418 results on '"O. Abramsky"'
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2. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain
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H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. Zucconl, Javier Muruzabal, R. R. Allen, R. Rivolta, K. Haugaard, A. Nespolo, K. Hoang-Xuang, G. Bussone, T. Avramidis, E. Corsini, Christiana Franke, T. Vinogradova, H. Boot, K. Vestergaard, G. H. Jansen, N. Argentino, M. Raltzig, W. Linssen, Mark B. Pepys, P. Roblot, L. Lauritzen, E. Fainardi, D. Morin, T. X. Arbizu Urdiain, J. Wollenhaupt, S. Bostantjopoulou, G. Pavesi, A. D. Forman, Giovanni Fabbrini, D. Jean, J. J. Archelos, M. I. Blanchs, M. Del Gobbo, Anna Carla Turconi, Ch. Derouesné, Elio Scarpini, A. Visbeck, P. Castejon, J. P. Renou, F. Mounier-Vehier, G. Potagas, Ch. Duyckaerts, A. Filla, R. Schneider, G. Ronen, K. Nagata, J. P. Vedel, A. Henneberg, G. van Melle, C. Baratti, H. Knott, M. C. Prevett, A. Bes, B. Metin, Jos V. Reempts, L. Martorell, Mefkure Eraksoy, H. O. Handwerker, D. S. Younger, O. Oktem, D. Frongillo, C. Soriano-Soriano, L. Niehaus, F. Zipp, A. Tartaro, S Newman, R. H. Browne, P. Davous, R. Sanchez, M. Muros, M. E. Kornhuber, A. Lavarone, M. Mohr, M. R. Garcia, S. Russell, H. Kellar-Wood, M. R. Tola, B. Ostermeyer, Ch. Tzekov, K. Sartor, E. B. Ringelstein, P. P. Gazzaniga, Paul Krack, H. Fidaner, H. Rico, T. Dbaiss, F. Alameda, E. Torchiana, L. Rumbach, I. Charques, J. M. Bogaard, C. D. Frith, L. J. Rappelle, R. Brenner, A. Joutel, K. Fuxe, G. HÄcker, M. J. Blaser, J. Valls-SolÇ, G. Ulm, M. Alberdi, A. Bock, F. W. Bertelsmann, U. Wieshmann, J. Visa, J. R. Lupski, D. D'Amico, L. M. P. Ramos, A. A. Vanderbark, R. Horn, M. Warmuth, Dietmar Kühne, Mark S. Palmer, C. Ehrenheim, E. Canga, S. Viola, O. Scarpino, P. Naldi, R. Almeida, A. A. Raymond, J. Gamez, Stephan Arnold, A. DiGiovanni, J. Dalmau, C. C. Chari, H. F. Beer, J. C. Koetsier, J. Iriarte, E. Yunis, J. Casadevall, E. Le Guern, E. Stenager, S. R. Benbadis, J. M. Warter, F. Burklin, I. Theodorou, L. Johannesen, G. A. Graveland, X. Leclerc, I. Vecchio, L. Ozelius, G. Nicoletti, R. K. Gherardi, E. Esperet, M. L. Delodovici, F. Cattin, F. Paiau, Giorgio Sacilotto, C. A. J. Broere, D. Chavdarov, J. P. Willmer, C. H. Hawkes, Th. Naegele, E. Ellie, E. Dartigues, M. J. Guardiola, S. Hesse, Z. Levic, Marco Rovaris, P. Saugeir-Veber, B. A. Yaqub, H. F. Durwen, R. Larumbe, J. Ballabrina, M. Sendtner, J. Röther, M. Horstink, C. Kluglein, M.P. Montesi, H. Apaydin, J. Montoya, E. Waubant, Ch. Verellen-Dunoulin, A. Nicolai, J. Lopez-Delval, R. Lemon, G. Cantinho, E. Granieri, A. Zeviani, Wolfgang H. Oertel, U. Ficola, V. Di Piero, V. Fragola, K. Sabev, M. V. Guitera, I. Turki, F. Bolgert, P. Ingrand, J. M. Gobernado, L. M. E. Grimaldi, S. Baybas, B. Eymard, Y. Rolland, Y. Robitaille, Ta. Pampols, P. J. Koehler, A. Carroacedo, J. Vilchez, S. Di Vittorio, I. R. Rise, T. Nagy, M. Kuffner, E. Palazzini, A. Ott, J. Pruim, T. X. Arbizu, E. Manetti, C. Cervera, S. Felber, G. Gursoy, J. Scholz, G. A. Buscaino, M. S. Chen, A. Pascual, J. Hazan, J. U. Gajda, J. G. Cea, G. Bottini, G. Damalik, F. Le Doze, G. Bonaldi, J. M. Hew, C. Messina, A. M. Kennedy, J. M. Carney, N. M. F. Murray, M. Parent, M. Koepp, V. Dimova, D. De Leo, K. Jellinger, G. Salemi, S. Mientus, M. L. Hansen, F. Mazzucchelli, J. Vieth, M. Mauri, E. Bartels, L. Johannsen, C. Humphreys, J. Emile, D. N. Landon, E. Kansu, R. Sanchez-Pernaute, Rsj Frackowiak, M. Gonzalez Torres, L. Oller, C. Machedo, J. Kother, M. Billiard, H. Durak, T. Schindler, A. Frank, A. Uncini, A. Sbriccoli, C. Farinas, D. W. Paty, N. Fast, A. T. Zangaladze, A. Kerkhofs, J. M. Pino Garcia, I. De la Fuente, B. Marini, L. Gomez, I. Rubio, Alessandra Bardoni, C. Brodie, P. Acin, U. Sliwka, S. A. Hawkins, S. Tardieu, F. Vitullo, J. M. Pereira Monteino, R. Gagliardi, T. Jezewski, A. Cano, T. Lempert, F. Abad Alegria, G. Rotondo, D. Ince, C. Martinez Parra, Y. Huang, H. Luders, Y. Steinvil, F. G. A. Van Der Meche, R. Bianchi, A. Sanchez, T. Sevilla, J. M. Ketelslegers, A. Domzal-Stryga, M. Pandolfo, M. O. Josse, K. W. Neff, I. Blanco, G. W. Bruyn, O. W. Witte, J. L. Thibault, G. Andersen, J. Pariset, A. Marcone, R. J. M. Lane, A. Hofman, M. Verin, T. Matilla, P. Bedoucha, J. Roche, M. Lai, M. Collard, A. Ugarte, F. Gallecho, D. Silbersweig, C. Kennard, J. P. Azulay, T. W. Ho, P. L. I. Dellemijn, R. Girardello, F. Baas, B. Voss, F. Rozenberg, E. M. Brocker, V. Stanev, A. A. J. Soeterboek, A. Marra, A. Rey, E. Ertem, M. Sawradewicz-Rybak, J. De Keyser, P. Cavallari, F. Proust, Y. Chevalier, H. C. Hansen, D. Leys, C. A. Davie, K. Hoang-Xuan, C. Bairati, H. van Crevel, Thomas T. Warner, B. Bompais, A. Dobbeleir, T Campbell, C. Macko, C. J. M. Klijn, M. Dussallant, T. P. Berlit, W. Rozenbaum, M. J. van den Bent, W. A. Rocca, M. Muller, H. Hundemer, U. Zifko, M. Campera, F. Drislane, D. Ranoux, T. M. Kloss, Anil Kumar, I. Ruolt, C. Bargnani, B. Marescau, N. A. Losseff, S. Notermans, B. Kint, E. T. Burke, C. Aykut, J. Matias Guiu, P. Maquet, T. Drogendijk, M. Leone, K. von Ammon, M. Pepeliarska, C. Prados, L. DiGiamberardino, T. Logtenberg, G. Lenoir, I. Castaldo, Damhaut, M. Radionova, G. Sirabian, R. Navon, Giovanni Antonini, K. Al Moutaery, E. Chamas, R. Schönhuber, M. Giannini, B. Debilly, I. Labatut, H. Henon, J. A. Egido, M. Baudrimont, J. N. Lorenzo, J. E. C. Bromberg, R. Antonacci, J. J. Vilchez, T. Moulin, B. Rautenstrauss, Giovanni Meola, J. Noth, S Mammi, P. Laforet, F. Lopez, C. Gehring, S. Bort, G. Rancurel, D. Decamps, S. Kostadinova, Y. Shapira, B. Neundoerfer, D. Chavrot, M. Solimena, J. P. Salier, W. Deberdt, R. Hoff-Jörgensen, A. Messina, S. Meairs, G. Rosoklija, E. Nelis, I. Bertran, C. Ertekin, J. Lohmeyer, Mitermayer Galvao dos Reis, L. Calo, E. Maccagnano, A. P. Hays, J. Verlooy, M. G. Forno, T. Blanco, L. Bail, Gabriella Silvestri, J. Montero, F. Bertrand, R. T. Ghnassia, C. Besses, T. Sereghy, F. Shalit, G. Bogliun, S. Braghi, St. Baykouchev, C. Franke, A. Lasa, L. C. Archard, J. Kriebel, S. Shaunak, M. Nocito, Alexander Tsiskaridze, E. Manfredini, T. Seigal, David G. Gadian, M. Barlas, J. D. Degos, C. Seeber, J. Caemert, J. L. Mas, R. B. Pepinsky, M. G. D'Angelo, N. Baumann, S. Yorifuji, H. P. Endtz, M. A. Cassatella, R. A. C. Hughes, V. Golzi, A. Bittencourt, A. Ferreira, M. Sanson, C. Alper, M. Vermeulen, M. A. A. van Walderveen, E. Alexiou, C. H. Lucas, M. Fiorelli, Y. N. Debbink, R. Gil, S. Congia, T. Banerjee, J. M. Bouchard, A. N. Pinto, A. Ceballos-Baumann, G. Grollier, P. I. M. Schmitz, M. D. Catata, N. Lahat, N. S. Rao, P. Papathanasopoulos, J. Valls-Solé, D. Claus, G. Schroter, A. Castro, C. Videbaek, R. Martinez Dreke, A. D. Platts, M. Hermesl, A. C. PeÇanha-Martins, M. Cardoso Silva, P. Masnou, M. J. A. Tanner, Ch. Confavreux, B. Mishu, H. Rasmussen, L. Valenciano, Carlo Pozzilli, S. W. Li, V. Salzman, Y. Vashtang, Massimo Franceschi, M. Severo, G. Deuschl, S. Setien, G. Mariani, A. Protti, J. Castillo, M. J. B. Taphoorn, M. Frontali, I. Milonas, D. Decoq, J. A. Navarro, S. Castellvi-Pel, C. Ertikin, M. Urtasun, Y. Lajat, B. E. Kendall, E. Verdu, B. Gueguen, E. Boisen, R. Couderc, A Danek, JM Stevens, F. Nicoli, L. Feltri, M. L. Vazquez-Andre, J. A. Morgan-Hughes, L. D'Angelo, F. Y. Liew, L. F. Pascual, J. Patrignani Ochoa, Vittorio Martinelli, J. Cophignon, L. Zhang, S. Martin, J. F. Meder, H. C. Buschmann, L. Bertin, J. van Gijn, A. Barreiro, A. Cools, C. Leon, A. Berod, E. A. Anllo, E. Zanette, L. Petrov, R. Barona, B. Gallicchio, P. J. Cozzone, N. Diederich, G. Cancel, L. Schelosky, P. Orizaola, K. Yulug, S. Ozer, Valeria A. Sansone, B. Guiraud-Chaumeil, K. Voigt, P. Labauge, M. Eoli, J. Zhu, J. Aguirre, M. Ferrarini, B. Zyluk, E. Planas, A. Cadilha, C. Tortorella, H. Bismuth, C. E. Counsell, A. Laun, A. Ferlini, Rio J. Montalban, N. Biary, L. Becker, M. Fardeau, M. Poloni, V. M. S. de Bruin, C. Fornada, J. Barros, E. Ganzmann, E. Touze, D. Wallach, J. Peila, H. Fujimura, M. T. Iba-Zizen, G. Macchi, C. Villoslada, R. Gouider, Ph. Rondepierre, P. Grummich, P. Chiodi, C. Conte, M. Michels, P. Annunziata, G. Semana, C. Sommer, J. Vajsar, D. Zekin, J. Kulisevsky, David G. Munoz, B. Jacotot, M. Magoni, A. Luxen, T. Garcia-Silva, S. Di Cesare, Christophe Tzourio, M. Gomori, I. Picomell, L. Santoro, F. Villa, Giovanni Pennisi, T. Ribalta, J. M. Molto, L. Marzorati, P. Loiseau, F. Gemignani, A. Gironell, J. Wissel, A. Prusinski, F. Cailloux, P. Villanueva-Hemandez, P. Cozzone, T. Del Ser, J. Sans-Sabrafen, M. Zappia, P. W. A. Willems, G. Tchernia, D. Gardeur, R. Bauer, F. Palomo, H. Metz, S. Lamoureux, C. Chastang, I. Reinhard, A. Goldfarb, S. Harder, Jordi Río, C. Ozkara, E. Tekinsoy, P. Vontobell, J. De Recondo, M. Rabasa, L. Lacomblez, F. Boon, Dgt Thomas, V. Palma, Renato Mantegazza, A. Dervis, M. Nueckel, B. YalÇinerner, I. Duran, G. Dalla Volta, A. Zubimendi, J. Pinheiro, A. Marbini, Xavier Montalban, H. Wekerle, X. Pereira Monteino, F. Crespo, F. Koskas, N. Battistini, C. Ruiz, H. Offner, J. de Pommery, P. Kanovsky, J. Y. Barnett, J. Pardo, G. Tomei, R. Rene, H. M. Lokhorst, P. Thajeb, H. Bilgin, D. McGehee, R. Fahsold, L. Morgante, Katie Sidle, C. Delwaide, M. N. Diaye, P. H. Rice, A. Creange, C. Sabev, K. Stephan, K. WeilBenborn, G. Magnani, L. Grymonprez, F. Cardellach, M. Kaps, N. G. Meco, F. Vega, V. Bonifati, A. Desomer, M. Baldy-Moulinier, G. Kvale, F. J. Authier, B. Yegen, T. Ho, J. M. Rozet, E. A. Cabanis, L. Bruce, L. Ambrosoli, M. A. Petrella, M. Hernandez, P. Timmings, H. B. van der Worp, F. Mahieux, A. Urbano-Marquez, D. A. Krendel, A. A. Garcia, R. Divari, R. Michalowicz, M. R. Piedmonte, M. Bondavalli, M. Zanca, P. F. Ippel, Onofre Combarros, B. Tavitian, E. Hirsch, I. Anastasopoulos, A. Roses, A. Köhler, P. Vienna, V. Timmerman, P. Sergi, F. Cornelio, A. Di Pasquale, R. Verleger, S. Castellvirel, J. Proano, B. van Moll, F. Rubio, W. Hacke, I. Lavenu, L. Zetta, M. W. Tas, N. Bittmann, M. Bonamini, O. R. Hommes, V. Dousset, N. Afsar, S. Belal, R. R. Myers, J. Goes, Giuseppe Vita, E. Clementi, V. G. Karepov, M. Jueptner, A Vincent, P. Emmrich, Th. Heb, A. Caballo, J. Gallego, T. Mokrusch, C. Perla, L. Gebuhrer, O. Titlbach, Alessandro Prelle, A. Czlonkowska, M. Russo, D. Hadjiev, T. S. Chkhikvishvili, M. Oehlschlager, G. Becker, I. Günther, E. N. Stenager, J. Garcia Agundez, J. Casademont, J. Batlle, S. Podobnik-Sarkanji, C. Alonso-Villaverde, B. Delaguillaume, B. Genc, B. Mazoyer, A. Rodriguez-Al-barino, Ch. Hilger, B. Ferrero, R. Price, W. Grisold, L. Fuhry, D. Oulbani, D. Ewing, A. Petkov, W. Walther, A. Gokyigit, John Newsom-Davis, J. Tayot, D. Seliak, G. Pelliccioni, D. Campagne, K. Kessler, F. Boureau, D. Perani, J. P. N'Guyen, N. Tchalucova, B. A. Antin-Ozerkis, C. Lacroix, B. D. Aronovich, I. H. Jenkins, E. A. dos Reis, M. Hortells, H. M. Meinck, H. Ch. Buschmann, S. C. J. M. Jacobs, T. Wetter, P. Creissard, N. Martinez, J. Weidenfeldl, H. J. Sturenburg, G. Damlacik, V. Gracia, J. C. Turpin, A. Pou-Serradell, J. P. Vincent, T. Gagoshidze, U. Ozkutlu, M. McLeod, K. Siegfried, I. Tchaoussoglou, J. Hildebrand, S. Kowalska, M. C. Picot, G. Galardin, L. Crevits, F. Andreetta, S. Larumbe-Lobalde, G. de la Sierra, J. C. Alvarez-Cermeno, R. J. Seitz, P. L. Oey, L. Ptacek, A. M. J. Paans, A. Wirrwar, A. Schmied, J. Uilchez, H. Tounsi, D. Hipola, V. Avoledo, Y. Hirata, P. Vermersch, T. M. Aisonobe, J. Valls-SoIè, H. Staunton, J. Dichgans, R. Karabudak, I. Dones, G. Porta, E. Janssens, Maria Martinez, J. M. Fernandez-Real, R. Villagra, Y. Yoshino, C. Kabus, K. Schimrigk, I. Girard-Buttaz, F. Piccoli, F. Aichner, P. Zuchegna, S. M. Al Deeb, F. Bono, N. Busquets, A. Jobert, Patrizia Ciscato, M. Martin, L. Polman, S. Darbra, V. Le Cam-Duchez, F. Baldissera, B. Baykan-Kurt, D. Guez, M. Bratoeva, H. Matsui, M. Mila, H. Perron, L. Bjorge, G. Husby, Steven T. DeKosky, D. R. Cornblath, J. M. Gabriel, J. J. Poza, Y. Wu, A. Toscano, R. P. Kleyweg, J. Kuhnen, S. O. Confort-Gouny, A. Barcelo, A. M. Conti, C. Fiol, C. Steichen-Wiehn, J. Rodes, M. Cavenaile, C. Vedeler, M. Drlicek, C. Argentino, M. L. Peris, A. Cervello, A. Z. GinaÏ, S. Yancheva, D. Passingham, S. Aoba, D. L. Lopez, T. Rechlin, K. Sonka, L. Grazzi, V. Folnegovic-Smalc, Maurizio Moggio, S. Rivaud, F. G. I. Jennekens, C. H. Hartard, H. Meierkord, G. Stocklin, M. D. Catala, W. C. McKay, E. Salmon, C. Navarro, I. Pastor, L. Canafoglia, M. De