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2. Royal academy of medicine in Ireland international conference on homocysteine metabolism from basic science to clinical medicine: Proceedings of meeting held at Dromoland Castle, Co. Clare on July 2nd–6th, 1995
- Author
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Björkegren, K., Bergmark, C., de Faire, U., Mansoor, M. Azam, Svardal, A., Bostom, A. G., Roubenoff, R., Dellaripa, P., Nadeau, M. R., Sutherland, P., Wilson, P. W. F., Jacques, P. F., Selhub, J., Rosenberg, I. H., Bostom, A. G., Brosnan, J. T., Hall, B., Nadeau, M. R., Selhub, J., Bostom, A. G., Shemin, D., Lapane, K. L., Sutherland, P., Nadeau, M. R., Wilson, P. W. F., Selhub, J., Bostom, A. G., Shemin, D., Nadeau, M. R., Selhub, J., Bostom, A. G., Selhub, J., Jacques, P. F., Nadeau, M. R., Williams, R. R., Ellison, R. C., Cuskelly, G. J., McNulty, H., Strain, J. J., McPartlin, J. M., Scott, J. M., Chadefaux-Vekemans, B., Coudé, M., Aupetit, J., Kamoun, P., Coudé, M., Aral, B., Zabot, M. T., Aupetit, J., Kamoun, P., Chadefaux-Vekemans, B., Calaf, R., Ghiringelli, O., Barlatier, A., Charpiot, P., Rolland, P. H., Garçon, D., Charpiot, P., Augier, T., Chareyre, C., Rolland, P. H., Garçon, D., Chango, A., Hodez, F., Tronel, H., Nuel, G., Michel, F., Frémont, S., Méjean, L., Nicolas, J. P., Candito, M., Chambon, P., Gibelin, P., Amsellem, J., Baudouy, M., Morand, P., Candito, M., Chambon, P., Pringuey, D., Aubin-Brunet, V., Beaulieu, F., Darcourt, G., Bedoucha, P., Alchaar, H., Chatel, M., Candito, M., de Valk, H. W., van der Griend, R., Eeden, M. K. G. van, de Groot, E., Duran, M., Smeitink, J. A. M., de Klerk, J. B. C., Wittebol-Post, D., Rolland, M. -O., Haas, F. J. L. M., Meuwissen, O. J. A. Th., Banga, J. D., Poll-The, B. T., de Vries, J. I. P., Dekker, G. A., van Geijn, H. P., Huigens, P. C., Jakobs, C., von Blomberg, B. M. E., Deulofeu, R., Giralt, M., Aibar, C., Bauchet, C., Ballesta, A. M., Varela, G., Vila, N., Chamorro, A., Casals, F. J., Cremades, J. Diaz, Daly, L., Meleady, R., Graham, I., den Heijer, M., Brouwer, I. A., Gerrits, W. B. J., Bos, G. M. J., Blom, H. J., den Heijer, M., Bos, G. M. J., Koster, T., Vandenbroucke, J. P., Blom, H. J., Briët, E., Rosendaal, F. R., Fischer, G., Behrend, C., Bartholmes, P., Fermo, I., Paroni, R., Vigano, S., D’Angelo, A., Fermo, I., Paroni, R., Vigano, S., D’Angelo, A., Franken, D. G., Boers, G. H. J., Blom, H. J., Hamel, B. C. J., Franken, D. G., Boers, G. H. J., Blom, H. J., Ruijs, J. H. J., Franken, D. G., Blom, H. J., Boers, G. H. J., Tangerman, A., Guttormsen, A. B., Ueland, P. M., Refsum, H., Svarstad, E., Gao, W., Goldman, E., Jakubowski, H., Sebastio, G., Sperandeo, M. P., de Franchis, R., Andria, G., Garrow, T. A., Hladovec, J., Sommerova, Z., Písariková, A., Halsted, C. H., Villanueva, J., Chandler, C. J., Stabler, S. P., Allen, R. H., Muskhelishvili, L., James, S. J., Poirer, L., Jacobsen, D. W., Savon, S. R., DiCorleto, P. E., Jourdheuil-Rahmani, D., Rolland, P. H., Garçon, D., Joosten, E., Riezler, R., Allen, R., Joosten, E., Riezler, R., Allen, R., Marquardt, T., Ullrich, K., Harms, E., Koch, H. G., Koch, H. G., Evers, S., Grotemeyer, K. H., Vogelpohl, L., von Eckardstein, A., Ullrich, K., Deufel, T., Kraus, J., Harms, E., Kozich, V., Janosik, M., Sokolová, J., Bukovská, G., Kraus, J. P., Kluitmans, L. A. J., van den Heuvel, L. P., Stevens, E., Trubels, J. M. F., Blom, H. J., Boers, G. H. J., van Oost, B. A., Kraus, J. P., Kittner, S., Macko, R., Hebel, J. R., Rohr, J., Malinow, M. R., Upson, B., Buchholz, D., Earley, C., Johnson, C., Price, T. R., Rosario, J., Sloan, M., Stern, B., Wityk, R., Wozniak, M., Sherwin, R., Stolley, P., Kluijtmans, L., Heuvel, L. van den, Stevens, E., Trijbels, F., Blom, H., Boers, G., van Oost, B., den Heijer, M., Rozen, R., Löhrer, F., Angst, C., Fowler, B., Zaugg, M., Brunner, F., Haefeli, W. E., Nedrebø, B., Ericsson, U. -B., Ueland, P. M., Refsum, H., Lien, E. A., London, J., Paly, E., Paul, V., Paris, D., Kamoun, P., Chassé, J. F., Møller, J., Rasmussen, K., Meleady, R., Graham, I., Daly, L., Verhoef, P., Meleady, R., Graham, I., Daly, L., McMartin, K. E., Phifer, T. J., Alexander, J. S., Middlebrooks, M., Childress, L. E., Nicolas, J. P., Tronel, H., Chango, A., Fremont, S., Felden, F., Guerci, B., Creton, C., Drouin, P., Oakley, G. P., Elias, P. R. P., Hann, A. C., Curtis, C. G., Rose, F. A., Tudball, N., Parrot-Roulaud, F., Cochet, C., Catargi, B., Leprat, F., Latapie, J. -L., Perna, A. F., De Santo, N. G., Ingrosso, D., Galletti, P., Zappia, V., Parrot-Roulaud, F., Sassoust, G., Boissieras, P., Blom, H. J., Majors, A. K., Ehrhart, L. A., Pezacka, E. H., Perry, I. J., Morris, R. W., Ebrahim, S. B., Shaper, A. G., Refsum, H., Ueland, P. M., Pietrzik, K., Dierkes, J., Kroesen, M., Bung, P., Rasmussen, K., Moller, J., Rasmussen, K., Remacha, A., Garcia-Die, F., Cadafalch, J., Barceló, H. J., Parellada, H., Regland, B., Gottfries, C. -G., Andersson, M., Bagby, J., Dyrehag, L. -E., Abrahamsson, L., Ronge, E., Kjellman, B., Frosst, P., Christensen, B., Goyette, P., Rosenblatt, D. S., Genest, J., Rozen, R., Riedel, B., Ueland, P. M., Svardal, A. M., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X. W., Xie, L., Dudman, N., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X. W., Xie, L., Dudman, N., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X., Xie, L., Dudman, N., Smith, B., Kohlman-Trigoboff, D., Simsir, S., Stabler, S. P., Allen, R. H., Strydom, A. J. C., Schlüssel, E., Preibisch, G., Elstner, E. F. E., Pütter, S., Spuijbroek, M. D. E. H., Goddijn-Wessel, T. A. W., Wouters, M. G. A. J., Molen, E. F. v. d., Blom, H. J., Boers, G. H. J., Steegers-Theunissen, R. P. M., Trijbels, J. M. F., Thomas, C. M. G., Eskes, T. K. A. B., Tsai, M. Y., Hanson, N., Key, N., Schwichtenberg, K., Garg, U., Todesco, L., Fowler, B., Pollaert, N., Haefeli, W. E., Thorand, B., Hages, M., Pietrzik, K., Bung, P., Holzgreve, W., Vila, N., Chamorro, A., Deulofeu, R., Aibar, C., Giralt, M., Ballesta, A. M., van der Mooren, M. J., Wouters, M. G. A. J., Schellekens, L. A., Eskes, T. K. A. B., Rolland, R., Blom, H. J., Put, N. v. d., Trijbels, F., Heuvel, L. v. d., Blom, H., Eskes, T., Steegers-Theunissen, R., Mariman, E., Heyer, M. d., Rozen, R., Daher, R., Van Lente, F., Vilkovsky, A. B., Maev, I. V., Richter, E. L., Kirnus, M. D., Varela-Moreiras, G., Alonso-Aperte, E., Rubio, M., Gassó, M., Deulofeu, R., Alvarez, L., Caballeria, J., Rodés, J., Mato, J. M., van Aerts, L. A. G. J. M., Peereboom-Stegeman, J. H. J. Copius, Noordhoek, J., Eskes, T. K. A. B., Molen, E. F. v. d., Spuijbroek, M. D. E. H., Eskes, T. K. A. B., Heuvel, L. P. v. d., Monnens, L. A. H., Blom, H. J., van Guidener, C., Janssen, M. J. F. M., Surachno, J., Stehouwer, C. D. A., van den Berg, M., Bierdrager, E., Rauwerda, J. A., Wilcken, B., Hammond, J., Wouters, M. G. A. J., Hamilton, C. J. C. M., Blom, H. J., Boers, G. H. J., Thomas, C. M. G., Borm, G. F., Eskes, T. K. A. B., Wang, H., Tsai, J. -C., Perrella, M. A., Yoshizumi, M., Sibinga, N. E. S., Haber, E., Chang, T. H. -T., Schlegel, R., Lee, M. -E., Woodside, J., McMaster, D., Yarnell, J., Young, I., Mercer, C., Byrne, K., Evans, A., Gey, F., Gao, X. M., Dougan, G., Wordsworth, P., McMichael, A., Young, P. B., Kennedy, D. G., Molloy, A. M., Scott, J. M., Ward, P., Naughten, E., Cahalane, S., Murphy, D., Mayne, P., Chauveau, P., Chadefaux-Vekemans, B., Coudé, M., Aupetit, J., Kamoun, P., Jungers, P., van Asselt, D. Z. B., Blom, H. J., de Wild, G. M., van Staveren, W. A., Hoefnagels, W. H. L., Naruszewicz, M., Staniewicz, A., Dziewanowski, K., Evrovski, J., Cole, D. E. C., Callaghan, Michael, Lindgren, A., Brattström, L., Hultberg, B., Verhoef, P., Hennekens, C. H., Allen, R. H., Stabler, S. P., Willett, W. C., Stampfer, M. J., Frantzen, F., Sundrehagen, E., Verhoef, P., Kok, F. J., Stampfer, M. J., Willett, W. C., Gaziano, J. M., Hennekens, C. H., Allen, R. H., Stabler, S. P., Reynolds, R. D., Hsu, R. -J., Shane, B., Robinson, K., Kottke-Marchant, K., Green, R., Gupta, A., Jacobsen, D., Robinson, K., Mayer, E., Gupta, A., Miller, D., Marchant, K., Green, R., Jacobsen, D., Greene, R., Chong, Y. -Y., Jacobsen, D., Robinson, K., Gupta, M., Sheppard, C. A., Matthews, R. G., Goyette, P., Frosst, P., Rozen, R., Verhoef, P., Kok, F. J., Kruyssen, H. A. C. M., Witteman, J. C. M., Ueland, P. M., Boushey, C., Beresford, S., Omenn, G., Motulsky, A. G., Nygard, O., Vollset, S. E., Kvale, G., Stensvold, I., Ueland, P. M., Refsum, H., Fiskerstrand, T., Ueland, P. M., Refsum, H., Bugge, K. H., Oshaug, A., Bjønnes, C. H., Refsum, H., Wu, J. T., Wu, L. L., and Wilson, L. W.
