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Derlon J. M., Petit-taboué M. C., Dauphin F., Courtheoux P., Chapon F., Creissard P., Darcel F., Houtteville J. P., Kaschten, B., Sadzot, B., Stevenaert, A., Tjuvajev, Juri G., Macapinlac, Homer A., Daghighian, Farhad, Ginos, James Z., Finn, Ronald D., Jiaju Zhang, M. S., Beattie, Bradley, Graham, Martin, Larson, Steven M., Blasberg, Ronald G., Levivier, M., Goldman, S., Pirotte, B., Brucher, J. M., Balériaux, D., Luxen, A., Hildebrand, J., Brotchi, J., Go K. G., Kamman R. L., Mooyaart E. L., Heesters M. A. A. M., Sijens, P. E., Oudksrk, M., van Dijk, P., Levendag, P. C., Vecht, Ch. J., Metz, R. J., Kennedy, D. N., Rosen, B. R., Hochberg, F. H., Fishman, A. J., Filipek, P. A., Caviness, V. S., Gross, M. W., Weinzierl, F. X., Trappe, A. E., Goebel, W. E., Frank, A. M., Becker, Georg, Krone, Andreas, Schmidt, Karsten, Hofmann, Erich, Bogdahn, Ulrich, Bencsch, H., Fclber, S., Finkenstedt, G., Kremser, C., Sfockhammer, G., Aichner, F., Bogdahn U., Fröhlich T., Becker G., Krone A., Schlief R., Schürmann J., Jachimczak P., Hofmann E., Roggendorf W., Roosen K., Carapella, C. M., Carpinelli, G., Passalacqua, R., Raus, L., Giannini, M., Mastrostefano, R., Podo, F., Tofani, A., Maslrostefano, R., Mottoles, M., Ferraironi, A., Scelsa, M. G., Oppido, P., Riccio, A., Maini, C. L., Collombier, L., Taillandier, L., Dcbouverie, M., Laurens, M. H., Thouvenot, P., Weber, M., Bertrand, A., Cruickshank G. S., Patterson J., Hadley D., De Witte, Olivier, Hildebrand, Jerzy, Luxen, André, Goldman, Serge, Ernestus, R. -I., Bockhorst, K., Eis, M., Els, T., Hoehn-Berlage, M., Gliese, M., Fründ, R., Geissler, A., Woertgen, C., Holzschuh, M., Goldman, Serge, Levivier, M., Pirotte, B., Brucher, J. M., Luxen, A., Brotchi, J., Hildebrand, J., Hausmann, O., Merlo, A., Jerrnann, E., Uirich, J., Chiquet-Ehrismann, R., Müller, J., Mäcke, H., Gratzl, O., Herholz, K., Ghaemi, M., Würker, M., Pietrzyk, U., Heiss, W. -D., Kotitschke, K., Brandl, M., Tonn, J. C., Haase, A., Bogdahn, U., Kotitschke, K., Muigg, S., Felber, S., Aichner, F., Haase, A., Bogdahn, U., Krone A., Becker G., Woydt M., Roggendorf W., Hofmann E., Bogdahn U., Roosen K., Lanfermann, Heinrich, Heindel, Walter, Kugel, Harald, Erneslus, Ralf -Ingo, Röhn, Gabricle, Lackner, Klaus, Metz, R. J., Kennedy, D. N., Pardo, F. S., Kutke, S., Sorensen, A. G., Hochberg, F. H., Fishman, A. J., Filipek, P. A., Rosen, B. R., Caviness, V. S., Mechtler, L. L., Withiam-Lench, S., Shin, K., Klnkel, W. R., Patel, M., Truax, B., Kinkel, P., Shin, K., Mechtler, L., Ricci M., Pantano P., Maleci A., Pierallini S., Di Stefano D., Bozzao L., Cantore G. P., Röhn, Gabriele, Els, T., Schröder, R., Hoehn-Berlage, M., Ernestus, R. -I., Ruda, R., Mocellini, C., Soffietti, R., Campana, M., Ropolo, R., Riva, A., de Filippi, P. G., Schiffer, D., Salgado D., Rodrigues M., Salgado L., Fonseca A. T., Vieira M. R., Bravo Marques J. M., Satoh, H., Uozumi, T., Kiya, K., Kurisu, K., Arita, K., Sumida, M., Ikawa, F., Tzuk-Shina, Tz., Gomori, J. M., Rubinstein, R., Lossos, A., Siegal, T., Vaalburg, W., Paans, A. M. J., Willemsen, A. T. M., van Waarde, A., Pruim, J., Visser, G. M., Go, K. G., Valentini, S., Ting, Y. L. T., De Rose, R., Chidichimo, G., Corricro, G., van Lcycn-Pilgram, Karin, Erncslus, Ralf -Ingo, Klug, Norfried, van Leyen-Pilgram, K., Ernestus, R. -I., Schröder, R., Klug, N., Woydt M., Krone A., Tonn J. C., Becker G., Neumann U., Roggendorf W., Roosen K., Plate, Karl H., Breier, Georg, Millaucr, Birgit, Weich, Herbert A., Ullrich, Axel, Risau, Werner, Roosen N., Chopra R. K., Mikkelsen T., Rosenblum S. D., Yan P. S., Knight R., Windham J., Rosenblum M. L., Schiffer, D., Attanasio, A., Cavalla, P., Chio, A., Giordana, M. T., Migheli, A., Amberger, V., Hensel, T., Schwab, M. E., Cervoni, Luigi, Celli, Paolo, Tarantino, Roberto, Huettner, C., Tonn, J. C., Berweiler, U., Roggendorf, W., Salmon, I., Rorive, S., Rombaut, K., Pirotte, B., Haot, J., Brotchi, J., Kiss, R., Maugard-Louboutin C., Charrier J., Fayet G., Sagan C., Cuillioere P., Ricolleau G., Martin S., Menegalli-Bogeelli D., Lajat Y., Resche F., Molnàr, Péter, Bárdos, Helga, Ádány, Róza, Rogers, J. P., Pilkington, G. J., Pollo, B., Giaccone, G., Allegranza, A., Bugiani, O., Prim, J., Badia, J., Ribas, E., Coello, F., Shezen, E., Lossos, A., Abramsky, O., Siegal, T., Scerrati M., Roselli R., Iacoangeli M., Pompucci A., Rossi G. F., Deeb, Saleh M. Al., Koreich, Osama, Yaqub, Basim, Moutaery, Khalaf R. Al., Giordana, M. T., Cavalla, P., Chio, A., Marino, S., Vigliani, M. C., Schiffer, D., Deburghgraeve, V., Darcel, F., Gedouin, D., Hassel, M. Ben, Guegan, Y., Jeremic, B., Grujicic, D., Antunovic, V., Matovic, M., Shibamoto, Y., Kallio, Merja, Huhmar, Helena, Kudoh, Ch., Detta, A., Sugiura, K., Hitchcock, E. R., Mastrostefano, R., Di Russo, R., Cipriani§, M., Occhipinti, E. M., Conti, E. M. S., Clowegeser A., Ortler M., Seiwald M., Kostron H., Rajan B., Ross G., Lim C., Ashlcy S., Goode D., Traish D., Brada M., Sanden, G. A. C. vd, Schouten, L. J., Coebergh, J. W. W., Razenberg, P. P. A., Twijnstra, A., Snilders-Keilholz, A., Voormolen, J. H. C., Hermans, J., Leer, J. W. H., Taillandier, L., Baylac, F., Dcbouvcrie, M., Anxionnal, R., Bracard, S., Vignand, J. M., Duprcz, A., Weber, M., Winking, M., Böker, D. K., Simmet, T., Rothbart, David, Strugar, John, Balledux, Jeroen, Criscuolo, Gregory R., Jachimczak, Piotr, Blesch, Armin, Heβdörfer, Birgit, Bogdahn, Ulrich, Ernestus, Ralf -Ingo, Schröder, Roland, Klug, Norfrid, Krouwer, H. G. J., Duinen, S. G. v., Algra, A., Zentner, J., Wolf, H. K., Ostertun, B., Hufnagel, A., Campos, M. G., Solymosi, L., Schramm, J., Newlands, E. S., O'Reilly, S. M., Brampton, M., Soffietti, R., Chio, A., Mocellini, C., Ruda, R., Vigliani, M. C., Schiffer, D., Sciolla, R., Seliak, D., Henriksson, R., Bergenheim, A. T., Björk, P., Gunnarsson, P. -O., Hariz, Ml., Grant, R., Collie, D., Gregor A., Ebmeier K. P., Jarvis G., Lander F., Cull A., Sellar R., Brada, M., Thomas, C., Elyan, S., Hines, F., Ashley, S., Stenning, S., Bernstein J. J., Goldberg W. J., Roelcke U., Von Ammon K., Hausmann O., Radu E. W., Kaech D., Leenders K. L., Fitzek, II, M. M., Aronen J. Efird, Hochberg, F., Gruber, M., Schmidt, E., Rosen, B., Flschman, A., Pardo, P., Afra U. M. U., Sipos, L., Slouik, F., Boiardi A., Salmaggi A., Pozzi A., Farinotti L., Fariselli L., Silvani A., Brandes, A., Scelzi, E., Rigon, A., Zampieri, P., Pignataro, M., Amanzo, P. D'., Amista, P., Rotilio, A., Fiorentino, M. V., Thomas, R., Brazil, L., O'Connor, A. M., Ashley, S., Brada, M., Salvati, Maurizio, Cervoni, Luigi, Puzzilli, Fabrizio, Cervoni, Luigi, Salvati, Maurizio, Raguso, Michele, Cruickshank G. S., Duckworth R., Rumpling R., Rottuci M., Fariselli L., Boiardi A., Broggi G., Plrint, N. G., Sabattini, E., Manetto, V., Gambacorta, H., Poggi, S., Pileri, S., Ferracini, R., Grant, R., Plev D. V., Hopf N. J., Knosp E., Bohl J., Perncczky A., Kiss, R., Salmon, I., Catnby, I., Dewitte, O., Brotchi, J., Pasteels, J. L., Camby, I., Salmon, I., Darro, F., Danguy, A., Brotchi, J., Pasteels, J. L., Kiss, R., Kiu, M. C., Lai, G. M., Yang, T. S., Ng, K. T., Chen, J. S., Chang, C. N., Leung, W. M., Ho, Y. S., Rychter, M. Deblec, Klimek, A., Liberski, P. P., Karpinaka, A., Krauseneck P., Schöffel V., Müller B., Kreth, F. W., Faist, M., Warnke, P. C., Ostertag, C. B., Nielen, K. M. B. v., Visscr, M. C., Lebrun C., Lonjon M., Desjardin T., Michiels J. F., Chanalet Sa. Lagrange J. L., Roche J. L., Chatel M., Mastronardi L., Puzzilli F., Osman Farah J., Lunardi P., Matsutani, M., Ushio, Y., Takakura, K., Menten, Johan, Hamers, Han, Ribot, Jacques, Dom, René, Tcepen, Hans, Müller B., Weidner N., Krauseneck P., Naujocks, G., van Roost, D., Wiestler, O. D., Kuncz, A., Nieder, C., Setzel-Sesterhein, M., Niewald, M., Schnabel, I., O'Neill, K. S., Kitchen, N. D., Wilkins, P. R., Marsh, H. T., Pierce, E., Doshi, R., Deane, R., Previtali, S., Quattrini, A., Nemni, R., Ducati, A., Wrabetz, L., Canal, N., Punt, C. J. A., Stamatakis, L., Giroux, B., Rutten, E., Quigley, Matthew R., Beth Sargent P. A. -C., Flores, Nicholas, Simon, Sheryl, Maroon, Joseph C., Quigley, Matthew R., Beth Sargent P. A. -C., Flores, Nicholas, Maroon, Joseph C., Rocca A. A., Gervasoni C., Castagna A., Picozzi P., Giugni E., Rocca A. A., Tonnarelli G. P., Ducati A., Mangili F., Truci G., Canal N., Giovanelli M., Roelcke U., Von Ammon K., Radu E. W., Leenders K. L., Sachsenheimer, W., Bimmler, T., Seiwald M., Eiter H. Rhomberg W., Ortler M., Obwegesser A., Kostron H., Steilen H., Henn W., Moringlane J. R., Kolles H., Feiden W., Zang K. D., Sleudel W. I., Steinbrecher, Andreas, Schabet, Martin, Heb, Clemens, Bamberg, Michael, Dichgans, Johannes, Stragliotto, G., Delattre, J. Y., Poisson, M., Zampieri, P., Brandes, A., Rigon, A., Tosatto, L., D'Amanzo, P., Menicucci, N., Rotilio, A., Mingrino, S., Steudel, W. I., Feld, R., Henn, W., Zang, K. D., Maire, J. Ph., Caudry, M., Guerin, J., Celerier, D., Salem, N., Demeaux, H., Fahregat, J. F., Kusak, M. E., Bucno, A., Albisua, J., Jerez, P., Sarasa, J. L., Garefa, R., de Campos, J. M., Kusak, M. E., de Campos, J. M., Bueno, A., García-Delgado, R., Sarasa, J. L., García-Sola, R., Lantsov A. A., Shustova T. I., Lcnartz, D., Wellenreuther, R., von Deirnling, A., Köning, W., Menzel, J., Scarpa, S., Manna, A., Reale, M. G., Oppido, P. A., Carapella, C. M., Frati, L., Valery, C. A., Ichen, M., Foncin, J. P., Soubrane, C., Khayat, D., Philippon, J., Vaz, R., Cruz, C., Weis S., Protopapa D., März R., Winkler P. A., Reulen H. J., Bise K., Beuls E., Berg J., Deinsberger, W., Böker, D. K., Samii, M., Caudry, M., Darrouzet, V., Guérin, J., Trouette, R., Causse, N., Bébéar, J. P., Parker, F., Vallee, J. N., Carlier, R., Zerah, M., Lacroix-Jousselin, C., Piepmeier, Joseph M., Kveton, John, Czibulka, Agnes, Tigliev G. S., Chernov M. P., Maslova L. N., Valdueza, José M., Jänisch, Werner, Bock, Alexander, Harms, Lutz, Bessell, E. M., Graus, F., Punt, J., Firth, J., Hope, T., Koriech, Osama, Al Deeb, Saleh, Al Moutaery, Khalaf, Yaqub, B., Silvani A., Salmaggi A., Pozzi A., Franzini A., Boiardi A., Goldbrunner, R., Warmuth-Metz, M., Paulus, W., Tonn, J. -Ch., Roosen, K., Strik I. I., Müller B., Markert C., Pflughaupt K. -W., Krauseneck P., O'Neill, B. P., Dinapoli, R. P., Voges, J., Sturm, V., Deuß, U., Traud, C., Treuer, H., Lehrke, R., Kim, D. G., Müller, R. P., Alexandrov Yu. S., Moutaery, K., Aabed, M., Koreich, O., Ross, G. M., Rajan, B., Traish, D., Ashley, S., Ford, D., Brada, M., Schmeets, I. L. O., Jager, J. J., Pannebakker, M. A. G., de Jong, J. M. A., van Lindert, E., Knosp, E., Kitz, K., Blond, S., Dubois, F., Assaker, R., Baranzelli, M. C., Sleiman, M., Pruvo, J. P., Coche-Dequeant, B., Matsutani M., Takakura K., Sano K., PetriČ-Grabnar, G., Jereb, B., Župančič, N., Koršič, M., Rainov N. G., Burkert W., Ushio, Yukitaka, Kochi, Masato, Itoyama, Youichi, de