Braekeleer, P. K. Thomas, C. Mocellini, C. Pierre-Jerome, M. C. Dalakas, P. Pollak, M. Levivier, Niall Quinn, G. E. Rivolta, Z. Tunca, H. Zeumer, J. Garcia Tena, St. Guily, P. Gaudray, Johannes Kornhuber, V. Petrunjashev, R. Montesanti, R. J. Abbott, H. Petit, G. Kiteva-Trencevska, F. Carletto, C. Ramo, I. M. Pino, P. Beau, G. F. Mennuni, F. Moschian, F. Meneghini, B. Zdziarska, B. Fontaine, C. Stephens, G. Meco, K. Reiners, G. Badlan, M. Sessa, I. Degaey, S. M. Hassan, C. Albani, F. Caroeller, M. Schroeder, G. Savettieri, A. Novelletto, R. Kurita, P. Oschmann, I. Plaza, M. Oliveres, Simone Spuler, A. Molins, M. Schwab, J. R. Kalden, C. P. Gennaula, Y. Baklan, O. Picard, J. M. Léger, B. Mokri, E. Ghidoni, M. Jacob, D. Deplanque, W. JÄnisch, C. De Andres, P. De Deyn, G. Guomundsson, B. Herron, J. Barado, J. L. Gastaut, Guglielmo Scarlato, F. Poron, Nicola Jones, H. Teisserenc, C. P. Hawkins, A. J. Steck, H. C. Chandler, S. Blanc, J. H. Faiss, Jm. Soler Insa, I. Sarova-Ponchas, M. Malberin, A. Sackmann, G. De Vuono, K. Kaiser-Rub, K. Badhia, E. Szwabowska-Orzeszko, S. Ramm, C. Jodice, G. Franck, J. Marta-Moreno, R. Sciolla, C. Fritz, A. Attaccalite, F. Weber, E. Neuman, M. Cannata, A. Rodriguez, I. Nachainkin, R. Raffaele, T. S. Yu, N. Losseff, E. Fabrizio, C. Khati, M. Keipes, M. P. Ortega, M. Ramos-Alvarez, E. Brambilla, A. Tarasov, K. H. Wollinsky, O. B. Paulson, F. Boller, G. Bozzato, H. Wagnur, R. Canton, D. Testa, E. Kutluaye, M. Calopa, D. Smadja, G. Malatesta, F. Baggi, A. Stracciari, G. Daral, G. Avanzini, J. Perret, J. Arenas, P. Boon, I. Gomes, A. Vortmeyer, P. Cesaro, S. Venz, E. Bernd Ringelstein, N. Milani, D. Laplane, P. Seibel, E. Tournier-Lasserve, Alexis Brice, L. Motti, E. Wascher, R. J. Abbot, F. Miralles, A. Turon, P. De Camilli, G. Luz, G. C. Guazzi, S. Tekin, F. Lesoin, T. Kryst, N. Lannoy, F. Gerstenbrand, S. Ballivet, H. A. M. van Diemen, J. Lopez-ArLandis, P. Bell, A. Silvani, M. A. Garcia, S. Vorstrup, D. Langdon, S. Ueno, B. Sander, V. Ozurk, C. Gurses, P. Berlit, J. M. Martinez-Lage, M. Treacy, S. O. Rodiek, S. Cherninkova, J. Grimaud, P. Marozzi, K. Hasert, S. Goldman, S. H. Ingwersen, A. Taghavy, T. Roig, R. Harper, I. Sarova-Pinchas, Anthony H.V. Schapira, R. Lebtahi, A. Vidaller, B. Stankov, D. Link, J. p. Malin, V. Petrova, Ludwig Kappos, J. L. Ochoa, T. Torbergsen, M. Carpo, M. Donato, Simon Shorvon, J. Mieszkowski, J. Perez-Serra, Raymond Voltz, G. Comi, S. Rafique, A. Perez-Sempere, N. Khalfallah, S. Bailleul, M. Borgers, S. Banfi, S. Mossman, A. Laihinen, G. Filippini, R. A. Grunewald, E. Stern, H. D. Herrmann, A. G. Droogan, P. Xue, A. Grilo, L. La Mantia, J. H. J. Wokke, S. Pizzul, Kie Kian Ang, S. Rapaport, W. Szaplyko, B. Romero, P. Brunet, A. 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Valalentino, D. Guidetti, B. Buchwald, C. H. Lücking, D. Gauvreau, F. Pfaff, A. Ben Younes-Chennoufi, R. Kiefer, R. Massot, K. A. Hossmann, L. Werdelin, P. J. Baxter, U. Ziflo, S. Allaria, C. D. Marsden, M. Cabaret, S. P. Mueller, E. Calabrese, R. Colao, S. I. Bekkelund, M. Yilmaz, O. Oktem-Tanor, R. Gine, M. E. Scheulen, J. Beuuer, A. Melo, Z. Gulay, M. D. Have, C. Frith, D. Liberati, J. Gozlan, P. Rondot, Ch. Brunholzl, M. Pocchiari, J. Pena, L. Moiola, C. Salvadori, A. Cabello, T. Catarci, S. Webb, C. Dettmers, N. A. Gregson, Alexandra Durr, F. Iglesias, U. Knorr, L. Ferrini-Strambi, F. Kruggel, P. Allard, A. Coquerel, P. Genet, F. Vinuels, C. Oberwittler, A. Torbicki, P. Leffers, B. Renault, B. Fauser, C. Ciano, G. Uziel, J. M. Gibson, F. Anaya, C. Derouesné, C. N. Anagnostou, M. Kaido, W. Eickhoff, G. Talerico, M. L. Berthier, A. Capdevila, M. Alons, D. Rezek, E. Wondrusch, U. Kauerz, D. Mateo, M. A. Chornet, Holon, N. Pinsard, I. Doganer, E. Paoino, H. Strenge, C. Diaz, J. R. 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Garcia de Yebenes, N. K. Olsen, P. Hitzenberger, S. Einius, Aj Thompson, Ch. J. Vecht, T. Crepin-Leblond, Klaus L. Leenders, A. Di Muzio, L. Georgieva, René Spiegel, K. Sabey, D. Ménégalli, J. Meulstee, U. Liszka, P. Giral, C. Sunol, J. M. Espadaler, A. D. Crockar, K. Varli, G. Giraud, P. J. Hülser, A. Benazzouz, A. Reggio, M. Salvatore, K. Genc, M. Kushnir, S. Barbieri, J. Ph. Azulay, M. Gianelli, N. Bathien, A. AlMemar, F. Hentati, I. Ragueneau, F. Chiarotti, R. C. F. Smits, A. K. Asbury, F. Lacruz, B. Muller, Alan J. Thompson, Gordon Smith, K. Schmidt, C. Daems Monpeun, Juergen Weber, A. Arboix, G. R. Fink, A. M. Cobo, M. Ait Kaci Ahmed, E. Gencheva, Israel-Biet, G. Schlaug, P. De Jonghe, Philip Scheltens, K. Toyka, P. Gonzalez-Porque, A. Cila, J. M. Fernandez, P. Augustin, J. Siclia, S. Medaglini, D. E. Ziogas, A. Feve, L. Kater, G. J. E. Rinkel, D. Leppert, Rüdiger J. Seitz, S. Ried, C. Turc-Carel, G. Smeyers, F. Godinho, M. Czygan, M. Rijntjes, E. Aversa, M. 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Meinardi, F. Carrara, J. Kuehnen, C. Peiro, H. Lassmann, K. Skovgaard Olsen, A. McDonald, L. Sciulli, A. Cobo, A. Monticelli, B. Conrad, J. Bagunya, J. Benitez, V. Desnizza, B. Dupont, O. Delrieu, D. Moraes, J. J. Heimans, F. Garcia Rio, M. Matsumto, A. Fernandez, R. Nermni, R. Chalmers, M. J. Marchau, F. Aguado, P. Velupillai, P. J. Martin, P. Tassan, V. Demarin, A. Engelien, T. Gerriets, Comar, J. L. Carrasco, J. P. Pruvo, A. Lopez de Munain, D. Pavitt, J. Alarcon, Chris H. Polman, B. Guldin, N. Yeni, Hartmut Brückmann, N. Wilczak, H. Szwed, R. Causaran, G. Kyriazis, M. E. Westarp, M. Gasparini, N. Pecora, J. M. Roda, E. Lang, V. Scaioli, David R. Fish, D. Caputo, O. Gratzl, R. Mercelis, A. Perretti, G. Steimetz, I. Link, C. Rigoletto, A. Catafau, G. Lucotte, M. Buti, G. Fagiolari, A. Piqueras, C. Godinot, J. C. Meurice, Erodriguez J. Dominigo, F. Lionnet, H. Grzelec, David J. Brooks, P. M. G. Munro, F. X. Weilbach, M. Maiwald, W. Split, B. Widjaja-Cramer, V. Ozturk, J. Colas, E. Brizioli, J. Calleja, L. Publio, M. Desi, R. Soffietti, P. Cortinovis-Tourniaire, E. F. Gonano, G. Cavaletti, S. Uselli, K. Westerlind, H. Betuel, C. O. Dhiver, H. Guggenheim, M. Hamon, R. Fazio, P. Lehikoinen, A. Esser, B. Sadzot, G. Fink, Angelo Antonini, D. Bendahan, V. Di Carlo, G. Galardi, A. F. Boller, M. Aksenova, Del Fiore, V. de la Sayette, H. Chabriat, A. Nicoletti, A. Dilouya, M. L. Harpin, E. Rouillet, J. Stam, A. Wolters, M. R. Delgado, Eduardo Tolosa, G. Said, A. J. Lees, L. Rinaldi, A. Schulze-Bonhage, MA Ron, C. Lefebvre, E. W. Radü, R. Alvarez, M. L. Bots, P. Reganati, S. Palazzi, A. Poggi, N. J. Scolding, V. Sazdovitch, T. Moreau, E. Maes, M. A. Estelies, P. Petkova, Jose-Felix Marti-Masso, G De La Meilleure, N. Mullatti, M. Rodegher, N. C. Notermans, T. A. T. Warner, S. Aktan, J. P. Louboutin, L. Volpe, C. Scheidt, W. Aust, C. M. Wiles, U. Schneider, S. K. Braekken, W. R. Willems, K. Usuku, Peter M. Rothwell, C. Talamon, M. L. Sacchetti, A. Codina, M. H. Marion, A. 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Riva, M. H. Mahagne, M. Ozturk, Ve. Drory, N. Konic, C. Jungreis, A. Pou Serradell, J. L. Gauvrit, G. J. Chelune, S. Hermandez, T. Dingus, L. Hewer, Ch. Koch, M. N. Metz-Lutz, G. Parlato, M. Sinaki, Charles Pierrot-Deseilligny, H. C. Diener, J. Broeckx, J. Weill-Fulazza, M. L. Villar, M. Rizzo, O. Ganslandt, C. Duran, N. A. Fletcher, G. Di Giovacchino, Susan T. Iannaccone, C. Kolig, N. Fabre, H. A. Crockard, Rita Bella, M. Tazir, E. Papagiannuli, K. Overgaard, Emma Ciafaloni, I. Lorenzetti, F. Viader, P. A. H. Millac, I. Montiel, L. H. Visser, M. Palomar, P. L. Murgia, H. Pedersen, Rafael Blesa, S. Seddigh, W. O. Renier, I. Lemahieu, H. M. L. Jansen, L. Rosin, J. Galofre, K. Mattos, M. Pondal, G. M. Hadjigeorgiou, D. Francis, L. Cantin, D. Stegeman, M. Rango, A. B. M. F. Karim, S. Schraff, B. Castellotti, I. Iriarte, E. Laborde, T. J. Tjan, R. Mutani, D. Toni, B. Bergaasco, J. G. Young, C. Klotzsch, A. Zincone, X. Ducrocq, M. Uchuya, O. J. Kolar, A. Quattrone, T. 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Butterfield, P. P. Costa, F. deRino, F. Bamonti, J. M. Cesar, C. H. Lahoz, I. Mosely, M. Starck, M. H. Lemaitre, K. M. Stephan, S. Tex, R. Bokonjic, I. Mollee, L. Pastena, M. Gutierrez, F. Boiler, M. C. Martinez-Para, M. Velicogna, O. Obuz, A. Grinspan, M. Guarino, L. M. Cartier, E. Ruiz, D. Gambi, S. Messina, M. Villa, Michael G. Hanna, J. Valk, Leone Pascual, M. Clanet, Z. Argov, B. Ryniewicz, E. Magni, B. Berlanga, K. S. Wong, C. Gellera, C. Prevost, F. Gonzalez-Huix, R. Petraroli, J. E. G. Benedikz, I. Kojder, C. Bommelaer, L. Perusse, M. R. Bangioanni, Guy M. McKhann, A. Molina, C. Fresquet, E. Sindern, Florence Pasquier, M. J. Rosas, M. Altieri, O. Simoncini, M. Koutroumanidis, C. A. F. Tulleken, M. Dary-Auriol, S. Oueslati, H. Kruyer, I. Nishisho, C. R. Horning, A. Vital, G. V. Czettritz, J. Ph. Neau, B. Mihout, A. Ameri, M. Francis, S. Quasthoff, D. Taussig, S. Blunt, P. Valentin, C. Y. Gao, O. Heinzlef, H. d'Allens, C. Coudero, M. Erfas, G. Borghero, P. J. Modrego Pardo, M. C. Patrosso, N. L. Gershfeld, P. A. J. M. Boon, O. Sabouraud, M. Lara, J. Svennevig, G. L. Lenzi, A. Barrio, H. Villaroya, JosÇ M. Manubens, O. Boespflug-Tanguy, M. Carreras, D. A. Costiga, J. P. Breux, S. Lynn, C. Oliveras Ley, A. G. Herbaut, J. Nos, C. Tornali, Y. A. Hekster, J. L. Chopard, J. M. Manubens, P. Chemouilli, A. Jovicic, F. Dworzak, S. Smirne, S. E. Soudain, B. Gallano, D. Lubach, G. Masullo, G. Izquierdo, A. Pascual Leone Pascual, A. Sessa, V. Freitas, O. Crambes, L. Ouss, G. W. Van Dijk, P. Marchettini, P. Confalonieri, M. Donaghy, A. Munnich, M. Corbo, and M. E. L. van der Burg
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J. M. Derlon, M. C. Petit-taboué, F. Dauphin, P. Courtheoux, F. Chapon, P. Creissard, F. Darcel, J. P. Houtteville, B. Kaschten, B. Sadzot, A. Stevenaert, Juri G. Tjuvajev, Homer A. Macapinlac, Farhad Daghighian, James Z. Ginos, Ronald D. Finn, M. S. Jiaju Zhang, Bradley Beattie, Martin Graham, Steven M. Larson, Ronald G. Blasberg, M. Levivier, S. Goldman, B. Pirotte, J. M. Brucher, D. Balériaux, A. Luxen, J. Hildebrand, J. Brotchi, K. G. Go, R. L. Kamman, E. L. Mooyaart, M. A. A. M. Heesters, P. E. Sijens, M. Oudksrk, P. van Dijk, P. C. Levendag, Ch. J. Vecht, R. J. Metz, D. N. Kennedy, B. R. Rosen, F. H. Hochberg, A. J. Fishman, P. A. Filipek, V. S. Caviness, M. W. Gross, F. X. Weinzierl, A. E. Trappe, W. E. Goebel, A. M. Frank, Georg Becker, Andreas Krone, Karsten Schmidt, Erich Hofmann, Ulrich Bogdahn, H. Bencsch, S. Fclber, G. Finkenstedt, C. Kremser, G. Sfockhammer, F. Aichner, U. Bogdahn, T. Fröhlich, G. Becker, A. Krone, R. Schlief, J. Schürmann, P. Jachimczak, E. Hofmann, W. Roggendorf, K. Roosen, C. M. Carapella, G. Carpinelli, R. Passalacqua, L. Raus, M. Giannini, R. Mastrostefano, F. Podo, A. Tofani, R. Maslrostefano, M. Mottoles, A. Ferraironi, M. G. Scelsa, P. Oppido, A. Riccio, C. L. Maini, L. Collombier, L. Taillandier, M. Dcbouverie, M. H. Laurens, P. Thouvenot, M. Weber, A. Bertrand, G. S. Cruickshank, J. Patterson, D. Hadley, Olivier De Witte, Jerzy Hildebrand, André Luxen, Serge Goldman, R. -I. Ernestus, K. Bockhorst, M. Eis, T. Els, M. Hoehn-Berlage, M. Gliese, R. Fründ, A. Geissler, C. Woertgen, M. Holzschuh, O. Hausmann, A. Merlo, E. Jerrnann, J. Uirich, R. Chiquet-Ehrismann, J. Müller, H. Mäcke, O. Gratzl, K. Herholz, M. Ghaemi, M. Würker, U. Pietrzyk, W. -D. Heiss, K. Kotitschke, M. Brandl, J. C. Tonn, A. Haase, S. Muigg, S. Felber, M. Woydt, Heinrich Lanfermann, Walter Heindel, Harald Kugel, Ralf -Ingo Erneslus, Gabricle Röhn, Klaus Lackner, F. S. Pardo, S. Kutke, A. G. Sorensen, L. L. Mechtler, S. Withiam-Lench, K. Shin, W. R. Klnkel, M. 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Cancer Research ,Neurology ,Oncology ,Neurology (clinical) - Published
- 1994
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4. Clinical Efficacy of Plasma-Exchange in Patients with Progressive forms of Multiple Sclerosis and NMO-Spectrum Disease
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P, Petrou, primary, Hur T, Ben, additional, Dembinsky A, Vaknin, additional, O, Abramsky, additional, and D, Karussis, additional
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5. [256 scientific ties between Jews and Germans, Israel and Germany from the 20th century until today Conference held in Jerusalem on November 17th 2008]
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O, Abramsky