- Published
- 1995
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3. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain: Abstracts of Symposia and free communications
- Author
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Harms, L., Bock, A., JÄnisch, W., Valdueza, J., Weber, J., Link, I., De Keyser, J., Goossens, A., Wilczak, N., Vedeler, C., Bjorge, L., Uvestad, E., Conti, G., Williams, K., Ginsberg, L., Rafique, S., Rapoport, S. I., Gershfeld, N. L., De La Meilleure, G., Crevits, L., Faiss, J. H., Heye, N., Blanke, J., Sackmann, A., Kastrup, O., Doornbos, R., van der Worp, H. B., Kappelle, L. J., Bar, P. R., Davie, C. A., Barker, G. J., Brenton, D., Miller, D. H., Thompson, A. J., Block, F., Schwarz, M., Delodovici, L., Baruzzi, F., Bonaldi, G., Dario, A., Marra, A., Mercuri, A., Dworzak, F., Cavallari, P., Confalonieri, P., Zuffi, M., Antozzi, C., Cornelio, F., Baldissera, F., Chassande, B., Ameri, A., Eymard, B., Poisson, M., Vérier, A., Brunet, P., Congia, S., Murgia, P. L., Cannas, A., Borghero, G., Uselli, S., Mellino, G., Ferrai, R., Lampis, R., Massa, R., Muzzetto, B., Giannini, F., Rossi, S., Cioni, R., d'Aniello, C., Guarneri, A., Battistini, N., Ceriani, F., Del Santo, A., Poloni, M., Campo, J. F., Iglesias, F., Guitera, M. V., Farinas, C., Pascual, J., Leno, C., Berciano, J., Thorpe, I. W., Kendall, B. E., McDonald, W. I., Moulignier, A., Dromer, F., Baudrimont, M., Dupont, B., Gozlan, J., El Amrani, M., Petit, J. C., Roullet, E., Sterzi, R., Causaran, R., Protti, A., Riva, M., Erminio, F., Arena, O., Villa, F., Maccagnano, E., Miletta, M., Spinelli, F., Ben-Hur, T., Weidenfeldl, J., Rao, N. S., Chari, C. C., Laforet, P., Matheron, S., Adams, D., Chemouilli, Ph., Desi, M., Said, G., Davous, P., Lionnet, F., Pulik, M., Genet, P., Rozenberg, F., Cartier, L. M., Castillo, J. L., Cea, J. G., Villagra, R., de Saint Martin, L., Mahieux, F., Manifacier, M. J., Mattos, K., Queiros, C., Publio, L., Vinhas, V., PeÇanha-Martins, A. C., Melo, A., Liska, U., Zifko, U., Budka, H., Drlicek, M., Grisold, W., Kaufmann, R., Kaiser, R., Czygan, M., Gomes, I., Jones, N., Cunha, S., EmbiruÇu, E. Katiane, Vieira, V., Araujo, I., Alexandra, M., Ferreira, A., Goes, J., Chemouilli, P., Israel-Biet, Masson, H., Lacroix, C., Gasnault, J., Hildebrandt-Müller, B., Oschmann, P., Krack, P., Willems, W. R., Dorndorf, W., Freitas, V., Bittencourt, A., Fernandes, D., Nascimento, M. H., Severo, M., Moraes, D., Muller, M., Hasert, K., Merkelbach, S., Schimrigk, K., van Oosten, B. W., Lai, M., Polman, C. H., Bertelsmann, F. W., Hodgkinson, S., Cabre, P. H., Volpe, L., Smadja, D., Vernant, J. P., Villaroya, H., Violleau, K., Younes-Chennoufi, A. Ben, Baumann, N., Villanueva-Hemandez, P., Ballabriga, J., Basart, E., Arbizu, T. X., Perez-Serra, J., Vinuels, F., Giron, J. M., Castilla, J. M., Redondo, L., Izquierdo, G., Lauer, K., Henneberg, A., Bittmann, N., Link, D., Wollinsky, K. H., Mobner, R., Fassbender, K., Kuhnen, J., Schwartz, A., Hennerici, M., Miller, A., Lider, O., Abramsky, O., Weiner, H. L., Offner, H., Vanderbark, A. A., Paoino, E., Fainardi, E., Addonizio, M. C., Ruppi, P., Tola, M. R., Granieri, E., Carreras, M., Sazdovitch, V., Joutel, A., Verdier-taillefer, M. H., Heinzlef, O., Radder, C., Tournier-Lasserve, E., Brenner, R. E., Munro, P. M. G., Williams, S. C. R., Bell, J. D., Hawkins, C. P., Filippi, M., Campi, A., Dousset, V., Canal, N., Comi, G., Zhu, J., Weber, F., Retska, R., List, J., Zhang, L., Brock, M., Taphoorn, M. J. B., Heimans, J. J., van der Veen, E. A., Karim, A. B. M. F., Sarazin, M., Argentino, N., Delattre, J. Y., Derkinderen, P., Buchwald, B., Schroter, G., Serve, G., Franke, C. H., Conrad, B., Kitchen, N. D., Thomas, D. G. T., Forman, A. D., Ang, Kie- Kian, Price, R., Stephens, C., Salmaggi, A., Nermni, R., Silvani, A., Forno, M. G., Luksch, R., Boiardi, A., Grzelec, H., Fryze, C., Nowacki, P., Zdziarska, B., Sanson, M., Merel, P., Richard, S., Rouleau, G., Thomas, G., Olsen, N. K., Pfeiffer, P., Egund, N., Bentzen, S. M., Johannesen, L., Mondrup, K., Rose, C., Zyluk, B., Wondrusch, E., Berger, O., Fast, N., Jellinger, K., Lindner, K., Urman, A., Thibault, J. L., Duyckaerts, Ch., Strik, H., Muller, B., Richter, E., Krauseneck, P., Steinbrecher, A., Schabet, M., Hess, C., Bamberg, M., Dichgans, J., Counsell, C. E., McLeod, M., Grant, R., Creel, G. B., Claus, D., Sieber, E., Engelhardt, A., Rechlin, T., Thierauf, P., Neubauer, U., Peresson, M., Di Giovacchino, G., Romani, G. L., Di Silverio, F., Danek, A., Kuffner, M., Hoermann, R., Schopohl, J., Laska, M., Heye, B., Zangaladze, A. T., Valls-SoIè, J., Cammarota, A., Alvarez, R., Tolosa, E., Hallett, M., Ulbricht, D., Ganslandt, O., Kober, H., Vieth, J., Grummich, P., Pongratz, H., Brigel, C., Fahlbusch, R., Serra, F. P., Palma, V., Nolfe, G., Buscaino, G. A., Rothstein, T. L., Gibson J. M., Morrison P. M., Collins A. D., Eiselt, M., Wagnur, H., Zwiener, U., Schindler, T., Efendi, H., Ertekin, C., Erfas, M., Larsson, L. E., Sirin, H., AraÇ, N., Toygar, A., Demir, Y., Seddigh, S., Vogt, T. H., Hundemer, H., Visbeck, A., Pastena, L., Faralli, F., Mainardi, G., Gagliardi, R., Linden, D., Berlit, P., Lopez, O. L., Becker, J. T., Jungreis, C., Brenner, R., Rezek, D., Dekesky, S. T., Estol, C., Boller, F., Fernandez, J. M., Mederer, S., Batlle, J., Turon, A., Codina, A., Hitzenberger, P., Vila, N., Valls-SolÇ, J., Chamorro, A., Pouget, J., Schmied, A., Morin, D., Azulay, J. Ph., Vedel, J. P., Montalt, J., Escudero, J., Barona, R., Campos, A., Varli, K., Ertem, E., Uludag, B., Yagiz, A., Privorkin, Z., Steinvil, Y., Kott, E., Combarros, O., Sanchez-Pernaute, R., Orizaola, P., Mokrusch, Th., Kutluaye, E., Selcuki, D., Ertikin, C., Zettl, U., Gold, R., Harvey, G. K., Hartung, H. P., Toyka, K. V., Wokke, J. H. J., Oey, P. L., Ippel, P. F., Jansen, G. H., Franssen, H., Toyooka, K., Fujimura, H., Ueno, S., Yoshikawa, H., Yorifuji, S., Yanagihara, T., Talamon, C., Tzourio, C., Kiefer, R., Jung, S., Toyka, K., Ruolt, I., Tranchant, C., Mohr, M., Warter, J. M., Younger, D. S., Rosoklija, G., Hays, A. P., Kurita, R., Hasegawa, O., Matsumto, M., Komiyama, A., Nara, Y., Oueslati, S., Belal, S., Turki, I., Ben Hamida, C., Hentati, F., Ben Hamida, M., Kwiecinski, H., Krolicki, L., Domzal-Stryga, A., Dellemijn, P. L. I., van Deventer, P., van Moll, B., Drogendijk, T., Vecht, Ch. J., Nemni S., Amadio, Fazio, R., Galardin, G., Delodovici, M. L., Peghi, E., Monticelli, M. L., Sessa, A., Viguera, M. L., Palomar, M., Gamez, J., Cervera, C., Navarro, C., Serena, J., Duran, I., Fernandez, A. L., Comabella, M., Nos, C., Rio, J., Montalban, J., Navarro, X., Verdu, E., Darbra, S., Buti, M., Mrabet, A., Fredj, M., Gouider, R., Tounsi, H., Khalfallah, N., Haddad, A., Dbaiss, T., Ghnassia, R., Rouillet, E., Chedru, F., Porsche, H., Strenge, H., Li, S. W., Young, Y. P., Garcia, A. A., Baron, P., Scarpini, E., Bianchi, R., Conti, A., Livraghi, S., Rees, J. H., Gregson, N. A., Hughes, R. A. C., Sedano, M. J., Calleja, J., Canga, E., Bahou, Y., Biary, N., Al Deeb, S. M., Guern, E. L. E., Gugenheim, M., Tardieu, S., Aisonobe, T. M., Agid, Y., Bouche, P., Brice, A., Rautenstrauss, B., Nelis, E., Grehl, H., Van Broeckhoven, C., Pfeiffer, R. A., Liehr, T., Ganzmann, E., Gehring, C., Neundörfer, B., Geremia, L., Doronzo, R., Sacilotto, G., Sergi, P., Pastorino, G. C., Scarlato, G., Planté-Bordeneuve, V., Mantel, A., Baas, F., Moser, H., Antonini, A., Psylla, M., Günther, I., Vontobell, P., Beer, H. F., Leenders, K. L., Chaudhuri, K. Ray, Parker, J., Pye, I. F., Millac, P. A. H., Abbott, R. J., Sutter, M., Albani, C., de Rijk, M. C., Breteler, M. M. B., Graveland, G. A., van der Mechè, F. G. A., Hofman, A., Keipes, M., Hilger, Ch., Diederich, N., Metz, H., Hentges, F., Pollak, P., Benabid, A. L., Limousin, P., Hoffmann, D., Benazzouz, A., Perret, J., Laihinen, A., Rinne, J. O., Ruottinen, H., Nagren, K., Lehikoinen, P., Oikonen, V., Ruotsalainen, U., Rinne, U. K., Cocozza, S., Pizzuti, A., Cavalcanti, F., Monticelli, A., Pianese, L., Redolfi, E., Paiau, F., Di Donato, S., Pandolfo, M., Palau, F., Monros, E., De Michele, G., Smeyers, P., Lopez-ArLandis, J., Uilchez, J., Filla, A., Genis, D., Matilla, T., Volpini, V., Blanchs, M. I., Davalos, A., Molins, A., Rosell, J., Estivill, X., De Jonghe, P., Smeyers, G., Krols, L., Mercelis, R., Hazan, J., Weissenbach, J., Martin, J. J., Warner, T. A. T., Williams, L., Orb, A. S., Harding, A. E., Giunti, P., Sweeney, M. G., Spadaro, M., Jodice, C., Novelletto, A., Malaspina, P., Frontali, M., Salmon, E., Gregoire, Del Fiore, Comar, Franck, G., Scheltens, P. H., Siegfried, K., Dartigues, E., De Deyn, P., Horn, R., Nelson, I., Hanna, M. G., Morgan-Hughes, J. A., Collinge, J., Palmer, M. S., Campbell, T., Mahal, S., Sidle, K., Humphreys, C., Tavitian, B., Pappata, S., Jobert, A., Crouzel, A. M., DiGiamberardino, L., Steimetz, G., Barbanti, P., Fabbrini, G., Salvatore, M., Buzzi, M. G., Di Piero, V., Petraroli, R., Sbriccoli, A., Pocchiari, M., Macchi, G., Lenzi, G. L., Spiegel, R., Maguire, P., Schmid, W., Ott, A., Bots, M. L., Grobbe, D. E., Hofman, A., Howard, R. S., Russell, S., Losseff, N., Hirsch, N. P., Couderc, R., Bailleul, S., Nargeot, M. C., Touchon, J., Picot, M. C., Rizzo, M., Watson, G., McGehee, D., Dingus, T., Kappos, L., Radü, E. W., Haas, J., Hartard, C. H., Spuler, S., Yousry, T., Voltz, R., Scheller, A., Holler, E., Hohlfeld, R., Scolding, N. J., Sussman, J., Kolar, O. J., Farlow, M. 