. Stolpovskiy av, P. Strmen ak, A. A. P. Suaide dk, M. A. Subieta Vásquez y, T. Sugitate ar, C. Suire au, R. Sultanov ay, M. Šumbera ca, T. Susa co, T. J. M. Symons bs, A. Szanto de Toledo dk, I. Szarka ak, A. Szczepankiewicz dh, M. Szyman ́ ski dw, J. Takahashi dl, M. A. Tangaro af, J. D. Tapia Takaki au, A. Tarantola Peloni be, A. Tarazona Martinez ah, A. Tauro ah, G. Tejeda Muñoz c, A. Telesca ah, A. Ter Minasyan cq, C. Terrevoli af, J. Thäder cn, D. Thomas ax, R. Tieulent dm, A. R. Timmins dn, D. Tlusty al, A. Toia an, ac, cw, H. Torii dq, L. Toscano cv, V. Trubnikov d, D. Truesdale t, W. H. Trzaska aq, T. Tsuji dq, A. Tumkin cp, R. Turrisi cw, T. S. Tveter v, J. Ulery be, K. Ullaland s, J. Ulrich bl, A. Uras dm, G. M. Urciuoli db, G. L. Usai x, M. Vajzer al, M. Vala bk, L. Valencia Palomo au, P. Vande Vyvre ah, J. W. Van Hoorne ah, M. van Leeuwen ax, L. Vannucci br, A. Vargas c, R. Varma as, M. Vasileiou cf, A. Vasiliev cq, V. Vechernin dv, M. Veldhoen ax, M. Venaruzzo w, E. Vercellin y, S. Vergara c, R. Vernet i, M. Verweij ax, L. Vickovic df, G. Viesti ac, J. Viinikainen aq, Z. Vilakazi cg, O. Villalobos Baillie cs, Y. Vinogradov cp, L. Vinogradov dv, A. Vinogradov cq, T. Virgili ad, Y. P. Viyogi dt, A. Vodopyanov bk, M. A. Völkl cj, S. Voloshin dx, K. Voloshin ay, G. Volpe ah, B. von Haller ah, I. Vorobyev dv, D. Vranic cn, J. Vrláková am, B. Vulpescu bo, A. Vyushin cp, B. Wagner s, V. Wagner al, R. Wan h, Y. Wang h, M. Wang h, Y. Wang cj, K. Watanabe dr, M. Weber dn, J. P. Wessels ah, U. Westerhoff bg, J. Wiechula ds, J. Wikne v, M. Wilde bg, G. Wilk bv, M. C. S. Williams cx, B. Windelband cj, L. Xaplanteris Karampatsos di, C. G. Yaldo dx, Y. Yamaguchi dq, S. Yang s, P. Yang h, H. Yang o, S. Yasnopolskiy cq, J. Yi cm, Z. Yin h, I. K. Yoo cm, J. Yoon eb, W. Yu be, X. Yuan h, I. Yushmanov cq, V. Zaccolo by, C. Zach al, C. Zampolli cx, S. Zaporozhets bk, A. Zarochentsev dv, P. Závada bb, N. Zaviyalov cp, H. Zbroszczyk dw, P. Zelnicek bd, I. S. Zgura bc, M. Zhalov cc, H. Zhang h, X. Zhang bs, bo, h, Y. Zhang h, D. Zhou h, F. Zhou h, Y. Zhou ax, H. Zhu h, J. Zhu h, X. Zhu h, A. Zichichi ab, A. Zimmermann cj, G. Zinovjev d, Y. Zoccarato dm, M. Zynovyev d, M. Zyzak, CAMERINI, Paolo, FRAGIACOMO, ENRICO, LEA, RAMONA, LUPARELLO, GRAZIA, MARGAGLIOTTI, GIACOMO, PIANO, STEFANO, RUI, RINALDO, E., Abbas a, B., Abelev bt, J., Adam al, D., Adamová ca, A. M., Adare dz, M. M., Aggarwal ce, G., Aglieri Rinella ah, M., Agnello cv, Ck, A. G., Agocs dy, A., Agostinelli ab, Z., Ahammed dt, A., Ahmad Masoodi r, N., Ahmad r, S. U., Ahn bm, S. A., Ahn bm, I., Aimo y, Cv, Ck, M., Ajaz p, A., Akindinov ay, D., Aleksandrov cq, B., Alessandro cv, A., Alici cx, M, A., Alkin d, E., Almaráz Aviña bi, J., Alme aj, T., Alt an, V., Altini af, S., Altinpinar, I., Altsybeev dv, C., Andrei bw, A., Andronic cn, V., Anguelov cj, J., Anielski bg, C., Anson t, T., Anticˇic ́ co, F., Antinori cw, P., Antonioli cx, L., Aphecetche dd, H., Appelshäuser be, N., Arbor bp, S., Arcelli ab, A., Arend be, N., Armesto q, R., Arnaldi cv, T., Aronsson dz, I. C., Arsene cn, M., Arslandok be, A., Asryan dv, A., Augustinus ah, R., Averbeck cn, T. C., Awes cb, J., Äystö aq, M. D., Azmi r, Cg, M., Bach an, A., Badalà cu, Y. W., Baek bo, Ao, R., Bailhache be, R., Bala ch, Cv, A., Baldisseri o, F., Baltasar Dos Santos Pedrosa ah, J., Bán az, R. C., Baral ba, R., Barbera aa, F., Barile af, G. G., Barnaföldi dy, L. S., Barnby c, V., Barret bo, J., Bartke dh, M., Basile ab, N., Bastid bo, S., Basu dt, B., Bathen bg, G., Batigne dd, B., Batyunya bk, P. C., Batzing v, C., Baumann be, I. G., Bearden by, H., Beck be, N. K., Behera a, I., Belikov bj, F., Bellini ab, R., Bellwied dn, E., Belmont Moreno bi, G., Bencedi dy, S., Beole y, I., Berceanu bw, A., Bercuci bw, Y., Berdnikov cc, D., Berenyi dy, A. A. E., Bergognon dd, R. A., Bertens ax, D., Berzano y, L., Betev ah, A., Bhasin ch, A. K., Bhati ce, J., Bhom dr, N., Bianchi bq, L., Bianchi y, C., Bianchin ax, J., Bielcˇík al, J., Bielcˇíková ca, A., Bilandzic by, S., Bjelogrlic ax, F., Blanco k, F., Blanco dn, D., Blau cq, C., Blume be, M., Boccioli ah, S., Böttger bd, A., Bogdanov bu, H., Bøggild by, M., Bogolyubsky av, L., Boldizsár dy, M., Bombara am, J., Book be, H., Borel o, A., Borissov dx, F., Bossú cg, M., Botje bz, E., Botta y, E., Braidot b, P., Braun Munzinger cn, M., Bregant dd, T., Breitner bd, T. A., Broker be, T. A., Browning cl, M., Broz ak, R., Brun ah, E., Bruna y, G. E., Bruno af, D., Budnikov cp, H., Buesching be, S., Bufalino y, P., Buncic ah, O., Busch cj, Z., Buthelezi cg, D., Caffarri ac, Cw, X., Cai h, H., Caines dz, E., Calvo Villar ct, Camerini, Paolo, V., Canoa Roman l, G., Cara Romeo cx, F., Carena ah, W., Carena ah, N., Carlin Filho dk, F., Carminati ah, A., Casanova Díaz bq, J., Castillo Castellanos o, J. F., Castillo Hernandez cn, E. A. R., Casula x, V., Catanescu bw, C., Cavicchioli ah, C., Ceballos Sanchez j, J., Cepila al, P., Cerello cv, B., Chang aq, Eb, S., Chapeland ah, J. L., Charvet o, S., Chattopadhyay dt, S., Chattopadhyay cr, M., Cherney cd, C., Cheshkov ah, Dm, B., Cheynis dm, V., Chibante Barroso ah, D. D., Chinellato dn, P., Chochula ah, M., Chojnacki by, S., Choudhury dt, P., Christakoglou bz, C. H., Christensen by, P., Christiansen ag, T., Chujo dr, S. U., Chung cm, C., Cicalo cy, L., Cifarelli ab, F., Cindolo cx, J., Cleymans cg, F., Colamaria af, D., Colella af, A., Collu x, G., Conesa Balbastre bp, Z., Conesa del Valle ah, Au, M. E., Connors dz, G., Contin w, J. G., Contreras l, T. M., Cormier dx, Y., Corrales Morales y, P., Cortese ae, I., Cortés Maldonado c, M. R., Cosentino b, F., Costa ah, M. E., Cotallo k, E., Crescio l, P., Crochet bo, E., Cruz Alaniz bi, R., Cruz Albino l, E., Cuautle bh, L., Cunqueiro bq, A., Dainese ac, H. H., Dalsgaard by, R., Dangh, A., Danubc, K., Dascr, I., Dasau, S., Dase, D., Dascr, A., Dashdl, S., Dasha, S., Dedt, G. O. V., de Barros dk, A., De Caro ad, G., de Cataldo da, J., de Cuveland an, A., De Falco x, D., De Gruttola ad, H., Delagrange dd, A., Deloff bv, N., De Marco cv, E., Dénes dy, S., De Pasquale ad, A., Deppman dk, G. D., Erasmo af, R., de Rooij ax, M. A., Diaz Corchero k, D., Di Bari af, T., Dietel bg, C., Di Giglio af, S., Di Liberto db, A., Di Mauro ah, P., Di Nezza bq, R., Divià