Campos, J. M., Kusak, M. E., Sarasa, J. L., García, R., Bueno, A., Ferrando, L., Hoang-Xuan, K., Sanson, M., Merel, P., Delattre, J. Y., Poisson, M., Delattre, O., Thomas, G., Hoang-Xuan, K., Delattre, J. Y., Poisson, M., Thomas, G., Haritz, D., Obersen, B., Grochulla, F., Gabel, D., Haselsberger K., Radner H., Pendl G., Brada, M., Laing, R. W., Warrington, A. P., Nowak, P. J. C. M., Kolkman-Deurloo, I. K. K., Visser, A. G., Berge, Hv. d., Niël, C. G. J. H., Levendag, P. C., Bergström P., Hariz M., Löfroth P. -O., Bergenheim T., Henriksson R., Blond, S., Assaker, R., Cortet-rudelli, C., Dewailly, D., Coche-dequeant, B., Castelain, B., Dinapoli, R., Shaw, E., Coffey, R., Earle, J., Foote, R., Schomberg, P., Gorman, D., Girard N., Courel M. N., Delpech B., Haselsberger K., Friehs G. M., Schröttner O., Pendl G., Pötter, R., hawliczek, R., Sperveslage, P., Prott, F. J., Wachter, S., Dieckmann, K., Würker, M., Herholz, K., Pietrzyk, U., Voges, J., Treuer, H., Sturm, V., Bauer, B., Heiss, W. -D., Jund, R., Zimmermann, F., Feldmann, H. J., Gross, M. W., Kneschaurek, P., Molls, M., Lederman, G., Lowry, J., Wertheim, S., Voulsinas, L., Fine, M., Lederman, G., Lowry, J., Wertheim, S., Fine, M., Voutsinas, I., Qian, G., Rashid, H., Lederman, G., Lowry, J., Wertheim, S., Fine, M., Voulsinas, L., Qian, G., Rashid, H., Moutaery, K., Aabed, M., Koreich, O., Scerrati M., Montemaggi P., Iacoangeli M., Pompucci A., Roselli R., Trignani R., Rossi G. F., Shin, K., Mechtler, L., West, C., Grand, W., Shin, K., Sibata, C., West, C., Mechtler, L., Grand, W., Thomas, R., Guerrero, D., James, N., Ashley, S., Gregor, A., Brada, M., Voges, J., Sturm, V., Bramer, R., Pahlke, H., Lehrke, R., Treuer, H., Banik, N., Kim, D. G., Hövels, M., Bernsen H. J. J. A., Rijken P. F. J. W., Van der Sanden B. P. J., Hagemeier N. E. M., Van der Kogel A. J., Koehler P. J., Verbiest H., Jager J., Vecht Ch. J., Ross G. M., McIlwrath A., Brown R., Mottolesb, C., Pierre'Kahn, A., Croux, M., Roche, J. L., Marchai, J., Delhemes, P., Tremoulet, M., Stilhart, B., Chazai, J., Caillaud, P., Ravon, R., Passacha, J., Bouffet, E., Dirven C. M. F., Mooy J. J. A., Molenaar W. M., Lewandowicz, G. M., Grant, N., Harkness, W., Hayward, R., Thomas, D. G. T., Darling, J. L., Delepine, N., Subovici I. I., Cornille B., Markowska S., Alkallaf JC. Desbois, KühI, J., Niethammer, D., Spaar, H. J., Gnekow, A., Havers, W., Berthold, F., Graf, N., Lampert, F., Maass, E., Mertens, R., Schöck, V., Aguzzi, A., Boukhny, A., Smirtukov, S., Prityko, A., Hoiodov, B., Geludkova, O., Nikanorov, A., Levin, P., Rothbart, David, Balledux, Jeroen, Criscuolo, Gregory R., D'haen, B., Van Calenbergh, F., Casaer, P., Dom, R., Menten, J., Goffin, J., Plets, C., Hertel, A., Hernaiz, P., Seipp, C., Siegler, K., Baum, R. P., Maul, F. D., Schwabe, D., Jacobi, G., Kornhuber, B., Hör, G., Menten, J., Casaer, P., Pilkington, G. J., Merzak, A., Rooprai, H. K., Bullock, P., van Domburg P. H. M. F., Wesseling P., Thijssen H. O. M., Wolff, J. E. A., Boos, J., Krähling, K. H., Gressner-Brocks, V., Jürgens, H., Schlegel, J., Scherthan, H., Arens, N., Stumm, Gabi, Kiessling, Marika, Merzak, A., Koochekpour, S., Pilkington, G. J., Reifenberger, G., Reifenberger, J., Liu, L., James, C. D., Wechsler, W., Collins, V. P., Fabel-Schulte, Klaus, Jachimczak, Plotr, Heßdörfer, Birgitt, Baur, Inge, Schlingensiepen, Karl -Hermann, Brysch, Wolgang, Bogdahn, Ulrich, Blesch A., Bosserhoff A. K., Apfel R., Lottspeich F., Jachimczak P., Büttner R., Bogdahn U., Cece, R., Barajon, I., Tazzari, S., Cavaletti, G., Torri-Tarelli, L., Tredici, G., Hecht, B., Turc-Carel, C., Atllas, R., Chatel, M., Gaudray, P., Gioanni, J., Hecht, F., Balledux, Jeroen, Rothbart, David, Criscuolo, Gregory R., de Campos, J. M., Kusak, M. E., Rey, J. A., Bello, M. J., Sarasa, J. L., Dubois, F., Blond, S., Parent, M., Assaker, R., Gosselin, P., Christiaens, J. L., Feld, R., Moringlane, J. R., Steudel, W. I., Schaudies, J. R., Janka M., Tonn J. C., Fischer U., Meese E., Roosen K., Remmelink, M., Salmon, I., Cras, P., Pasteels, J. L., Brotchi, J., Kiss, R., Bensadoun R. J., Frenay M., Formento J. L., Milano G., Lagrange J. L., Grellier P., Lee, J. -Y., Ernestus, R. -I., Riese, H. -H., Cervós-Navarro, J., Reutter, W., Lippitz, B., Scheitinger, C., Scholz, M., Weis, J., Gilsbach, J. M., Füzesi, L., Koochekpour, S., Merzak, A., Pilkington, G. J., Sanson, M., Li, Y. J., Hoang-Xuan, K., Delattre, J. Y., Poisson, M., Hamelin, R., Van de Kelft, Erik, Dams, Erna, Martin, Jean -Jacques, Willems, Patrick, Lehrke R., Voges J., Treuer H., Erdmann J., Müller R. P., Sturm V., Wurm R. E., Warrington A. P., Laing R. W., Sardell S., Hines F., Graham J. D., Brada M., Ushio, Yukitaka, Kuratsu, Jun -ichi, Kochi, Masato, Kitz K., Aichholzer M., Rössler K., Alesch F., Ertl A., Sorensen, P. S., Helweg-Larsen, S., Mourldsen, H., Hansen, H. H., El Sharoum, S. Y., Berfelo, M. W., Theunissen, P. H. M. H., Jager, J. J., de Jong, J. M. A., Fedorcsák, I., Nyáry, I., Osztie, É., Horvath, Á., Kontra, G., Frenay M., Burgoni-chuzel J., Paquis P., Lagrange J. L., Helweg-Larsen, S., Hansen, SW., Sørensen, PS., Salmon, I., Kiss, R., Krauseneck P., Müller B., Morche M., Tonn J. C., Lagerwaard, F. J., Levendag, P. C., Eijkenboom, W. M. H., Schmilz, P. I. M., Lentzsch S., Weber F., Franke J., Dörken B., Lunardi P., Schettini G., Osman Farah J., Qasho R., Mocellini, C., Ruda, R., Soffietti, R., Garabello, D., Sales, S., De