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X., Francis, D., Mosely, I., Hansen, H. C., Helmke, K., Kunze, K., Sadzot, B., Maquet, P., Lemaire, Plenevaux, Damhaut, Sommer, C., Myers, R. R., Berta, E., Mantegazza, R., Argov, Z., Shapira, Y., Wirguin, I., Beuuer, J., Franke, C., Roberts, M., Willison, H., Vincent, A., Newsom-Davis, J., Morrison, K. E., Damels, R., Francis, M., Campbell, L., Davies, K. E., Kohler, W., Bucka, C., Hertel, G., Kanovsky, P., Auer, D., Ackermann, H., Klose, U., Naegele, Th., Bien, S., Voigt, K., Fink, G. R., Stephan, K. M., Wise, R. J. S., Mullatti, N., Hewer, L., Frackowiak, R. S. J., Weiller, C. S., Rijnites, M., Jueptner, M., Bauermann, T., Krams, M., Diener, H. C., van Walderveen, M. A. A., Barkhof, F., Hommes, O. R., Valk, J., Willmer, J. P., Guzman, D. A., Passingham, R. E., Silbersweig, D., Ceballos-Baumann, A., Frith, C. D., Frackowiak, R., Lucas, C. H., Goullard, L., Marchau, M. J., Godefroy, O., Rondepierre, P. H., Chamas, E., Mounier-Vehier, F., Leys, D., Renato, J., Verdugo, M. S. C., Campero, M., Jose, L., Ochoa, D. S. C., Vivancos, F., Tejedor, E. Diez, Martinez, N., Roda, J., Frank, A., Barreiro, P., Satoh, Y., Nagata, K., Maeda, T., Hirata, Y., YalÇinerner, B., Ozkara, C., Ozer, F., Ozer, S., Hanoglu, L., Zunker, P., Pozo, J. L., Oberwittler, C., Schick, A., Buschmann, H. -Ch., Ringelstein, E. Bernd, Lara, M., Anzola, G. P., Magoni, M., Volta, G. Dalla, Tarasov, A., Feigin, V., Beaudry, M. G., Carrier, S., Chicoutimi, Henriques, I. L., Bogoussslavsky, J., van Melle, G., Mathieu, J., Perusse, L., Allard, P., Prevost, C., Cantin, L., Bouchard, J. M., De Braekeleer, M., Agbo, C., Neau, J. P., Tantot, A. M., Dary-Auriol, M., Ingrand, P., Gil, R., Baltadjiev, D., Zekin, D., Sabey, K., Gennaula, C. P., Pope, B. A., Caparros-Lefebvre, D., Girard-Buttaz, I., Pruvo, J. P., Petit, H., Hipola, D., Martin, M., Giménez-Roldan, S., Ivanez, V., Japaridze, G., Carrasco, J. L., Picomell, I., Herranz, J. L., Macias, J. A., Nieto, M., Noya, M., Oller, L., Kiteva-Trencevska, G., Delgado, M. R., Liu, H., Luengo, A., Parra, J., Colas, J., Fernandez, M. J., Manzanares, R., Kornhuber, M. E., Malashkhia, V., Orkodashili, G., Martinez, M., Bonaventura, I., Porta, G., Martinez, I., Fernandez, A., Aguilar, M., Masnou, P., Drouet, A., Dreyfus, M., Cartron, J., Morel-Kopp, M. C., Tchernia, G., Kaplan, C., Lammers, M. W., Hekster, Y. A., Keyser, A., Meinardi, H., Renier, W. O., Boon, P. A. J. M., Have, M. D., Kint, B., Cruz, P., Cadilha, A., Almeida, R., Goncalves, M., Pimenta, M., Ramos, L. M. P., Polder, T. W., Broere, C. A., Polman, L., Rother, I., Rother, M., Schlaug, G., Arnold, S., Holthausen, H., Wunderlich, G., Ebner, A., Luders, H., Witte, O. W., Seitz, R. J., Serra, L. L., Gallicchio, B., Rotondi, F., Wieshmann, U., Meierkord, H., Sabev, K., Di Carlo, V., Gueguen, B., Derouesné, Ch., Ancri, D., Bourdel, M. C., Guillou, S., Aliaga, R., Chornet, M. A., Rodrigo, A., Pascual, A. Pascual -Leone, Catala, M. D., Pascual-Leone, A., Benbadis, S. R., Dinner, D. S., Chelune, G. J., Lüders, H. O., Piedmonte, M. R., Blanco, T., Lopez, M. P., Romero, B., Deltoro, A., Pascual, A., Pascual, Leone, Bolgert, F., Josse, M. O., Tassan, P., Touze, E., Laplane, D., Godenberg, F., Brizioli, E., Del Gobbo, M., Pelliccioni, G., Scarpino, O., Durak, H., Damlacik, G., Tunca, Z., Fidaner, H., Yurekli, Y., Yemez, B., Kaygisiz, A., Anllo, E. A., Esperet, E., Giovagnoli, A. R., Casazza, M., Spreafico, R., Avanzini, G., Mascheroni, S., Vecchio, I., Tornali, C., Antonuzzo, A., Grasso, A. A., Bella, R., Pennisi, G., Raffaele, R., Broeckx, J., Schildermans, F., Hospers, W., Deberdt, W., Carney, J. M., Aksenova, M., Chen, M. S., Juncadella, M., Busquets, N., De la Fuente, I., Rodriguez, A., Rubio, F., Soler, R., Khati, C., Pillon, B., Deweer, B., Malapani, C., Malichard, N., Dubois, B., Rancurel, G., Lopez, D. L., Jungreia, G., DeKosky, S. T., Boiler, F., Weiller, C., Rijntjes, M., Mueller, S. P., Maguire, E. A., Burke, E. T., Staunton, H., Phillips, J., Rousseaux, M., Pena, J., Bertran, I., Santacruz, P., Lopez, R., Catafau, A., Lomena, F., Blesa, R., Rampello, L., Nicoletti, A., Cabaret, M., Lesoin, F., Steinling, M., Tournev, I., Maier-Hauff, K., Schroeder, M., Wolf, A., Cochin, J. P., Noel, I., Augustin, P., Auzou, P., Hannequin, D., Maria, V., Lopez-Bresnahan, Danielle, D. M., Antin-Ozerkis B. A., Bartels, E., Rodiek, S. O., Flugel, K. A., Campos, D. M., Salas-Puig, J., Del Rio, J. Sanhez, Vidal, J. A., Lahoz, C. H., Eraksoy, M., Barlas, O., Barlas, M., Bayindir, C., Ozcan, H., Birbamer, G., Gerstenbrand, F., Felber, S., Luz, G., Aichner, F., Seidel, G., Kaps, M., Hutzelmann, A., Gerriets, T., Kruggel, F., Martin, P. J., Gaunt, M. E., Abbot, R. J., Naylor, A. R., Meary, E., Dilouya, A., Meder, J. F., De Recondo, J., Lebtahi, R., Neff, K. W., Meairs, S., Viola, S., Matta, E., Aquilone, L., Rise, I. R., Authier, F. J., Kondo, H., Ghnassia, R. T., Degos, J. D., Gherardi, R. K., Bardoni A., Ciafaloni E., Comi G. P., Bresolin N., Robotti M., Moggio M., Rigoletto C., Roses A., Scarlato G., Castelli, E., Turconi, A., Bresolin, N., Perani, D., Felisari, G., Chariot, P., de Pinieux, G., Astier, A., Jacotot, B., Gherardi, R., Fischer-Gagnepain, V., Louboutin, J. P., Crespo, F., Florea-Strat, A., Fromont, G., Sabourin, J. -C., Gonano, E. -F., Moroni, I., Prelle, A., Iannaccone, S., Quattrini, A., deRino, F., Sessa, M., Golzi, V., Smirne, S., Nemni, R., Turpin, J. C., Lucotte, G., Jacobs, S. C. J. M., Willems, P. W. A., Bootsma, A. L., Lasa, A., Calaf, M., Baiget, M., Gallano, B., Fichter-Gagnepain, V., Mazzucchelli, F., D'Angelo, M. G., Velicogna, M., Bet, L., Comi, G. P., Bordoni, A., Gonano, E. F., Bazzi, P., Rapuzzi, S., Moggio, M., Fagiolari, G., Ciscato, P., Messina, A., Battistel, A., Ryniewicz, B., Sangla, I., Desnuelle, C., Paquis, V., Cozzone, P. J., Bendahan, D., Sturenburg, H. J., Kohncke, G., Castellli, E., Linssen, W., Stegeman, D., Binkhorst, R., Notermans, S., Jaspert, A., Fahsold, R., de Munain, A. Lopez, Cobo, A., Martorell, L., Poza, J. J., Navarrete Palau, D., Emparanza, J. I., Sanchez-Roy, R., Vilchez, J. J., Hernandez, M., Tena, J. Garcia, Perla, C., Koutroumanidis, M., Papathanasopoulos, P., Papadimitriou, A., Papapetropoulos, T. H., Divari, R., Hadjigeorgiou, G. M., Anastasopoulos, I., Sansone, V., Rotondo, G., Meola, G., Rigoletto, C., Messina, S., Szwabowska-Orzeszko, E., Jozwiak, S., Michalowicz, R., Szaplyko, W., Petrella, M. A., Della Marca, G., Masullo, G., Mennuni, G. F., Kompf, D., Wascher, E., Verleger, R., Kaido, M., Soga, F., Toyooka, H., Bayon, C., Rubio, J., Carlomagno, S., Parlato, V., Santoro, A., Lavarone, A., Bonavita, V., Pentore, R., Venneri, A., Pasquier, F., Lebert, F., Grymonprez, L., Lefebvre, C., Van der Linden, M., Derouesné, C., Renault, B., Lacomblez, L., Homeyer, P., Ouss, L., Neuman, E., Malbezin, M., Barrandon, S., Guez, D., Stevens, M., van Swieten, J. C., Franke, C. L., Sanchez, A., Castellvirel, S., Mila, M., Jimenez, D., Pallesta, F., Ruiz, P. J. Garcia, Barrio, A., Barroso, T., Benitez, J., de Yebenes, J. Garcia, Manubens, J. M., Martinez-Lage, J. M., Larumbe, R., Muruzabal, J., Lacruz, F., Quesada, Pedro, Gallego, J., Ferini-Strambi, L., Marcone, A., Garancini, P., Tedesi, B., Jacob, B., Rozewicz, L., Langdon, D., Davie, C., Ron, M., Thompson, A., Koepp, M. J., Hansen, M. L., Guldin, B., Pressler, R. M., Ried, S., Scholz, C., Monaco, F., Gianelli, M., Schiavalla, M. P., Naldi, P., Cantello, R., Torta, R., Verze, L., Mutani, R., Knott, H., Ferbert, A., Schulze-Bonhage, A., Aust, W., Di Mascio, R., Marchioli, R., Vitullo, F., Di Pasquale, A., Sciulli, L., Kramer, V., Tognoni, G., Santacruz, P., Lopez, R., Marti, M. J., Charques, I., Catafau, A., Lomeila, F., Peila, J., Bertran, I., Blesa, R., Krendel, D. A., Costiga, D. A., Koeppen, S., Korn, W. M., Brugge, S., Schmitz, D., Scheulen, M. E., King, R. H. M., Robertson, A. M., Thomas, P. K., Kerkhofs, A., Vermersch, P., Dereeper, O., Daems Monpeun, C., Parent, M., Deplanque, D., Petit, H., Campero, M., Serra, J., Ochoa, J. L., Martinez-Matos, J. A., Montero, J., Olivé, M., Rene, R., Vidaller, A., Gugenheim, M., Gouider, R., Le Guern, E., Brice, A., Agid, Y., Bouche, P., Grisold, W., Ziflo, U., Drlicek, M., Budka, H., Jellinger, K., Zielinski, C. H., Ginsberg, L., King, R. H. M., Workman, J., Platts, A. D., Thomas, P. K., Gherardi, R. K., Florea-Strat, A., Poron, F., Sabourin, J. -C., Fazio, R., Nemni, R., Franceschi, M., Lorenzetti, I., Rinaldi, L., Canal, N., Weilbach, F. X., Sennlaub, A., Jung, S., Gold, R., Toyka, K. V., Hartung, H. P., Giegerich, G., Ellie, E., Vital, A., Steck, A. J., Vital, C., Julien, J., Doneda, P., Pizzul, S., Scarpini, E., Chiodi, P., Ramacci, M. T., Livraghi, S., Maimone, D., Annunziata, P., Salvadori, C., Guazzi, G. C., Arne-Bes, M. C., Delisle, M. B., Fabre, N., Hurtevent, J. F., Bes, A., Baudoin-Martin, D., Laborde, E., Viallet, F., Creisson, C., Crespi, V., Bogliun, G., Marzorati, L., Zincone, A., D'Angelo, L., Liberani, A., Merlini, M., Rivolta, R., Creange, A., Sabourin, J. -C., Theodorou, I., Gherardi, R. K., Conti, A. M., Malosio, M. L., Baron, P. L., Scarlato, G., Chorao, R., Rosas, M. J., Leite, I., Callea, L., Donati, E., Bargnani, C., Bud, M., Verdu, E., Navarro, X., Braun, S., Einius, S., Poindron, P., Warier, J. M., Bradley, J., Bekkelund, S. I., Torbergsen, T., Mellgren, S. I., Carlomagno, S., Parlato, V., Santoro, A., Lavarone, A., Boller, F., Bonavita, V., Engelhardt, A., Lörler, H., Robeck, S., Kluglein, C., Comi, G., Avoledo, V., Locatelli, T., Leocani, L., Galardi, G., Magnani, G., Medaglini, S., Chkhikvishvili, T. S., Zangaladze, A., Bratoeva, M., Kovachev, P., Chavdarov, D., Artemis, N., Karacostas, D., Milonas, I., Arpa, J., Lopez-Pajares, R., Cruz-Matinez, A., Sarria, J., Palomo, F., Alonso, M., Rodriguez-Al-barino, A., Lacasa, T., Nos, J., Barreiro, P., Martinez, A. Cruz, Villoslada, C., Alons, M., Taghavy, A., Hamer, H., Kratzer, A., Dethy, S., Pauwels, T., Monclus, M., Luxen, A., Goldman, S., Ziegler, M., Crambes, O., Ragueneau, I., Arnaud, F., Zappia, M., Montesanti, R., Colao, R., Palmieri, A., Branca, D., Nicoletti, G., Rizzo, M., Parlato, G., Quattrone, A., Vanacore, N., Zuchegna, P., Bonifati, V., Meco, G., Scholz, J., Friedrich, H. -J., Rohl, A., Ulm, G., Vieregge, P., Savettieri, G., Rocca, W. A., Meneghini, F., Grigoletto, F., Morgante, L., Reggio, A., Salemi, G., Di Pierri, R., OzckmekÇi, S., Ertan, S., Yeni, N., Apaydin, H., Erkol, G., Kiziltan, G., Denktas, F., Ranoux, D., de Recondo, J., Ostergaard, L., Werdelin, L., Odin, P., Lindvall, O., Dupont, E., Christensen, P. B., Boisen, E., Jensen, N. B., Schmiegelow, M., Ingwersen, S. H., Matias-Guiu, J., Canet, T., Falip, R., Martin, R., Galiano, L., Voloshin, M. Y., Burchinskaya, L. F., Cabrera-Valdivia, F., Jimenez-Jimenez, F. J., Molina, J. A., Fernandez-Calle, P., Vazquez, A., Canizares-Liebana, F., Larumbe-Lobalde, S., Ayuso-Peralta, L., Rabasa, M., Codoceo, R., Arrieta, F. J., Aguilar, M. V., Jorge-Santamaria, A., Martinez-Para, M. C., Alarcon, J., Mateo, D., Gimenez-Roldan, S., Gencheva, E., Tzonev, T. z., Georgiev, G., Petkova, P., Gasparini, M., Vanacore, N., Meco, N. G., de la Sierra, G., Aguado, F., Revilla, M., Varela, L., Rico, H., Feve, A., N'Guyen, J. 