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Germany ,Jews ,Science ,Interpersonal Relations ,Congresses as Topic ,History, 20th Century ,Israel ,History, 21st Century - Published
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6. Natalizumab plus interferon beta-1a reduces lesion formation in relapsing multiple sclerosis
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Ernst Wilhelm, Radue, William, H. Stuart, Peter, A. Calabresi, Christian, Confavreux, Steven, L. Galetta, Richard, A. Rudick, Fred, D. Lublin, Bianca, Weinstock Guttman, Daniel, R. Wynn, Elizabeth, Fisher, Athina, Papadopoulou, Frances, Lynn, Michael, A. Panzara, Alfred, W. Sandrock, For, the SENTINEL Investigators including F. Fazekas, Enzinger, C., Seifert, T., Storch, M., Strasser Fuchs, S., Berger, T., Dilitz, E., Egg, R., Deisenhammer, F., Decoo, D, Lampaert, J., Bartholome, E., Bier, J., Stenager, E., Rasmussen, M., Binzer, M., Shorsh, K., Christensen, M., Ravnborg, M., Soelberg Sørensen, P., Blinkenberg, M., Petersen, B., Hansen, H. J., Bech, E., Petersen, T., Kirkegaard, M., Finland:, J. Eralinna, Ruutiainen, J., Soilu Hänninen, M., Säkö, E., Laaksonen, M., Reunanen, M., Remes, A., Keskinarkaus, I., Moreau, T., Noblet, M., Rouaud, O., Couvreur, G., Edan, G., Lepage, E., Drapier, S., De Burghgraeve, V., Yaouanq, J., Merienne, M., Cahagne, V., Gout, O., Deschamps, R., Le Canuet, P., Moulignier, A., Vermersch, P., De Seze, J., Stojkovic, T., Griffié, G., Engles, Ferriby, D., Debouverie, M., Pittion Vouyouvitch, S., Lacour, J. C., Pelletier, J., Feuillet, L., Suchet, L., Dalecky, A., Tammam, D., Lubetzki, C., Youssov, K., Mrejen, S., Charles, P., Yaici, S., Clavelou, P., Aufauvre, D., Renouil Guy, N., Cesaro, P., Degos, F., Benisty, S., Rumbach, L., Decavel, P., Confavreux, C., Blanc, S., Aubertin, P., Riche, G., Brochet, B., Ouallet, J. C., Anne, O., Menck, S., Grupe, Guttman, Lensch, E., Fucik, E., Heitmann, S., Hartung, H. P., Schröter, M., Kurz, F. M. W., Heidenreich, F., Trebst, C., Pul, R., Hohlfeld, R., Krumbholz, M., Pellkofer, H., Haas, J., Segert, A., Meyer, R., Anagnostou, P., Kabus, C., Poehlau, D., Schneider, K., Hoffmann, V., Zettl, U., Steinhagen, V., Adler, S., Steinbrecher E. Rothenfusser Körber, A. Steinbrecher E. Rothenfusser Körber, Zellner, Baum, K., Günther, A., Bläsing, H., Stoll, G., Gold, R., Bayas, A., Kleinschnitz, C., Limmroth, V., Katsarava, Z., Kastrup, O., Haller, P., Stoeve, S., Höbel, D., Oschmann, P., Voigt, K., Burger, C. V., Israel:, O. Abramsky, Karusiss, D., Achiron, A., Kishner, I., Stern, Y., Sarove Pinhas, I., Dolev, M., Magalashvili, D., Pozzili, : C., Lenzi, D., Scontrini, A., Millefiorini, E., Buttinelli, C., Gallo, P., Ranzato, F., Tiberio, M., Perini, P., Laroni, Alice, Marrosu, M., Cocco P. Marchi, E. Cocco P. Marchi, Spinicci, G., Massole, S., Mascia, M., Floris, G., Trojano, M., Bellacosa, A., Paolicelli, D., Bosco Zimatore, G., Simone, I. L., Giorelli, M., Di Monte, E., Mancardi, GIOVANNI LUIGI, Pizzorno, M., Murialdo, A., Narciso, E., Capello, A., Comi, G., Martinelli, V., Rodegher, M., Esposito, F., Colombo, B., Rossi, P., Polman, C. H., Jasperse, M. M. S., Zwemmer, J. N. P., Nielsen, J., Kragt, J. J., Jongen, P. J. H., De Smet, E., Tacken, H., Frequin, S. T. F. M., Siegers, H. P., Mauser, H. W., Fernandez Fernandez, O., León, A., Romero, F., Alonso, A., Tamayo, J., Montalban, X., Nos, C., Pelayo, R., Tellez, N., Rio, J., Tintore, M., Arbizu, T., Romero, L., Moral, E., Martinez, S., Switzerland:, L. Kappos, Achtnichts, L., Wilmes, S., Turkey:, R. Karabudak, Kurne, A., Erdem, S., Siva, A., Saip, S., Altintas, A., Atamer, A., Eraksoy, M., Bilgili, F., Topcular, B., Giovannoni, G., Lim, E. T., Lava, N., Murnane, M., Dentinger, M., Zimmerman, E., Reiss, M., Gupta, V., Scott, T., Brillman, J., Kunschner, L., Wright, D., Perel, A., Babu, A., Rivera, V., Killian, J., Hutton, G., Lai, E., Picone, M., Cadivid, D., Kamin, S., Shanawani, M., Gauthier, S., Morgan, A., Buckle, G., Margolin, D., Weinstock Guttman, B., Kwen, P. L., Garg, N., Munschauer, F., Khatri, B., Rassouli, M., Saxena, V., Ahmed, A., Turner, A., Fox, E., Couch, C., Tyler, R., Horvit, A., Fodor, P., Humphries, S., Wynn, D., Nagar, C., O'Brien, D., Allen, N., Turel, A., Friedenberg, S., Carlson, J., Hosey, J., Crayton, H., Richert, J., Tornatore, C., Sirdofsky, M., Greenstein, J., Shpigel, Y., Mandel, S., Adbelhak, T., Schmerler, M., Zadikoff, C., Rorick, M., Reed, R., Elias, S., Feit, H., Angus, E., Sripathi, N., Herbert, J., Kiprovski, K., Qu, X., Del Bene, M., Mattson, D., Hingtgen, C., Fleck, J., Horak, H., Javerbaum, J., Elmore, R., Garcia, E., Tasch, E., Gruener, G., Celesia, G., Chawla, J., Miller, A., Drexler, E., Keilson, M., Wolintz, R., Drasby, E., Muscat, P., Belden, J., Sullivan, R., Cohen, J., Stone, L., Marrie, R. A., Fox, R., Hughes, B., Babikian, P., Jacoby, M., Doro, J., Puricelli, M., Rossman, H., Boudoris, W., Belkin, M., Pierce, R., Eggenberger, E., Birbeck, G., Martin, J., Kaufman, D., Stuart, W., English, J. B., Stuart, D. S., Gilbert, R. W., Kaufman, M., Putman, S., Diedrich, A., Follmer, R., Pelletier, D., Waubant, E., Cree, B., Genain, C., Goodin, D., Guarnaccia, J., Patwa, H., Rizo, M., Kitaj, M., Blevins, J., Smith, T., Mcgee, F., Honeycutt, W., Brown, M., Isa, A., Nieves Quinones, D., Krupp, L., Smiroldo, J., Zarif, M., Perkins, C., Sumner, A., Fisher, A., Gutierrez, Jacoby, R., Svoboda, S., Dorn, D., Groeschel, A., Steingo, B., Kishner, R., Cohen, B., Melen, O., Simuni, T., Zee, P., Cohan, S., Yerby, M., Hendin, B., Levine, T., Tamm, H., Travis, L. H., Freedman, S. M., Tim, R., Ferrell, W., Stefoski, D., Stevens, S., Katsamakis, G., Topel, J., Ko, M., Gelber, D., Fortin, C., Green, B., Logan, W., Carpenter, D., Temple, L., Sadiq, S., Sylvester, A., Sim, G., Mihai, C., Vertino, M., Jubelt, B., Mejico, L., Phillips, J. T., Martin, A., Heitzman, D., Greenfield, C. F., Riskind, P., Cabo, A., Paskavitz, J., Moonis, M., Bashir J. Brockington, K. Bashir J. Brockington, Nicholas, A., Slaughter, R., Archer S. Harik, R. Archer S. Harik, Haddad, N., Pippenger, M. A., Van den Noort, S., Thai, G., Olek, M., Demetriou, M., Shin, R., Calabresi, P., Rus, H., Bever, C., Johnson, K., Sheremata, W., Delgado, S., Sherbert, R., Herndon, R., Uschmann, H., Chandler, A., Markowitz, C., Jacobs, D., Balcer, L., Mitchell, G., Chakravorty, S., Heyman, R., Stauber, Z., Goodman, A., Segal, B., Schwid, S., Samkoff, L., Levin, M., Jacewicz, M., Menkes, D., Pulsinelli, W., Frohman, E., Racke, M., Hawker, K., Ulrich, R., Panitch, H., Hamill, R., Tandon, R., Dulaney, E., Simnad, V., Miller, J., Wooten, G. F., Harrison, M., Bowen, J., Doherty, M., Wundes, A., Garden, G. A., Distad, J., Kachuck, N., Berkovich, R., Burnett, M., Sahai, S., Bandari, D., Weiner, L., Storey, J. R., Beesley, B., Hart, D., Moses, H., Sriram, S., Fang, J., O'Duffy, A., Kita, M., Taylor, L., Elliott, M., Roberts, J., Jeffery, D., Maxwell, S., Lefkowitz, D., Kumar, S., Sinclair, M., Neurology, and NCA - Multiple Sclerosis and Other Neuroinflammatory Diseases
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Adult ,Male ,medicine.medical_specialty ,Multiple Sclerosis ,Adolescent ,Relapsing-Remitting ,Placebo ,Antibodies, Monoclonal, Humanized ,Gastroenterology ,Antibodies ,Central nervous system disease ,Pharmacotherapy ,Natalizumab ,Multiple Sclerosis, Relapsing-Remitting ,pathology/therapy ,Drug Therapy ,Internal medicine ,Monoclonal ,Medicine ,Humans ,Immunologic Factors ,Humanized ,medicine.diagnostic_test ,business.industry ,Multiple sclerosis ,Patient Selection ,Interferon beta-1a ,Antibodies, Monoclonal ,Brain ,Magnetic resonance imaging ,Interferon-beta ,Middle Aged ,medicine.disease ,Magnetic Resonance Imaging ,Surgery ,Treatment Outcome ,Neurology ,therapeutic use ,Combination ,Drug Therapy, Combination ,pathology ,Female ,Neurology (clinical) ,Adolescent, Adult, Antibodies ,Humanized, Antibodies ,therapeutic use, Brain ,pathology, Drug Therapy ,Combination, Female, Humans, Immunologic Factors ,therapeutic use, Interferon-beta ,therapeutic use, Magnetic Resonance Imaging, Male, Middle Aged, Multiple Sclerosis ,pathology/therapy, Patient Selection, Treatment Outcome ,business ,medicine.drug - Abstract
The SENTINEL study showed that the addition of natalizumab improved outcomes for patients with relapsing multiple sclerosis (MS) who had experienced disease activity while receiving interferon beta-1a (IFNbeta-1a) alone. Previously unreported secondary and tertiary magnetic resonance imaging (MRI) measures are presented here. Patients received natalizumab 300 mg (n=589) or placebo (n=582) intravenously every 4 weeks plus IFNbeta-1a 30 microg intramuscularly once weekly. Annual MRI scans allowed comparison of a range of MRI end points versus baseline. Over 2 years, 67% of patients receiving natalizumab plus IFNbeta-1a remained free of new or enlarging T2-lesions compared with 30% of patients receiving IFNbeta-1a alone. The mean change from baseline in T2 lesion volume over 2 years decreased in patients receiving natalizumab plus IFNbeta-1a and increased in those receiving IFNbeta-1a alone (-277.5mm(3) versus 525.6mm(3); p0.001). Compared with IFNbeta-1a alone, add-on natalizumab therapy resulted in a smaller increase in mean T1-hypointense lesion volume after 2 years (1821.3mm(3) versus 2210.5mm(3); p0.001), a smaller mean number of new T1-hypointense lesions over 2 years (2.3 versus 4.1; p0.001), and a slower rate of brain atrophy during the second year of therapy (-0.31% versus -0.40%; p=0.020). Natalizumab add-on therapy reduced gadolinium-enhancing, T1-hypointense, and T2 MRI lesion activity and slowed brain atrophy progression in patients with relapsing MS who experienced disease activity despite treatment with IFNbeta-1a alone.
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- 2010
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7. Oral laquinimod in patients with relapsing-remitting multiple sclerosis: 36-week double-blind active extension of the multi-centre, randomized, double-blind, parallel-group placebo-controlled study
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G, Comi, O, Abramsky, T, Arbizu, A, Boyko, R, Gold, E, Havrdová, S, Komoly, K, Selmaj, B, Sharrack, M, Filippi, R, Vuotto, Comi, Giancarlo, Abramsky, O, Arbizu, T, Boyko, A, Gold, R, Havrdova, E, Komoly, S, Selmaj, K, Sharrack, B, and Filippi, Massimo
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medicine.medical_specialty ,Placebo-controlled study ,Administration, Oral ,Quinolones ,Placebo ,Central nervous system disease ,Disability Evaluation ,chemistry.chemical_compound ,Multiple Sclerosis, Relapsing-Remitting ,Double-Blind Method ,Oral administration ,Internal medicine ,medicine ,Humans ,Immunologic Factors ,In patient ,business.industry ,Multiple sclerosis ,Brain ,medicine.disease ,Magnetic Resonance Imaging ,Surgery ,Neurology ,Relapsing remitting ,chemistry ,Neurology (clinical) ,business ,Laquinimod - Abstract
Background: Laquinimod, an oral novel immunomodulator, was shown to reduce MRI-measured disease activity in relapsing—remitting MS (RRMS) patients. Objectives: To determine whether the safety and efficacy profile of laquinimod, as shown in a placebo-controlled 36-week trial (LAQ/5062), is sustained and reproducible. Methods: Two hundred and fifty seven patients entered the extension phase in which MRI was performed at the beginning and at the end of the active extension phase. Clinical assessments were performed at weeks 4, 12 and every 12 weeks thereafter. Results: Two hundred and thirty nine (93%) patients completed the extension phase and 222 (86.3%) had a final scan available. Gadolinium-enhanced (GdE) T1 lesions were significantly reduced for patients switching from placebo to 0.3/ 0.6 mg doses (52%, p = 0.0006). In patients initially randomized to 0.6 mg in LAQ/5062 the reduction of MRI activity observed in the placebo-controlled phase was maintained in the extension. The proportion of GdE-free patients for those who switched from placebo increased from a baseline of 31% to 47% at the end of the extension phase ( p = 0.01). The most prominent safety signal was elevations of liver enzymes, reversible in all cases. Conclusions: The good efficacy and the excellent safety and tolerability profiles of laquinimod 0.6 mg/day are confirmed in this extension study.