ah, Ø., Djuvsland, A., Dobrin dx, Ag, Ax, T., Dobrowolski bv, B., Dönigus cn, O., Dordic v, O., Driga dd, A. K., Dubey dt, A., Dubla ax, L., Ducroux dm, P., Dupieux bo, A. K., Dutta Majumdar cr, D., Elia da, D., Emschermann bg, H., Engel bd, B., Erazmus ah, Dd, H. A., Erdal aj, D., Eschweiler an, B., Espagnon au, M., Estienne dd, S., Esumi dr, D., Evans c, S., Evdokimov av, G., Eyyubova v, D., Fabris ac, J., Faivre bp, D., Falchieri ab, A., Fantoni bq, M., Fasel cj, D., Fehlker, L., Feldkamp bg, D., Felea bc, A., Feliciello cv, B., Fenton Olsen b, G., Feofilov dv, A., Fernández Téllez c, A., Ferretti y, A., Festanti ac, J., Figiel dh, M. A. S., Figueredo dk, S., Filchagin cp, D., Finogeev aw, F. M., Fionda af, E. M., Fiore af, E., Floratos cf, M., Floris ah, S., Foertsch cg, P., Foka cn, S., Fokin cq, Fragiacomo, Enrico, A., Francescon ah, Ac, U., Frankenfeld cn, U., Fuchs ah, C., Furget bp, M., Fusco Girard ad, J. J., Gaardhøje by, M., Gagliardi y, A., Gago ct, M., Gallio y, D. R., Gangadharan t, P., Ganoti cb, C., Garabatos cn, E., Garcia Solis n, C., Gargiulo ah, I., Garishvili bt, J., Gerhard an, M., Germain dd, C., Geuna o, A., Gheata ah, M., Gheata bc, Ah, B., Ghidini af, P., Ghosh dt, P., Gianotti bq, M. R., Girard dw, P., Giubellino ah, E., Gladysz Dziadus dh, P., Glässel cj, R., Gomez dj, L, E. G., Ferreiro q, L. H., González Trueba bi, P., González Zamora k, S., Gorbunov an, A., Goswami ci, S., Gotovac df, L. K., Graczykowski dw, R., Grajcarek cj, A., Grelli ax, A., Grigoras ah, C., Grigoras ah, V., Grigoriev bu, A., Grigoryan b, S., Grigoryan bk, B., Grinyov d, N., Grion cz, P., Gros ag, J. F., Grosse Oetringhaus ah, J. Y., Grossiord dm, R., Grosso ah, F., Guber aw, R., Guernane bp, B., Guerzoni ab, M., Guilbaud dm, K., Gulbrandsen by, H., Gulkanyan b, T., Gunji dq, R., Gupta ch, A., Gupta ch, R., Haake bg, Ø., Haaland, C., Hadjidakis au, M., Haiduc bc, H., Hamagaki dq, G., Hamar dy, B. H., Han u, L. D., Hanratty c, A., Hansen by, Z., Harmanová Tóthová am, J. W., Harris dz, M., Hartig be, A., Harton n, D., Hatzifotiadou cx, S., Hayashi dq, A., Hayrapetyan ah, B, S. T., Heckel be, M., Heide bg, H., Helstrup aj, A., Herghelegiu bw, G., Herrera Corral l, N., Herrmann cj, B. A., Hess d, K. F., Hetland aj, B., Hicks dz, B., Hippolyte bj, Y., Hori dq, P., Hristov ah, I., Hrˇivnácˇová au, M., Huang, T. J., Humanic t, D. S., Hwang u, R., Ichou bo, R., Ilkaev cp, I., Ilkiv bv, M., Inaba dr, E., Incani x, P. G., Innocenti ah, G. M., Innocenti y, M., Ippolitov cq, M., Irfan r, C., Ivan cn, V., Ivanov cc, A., Ivanov dv, M., Ivanov cn, O., Ivanytskyi d, A., Jachołkowski aa, P. M., Jacobs b, C., Jahnke dk, H. J., Jang bm, M. A., Janik dw, P. H. S. Y., Jayarathna dn, S., Jena a, D. M., Jha dx, R. T., Jimenez Bustamante bh, P. G., Jones c, H., Jung ao, A., Jusko c, A. B., Kaidalov ay, S., Kalcher an, P., Kalinˇák az, T., Kalliokoski aq, A., Kalweit ah, J. H., Kang eb, V., Kaplin bu, S., Kar dt, A., Karasu Uysal ah, Ea, Bn, O., Karavichev aw, T., Karavicheva aw, E., Karpechev aw, A., Kazantsev cq, U., Kebschull bd, R., Keidel ec, B., Ketzer be, Dg, K. H., Khan p, M. M., Khan r, P., Khan cr, S. A., Khan dt, A., Khanzadeev cc, Y., Kharlov av, B., Kileng aj, M., Kim eb, S., Kim u, B., Kim eb, T., Kim eb, D. J., Kim aq, D. W., Kim ao, Bm, J. H., Kim u, J. S., Kim ao, M., Kim ao, S., Kirsch an, I., Kisel an, S., Kiselev ay, A., Kisiel dw, J. L., Klay g, J., Klein cj, C., Klein Bösing bg, M., Kliemant be, A., Kluge ah, M. L., Knichel cn, A. G., Knospe di, M. K., Köhler cn, T., Kollegger an, A., Kolojvari dv, M., Kompaniets dv, V., Kondratiev dv, N., Kondratyeva bu, A., Konevskikh aw, V., Kovalenko dv, M., Kowalski dh, S., Kox bp, G., Koyithatta Meethaleveedu a, J., Kral aq, I., Králik az, F., Kramer be, A., Kravcˇáková am, M., Krelina al, M., Kretz an, M., Krivda c, Az, F., Krizek aq, M., Krus al, E., Kryshen cc, M., Krzewicki cn, V., Kucera ca, Y., Kucheriaev cq, T., Kugathasan ah, C., Kuhn bj, P. G., Kuijer bz, I., Kulakov be, J., Kumar a, P., Kurashvili bv, A., Kurepin aw, A. B., Kurepin aw, A., Kuryakin cp, S., Kushpil ca, V., Kushpil ca, H., Kvaerno v, M. J., Kweon cj, Y., Kwon eb, P., Ladrón de Guevara bh, I., Lakomov au, R., Langoy, Du, S. L., La Pointe ax, C., Lara bd, A., Lardeux dd, P., La Rocca aa, Lea, Ramona, M., Lechman ah, S. C., Lee ao, G. R., Lee c, I., Legrand ah, J., Lehnert be, R. C., Lemmon dc, M., Lenhardt cn, V., Lenti da, H., León bi, M., Leoncino y, I., León Monzón dj, P., Lévai dy, S., Li bo, H, J., Lien, R., Lietava c, S., Lindal v, V., Lindenstruth an, C., Lippmann cn, M. A., Lisa t, H. M., Ljunggren ag, D. F., Lodato ax, P. I., Loenne, V. R., Loggins dx, V., Loginov bu, D., Lohner cj, C., Loizides b, K. K., Loo aq, X., Lopez bo, E., López Torres j, G., Løvhøiden v, X. G., Lu cj, P., Luettig be, M., Lunardon ac, J., Luo h, Luparello, Grazia, C., Luzzi ah, K., Ma h, R., Ma dz, D. M., Madagodahettige Don dn, A., Maevskaya aw, M., Mager bf, D. P., Mahapatra ba, A., Maire cj, M., Malaev cc, I., Maldonado Cervantes bh, Ludmila Malinina, Bk, D., Mal’Kevich ay, P., Malzacher cn, A., Mamonov cp, L., Manceau cv, L., Mangotra ch, V., Manko cq, F., Manso bo, V., Manzari da, Y., Mao h, M., Marchisone bo, Y, J., Mareš bb, Margagliotti, Giacomo, Cz, A., Margotti cx, A., Marín cn, C., Markert di, M., Marquard be, I., Martashvili dp, N. A., Martin cn, P., Martinengo ah, M. I., Martínez c, G., Martínez García dd, Y., Martynov d, A., Mas dd, S., Masciocchi cn, M., Masera y, A., Masoni cy, L., Massacrier dd, A., Mastroserio af, A., Matyja dh, C., Mayer dh, J., Mazer dp, M. A., Mazzoni db, F., Meddi z, A., Menchaca Rocha bi, J., Mercado Pérez cj, M., Meres ak, Y., Miake dr, K., Mikhaylov bk, Ay, L., Milano ah, Jovan Milosevic, V, A., Mischke ax, A. N., Mishra ci, At, D., Mis ́kowiec cn, C., Mitu bc, S., Mizuno dr, J., Mlynarz dx, B., Mohanty dt, Bx, L., Molnar dy, Bj, L., Montaño Zetina l, M., Monteno cv, E., Montes k, T., Moon eb, M., Morando ac, D. A., Moreira De Godoy dk, S., Moretto ac, A., Morreale aq, A., Morsch ah, V., Muccifora bq, E., Mudnic df, S., Muhuri dt, M., Mukherjee dt, H., Müller ah, M. G., Munhoz dk, S., Murray cg, L., Musa ah, J., Musinsky az, B. K., Nandi a, R., Nania cx, E., Nappi da, C., Nattrass dp, T. K., Nayak dt, S., Nazarenko cp, A., Nedosekin ay, M., Nicassio af, Cn, M., Niculescu