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L., Giannini, P., Liguori, M., Lucivero, V., Picciola, E., Tortorella, C., Drislane, F., Wang, A. Ming, Di Mascio, R., Marchioli, R., Vitullo, F., Di Pasquale, A., Sciulli, L., Kramer, V., Tognoni, G., Levivier, M., del Olmo, A., Caballero, E., Degaey, I., de Bruijn, S. F. T. M., Tchaoussoglou, I., Bastianello, S., Pozzilli, C., Cervello, A., Catala, N., Koskas, F., Kieffer, E., Botia, E., Vivancos, J., Leon, T., Segura, T., Ramo, C., Lopez, F., Karepov, V. G., Gur, A. J., Berlanga, B., Gracia, V., Fiol, C., Kurtel, H., Ozkutlu, U., Yegen, B., Grau, A. J., Buggle, F., Heindle, S., Steichen-Wiehn, C., Banerjee, T., Maiwald, M., Becher, H., Villafana, W., Medina, F., Fernandez-Real, J. M., Soler, S., Planas, E., Iceman, E., Doganer, I., Badlan, G., Genc, B., Yulug, K., Ideman, E., Dural, H., Kutlul, K., Damalik, G., Baklan, Y., Metin, B., Tekinsoy, E., Iriarte, I., Subira, M. L., Crockar, A. D., Treacy, M., McNell, T. A., Grazzi, L., Ediboglu, N., Bilgin, H., Ertas, S., Goument, J. -P., Basset, C., Campos, Y., Garcia-Silva, T., Cabello, A., Bussaglia, E., Tizzano, E., Colomer, J., Gimbergues, P., Campagne, D., Bommelaer, C., Delaguillaume, B., Ramtami, H., Ait-Kaci-Ahmed, M., Pascual L. F., Fernandez T., Hortells M., Sanz C., Morales F., Lauritzen, L., Picard, F., Sellal, F., Collard, M., Avramidis, T., Alexiou, E., Anastopoulos, T., Frongillo, D., Delfino, F. A., Cannata, M., Calo, L., Vichi, R., Antonini, G., Fragola, V., Cannata, D., Salas, M., Ruiz, C., Angelard, B., Lacau, J., Guily, St., Sendtner, M., Goadsby, Peter J., Quin, N. P., Gadian, D. G., Roland, P. E., Seitz, Rudiger J., Frackowiak, Richard S. J., Becker, G., Krone, A., Schmidt, K., Hofmann, E., Bogdahn, U., Rosenfeld, M. R., Meneses, P., Kaplitt, M. G., Dalmau, J., Posner, J., Cordon-Cardon, C., Hoang-Xuan, K., Vega, F., Nishisho, I., Moisan, J. P., Theillet, C., Delattre, O., Zhu, Jiahong, Walther, W., Posner, J. B., Roelcke, U., von Ammon, K., Pellikka, R., Lucking, C. H., Walon, C., Boucquey, D., -Van Rijckevorsel, K. Harmant, Lannoy, N., Verellen-Dunoulin, Ch., Liszka, U., Cavaletti, G., Casati, B., Kolig, C., Bogliun, G., Marzorati, L., Johannsen, L., Chio, A., Ruda, R., Vigliani, M. C., Sciolla, R., Seliak, D., Hoang-Xuang, K., Villanueva, J. A., Montalban, X., Arboix, A., Colosimo, C., Albanese, A., Hughes, A. J., de Bruin, V., Lees, A. J., Kowalski, J. W., Banfi, S., Santoro, L., Perretti, A., Castaldo, I., Barbieri, F., Campanella, G., Bhatia, K. P., Mardsen, C. D., de Bruin, V. S., Machedo, C., Ceballos-Baumann, D., Marsden, C. D., Brooks, D. B. J., Wennlng, G. K., Quinn, N., McDonald, W. l., Warner, T. T., Bain, P. C., Davis, M. B., Conway, D., Shaunak, S., O'Sullivan, E., Crawford, T., Lawden, M., Blunt, S., Rapoport, A., Sarova-Pinchas, I., de Beyl, D. Zegers, Mavroudakis, N., Blanc, S., Godinot, C., Lenoir, G., Barkhof, M. S. F., Tas, M. W., Baron, P. L., Constantin, C., Cassatella, M. A., Langdon, D. W., Webb, S., Gasparini, P., Zeviani, A., Kidd, D., Mammi, S., Cahalon, L., Hershkoviz, R., Lahat, N., Wallach, D., Annunziata, P., Martino, T., Maimone, D., Guazzi, G. C., Porrini, A. M., Dell'Arciprete, L., Rothwell, P. M., Stewart, R. R. C., Cull, R. E., Willmes, K., Poeck, K., Russell, D., Braekken, S. K., Brucher, R., Svennevig, J., Hermesl, M., Bruckmann, H., Biraben, A., Sliwka, U., Meyer, B., Schondube, F., Noth, J., Lavenu, I., Lammers, C., Waldecker, B., Haberbosch, W., Stam, J., Schneider, R., Gautier, J. C., Berlit, T. P., Fauser, B., Kuhne, D., Geraud, G., Danielli, A., Larrue, V., Bes, A., Timmerman, E., Bono, F., Bruni, A. C., Valalentino, P., Montesi, M. P., Talerico, G., Zappia, M., Sabatelli, M., Quattrone, A., Pareyson, D., Lorenzetti, D., Sghirlanzoni, A., Castellotti, B., Lupski, J. R., Archidiacono, N., Antonacci, R., Marzella, R., Rocchi, M., Samuel, D., Goulon-Goeau, C., Costa, P. P., Bismuth, H., Said, G., De Jongh P., Lofgren A., Timmerman V., Vance J. M., Van Broeckhoven C., Martin J. -J., Martinez, A. Cruz, Bort, S., Arpa, J., Misra, P., King, R. H. M., Badhia, K., Anderson, M., Caballo, A., Vichez, J., Gabriel, J. M., Erne, B., Miescher, G. C., Ulrich, J., Vital, A., Vital, C., Steck, A., Petry, K., Labatut, I., Hilmi, S., Ellie, E., Ferrini-Strambi, L., Zucconl, M., Marchettini, P., Palazzi, S., Oehlschlager, M., Pepinsky, R. B., Gemignani, F., Marbini, A., Pavesi, G., Di Vittorio, S., Manganelli, P., Mancia, D., Vermersh, P., Roche, J., Durocher, A. M., Dewailly, Ph., Dettmers, C., Fink, G., Lemon, R., Stephan, K., Passingham, D., Weder, B., Knorr, U., Huang, Y., Butterfield, D. A., Peris, M. L., Peiro, C., Pascual, A. Pascual-Leone, Bottini, G., Folnegovic-Smalc, V., Knezevic, S., Bokonjic, R., Ersmark, B., Torres, M. Gonzalez, Guiraud-Chaumeil, B., Haugaard, K., Jovicic, A., Chr, Lang, Levic, Z., Parra, C. Martinez, Ochoa, J. Patrignani, Titlbach, O., Wikkelso, C., Caparros-Lefevre, D., Debachy, B., Verier, A., Cantinho, G., Santos, A. I., Godinho, F., Bagunya, J., Roig, T., Ensenyat, A., Santiag, O., Trabucchi, H., De Leo, D., Koch, Ch., Zeumer, H., Matkovic, Z., Morris, P., Donaghy, M., Köhler, W., Kammer, T., Röther, J., Navon, R., Fontaine, B., Wu, Y., Capdevila, A., Guardiola, M. J., van Dijk, G. W., Notermans, N. C., Kruize, A. A., Kater, L., Bertelt, C., Hesse, S., Friedrich, H., Mauritz, K. -H., Giron, L. T., Watanabe, I. S., Ewing, D., Koepp, M., Lempert, T., Sander, B., Kauerz, U., Mehdorn, H. M., Hezel, J., Eickhoff, W., Kryst, T., Timsit, S., Gardeur, D., Reis, Mitermayer Galvao dos, Secor, E., Filho, A. Andrade, Silva, M. Cardoso, Santos, S. R. Silveira, Vasilaski, G., Reis, E. A. dos, Velupillai, P., Harn, D. A., Tigera, J. Garcia, Dreke, R. Martinez, Crespo, R. Piedra, Besses, C., Acin, P., Massons, J., Florensa, L., Oliveres, M., Sans-Sabrafen, J., Wicklein, E. M., Pleiffer, G., Kunre, K., Dieterich, M., Brandt, Th., Guarino, M., Stracciari, A., Pazzaglia, P., D'Alessandro, R., Santilli, I., Donato, M., The European Velnacrine Study Group, The Dutch Guillain-Barré study group, The COP-1 Multicenter Clinical and Research Group Study, and European Study Group
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- 1994
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4. Troubles cognitifs et sclérose en plaques rémittente : intérêt de leur détection précoce
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Grégoire Malandain, C. Bensa, C. Bertogliati, P. Bedoucha, Christine Lebrun, and Stéphane Chanalet
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Gynecology ,medicine.medical_specialty ,Neurology ,business.industry ,Medical screening ,Medicine ,Early detection ,Neurology (clinical) ,business - Abstract
Resume Introduction L’atteinte cognitive est frequente dans la SEP remittente, mais elle est souvent diagnostiquee apres desinsertion sociale et professionnelle. Methodes Nous avons evalue le profil cognitif d’une population homogene de 32 patients presentant une sclerose en plaques remittente evoluant depuis moins de 5 ans avec plainte mnesique spontanee. Les patients etaient apparies en âge et niveau scolaire a 20 temoins et 16 d’entre eux ont ete suivis pendant 2 ans (3 instants), avec une batterie de tests neuropsychologiques, un examen clinique, une IRM cerebrale. Les tests neuropsychologiques utilises testaient les capacites mnesiques verbales et visuospatiales, l’attention, les fonctions executives, le langage, et les praxies visuo-constructives. Les charges lesionnelles en IRM ont ete quantifiees a l’aide d’outils de segmentation semi-automatique et verifiees par contourage manuel. Resultats Quatre-vingt pour cent des patients de la cohorte presentaient des troubles cognitifs, pourcentage superieur a celui decrit dans la litterature. Ces troubles predominaient sur la memoire verbale, l’attention, les fonctions executives. Les patients dont les IRM cerebrales remplissaient initialement les criteres de Barkhof et ceux qui avaient des lesions calleuses montraient une atteinte mnesique plus marquee. Il existait un lien statistique entre la presence de plaques dans la fosse posterieure et l’existence de troubles attentionnels. Il n’a pas ete retrouve de lien avec la charge lesionnelle globale en T1 et en T2. Lors du suivi, nous avons constate une amelioration des performances mnesiques, attentionnelles, et du nombre de domaines cognitifs atteints pour chaque patient. Cette amelioration, alors que le niveau de handicap mesure par l’EDSS restait stable, souligne l’importance de l’effet test-retest. Conclusion La majorite des patients testes a la phase precoce de la maladie presente un deficit cognitif leger. Une detection rapide, des propositions therapeutiques, et la reconnaissance des troubles sont indispensables pour optimiser la prise en charge des patients. Cette etude se poursuit actuellement pour evaluer le statut clinique et IRM sur 5 ans.