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- 2010
8. Prevention of experimental autoimmune encephalomyelitis and induction of tolerance with acute immunosuppression followed by syngeneic bone marrow transplantation
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D M Karussis, S Slavin, D Lehmann, R Mizrachi-Koll, O Abramsky, and A Ben-Nun
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Immunology ,Immunology and Allergy - Abstract
Experimental autoimmune encephalomyelitis (EAE) is an inducible autoimmune disease widely used as a model of the acute/relapsing stage of multiple sclerosis. In the present study we examined the effect of acute immunosuppression induced by total body irradiation (TBI) (900 to 1100 centigray (cGy)) or by a single high dose of cyclophosphamide (CY) (300 mg/kg), followed by syngeneic bone marrow transplantation (SBMT), on the development of EAE in SJL/J mice. EAE was induced in SJL/J mice by immunization with spinal cord homogenate in adjuvant. Treatment with TBI (900 cGy) and SBMT on day 6 postimmunization caused a delayed onset and a marked reduction in the incidence and severity of EAE. A higher dose of irradiation (1100 cGy) or the administration of CY followed by SBMT completely abrogated the development of paralysis. None of the 21 mice treated with CY and SBMT, and only 1 of 7 mice treated with TBI (1100 cGy) and SBMT developed clinical signs of EAE during a period of 3 months. Furthermore, mice treated with CY and SBMT became resistant to rechallenge with the same encephalitogenic inoculum. In addition, the lymphocytes obtained from these mice did not proliferate in vitro in response to myelin basic protein or tuberculin-purified protein derivative, unlike lymphocytes from immunized but untreated animals. This absence of reactivity was not associated with alterations in the proportion of the L3T4 and Lyt-2 T-cell subsets nor with a loss in T cell competence as evidenced by the full response of lymphocytes to the T cell mitogen Con A and to a nonrelevant Ag (OVA). Our results indicate that the elimination of effector lymphocytes either by myeloablative doses of CY or ionizing irradiation followed by rescue with SBMT inhibits the development of the autoimmune process in EAE and leads to induction of tolerance to the immunizing Ag by newly developing lymphocytes. This approach of combining immunoablation and reconstitution with autologous bone marrow transplantation may be applicable in the treatment of life-threatening neurologic autoimmune diseases.
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- 1992
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9. Expression of alpha-smooth muscle actin in murine bone marrow stromal cells
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Amnon Peled, O. Abramsky, Elias Shezen, Dov Zipori, and Haim Ovadia
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Pathology ,medicine.medical_specialty ,Stromal cell ,Population ,Blotting, Western ,Immunology ,Radioimmunoassay ,Fluorescent Antibody Technique ,Bone Marrow Cells ,Biology ,Biochemistry ,Cell Line ,Immunoenzyme Techniques ,Mice ,Bone Marrow ,medicine ,Animals ,Vimentin ,education ,Actin ,education.field_of_study ,Hematopoietic Tissue ,Antibodies, Monoclonal ,Muscle, Smooth ,Cell Biology ,Hematology ,Actins ,Cell biology ,Clone Cells ,Haematopoiesis ,medicine.anatomical_structure ,Cell culture ,Bone marrow ,Myofibroblast - Abstract
Human fibrotic bone marrow (BM) stroma has been shown to contain alpha- smooth muscle actin (alpha-SMA)-positive cells. These closely resemble myofibroblasts that were described in other fibrotic tissues. We studied the expression of alpha-SMA in a series of murine BM-derived stromal cell lines to investigate the cellular origin and functional significance of myofibroblast-like cells in hematopoietic tissues. Although these cell lines differed in their biologic properties, most of them expressed alpha-SMA under certain conditions. Cells expressing alpha-SMA constituted a minor population in post-confluent, growth- arrested cultures. However, the incidence of cells expressing alpha-SMA increased significantly when cultures were transferred to nonconfluent conditions. A similar increase in alpha-SMA-positive cells occurred after a strip of cells was scraped away from the confluent cell layer; the cells of the affected area acquired alpha-SMA-positive contractile phenotype. The relationship between alpha-SMA expression and hematopoietic activity was studied using a cloned cell line of BM origin (14F1.1). The ability of these endothelial-adipocyte cells to support hematopoiesis in vitro was maximal under confluent conditions, whereas their expression of alpha-SMA under such conditions was residual. Moreover, in long-term BM cultures supported by confluent 14F1.1 cells, stromal areas associated with proliferating hematopoietic precursors, known as “cobblestone areas,” were devoid of alpha-SMA- positive cells. These observations suggest that the expression of alpha- SMA is reversible and inversely related to hematopoietic activity.
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- 1991
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10. The incidence and significance of anti-natalizumab antibodies: results from AFFIRM and SENTINEL
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Calabresi, Pa, Giovannoni, G, Confavreux, C, Galetta, Sl, Havrdova, E, Hutchinson, M, Kappos, L, Miller, Dh, O'Connor, Pw, Phillips, Jt, Polman, Ch, Radue, Ew, Rudick, Ra, Stuart, Wh, Lublin, Fd, Wajgt, A, Weinstock Guttman, B, Wynn, Dr, Lynn, F, Panzara, Ma, Affirm, Investigators, Fazekas, SENTINEL Investigators including: F., Enzinger, C., Seifert, T., Storch, M., Strasser Fuchs, S., Berger, T., Dilitz, E., Egg, R., Eisenhammer, F., Decoo J. Lampaert, D. Decoo J. Lampaert, Bartholome J. Bier, E. Bartholome J. Bier, Stenager, E., Rasmussen, M., Binzer, M., Shorsh, K., Christensen, M., Ravnborg, M., Soelberg Sørensen, P., Blinkenberg, M., Petersen, B., Hansen, H. J., Bech, E., Petersen, T., Kirkegaard, M., Eralinna, J., Ruutiainen, J., Soilu Hänninen, M., Säkö, E., Laaksonen, M., Reunanen, M., Remes, A., Keskinarkaus, I., Moreau, T., Noblet, M., Rouaud, O., Couvreur, G., Edan, G., Lepage, E., Drapier, S., De Burghgraeve, V., Yaouanq, J., Merienne, M., Cahagne, V., Gout, O., Deschamps, R., Le Canuet, P., Moulignier, A., Vermersch, P., De Seze, J., Stojkovic, T., Griffié, G., Engles, A., Ferriby, D., Debouverie, M., Pittionvouyouvitch, S., Lacour, J. C., Pelletier, J., Feuillet, L., Suchet, L., Dalecky, A., Tammam, D., Lubetzki, C., Youssov, K., Mrejen, S., Charles, P., Yaici, S., Clavelou, P., Aufauvre, D., Renouil Guy, N., Cesaro, P., Degos, F., Benisty, S., Rumbach P. Decavel, L. Rumbach P. Decavel, Confavreux, C., Blanc, S., Aubertin, P., Riche, G., Brochet, B., Ouallet, J. C., Anne, O., Menck, S., Grupe, A., Guttman, E., Lensch, E., Fucik, E., Heitmann, S., Hartung, H. P., Schröter, M., Kurz, F. M. W., Heidenreich, F., Trebst, C., Pul, R., Hohlfeld, R., Krumbholz, M., Pellkofer, H., Haas, J., Segert, A., Meyer, R., Anagnostou, P., Kabus, C., Poehlau, D., Schneider, K., Hoffmann, V., Zettl, U., Steinhagen, V., Adler, S., Steinbrecher, A., Rothenfusser Körber, E., Zellner, R., Baum, K., Günther, A., Bläsing, H., Stoll, G., Gold, R., Bayas, A., Kleinschnitz, C., Limmroth, V., Katsarava, Z., Kastrup, O., Haller, P., Stoeve, S., Höbel, D., Oschmann, P., Voigt, K., Burger, C. V., Abramsky D. Karusiss, O. Abramsky D. Karusiss, Achiron, A., Kishner, I., Stern, Y., Sarove Pinhas, I., Dolev, M., Magalashvili, D., Pozzili, C., Lenzi, D., Scontrini, A., Millefiorini, E., Buttinelli, C., Gallo, P., Ranzato, F., Tiberio, M., Perini, P., Laroni, Alice, Marrosu, M., Cocco P. Marchi, E. Cocco P. Marchi, Spinicci, G., Massole, S., Mascia, M., Floris, G., Trojano, M., Bellacosa, A., Paolicelli, D., Bosco Zimatore, G., Simone, I. L., Giorelli, M., Di Monte, E., Mancardi, GIOVANNI LUIGI, Pizzorno, M., Murialdo, A., Narciso, E., Capello, A., Comi, G., Martinelli, V., Rodegher, M., Esposito, F., Colombo, B., Rossi, P., Polman, C. H., Jasperse, M. M. S., Zwemmer, J. N. P., Nielsen, J., Kragt, J. J., Jongen, P. J. H., De Smet, E., Tacken, H., Frequin, S. T. F. M., Siegers, H. P., Mauser, H. W., Fern ez Fern ez, O., León, A., Romero, F., Alonso, A., Tamayo, J., Montalban, X., Nos, C., Pelayo, R., Tellez, N., Rio, J., Tintore, M., Arbizu, T., Romero, L., Moral, E., Martinez, S., Kappos, L., Achtnichts, L., Wilmes, S., Karabudak, R., Kurne, A., Erdem, S., Siva, A., Saip, S., Altintas, A., Atamer, A., Eraksoy, M., Bilgili, F., Topcular, B., Giovannoni ET Lim, G. Giovannoni E. T. Lim, Lava, N., Murnane, M., Dentinger, M., Zimmerman, E., Reiss V. Gupta, M. Reiss V. Gupta, Scott, T., Brillman, J., Kunschner, L., Wright, D., Perel A. Babu, A. Perel A. Babu, Rivera, V., Killian, J., Hutton, G., Lai, E., Picone, M., Cadivid, D., Kamin, S., Shanawani, M., Gauthier, S., Morgan, A., Buckle, G., Margolin, D., Weinstock Guttman, B., Kwen, P. L., Garg, N., Munschauer, F., Khatri, B., Rassouli, M., Saxena, V., Ahmed, A., Turner, A., Fox, E., Couch, C., Tyler, R., Horvit, A., Fodor S. Humphries, P. Fodor S. Humphries, Wynn, D., Nagar, C., O’Brien, D., Allen, N., Turel, A., Friedenberg, S., Carlson, J., Hosey, J., Crayton, H., Richert, J., Tornatore, C., Sirdofsky, M., Greenstein, J., Shpigel, Y., S. M, El, Adbelhak, T., Schmerler, M., Zadikoff, C., Rorick, M., Reed, R., Elias, S., Feit, H., Angus, E., Sripathi, N., Herbert, J., Kiprovski, K., Qu, X., Del Bene, M., Mattson, D., Hingtgen, C., Fleck, J., Horak, H., Kaiser, J. Javerbaum, Elmore, R., Garcia, E., Tasch, E., Gruener, G., Celesia, G., Chawla, J., Miller, A., Drexler, E., Keilson, M., Wolintz, R., Drasby, E., Muscat, P., Belden, J., Sullivan, R., Cohen, J., Stone, L., Marrie, R. A., Fox, R., Hughes, B., Babikian, P., Jacoby, M., Doro, J., Puricelli, M., Rossman, H., Boudoris, W., Belkin, M., Pierce, R., Eggenberger, E., Birbeck, G., Martin, J., Kaufman, D., Stuart, W., English, J. B., Stuart, D. S., Gilbert, R. W., Kaufman, M., Putman, S., Diedrich, A., Follmer, R., Pelletier, D., Waubant, E., Cree, B., Genain, C., Goodin, D., Guarnaccia, J., Patwa, H., Rizo, M., Kitaj, M., Blevins, J., Smith, T., Mcgee, F., Honeycutt, W., Brown, M., Isa, A., Nieves Quinones, D., Krupp, L., Smiroldo, J., Zarif, M., Perkins, C., Sumner, A., Fisher, A., Gutierrez, A., Jacoby, R., Svoboda, S., Dorn, D., Groeschel, A., Steingo R. Kishner, B. Steingo R. Kishner, Cohen, B., Melen, O., Simuni, T., Zee, P., Cohan M. Yerby, S. Cohan M. Yerby, Hendin, B., Levine, T., Tamm, H., Travis, L. H., Freedman, S. M., Tim, R., Ferrell, W., Stefoski, D., Stevens, S., Katsamakis, G., Topel, J., KoD Gelber C. Fortin, M. K. o. D. Gelber C. Fortin, Green, B., Logan, W., Carpenter, D., Temple, L., Sadiq, S., Sylvester, A., Sim, G., Mihai, C., Vertino, M., Jubelt, B., Mejico, L., Phillips, J. T., Martin, A., Heitzman, D., Greenfield, C. F., Riskind, P., Cabo, A., Paskavitz, J., Moonis, M., Bashir, K., Brockington, J., Nicholas, A., Slaughter, R., Archer, R., Harik, S., Haddad, N., Pippenger, M. A., Van den Noort, S., Thai, G., Olek, M., Demetriou, M., Shin, R., Calabresi, P., Rus, H., Bever, C., Johnson, K., Sheremata, W., Delgado, S., Sherbert, R., Herndon, R., Uschmann, H., Ch ler, A., Markowitz, C., Jacobs, D., Balcer, L., Mitchell, G., Chakravorty, S., Heyman, R., Stauber, Z., Goodman, A., Segal, B., Schwid, S., Samkoff, L., Levin, M., Jacewicz, M., Menkes, D., Pulsinelli, W., Frohman, E., Racke, M., Hawker, K., Ulrich, R., Panitch, H., Hamill, R., R. T, On, Dulaney, E., Simnad, V., Miller, J., Wooten, G. F., Harrison, M., Bowen, J., Doherty, M., Wundes, A., Garden, G. A., Distad, J., Kachuck, N., Berkovich, R., Burnett, M., Sahai, S., Ari, D. B, Weiner, L., Storey, J. R., Beesley, B., Hart, D., Moses, H., Sriram, S., Fang, J., O’Duffy, A., Kita, M., Taylor, L., Elliott, M., Roberts, J., Jeffery, D., Maxwell, S., Lefkowitz, D., Kumar, S., Sinclair EW Radue, M. S. i. n. c. l. a. i. r. E. W. Radue, de Vera, A., Bacelar, O., Kuster, P., and Kappos, L. .
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medicine.medical_specialty ,Multiple Sclerosis ,Enzyme-Linked Immunosorbent Assay ,Relapsing-Remitting ,Antibodies, Monoclonal, Humanized ,Gastroenterology ,Antibodies ,law.invention ,Disability Evaluation ,Natalizumab ,Multiple Sclerosis, Relapsing-Remitting ,Randomized controlled trial ,Double-Blind Method ,law ,Antibody Specificity ,Internal medicine ,Monoclonal ,medicine ,Secondary Prevention ,Humans ,Adverse effect ,Antibodies, Blocking ,Humanized ,Antibodies, Monoclonal ,Brain ,Flow Cytometry ,Interferon-beta ,Magnetic Resonance Imaging ,Placebo Effect ,Treatment Outcome ,Neuroscience (all) ,Expanded Disability Status Scale ,business.industry ,Multiple sclerosis ,Incidence (epidemiology) ,Interferon beta-1a ,medicine.disease ,Blocking ,Multiple sclerosis functional composite ,Immunology ,Neurology (clinical) ,business ,medicine.drug - Abstract
Objective: To determine the incidence and clinical effects of antibodies that develop during treatment with natalizumab. Methods: In two randomized, double-blind, placebo-controlled studies (natalizumab safety and efficacy in relapsing remitting multiple sclerosis [MS, AFFIRM] and safety and efficacy of natalizumab in combination with interferon β-1a [INFβ1a] in patients with relapsing remitting MS [SENTINEL]) of patients with relapsing multiple sclerosis, blood samples were obtained at baseline and every 12 weeks to determine the presence of antibodies against natalizumab. Antibodies to natalizumab were measured using an ELISA. Patients were categorized as “transiently positive” if they had detectable antibodies (≥0.5 μg/mL) at a single time point or “persistently positive” if they had antibodies at two or more time points ≥6 weeks apart. Results: In the AFFIRM study, antibodies were detected in 57 of 625 (9%) of natalizumab-treated patients: Twenty (3%) were transiently positive and 37 (6%) were persistently positive. Persistently positive patients showed a loss of clinical efficacy as measured by disability progression ( p ≤ 0.05), relapse rate ( p = 0.009), and MRI ( p ≤ 0.05) compared with antibody-negative patients. In transiently positive patients, full efficacy was achieved after approximately 6 months of treatment, the time when patients were becoming antibody negative. The incidence of infusion-related adverse events was significantly higher in persistently positive patients. Results of SENTINEL were similar to AFFIRM, except with regard to sustained disability progression; differences between persistently positive and antibody-negative patients were not statistically significant. Conclusions: The incidence of persistent antibody positivity associated with natalizumab is 6%. Reduced clinical efficacy is apparent in persistently positive patients. Patients with a suboptimal clinical response or persistent infusion-related adverse events should be considered for antibody testing. GLOSSARY: BLQ = below the limit of quantification; EDSS = Expanded Disability Status Scale; Gd+ = gadolinium enhancing; IFNβ1a = interferon β-1a; MS = multiple sclerosis; MSFC = multiple sclerosis functional composite; OD = optical density.
