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18. TRANSPLANTATION BASIC SCIENCE, ALLOGENIC AND XENOGENIC TOLERANCE

Author

Berthelot, L., primary, Robert, T., additional, Tabary, T., additional, Vuiblet, V., additional, Drame, M., additional, Toupance, O., additional, Rieu, P., additional, Monteiro, R. C., additional, Toure, F., additional, Ferrario, S., additional, Cantaluppi, V., additional, De Lena, M., additional, Dellepiane, S., additional, Beltramo, S., additional, Rossetti, M., additional, Manzione, A. M., additional, Messina, M., additional, Gai, M., additional, Dolla, C., additional, Biancone, L., additional, Camussi, G., additional, Pontrelli, P., additional, Oranger, A. R., additional, Accetturo, M., additional, Rascio, F., additional, Gigante, M., additional, Castellano, G., additional, Schena, A., additional, Fiorentino, M., additional, Zito, A., additional, Zaza, G., additional, Stallone, G., additional, Gesualdo, L., additional, Grandaliano, G., additional, Pattonieri, E. F., additional, Gregorini, M., additional, Corradetti, V., additional, Rocca, C., additional, Milanesi, S., additional, Peloso, A., additional, Ferrario, J., additional, Cannone, M., additional, Bosio, F., additional, Maggi, N., additional, Avanzini, M. A., additional, Minutillo, P., additional, Paulli, M., additional, Maestri, M., additional, Rampino, T., additional, Dal Canton, A., additional, Wu, K. S. T., additional, Coxall, O., additional, Luque, Y., additional, Candon, S., additional, Rabant, M., additional, Noel, L.-H., additional, Thervet, E., additional, Chatenoud, L., additional, Snanoudj, R., additional, Anglicheau, D., additional, Legendre, C., additional, Zuber, J., additional, Hruba, P., additional, Brabcova, I., additional, Krepsova, E., additional, Slatinska, J., additional, Sekerkova, A., additional, Striz, I., additional, Zachoval, R., additional, Viklicky, O., additional, Scholbach, T. M., additional, Wang, H.-K., additional, Loong, C.-C., additional, Yang, A.-H., additional, Wu, T.-H., additional, Guberina, H., additional, Rebmann, V., additional, Dziallas, P., additional, Dolff, S., additional, Wohlschlaeger, J., additional, Heinemann, F. M., additional, Witzke, O., additional, Zoet, Y. M., additional, Claas, F. H. J., additional, Horn, P. A., additional, Kribben, A., additional, Doxiadis, I. I. N., additional, Prasad, N., additional, Yadav, B., additional, Agarwal, V., additional, Jaiswal, A., additional, Rai, M., additional, Hope, C. M., additional, Coates, P. T., additional, Heeger, P. S., additional, Carroll, R., additional, Masola, V., additional, Secchi, M. F., additional, Onisto, M., additional, Gambaro, G., additional, Lupo, A., additional, Matsuyama, M., additional, Kobayashi, T., additional, Yoneda, Y., additional, Chargui, J., additional, Touraine, J. L., additional, Yoshimura, R., additional, Vizza, D., additional, Perri, A., additional, Lupinacci, S., additional, Toteda, G., additional, Lofaro, D., additional, Leone, F., additional, Gigliotti, P., additional, La Russa, A., additional, Papalia, T., additional, Bonofilgio, R., additional, Sentis Fuster, A., additional, Kers, J., additional, Yapici, U., additional, Claessen, N., additional, Bemelman, F. J., additional, Ten Berge, I. J. M., additional, Florquin, S., additional, Glotz, D., additional, Rostaing, L., additional, Squifflet, J.