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- 2006
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5. DNA-Encoded Library-Derived DDR1 Inhibitor Prevents Fibrosis and Renal Function Loss in a Genetic Mouse Model of Alport Syndrome.
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Richter, Hans, Satz, Alexander L., Bedoucha, Marc, Buettelmann, Bernd, Petersen, Ann C., Harmeier, Anja, Hermosilla, Ricardo, Hochstrasser, Remo, Burger, Dominique, Gsell, Bernard, Gasser, Rodolfo, Huber, Sylwia, Hug, Melanie N., Kocer, Buelent, Kuhn, Bernd, Ritter, Martin, Rudolph, Markus G., Weibel, Franziska, Molina-David, Judith, and Kim, Jin-Ju
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- 2019
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6. Arthroplastie de la hanche par cupules couplées
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Gérard, Y., Segal, Ph., and Bedoucha, J. S.
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- 1977
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7. Thrombose veineuse cérébrale et drépanocytose : caractéristiques cliniques, facteurs associés et prise en charge spécifique
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Bedoucha, Laurine, Reiner, Peggy, Guey, Stéphanie, Jouvent, Eric, Mazighi, Mikael, and Crassard, Isabelle
- Abstract
La drépanocytose est associée à une augmentation du risque de thrombose veineuse. La survenue de thrombose veineuse cérébrale (TVC) a, cependant, rarement été rapportée.
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- 2023
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8. [Early detection of cognitive impairment in relapsing-remitting multiple sclerosis: functional-anatomical correlations and longitudinal follow-up]
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C, Bensa, C, Bertogliati, S, Chanalet, G, Malandain, P, Bedoucha, and C, Lebrun
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Adult ,Cohort Studies ,Male ,Multiple Sclerosis, Relapsing-Remitting ,Humans ,Female ,Longitudinal Studies ,Middle Aged ,Neuropsychological Tests ,Cognition Disorders ,Magnetic Resonance Imaging ,Demography - Abstract
Cognitive impairment is frequent in relapsing remitting Multiple Sclerosis and is often diagnosed after disruption of occupational and social relations.We studied at baseline a homogeneous population of 32 RRMS patients, diagnosed for less than 5 years, with spontaneous memory complaints, and 20 controls. Sixteen patients were followed for 2 years, combining physical examination, neuropsychological tests, and brain MRI. Neuropsychological tests used evaluated memory capacities, attentional capacities, executive functions, language, and visuo-constructive praxis. Lesion load on brain MRI was measured with semi-automatic segmentation procedures and manual control.Eighty percent of patients presented cognitive impairment, and this proportion was higher than that found in the literature. These disorders were more marked for verbal episodic memory, attention, and executive functions. Patients with brain MRI that initially fulfilled the Barkhof criteria and those with callous lesions had more memory disorders. No link between global T1 and T2 lesion loads and neuropsychological scores was found. A statistical link between posterior fossa lesions and attentional disorders was shown. In the longitudinal follow-up, patients had better performances in memory and attentional domains, and a lower number of cognitive domains with dysfunction for each patient. This improvement on neuropsychological tests, whereas EDSS levels were stable, underlined a possible test-retest effect.During the initial phase of the disease, most of the relapsing remitting patients present a mild cognitive impairment. Early detection, therapeutic propositions, and recognition of disorders are necessary.
- Published
- 2006
9. Mise en place d’une activité de conciliation des traitements médicamenteux à l’admission dans un service de chirurgie orthopédique
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Biasolo, C., Dumoulin, C., Bedoucha, C., Dulin, R., Gayral, M., and Marion, A.-C.
- Abstract
La Conciliation des traitements médicamenteux (CTM), associée à l’analyse pharmaceutique, est une pratique connue pour lutter contre l’iatrogénie médicamenteuse. Dans une volonté de démarrer cette activité, la Phrmacie à usage intérieur (PUI) du Centre hospitalier de Libourne a priorisé ses actions en chirurgie orthopédique, identifié comme secteur à risque d’erreurs médicamenteuses (absence de médecin en continu dans les unités, importante rotation des équipes et nombreuses admissions par les urgences).
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- 2022
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10. Le livret des chimiothérapies injectables : un nouvel outil indispensable à la formation continue du personnel ?
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Dumoulin, C., Biasolo, C., Feuerstein, E., Bedoucha, C., Gayral, M., Barnetche, S., Gratelle, M.-A., Dulin, R., and Marion, A.-C.
- Abstract
Le circuit des chimiothérapies injectables comporte une série d’activités à risque de leur préparation à leur administration. La pluridisciplinarité et le turnover des intervenants tout au long du processus nécessitent la mise en place d’outils de formation.
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- 2022
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11. [Cerebral vascular complication of hyperhomocysteinemia. Controlling thromboembolic complications with folates]
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M, Candito, P, Bedoucha, D, Jambou, A, Appert-Flory, F, Fisher, F, Parrot-Roulaud, J, Bayle, E, Van Obberghen, and M, Chatel
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Adult ,Methylenetetrahydrofolate Dehydrogenase (NADP) ,Leg ,Folic Acid ,Homozygote ,Mutation ,Factor V ,Humans ,Female ,Thrombosis ,Intracranial Embolism and Thrombosis ,Homocysteine - Abstract
Young patients who experience cardiovascular events may have raised levels of homocysteine. There may be several causes for this hyperhomocysteinemia.Cerebrovascular disease occurred in a 40-year-old female smoker with hyperhomocysteinemia. This patient subsequently had several episodes of thromboembolism involving the brain and lower limb arteries. Prothrombin concentration was difficult to control with antivitamin K anticoagulants. Investigations to identify a genetic cause of hyperhomocysteinemia revealed that she was homozygous for the C677T mutation on the methylenetetrahydrofolate reductase gene. There was no G1691A mutation of the factor V gene, a risk factor for familial thrombosis. Supplementation with folic acid successfully halted episodes of thromboembolism (follow-up 2 years) and prothrombin levels stabilized under treatment.The C677T mutation, which is common in the general population (15.7%), cannot explain the effect of folate supplementation alone. Other mutations affecting homocysteine metabolism could have a potentializing effect on vascular events.
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- 1997
12. Total plasma homocysteine determination by liquid chromatography before and after methionine loading. Results in cerebrovascular disease
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M, Candito, P, Bedoucha, M H, Mahagne, G, Scavini, and M, Chatel
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Adult ,Male ,Cerebrovascular Disorders ,Methionine ,Humans ,Female ,Fasting ,Middle Aged ,Chromatography, Ion Exchange ,Homocysteine - Abstract
Elevated homocysteine (HCY) levels in tissues and blood are associated with premature occlusive diseases. A number of techniques have been developed to assay HCY, including high-performance liquid chromatography (HPLC) with fluorimetric or electrochemical detection, and radioenzymatic methods. The present study evaluated the adaptation of a liquid chromatographic, ion-exchange technique with postcolumn derivatization using ninhydrin. Fasting and moreover post-methionine load total plasma HCY were assayed in 50 patients three months after a stroke and in 20 age-matched controls. Ion-exchange liquid chromatography was performed on an amino acid analyzer using a modified procedure to improve methionine and HCY separation. HCY values in the fasting state were moderately but significantly increased (P0.05) in the patients compared to the controls: 10.5+/-3.4 versus 9.3+/-2.3 micromol/l. The difference between the two groups was amplified in post-load HCY results, which were significantly increased (P0.05) in the patients: 41.6+/-17.8 versus 29.2+/-5.5 micromol/l in controls. The relationship between cerebrovascular disease and impaired HCY metabolism has previously been emphasized by other investigators. Our findings suggest that certain inherited and/or acquired HCY disorders observed in the fasting state (14%) and especially in post-methionine load conditions (32%) may occur during acute disease, and that total plasma HCY can be determined by ion-exchange chromatography even after oral methionine loading.
- Published
- 1997
13. Treatment-free remission following frontline nilotinib in patients with chronic myeloid leukemia in chronic phase: results from the ENESTfreedom study
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Hochhaus, A, Masszi, T, Giles, F J, Radich, J P, Ross, D M, Gómez Casares, M T, Hellmann, A, Stentoft, J, Conneally, E, García-Gutiérrez, V, Gattermann, N, Wiktor-Jedrzejczak, W, le Coutre, P D, Martino, B, Saussele, S, Menssen, H D, Deng, W, Krunic, N, Bedoucha, V, and Saglio, G
- Abstract
The single-arm, phase 2 ENESTfreedom trial assessed the potential for treatment-free remission (TFR; i.e., the ability to maintain a molecular response after stopping therapy) following frontline nilotinib treatment. Patients with Philadelphia chromosome-positive chronic myeloid leukemia in chronic phase with MR4.5(BCR-ABL1⩽0.0032% on the International Scale (BCR-ABL1IS)) and ⩾2 years of frontline nilotinib therapy were enrolled. Patients with sustained deep molecular response during the 1-year nilotinib consolidation phase were eligible to stop treatment and enter the TFR phase. Patients with loss of major molecular response (MMR; BCR-ABL1IS⩽0.1%) during the TFR phase reinitiated nilotinib. In total, 215 patients entered the consolidation phase, of whom 190 entered the TFR phase. The median duration of nilotinib before stopping treatment was 43.5 months. At 48 weeks after stopping nilotinib, 98 patients (51.6%; 95% confidence interval, 44.2–58.9%) remained in MMR or better (primary end point). Of the 86 patients who restarted nilotinib in the treatment reinitiation phase after loss of MMR, 98.8% and 88.4%, respectively, regained MMR and MR4.5by the data cutoff date. Consistent with prior reports of imatinib-treated patients, musculoskeletal pain-related events were reported in 24.7% of patients in the TFR phase (consolidation phase, 16.3%).
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- 2017
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14. [Transesophageal echocardiography in the etiological evaluation of ischemic cerebral vascular accidents. Value in young subjects]
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E, Ferrari, S, Sarzotti, P, Gibelin, M H, Mahagne, P, Thomas, P, Bedoucha, M, Baudouy, and P, Morand
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Adult ,Male ,Mitral Valve Prolapse ,Heart Diseases ,Arteriosclerosis ,Thrombosis ,Middle Aged ,Brain Ischemia ,Heart Septum ,Humans ,Female ,Heart Aneurysm ,Cardiomyopathies ,Echocardiography, Transesophageal - Abstract
We conducted this study to evaluate the role of transoesophageal echocardiography in the aetiologic diagnosis of ischaemic cerebral vascular events in young subjects.Over a 16-month period, 70 consecutive patients under 55 (mean age 49 years; range 32-55; 34 females, 36 males) underwent transoesophageal echocardiography as part of a complete work-up after a recent (1 month) cerebral event considered to be ischaemic in nature. Exclusion criteria were age over 55, vascular stenosis or ulcerated plaque, embologenic heart disease and valve prosthesis. 24-h Holter recordings were also obtained in all patients.The cerebral event was temporary in 11 subjects and permanent in the other 59. The ischaemic nature of the event was confirmed in all patients with computed tomography or magnetic resonance imagery. All patients were in sinus rhythm at examination and supraventricular paroxysmal arrhythmia was observed in 7 during the Holter recordings. The transoesophageal echocardiography was normal in 37 patients (52%) and pathologic in 33 (48%). The source of the embolus was identified in 4 cases (6%) and the probable cause of the cerebral event was found in 29 (42%). Among the abnormal structures observed were permeable oval foramens, inter-atrial septum aneurysms and plaques on the ascending aorta.In our selected population of patients under 55 years of age, transoesophageal echocardiography detected the certain or probable source of the ischaemic cerebral event in 48% of the cases, a diagnostic yield better than most other methods. Nevertheless, there is no known therapeutic response to several of the potential sources of embolus observed.