Lucchi, R., Vasario, E., Schiffer, D., Muracciole, X., Régis, J., Manera, L., Peragut, J. C., Juin, P., Sedan, R., Nieder, C., Niewald, M., Walter, K., Schnabel, K., Nieder, C., Niewald, N., Nestle, U., Schnabel, K., Berberich, W., Oschmann, P., Theißen R. D., Reuner K. H., Kaps M., Dorndorf W., Martin, K. K., Akinwunmi, J., Rooprai, H. K., Kennedy, A., Linke, A., Ognjenovic, N., Pilkington, G. J., Svadovsky A. I., Peresedov V. V., Bulakov A. A., Butyalko M. Y., Zhirnova I. G., Labunsky D. A., Gnazdizky V. V., Gannushkina I. V., Taphoorn, M. J. B., Potman, R., Barkhof, F., Weerts, J. G., Karim, A. B. M. F., Heimans, J. J., van de Pol, M., van Aalst, V. C., Wilmink, J. T., Twijnstra, A., van der Sande, J. J., Boogerd, W., Kröger, R., Jäger A., Wismeth C., Dekant A., Brysch W., Schlingensiepen K. H., Jachimczak P., Bogdahn U., Pirolte, B., Cool, V., Gérard, C., Levivier, M., Dargent, J. L., Goldman, S., Brotchi, J., Hildebrand, J., Velu, T., Herrlinger, U., Schabet, M., Ohneseit, P., Buchholz, R., Zhu, Jianhong, Reszka, Regina, Weber, Friedrich, Walther, Wolfgang, Zhang, L. I., Brock, Mario, Roosen N., Rock J. P., Zeng H., Feng J., Fenstermacher J. D., Rosenblum M. L., Siegal, T., Gabizon, A., Beljanski M., Crochet S., Bergenheim, A. T., Zackrisson, B., Elfverson, J., Bergström, P., Henriksson, R., Butti, G., Baetta, R., Magrassi, L., De Renzis, M. R., Soma, M. R., Davegna, C., Pezzotta, S., Paoletti, R., Fumagalli, R., Infuso, L., Sankar, A. A., Darling, J. L., Thomas, D. G. T., Defer, G. -L., Brugières, P., Gray, F., Chomienne, C., Poirier, J., Degos, L., Degos, J. D., Colombo, Bruno M., DiDonato, Stefano, Finocchiaro, Gaetano, Hebeda, K. M., Sterenborg, H. J. C. M., Saarnak, A. E., Wolbers, J. G., van Gemert, M. J. C., Kaaijk P., Troost D., Leenstra S., Das P. K., Bosch D. A., Kostron H., Hochleitner B. W., Obwegeser A., Ortler M., Seiwald M., Vooys, W., Krouwer, H. G. J., de Gast, G. C., Marx, J. J. M., Osman Farah J., Lunardi P., Puzzilli F., Menovsky, T., Beek, J. F., Wolbers, J. G., van Gemert, M. J. C., Naujocks, G., Wiestler, O. D., Schirrmacher, V., Schramm, J., Schmitz, A., Eis-Hübinger, A. M., Piepmeier, p. h., Pedersen, Patricia, Greer, Charles, Quigley, Matthew R., Shih, Tommy, Elrifal, Amr, Rothfus, William, Maroon, Joseph C., Rohertson, L., Rampling, R., Whoteley, T. L., Piumb, J. A., Kerr, D. J., Falina, P. A., Crossan, I. M., Roosen N., Rock J. P., Feng J., Zeng H., Ho K. L., Fenstermacher J. D., Rosenblum M. L., Ruchoux, M. M., Vincent, S., Jonca, F., Plouet, J., Lecomte, M., Samid, D., Thibault, A., Ram, Z., Oldfield, E. H., Myers, C. E., Reed, E., Schabet, M., Herrlinger, U., Buchholz, R., Shoshan, Y., Siegal, T., Siegal, T., Shezen, E., Siegal, Tz., Stockhammer, G., Rosenblum, M., Samid, D., Lieberman, F., Terzis, A. J. A., Bjerkvig, R., Laerum, O. D., Arnold, H., Thibault, A., Samid, D., Figg, W. D., Myers, C. E., Reed, E., Thomas, R., Flux, G., Chittenden, S., Doshi, P., Brazil, L., Thomas, D. G. T., Bignor, D., Zalutsky, M., Brada, M., Tjuvajev, Juri, Kaplitt, Michael, Desai, Revathi, Bradley, M. S., Bettie B. S., Gansbacher, Bernd, Blasberg, Ronald, Haugland, H. K., Saraste, J., Rooseni, K., Laerum, O. D., Vincent, A. J. P. E., Avezaat, C. J. J., Bout, A., Noteboom, J. L., Vecht, C. h., Valerio, D., Hoogerbrugge, P. M., Weber, F., Reszka, R., Zhu, J., Walther, W., List, J., Schulz, W., Wolbers, J. G., Sterenborg, I. I. J. C. M., Kamphorst, W., van Gemert, M. J. C., van Alplien, H. A. M., Salander P., Bergenheim T., Henriksson R., Grant, R., Brazil, L., Thomas, R., Guerrero, D., Laing, R., Ashley, S., Brada, M., Schmidt B., Bauer B., Grau G., Bohnstedt, T., Frydrych A., Franz K., Lorenz R., Brandes, A., Amanzo, P. D'., Zampieri, P., Rigon, A., Scelzi, E., Rotilio, A., Berti, F., Paccagnella, A., Fiorentino, M. V., Müller B., Krauseneck P., van Deventer, P. L., Dellemijn, P. L. I., van den Bent, M. J., Vecht, Ch. J., Kansen, P. J., Tredici, G., Petruccioli, N. G., Cavaletti, G., Cavalletti, E., Kiburg, B., Müller, L. J., Moorer-van Delft, C. M., Heimans, J. J., Boer, H. H., Pace A., Bove L., Pietrangeli A., Innocenti P., Aloe A., Nardi M., Jandolo B., Kellie S. J., De Graaf S. S. N., Bloemhof H., Roebuck D., Dalla Pozza L., Uges D. D. R., Johnston I., Besser M., Chaseling R. A., Koeppen, S., Gründemann, S., Lossos, A., Siegal, T., Nitschke M., Vieregge P., Reusche E., Rob P., Kömpf D., Postma, T. J., Vermorken, J. B., Heimans, J. J., Rampling R. P., Dunlop D. J., Steward M. S., Campbell S. M., Roy S., Hilkens, P. H. E., Verweij, J., van Putten, W. L. J., Vecht, Ch. J., van den Bent, M. J., Hilkens, P. H. E., Moll, J. W. B., van der Burg, M. E. L., Planting, A. S. T., van Putten, W. L. J., Vecht, Ch. J., van den Bent, M. J., Wondrusch E., Zifko U., Drlicek M., Liszka U., Grisold W., Zifko U., Fazeny B., Dittrich Ch., Wondrusch E., Grisold W., Verschuuren, Jan J., Meneses, Patricio I., Rosenfeld, Myrna R., Kaplitt, Michael G., Posner, Jerome B., Dalmau, Josep, Sillevis Smitt P. A. E., Manley G., Posner J. B., Cavaletti, G., Bogliun, G., Margorati, L., Bianchi, G., Drlicek, M., Liska, U., Casati, B., Kolig, C., Grisold, H., Graus, F., Reñe, R., Uchuya, M., Valldeoriola, F., Delattre, J. Y., Benedetti de Cosentiro C., Ortale D., Martinez R., Lambre J., Cagnolati S., Vinai C., Salmaggi A., Nemni R., Silvani A., Forno M. G., Luksch R., Confalonieri P., Boiardi A., Nitschke M., Scholz J., Vieregge P., Kömpf D., Hochberg F. H., Pfeiffer, G., Netzer, J., Hansen, Ch., Eggers, Ch., Hagel Ch., Kunze, K., Verschuuren, Jan J., Rosenblum, Marc K., Lieberman, Frank S., Posner, Jerome B., and Dalmau, Josep