bc, B. S., Nielsen by, T., Niida dr, S., Nikolaev cq, V., Nikolic co, S., Nikulin cq, V., Nikulin cc, B. S., Nilsen cd, M. S., Nilsson v, F., Noferini cx, P., Nomokonov bk, G., Nooren ax, A., Nyanin cq, A., Nyatha a, C., Nygaard by, J., Nystrand, A., Ochirov dv, H., Oeschler bf, Ah, Cj, S., Oh dz, S. K., Oh ao, J., Oleniacz dw, A. C., Oliveira Da Silva dk, C., Oppedisano cv, A., Ortiz Velasquez ag, Bh, A., Oskarsson ag, P., Ostrowski dw, J., Otwinowski cn, K., Oyama cj, K., Ozawa dq, Y., Pachmayer cj, M., Pachr al, F., Padilla y, P., Pagano ad, G., Paic ́ bh, F., Painke an, C., Pajares q, S. K., Pal dt, A., Palaha c, A., Palmeri cu, V., Papikyan b, G. S., Pappalardo cu, W. J., Park cn, A., Passfeld bg, D. I., Patalakha av, V., Paticchio da, B., Paul cr, A., Pavlinov dx, T., Pawlak dw, T., Peitzmann ax, H., Pereira Da Costa o, E., Pereira De Oliveira Filho dk, D., Peresunko cq, C. E., Pérez Lara bz, D., Perrino af, W., Peryt dw, A., Pesci cx, Y., Pestov f, V., Petrácˇek al, M., Petran al, M., Petris bw, P., Petrov c, M., Petrovici bw, C., Petta aa, Piano, Stefano, M., Pikna ak, P., Pillot dd, O., Pinazza ah, L., Pinsky dn, N., Pitz be, D. B., Piyarathna dn, M., Planinic co, M., Płoskon ́ b, J., Pluta dw, T., Pocheptsov bk, S., Pochybova dy, P. L. M., Podesta Lerma dj, M. G., Poghosyan ah, K., Polák bb, B., Polichtchouk av, N., Poljak ax, Co, A., Pop bw, S., Porteboeuf Houssais bo, V., Pospíšil al, B., Potukuchi ch, S. K., Prasad dx, R., Preghenella cx, F., Prino cv, C. A., Pruneau dx, I., Pshenichnov aw, G., Puddu x, V., Punin cp, M., Putiš am, J., Putschke dx, H., Qvigstad v, A., Rachevski cz, A., Rademakers ah, T. S., Räihä aq, J., Rak aq, A., Rakotozafindrabe o, L., Ramello ae, S., Raniwala ci, R., Raniwala ci, S. S., Räsänen aq, B. T., Rascanu be, D., Rathee ce, W., Rauch ah, K. F., Read dp, J. S., Real bp, K., Redlich bv, R. J., Reed dz, A., Rehman, P., Reichelt be, M., Reicher ax, R., Renfordt be, A. R., Reolon bq, A., Reshetin aw, F., Rettig an, J. P., Revol ah, K., Reygers cj, L., Riccati cv, R. A., Ricci br, T., Richert ag, M., Richter v, P., Riedler ah, W., Riegler ah, F., Riggi aa, Cu, M., Rodríguez Cahuantzi c, A., Rodriguez Manso bz, K., Røed, V, E., Rogochaya bk, D., Rohr an, D., Röhrich, R., Romita cn, Dc, F., Ronchetti bq, P., Rosnet bo, S., Rossegger ah, A., Rossi ah, P., Roy cr, C., Roy bj, A. J., Rubio Montero k, Rui, Rinaldo, R., Russo y, E., Ryabinkin cq, A., Rybicki dh, S., Sadovsky av, K., Šafarˇík ah, R., Sahoo at, P. K., Sahu ba, J., Saini dt, H., Sakaguchi ar, S., Sakai b, D., Sakata dr, C. A., Salgado q, J., Salzwedel t, S., Sambyal ch, V., Samsonov cc, X., Sanchez Castro bj, L., Šándor az, A., Sandoval bi, M., Sano dr, G., Santagati aa, R., Santoro ah, J., Sarkamo aq, D., Sarkar dt, E., Scapparone cx, F., Scarlassara ac, R. P., Scharenberg cl, C., Schiaua bw, R., Schicker cj, H. R., Schmidt d, C., Schmidt cn, S., Schuchmann be, J., Schukraft ah, T., Schuster dz, Y., Schutz ah, K., Schwarz cn, K., Schweda cn, G., Scioli ab, E., Scomparin cv, R., Scott dp, P. A., Scott c, G., Segato ac, I., Selyuzhenkov cn, S., Senyukov bj, J., Seo cm, S., Serci x, E., Serradilla k, Bi, A., Sevcenco bc, A., Shabetai dd, G., Shabratova bk, R., Shahoyan ah, N., Sharma dp, S., Sharma ch, S., Rohni ch, K., Shigaki ar, K., Shtejer j, Y., Sibiriak cq, E., Sicking bg, S., Siddhanta cy, T., Siemiarczuk bv, D., Silvermyr cb, C., Silvestre bp, G., Simatovic bh, G., Simonetti ah, R., Singaraju dt, R., Singh ch, S., Singha dt, V., Singhal dt, B. C., Sinha dt, T., Sinha cr, B., Sitar ak, M., Sitta ae, T. B., Skaali v, K., Skjerdal, R., Smakal al, N., Smirnov dz, R. J. M., Snellings ax, C., Søgaard ag, R., Soltz bt, M., Song eb, J., Song cm, C., Soos ah, F., Soramel ac, I., Sputowska dh, M., Spyropoulou Stassinaki cf, B. K., Srivastava cl, J., Stachel cj, I., Stan bc, G., Stefanek bv, M., Steinpreis t, E., Stenlund ag, G., Steyn cg, J. H., Stiller cj, D., Stocco dd, M., Stolpovskiy av, P., Strmen ak, A. A. P., Suaide dk, M. A., Subieta Vásquez y, T., Sugitate ar, C., Suire au, R., Sultanov ay, M., Šumbera ca, T., Susa co, T. J. M., Symons b, A., Szanto de Toledo dk, I., Szarka ak, A., Szczepankiewicz dh, M., Szyman ́ ski dw, J., Takahashi dl, M. A., Tangaro af, J. D., Tapia Takaki au, A., Tarantola Peloni be, A., Tarazona Martinez ah, A., Tauro ah, G., Tejeda Muñoz c, A., Telesca ah, A., Ter Minasyan cq, C., Terrevoli af, J., Thäder cn, D., Thomas ax, R., Tieulent dm, A. R., Timmins dn, D., Tlusty al, A., Toia an, Ac, Cw, H., Torii dq, L., Toscano cv, V., Trubnikov d, D., Truesdale t, W. H., Trzaska aq, T., Tsuji dq, A., Tumkin cp, R., Turrisi cw, T. S., Tveter v, J., Ulery be, K., Ullaland, J., Ulrich bl, Bd, A., Uras dm, G. M., Urciuoli db, G. L., Usai x, M., Vajzer al, Ca, M., Vala bk, L., Valencia Palomo au, P., Vande Vyvre ah, J. W., Van Hoorne ah, M., van Leeuwen ax, L., Vannucci br, A., Vargas c, R., Varma a, M., Vasileiou cf, A., Vasiliev cq, V., Vechernin dv, M., Veldhoen ax, M., Venaruzzo w, E., Vercellin y, S., Vergara c, R., Vernet i, M., Verweij ax, L., Vickovic df, G., Viesti ac, J., Viinikainen aq, Z., Vilakazi cg, O., Villalobos Baillie c, Y., Vinogradov cp, L., Vinogradov dv, A., Vinogradov cq, T., Virgili ad, Y. P., Viyogi dt, A., Vodopyanov bk, M. A., Völkl cj, S., Voloshin dx, K., Voloshin ay, G., Volpe ah, B., von Haller ah, I., Vorobyev dv, D., Vranic cn, J., Vrláková am, B., Vulpescu bo, A., Vyushin cp, B., Wagner, V., Wagner al, R., Wan h, Y., Wang h, M., Wang h, Y., Wang cj, K., Watanabe dr, M., Weber dn, J. P., Wessels ah, Bg, U., Westerhoff bg, J., Wiechula d, J., Wikne v, M., Wilde bg, G., Wilk bv, M. C. S., Williams cx, B., Windelband cj, L., Xaplanteris Karampatsos di, C. G., Yaldo dx, Y., Yamaguchi dq, S., Yang, P., Yang h, H., Yang o, Ax, S., Yasnopolskiy cq, J., Yi cm, Z., Yin h, I. K., Yoo cm, J., Yoon eb, W., Yu be, X., Yuan h, I., Yushmanov cq, Zaccolo by, V., C., Zach al, C., Zampolli cx, S., Zaporozhets bk, A., Zarochentsev dv, P., Závada bb, N., Zaviyalov cp, H., Zbroszczyk dw, P., Zelnicek bd, I. S., Zgura bc, M., Zhalov cc, H., Zhang h, X., Zhang b, Bo, H, Y., Zhang h, D., Zhou h, F., Zhou h, Y., Zhou ax, H., Zhu h, J., Zhu h, X., Zhu h, A., Zichichi ab, A., Zimmermann cj, G., Zinovjev d, Y., Zoccarato dm, M., Zynovyev d, and M., Zyzak