- Published
- 1994
15. Incretin-like effects of small molecule trace amine-associated receptor 1 agonists.
- Author
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Raab, Susanne, Wang, Haiyan, Uhles, Sabine, Cole, Nadine, Alvarez-Sanchez, Ruben, Künnecke, Basil, Ullmer, Christoph, Matile, Hugues, Bedoucha, Marc, Norcross, Roger D., Ottaway-Parker, Nickki, Perez-Tilve, Diego, Conde Knape, Karin, Tschöp, Matthias H., Hoener, Marius C., and Sewing, Sabine
- Abstract
Objective Type 2 diabetes and obesity are emerging pandemics in the 21st century creating worldwide urgency for the development of novel and safe therapies. We investigated trace amine-associated receptor 1 (TAAR1) as a novel target contributing to the control of glucose homeostasis and body weight. Methods We investigated the peripheral human tissue distribution of TAAR1 by immunohistochemistry and tested the effect of a small molecule TAAR1 agonist on insulin secretion in vitro using INS1E cells and human islets and on glucose tolerance in C57Bl6, and db/db mice. Body weight effects were investigated in obese DIO mice. Results TAAR1 activation by a selective small molecule agonist increased glucose-dependent insulin secretion in INS1E cells and human islets and elevated plasma PYY and GLP-1 levels in mice. In diabetic db/db mice, the TAAR1 agonist normalized glucose excursion during an oral glucose tolerance test. Sub-chronic treatment of diet-induced obese (DIO) mice with the TAAR1 agonist resulted in reduced food intake and body weight. Furthermore insulin sensitivity was improved and plasma triglyceride levels and liver triglyceride content were lower than in controls. Conclusions We have identified TAAR1 as a novel integrator of metabolic control, which acts on gastrointestinal and pancreatic islet hormone secretion. Thus TAAR1 qualifies as a novel and promising target for the treatment of type 2 diabetes and obesity. [ABSTRACT FROM AUTHOR]
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- 2016
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16. P2-16 Caractéristiques des patients avec et sans traitement antipsychotique dans la cohorte PHRC-REAL
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P.H. Robert, O. Guerin, Michel Benoit, P. Bedoucha, P. Brocker, Laurent Lechowski, R. Boulhassas, C. Bertogliati, and V. Lafont
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Neurology ,Neurology (clinical) - Published
- 2005
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17. mTORC1 Inhibition Corrects Neurodevelopmental and Synaptic Alterations in a Human Stem Cell Model of Tuberous Sclerosis
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Costa, Veronica, Aigner, Stefan, Vukcevic, Mirko, Sauter, Evelyn, Behr, Katharina, Ebeling, Martin, Dunkley, Tom, Friedlein, Arno, Zoffmann, Sannah, Meyer, Claas A., Knoflach, Frédéric, Lugert, Sebastian, Patsch, Christoph, Fjeldskaar, Fatiha, Chicha-Gaudimier, Laurie, Kiialainen, Anna, Piraino, Paolo, Bedoucha, Marc, Graf, Martin, Jessberger, Sebastian, Ghosh, Anirvan, Bischofberger, Josef, and Jagasia, Ravi
- Abstract
Hyperfunction of the mTORC1 pathway has been associated with idiopathic and syndromic forms of autism spectrum disorder (ASD), including tuberous sclerosis, caused by loss of either TSC1or TSC2. It remains largely unknown how developmental processes and biochemical signaling affected by mTORC1 dysregulation contribute to human neuronal dysfunction. Here, we have characterized multiple stages of neurogenesis and synapse formation in human neurons derived from TSC2-deleted pluripotent stem cells. Homozygous TSC2deletion causes severe developmental abnormalities that recapitulate pathological hallmarks of cortical malformations in patients. Both TSC2+/−and TSC2−/−neurons display altered synaptic transmission paralleled by molecular changes in pathways associated with autism, suggesting the convergence of pathological mechanisms in ASD. Pharmacological inhibition of mTORC1 corrects developmental abnormalities and synaptic dysfunction during independent developmental stages. Our results uncouple stage-specific roles of mTORC1 in human neuronal development and contribute to a better understanding of the onset of neuronal pathophysiology in tuberous sclerosis.
- Published
- 2016
- Full Text
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18. Instruction de gradation des soins : une opportunité pour ancrer les activités de pharmacie clinique dans le parcours des patients atteints de cancer
- Author
-
Cormier, Nicolas, Bedoucha, Clément, Roux-Marson, Clarisse, Valery, Antoine, and Dufossez, François
- Abstract
La stratégie décennale de lutte contre les cancers lancée en 2021 met l’accent sur la structuration des soins de support comme axe fort pour lutter contre les effets secondaires des traitements et offrir aux patients des parcours plus fluides. Dans le même temps, l’instruction gradation des prises en charge ambulatoires parue en 2020, a introduit de nouvelles règles de facturation pour les prises en charges en hôpital de jour (HDJ), qui facilitent l’intervention de plusieurs professionnels de santé (médicaux, paramédicaux ou socio-éducatifs) de manière coordonnée auprès du patient. Parmi ces professionnels, le pharmacien a particulièrement sa place au sein des équipes pluridisciplinaires en cancérologie puisque les thérapies anticancéreuses prises par voie orale requièrent une adhésion thérapeutique et un continuum de prise en charge avec les professionnels de ville. Jusqu’à présent, ces activités de pharmacie clinique, qui incluent la réalisation de bilans de médication, l’élaboration de plans pharmaceutiques personnalisés et la conduite d’entretiens pharmaceutiques auprès des patients, peinaient à se développer de manière pérenne faute d’un mode de financement au sein des établissements de santé. L’instruction gradation représente désormais une réelle opportunité pour soutenir les actions de pharmacie clinique, notamment dans les HDJ. Dans la perspective de faire gagner du temps aux équipes hospitalières souhaitant consolider ou initier une telle activité, des points de vigilance et des facteurs facilitateurs sont à considérer.
- Published
- 2023
- Full Text
- View/download PDF
19. Accompagnement pharmaceutique des patients en sortie de chirurgie orthopédique
- Author
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Biasolo, C., Dumoulin, C., Bedoucha, C., Dulin, R., Gayral, M., and Marion, A.-C.
- Abstract
Dans une volonté de développer des activités de pharmacie clinique, la Pharmacie à usage intérieur (PUI) du Centre hospitalier de Libourne a priorisé ses actions dans les services de chirurgie, plus à risque d’incidents iatrogènes. Une première activité de conciliation des traitements médicamenteux (CTM) à l’admission a été mise en place. L’analyse pharmaceutique qui l’accompagne inclut tous les patients de chirurgie orthopédique (traumatologie et programmée). Le suivi des thérapeutiques à risque (anti-infectieux dans le cadre des infections ostéo-articulaires (IOA) et anticoagulants lors du relais oral/injectable) est particulièrement appliqué. Pour les patients concernés, une activité de CTM en sortie d’hospitalisation est mise en œuvre.
- Published
- 2022
- Full Text
- View/download PDF
20. Bilan à 10 mois de la mise en place de consultations tripartites : quel est l’impact du pharmacien ?
- Author
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Thomelin, L., Dumoulin, C., Bedoucha, C., Biasolo, C., Gayral, M., Dulin, R., and Marion, A.-C.
- Abstract
Les thérapies anticancéreuses orales (TAO) connaissent un essor considérable depuis plusieurs années. Le traitement ambulatoire nécessite une observance irréprochable et un accompagnement éducatif du patient pour le bon usage de son traitement. Les consultations tripartites médecin, pharmacien, infirmier diplômé d’état (IDE) sont une des activités pivot de ce parcours patient.
- Published
- 2022
- Full Text
- View/download PDF
21. Impact of genioplasty during puberty on the upper airways
- Author
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Bedoucha, Valérie, Boutin, François, and Frapier, Laure
- Abstract
Mouth breathing is a functional disorder that affects craniofacial and dento-alveolar growth and also upper airway (UA) anatomy. This is apparent mainly in dimensional abnormalities of the UA caused by hypertrophy of Waldeyer's ring and excessive vertical development of the lower part, giving rise to labial incompetence that perpetuates the functional disorder. The main aim of this study was to evaluate the development of the oropharyngeal structures in young hyperdivergent patients who had undergone functional genioplasty in the context of orthodontic treatment.
- Published
- 2015
- Full Text
- View/download PDF
22. Impact de la génioplastie en période pubertaire sur les voies aériennes supérieures
- Author
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Bedoucha, Valérie, Boutin, François, and Frapier, Laure
- Abstract
La ventilation orale est une dysfonction qui retentit sur la croissance craniofaciale et dento-alvéolaire ainsi que sur l’anatomie des voies aériennes supérieures (VAS). Elle se manifeste notamment par un mauvais calibrage des VAS perturbé par l’hypertrophie de l’anneau de Waldeyer et par un excès vertical de l’étage inférieur responsable d’une béance labiale qui entretient la dysfonction. L’objectif principal de cette étude était d’évaluer l’évolution de la sphère oropharyngée chez de jeunes patients hyperdivergents ayant bénéficié d’une génioplastie fonctionnelle dans le cadre d’un traitement orthodontique.
- Published
- 2015
- Full Text
- View/download PDF
23. Pathogénie et traitement du syndrome de Lance et Adams Étude de trois cas avec effet à long-terme du piracetam
- Author
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C. Desnuelle, P. Bedoucha, M. Lanteri-Minet, M. Chatel, and M. H. Mahagne
- Subjects
Long lasting ,business.industry ,Anesthesia ,Gastroenterology ,Internal Medicine ,medicine ,Piracetam ,Open label ,medicine.symptom ,business ,Myoclonus ,medicine.drug - Abstract
We report three patients presenting the typical features of Lance-Adams syndrome (LAS) treated with piracetam (24g/d) in open trial. Our findings clearly reveal the beneficial (reduction of the myoclonus clinical score from 42 %, 72 % and 92 % respectively) and long lasting (follow-up from 2 years) effect of piracetam for the treatment of LAS.
- Published
- 1992
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- View/download PDF
24. Diabetic KKAy mice exhibit increased hepatic PPARg1 gene expression and develop hepatic steatosis upon chronic treatment with antidiabetic thiazolidinediones
- Author
-
Bedoucha, M., Atzpodien, E., and Boelsterli, U. A.
- Published
- 2001
- Full Text
- View/download PDF
25. Down-regulation by troglitazone of hepatic tumor necrosis factor-a and interleukin-6 mRNA expression in a murine model of non-insulin-dependent diabetes
- Author
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Sigrist, S., Bedoucha, M., and Boelsterli, U. A.
- Published
- 2000
- Full Text
- View/download PDF
26. Baculovirus cDNA libraries for expression cloning of genes encoding cell-surface antigens
- Author
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Granziero, L., Nelboeck, P., Bedoucha, M., Lanzavecchia, A., and Reid, H. H.
- Published
- 1997
- Full Text
- View/download PDF
27. Total plasma homocysteine determination by liquid chromatography before and after methionine loading. Results in cerebrovascular disease
- Author
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Candito, M., Bedoucha, P., Mahagne, M. H., Scavini, G., and Chatel, M.
- Published
- 1997
- Full Text
- View/download PDF
28. 2-dimensional immunoelectrophoresis of CSF proteins
- Author
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P, Martin, P, Chambon, A M, Michel, and P, Bedoucha
- Subjects
Brain Diseases ,Epilepsy ,Brain Neoplasms ,Immune Sera ,Nerve Compression Syndromes ,Cerebrospinal Fluid Proteins ,Parkinson Disease ,Paresis ,Cerebrovascular Disorders ,Meningoencephalitis ,Tabes Dorsalis ,Humans ,Polyradiculopathy ,Immunoelectrophoresis ,Immunoelectrophoresis, Two-Dimensional - Abstract
Two-dimensional electrophoresis isolates the various proteins in the CSF in peaks ; this a method which gives very reliable results ; the height of the peaks has a certain quantitative value, similar to that obtained with electro-immunodiffusion. The peaks visible in the CSF can be increased separately -- mainly the "alpha 2", "alpha 2 beta", the IgA and IgG peaks -- in another type of recording, the height and number of the peaks may be increased, indicating the presence in the CSF of normally absent protein originating in the serum. An increase in the "alpha 2" or "alpha 2 beta" peaks is not specific, but it is always indicative that the development of a neurological process is under way ; the increase of IgG and IgA retains its character of great specificity in evolutive inflammatory conditions. Multiple peaks indicate the passage of serum proteins into the CSF in oedematous and destructive processes, in expansive or compressive processes and in polyradiculoneuritis. This method with its well-codified technique, which may be carried out on an unconcentrated CSF without risk of denaturing the proteins, may be carried out routinely in clinical practice with human anti-serum immune serum or with more specific serum, anti CSF for example, which seems to give quite reliable results.
- Published
- 1976
29. [A case of myopathy with carnitine deficiency]
- Author
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P, Martin, H, Carrier, J F, Renaud, B, Kullmann, E, Delpont, G, Romey, B, Cartier, and P, Bedoucha
- Subjects
Muscular Diseases ,Histocytochemistry ,Carnitine ,Culture Techniques ,Muscles ,Action Potentials ,Humans ,Female ,Lipid Metabolism - Abstract
Clinical and biological criteria of myopathies associated with carnitine deficiency allow to distinguish a muscular and a systemic form of the condition. In this report, the results of clinical, pathological and electrophysiological data obtained from a patient with carnitine deficiency-linked myopathy are described. The patient was a 23-year-old girl who was previously known to suffer from muscle weakness when suddenly acidosis associated with a severe drop in plasma carnitine appeared. In addition there were hypermetabolic symptoms similar to those described in Luft's syndrome. Biopsy from the quadriceps femoris muscle before treatment revealed that all type I fibers were either hypotrophic or atrophic. They showed lipid overloading manifested by triglyceride droplets adjacent to the mitochondrial membrane. Furthermore, the level of soluble muscle carnitine was 83 p. 100 less than in controls and membrane linked muscle carnitine was also 73.5 p. 100 less than in controls. The patient rapidly recovered after the initiation of daily treatment with 4.40 g carnitine chlorhydrate associated with 50 g Lipogram 20. Nine months later, lipid overloading completely disappeared and the level of plasma carnitine returned to near normal whereas the level of both soluble and linked carnitine remained very low. To provide more information on the origin of the myopathy (myogenic, neurogenic or humoral) we carried out an electrophysiological investigation of cultured skeletal muscle cells from the patient and from biopsies of patients not known to be suffering from myopathy. The electrophysiological data showed that the patient myotubes were less polarized than myotubes from control patients. Furthermore, the amplitude of the action potential was smaller than the amplitude of the action potential measured in control cells. Daily addition of 50 microM carnitine chlorhydrate to the cultured myotubes induced a recovery of the action potential amplitude. Taken together these results indicate that the carnitine deficiency reported here was probably of systemic origin in addition to a myogenic component. Muscle deficiency could be either linked to an alteration in the carnitine pathway or to overconsumption of carnitine by muscle. This latter point is discussed.