Published
1994
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6. Messenger RNA expression of the immunosuppressive cytokine IL-10 in human gliomas

Author

Huettner, C., Paulus, W., and Roggendorf, W.

Subjects
Base Sequence, Brain Neoplasms, Interleukin-6, Molecular Sequence Data, Brain, Glioma, Polymerase Chain Reaction, Interleukin-10, Tumor Cells, Cultured, Humans, RNA, Messenger, Glioblastoma, Research Article, Neoplasm Staging
Abstract

Interleukin 10 (IL-10) was initially discovered on the basis of its ability to suppress cytokine synthesis. Additionally, it can exert immunosuppressive effects on a variety of cell types. Because patients with malignant gliomas present with a general impairment of the immune system, we investigated IL-10 expression in the glioma tissue. Because expression of IL-10 and IL-6 is associated in hematopoietic cells and IL-6 can act as an autocrine growth stimulator for glioblastoma cell lines, we looked in addition for a relationship between IL-10 and IL-6 expression. Using a quantitative reverse transcriptase polymerase chain reaction, IL-10 and IL-6 mRNA levels were determined in 37 glial tumors of different grades including 2 recurrencies, 3 specimens from normal brain tissue, and 3 glioblastoma cell lines. Expression of IL-10 mRNA was demonstrable in all tumors as well as in normal brain. High grade tumors and recurrent cases expressed significantly higher amounts of IL-10-specific mRNA compared with low grade tumors, whereas 2 of 3 cell lines showed only weak constitutive expression, mRNA for IL-6 was found in 86.5% of all gliomas with a correlation concerning the expression levels for both cytokines in 69% of gliomas. We suggest that IL-10 may contribute to the progression of astrocytomas by suppressing the patient's immune response, whereas IL-6 provides an additional growth advantage.

Published
1995

7. DEVELOPMENT STATUS OF A MAGLEV CENTRIFUGAL LVAD

Author

Loree, H., primary, Bourque, K., additional, Dague, C., additional, Poirier, V., additional, Farrar, D., additional, Fleischli, A., additional, Gempp, T., additional, Hahn, J., additional, Siebenhaar, A., additional, Steinacher, V., additional, Shoeb, R, additional, and Huettner, C., additional

Published
2003
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9. Induction of Fetal Hemoglobin Synthesis With Recombinant Human Erythropoietin in Anemic Patients With Heterozygous Beta-Thalassemia During Pregnancy

Author

Breymann, C., Fibach, E., Visca, E., Huettner, C., Huch, A., and Huch, R.

Abstract

Objective: Recombinant human erythropoietin (rhEPO) increases fetal hemoglobin synthesis in nonpregnant thalassaemic patients. We used rhEPO in 4 pregnant patients with heterozygous β-thalassemia and anemia to study its effect on erythropoiesis, F cell production, and HbF synthesis.Methods: Patients were treated with a combination therapy of rhEPO and iron. The effect on HbF synthesis was assessed by the percentage of F reticulocytes, F cells, and total HbF, erythropietis by reticulocyte count, and hemoglobin measurements and iron status by ferritin levels, transferrin saturation, and percentage of hypochromic red cells.Results: RhEPO caused an increase of F reticulocytes (1.5 to 10.5 fold), F cells (5.0 to 7.7 fold), and HbF (1.4 to 2.2 fold). All patients showed an increase of young, immature reticulocytes and had elevated reticulocytes at the end of therapy. Hemoglobin increased with a range from 0.3 to 1.5 g/dL. Transferrin saturation and ferritin levels were normal at the end of the study. There was an increase of the percentage of hypochromic red cells, indicating functional iron deficiency after rhEPO administration despite supplemental iron.Conclusions: RhEPO stimulates both HbF synthesis and erythropoiesis in pregnant patients with heterozygous β-thalassemia and anemia. Since it is known that high HbF levels ameliorate thalassemia symptoms in nonpregnant patients, use of rhEPO for the treatment of severe anemia in thalassaemic patients during pregnancy might be further evaluated.

Published
1999
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10. Fractionation of inducible alkane hydroxylase activity in Pseudomonas putida and characterization of hydroxylase-negative plasmid mutations

Author

Benson, S, Fennewald, M, Shapiro, J, and Huettner, C

Abstract

The plasmid-determined inducible alkane hydroxylase of Pseudomonas putida resolved into particulate and soluble fractions. Spinach reductase and spinach ferredoxin could replace the soluble hydroxylase component. Two alkane hydroxylase mutants show in vitro complementation (S. Benson and J. Shapiro, J. Bacteriol., 123: 759-760, 1975): one, alk-7, lacks an active soluble component and the other, alk-181, lacks an active particulate component. Together with previous results on a particulate alcohol dehydrogenase enzyme (Benson and Shapiro, J. Bacteriol., 126: 794-798, 1976), these results allowed us to assay three plasmid-determined inducible activities: soluble alkane hydroxylase (alkA+), particulate alkane hydroxylase (alkB+), and particulate alcohol dehydrogenase (alkC+). Growth tests and in vitro complementation assays revealed three groups of plasmid mutations that block expression of alkane hydroxylase activity: alkA, which so far includes only the alk-7 mutation; alkB, which includes alk-181 and 11 other mutations; and a pleiotropic-negative class, which includes nine mutations that lead to loss of alkA+, alkB+, and alkC+ activities. Thus, the alk+ gene cluster found on IncP-2 plasmids contains at least four cistrons. We believe it is significant that two of these determined the presence of membrane proteins. The accompanying paper shows that these loci are part of a single regulon.

Published
1977
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11. Tailoring the Adsorption of ACE-Inhibiting Peptides by Nitrogen Functionalization of Porous Carbons.