-P., additional, Merville, P., additional, Belmokhtar, C., additional, Le Ny, G., additional, Lebranchu, Y., additional, Papazova, D. A., additional, Friederich-Persson, M., additional, Koeners, M. P., additional, Joles, J. A., additional, Verhaar, M. C., additional, Trivedi, H. L., additional, Vanikar, A. V., additional, Dave, S. D., additional, Suarez Alvarez, B., additional, Garcia Melendreras, S., additional, Carvajal Palao, R., additional, Diaz Corte, C., additional, Ruiz Ortega, M., additional, Lopez-Larrea, C., additional, Yadav, A. K., additional, Bansal, D., additional, Kumar, V., additional, Minz, M., additional, Jha, V., additional, Kaminska, D., additional, Koscielska-Kasprzak, K., additional, Chudoba, P., additional, Mazanowska, O., additional, Banasik, M., additional, Zabinska, M., additional, Boratynska, M., additional, Lepiesza, A., additional, Korta, K., additional, Klinger, M., additional, Csohany, R., additional, Prokai, A., additional, Pap, D., additional, Balicza-Himer, N., additional, Vannay, A., additional, Fekete, A., additional, Kis-Petik, K., additional, Peti-Peterdi, J., additional, Szabo, A., additional, Masajtis-Zagajewska, A., additional, Muras, K., additional, Niewodniczy, M., additional, Nowicki, M., additional, Pascual, J., additional, Srinivas, T. R., additional, Chadban, S., additional, Citterio, F., additional, Henry, M., additional, Oppenheimer, F., additional, Lee, P.-C., additional, Tedesco-Silva, H., additional, Zeier, M., additional, Watarai, Y., additional, Dong, G., additional, Hexham, M., additional, Bernhardt, P., additional, Vincenti, F., additional, Rocchetti, M. T., additional, Su owicz, J., additional, Wojas-Pelc, A., additional, Ignacak, E., additional, Janda, K., additional, Krzanowski, M., additional, Su owicz, W., additional, Mitsuhashi, M., additional, Murakami, T., additional, Benso, A., additional, Leuning, D., additional, Reinders, M., additional, Lievers, E., additional, Duijs, J., additional, Van Zonneveld, A. J., additional, Van Kooten, C., additional, Engelse, M., additional, Rabelink, T., additional, Assounga, A., additional, Omarjee, S., additional, Ngema, Z., additional, Ersoy, A., additional, Gultepe, A., additional, Isiktas Sayilar, E., additional, Akalin, H., additional, Coskun, F., additional, Oner Torlak, M., additional, Ayar, Y., additional, Riegersperger, M., additional, Plischke, M., additional, Steinhauser, C., additional, Jallitsch-Halper, A., additional, Sengoelge, G., additional, Winkelmayer, W. C., additional, Sunder-Plassmann, G., additional, Foedinger, M., additional, Kaziuk, M., additional, Kuz'Niewski, M., additional, B Tkowska- Prokop, A., additional, Pa Ka, K., additional, Dumnicka, P., additional, Kolber, W., additional, and Su Owicz, W., additional