Subjects
Charged-particle density, Heavy-ion collisions, LHC, Wide rapidity coverage, Nuclear and High Energy Physics, HEAVY-ION COLLISIONS, Charged-Particle Density, Heavy ions collisions, charged-particle density, Nuclear Experiment
Abstract

We present the first wide-range measurement of the charged-particle pseudorapidity density distribution, for different centralities (the 0–5%, 5–10%, 10–20%, and 20–30% most central events) in Pb–Pb collisions at √sNN = 2.76 TeV at the LHC. The measurement is performed using the full coverage of the ALICE detectors, −5.0 < η < 5.5, and employing a special analysis technique based on collisions arising from LHC ‘satellite’ bunches. We present the pseudorapidity density as a function of the number of participating nucleons as well as an extrapolation to the total number of produced charged particles (Nch = 17 165 ± 772 for the 0–5% most central collisions). From the measured dNch/dη distribution we derive the rapidity density distribution, dNch/dy, under simple assumptions. The rapidity density distribution is found to be significantly wider than the predictions of the Landau model. We assess the validity of longitudinal scaling by comparing to lower energy results from RHIC. Finally the mechanisms of the underlying particle production are discussed based on a comparison with various theoretical models.

Published
2013

3. Identification of unique adaptive immune system signature in acute coronary syndromes

Author

Liuzzo, Giovanna, Montone, Ra, Gabriele, M, Pedicino, D, Giglio, Af, Trotta, F, Galiffa, Va, Previtero, M, Severino, A, Biasucci, Lm, Crea, F., Liuzzo, Giovanna (ORCID:0000-0002-5714-0907), Liuzzo, Giovanna, Montone, Ra, Gabriele, M, Pedicino, D, Giglio, Af, Trotta, F, Galiffa, Va, Previtero, M, Severino, A, Biasucci, Lm, Crea, F., and Liuzzo, Giovanna (ORCID:0000-0002-5714-0907)

Published
2013

4. Infections, immunity and atherosclerosis: Pathogenic mechanisms and unsolved questions

Author

Pedicino, Daniela, Giglio, Af, Galiffa, Va, Cialdella, P, Trotta, F, Graziani, F, Liuzzo, Giovanna, Liuzzo, Giovanna (ORCID:0000-0002-5714-0907), Pedicino, Daniela, Giglio, Af, Galiffa, Va, Cialdella, P, Trotta, F, Graziani, F, Liuzzo, Giovanna, and Liuzzo, Giovanna (ORCID:0000-0002-5714-0907)

Abstract

The role of inflammation and immunity in the pathogenesis and clinical manifestations of atherosclerotic disease has been widely studied. Common infectious diseases can be associated with a chronic inflammatory state which is the hallmark of atherosclerosis, thus suggesting a possible link between the two pathological conditions. Therefore, a great number of studies have tested the "infection hypothesis", but their results are conflicting. Nevertheless, several molecular and biological mechanisms possibly involved in the complex relationship between infections, immune response, vascular wall damage and atherosclerosis onset and progression have been described. The purpose of this article is to offer an overview of the principal mechanisms and molecular pathways that probably constitute the most relevant biological substrate on which the infection hypothesis is founded; some of these mechanisms are not fully understood yet. Nevertheless, their comprehension could be essential for the development of new preventive and therapeutic strategies.