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- 2007
11. The incidence and significance of anti-natalizumab antibodies. Results from the AFFIRM and SENTINEL
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Calabresi, Pa, Giovannoni, G, Confavreux, C, Galetta, Sl, Havrdova, E, Hutchinson, M, Kappos, L, Miller, Dh, O'Connor, Pw, Phillips, Jt, Polman, Ch, Radue, Ew, Rudick, Ra, Stuart, Wh, Lublin, Fd, Wajgt, A, Weinstock Guttman, B, Wynn, Dr, Lynn, F, Panzara, Ma, Fazekas, The following investigators participated in the SENTINEL study: F., Enzinger, * C., Seifert, T., Storch, M., Strasser Fuchs, S., Berger, T., Dilitz, * E., Egg, R., Deisenhammer, F., Lampaert, D. Decoo* J., Bier, E. Bartholome* J., Stenager, Denmark: E., Rasmussen, * M., Binzer, M., Ravnborg, M., Soelberg Sørensen, * P., Blinkenberg, M., Petersen, B., Hansen, H. J., Bech, * E., Petersen, T., Kirkegaard, M., Eralinna, J., Ruutiainen, * J., Soilu Hänninen, M., Reunanen, M., Remes, * A., Keskinarkaus, I., Moreau, T., Noblet, * M., Rouaud, O., Couvreur, G., Edan, G., Lepage, * E., Drapier, S., De Burghgraeve, V., Yaouanq, J., Gout, O., Deschamps, * R., Le Canuet, P., Moulignier, A., Vermersch, P., De Seze, * J., Stojkovic, T., Griffié, G., Engles, A., Ferriby, D., Debouverie, M., Pittion Vouyouvitch, * S., Lacour, J. C., Pelletier, J., Feuillet, * L., Suchet, L., Dalecky, A., Tammam, D., Lubetzki, C., Youssov, * K., Mrejen, S., Charles, P., Yaici, S., Clavelou, P., Aufauvre, * D., Renouil Guy, N., Cesaro, P., Degos, * F., Benisty, S., Decavel, L. Rumbach* P., Confavreux, C., Blanc, * S., Aubertin, P., Riche, G., Brochet, B., Ouallet, * J. C., Anne, O., Menck, S., Grupe, * A., Guttman, E., Lensch, E., Fucik, * E., Heitmann, S., Hartung, H. P., Schröter, * M., Kurz, F. M. W., Heidenreich, F., Trebst, * C., Pul, R., Hohlfeld, R., Krumbholz, * M., Pellkofer, H., Haas, J., Segert, * A., Meyer, R., Anagnostou, P., Kabus, C., Poehlau, D., Schneider, * K., Hoffmann, V., Zettl, U., Steinhagen, * V., Adler, S., Steinbrecher, A., Rothenfusser Körber, * E., Zellner, R., Baum, K., Günther, * A., Bläsing, H., Stoll, G., Gold, * R., Bayas, * A., Kleinschnitz, C., Limmroth, V., Katsarava, * Z., Kastrup, O., Haller, P., Stoeve, * S., Höbel, D., Oschmann, P., Voigt, * K., Burger, C. V., Karusiss, O. Abramsky* D., Achiron, A., Kishner, * I., Stern, Y., Sarove Pinhas, I., Dolev, M., Magalashvili, D., Pozzili, C., Lenzi, * D., Scontrini, A., Millefiorini, E., Buttinelli, C., Gallo, Paolo, Ranzato, * F., Tiberio, M., Perini, P., Laroni, A., Marrosu, M., Marchi, * E. Cocco P., Spinicci, G., Massole, S., Mascia, M., Floris, G., Trojano, M., Bellacosa, * A., Paolicelli, D., Bosco Zimatore, G., Simone, I. L., Giorelli, M., Di Monte, E., Mancardi, G., Pizzorno, * M., Murialdo, A., Narciso, E., Capello, A., Comi, G., Martinelli, * V., Rodegher, M., Esposito, F., Colombo, B., Rossi, P., Polman, C. H., Jasperse, * M. M. S., Zwemmer, J. N. P., Nielsen, J., Kragt, J. J., Jongen, P. J. H., De Smet, * E., Tacken, H., Frequin, S. T. F. M., Siegers, * H. P., Mauser, H. W., Fernandez Fernandez, O., León, * A., Romero, F., Alonso, A., Tamayo, J., Montalban, X., Nos, * C., Pelayo, R., Tellez, N., Rio, J., Tintore, M., Arbizu, T., Romero, * L., Moral, E., Martinez, S., Kappos, L., Achtnichts, * L., Wilmes, S., Karabudak, R., Kurne, * A., Erdem, S., Siva, A., Saip, * S., Altintas, A., Atamer, A., Eraksoy, M., Bilgili, * F., Topcular, B., Lim, G. Giovannoni* E. T., Lava, N., Murnane, * M., Dentinger, M., Zimmerman, E., Gupta, M. Reiss* V., Scott, T., Brillman, * J., Kunschner, L., Wright, D., Babu, A. Perel* A., Rivera, V., Killian, * J., Hutton, G., Lai, E., Picone, Bernard W. M., Cadivid, * D., Kamin, S., Shanawani, M., Gauthier, S., Morgan, * A., Buckle, G., Margolin, D., Weinstock Guttman, B., Kwen, * P. L., Garg, N., Munschauer, F., Khatri, B., Rassouli, * M., Saxena, V., Ahmed, A., Turner, A., Fox, E., Couch, * C., Tyler, R., Horvit, A., Humphries, P. Fodor* S., Wynn, D., Nagar, * C., O’Brien, D., Allen, N., Turel, A., Friedenberg, * S., Carlson, J., Hosey, J., Crayton, H., Richert, * J., Tornatore, C., Sirdofsky, M., Greenstein, J., Shpigel, * Y., Mandel, S., Adbelhak, T., Schmerler, M., Zadikoff, * C., Rorick, M., Reed, R., Elias, S., Feit, * H., Angus, E., Sripathi, N., Herbert, J., Kiprovski, * K., Qu, X., Del Bene, M., Mattson, D., Hingtgen, * C., Fleck, J., Horak, H., Javerbaum, J., Elmore, * R., Garcia, E., Tasch, E., Gruener, G., Celesia, * G., Chawla, J., Miller, A., Drexler, * E., Keilson, M., Wolintz, R., Drasby, E., Muscat, * P., Belden, J., Sullivan, R., Cohen, J., Stone, * L., Marrie, R. A., Fox, R., Hughes, B., Babikian, * P., Jacoby, M., Doro, J., Puricelli, M., Rossman, H., Boudoris, * W., Belkin, M., Pierce, R., Eggenberger, E., Birbeck, * G., Martin, J., Kaufman, D., Stuart, W., English, * J. B., Stuart, D. S., Gilbert, R. W., Kaufman, MS M., Putman, . *. S., Diedrich, A., Follmer, R., Pelletier, D., Waubant, * E., Cree, B., Genain, C., Goodin, D., Guarnaccia, J., Patwa, * H., Rizo, M., Kitaj, M., Blevins, Neurolo J., Smith, * T., Mcgee, F., Honeycutt, W., Brown, * M., Isa, A., Nieves Quinones, D., Krupp, L., Smiroldo, * J., Zarif, M., Perkins, C., Sumner, A., Fisher, A., Gutierrez, A., Jacoby, R., Svoboda, * S., Dorn, D., Groeschel, A., Kishner, B. Steingo* R., Cohen, B., Melen, * O., Simuni, T., Zee, P., Yerby, S. Cohan* M., Hendin, B., Levine, * T., Tamm, H., Travis, L. H., Freedman, S. M., Tim, * R., Ferrell, W., Stefoski, D., Stevens, * S., Katsamakis, G., Topel, J., Ko, M., Fortin, D. Gelber* C., Green, B., Logan, * W., Carpenter, D., Temple, L., Sadiq, S., Sylvester, * A., Sim, G., Mihai, C., Vertino, * M., Jubelt, B., Mejico, L., Phillips, J. T., Martin, * A., Heitzman, D., Greenfield, C. F., Riskind, P., Cabo, * A., Paskavitz, J., Moonis, M., Bashir, K., Brockington, * J., Nicholas, A., Slaughter, R., Archer, R., Harik, * S., Haddad, N., Pippenger, M. A., Van den Noort, S., Thai, * G., Olek, M., Demetriou, M., Shin, R., Cala bresi, * P., Rus, H., Bever, C., Johnson, K., Sheremata, W., Delgado, * S., Sherbert, R., Herndon, R., Uschmann, * H., Chandler, A., Markowitz, C., Jacobs, * D., Balcer, L., Mitchell, G., Chakra vorty, * S., Heyman, R., Stauber, Z., Goodman, A., Segal, * B., Schwid, S., Samkoff, L., Levin, M., Jacewicz, * M., Menkes, D., Pulsinelli, W., Frohman, E., Racke, * M., Hawker, K., Ulrich, R., Panitch, H., Hamill, * R., Tandon, R., Dulaney, E., Simnad, V., Miller, * J., Wooten, G. F., Harrison, M., Bowen, J., Doherty, * M., Wundes, A., Garden, G. A., Distad, J., Kachuck, N., Berkovich, * R., Burnett, M., Sahai, S., Bandari, D., Weiner, L., Storey, J. R., Beesley, * B., Hart, D., Moses, H., Sriram, * S., Fang, J., O’Duffy, A., Kita, M., Taylor, * L., Elliott, M., Roberts, J., Jeffery, D., Maxwell, * S., Lefkowitz, D., Kumar, S., and Sinclair, M.
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- 2007
12. Occurrence of CNS demyelinating disease in patients with myasthenia gravis
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M. Gotkine, Y. Fellig, and O. Abramsky
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Adult ,Aged, 80 and over ,Male ,Adolescent ,Brain ,Demyelinating Autoimmune Diseases, CNS ,Middle Aged ,Magnetic Resonance Imaging ,Spinal Cord ,Myasthenia Gravis ,Humans ,Female ,Neurology (clinical) ,Child ,Aged ,Retrospective Studies - Abstract
An increased incidence of multiple sclerosis (MS) has been reported in patients with myasthenia gravis (MG). We reviewed records of 214 patients with MG. CNS demyelinating disease (CNSDD) occurred in five patients (2.3%). CNSDD always occurred after the diagnosis of MG. Myelitis (including recurrent myelitis) was the most common CNS manifestation. All patients had antinuclear antibodies. CNSDD occurs more frequently in patients with MG and may be related to immune-modulating treatments including thymectomy.
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- 2006
13. Natalizumab plus interferon beta-1a for relapsing multiple sclerosis
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Richard, A. Rudick, William, H. Stuart, Peter, A. Calabresi, Christian, Confavreux, Steven, L. Galetta, Ernst Wilhelm, Radue, Fred, D. Lublin, Bianca, Weinstock Guttman, Daniel, R. Wynn, Frances, Lynn, Msc, M. S. c., Michael, A. Panzara, Alfred, W. Sandrock, For, the SENTINEL Investigators including: F. Fazekas, Enzinger, C., Seifert, T., Storch, M., Strasser Fuchs, S., Berger, T., Dilitz, E., Egg, R., Eisenhammer, F., Decoo J. Lampaert, D. Decoo J. Lampaert, Bartholome J. Bier, E. Bartholome J. Bier, Stenager, E., Rasmussen, M., Binzer, M., Shorsh, K., Christensen, M., Ravnborg, M., Soelberg Sørensen, P., Blinkenberg, M., Petersen, B., Hansen, H. J., Bech, E., Petersen, T., Kirkegaard, M., Eralinna, J., Ruutiainen, J., Soilu Hänninen, M., Säkö, E., Laaksonen, M., Reunanen, M., Remes, A., Keskinarkaus, I., Moreau, T., Noblet, M., Rouaud, O., Couvreur, G., Edan, G., Lepage, E., Drapier, S., De Burghgraeve, V., Yaouanq, J., Merienne, M., Cahagne, V., Gout, O., Deschamps, R., Le Canuet, P., Moulignier, A., Vermersch, P., De Seze, J., Stojkovic, T., Griffié, G., Engles, A., Ferriby, D., Debouverie, M., Pittionvouyouvitch, S., Lacour, J. C., Pelletier, J., Feuillet, L., Suchet, L., Dalecky, A., Tammam, D., Lubetzki, C., Youssov, K., Mrejen, S., Charles, P., Yaici, S., Clavelou, P., Aufauvre, D., Renouil Guy, N., Cesaro, P., Degos, F., Benisty, S., Rumbach P. Decavel, L. Rumbach P. Decavel, Confavreux, C., Blanc, S., Aubertin, P., Riche, G., Brochet, B., Ouallet, J. C., Anne, O., Menck, S., Grupe, A., Guttman, E., Lensch, E., Fucik, E., Heitmann, S., Hartung, H. P., Schröter, M., Kurz, F. M. W., Heidenreich, F., Trebst, C., Pul, R., Hohlfeld, R., Krumbholz, M., Pellkofer, H., Haas, J., Segert, A., Meyer, R., Anagnostou, P., Kabus, C., Poehlau, D., Schneider, K., Hoffmann, V., Zettl, U., Steinhagen, V., Adler, S., Steinbrecher, A., Rothenfusser Körber, E., Zellner, R., Baum, K., Günther, A., Bläsing, H., Stoll, G., Gold, R., Bayas, A., Kleinschnitz, C., Limmroth, V., Katsarava, Z., Kastrup, O., Haller, P., Stoeve, S., Höbel, D., Oschmann, P., Voigt, K., Burger, C. V., Abramsky D. Karusiss, O. Abramsky D. Karusiss, Achiron, A., Kishner, I., Stern, Y., Sarove Pinhas, I., Dolev, M., Magalashvili, D., Pozzili, C., Lenzi, D., Scontrini, A., Millefiorini, E., Buttinelli, C., Gallo, P., Ranzato, F., Tiberio, M., Perini, P., Laroni, Alice, Marrosu, M., Cocco P. Marchi, E. Cocco P. Marchi, Spinicci, G., Massole, S., Mascia, M., Floris, G., Trojano, M., Bellacosa, A., Paolicelli, D., Bosco Zimatore, G., Simone, I. L., Giorelli, M., Di Monte, E., Mancardi, GIOVANNI LUIGI, Pizzorno, M., Murialdo, A., Narciso, E., Capello, A., Comi, G., Martinelli, V., Rodegher, M., Esposito, F., Colombo, B., Rossi, P., Polman, C. H., Jasperse, M. M. S., Zwemmer, J. N. P., Nielsen, J., Kragt, J. J., Jongen, P. J. H., De Smet, E., Tacken, H., Frequin, S. T. F. M., Siegers, H. P., Mauser, H. W., Fern ez Fern ez, O., León, A., Romero, F., Alonso, A., Tamayo, J., Montalban, X., Nos, C., Pelayo, R., Tellez, N., Rio, J., Tintore, M., Arbizu, T., Romero, L., Moral, E., Martinez, S., Kappos, L., Achtnichts, L., Wilmes, S., Karabudak, R., Kurne, A., Erdem, S., Siva, A., Saip, S., Altintas, A., Atamer, A., Eraksoy, M., Bilgili, F., Topcular, B., Giovannoni ET Lim, G. Giovannoni E. T. Lim, Lava, N., Murnane, M., Dentinger, M., Zimmerman, E., Reiss V. Gupta, M. Reiss V. Gupta, Scott, T., Brillman, J., Kunschner, L., Wright, D., Perel A. Babu, A. Perel A. Babu, Rivera, V., Killian, J., Hutton, G., Lai, E., Picone, M., Cadivid, D., Kamin, S., Shanawani, M., Gauthier, S., Morgan, A., Buckle, G., Margolin, D., Weinstock Guttman, B., Kwen, P. L., Garg, N., Munschauer, F., Khatri, B., Rassouli, M., Saxena, V., Ahmed, A., Turner, A., Fox, E., Couch, C., Tyler, R., Horvit, A., Fodor S. Humphries, P. Fodor S. Humphries, Wynn, D., Nagar, C., O’Brien, D., Allen, N., Turel, A., Friedenberg, S., Carlson, J., Hosey, J., Crayton, H., Richert, J., Tornatore, C., Sirdofsky, M., Greenstein, J., Shpigel, Y., S. M, El, Adbelhak, T., Schmerler, M., Zadikoff, C., Rorick, M., Reed, R., Elias, S., Feit, H., Angus, E., Sripathi, N., Herbert, J., Kiprovski, K., Qu, X., Del Bene, M., Mattson, D., Hingtgen, C., Fleck, J., Horak, H., Kaiser, J. Javerbaum, Elmore, R., Garcia, E., Tasch, E., Gruener, G., Celesia, G., Chawla, J., Miller, A., Drexler, E., Keilson, M., Wolintz, R., Drasby, E., Muscat, P., Belden, J., Sullivan, R., Cohen, J., Stone, L., Marrie, R. A., Fox, R., Hughes, B., Babikian, P., Jacoby, M., Doro, J., Puricelli, M., Rossman, H., Boudoris, W., Belkin, M., Pierce, R., Eggenberger, E., Birbeck, G., Martin, J., Kaufman, D., Stuart, W., English, J. B., Stuart, D. S., Gilbert, R. W., Kaufman, M., Putman, S., Diedrich, A., Follmer, R., Pelletier, D., Waubant, E., Cree, B., Genain, C., Goodin, D., Guarnaccia, J., Patwa, H., Rizo, M., Kitaj, M., Blevins, J., Smith, T., Mcgee, F., Honeycutt, W., Brown, M., Isa, A., Nieves Quinones, D., Krupp, L., Smiroldo, J., Zarif, M., Perkins, C., Sumner, A., Fisher, A., Gutierrez, A., Jacoby, R., Svoboda, S., Dorn, D., Groeschel, A., Steingo R. Kishner, B. Steingo R. Kishner, Cohen, B., Melen, O., Simuni, T., Zee, P., Cohan M. Yerby, S. Cohan M. Yerby, Hendin, B., Levine, T., Tamm, H., Travis, L. H., Freedman, S. M., Tim, R., Ferrell, W., Stefoski, D., Stevens, S., Katsamakis, G., Topel, J., KoD Gelber C. Fortin, M. K. o. D. Gelber C. Fortin, Green, B., Logan, W., Carpenter, D., Temple, L., Sadiq, S., Sylvester, A., Sim, G., Mihai, C., Vertino, M., Jubelt, B., Mejico, L., Phillips, J. T., Martin, A., Heitzman, D., Greenfield, C. F., Riskind, P., Cabo, A., Paskavitz, J., Moonis, M., Bashir, K., Brockington, J., Nicholas, A., Slaughter, R., Archer, R., Harik, S., Haddad, N., Pippenger, M. A., Van den Noort, S., Thai, G., Olek, M., Demetriou, M., Shin, R., Calabresi, P., Rus, H., Bever, C., Johnson, K., Sheremata, W., Delgado, S., Sherbert, R., Herndon, R., Uschmann, H., Ch ler, A., Markowitz, C., Jacobs, D., Balcer, L., Mitchell, G., Chakravorty, S., Heyman, R., Stauber, Z., Goodman, A., Segal, B., Schwid, S., Samkoff, L., Levin, M., Jacewicz, M., Menkes, D., Pulsinelli, W., Frohman, E., Racke, M., Hawker, K., Ulrich, R., Panitch, H., Hamill, R., R. T, On, Dulaney, E., Simnad, V., Miller, J., Wooten, G. F., Harrison, M., Bowen, J., Doherty, M., Wundes, A., Garden, G. A., Distad, J., Kachuck, N., Berkovich, R., Burnett, M., Sahai, S., Ari, D. B, Weiner, L., Storey, J. R., Beesley, B., Hart, D., Moses, H., Sriram, S., Fang, J., O’Duffy, A., Kita, M., Taylor, L., Elliott, M., Roberts, J., Jeffery, D., Maxwell, S., Lefkowitz, D., Kumar, S., Sinclair EW Radue, M. S. i. n. c. l. a. i. r. E. W. Radue, de Vera, A., Bacelar, O., Kuster, P., and Kappos, L. .