Published
2014
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21. Transplantation - basic

Author

Hruba, P., primary, Brabcova, I., additional, Krejcik, Z., additional, Stranecky, V., additional, Honsova, E., additional, Viklicky, O., additional, Rocchetti, M. T., additional, Pontrelli, P., additional, Rascio, F., additional, Fiorentino, M., additional, Stallone, G., additional, Gesualdo, L., additional, Grandaliano, G., additional, Lemy, A., additional, Lionet, A., additional, Noel, C., additional, Couzi, L., additional, Taupin, J.-L., additional, Merville, P., additional, Hiesse, C., additional, Suberbielle-Boissel, C., additional, De Meyer, M., additional, Latinne, D., additional, Racape, J., additional, Wissing, K. M., additional, Claas, F. H. J., additional, Toungouz, M., additional, Abramowicz, D., additional, Caballero, A., additional, Ruiz-Esteban, P., additional, Leon, M., additional, Palma-Merida, E., additional, Burgos, D., additional, Cabello, M., additional, Gonzalez-Molina, M., additional, Torres, A., additional, Hernandez, D., additional, Janssen, E. H. C. C., additional, Ledeganck, K. J., additional, Hoenderop, J. G. J., additional, Verpooten, G. A. L., additional, and De Winter, B. Y., additional

Published
2013
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25. Genetic diseases