Published
2012

5. Restricted T-Cell Repertoire in the Epicardial Adipose Tissue of Non-ST Segment Elevation Myocardial Infarction Patients.

Author

Pedicino D, Severino A, Di Sante G, De Rosa MC, Pirolli D, Vinci R, Pazzano V, Giglio AF, Trotta F, Russo G, Ruggio A, Pisano E, d'Aiello A, Canonico F, Ciampi P, Cianflone D, Cianfanelli L, Grimaldi MC, Filomia S, Luciani N, Glieca F, Bruno P, Massetti M, Ria F, Crea F, and Liuzzo G

Subjects
Adipose Tissue, Epitopes, HLA-A3 Antigen, Humans, Leukocytes, Mononuclear, Proteome, T-Lymphocytes, Acute Coronary Syndrome, Non-ST Elevated Myocardial Infarction
Abstract

Aims: Human epicardial adipose tissue, a dynamic source of multiple bioactive factors, holds a close functional and anatomic relationship with the epicardial coronary arteries and communicates with the coronary artery wall through paracrine and vasocrine secretions. We explored the hypothesis that T-cell recruitment into epicardial adipose tissue (EAT) in patients with non-ST segment elevation myocardial infarction (NSTEMI) could be part of a specific antigen-driven response implicated in acute coronary syndrome onset and progression., Methods and Results: We enrolled 32 NSTEMI patients and 34 chronic coronary syndrome (CCS) patients undergoing coronary artery bypass grafting (CABG) and 12 mitral valve disease (MVD) patients undergoing surgery. We performed EAT proteome profiling on pooled specimens from three NSTEMI and three CCS patients. We performed T-cell receptor (TCR) spectratyping and CDR3 sequencing in EAT and peripheral blood mononuclear cells of 29 NSTEMI, 31 CCS, and 12 MVD patients. We then used computational modeling studies to predict interactions of the TCR beta chain variable region (TRBV) and explore sequence alignments. The EAT proteome profiling displayed a higher content of pro-inflammatory molecules (CD31, CHI3L1, CRP, EMPRINN, ENG, IL-17, IL-33, MMP-9, MPO, NGAL, RBP-4, RETN, VDB) in NSTEMI as compared to CCS ( P < 0.0001). CDR3-beta spectratyping showed a TRBV21 enrichment in EAT of NSTEMI (12/29 patients; 41%) as compared with CCS (1/31 patients; 3%) and MVD (none) (ANOVA for trend P < 0.001). Of note, 11/12 (92%) NSTEMI patients with TRBV21 perturbation were at their first manifestation of ACS. Four patients with the first event shared a distinctive TRBV21-CDR3 sequence of 178 bp length and 2/4 were carriers of the human leukocyte antigen (HLA)-A*03:01 allele. A 3D analysis predicted the most likely epitope able to bind HLA-A3*01 and interact with the TRBV21-CDR3 sequence of 178 bp length, while the alignment results were consistent with microbial DNA sequences., Conclusions: Our study revealed a unique immune signature of the epicardial adipose tissue, which led to a 3D modeling of the TCRBV/peptide/HLA-A3 complex, in acute coronary syndrome patients at their first event, paving the way for epitope-driven therapeutic strategies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Pedicino, Severino, Di Sante, De Rosa, Pirolli, Vinci, Pazzano, Giglio, Trotta, Russo, Ruggio, Pisano, d’Aiello, Canonico, Ciampi, Cianflone, Cianfanelli, Grimaldi, Filomia, Luciani, Glieca, Bruno, Massetti, Ria, Crea and Liuzzo.)

Published
2022
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6. Alterations of Hyaluronan Metabolism in Acute Coronary Syndrome: Implications for Plaque Erosion.

Author

Pedicino D, Vinci R, Giglio AF, Pisano E, Porto I, Vergallo R, Russo G, Ruggio A, D'Aiello A, Flego D, Annibali G, Trotta F, Piacentini R, Niccoli G, Liuzzo G, and Crea F

Subjects
Acute Coronary Syndrome genetics, Aged, Case-Control Studies, Cell Adhesion Molecules metabolism, Female, GPI-Linked Proteins genetics, GPI-Linked Proteins metabolism, Gene Expression, Humans, Hyaluronan Receptors genetics, Hyaluronan Receptors metabolism, Hyaluronoglucosaminidase metabolism, Leukocytes, Mononuclear metabolism, Male, Middle Aged, Protein Splicing, RNA, Messenger metabolism, Tomography, Optical Coherence, Acute Coronary Syndrome metabolism, Cell Adhesion Molecules genetics, Hyaluronoglucosaminidase genetics, Plaque, Atherosclerotic diagnostic imaging
Abstract

Background: Superficial erosion currently causes at least one-third of acute coronary syndromes (ACS), and its incidence is increasing. Yet, the underlying mechanisms in humans are still largely unknown., Objectives: The authors sought to assess the role of hyaluronan (HA) metabolism in ACS., Methods: Peripheral blood mononuclear cells were collected from ACS (n = 66), stable angina (SA) (n = 55), and control (CTRL) patients (n = 45). The authors evaluated: 1) gene expression of hyaluronidase 2 (HYAL2) (enzyme degrading high-molecular-weight HA to its proinflammatory 20-kDa isoform) and of CD44v1, CD44v4, and CD44v6 splicing variants of HA receptor; and 2) HYAL2 and CD44 protein expression. Moreover, they compared HYAL2 and CD44 gene expression in ACS patients with plaque erosion (intact fibrous cap and thrombus) and in ACS patients with plaque rupture, identified by optical coherence tomography analysis., Results: Gene expression of HYAL2, CD44v1, and CD44v6 were significantly higher in ACS as compared with SA (p = 0.003, p < 0.001, and p = 0.033, respectively) and CTRL subjects (p < 0.001, p < 0.001, and p = 0.009, respectively). HYAL2 protein expression was significantly higher in ACS than in SA (p = 0.017) and CTRL (p = 0.032), whereas no differences were found in CD44 protein expression. HYAL2 and CD44v6 gene expression was significantly higher in patients with plaque erosion than in those with plaque rupture (p = 0.015 and p = 0.029, respectively)., Conclusions: HYAL2 and CD44v6 splicing variants seem to play an important role in ACS, in particular when associated with plaque erosion. After further validation, HYAL2 might represent a potentially useful biomarker for the noninvasive identification of this mechanism of coronary instability., (Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Published
2018
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7. Inflammasome, T Lymphocytes and Innate-Adaptive Immunity Crosstalk: Role in Cardiovascular Disease and Therapeutic Perspectives.