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Adult ,Male ,Infusions ,medicine.medical_specialty ,Multiple Sclerosis ,Adolescent ,Combination therapy ,Integrin alpha4 ,Peripheral edema ,Progressive Multifocal ,Relapsing-Remitting ,Gastroenterology ,Antibodies ,Natalizumab ,Drug Therapy ,Leukoencephalopathy ,Internal medicine ,Monoclonal ,Secondary Prevention ,medicine ,Humans ,Humanized ,Proportional Hazards Models ,Expanded Disability Status Scale ,business.industry ,Antibodies, Monoclonal ,Antibodies, Monoclonal, Humanized ,Brain ,Cell Adhesion Molecules ,Disease Progression ,Drug Therapy, Combination ,Female ,Infusions, Intravenous ,Interferon-beta ,JC Virus ,Leukoencephalopathy, Progressive Multifocal ,Middle Aged ,Multiple Sclerosis, Relapsing-Remitting ,Medicine (all) ,Progressive multifocal leukoencephalopathy ,Multiple sclerosis ,Hazard ratio ,Interferon beta-1a ,General Medicine ,medicine.disease ,Surgery ,Combination ,medicine.symptom ,Intravenous ,business ,medicine.drug - Abstract
Background Interferon beta is used to modify the course of relapsing multiple sclerosis. Despite interferon beta therapy, many patients have relapses. Natalizumab, an α 4 integrin antagonist, appeared to be safe and effective alone and when added to interferon beta-1a in preliminary studies. Methods We randomly assigned 1171 patients who, despite interferon beta-1a therapy, had had at least one relapse during the 12-month period before randomization to receive continued interferon beta-1a in combination with 300 mg of natalizumab (589 patients) or placebo (582 patients) intravenously every 4 weeks for up to 116 weeks. The primary end points were the rate of clinical relapse at 1 year and the cumulative probability of disability progression sustained for 12 weeks, as measured by the Expanded Disability Status Scale, at 2 years. Results Combination therapy resulted in a 24 percent reduction in the relative risk of sustained disability progression (hazard ratio, 0.76; 95 percent confidence interval, 0.61 to 0.96; P = 0.02). Kaplan–Meier estimates of the cumulative probability of progression at two years were 23 percent with combination therapy and 29 percent with interferon beta-1a alone. Combination therapy was associated with a lower annualized rate of relapse over a two-year period than was interferon beta-1a alone (0.34 vs. 0.75, P
- Published
- 2006
14. Randomized study of once-weekly interferon beta-1la therapy in relapsing multiple sclerosis: three-year data from the OWIMS study
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Gordon S. Francis, Jean Pelletier, Pierre Duquette, Patrick O'Connor, Mark S. Freedman, G. Comi, O Abramsky, F O'Brien, E Acm Sanders, Luanne M. Metz, G Pa Rice, J-P Bouchard, and T J Murray
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Oncology ,Adult ,Male ,medicine.medical_specialty ,Pathology ,Placebo ,Antibodies ,law.invention ,Central nervous system disease ,03 medical and health sciences ,0302 clinical medicine ,Multiple Sclerosis, Relapsing-Remitting ,Randomized controlled trial ,Adjuvants, Immunologic ,Interferon ,law ,Internal medicine ,medicine ,Humans ,030212 general & internal medicine ,medicine.diagnostic_test ,business.industry ,Multiple sclerosis ,Interferon beta-1a ,Magnetic resonance imaging ,Interferon-beta ,medicine.disease ,Magnetic Resonance Imaging ,Clinical trial ,Treatment Outcome ,Neurology ,Female ,Neurology (clinical) ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Background: Once weekly interferon β-1a for multiple sclerosis (OWIMS) demonstrated modest, but significant, magnetic resonance imaging (MRI) benefit of once-weekly (qw) interferon (IFN) β-1a at 48 weeks, but no significant effect on relapses. Objective: An OWIMS extension permitted assessment of longer-term efficacy/safety of qw IFN β-1a in relapsing-remitting multiple sclerosis (RRMS). Methods: Placebo patients were rerandomized to IFN β-1a, 22 or 44 mcg qw, for two additional 48-week intervals. Primary outcome was MRI lesion activity. Relapse rate and other MRI measures were secondary outcomes. Results: After three years, median (mean) T2 lesion count/patient/scan was 1.3 (2.6) for 44 mcg, 1.7 (3.3) for 22 mcg, 1.7 (3.4) for placebo/22 mcg, 2.0 (3.6) for placebo/44 mcg (all differences not significant). Annualized relapse rates were lowest for 44 mcg (0.77) versus other groups (0.83-0.86, not significant). Persistent neutralizing antibodies did not affect relapse rates, but MRI active lesions were increased in antibody-positive patients receiving 44 mcg compared to antibody negative patients. Conclusions: In RRMS, once weekly IFN β-1a, particularly 44 mcg, can induce a significant MRI, but not relapse, effect, compared with placebo. No significant dose effect was seen. In contrast to the significant effect observed with three-times-weekly dosing of subcutaneous IFN β-1a compared with placebo, this study confirms the lack of meaningful clinical benefit with once-weekly dosing.
- Published
- 2005
15. The Ras-pathway inhibitor, S-trans-trans-farnesylthiosalicylic acid, suppresses experimental allergic encephalomyelitis
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H Niv, Nikolaos Grigoriadis, O Abramsky, R Mizrachi-Koll, Dimitrios Karussis, Yoel Kloog, and Joab Chapman
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Proteolipid protein 1 ,Encephalomyelitis, Autoimmune, Experimental ,Encephalomyelitis ,medicine.medical_treatment ,Immunology ,Down-Regulation ,Lymphocyte proliferation ,Biology ,Pharmacology ,Lymphocyte Activation ,Drug Administration Schedule ,Mice ,Downregulation and upregulation ,Antigen ,medicine ,Immunology and Allergy ,Animals ,Paralysis ,Lymphocytes ,Enzyme Inhibitors ,Receptor ,Cells, Cultured ,Myelin Sheath ,Dose-Response Relationship, Drug ,Experimental autoimmune encephalomyelitis ,Immunosuppression ,medicine.disease ,Farnesol ,Salicylates ,Survival Rate ,Treatment Outcome ,Neurology ,Antigens, Surface ,ras Proteins ,Female ,Neurology (clinical) ,Cell Division ,Myelin Proteins - Abstract
Aim: To evaluate the effects of the synthetic Ras-pathway inhibitor, S-trans-trans-farnesylthiosalicylic acid (FTS) on acute and chronic experimental autoimmune encephalomyelitis (EAE and CR-EAE). Background: Treatment of EAE and MS is based on immunosuppression aiming at downregulation of the proliferating myelin-reactive lymphocytes. One of the pathways of lymphocyte activation involves the GTP-binding protein Ras. FTS destabilizes the attachment of Ras to the cell membrane, resulting in an inhibition of the Ras-mediated signal transduction pathways. Materials and methods: EAE was induced in SJL/J mice by immunization with spinal cord homogenate (MSCH) in adjuvant and two i.v. boosts of pertussis antigen and CR-EAE with passive transfer of proteolipid protein (PLP)-activated lymphocytes. Animals were treated daily starting either from the day of EAE-induction (or cell transfer) or at a later stage, with i.p. injections of FTS (5 mg/kg/day). The clinical severity of the disease was evaluated daily and scored using a 0–6 scale. Results: In six separate experiments, 27 of the 38 (71.7%) vehicle-treated animals developed clinical signs of EAE compared to 17/38 (44.7%) of the FTS-treated mice (p=0.02, t-test). The maximal average score in the control group was 2.94±2.2, whereas in the FTS group it was significantly lower (1.63±2.2, p=0.01). Mortality was 26.3% and 10.5% in the two groups, respectively (p=0.03). When treatment was initiated at a later stage, just before the onset of the clinical signs, the protective effect was even more pronounced. A significant suppression of clinical signs was also observed in the CR-EAE model (p=0.02). Lymphocyte proliferation assays demonstrated a more than twofold decrease in the reactivity to myelin antigens (MBP and PLP) and downregulation of the activated lymphocytes (expressing the CD62L, and IA-k-MHC Class I markers and the Vb17 T-cell receptor) in the FTS-treated group; in vitro FTS suppressed the Ras activity of lymphocytes and inhibited the proliferative ability of the lymphocytes in a dose-dependent manner. Conclusions: FTS suppresses EAE by downregulation of myelin-reactive activated T-lymphocytes. Since FTS did not induce generalized immunosuppressive effects, it may offer significant advantages over the broad immunosuppressive modalities and may be a candidate treatment for autoimmune diseases, such as MS.
- Published
- 2001
16. Inhibition of nitric oxide production for down-regulation of CNS inflammation and demyelination
- Author
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T, Brenner, F, Pinto, O, Abramsky, and R, Gallily
- Subjects
Neuritis ,Central Nervous System Diseases ,Animals ,Down-Regulation ,Nitric Oxide ,Demyelinating Diseases - Published
- 2001
17. [Paraneoplastic autoimmune syndromes of the nervous system]
- Author
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A, Ashkenazi, H, Ovadia, and O, Abramsky
- Subjects
Lambert-Eaton Myasthenic Syndrome ,Humans ,Paraneoplastic Cerebellar Degeneration ,Autoantibodies ,Autoimmune Diseases - Published
- 2001
18. Evidence for the genetic role of human leukocyte antigens in low frequency DRB1*1501 multiple sclerosis patients in Israel
- Author
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A, Karni, Y, Kohn, C, Safirman, O, Abramsky, L, Barcellos, J R, Oksenberg, E, Kahana, D, Karussis, J, Chapman, and C, Brautbar
- Subjects
Multiple Sclerosis ,HLA-DR Antigens ,HLA-DQ alpha-Chains ,Linkage Disequilibrium ,Medical Records ,Nuclear Family ,Haplotypes ,HLA Antigens ,HLA-DQ Antigens ,HLA-DQ beta-Chains ,Humans ,Family ,Israel ,Lod Score ,Alleles ,HLA-DRB1 Chains - Abstract
A strong association exists between multiple sclerosis (MS) and the DRB1*1501 haplotype, in most populations. Linkage of Multiple Sclerosis (MS) with the MHC or HLA region on chromosome 6p21 has previously been observed in DRB1*1501 positive MS families. A group of 13 Israeli multiplex MS families with a very low frequency of DRB1*1501 haplotype were examined in this study. Association and a linkage test were performed in order to identify a non-DRB1*1501 effect of HLA on susceptibility for MS. MS multiplex families and healthy controls were molecularly typed for six highly polymorphic markers located within the MHC region: DRB1, DQA1 and DQB1, BAT-2, MIB and D6S248. Data analyses included: (a) an association study comparing the patient group with both healthy relative, and healthy control groups (b) a transmission test for linkage disequilibrium (TDT) of the MS-associated alleles in the multiplex families, and (c) multipoint non-parametric linkage (NPL) and parametric LOD score analyses using the GENEHUNTER program. The DRB1*1303 allele was significantly more frequent among the MS patients. There was a trend towards transmission disequilibrium of DRB1*1303, but was not statistically significant. Allele sharing and LOD score analyses revealed no evidence for linkage. The high frequency of DRB1*1303 observed in our family patients provides evidence to support the association with this allele that previously described in sporadic non-Ashkenazi MS patients. Thus, DRB1*1303 may serve as genetic risk factor for MS. Our study exemplifies the genetic heterogeneity in MS as there is a genetic effect of HLA on MS susceptibility in our low frequency DRB1*1501 patients.
- Published
- 2000
19. Immunosuppressive and Immunomodulating Therapeutic Approaches for Induction of Self-Tolerance in Experimental Autoimmune Encephalomyelitis (EAE and CR-EAE) and Multiple Sclerosis
- Author
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D. Karussis and O. Abramsky
- Subjects
business.industry ,Multiple sclerosis ,Self Tolerance ,Experimental autoimmune encephalomyelitis ,Immunology ,medicine ,medicine.disease ,business - Published
- 1999
- Full Text
- View/download PDF
20. Occurrence of CNS demyelinating disease in patients with myasthenia gravis
- Author
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B. G. Weinshenker, A. Jacob, I. Kister, J. Herbert, M. L. Swerdlow, R. Bergamaschi, G. Piccolo, J. Oger, K. Ikeda, Y. Araki, Y. Iwasaki, I . Kister, J . Herbert, M .L. Swerdlow, R . Bergamaschi, G . Piccolo, J . Oger, M. Gotkine, and O. Abramsky
- Subjects
medicine.medical_specialty ,Anti-nuclear antibody ,business.industry ,Incidence (epidemiology) ,medicine.medical_treatment ,Multiple sclerosis ,Central nervous system ,Myelitis ,Retrospective cohort study ,medicine.disease ,Gastroenterology ,Myasthenia gravis ,Thymectomy ,medicine.anatomical_structure ,Internal medicine ,Immunology ,Medicine ,Neurology (clinical) ,business - Abstract
An increased incidence of multiple sclerosis (MS) has been reported in patients with myasthenia gravis (MG). We reviewed records of 214 patients with MG. CNS demyelinating disease (CNSDD) occurred in five patients (2.3%). CNSDD always occurred after the diagnosis of MG. Myelitis (including recurrent myelitis) was the most common CNS manifestation. All patients had antinuclear antibodies. CNSDD occurs more frequently in patients with MG and may be related to immune-modulating treatments including thymectomy.
- Published
- 2007
- Full Text
- View/download PDF
21. Control of stroma-dependent hematopoiesis by basic fibroblast growth factor: stromal phenotypic plasticity and modified myelopoietic functions
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D, Sternberg, A, Peled, E, Shezen, O, Abramsky, W, Jiang, F, Bertolero, and D, Zipori
- Subjects
Cytoskeletal Proteins ,Extracellular Matrix Proteins ,Mice ,Phenotype ,Adipocytes ,Animals ,Bone Marrow Cells ,Fibroblast Growth Factor 2 ,Stromal Cells ,Hematopoietic Stem Cells ,Cell Line ,Hematopoiesis - Abstract
It has been suggested that basic fibroblast growth factor (bFGF) affects hematopoietic cells directly and that it may also act indirectly by modulating stromal cell functions. We tested the response of phenotypically and functionally distinct stromal cell clones to this cytokine. We studied cell phenotype, the composition and organization of cytoskeleton and extracellular matrix, the ability to repopulate 'wounded areas', the expression of cytokine genes, and the capacity of the stroma to support long-term hematopoiesis in vitro. Although the impact of bFGF on cell growth was small, it induced a prominent morphological change in three stromal cell types that we tested. We analyzed the molecular basis for this change: bFGF modified the protein expression of alpha-smooth muscle actin (alpha-SMA), tropomyosin, alpha-tubulin, fibronectin and paxillin in a distinct manner characteristic of each of the stromal cell types. Immunofluorescence analysis of these proteins revealed profound changes in the cytoskeleton and extracellular matrix (ECM) networks accompanied by increased ability of the 14F1.1 stromal cells to scatter in in vitro 'wounded' areas. Furthermore, although only limited changes were monitored in the expression of cytokine genes, the ability of the stromal cells to support hematopoiesis was markedly modified. Thus bFGF profoundly changes the cellular organization of stromal cells, their adhesion and their motility properties. These changes are associated with modified capacity to support hematopoiesis in culture.