Author

Inazu, T., primary, Kawahara, T., additional, Endou, H., additional, Anzai, N., additional, Sebesta, I., additional, Stiburkova, B., additional, Ichida, K., additional, Hosoyamada, M., additional, Testa, A., additional, Leonardis, D., additional, Catalano, F., additional, Pisano, A., additional, Mafrica, A., additional, Spoto, B., additional, Sanguedolce, M. C., additional, Parlongo, R. M., additional, Tripepi, G., additional, Postorino, M., additional, Enia, G., additional, Zoccali, C., additional, Mallamaci, F., additional, Working Group*, M., additional, Luque de Pablos, A., additional, Garcia-Nieto, V., additional, Lopez-Menchero, J. C., additional, Ramos-Trujillo, E., additional, Gonzalez-Acosta, H., additional, Claverie-Martin, F., additional, Arsali, M., additional, Demosthenous, P., additional, Papazachariou, L., additional, Athanasiou, Y., additional, Voskarides, K., additional, Deltas, C., additional, Pierides, A., additional, Lee, S., additional, Jeong, K. H., additional, Ihm, C., additional, Lee, T. W., additional, Lee, S. H., additional, Moon, J. Y., additional, Wi, J. G., additional, Lee, H. J., additional, Kim, E. Y., additional, Rogacev, K., additional, Friedrich, A., additional, Hummel, B., additional, Berg, J., additional, Zawada, A., additional, Fliser, D., additional, Geisel, J., additional, Heine, G. H., additional, Brabcova, I., additional, Dusilova-Sulkova, S., additional, Krejcik, Z., additional, Stranecky, V., additional, Lipar, K., additional, Marada, T., additional, Stepankova, J., additional, Viklicky, O., additional, Buraczynska, M., additional, Zukowski, P., additional, Zaluska, W., additional, Kuczmaszewska, A., additional, Ksiazek, A., additional, Gaggl, M., additional, Weidner, S., additional, Hofer, M., additional, Kleinert, J., additional, Fauler, G., additional, Wallner, M., additional, Kotanko, P., additional, Sunder-Plassmann, G., additional, Paschke, E., additional, Heguilen, R., additional, Albarracin, L., additional, Politei, J., additional, Liste, A. A., additional, Bernasconi, A., additional, Kusano, E., additional, Russo, R., additional, Pisani, A., additional, Messalli, G., additional, Imbriaco, M., additional, Prikhodina, L., additional, Ryzhkova, O., additional, Polyakov, V., additional, Lipkowska, K., additional, Ostalska-Nowicka, D., additional, Smiech, M., additional, Jaroniec, M., additional, Zaorska, K., additional, Szaflarski, W., additional, Nowicki, M., additional, Zachwieja, J., additional, D'arrigo, G., additional, Moskowitz, J., additional, Piret, S., additional, Tashman, A., additional, Velez, E., additional, Lhotta, K., additional, Thakker, R., additional, Cox, J., additional, Kingswood, J., additional, Mbundi, J., additional, Attard, G., additional, Patel, U., additional, Saggar, A., additional, Elmslie, F., additional, Doyle, T., additional, Jansen, A., additional, Jozwiak, S., additional, Belousova, E., additional, Frost, M., additional, Kuperman, R., additional, Bebin, M., additional, Korf, B., additional, Flamini, R., additional, Kohrman, M., additional, Sparagana, S., additional, Wu, J., additional, Ford, J., additional, Shah, G., additional, Franz, D., additional, Zonnenberg, B., additional, Cheung, W., additional, Urva, S., additional, Wang, J., additional, Kingswood, C., additional, Budde, K., additional, Kofman, T., additional, Narjoz, C., additional, Raimbourg, Q., additional, Roland, M., additional, Loriot, M.-A., additional, Karras, A., additional, Hill, G. S., additional, Jacquot, C., additional, Nochy, D., additional, Thervet, E., additional, Jagodzinski, P., additional, Mostowska, M., additional, Oko, A., additional, Nicolaou, N., additional, Kevelam, S., additional, Lilien, M., additional, Oosterveld, M., additional, Goldschmeding, R., additional, Van Eerde, A., additional, Pfundt, R., additional, Sonnenberg, A., additional, Ter Hal, P., additional, Knoers, N., additional, Renkema, K., additional, Storm, T., additional, Nielsen, R., additional, Christensen, E., additional, Frykholm, C., additional, Tranebjaerg, L., additional, Birn, H., additional, Verroust, P., additional, Neveus, T., additional, Sundelin, B., additional, Hertz, J. M., additional, Holmstrom, G., additional, Ericson, K., additional, Fabris, A., additional, Cremasco, D., additional, Zambon, A., additional, Muraro, E., additional, Alessi, M., additional, D'angelo, A., additional, Anglani, F., additional, Del Prete, D., additional, Alkmim Teixeira, A., additional, Quinto, B. M., additional, Jose Rodrigues, C., additional, Beltrame Ribeiro, A., additional, Batista, M., additional, Kerti, A., additional, Csohany, R., additional, Szabo, A., additional, Arkossy, O., additional, Sallai, P., additional, Moriniere, V., additional, Vega-Warner, V., additional, Lakatos, O., additional, Szabo, T., additional, Reusz, G., additional, Tory, K., additional, Addis, M., additional, Tosetto, E., additional, Meloni, C., additional, Ceol, M., additional, Cristofaro, R., additional, Melis, M. A., additional, Vercelloni, P., additional, Marra, G., additional, Kaniuka, S., additional, Nagel, M., additional, Wolyniec, W., additional, Obolonczyk, L., additional, Swiatkowska-Stodulska, R., additional, Sworczak, K., additional, Rutkowski, B., additional, Chen, C., additional, Jiang, L., additional, Chen, L., additional, Fang, L., additional, Mozes M., M., additional, Boosi, M., additional, Rosivall, L., additional, Kokeny, G., additional, Diana, R., additional, Gross, O., additional, Johanna, T., additional, Rainer, G., additional, Ayse, C., additional, Henrik, H., additional, Gerhard-Anton, M., additional, Nabil, M., additional, Intissar, E., additional, Belge, H., additional, Bloch, J., additional, Dahan, K., additional, Pirson, Y., additional, Vanhille, P., additional, and Demoulin, N., additional