Author

Huettner C, Hagemann D, Troschke E, Hippauf F, Borchardt L, Oswald S, Henle T, and Kaskel S

Subjects
Adsorption, Hydrolysis, Lactalbumin metabolism, Porosity, Tryptophan chemistry, Angiotensin-Converting Enzyme Inhibitors chemistry, Carbon chemistry, Nitrogen chemistry, Peptides chemistry, Peptidyl-Dipeptidase A metabolism
Abstract

Bioactive peptides, such as isoleucyl-tryptophan (IW), exhibit a high potential to inhibit the angiotensin-converting enzyme (ACE). Adsorption on carbon materials provides a beneficial method to extract these specific molecules from the complex mixture of an α-lactalbumin hydrolysate. This study focuses on the impact of nitrogen functionalization of porous carbon adsorbents, either via pre- or post-treatment, on the adsorption behavior of the ACE-inhibiting peptide IW and the essential amino acid tryptophan (W). The commercially activated carbon Norit ROX 0.8 is compared with pre- and postsynthetically functionalized N-doped carbon in terms of surface area, pore size, and surface functionality. For prefunctionalization, a covalent triazine framework was synthesized by trimerization of an aromatic nitrile under ionothermal conditions. For the postsynthetic approach, the activated carbon ROX 0.8 was functionalized with the nitrogen-rich molecule melamine. The batch adsorption results using model mixtures containing the single components IW and W could be transferred to a more complex mixture of an α-lactalbumin hydrolysate containing a huge number of various peptides. For this purpose, reverse-phase high-pressure liquid chromatography with fluorescence detection was used for identification and quantification. The treatment with the three different carbon materials leads to an increase in the ACE-inhibiting effect in vitro. The modified surface structure of the carbon via pre- or post-treatment allows separation of IW and W due to the certain selectivity for either the amino acid or the dipeptide.

Published
2019
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12. Altered microenvironmental regulation of leukemic and normal stem cells in chronic myelogenous leukemia.

Author

Zhang B, Ho YW, Huang Q, Maeda T, Lin A, Lee SU, Hair A, Holyoake TL, Huettner C, and Bhatia R

Subjects
Animals, Benzamides, Cell Cycle, Chemokines metabolism, Cytokines metabolism, Fusion Proteins, bcr-abl genetics, Imatinib Mesylate, Leukemia, Myelogenous, Chronic, BCR-ABL Positive pathology, Mice, Mice, Transgenic, Neoplastic Stem Cells metabolism, Neoplastic Stem Cells pathology, Piperazines pharmacology, Protein Kinase Inhibitors pharmacology, Protein-Tyrosine Kinases antagonists & inhibitors, Pyrimidines pharmacology, Tumor Microenvironment drug effects, Gene Expression Regulation, Neoplastic, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Tumor Microenvironment genetics
Abstract

We characterized leukemia stem cells (LSC) in chronic phase chronic myelogenous leukemia (CML) using a transgenic mouse model. LSC were restricted to cells with long-term hematopoietic stem cell (LTHSC) phenotype. CML LTHSC demonstrated reduced homing and retention in the bone marrow (BM), related to decreased CXCL12 expression in CML BM, resulting from increased G-CSF production by leukemia cells. Altered cytokine expression in CML BM was associated with selective impairment of normal LTHSC growth and a growth advantage to CML LTHSC. Imatinib (IM) treatment partially corrected abnormalities in cytokine levels and LTHSC growth. These results were validated using human CML samples and provide improved understanding of microenvironmental regulation of normal and leukemic LTHSC and their response to IM in CML., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Published
2012
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13. Reversibility of acute B-cell leukaemia induced by BCR-ABL1.

Author

Huettner CS, Zhang P, Van Etten RA, and Tenen DG

Subjects
Adult, Animals, Bone Marrow Cells pathology, Humans, Immunoblotting, Mice, Mice, Transgenic, Neoplasm Transplantation, Burkitt Lymphoma genetics, Fusion Proteins, bcr-abl genetics
Abstract

Cancer is thought to arise from multiple genetic events that establish irreversible malignancy. A different mechanism might be present in certain leukaemias initiated by a chromosomal translocation. We have taken a new approach to determine if ablation of the genetic abnormality is sufficient for reversion by generating a conditional transgenic model of BCR-ABL1 (also known as BCR-ABL)-induced leukaemia. This oncogene is the result of a reciprocal translocation and is associated with different forms of leukaemia. The most common form, p210 BCR-ABL1, is found in more than 90% of patients with chronic myelogenous leukaemia (CML) and in up to 15% of adult patients with de novoacute lymphoblastic leukaemia (ALL). Efforts to establish a useful transgenic model have been hampered by embryonic lethality when the oncogene is expressed during embryogenesis, by reduced penetrance or by extremely long latency periods. One model uses the 'knock-in' approach to induce leukaemia by p190 BCR-ABL1(ref. 10). Given the limitations of models with p210, we used a different experimental approach. Lethal leukaemia developed within an acceptable time frame in all animals, and complete remission was achieved by suppression of BCR-ABL1expression, even after multiple rounds of induction and reversion. Our results demonstrate that BCR-ABL1is required for both induction and maintenance of leukaemia.

Published
2000
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14. Multiple control elements are required for expression of the human CD34 gene.

Author

Radomska HS, Satterthwaite AB, Burn TC, Oliff IA, Huettner CS, and Tenen DG

Subjects
Animals, Base Sequence, Cell Line, Chromatin genetics, Chromosome Mapping, DNA chemistry, DNA genetics, DNA Methylation, DNA Primers genetics, Enhancer Elements, Genetic, Humans, Introns, Locus Control Region, Mice, Molecular Sequence Data, Promoter Regions, Genetic, RNA, Messenger genetics, Reverse Transcriptase Polymerase Chain Reaction, Antigens, CD34 genetics, Gene Expression Regulation
Abstract

Two cis regulatory elements of the human CD34 gene, the promoter and a 3' enhancer, have previously been described. In transient transfection assays, the promoter was not sufficient to direct cell type specific expression. In contrast, the 3' enhancer was active only in CD34+ cell lines, suggesting that this element might be responsible for stem cell-restricted expression of the CD34 gene. In the current work, through deletion and transient transfection experiments, we delineated the core enhancer sequence. We examined the role of this element upon stable integration. Our data suggested the presence of additional control elements. In order to identify them, using DNaseI hypersensitivity and methylation studies, we determined the chromatin structure of the entire CD34 locus. Amongst a number of DNaseI hypersensitive sites, we detected a strong CD34+ cell type-specific site in intron 4. This region, however, did not work as an enhancer by itself. By analyzing stable transfectants and transgenic animals, we demonstrated that the 3' enhancer and intron 4 hypersensitive regions, either alone or together, did not function as a locus control region upon chromosomal integration. In contrast, a 160kb genomic fragment encompassing the entire CD34 gene contained regulatory elements sufficient for high-level CD34 mRNA expression in murine stable lines. Our data indicate that combinatorial action of multiple, proximal and long-range, cis elements is necessary for proper regulation of CD34 expression.

Published
1998
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15. Expression of matrix metalloproteinases in human glioma cell lines in the presence of IL-10.

Author

Wagner S, Stegen C, Bouterfa H, Huettner C, Kerkau S, Roggendorf W, Roosen K, and Tonn JC

Subjects
Brain Neoplasms drug therapy, Brain Neoplasms pathology, Cell Line, Endopeptidases biosynthesis, Endopeptidases isolation & purification, Extracellular Matrix drug effects, Glioma drug therapy, Glioma pathology, Humans, Metalloendopeptidases biosynthesis, RNA, Messenger biosynthesis, RNA, Neoplasm biosynthesis, Recombinant Proteins pharmacology, Reverse Transcriptase Polymerase Chain Reaction, Brain Neoplasms enzymology, Extracellular Matrix enzymology, Glioma enzymology, Interleukin-10 pharmacology, Metalloendopeptidases metabolism
Abstract