Author

Pedicino D, Giglio AF, Ruggio A, Massaro G, D'Aiello A, Trotta F, Lucci C, Graziani F, Biasucci LM, Crea F, and Liuzzo G

Subjects
Animals, Cardiovascular Agents therapeutic use, Cardiovascular Diseases metabolism, Cardiovascular Diseases therapy, Humans, Immunologic Factors therapeutic use, Immunotherapy methods, Inflammasomes drug effects, Inflammasomes metabolism, Inflammation Mediators immunology, Inflammation Mediators metabolism, Signal Transduction, T-Lymphocytes drug effects, T-Lymphocytes metabolism, Adaptive Immunity drug effects, Cardiovascular Diseases immunology, Immunity, Innate drug effects, Inflammasomes immunology, T-Lymphocytes immunology
Abstract

Over the past few decades, lot of evidences have shown atherosclerosis as a chronic progressive disease with an exquisite inflammatory feature. More recently, the role of innate immune response in the onset and progression of coronary artery disease (CAD) and an adaptive immunity imbalance, mostly involving T cell sub-sets, have been documented. Therefore, like in many other inflammatory and autoimmune disorders, an altered innate-adaptive immunity crosstalk could represent the key of the inflammatory burden leading to atherosclerotic plaque formation and progression and to the breakdown of plaque stability. In this review, we will address the role of inflammasome in innate immunity and in the imbalance of adaptive immunity. We will discuss how this altered immune crosstalk is related to CAD onset and progression. We will also discuss how unravelling the key molecular mechanisms is of paramount importance in the development of therapeutic tools to delay the chronic progression and prevent the acute destabilization of atherosclerotic plaque., Competing Interests: None., (Georg Thieme Verlag KG Stuttgart · New York.)

Published
2018
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8. Indoleamine 2,3-Dioxygenase (IDO) Enzyme Links Innate Immunity and Altered T-Cell Differentiation in Non-ST Segment Elevation Acute Coronary Syndrome.

Author

Zara C, Severino A, Flego D, Ruggio A, Pedicino D, Giglio AF, Trotta F, Lucci C, D'Amario D, Vinci R, Pisano E, La Rosa G, Biasucci LM, Crea F, and Liuzzo G

Subjects
Acute Coronary Syndrome pathology, Adult, Aged, Aged, 80 and over, Cell Differentiation, Cells, Cultured, Dendritic Cells immunology, Dendritic Cells pathology, Female, Humans, Lymphocyte Activation, Male, Middle Aged, Monocytes immunology, Monocytes pathology, Non-ST Elevated Myocardial Infarction pathology, T-Lymphocyte Subsets pathology, Acute Coronary Syndrome immunology, Immunity, Innate, Indoleamine-Pyrrole 2,3,-Dioxygenase immunology, Non-ST Elevated Myocardial Infarction immunology, T-Lymphocyte Subsets immunology
Abstract

Atherosclerosis is a chronic inflammatory disease characterized by a complex interplay between innate and adaptive immunity. Dendritic cells (DCs) play a key role in T-cell activation and regulation by promoting a tolerogenic environment through the expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (IDO), an intracellular enzyme involved in tryptophan catabolism. IDO expression and activity was analyzed in monocytes derived DCs (MDDCs) from non-ST segment elevation myocardial infarction (NSTEMI) patients, stable angina (SA) patients and healthy controls (HC) by real-time quantitative polymerase chain reaction (RT-qPCR) before and after in vitro maturation with lipopolysaccharide (LPS). The amount of tryptophan catabolite; kynurenine; was evaluated in the culture supernatants of mature-MDDCs by ELISA assay. Autologous mixed lymphocyte reaction (MLR) between mature-MDDCs and naïve T-cells was carried out to study the differentiation towards T-helper 1 (Th1) and induced regulatory T-cells (iTreg). Analysis of IDO mRNA transcripts in mature-MDDCs revealed a significant reduction in cells isolated from NSTEMI (625.0 ± 128.2; mean ± SEM) as compared with those from SA (958.5 ± 218.3; p = 0.041) and from HC (1183.6 ± 231.6; p = 0.034). Furthermore; the concentration of kynurenine was lower in NSTEMI patients (2.78 ± 0.2) and SA (2.98 ± 0.25) as compared with HC (5.1 ± 0.69 ng/mL; p = 0.002 and p = 0.016; respectively). When IDO-competent mature-MDDCs were co-cultured with allogeneic naïve T-cells, the ratio between the percentage of generated Th1 and iTreg was higher in NSTEMI (4.4 ± 2.9) than in SA (1.8 ± 0.6; p = 0.056) and HC (0.9 ± 0.3; p = 0.008). In NSTEMI, the tolerogenic mechanism of the immune response related to IDO production by activated MDDCs is altered, supporting their role in T-cell dysregulation., Competing Interests: The authors declare no conflicts of interest.

Published
2017
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9. Epicardial adipose tissue microbial colonization and inflammasome activation in acute coronary syndrome.

Author

Pedicino D, Severino A, Ucci S, Bugli F, Flego D, Giglio AF, Trotta F, Ruggio A, Lucci C, Iaconelli A, Paroni Sterbini F, Biasucci LM, Sanguinetti M, Glieca F, Luciani N, Massetti M, Crea F, and Liuzzo G

Subjects
Aged, Colony Count, Microbial methods, Coronary Vessels pathology, DNA, Bacterial isolation & purification, Female, Humans, Interleukin-1beta analysis, Italy, Male, Middle Aged, NLR Family, Pyrin Domain-Containing 3 Protein analysis, Statistics as Topic, Acute Coronary Syndrome diagnosis, Acute Coronary Syndrome immunology, Acute Coronary Syndrome surgery, Adipose Tissue immunology, Adipose Tissue microbiology, Adipose Tissue pathology, Coronary Artery Bypass methods, Inflammasomes physiology, Microbiota physiology, Pericardium immunology, Pericardium microbiology, Pericardium pathology
Abstract

Background: Epicardial adipose tissue (EAT) has a close functional and anatomic relationship with epicardial coronary arteries. Accumulating evidence suggests that host microbiome alterations may play a role in several inflammatory/immune disorders, triggering a robust proinflammatory response also involving interleukin-1β (IL-1β) and the NALP3 inflammasome. In the current study, we explore the hypothesis that in patients with non-ST elevation acute coronary syndrome (ACS), EAT contains potentially pro-atherosclerotic bacteria that might elicit inflammasome activation., Methods: EAT samples were obtained during coronary artery bypass grafting from ACS (n=18) and effort stable angina (SA; n=16) patients, and as controls, from patients with angiographically normal coronary arteries undergoing surgery for mitral insufficiency (MVD; n=13). In all patients, NALP3 and proIL-1β mRNA expressions were evaluated with qRT-PCR. In 3 patients from each group, EAT microbiota composition was determined using next-generation sequencing technologies., Results: In EAT, mRNA expression of both NALP3 and pro-IL1β was significantly higher in ACS than in SA and MVD (P=0.028 and P=0.005, respectively). A broad range of bacterial species (n=76) was identified in both ACS and SA, with different predominant species. In contrast, microbial DNA was barely observed in MVD., Conclusions: Our study demonstrated the presence of bacterial DNA directly into EAT, surrounding diseased coronary arteries, of patients with ACS. Furthermore, ACS is associated with NALP3/inflammasome pathway activation in EAT. Our data suggest that the EAT environment is susceptible to microbial colonization that might stimulate a proinflammatory response. These findings add new elements to the pathogenesis of ACS and suggest novel therapeutic targets., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Published
2017
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10. Atorvastatin inhibits the immediate-early response gene EGR1 and improves the functional profile of CD4+T-lymphocytes in acute coronary syndromes.