- Published
- 1996
22. Creutzfeldt-Jakob disease
- Author
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J, Jacobs, O, Abramsky, and R, Gabison
- Subjects
Carrier State ,Humans ,Transfusion Reaction ,Blood Donors ,Creutzfeldt-Jakob Syndrome - Published
- 1996
23. Immunomodulation of autoimmunity in MRL/lpr mice with syngeneic bone marrow transplantation (SBMT)
- Author
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U Vourka-Karussis, Dimitrios Karussis, O Abramsky, A. Ben-Nun, Dan Lehmann, and S Slavin
- Subjects
Male ,Pathology ,medicine.medical_specialty ,Cyclophosphamide ,Lymphoid Tissue ,medicine.medical_treatment ,Immunology ,Autoimmunity ,Kidney ,Autoimmune Diseases ,Mice ,immune system diseases ,medicine ,Immunology and Allergy ,Animals ,Lupus Erythematosus, Systemic ,Bone Marrow Transplantation ,Autoimmune disease ,Lupus erythematosus ,business.industry ,Immunosuppression ,Total body irradiation ,Syngeneic Bone Marrow Transplantation ,medicine.disease ,Survival Analysis ,Mice, Mutant Strains ,Transplantation ,Proteinuria ,medicine.anatomical_structure ,surgical procedures, operative ,Antibodies, Antinuclear ,Female ,Bone marrow ,business ,medicine.drug ,Research Article - Abstract
SUMMARY MRL-lpr/lpr mice spontaneously develop a severe autoimmune syndrome, characterized by massive generalized lymphadenopathy, arthritis, arteritis, dermatitis and immune complex-mediated glomerulonephritis. Bone marrow transplantation (BMT) from MHC-matched systemic lupus erythematosus (SLE)-resistant donors to susceptible recipients has proved effective in correcting autoimmune manifestations in autoimmune-prone mice. We investigated the effect of syngeneic BMT from MRL/lpr (donor) to immunocompromised MRL/lpr (recipient), after purging the bone marrow inoculum with MoAbs against mature T cells (anti-Thy 1.2). All the untreated mice developed lymphadenopathy and by the age of 36 weeks five of the eight were dead; in contrast, all the mice which underwent syngeneic BMT following acute immunosuppression with total body irradiation (900 cGy) (TBI) remained disease-free. In an additional experiment, it was found that conditioning with cyclophosphamide (CY) before BMT was more effective than TBI in inhibiting delayed-onset autoimmune manifestations (mean survival 350 days in the CY group and 305 days in the TBI group, versus 197 days in untreated controls). Under both immunosuppressive regimens T cell-depleted bone marrow grafts produced far better results than did unmanipulated BMT. Following syngeneic BMT the incidence of proteinuria and the level of serum anti-DNA (dd) antibodies were significantly reduced, compared with that of the age-matched untreated controls. CY was more effective than TBI in reducing the anti-DNA titres. Likewise. T depletion of bone marrow inocula before BMT induced a more drastic drop in autoantibodies, following both CY and TBI conditioning protocols. After syngeneic BMT (either CY or TBI) no signs of lymphadenopathy were observed even at an advanced age. Upon histopathological examination, the BMT-treated mice displayed normal glomeruli with occasional minimal signs of glomerulonephritis. Syngeneic T cell-depleted BMT following acute cytoreduction of anti-self immune lymphocytes may represent a new therapeutic approach for drug-resistant autoimmune diseases.
- Published
- 1995
24. Immunomodulation of autoimmunity by linomide
- Author
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D M, Karussis, D, Lehmann, S, Slavin, T, Kalland, U, Vourka-Karussis, R, Mizrachi-Koll, H, Ovadia, and O, Abramsky
- Subjects
Mice ,Encephalomyelitis, Autoimmune, Experimental ,Adjuvants, Immunologic ,Recurrence ,Hydroxyquinolines ,Administration, Oral ,Animals ,Autoimmunity ,Killer Cells, Lymphokine-Activated ,Rats - Published
- 1995
25. Inoculation of BCL1 lymphoma cells into CSJL/J F1 mice inhibits acute experimental autoimmune encephalomyelitis
- Author
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O, Abramsky, D M, Karussis, R, Mizrachi-Koll, and D, Lehmann
- Subjects
Immunosuppression Therapy ,B-Lymphocytes ,Encephalomyelitis, Autoimmune, Experimental ,Lymphoma, B-Cell ,Vaccination ,Mice, Inbred Strains ,CD5 Antigens ,Lymphocyte Activation ,Immunotherapy, Adoptive ,Antibodies, Anti-Idiotypic ,Cell Line ,Mice ,Antigens, CD ,Acute Disease ,Animals ,Female ,Interleukin-5 ,Multiple Myeloma - Abstract
T cell vaccination, which protects rodents against experimental autoimmune encephalomyelitis (EAE), has been shown to induce anti-idiotypic response in the T cell compartment. CD5 B cells (B1 cells) are the main source of natural autoantibodies, and are often characterized by high idiotypic connectivity. In this study we examined the possibility that idiotypic connectivity in the B cell compartment may also play a role in the regulation of EAE. We inoculated CSJLF1 mice (H-2d,s) with a CD5 B cell line, the BCL1 lymphoma cells (H-2d), and subsequently induced EAE. The injection of as few as 1,000 BCL1 lymphoma cells significantly blocked the development of EAE. Injection of CD5-negative myeloma cells (SP2) had no effect on the pathogenesis of the disease. Unlike control animals, lymphocytes from BCL1 lymphoma-injected mice significantly proliferate in response to interleukin-5, a growth factor to CD5 B cells. The proliferative response of lymphocytes from BCL1 inoculated mice to mitogenic stimulation was rather unchanged, indicating that no general immunosuppression has been induced by inoculating BCLJ lymphoma. These experiments suggest that CD5 B cells may be involved in the regulation of EAE.
- Published
- 1994
26. Immunohematopoietic reconstitution by allogeneic and autologous bone marrow grafts as a means for induction of specific unresponsiveness to donor-specific allografts and modified self in autoimmune disorders
- Author
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S, Slavin, D, Karussis, L, Weiss, U, Vourka-Karussis, and O, Abramsky
- Subjects
Isoantigens ,Mice, Inbred BALB C ,Encephalomyelitis, Autoimmune, Experimental ,T-Lymphocytes ,Antibodies, Monoclonal ,Mice, Inbred Strains ,Skin Transplantation ,Hematopoietic Stem Cells ,Transplantation, Autologous ,Lymphocyte Depletion ,Mice, Inbred C57BL ,Mice ,Animals ,Transplantation, Homologous ,Crosses, Genetic ,Whole-Body Irradiation ,Bone Marrow Transplantation - Published
- 1993
27. Prolonged sleep-deprivation induced disturbed liver functions serum lipid levels, and hyperphosphatemia
- Author
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G. Glazer, Y. Ilan, Peretz Lavie, O. Abramsky, and G. Martinowitz
- Subjects
Adult ,Male ,medicine.medical_specialty ,Evening ,Time Factors ,Clinical Biochemistry ,Biology ,Biochemistry ,Phosphates ,Hyperphosphatemia ,chemistry.chemical_compound ,Internal medicine ,medicine ,Humans ,Aspartate Aminotransferases ,Apolipoproteins A ,Morning ,Hydrocortisone ,Apolipoproteins B ,Triglyceride ,Alanine Transaminase ,General Medicine ,medicine.disease ,Lipids ,Sleep deprivation ,Endocrinology ,chemistry ,Liver ,Sleep Deprivation ,Liver function ,medicine.symptom ,Lipoproteins, HDL ,Glucocorticoid ,medicine.drug - Abstract
Sixty-four healthy young male volunteers were kept awake from 76 to 80 h. Blood tests conducted at the start and conclusion of the continuous sleep deprivation revealed an increase of 170% in mean SGOT, 58.5% in mean SGPT and 37.5% in mean plasma phosphorus levels. Triglyceride levels decreased by 16%, while HDL levels increased by 18% and the apoB/apoA ratio decreased by 12%. Morning plasma cortisol showed a significant increase during the experiment while evening cortisol showed a significant decrease. Morning T3 levels increased from the first to second day and decreased on the third day. There were no significant changes in other plasma electrolyte levels.
- Published
- 1992
28. [The trimolecular complex as a target for specific immunotherapy in experimental autoimmune encephalomyelitis--applications for multiple sclerosis and other human autoimmune disease]
- Author
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A, Miller, H L, Weiner, and O, Abramsky
- Subjects
Major Histocompatibility Complex ,Encephalomyelitis, Autoimmune, Experimental ,Multiple Sclerosis ,T-Lymphocytes ,Receptors, Antigen, T-Cell ,Humans ,Immunotherapy ,Autoimmune Diseases - Published
- 1992
29. [Physicians-researchers will vanish?]
- Author
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Y, Shoenfeld, H, Boichis, and O, Abramsky
- Subjects
Physicians ,Humans ,Research Personnel ,Forecasting - Published
- 1992
30. CSF ACETYLCHOLINE RECEPTOR ANTIBODY INDEX IN MYASTHENIA GRAVIS AND CONTROLS
- Author
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O. Abramsky, Slavenka Kam-Hansen, and Hans Link
- Subjects
Neurology ,Acetylcholine receptor antibody ,business.industry ,Immunology ,medicine ,Neurology (clinical) ,General Medicine ,medicine.disease ,business ,Myasthenia gravis - Published
- 2009
- Full Text
- View/download PDF
31. Acute inflammatory demyelinating polyneuropathy following bone marrow transplantation
- Author
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S, Eliashiv, T, Brenner, O, Abramsky, R, Shahin, E, Agai, E, Naparstek, and I, Steiner
- Subjects
Adult ,Male ,Adolescent ,T-Lymphocytes ,Polyradiculoneuropathy ,Graft vs Host Disease ,Autoimmunity ,Precursor Cell Lymphoblastic Leukemia-Lymphoma ,Leukemia, Myelogenous, Chronic, BCR-ABL Positive ,Humans ,Transplantation, Homologous ,Female ,Myelin Proteins ,Bone Marrow Transplantation - Abstract
Acute inflammatory demyelinating polyneuropathy (AIDP) appeared in two patients following allogeneic bone marrow transplantation (BMT). In one transplanted patient (but not in the donor) T cells were sensitized against peripheral nervous system myelin. This could reflect a change in the T cell repertoire in a different milieu. In this context, AIDP might be part of graft-versus-host disease or another associated autoimmune disorder following BMT.
- Published
- 1991
32. Peripheral neuropathy and folate deficiency as the first sign of Crohn's disease
- Author
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A. Lossos, O. Abramsky, Z. Ackerman, and Zohar Argov
- Subjects
Adult ,Male ,Crohn's disease ,medicine.medical_specialty ,Systemic disease ,Crohn disease ,business.industry ,Intestinal biopsy ,Gastroenterology ,Peripheral Nervous System Diseases ,Disease ,Folic Acid Deficiency ,medicine.disease ,Surgery ,Peripheral neuropathy ,Serum folate ,Crohn Disease ,Internal medicine ,medicine ,Humans ,Sensory peripheral neuropathy ,business - Abstract
A 33-year-old man developed severe sensory peripheral neuropathy associated with low serum folate levels. No systemic disease was identified on the initial evaluation, but 21/2 years later he developed clinical and radiological features of Crohn's disease, confirmed by intestinal biopsy. Thus, sensory polyneuropathy may occur as the first manifestation of Crohn's disease.
- Published
- 1991
33. Development of experimental allergic encephalomyelitis during steroid administration. Outcome of neurological immune-mediated disorders under immunosuppressive therapy
- Author
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I, Steiner, T, Brenner, R, Mizrachi-Kol, and O, Abramsky
- Subjects
Disease Models, Animal ,Encephalomyelitis, Autoimmune, Experimental ,Incidence ,Animals ,Methylprednisolone ,Severity of Illness Index ,Rats - Abstract
Glucocorticoids are frequently employed as immunosuppressive agents. Following clinical reports of occurrence and exacerbation of neurological immune-mediated conditions in patients receiving steroids, we studied the course of experimental allergic encephalomyelitis (EAE) in rats receiving methylprednisolone prior to and during disease induction and after the appearance of clinical signs. High methylprednisolone dose given prior to EAE induction significantly increased disease duration and the number of days at maximal disability. When the drug was given prior to and during the induction phase, both moderate and high doses exacerbated the EAE course. In contrast, treatment with methylprednisolone after the onset of clinical disease had a markedly beneficial effect. Thus, time of initiation, dosage and duration of treatment may differentially affect the course of EAE. Moreover, the natural course of a neurological immune-mediated condition may be worsened when it is triggered while the patient is under steroid treatment.
- Published
- 1991
34. Acetylcholine receptor-reactive T and B cells in myasthenia gravis and controls
- Author
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Hans Link, O. Abramsky, G. Andersson, Tomas Olsson, O. Olsson, T. Brenner, H. P. Ekre, Wei-Zhi Wang, and J. Sun
- Subjects
Male ,Proteolipid protein 1 ,T cell ,T-Lymphocytes ,Receptors, Antigen, T-Cell ,Receptors, Antigen, B-Cell ,Receptors, Nicotinic ,Interferon-gamma ,Leukocyte Count ,Antigen ,Myasthenia Gravis ,medicine ,Humans ,Interferon gamma ,B cell ,Acetylcholine receptor ,B-Lymphocytes ,biology ,General Medicine ,medicine.disease ,Thymectomy ,Myasthenia gravis ,Immunoglobulin Isotypes ,medicine.anatomical_structure ,Immunology ,biology.protein ,Female ,Antibody ,Nervous System Diseases ,medicine.drug ,Research Article - Abstract
Myasthenia gravis (MG) is strongly associated with antibodies to acetylcholine receptor (AChR), whereas the extent of T cell involvement is not settled. The number of cells secreting interferon-gamma (IFN-gamma) in response to AChR during 48 h culture of blood mononuclear cells (PBL) may reflect AChR-reactive T cells. Using an immunospot assay, we detected such cells in 23 of 30 patients with MG at a mean number of 1 per 33.333 PBL. AChR-reactive T cells were also found in patients with other neurological diseases (OND) and in healthy subjects but at lower frequencies and numbers. The T cell response to purified protein derivative and to PHA, and also to two major myelin proteins (basic protein and proteolipid protein) did not differ between MG and the two control groups, underlining the specificity of an augmented T cell reactivity to AChR in MG. Evaluation of the B cell response by enumerating anti-AChR IgG antibody secreting cells revealed such cells in 27 of 28 patients with MG at a mean value of 1 per 14,085 PBL. Cells secreting anti-AChR antibodies of the IgA and IgM isotypes were also detected in MG, but less frequently, at lower numbers, and only in conjunction with IgG antibody secreting cells. Anti-AChR antibody secreting cells were also found among patient with OND and in healthy controls, but at lower frequencies and numbers. These data confirm that AChR is a major target for autoimmune response in MG.
- Published
- 1991
35. Effect of experimental autoimmune encephalomyelitis on pregnancy: studies in rabbits and rats
- Author
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T, Brenner, S, Evron, and O, Abramsky
- Subjects
Encephalomyelitis, Autoimmune, Experimental ,Pregnancy Outcome ,Myelin Basic Protein ,Fetal Resorption ,Autoantigens ,Autoimmune Diseases ,Rats ,Pregnancy Complications ,Pregnancy ,Animals ,Female ,Rabbits ,Fetal Death ,Autoantibodies ,Demyelinating Diseases - Abstract
The influence of experimental autoimmune encephalomyelitis (EAE) on the course and outcome of pregnancy, and the effect of pregnancy on EAE development, was investigated in rabbits and rats. Animals were immunized with encephalitogenic antigen in complete Freund's adjuvant (CFA) either before or during pregnancy. Abortion or fetal resorption was observed in most of the rabbits immunized before or during pregnancy, but not in pregnant rabbits injected with CFA or saline alone. Fetal loss was higher in those rabbits that developed clinical EAE. In rats, fetal loss occurred only when immunization was carried out during the first half of pregnancy. The appearance of EAE in pregnant rabbits, but not in rats, was delayed until after abortion or termination of pregnancy. The incidence of EAE in rabbits was lower, with milder severity and longer duration. Serum antibody levels to myelin basic protein, the autoantigen of EAE, was lower in pregnant rabbits, but not in rats, as compared to non pregnant animals. These results indicate that in species where pregnancy has a suppressive influence on the development of experimental autoimmune demyelinating disease, immunization with the neuroantigen induces a high rate of fetal loss.