Matrix metalloproteinases have been implicated to play a vital role in glioma invasion as they degrade extracellular matrix to facilitate the subsequent migration of tumor cells into the surrounding brain tissue. The cytokine Interleukin-10 (IL-10) was detected recently in glial tumors in vivo. Expression of specific IL-10 mRNA as well as blood serum levels of IL-10 in glioma patients increased with malignancy suggesting a functional role of IL-10 in glioma progression. Moreover, glioma cell migration in vitro was enhanced in the presence of IL-10. We therefore investigated the expression of the matrix metalloproteinases (MMPs) stromelysin-1 (MMP-3), 72-kDa collagenase (MMP-2), 92-kDa collagenase (MMP-9), matrilysin (MMP-7) and the human macrophage metalloelastase (MMP-12). In addition, a possible relation between exposure of glioma cells to IL-10 and invasiveness of these cells due to MMP expression was analyzed. Experiments with Matrigel coated Boyden chambers revealed a pronounced dose dependent effect of IL-10 on glioma invasiveness. The synthetic MMP-inhibitor Marimastat markedly reduced cell invasion in the Boyden chambers confirming the significance of MMPs in the process of invasion. Subsequently, the expression level of MMPs and the serine protease uPA was investigated in 7 glioma cell lines (U373, GaMG, U251, GHE, SNB19, U138 and D54) by RT-PCR. In all but one cell line no enhancement of MMP expression by IL-10 was detected. Matrilysin in U373 cells was the only protease found to be upregulated in the presence of IL-10 dependent on cell density. The present data suggest that IL-10 related effects on the invasive properties of the cell lines are not directly mediated by an upregulation of matrix metalloproteinase expression.

Published
1998
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16. CCAAT/enhancer binding protein alpha is a regulatory switch sufficient for induction of granulocytic development from bipotential myeloid progenitors.

Author

Radomska HS, Huettner CS, Zhang P, Cheng T, Scadden DT, and Tenen DG

Subjects
CCAAT-Enhancer-Binding Proteins, Cell Differentiation, DNA-Binding Proteins genetics, Gene Expression, HL-60 Cells, HeLa Cells, Humans, Lymphocytes metabolism, Macrophages drug effects, Monocytes metabolism, Nuclear Proteins genetics, RNA, Messenger, Tetradecanoylphorbol Acetate pharmacology, Tumor Cells, Cultured, Up-Regulation, DNA-Binding Proteins biosynthesis, Granulocytes cytology, Hematopoietic Stem Cells cytology, Nuclear Proteins biosynthesis
Abstract

The transcription factor CCAAT/enhancer binding protein alpha (C/EBPalpha) regulates a number of myeloid cell-specific genes. To delineate the role of C/EBPalpha in human granulopoiesis, we studied its expression and function in human primary cells and bipotential (granulocytic/monocytic) myeloid cell lines. We show that the expression of C/EBPalpha initiates with the commitment of multipotential precursors to the myeloid lineage, is specifically upregulated during granulocytic differentiation, and is rapidly downregulated during the alternative monocytic pathway. Conditional expression of C/EBPalpha alone in stably transfected bipotential cells triggers neutrophilic differentiation, concomitant with upregulation of the granulocyte-specific granulocyte colony-stimulating factor receptor and secondary granule protein genes. Moreover, induced expression of C/EBPalpha in bipotential precursors blocks their monocytic differentiation program. These results indicate that C/EBPalpha serves as a myeloid differentiation switch acting on bipotential precursors and directing them to mature to granulocytes.

Published
1998
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17. Interleukin 10 is expressed in human gliomas in vivo and increases glioma cell proliferation and motility in vitro.

Author

Huettner C, Czub S, Kerkau S, Roggendorf W, and Tonn JC

Subjects
Brain embryology, Cell Division, Cell Movement, Glioma pathology, Humans, In Situ Hybridization, Organoids, Polymerase Chain Reaction methods, RNA, Messenger metabolism, RNA, Neoplasm metabolism, Tumor Cells, Cultured, Glioma metabolism, Interleukin-10 metabolism
Abstract

Interleukin 10 (IL-10) is a cytokine with a broad spectrum of immunosuppressive activity, but itoffs role in the oncogenesis of solid tumors is still unclear. In previous experiments we have shown that IL-10 specific mRNA is produced within glial tumors in vivo. The aim of the present study was to investigate the expression of the IL-10 protein in vivo and to identify the cells producing IL-10 within the tumor tissue. Expression levels significantly increased with malignancy of the gliomas. 87.5% of grade III and IV, but only 4% of grade II tumors expressed high levels of mRNA. Elevation of IL-10 serum levels was found in 11% of low grade and in 63.6% of high grade glioma patients. In situ hybridization analysis with combined immunohistochemistry revealed that: a) IL-10 is not produced by infiltrating B- or T- lymphocytes, b) both microglia and astroglia contributed to IL-10 expression in malignant gliomas in vivo. These data suggested the functional role of IL-10 in glioma progression. Therefore, the effects of IL-10 on proliferation and migration of glioma cells were determined in vitro. Two human glioma cell lines were grown as monolayer as well as spheroids in the presence of different concentrations of IL-10. IL-10 increased cell proliferation significantly in both culture systems with a dose optimum of 25 ng/ml. Glioma cell motility was enhanced with 25 ng/ml as the optimal dose. Adding the IL-10 specific antibody reversed both effects. We conclude from our data that IL-10 is involved in the progression of glial tumors, especially in the enhancement of tumor cell proliferation and migration which promotes infiltration of the surrounding tissue.

Published
1997

18. Presence of human herpesvirus type 6 in sporadic lymphoproliferative disorders. A comparative study.

Author

Hallas C, Neipel F, Huettner C, Schreiner D, Fleckenstein B, and Müller-Hermelink HK

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, DNA, Viral analysis, Humans, Infant, Lymphoproliferative Disorders genetics, Lymphoproliferative Disorders pathology, Middle Aged, Polymerase Chain Reaction, Herpesvirus 6, Human isolation & purification, Lymphoproliferative Disorders virology
Abstract

A supportive or causal role for human herpesvirus 6 (HHV-6) in lymphoproliferative disorders is still controversial. Different results were obtained in both tissue-based and serological investigations. We investigated 243 lymph node and salivary gland tissue biopsies for the presence of viral DNA by using a newly developed, highly sensitive nested polymerase chain reaction method. HHV-6 was detected in 39% of the non-Hodgkin's lymphomas, in 52% of Hodgkin's diseases, 64% of non-neoplastic lymph nodes, 23% of tumor metastases, and 50% of salivary gland biopsies. When correlating the patients' ages with the occurrence of HHV-6, we found a significantly higher percentage of positive samples in patients younger than 60 years of age (54%) than in older patients (35%). This age-related difference was found in all the lymphoproliferative disorders studied as well as in salivary gland biopsies. Taking patient's ages into account, we found no significant difference between the various groups of disorders concerning the percentage of HHV-6-positive samples.

Published
1996
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19. Effects of transforming growth factor-beta 1 on collagen synthesis, integrin expression, adhesion and invasion of glioma cells.