Author

Severino A, Zara C, Campioni M, Flego D, Angelini G, Pedicino D, Giglio AF, Trotta F, Giubilato S, Pazzano V, Lucci C, Iaconelli A, Ruggio A, Biasucci LM, Crea F, and Liuzzo G

Subjects
Acute Coronary Syndrome drug therapy, Blotting, Western, Cells, Cultured, Female, Flow Cytometry, Gene Expression drug effects, Gene Expression Profiling, Humans, Male, Middle Aged, Polymerase Chain Reaction, Acute Coronary Syndrome immunology, Atorvastatin therapeutic use, CD4-Positive T-Lymphocytes drug effects, Early Growth Response Protein 1 biosynthesis, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Lymphocyte Activation drug effects
Abstract

Background- Adaptive immune-response is associated with a worse outcome in acute coronary syndromes. Statins have anti-inflammatory activity beyond lowering lipid levels. We investigated the effects of ex-vivo and in-vivo atorvastatin treatment in acute coronary syndromes on CD4+T-cells, and the underlying molecular mechanisms.Approach and results- Blood samples were collected from 50 statin-naïve acute coronary syndrome patients. We assessed CD4+T-cell activation by flow-cytometry, the expression of 84 T-helper transcription-factors and 84 T-cell related genes by RT-qPCR, and protein expression by Western-blot, before and after 24-hours incubation with increasing doses of atorvastatin: 3-10-26 μg/ml (corresponding to blood levels achieved with doses of 10-40-80 mg, respectively). After incubation, we found a significant decrease in interferon-γ-producing CD4+CD28nullT-cells (P = 0.009) and a significant increase in interleukin-10-producing CD4+CD25highT-cells (P < 0.001). Atorvastatin increased the expression of 2 genes and decreased the expression of 12 genes (in particular, EGR1, FOS,CCR2 and toll like receptor-4; >3-fold changes).The in-vivo effects of atorvastatin were analyzed in 10 statin-free acute coronary syndrome patients at baseline, and after 24h and 48h of atorvastatin therapy (80 mg/daily): EGR1-gene expression decreased at 24h (P = 0.01) and 48h (P = 0.005); EGR1-protein levels decreased at 48h (P = 0.03).Conclusions-In acute coronary syndromes, the effects of atorvastatin on immune system might be partially related to the inhibition of the master regulator gene EGR1. Our finding might offer a causal explanation on why statins improve the early outcome in acute coronary syndromes.

Published
2017
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11. Reduced CD31 expression on CD14(+)CD16(+) monocyte subset in acute coronary syndromes.

Author

Flego D, Severino A, Trotta F, Copponi G, Manchi M, Pedicino D, Giglio AF, Crea F, and Liuzzo G

Subjects
Acute Coronary Syndrome metabolism, Humans, Monocytes immunology, Platelet Endothelial Cell Adhesion Molecule-1 immunology, Acute Coronary Syndrome immunology, Lipopolysaccharide Receptors immunology, Monocytes metabolism, Platelet Endothelial Cell Adhesion Molecule-1 biosynthesis, Receptors, IgG immunology
Published
2015
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12. Increased risk of myocardial infarction with dabigatran: fact or fiction?

Author

Giglio AF, Basile E, Santangeli P, Di Biase L, Trotta F, and Natale A

Subjects
Acute Coronary Syndrome blood, Acute Coronary Syndrome mortality, Atrial Fibrillation blood, Atrial Fibrillation complications, Atrial Fibrillation mortality, Dabigatran, Humans, Myocardial Infarction mortality, Risk Assessment, Risk Factors, Stroke blood, Stroke etiology, Stroke mortality, Treatment Outcome, Venous Thromboembolism blood, Venous Thromboembolism mortality, beta-Alanine adverse effects, Acute Coronary Syndrome drug therapy, Antithrombins adverse effects, Atrial Fibrillation drug therapy, Benzimidazoles adverse effects, Myocardial Infarction chemically induced, Stroke prevention & control, Venous Thromboembolism prevention & control, beta-Alanine analogs & derivatives
Abstract

Dabigatran is a direct, competitive inhibitor of thrombin recently approved for the prophylaxis of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. In some of the clinical trials evaluating the efficacy and safety of dabigatran in different clinical settings [i.e., prevention of venous thromboembolism (VTE) after orthopedic surgery, secondary prevention of VTE, and acute coronary syndromes (ACS)], a trend toward an increase in acute coronary events among patients receiving dabigatran has been reported, thus raising concerns of a possible relationship between dabigatran and myocardial infarction, especially in high-risk patients. However, as shown in our article, current evidence is inconclusive on this topic; more data are needed to detail this hypothetical association, and other considerations, such as the well-known protective effect of warfarin against ACS, should be taken into account as a possible explanation.

Published
2014
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14. Infections, immunity and atherosclerosis: pathogenic mechanisms and unsolved questions.

Author

Pedicino D, Giglio AF, Galiffa VA, Cialdella P, Trotta F, Graziani F, and Liuzzo G

Subjects
Animals, Humans, Immunity immunology, Atherosclerosis immunology, Atherosclerosis pathology, Autoimmunity immunology, Communicable Diseases immunology, Communicable Diseases pathology
Abstract

The role of inflammation and immunity in the pathogenesis and clinical manifestations of atherosclerotic disease has been widely studied. Common infectious diseases can be associated with a chronic inflammatory state which is the hallmark of atherosclerosis, thus suggesting a possible link between the two pathological conditions. Therefore, a great number of studies have tested the "infection hypothesis", but their results are conflicting. Nevertheless, several molecular and biological mechanisms possibly involved in the complex relationship between infections, immune response, vascular wall damage and atherosclerosis onset and progression have been described. The purpose of this article is to offer an overview of the principal mechanisms and molecular pathways that probably constitute the most relevant biological substrate on which the infection hypothesis is founded; some of these mechanisms are not fully understood yet. Nevertheless, their comprehension could be essential for the development of new preventive and therapeutic strategies., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Published
2013
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15. Inflammatory markers in heart failure: hype or hope?

Author

Cialdella P, Pedicino D, Gustapane M, Santangeli P, Narducci ML, Pelargonio G, Basile E, Giglio AF, Pazzano V, Vitulano N, and Bellocci F

Subjects
Anti-Inflammatory Agents therapeutic use, Biomarkers blood, Cardiovascular Agents therapeutic use, Heart Failure blood, Heart Failure drug therapy, Humans, Inflammation blood, Inflammation drug therapy, Heart Failure immunology, Inflammation immunology, Inflammation Mediators blood
Abstract

Heart failure is a growing global epidemic that involves in its pathophysiology a proinflammatory state. Since the first description of elevated cytokine levels in this setting, there has been increasing interest in understanding the role of these molecules in left-ventricular remodeling and function. Over the years, intense research on the 'cytokine theory' of heart failure has allowed evaluation of the role of inflammatory biomarkers not only as pathogenetic mediators, but also as potential tools in the diagnosis and risk stratification of heart failure patients. Whereas current evidence does not support the use of inflammatory biomarkers for the diagnosis of heart failure, the assessment of their levels and the connection between their changes and changes in clinical status and prognosis has been well validated. At present, the utility of anti-inflammatory therapies in heart failure is still debated, since trials of anti-inflammatory agents in this setting have pointed out controversial results. On the contrary, established treatments of heart failure, including β-blockers, renin-angiotensin system antagonists, and aldosterone-receptor blockers seem able to act by modulating cytokine expression, suggesting a new role for these molecules in guiding heart failure therapy. Therefore, the binomial topic of heart failure and inflammation still has a number of fields not completely explored: our aim is to update current knowledge and future perspectives.