- Published
- 1991
36. [Neurologic complications of primary Sjogren's syndrome]
- Author
-
D, Buskila, Y, Shoenfeld, L, Averbuch-Hiller, and O, Abramsky
- Subjects
Male ,Sjogren's Syndrome ,Central Nervous System Diseases ,Humans ,Middle Aged - Abstract
Primary Sjogren's syndrome has a wide clinical spectrum, ranging from an exocrinopathy to a systemic process and even extending to B-lymphocyte neoplasia. We describe a patient with this syndrome who developed central nervous system involvement manifested by involuntary dystonic movements of the mouth and larynx. We believe that the neurological involvement in this patient is part of his basic disease. Further studies are required to define more accurately the frequency, severity and spectrum of the neurological manifestations associated with primary Sjogren's syndrome.
- Published
- 1991
37. Autoimmune encephalomyelitis and the connection between the nervous and immune systems
- Author
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O, Abramsky, J, Weidenfeld, and H, Ovadia
- Subjects
Central Nervous System ,Neuroimmunomodulation ,Immune System ,Animals ,Humans ,Encephalomyelitis ,Autoimmune Diseases - Published
- 1990
38. Neural responses to antigenic challenges and immunomodulatory factors
- Author
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D, Saphier, H, Ovadia, and O, Abramsky
- Subjects
Male ,endocrine system ,animal structures ,Erythrocytes ,genetic structures ,Neuroimmunomodulation ,Hypothalamus ,Electroencephalography ,Preoptic Area ,Feedback ,Rats ,Thymus Hormones ,Interferon Type I ,Animals ,Antigens ,Corticosterone ,Cyclophosphamide ,Histamine ,Interleukin-1 ,Paraventricular Hypothalamic Nucleus ,Research Article - Abstract
In studies designed to examine the effects of the immune system, recordings of multi-unit electrical activity (MUA) in the central nervous system were made in the preoptic area/anterior hypothalamus (POA/AH) and paraventricular nucleus (PVN) of rats, following sheep red blood cell (SRBC) immunization. Peak increases in POA/AH MUA were observed on the fifth day following SRBC sensitization, the day on which serum antibodies were first detected. A significant increase in paraventricular nucleus (PVN) MUA was also observed on the sixth day. These changes in POA/AH and PVN MUA were found to be associated with increased plasma corticosterone levels on day 8. Induction of a second immune response to SRBC evoked a POA/AH MUA increase of extended duration but reduced amplitude, while administration of the immunosuppressive drug, cyclophosphamide, prevented both antibody generation and any increases in POA/AH MUA. These data suggest that activation of the immune system may provide signals, in the form of chemical messengers, which are able to alter neural activity in some regions of the brain that are important in neuroendocrine regulatory mechanisms. Accordingly, intracerebroventricular injections of thymic humoral factor or alpha-interferon decreased POA/AH MUA, increased EEG synchronization, and decreased plasma levels of corticosterone. Histamine and interleukin 1 did not alter POA/AH MUA but decreased EEG synchronization and increased plasma levels of corticosterone.
- Published
- 1990
39. Polyneuropathy associated with interferon beta treatment in patients with multiple sclerosis
- Author
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B. C. Kieseier, H.-P. Hartung, D. Ekstein, and O. Abramsky
- Subjects
Neurology (clinical) - Published
- 2006
- Full Text
- View/download PDF
40. Thalamic Anosognosia without Hemineglect
- Author
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D.M. Karussis, A. Lossos, Moshe Gomori, and O. Abramsky
- Subjects
medicine.medical_specialty ,business.industry ,media_common.quotation_subject ,Anosognosia ,medicine.disease ,Neglect ,Physical medicine and rehabilitation ,Neurology ,medicine ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine ,Psychiatry ,business ,Mri findings ,media_common - Abstract
We describe two patients with isolated anosognosia after right thalamic cerebrovascular accident and present the MRI findings.
- Published
- 1992
- Full Text
- View/download PDF
41. Early anticoagulation in patients with prosthetic heart valves and intracerebral hematoma
- Author
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E. F. M. Wijdicks, W. I. Schievink, R. D. Brown, C. Y. Mullany, R. R. Leker, and O. Abramsky
- Subjects
medicine.medical_specialty ,business.industry ,medicine.drug_class ,medicine.medical_treatment ,Anticoagulant ,Atrial fibrillation ,Heparin ,medicine.disease ,Surgery ,Discontinuation ,medicine.anatomical_structure ,Hematoma ,Mitral valve ,medicine ,Neurology (clinical) ,Neurosurgery ,Embolization ,business ,medicine.drug - Abstract
To the Editor: We noted with interest the article by Leker and Abramsky.1 We share their opinion that a survey of common practices in these patients might be helpful, but we are very concerned about their practice of early institution of heparin. Their article demonstrating good outcomes in four patients managed with early IV heparin was published almost simultaneously with our article in Neurosurgery .2 The conclusion of our review of 42 patients with intracranial hematomas and mechanical heart valves complements their case series. The management of these patients is complex because there are many variables that should be taken into account. Discontinuation of anticoagulation in patients with intracranial hemorrhage and a mechanical heart valve may lead to systemic embolization or valve thrombosis. The risk of embolization may be greater in patients with atrial fibrillation, caged-ball valve, mitral valve position, and the presence of reduced ventricular function. In addition, a history of emboli during low therapeutic INR values might further increase the risk of embolization when anticoagulation is discontinued. Leker and Abramsky1 correctly pointed out that no studies have addressed these dilemmas and only anecdotal cases or very small series …
- Published
- 1999
- Full Text
- View/download PDF
42. Intravenous immunoglobulin treatment in multiple sclerosis
- Author
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G. Francis, A. Achiron, Y. Barak, N. Gadoth, E. Melamed, A. Miller, I. Steiner, O. Abramsky, U. Gabbay, R. Gilad, S. Hassin-Baer, M. Gornish, A. Elizur, Y. Goldhammer, and I. Sarova-Pinhas
- Subjects
Pediatrics ,medicine.medical_specialty ,business.industry ,Multiple sclerosis ,Lesion volume ,medicine.disease ,Placebo ,Placebo group ,Lesion load ,Natural history ,Lesion ,Volume determination ,medicine ,Neurology (clinical) ,medicine.symptom ,business - Abstract
To the Editor: The report by Achiron et al.1 demonstrates the greatest reduction to date in relapse rate reported for patients with relapsing MS. This study supports data presented by Fazekas et al.2 but with an even more striking benefit. However, despite a dramatic impact on relapse rate and a trend to reduce disability, there was no impact on MRI, and in fact the score appears more favorable for the placebo than the treated patients. The reduced number of patients at year 2, particularly in the placebo group, may have contributed to this. However, the method of volume determination by the authors was unconventional and could create errors in determination of lesion volume. Has their method been cross-validated with currently accepted volume measurement methods, manual or automated?3,4 The authors state that the use of yearly T2 lesion load as an outcome measure is known to be insufficient. This statement would appear to contradict current standard practice. There are a large number of MR parameters used in following MS but the consensus for longer duration studies (greater than 6 months) is that T2 lesion burden is an appropriate outcome measure.4-6 Such analyses have demonstrated efficacy for both Betaseron7 and Rebif.8 The current authors may have intended to state that T2 lesion burden is not an appropriate outcome measure for exploratory studies, which are best analyzed using high-frequency gadolinium scanning. The fact that these scans were not performed by Achiron et al. is unfortunate but does not diminish the value of T2 lesion burden as an overall outcome in a 2-year study. The failure to find any change, particularly in the placebo group, in which every patient had attacks, is contrary to what has been found in natural history studies and in …
- Published
- 1999
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43. Suppression of experimental autoimmune encephalomyelitis (EAE) with low molecular weight heparin
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O. Abramsky, D. Karussis, and R. Mizrach-Koll
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Neurology ,Chemistry ,medicine.drug_class ,Immunology ,Experimental autoimmune encephalomyelitis ,medicine ,Immunology and Allergy ,Low molecular weight heparin ,Neurology (clinical) ,medicine.disease - Published
- 1998
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44. Epidural Anesthesia
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I. Steiner, Z. Argov, and O. Abramsky
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Neurology (clinical) - Published
- 1997
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45. The Frequency of Multiple Sclerosis in Jewish and Arab Populations in Greater Jerusalem.
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A. Karni, E. Kahana, N. Zilber, O. Abramsky, M. Alter, and D. Karussis
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MULTIPLE sclerosis ,RACIAL & ethnic attitudes ,MEDICAL imaging systems ,MAGNETIC resonance imaging - Abstract
AbstractA comparison of the incidence rate (IR) and the prevalence rate (PR) of multiple sclerosis (MS) in subgroups of the same ethnic origin, but born and living in different geographical areas, may delineate the relationship between environmental and genetic risk factors for MS. Previous epidemiological studies of MS in Israel did not include the Arab population and used diagnostic criteria that did not include MRI findings. Therefore, we studied the age-adjusted IR and PR of MS in a more recent sample in different population groups, including Arabs, of Greater Jerusalem. We found that the PR of MS in Israeli Jews is higher than previously described. Furthermore, the PR was significantly lower among immigrant Jews from Asia/Africa (A/A) than among native-born Jews of Asian/African origin (I-A/A). Since these groups have similar genetic susceptibilities to MS, the higher PR in the latter is probably due to environmental factors. Our study does not support the effect of latitude on the risk of developing MS since no difference in the PR was found between immigrant Jews from Europe/America (E/A) and native-born Jews of European/American origin (I-E/A). Among Arabs, the PR was similar to that among A/A. Therefore, we hypothesized similarity in environmental etiologic factors for MS between the countries of origin of A/A immigrants and of Arabs communities in Greater Jerusalem. The IR of I-E/A was higher than that of I-A/A and Arabs, although this difference did not reach statistical significance.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]
- Published
- 2003
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46. Treatment of acute hepatic encephalopathy with L-dopa
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G. Friedman, T. Chajek, E. M. Berry, and O. Abramsky
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Adult ,Levodopa ,Pregnancy ,business.industry ,MEDLINE ,Electroencephalography ,General Medicine ,medicine.disease ,Pregnancy Complications ,Acute hepatic failure ,Level of consciousness ,Clinical report ,Hepatic Encephalopathy ,Anesthesia ,medicine ,Humans ,Female ,business ,Hepatic encephalopathy ,Research Article ,medicine.drug - Abstract
Summary A clinical report of a 30-year-old woman who developed acute hepatic failure in the fifth month of pregnancy is presented. L-dopa administration resulted in a marked improvement in both level of consciousness and electroencephalogram. The literature dealing with L-dopa therapy in hepatic encephalopathy is reviewed.
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- 1977
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47. Chronic progressive myelopathy: its relation to the spinal progressive form of multiple sclerosis
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I. Steiner, D. Soffer, A. B. Pleet, O. Abramsky, and G. Feir
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Adult ,Male ,Pathology ,medicine.medical_specialty ,Multiple Sclerosis ,Oligoclonal IgG ,Sensation ,Immunoglobulins ,Disease course ,Diagnosis, Differential ,Muscular Atrophy, Spinal ,Myelopathy ,medicine ,Humans ,Spondylitis, Ankylosing ,Aged ,Motor Neurons ,business.industry ,Multiple sclerosis ,Oligoclonal Bands ,Retrospective cohort study ,General Medicine ,Middle Aged ,medicine.disease ,Spinal Cord ,Neurology ,Functional disability ,Immunoglobulin G ,Female ,Neurology (clinical) ,business - Abstract
— The causes and clinical features of chronic progressive myelopathy (CPM) were evaluated in a retrospective study of 107 patients. A special emphasis was put on those in whom no underlying cause for the myelopathy could be determined. Of 76 such, 39 (51%) had oligoclonal immunoglobulins (Ig) in the CSF and were therefore considered as possible MS, while the remainder, without oligoclonal Ig, were designated “myelopathy of unknown origin” (MUO). Our “possible MS” group was similar clinically to reported series of proven spinal MS, and it seems therefore, that the presence of oligoclonal Ig permits the recognition of a group of patiens with myelopathy who might be at a greater risk for MS. Patients with MUO differed from possible MS patients in several clinical characteristics, but most significantly in disease course and levels of functional disability which were more benign in the former. Myelopathy in possible MS patiens was also of a primary pyramidal and asymmetrical nature. It is therefore suggested that the segregation of patients with CPM of undetermined origin into 2 separate groups based on the presence or absence of oligoclonal Ig might be of prognostic significance.
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- 1988
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48. Evidence for the involvement of the central adrenergic system in interleukin l-induced adrenocortical response
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Haim Ovadia, O Abramsky, and Joseph Weidenfeld
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Pharmacology ,medicine.medical_specialty ,Adrenal cortex ,Antagonist ,Interleukin ,Adrenergic ,Propranolol ,Biology ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Internal medicine ,medicine ,Catecholamine ,Prazosin ,Oxidopamine ,medicine.drug - Abstract
The role of central catecholamines in the mediation of adrenocortical activation, induced by interleukin 1 (IL-1), was investigated by measuring ACTH and corticosterone in serum. Adult male rats were injected with either vehicle or the neurotoxin 6-hydroxydopamine (6-OHDA) into the lateral ventricle or the ventral noradrenergic ascending bundle. In vehicle-injected rats, 2 U of IL-1, injected intraventricularly, produced a 5- and 15-fold increase in ACTH and CS, respectively, in serum, 120 min after the injection of IL-1. In contrast, 6-OHDA, injected either intraventricularly or into the ventral noradrenergic ascending bundle, abolished the response to an intracerebral injection of IL-1. In addition, in rats pretreated with the α1-adrenergic antagonist, prazosin, IL-1 failed to activate the adrenocortical axis. In other rats pretreated with the β-adrenergic antagonist, propranolol, the adrenocortical response did not significantly differ from that of vehicle-pretreated rats. These results suggest that central adrenergic transmission, originating at the ventral noradrenergic ascending bundle and acting through α1-adrenergic receptors, is involved in the adrenocortical response to IL-1.
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- 1989
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49. Regulated expression of proenkephalin A in normal lymphocytes
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H Rosen, O Behar, O Abramsky, and H Ovadia
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Immunology ,Immunology and Allergy - Abstract
The expression of proenkephalin A (PEA), a neuropeptide-encoding gene, was examined in normal rat lymphocytes. With the use of Northern blot hybridization analysis of total RNA, PEA mRNA was found in normal cells derived from spleen, lymph nodes, and bone marrow. Cell sorting of the two main fractions of B and T cells derived from the spleen revealed that PEA is expressed in normal B cells (sIg+). The expression of PEA mRNA was markedly enhanced after a short incubation (3 h) of cells with LPS or Salmonella typhimurium. This was not the case when these cells were incubated with Con A during the same period of time; whereas, in thymocytes the presence of PEA mRNA was exclusively dependent upon mitogenic stimulus (Con A) and could be detected after 24 h of in vitro incubation. Extracts of cells were also found to contain immune reactive enkephalins, indicating that the PEA mRNA is translated. These results support the concept that neuropeptides, such as enkephalins, have a role in the modulation of the immune response and may participate in the bidirectional communication between the nervous and immune systems.
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- 1989
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50. LYMPHOCYTES SENSITISED TO BASIC ENCEPHALITOGEN IN PATIENTS WITH MULTIPLE SCLEROSIS UNRESPONSIVE TO STEROID THERAPY
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Michael Sela, Dvora Teitelbaum, O. Abramsky, Ruth Arnon, and Cynthia Webb
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Multiple Sclerosis ,Experimental allergic ,Encephalomyelitis ,In Vitro Techniques ,Lymphocyte Activation ,Autoantigens ,Autoimmune Diseases ,Immune system ,Adrenocorticotropic Hormone ,Antigen ,medicine ,Humans ,In patient ,Lymphocytes ,Cells, Cultured ,Immunity, Cellular ,business.industry ,Multiple sclerosis ,Brain ,Myelin Basic Protein ,General Medicine ,medicine.disease ,Steroid therapy ,Lymphocyte transformation ,Immunology ,Prednisone ,business - Abstract
Patients in various stages of multiple sclerosis (M.S.) were tested for peripheral-blood lymphocytes sensitised to purified basic brain encephalitogen (B.E.) by measuring specific transformation in vitro. These patients included thirteen who were having steroid therapy when tested. Lymphocyte transformation in response to B.E. was significant in five patients who, without exception, had not responded clinically to steroid therapy. The other eight patients, whose lymphocytes were not transformed by B.E., all improved markedly on steroid therapy. Fifteen patients tested when they were not receiving steroids all had negative lymphocyte-transformation tests. Included in this group were three of the five patients who responded positively after initiation of steroid treatment. Patients with other unrelated neurological disorders had negative tests whether or not they had been receiving steroid treatment at the time. Normal subjects were also negative. These findings demonstrate that some patients with M.S. show a cell-mediated immune response to the antigen which induces experimental allergic encephalomyelitis. They may also lead to new ideas on the efficacy and desirability of indiscriminate steroid therapy for patients with M.S.
- Published
- 1974
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