Published
2012
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26. Transplantation - basic

Author

Adamczak, M., primary, Koleganova, N., additional, Nyengaard, J. R., additional, Ritz, E., additional, Wiecek, A., additional, Slabiak Blaz, N., additional, Yi Chun, D. X., additional, Alexandre, H., additional, Sandrine, G.-S., additional, Olivier, T., additional, Isabelle, E., additional, Christophe, L., additional, Guy, T., additional, Pierre Francois, W., additional, Jean-Philippe, R., additional, Yvon, L., additional, Eric, R., additional, Muller-Krebs, S., additional, Weber, L., additional, Tsobaneli, J., additional, Reiser, J., additional, Zeier, M., additional, Schwenger, V., additional, Tinel, C., additional, Samson, M., additional, Bonnotte, B., additional, Mousson, C., additional, Machcinska, M., additional, Bocian, K., additional, Wyzgal, M., additional, Korczak-Kowalska, G., additional, Ju, M. K., additional, Huh, K. H., additional, Park, K. T., additional, Kim, S. J., additional, Cho, B. H., additional, Kim, C. D., additional, So, B. J., additional, Leee, S., additional, Kang, C. M., additional, Joo, D. J., additional, Kim, Y. S., additional, Zarzycki, M., additional, Sobich, A., additional, Matsuyama, M., additional, Hase, T., additional, Yoshimura, R., additional, Koshino, K., additional, Sakai, K., additional, Suzuki, T., additional, Nobori, S., additional, Ushigome, H., additional, Brikci-Nigassa, L., additional, Chargui, J., additional, Touraine, J.-L., additional, Yoshimura, N., additional, Cantaluppi, V., additional, Medica, D., additional, Figliolini, F., additional, Migliori, M., additional, Mannari, C., additional, Dellepiane, S., additional, Quercia, A. D., additional, Randone, O., additional, Tamagnone, M., additional, Messina, M., additional, Manzione, A. M., additional, Ranghino, A., additional, Biancone, L., additional, Segoloni, G. P., additional, Camussi, G., additional, Turk, T. R., additional, Zou, X., additional, Rauen, U., additional, De Groot, H., additional, Amann, K., additional, Kribben, A., additional, Eckardt, K.-U., additional, Bernhardt, W. M., additional, Witzke, O., additional, Lidia, G., additional, Wouter, C., additional, Eric, A., additional, Yann, L. M., additional, Christian, N., additional, Marie, E., additional, Pierre, M., additional, Zineb, A., additional, Miriana, D., additional, Annick, M., additional, Marc, A., additional, Daniel, A., additional, Wornle, M., additional, Ribeiro, A., additional, Motamedi, N., additional, Grone, H. J., additional, Cohen, C. D., additional, Schlondorff, D., additional, Schmid, H., additional, Teplan, V., additional, Banas, M., additional, Banas, B., additional, Steege, A., additional, Bergler, T., additional, Kruger, B., additional, Schnulle, P., additional, Yard, B., additional, Kramer, B. K., additional, Hoger, S., additional, Xavier, M. P., additional, Sampaio-Norton, S., additional, Gaiao, S., additional, Alves, H., additional, Oliveira, G., additional, Zaza, G., additional, Rascio, F., additional, Pontrelli, P., additional, Granata, S., additional, Rugiu, C., additional, Grandaliano, G., additional, Lupo, A., additional, Wohlfahrtova, M., additional, Brabcova, I., additional, Balaz, P., additional, Janousek, L., additional, Lodererova, A., additional, Honsova, E., additional, Wohlfahrt, P., additional, Viklicky, O., additional, Grabner, A., additional, Kentrup, D., additional, Edemir, B., additional, Sirin, Y., additional, Pavenstadt, H., additional, Schober, O., additional, Schlatter, E., additional, Schafers, M., additional, Schnockel, U., additional, Reuter, S., additional, Accetturo, M., additional, Gigante, M., additional, Tataranni, T., additional, Zito, A., additional, Schena, A., additional, Schena, F. P., additional, Stallone, G., additional, Gesualdo, L., additional, Maillard, N., additional, Masson, I., additional, Lena, A., additional, Manolie, M., additional, Christophe, M., additional, Lassen, C. K., additional, Keller, A. K., additional, Moldrup, U., additional, Bibby, B. M., additional, Jespersen, B., additional, Cvetkovic, T., additional, Velickovic Radovanovic, R., additional, Pavlovic, R., additional, Djordjevic, V., additional, Vlahovic, P., additional, Stefanovic, N., additional, Sladojevic, N., additional, Ignjatovic, A., additional, Rong, S., additional, Menne, J., additional, Haller, H., additional, Suszdak, P., additional, Tomczuk, P., additional, Gueler, F., additional, Nelli, S., additional, Sara, D., additional, Salma, E. K., additional, Naoufal, M., additional, Tarik, M., additional, Mohamed, Z., additional, Guislaine, M., additional, Mohamed Gharbi, B., additional, Benyounes, R., additional, Lu, X., additional, Shushakova, N., additional, Kirsch, T., additional, Bockmeyer, C. L., additional, Ramackers, W., additional, Wittig, J., additional, Agustian, P. A., additional, Klose, J., additional, Dammrich, M. E., additional, Kreipe, H., additional, Brocker, V., additional, Winkler, M., additional, and Becker, J. U., additional

Published
2012
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29. Transplantation: basic science and immune-tolerance