- Published
- 1986
30. [Bidimensional electrophoresis in the study of cerebrospinal fluid protein (author's transl)]
- Author
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A M, Michel, P, Chambon, A M, Soummer, P, Martin, and P, Bedoucha
- Subjects
Humans ,Immunoglobulins ,Cerebrospinal Fluid Proteins ,Immunoelectrophoresis ,Immunoelectrophoresis, Two-Dimensional - Abstract
The authors report 650 bidimensional electrophoreses of the cerebrospinal fluid (CSF). All examinations were carried out after prior concentration of CSF protein. The technic used is that described by Rebeyrotte in 1970. Four types of tracing were noted: -- Two tracings were unusual by the presence of a large peak in the alpha-2 region. -- One tracing was of the hypergamma type. -- One tracing was comparable to serum by the richness of the precipitations. A change in the first migration permitted us to obtain electrophoretic separations from 100 microlitres of pure CSF. The bidimensional immunoelectrophoresis tracings are comparable to those described previously.
- Published
- 1976
31. [Letter: Painless or nearly painless gaseous encephalography]
- Author
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P, Martin, M J, Vallade, and P, Bedoucha
- Subjects
Headache ,Humans ,Punctures ,Pneumoencephalography ,Cerebrospinal Fluid - Published
- 1976
32. 2-dimensional immunoelectrophoresis and cerebrospinal fluid protein profile in optic neuropathies and uveitis
- Author
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P, Martin, P, Bedoucha, J, Fantin, G, Denis, M, Borg, and A M, Michel
- Subjects
Uveitis ,Optic Nerve Diseases ,Humans ,Cerebrospinal Fluid Proteins ,Immunoelectrophoresis, Two-Dimensional - Published
- 1982
33. [Acute chorea and disseminated lupus erythematosus (author's transl)]
- Author
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P, Martin and P, Bedoucha
- Subjects
Adult ,Diagnosis, Differential ,Chorea ,Humans ,Lupus Erythematosus, Systemic ,Female ,Autoantibodies - Abstract
A case of acute chorea in a young woman with disseminated lupus erythematosus is described and 27 similar cases reported in the literature are reviewed. As in other neurological complications of the disease, signs of diffuse, labile angeitis (dysoric nodules) were present as well as antilymphocyte antibodies characteristics of these forms. Acute chorea is however a rare finding when compared with other types of complications. It keeps its clinical picture resembling that of Sydenham's chorea, and with which is can be compared also as regard the immunological syndromes frequently observed in acute rheumatic fever, and that which occasionally occurs during disseminated lupus erythematosus.
- Published
- 1981
34. Patient-Reported Quality of Life before and after Stopping Treatment in the ENESTfreedom Trial of Treatment-Free Remission for Patients with Chronic Myeloid Leukemia in Chronic Phase
- Author
-
Hochhaus, Andreas, Casares, Maria Teresa Gómez, Stentoft, Jesper, Conneally, Eibhlin, García-Gutiérrez, Valentin, Gattermann, Norbert, Wiktor-Jedrzejczak, Wieslaw, Le Coutre, Philipp D., Martino, Bruno, Saussele, Susanne, Giles, Francis J., Radich, Jerald P., Ross, David M., Menssen, Hans D., Deng, Weiping, Brandt, Patricia, Gnanasakthy, Ari, Bedoucha, Veronique, and Saglio, Giuseppe
- Abstract
Hochhaus: BMS: Honoraria, Research Funding; Novartis: Honoraria, Research Funding; Pfizer: Honoraria, Research Funding; ARIAD: Honoraria, Research Funding. Casares:Novartis: Consultancy, Speakers Bureau; BMS: Consultancy, Speakers Bureau; Ariad: Consultancy, Speakers Bureau. Stentoft:Pfizer: Research Funding; Ariad: Research Funding; Bristol-Myers-Squibb: Research Funding; Novartis: Research Funding. Conneally:Novartis: Honoraria, Membership on an entity's Board of Directors or advisory committees; BMS: Honoraria, Membership on an entity's Board of Directors or advisory committees; Pfizer: Honoraria, Membership on an entity's Board of Directors or advisory committees; Gilead: Honoraria, Membership on an entity's Board of Directors or advisory committees. García-Gutiérrez:Ariad: Consultancy, Research Funding; BMS: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding. Gattermann:Celgene: Consultancy, Honoraria, Research Funding; Novartis: Consultancy, Honoraria, Other: travel, accomodation expenses, Research Funding. Wiktor-Jedrzejczak:Sandoz: Consultancy; BMS: Research Funding; Novartis: Consultancy, Research Funding; Janssen-Cilag: Consultancy; Angelini: Consultancy; Novartis: Consultancy, Research Funding; Celgene: Consultancy; Amgen Inc.: Research Funding. Le Coutre:Ariad: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; BMS: Consultancy, Honoraria, Other: travel, accomodations, expenses; Novartis: Consultancy, Honoraria, Other: travel, accomocations, expenses, Research Funding. Saussele:ARIAD: Honoraria; Novartis: Honoraria, Other: Travel grants, Research Funding; Pfizer: Honoraria, Other: Travel grants; BMS: Honoraria, Other: Travel grants, Research Funding. Giles:Novartis: Consultancy, Research Funding. Radich:Ariad: Consultancy; BMS: Consultancy; Novartis: Consultancy, Research Funding. Ross:BMS: Honoraria; Novartis Pharmaceuticals: Honoraria, Research Funding. Menssen:Novartis Pharma AG: Employment. Deng:Novartis Phamaceuticals Corp.: Employment. Brandt:Novartis: Employment. Gnanasakthy:Novartis: Consultancy, Equity Ownership, Research Funding. Bedoucha:Novartis: Employment. Saglio:Novartis: Consultancy, Honoraria; BMS: Consultancy, Honoraria; Ariad: Consultancy, Honoraria; Pfizer: Consultancy, Honoraria; Roche: Consultancy, Honoraria.
- Published
- 2016
- Full Text
- View/download PDF
35. Hypertension artérielle pulmonaire et grossesse : à propos d’un cas
- Author
-
Bedoucha, M., Rois, M., Coustel, M.-A., Coatleven, F., and Horovitz, J.
- Abstract
L’hypertension artérielle pulmonaire (HTAP) est une maladie caractérisée par une obstruction progressive du lit vasculaire pulmonaire causant une augmentation des résistances vasculaires pulmonaires (RVP) et une insuffisance cardiaque droite secondaire. La grossesse chez la femme atteinte d’HTAP est un événement rare (1/100 000). Elle est responsable d’une mortalité et morbidité maternelle et fœtale très importantes avec un taux de mortalité maternelle compris entre 30 à 50 %. Par conséquent les experts contre-indiquent la grossesse chez ces femmes souffrant d’HTAP. Cependant, grâce à de récentes avancées dans le traitement spécifique de l’HTAP et à des soins pluridisciplinaires, le taux de mortalité maternelle dans HTAP semble avoir diminué.
- Published
- 2016
- Full Text
- View/download PDF
36. Isolated Ischemic Third-Nerve Palsy as a Warning Sign of Severe Internal Carotid Artery Stenosis
- Author
-
Mahagne, Maire-Hélène, Dunac, Antoine, Bedoucha, Pierre, and Chatel, Marcel
- Published
- 2002
- Full Text
- View/download PDF
37. Novel Mutation in Prion Protein Gene Causative of GerstmannStrausslerScheinker Disease
- Author
-
Delmont, Emilien, Peoc'h, Katell, Haik, Stephane, Brandel, Jean-Philippe, Hauw, Jean-Jacques, Chasseigneaux, Stephanie, Lenne, Martine, Laplanche, Jean-Louis, Chatel, Marcel, and Bedoucha, Piere
- Published
- 2006
38. Substitutions at residue 211 in the prion protein drive a switch between CJD and GSS syndrome, a new mechanism governing inherited neurodegenerative disorders.
- Author
-
Peoc'h K, Levavasseur E, Delmont E, De Simone A, Laffont-Proust I, Privat N, Chebaro Y, Chapuis C, Bedoucha P, Brandel JP, Laquerriere A, Kemeny JL, Hauw JJ, Borg M, Rezaei H, Derreumaux P, Laplanche JL, and Haïk S
- Subjects
- Amino Acid Substitution, Cloning, Molecular, Creutzfeldt-Jakob Syndrome pathology, Gerstmann-Straussler-Scheinker Disease pathology, Humans, Models, Molecular, Molecular Dynamics Simulation, Mutation, Phenotype, Phosphorylation, Plaque, Amyloid genetics, Plaque, Amyloid metabolism, Prions metabolism, Protein Conformation, Creutzfeldt-Jakob Syndrome genetics, Gerstmann-Straussler-Scheinker Disease genetics, Prions genetics
- Abstract
Human prion diseases are a heterogeneous group of fatal neurodegenerative disorders, characterized by the deposition of the partially protease-resistant prion protein (PrP(res)), astrocytosis, neuronal loss and spongiform change in the brain. Among inherited forms that represent 15% of patients, different phenotypes have been described depending on the variations detected at different positions within the prion protein gene. Here, we report a new mechanism governing the phenotypic variability of inherited prion diseases. First, we observed that the substitution at residue 211 with either Gln or Asp leads to distinct disorders at the clinical, neuropathological and biochemical levels (Creutzfeldt-Jakob disease or Gerstmann-Sträussler-Scheinker syndrome with abundant amyloid plaques and tau neurofibrillar pathology). Then, using molecular dynamics simulations and biophysical characterization of mutant proteins and an in vitro model of PrP conversion, we found evidence that each substitution impacts differently the stability of PrP and its propensity to produce different protease resistant fragments that may contribute to the phenotypical switch. Thus, subtle differences in the PrP primary structure and stability are sufficient to control amyloid plaques formation and tau abnormal phosphorylation and fibrillation. This mechanism is unique among neurodegenerative disorders and is consistent with the prion hypothesis that proposes a conformational change as the key pathological event in prion disorders.
- Published
- 2012
- Full Text
- View/download PDF
39. The apathy inventory: assessment of apathy and awareness in Alzheimer's disease, Parkinson's disease and mild cognitive impairment.
- Author
-
Robert PH, Clairet S, Benoit M, Koutaich J, Bertogliati C, Tible O, Caci H, Borg M, Brocker P, and Bedoucha P
- Subjects
- Aged, Awareness, Female, Humans, Male, Middle Aged, Mood Disorders psychology, Reproducibility of Results, Alzheimer Disease psychology, Cognition Disorders psychology, Mood Disorders diagnosis, Motivation, Parkinson Disease psychology, Psychiatric Status Rating Scales standards
- Abstract
Objective: This study was designed to establish the validity and reliability of the apathy inventory (IA), a rating scale for global assessment of apathy and separate assessment of emotional blunting, lack of initiative, and lack of interest., Method: Information for the IA can be obtained from the patient or from a caregiver. We evaluated 115 subjects using the IA, consisting of 19 healthy elderly subjects, 24 patients with Mild Cognitive Impairment (MCI), 12 subjects with Parkinson's disease (PD) and 60 subjects with Alzheimer's disease (AD)., Results: Internal consistency, item reliability, and between-rater reliability were high. A test-retest reliability study demonstrated that caregiver responses to IA questions were stable over short intervals. A concurrent validity study showed that the IA assesses apathy as effectively as the Neuro Psychiatric Inventory apathy domain. In the caregiver-based evaluation, AD subjects had significantly higher scores than controls, both for global apathy score and for the lack of interest dimension. When the AD patients were subdivided according to diagnostic criteria for apathy, apathetic patients had significantly higher scores than non apathetic patients. With the patient-based evaluations, no differences were found among the AD, MCI and control groups. The scores in the patient-based evaluations were only higher for the PD group versus the control subjects. The results also indicated that AD patients had poor awareness of their emotional blunting and lack of initiative., Conclusions: The IA is a reliable method for assessing in demented and non-demented elderly subjects several dimensions of the apathetic syndrome, and also the subject's awareness of these symptoms., (Copyright 2002 John Wiley & Sons, Ltd.)
- Published
- 2002
- Full Text
- View/download PDF
40. [Cerebral vascular complication of hyperhomocysteinemia. Controlling thromboembolic complications with folates].