Author

Paulus W, Baur I, Huettner C, Schmausser B, Roggendorf W, Schlingensiepen KH, and Brysch W

Subjects
Base Sequence, Blotting, Western, Cell Adhesion, Cell Count, Flow Cytometry, Gene Expression Regulation, Neoplastic, Humans, Molecular Sequence Data, Neoplasm Invasiveness, Oligonucleotides, Antisense, Polymerase Chain Reaction methods, Tumor Cells, Cultured, Collagen biosynthesis, Glioblastoma chemistry, Glioblastoma pathology, Integrins analysis, Transforming Growth Factor beta physiology
Abstract

Transforming growth factor-beta 1 (TGF-beta 1) as a potent modulator of cell-extracellular matrix (ECM) interactions may be related to poorly understood ECM-associated features of glioblastomas, such as diffuse brain invasion, rarity of extracranial metastasis and marked ECM production in vitro. We therefore studied TGF-beta 1 expression in glioblastoma biopsy specimens and cell lines by using reverse transcription-polymerase chain reaction (RT-PCR). The cell lines were also examined by Western blotting and immunocytochemistry. To determine effects of TGF-beta 1, glioma cell lines U-138MG and U-373MG were incubated for 48 hours with TGF-beta 1 (0.1, 1, 10 ng/ml) or with antisense phosphorothioate-oligodeoxynucleotides (APO) designed to specifically inhibit TGF-beta 1 gene expression. Thereafter, collagen synthesis was determined by isotopic labeling with 3H-proline; integrin expression by flow cytometry; adhesion on collagen types I and IV, laminin and fibronectin by adhesion assays; and invasion through reconstituted basement membrane by invasion assays. We found that TGF-beta 1 was expressed by all glioma cell lines at protein and mRNA levels. Pretreatment with TGF-beta 1 increased the amount of collagen synthesis/cell, upregulated the alpha 5 integrin chain of U-138MG cells, and facilitated adhesion on all ECM substrates, while invasion of U-138MG cells, but not that of U-373MG cells, was markedly reduced. Conversely, pretreatment with APO reduced TGF-beta 1 protein expression levels, inhibited adhesion and increased invasion of U-138MG cells, but did not affect collagen synthesis. We conclude that exogenously applied TGF-beta 1 exerts marked effects on ECM-related features of glioma cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1995
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20. Messenger RNA expression of the immunosuppressive cytokine IL-10 in human gliomas.

Author

Huettner C, Paulus W, and Roggendorf W

Subjects
Base Sequence, Brain metabolism, Brain Neoplasms pathology, Glioblastoma metabolism, Glioma pathology, Humans, Interleukin-6 metabolism, Molecular Sequence Data, Neoplasm Staging, Polymerase Chain Reaction, Tumor Cells, Cultured, Brain Neoplasms metabolism, Glioma metabolism, Interleukin-10 metabolism, RNA, Messenger metabolism
Abstract

Interleukin 10 (IL-10) was initially discovered on the basis of its ability to suppress cytokine synthesis. Additionally, it can exert immunosuppressive effects on a variety of cell types. Because patients with malignant gliomas present with a general impairment of the immune system, we investigated IL-10 expression in the glioma tissue. Because expression of IL-10 and IL-6 is associated in hematopoietic cells and IL-6 can act as an autocrine growth stimulator for glioblastoma cell lines, we looked in addition for a relationship between IL-10 and IL-6 expression. Using a quantitative reverse transcriptase polymerase chain reaction, IL-10 and IL-6 mRNA levels were determined in 37 glial tumors of different grades including 2 recurrencies, 3 specimens from normal brain tissue, and 3 glioblastoma cell lines. Expression of IL-10 mRNA was demonstrable in all tumors as well as in normal brain. High grade tumors and recurrent cases expressed significantly higher amounts of IL-10-specific mRNA compared with low grade tumors, whereas 2 of 3 cell lines showed only weak constitutive expression, mRNA for IL-6 was found in 86.5% of all gliomas with a correlation concerning the expression levels for both cytokines in 69% of gliomas. We suggest that IL-10 may contribute to the progression of astrocytomas by suppressing the patient's immune response, whereas IL-6 provides an additional growth advantage.

Published
1995

21. Collagens, integrins and the mesenchymal drift in glioblastomas: a comparison of biopsy specimens, spheroid and early monolayer cultures.

Author

Paulus W, Huettner C, and Tonn JC

Subjects
Base Sequence, Basement Membrane metabolism, Biopsy, Brain Neoplasms chemistry, Cell Differentiation physiology, Collagen biosynthesis, Collagen genetics, Glioblastoma chemistry, Humans, Immunohistochemistry, Integrins biosynthesis, Integrins genetics, Middle Aged, Molecular Sequence Data, Polymerase Chain Reaction, RNA, Messenger genetics, RNA, Messenger metabolism, RNA-Directed DNA Polymerase, Tumor Cells, Cultured, Brain Neoplasms pathology, Collagen physiology, Glioblastoma pathology, Integrins physiology
Abstract

To analyze the process of mesenchymal differentiation in vitro, we examined 5 human glioblastomas as biopsy specimens, monolayer cultures and 3-dimensional fragment spheroid cultures for the immunohistochemical expression of extracellular matrix (ECM) components (collagen types I, III-VI, laminin) and integrin receptors (beta 1, beta 2, beta 3 and beta 4 chains). mRNA for type-I and type-IV collagen alpha I chains was quantified using reverse transcription-polymerase chain reaction. In situ, glioma cells expressed beta 1, the common beta chain of most integrin ECM receptors, while ECM components were restricted to vascular elements. Early monolayer cultures showed a marked increase in ECM components (interstitial collagens more than basement membrane components), and coexpression of ECM components and glial fibrillary acidic protein (GFAP) by most cells. beta 2 and beta 3 integrins were upregulated in the primary cultures. In the fifth passages, GFAP-positive cells were decreased and collagen-expressing cells increased. The spheroids exhibited preserved GFAP staining, neoexpression of beta 4 integrin in some tumors, and variable ECM expression by glioma cells which was lower than that in monolayer cultures. ECM deposition usually commenced in central spheroid areas where the Ki-67 proliferation index was low. We conclude that different culture systems are characterized by distinct expression patterns for ECM components and receptors, and that mesenchymal features in cultured gliomas arise due to transdifferentiation of glioma cells.

Published
1994
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22. [Increased amounts of IL-10 mRNA in anaplastic astrocytomas and glioblastoma multiforme].

Author

Huettner C, Paulus W, and Roggendorf W

Subjects
Autopsy, Brain metabolism, Brain pathology, Brain Neoplasms immunology, Brain Neoplasms pathology, Glioblastoma immunology, Glioblastoma pathology, Humans, Polymerase Chain Reaction methods, RNA, Messenger analysis, Reference Values, Brain Neoplasms metabolism, Gene Expression, Glioblastoma metabolism, Interleukin-10 biosynthesis, RNA, Messenger biosynthesis
Abstract

Interleukin 10 (Il-10) was initially discovered on the basis of its ability to suppress cytokine synthesis. Additionally, it can exert immunosuppressive effects on a variety of cell types. Since patients with malignant gliomas present with a general impairment of the immune system, we sought to investigate if IL-10 is expressed in the glioma tissue. Using RT-PCR, IL-10 mRNA levels were determined in 37 glial tumors of different grades including 2 recurrencies, 3 specimens from normal brain tissue and 3 glioblastoma cell lines. Expression of IL-10 mRNA was demonstrable in all tumors as well as in normal brain. High grade tumors and recurrent cases expressed significantly higher amounts of IL-10 specific mRNA compared to low grade tumors, while 2 out of 3 cell lines showed only weak constitutive expression. We suggest, that IL-10 may contribute to the progression of astrocytomas by allowing the tumor cells to attenuate the T-cell immune response and evade immune detection.

Published
1994

23. Comparative aspects of glucose catabolism in Staphylococcus aureus and S. epidermidis.

Author

Blumenthal HJ, Huettner CF, and Montiel FA

Subjects
Aerobiosis, Coagulase biosynthesis, Fructosephosphates metabolism, Genetic Variation, Glucosephosphate Dehydrogenase metabolism, Isoenzymes metabolism, NAD metabolism, NADP metabolism, Niacinamide analogs & derivatives, Niacinamide pharmacology, Nicotinic Acids metabolism, Oxidation-Reduction, Phosphogluconate Dehydrogenase metabolism, Staphylococcus enzymology, Staphylococcus pathogenicity, Thiamine metabolism, Glucose metabolism, Staphylococcus metabolism
Published
1974
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