Author

Sugawara, M., primary, Ichimura, S., additional, Kokubo, K., additional, Shimbo, T., additional, Hirose, M., additional, Kobayashi, H., additional, Hribova, P., additional, Brabcova, I., additional, Honsova, E., additional, Viklicky, O., additional, Kute, V. B., additional, Shah, P. R., additional, Vanikar, A. V., additional, Gumber, M. R., additional, Patel, H. V., additional, Modi, P. R., additional, Trivedi, H. L., additional, Trivedi, V. B., additional, Nusrath, S., additional, Minz, M., additional, Walker Minz, R., additional, Sharma, A., additional, Singh, S., additional, Jha, V., additional, Joshi, K., additional, Richter, R., additional, Kohler, S., additional, Qidan, S., additional, Scheuermann, E., additional, Kachel, H.-G., additional, Gossmann, J., additional, Gauer, S., additional, Seifried, E., additional, Geiger, H., additional, Seidl, C., additional, Hauser, I. A., additional, Hanssen, L., additional, Frye, B., additional, Ostendorf, T., additional, Alidousty, C., additional, Djudjaj, S., additional, Boor, P., additional, Rauen, T., additional, Floege, J., additional, Mertens, P., additional, Raffetseder, U., additional, Garcia-Cenador, B., additional, Lopez-Novoa, J. M., additional, Iniguez, M., additional, Fernandez, V., additional, Perez de Obanos, P., additional, Ruiz, J., additional, Sanz-Gimenez, J. R., additional, Lopez-Marcos, J. F., additional, Garcia-Criado, J., additional, Van Craenenbroeck, A. H., additional, Anguille, S. H., additional, Jurgens, A., additional, Cools, N., additional, Van Camp, K., additional, Stein, B., additional, Nijs, G., additional, Berneman, Z., additional, Ieven, M., additional, Van Damme, P., additional, Van Tendeloo, V., additional, Verpooten, G. A., additional, Gohel, K., additional, Hegde, U., additional, Gang, S., additional, Rajapurkar, M., additional, Erdogmus, S., additional, Sengul, S., additional, Kocak, S., additional, Kurultak, I., additional, Kutlay, S., additional, Keven, K., additional, Erbay, B., additional, Erturk, S., additional, Kimura, S., additional, Imura, J., additional, Atsumi, H., additional, Fujimoto, K., additional, Chikazawa, Y., additional, Nakagawa, M., additional, Hayama, T., additional, Okuyama, H., additional, Yamaya, H., additional, Yokoyama, H., additional, Libetta, C., additional, Canevari, M., additional, Sepe, V., additional, Margiotta, E., additional, Meloni, F., additional, Martinelli, C., additional, Borettaz, I., additional, Esposito, P., additional, Portalupi, V., additional, Morosini, M., additional, Solari, N., additional, Dal Canton, A., additional, Rusai, K., additional, Schmaderer, C., additional, Hermans, R., additional, Lutz, J., additional, Heemann, U., additional, Baumann, M., additional, Cantaluppi, V., additional, Tamagnone, M., additional, Dellepiane, S., additional, Medica, D., additional, Dolla, C., additional, Messina, M., additional, Manzione, A. M., additional, Tognarelli, G., additional, Ranghino, A., additional, Biancone, L., additional, Camussi, G., additional, Segoloni, G. P., additional, Ozkurt, S., additional, Sahin, G., additional, Degirmenci, N., additional, Temiz, G., additional, Musmul, A., additional, Birdane, A., additional, Tek, M., additional, Tekin, N., additional, Akyuz, F., additional, Yalcin, A. U., additional, and Lopez-Valverde, A., additional

Published
2011
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30. Transplantation / Basic research

Author

Wornle, M., primary, Ribeiro, A., additional, Motamedi, N., additional, Nitschko, H., additional, Cohen, C. D., additional, Grone, H. J., additional, Schlondorff, D., additional, Schmid, H., additional, Kislat, C., additional, Schmidt, T., additional, Janssen, M., additional, Wolf, M., additional, Dirks, J., additional, Ahlenstiel, T., additional, Pape, L., additional, Fliser, D., additional, Sester, M., additional, Sester, U., additional, Urbanova, M., additional, Brabcova, I., additional, Girmanova, E., additional, Ondrej, V., additional, Gregorini, M., additional, Rampino, T., additional, Rocca, C., additional, Valsania, T., additional, Corradetti, V., additional, Bosio, F., additional, Bedino, G., additional, Carrara, C., additional, Pattonieri, E. F., additional, Soccio, G., additional, Esposito, P., additional, Dal Canton, A., additional, Becker, L. E., additional, Morath, C., additional, Schaier, M., additional, Gross, M.-L., additional, Bierhaus, A., additional, Waldherr, R., additional, Nawroth, P., additional, Zeier, M., additional, Tataranni, T., additional, Biondi, G., additional, Cariello, M., additional, Mangino, M., additional, Colucci, G., additional, Rutigliano, M., additional, Ditonno, P., additional, Schena, F. P., additional, Pertosa, G., additional, Gesualdo, L., additional, and Grandaliano, G., additional