- Author
-
Candito M, Bedoucha P, Jambou D, Appert-Flory A, Fisher F, Parrot-Roulaud F, Bayle J, Van Obberghen E, and Chatel M
- Subjects
- Adult, Factor V genetics, Female, Homocysteine genetics, Homocysteine metabolism, Homozygote, Humans, Intracranial Embolism and Thrombosis drug therapy, Leg blood supply, Methylenetetrahydrofolate Dehydrogenase (NADP) genetics, Mutation, Thrombosis drug therapy, Thrombosis prevention & control, Folic Acid therapeutic use, Homocysteine blood, Intracranial Embolism and Thrombosis blood
- Abstract
Background: Young patients who experience cardiovascular events may have raised levels of homocysteine. There may be several causes for this hyperhomocysteinemia., Case Report: Cerebrovascular disease occurred in a 40-year-old female smoker with hyperhomocysteinemia. This patient subsequently had several episodes of thromboembolism involving the brain and lower limb arteries. Prothrombin concentration was difficult to control with antivitamin K anticoagulants. Investigations to identify a genetic cause of hyperhomocysteinemia revealed that she was homozygous for the C677T mutation on the methylenetetrahydrofolate reductase gene. There was no G1691A mutation of the factor V gene, a risk factor for familial thrombosis. Supplementation with folic acid successfully halted episodes of thromboembolism (follow-up 2 years) and prothrombin levels stabilized under treatment., Discussion: The C677T mutation, which is common in the general population (15.7%), cannot explain the effect of folate supplementation alone. Other mutations affecting homocysteine metabolism could have a potentializing effect on vascular events.
- Published
- 1997
41. [Transesophageal echocardiography in the etiological evaluation of ischemic cerebral vascular accidents. Value in young subjects].
- Author
-
Ferrari E, Sarzotti S, Gibelin P, Mahagne MH, Thomas P, Bedoucha P, Baudouy M, and Morand P
- Subjects
- Adult, Arteriosclerosis complications, Arteriosclerosis diagnostic imaging, Brain Ischemia etiology, Cardiomyopathies complications, Cardiomyopathies diagnostic imaging, Female, Heart Aneurysm complications, Heart Diseases complications, Heart Diseases diagnostic imaging, Humans, Male, Middle Aged, Mitral Valve Prolapse complications, Thrombosis complications, Thrombosis diagnostic imaging, Brain Ischemia diagnostic imaging, Echocardiography, Transesophageal methods, Heart Aneurysm diagnostic imaging, Heart Septum diagnostic imaging, Mitral Valve Prolapse diagnostic imaging
- Abstract
Objectives: We conducted this study to evaluate the role of transoesophageal echocardiography in the aetiologic diagnosis of ischaemic cerebral vascular events in young subjects., Methods: Over a 16-month period, 70 consecutive patients under 55 (mean age 49 years; range 32-55; 34 females, 36 males) underwent transoesophageal echocardiography as part of a complete work-up after a recent (< 1 month) cerebral event considered to be ischaemic in nature. Exclusion criteria were age over 55, vascular stenosis or ulcerated plaque, embologenic heart disease and valve prosthesis. 24-h Holter recordings were also obtained in all patients., Results: The cerebral event was temporary in 11 subjects and permanent in the other 59. The ischaemic nature of the event was confirmed in all patients with computed tomography or magnetic resonance imagery. All patients were in sinus rhythm at examination and supraventricular paroxysmal arrhythmia was observed in 7 during the Holter recordings. The transoesophageal echocardiography was normal in 37 patients (52%) and pathologic in 33 (48%). The source of the embolus was identified in 4 cases (6%) and the probable cause of the cerebral event was found in 29 (42%). Among the abnormal structures observed were permeable oval foramens, inter-atrial septum aneurysms and plaques on the ascending aorta., Conclusions: In our selected population of patients under 55 years of age, transoesophageal echocardiography detected the certain or probable source of the ischaemic cerebral event in 48% of the cases, a diagnostic yield better than most other methods. Nevertheless, there is no known therapeutic response to several of the potential sources of embolus observed.
- Published
- 1994
42. [Sclerosis of varicose veins of the lower limbs causing ischemic cerebral accident].
- Author
-
Drai E, Ferrari E, Bedoucha P, Mihoubi A, Baudouy M, and Morand P
- Subjects
- Humans, Male, Middle Aged, Saline Solution, Hypertonic therapeutic use, Ischemic Attack, Transient etiology, Saline Solution, Hypertonic adverse effects, Sclerotherapy adverse effects, Varicose Veins therapy
- Published
- 1994
43. [Infarction of the caudate nucleus or anterior striato-capsular infarction?].
- Author
-
Milhaud D, Magnié MN, Roger PM, and Bedoucha P
- Subjects
- Adult, Aged, Aged, 80 and over, Cerebral Infarction complications, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Prognosis, Terminology as Topic, Tomography, X-Ray Computed, Caudate Nucleus, Cerebral Infarction diagnosis
- Abstract
Eight patients with caudate nucleus infarcts are reported. The main clinical findings were often transient facio-brachial weakness (6 patients), depression (4 patients), subcortical aphasia with decreased spontaneous verbal activity (2 patients), and aboulia (2 patients). The ischemic lesions of caudate nucleus often extend into the adjacent anterior limb of the internal capsule and the anterior putamen owing to vascularization pattern. The specific clinical picture of this entity also includes lesions of nearby white matter tracts. Risk factors, etiology of infarcts, clinical findings and prognosis were similar to those reported in striato-capsular infarcts. We suggest replacing the term caudate infarct by anterior striato-capsular infarct.
- Published
- 1994
44. [Neuroradiological exploration of posthypoxic intention and action myoclonus syndrome].
- Author
-
Lantéri-Minet M, Bedoucha P, Chanalet S, Mahagne MH, and Chatel M
- Subjects
- Humans, Magnetic Resonance Imaging, Syndrome, Tomography, X-Ray Computed, Myoclonus diagnostic imaging
- Published
- 1992
45. [Metal-induced brain embolism after gunshot wound of the heart].
- Author
-
Lantéri-Minet M, Bedoucha P, Mahagne MH, Chanalet S, Jourdan J, and Chatel M
- Subjects
- Adult, Female, Humans, Intracranial Embolism and Thrombosis diagnostic imaging, Time Factors, Tomography, X-Ray Computed, Foreign Bodies complications, Heart Injuries complications, Intracranial Embolism and Thrombosis etiology, Metals adverse effects, Wounds, Gunshot complications
- Published
- 1992
46. [Cholesterol emboli with neurologic manifestation in the spinal cord].
- Author
-
Desnuelle C, Lanteri-Minet M, Hofman P, Butori C, Bedoucha P, and Chatel M
- Subjects
- Aged, Aortic Aneurysm, Abdominal complications, Eosinophilia etiology, Humans, Male, Muscular Atrophy etiology, Paresis etiology, Cholesterol, Embolism, Fat complications, Spinal Cord Diseases etiology
- Abstract
A 71-year old man presented with a progressive chronic paraparesis combined with inflammatory biological features including hypereosinophilia and an aneurysm of the abdominal aorta. Disseminated cholesterol embolization of arterioles was evidenced by the identification of cholesterol crystals in biopsies of the quadriceps muscle and of an iliac lymph node. Despite the lack of post mortem study of the spinal cord, the presentation was highly suggestive of cholesterol emboli in the spinal arteries. Only ten documented cases have been reported.
- Published
- 1992
47. [Orbital apex syndrome disclosing naso-oculo-cerebral zygomycosis].
- Author
-
Mahagne MH, Hofman P, Bedoucha P, Lanteri Minet M, and Chatel M
- Subjects
- Aged, Amphotericin B therapeutic use, Diabetic Neuropathies etiology, Ethmoid Bone surgery, Ethmoid Sinusitis pathology, Ethmoid Sinusitis surgery, Humans, Male, Mucormycosis drug therapy, Orbital Diseases pathology, Orbital Diseases therapy, Syndrome, Ethmoid Sinusitis microbiology, Mucormycosis complications, Orbital Diseases etiology
- Abstract
In a 70-year-old male patient with untreated diabetes a febrile orbital apex syndrome of rapid onset revealed a rhino-orbito-cerebral zygomycosis. Biopsies of the ethmoidal mucosa showed numerous colonies of the Rhizopus genus. Despite medical treatment (amphotericin B) and surgery (ethmoidectomy), the patient died within one week. Rhino-cerebral zygomycosis is a rare disease which occurs in diabetic and immunocompromised patients.
- Published
- 1992
48. [A case of myopathy with carnitine deficiency].
- Author
-
Martin P, Carrier H, Renaud JF, Kullmann B, Delpont E, Romey G, Cartier B, and Bedoucha P
- Subjects
- Action Potentials, Culture Techniques, Female, Histocytochemistry, Humans, Lipid Metabolism, Muscles metabolism, Muscular Diseases physiopathology, Carnitine deficiency, Muscles pathology, Muscular Diseases pathology
- Abstract
Clinical and biological criteria of myopathies associated with carnitine deficiency allow to distinguish a muscular and a systemic form of the condition. In this report, the results of clinical, pathological and electrophysiological data obtained from a patient with carnitine deficiency-linked myopathy are described. The patient was a 23-year-old girl who was previously known to suffer from muscle weakness when suddenly acidosis associated with a severe drop in plasma carnitine appeared. In addition there were hypermetabolic symptoms similar to those described in Luft's syndrome. Biopsy from the quadriceps femoris muscle before treatment revealed that all type I fibers were either hypotrophic or atrophic. They showed lipid overloading manifested by triglyceride droplets adjacent to the mitochondrial membrane. Furthermore, the level of soluble muscle carnitine was 83 p. 100 less than in controls and membrane linked muscle carnitine was also 73.5 p. 100 less than in controls. The patient rapidly recovered after the initiation of daily treatment with 4.40 g carnitine chlorhydrate associated with 50 g Lipogram 20. Nine months later, lipid overloading completely disappeared and the level of plasma carnitine returned to near normal whereas the level of both soluble and linked carnitine remained very low. To provide more information on the origin of the myopathy (myogenic, neurogenic or humoral) we carried out an electrophysiological investigation of cultured skeletal muscle cells from the patient and from biopsies of patients not known to be suffering from myopathy. The electrophysiological data showed that the patient myotubes were less polarized than myotubes from control patients. Furthermore, the amplitude of the action potential was smaller than the amplitude of the action potential measured in control cells. Daily addition of 50 microM carnitine chlorhydrate to the cultured myotubes induced a recovery of the action potential amplitude. Taken together these results indicate that the carnitine deficiency reported here was probably of systemic origin in addition to a myogenic component. Muscle deficiency could be either linked to an alteration in the carnitine pathway or to overconsumption of carnitine by muscle. This latter point is discussed.
- Published
- 1986
49. [2-dimensional immunoelectrophoresis of CSF proteins].
- Author
-
Martin P, Chambon P, Michel AM, and Bedoucha P
- Subjects
- Brain Diseases cerebrospinal fluid, Brain Neoplasms cerebrospinal fluid, Cerebrovascular Disorders cerebrospinal fluid, Epilepsy cerebrospinal fluid, Humans, Immune Sera, Meningoencephalitis cerebrospinal fluid, Nerve Compression Syndromes cerebrospinal fluid, Paresis cerebrospinal fluid, Parkinson Disease cerebrospinal fluid, Polyradiculopathy cerebrospinal fluid, Tabes Dorsalis cerebrospinal fluid, Cerebrospinal Fluid Proteins analysis, Immunoelectrophoresis, Immunoelectrophoresis, Two-Dimensional
- Abstract
Two-dimensional electrophoresis isolates the various proteins in the CSF in peaks ; this a method which gives very reliable results ; the height of the peaks has a certain quantitative value, similar to that obtained with electro-immunodiffusion. The peaks visible in the CSF can be increased separately -- mainly the "alpha 2", "alpha 2 beta", the IgA and IgG peaks -- in another type of recording, the height and number of the peaks may be increased, indicating the presence in the CSF of normally absent protein originating in the serum. An increase in the "alpha 2" or "alpha 2 beta" peaks is not specific, but it is always indicative that the development of a neurological process is under way ; the increase of IgG and IgA retains its character of great specificity in evolutive inflammatory conditions. Multiple peaks indicate the passage of serum proteins into the CSF in oedematous and destructive processes, in expansive or compressive processes and in polyradiculoneuritis. This method with its well-codified technique, which may be carried out on an unconcentrated CSF without risk of denaturing the proteins, may be carried out routinely in clinical practice with human anti-serum immune serum or with more specific serum, anti CSF for example, which seems to give quite reliable results.
- Published
- 1976
50. [Acute chorea and disseminated lupus erythematosus (author's transl)].
- Author
-
Martin P and Bedoucha P
- Subjects
- Adult, Autoantibodies analysis, Chorea immunology, Diagnosis, Differential, Female, Humans, Lupus Erythematosus, Systemic immunology, Chorea etiology, Lupus Erythematosus, Systemic complications
- Abstract
A case of acute chorea in a young woman with disseminated lupus erythematosus is described and 27 similar cases reported in the literature are reviewed. As in other neurological complications of the disease, signs of diffuse, labile angeitis (dysoric nodules) were present as well as antilymphocyte antibodies characteristics of these forms. Acute chorea is however a rare finding when compared with other types of complications. It keeps its clinical picture resembling that of Sydenham's chorea, and with which is can be compared also as regard the immunological syndromes frequently observed in acute rheumatic fever, and that which occasionally occurs during disseminated lupus erythematosus.
- Published
- 1981
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