Published
2013
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16. Adaptive immunity, inflammation, and cardiovascular complications in type 1 and type 2 diabetes mellitus.

Author

Pedicino D, Liuzzo G, Trotta F, Giglio AF, Giubilato S, Martini F, Zaccardi F, Scavone G, Previtero M, Massaro G, Cialdella P, Cardillo MT, Pitocco D, Ghirlanda G, and Crea F

Subjects
Adult, Aged, Cardiovascular Diseases etiology, Cardiovascular Diseases pathology, Cell Line, Diabetes Mellitus, Type 1 complications, Diabetes Mellitus, Type 1 pathology, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 pathology, Female, Humans, Inflammation complications, Inflammation pathology, Insulin Resistance immunology, Insulin-Secreting Cells immunology, Insulin-Secreting Cells pathology, Male, Middle Aged, T-Lymphocyte Subsets immunology, T-Lymphocyte Subsets pathology, Adaptive Immunity immunology, Cardiovascular Diseases immunology, Diabetes Mellitus, Type 1 immunology, Diabetes Mellitus, Type 2 immunology, Inflammation immunology
Abstract

Diabetes mellitus (DM) is a pandemics that affects more than 170 million people worldwide, associated with increased mortality and morbidity due to coronary artery disease (CAD). In type 1 (T1) DM, the main pathogenic mechanism seems to be the destruction of pancreatic β -cells mediated by autoreactive T-cells resulting in chronic insulitis, while in type 2 (T2) DM primary insulin resistance, rather than defective insulin production due to β -cell destruction, seems to be the triggering alteration. In our study, we investigated the role of systemic inflammation and T-cell subsets in T1- and T2DM and the possible mechanisms underlying the increased cardiovascular risk associated with these diseases.

Published
2013
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17. [Catheter ablation as first-line therapy for atrial fibrillation: an analysis of available evidence].

Author

Santangeli P, Giglio AF, Di Biase L, and Natale A

Subjects
Humans, Atrial Fibrillation surgery, Catheter Ablation
Abstract

In patients with symptomatic atrial fibrillation refractory to antiarrhythmic therapy, catheter ablation is effective in restoring and maintaining sinus rhythm, in reducing hospitalization and improving quality of life. On the other hand, the role of catheter ablation as first-line therapy for atrial fibrillation is still controversial and has been recently evaluated by two randomized controlled trials and two consecutive case series. These studies showed the superiority of catheter ablation over antiarrhythmic therapy for the rhythm control of atrial fibrillation, with similar rates of complications between the two groups. According to these results, catheter ablation could be considered as first-line therapy for patients with symptomatic paroxysmal atrial fibrillation without significant heart disease.

Published
2013
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18. Reversible atrial gap junction remodeling during hypoxia/reoxygenation and ischemia: a possible arrhythmogenic substrate for atrial fibrillation.

Author

Severino A, Narducci ML, Pedicino D, Pazzano V, Giglio AF, Biasucci LM, Liuzzo G, Casella M, Bartoletti S, Dello Russo A, Pelargonio G, Santangeli P, Di Biase L, Natale A, and Crea F

Subjects
Cell Line, Heart Conduction System metabolism, Humans, Myocytes, Cardiac metabolism, Atrial Fibrillation metabolism, Connexin 43 metabolism, Gap Junctions metabolism, Heart Atria metabolism, Myocardial Ischemia metabolism, Myocardial Reperfusion Injury metabolism
Abstract

Alteration of cardiomyocyte gap-junctions and component connexins (Cx) has been suggested to contribute to the development of atrial fibrillation (AF), including postoperative AF. We tested different possible stimuli, such as hypoxia and ischemia, influencing Cx43 and Cx40 expression and distribution in cultured atrial cells (HL-1) and reversibility of these processes after reoxygenation. Western-blot analysis and immunostaining using anti-Cx43, anti-Cx40 and anti-zonula occludens polyclonal antibodies were performed. HL-1 cells exposed to hypoxia for 24 and 48 h showed a reduction of Cx43 protein levels by 75% and 90% respectively (p < 0.001). During reoxygenation following 24 h of hypoxia, Cx43 levels increased to reach the basal level within 48 h, while they remained at low level during reoxygenation following 48 h of hypoxia. Furthermore, atrial cardiomyocytes subjected to simulated ischemia (SI) were incubated in normoxic and hypoxic conditions for 3, 6, 9, 12 h. Atrial cardiomyocytes subjected to SI in addition to normoxia showed a progressive reduction of Cx43 levels beginning from 3 h. During SI and hypoxia, atrial Cx43 levels showed an initial decrease after 3 h with a subsequent rescue beginning from 6 h of exposure (p = 0.001). Hypoxia and ischemia per se downregulate Cx43 protein expression in atrial cardiomyocytes, but protein downregulation is reversible, depending on hypoxia duration and the association of the two triggers. These alterations characterize several conditions and might contribute to the generation of an arrhythmogenic substrate leading to AF onset and/or maintenance.

Published
2012
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19. Human epicardium-derived cells fuse with high efficiency with skeletal myotubes and differentiate toward the skeletal muscle phenotype: a comparison study with stromal and endothelial cells.

Author

Gentile A, Toietta G, Pazzano V, Tsiopoulos VD, Giglio AF, Crea F, Pompilio G, Capogrossi MC, and Di Rocco G

Subjects
Animals, Cell Fusion, Cell Nucleus metabolism, Cellular Reprogramming genetics, Coculture Techniques, Dystrophin metabolism, Endothelial Cells metabolism, Endothelial Cells transplantation, Gene Expression Regulation, Gene Knockdown Techniques, Humans, Interleukin-13 metabolism, Interleukin-4 metabolism, Mesoderm cytology, Mice, Mice, Inbred mdx, Muscle Fibers, Skeletal metabolism, MyoD Protein metabolism, Myoblasts cytology, Myoblasts metabolism, Organ Specificity genetics, Phenotype, Receptors, Interleukin-4 metabolism, Stromal Cells cytology, Stromal Cells metabolism, Stromal Cells transplantation, Vascular Cell Adhesion Molecule-1 metabolism, Cell Differentiation, Endothelial Cells cytology, Muscle Fibers, Skeletal cytology, Muscle, Skeletal cytology, Pericardium cytology
Abstract

Recent studies have underscored a role for the epicardium as a source of multipotent cells. Here, we investigate the myogenic potential of adult human epicardium-derived cells (EPDCs) and analyze their ability to undergo skeletal myogenesis when cultured with differentiating primary myoblasts. Results are compared to those obtained with mesenchymal stromal cells (MSCs) and with endothelial cells, another mesodermal derivative. We demonstrate that EPDCs spontaneously fuse with pre-existing myotubes with an efficiency that is significantly higher than that of other cells. Although at a low frequency, endothelial cells may also contribute to myotube formation. In all cases analyzed, after entering the myotube, nonmuscle nuclei are reprogrammed to express muscle-specific genes. The fusion competence of nonmyogenic cells in vitro parallels their ability to reconstitute dystrophin expression in mdx mice. We additionally show that vascular cell adhesion molecule 1 (VCAM1) expression levels of nonmuscle cells are modulated by soluble factors secreted by skeletal myoblasts and that VCAM1 function is required for fusion to occur. Finally, treatment with interleukin (IL)-4 or IL-13, two cytokines released by differentiating myotubes, increases VCAM1 expression and enhances the rate of fusion of EPDCs and MSCs, but not that of endothelial cells.

Published
2011
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