Published
2011
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31. Genetic diseases and molecular genetics

Author

Stekrova, J., primary, Reiterova, J., additional, Elisakova, V., additional, Merta, M., additional, Kohoutova, M., additional, Tesar, V., additional, Suvakov, S., additional, Damjanovic, T., additional, Dimkovic, N., additional, Pljesa, S., additional, Savic-Radojevic, A., additional, Pljesa-Ercegovac, M., additional, Matic, M., additional, Djukic, T., additional, Coric, V., additional, Simic, T., additional, Gigante, M., additional, d'Altilia, M., additional, Montemurno, E., additional, Schirinzi, A., additional, Bruno, F., additional, Netti, G. S., additional, Ranieri, E., additional, Stallone, G., additional, Infante, B., additional, Grandaliano, G., additional, Gesualdo, L., additional, Maritati, F., additional, Alberici, F., additional, Bonatti, F., additional, Oliva, E., additional, Sinico, R. A., additional, Moroni, G., additional, Leoni, A., additional, Gregorini, G., additional, Jeannin, G., additional, Possenti, S., additional, Tumiati, B., additional, Grasselli, C., additional, Brugnano, R., additional, Salvarani, C., additional, Fraticelli, P., additional, Pavone, L., additional, Pesci, A., additional, Guida, G., additional, Neri, T. M., additional, Buzio, C., additional, Malerba, G., additional, Martorana, D., additional, Vaglio, A., additional, Santucci, L., additional, Candiano, G., additional, Cremasco, D., additional, Tosetto, E., additional, Del Prete, D., additional, Bruschi, M., additional, Ghiggeri, G. M., additional, Anglani, F., additional, Rainone, F., additional, Soldati, L., additional, Terranegra, A., additional, Arcidiacono, T., additional, Aloia, A., additional, Dogliotti, E., additional, Vezzoli, G., additional, Maruniak-Chudek, I., additional, Zenker, M., additional, Chudek, J., additional, Obeidova, L., additional, Stekrova, J., additional, Lnenicka, P., additional, Iwanitskiy, L. V., additional, Krasnova, T. N., additional, Samokhodskaya, L. M., additional, Bernasconi, A. R., additional, Albarracin, L., additional, Liste, A. A., additional, Politei, J. M., additional, Heguilen, R. M., additional, Kaito, H., additional, Nozu, K., additional, Nakanishi, K., additional, Hashimura, Y., additional, Shima, Y., additional, Ninchoji, T., additional, Yoshikawa, N., additional, Iijima, K., additional, Matsuo, M., additional, Hur, E., additional, Gungor, O., additional, Bozkurt, D., additional, Bozgul, S. M. K., additional, Caliskan, H., additional, Dusunur, F., additional, Basci, A., additional, Akcicek, F., additional, Duman, S., additional, Li, Y., additional, Wang, C., additional, Nan, L., additional, Hruskova, Z., additional, Brabcova, I., additional, Lanska, V., additional, Honsova, E., additional, Hanzal, V., additional, Borovicka, V., additional, Rysava, R., additional, Zachoval, R., additional, Viklicky, O., additional, Miltenberger-Miltenyi, G., additional, Almeida, E., additional, Calado, J., additional, Carvalho, F., additional, Pereira, S., additional, Teixeira, C., additional, Jorge, S., additional, Viana, H., additional, Gomes da Costa, A., additional, Yang, C.-S., additional, Tseng, M.-H., additional, Yang, S.-S., additional, and Lin, S.-H., additional

Published
2011
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32. Association of advanced vasculopathy and transforming growth factor-beta1 gene expression with immunoglobulin A nephropathy progression

Author

Brabcova, I., primary, Tesar, V., additional, Honsova, E., additional, Lodererova, A., additional, Novotna, E., additional, Maixnerova, D., additional, Merta, M., additional, Burgelova, M., additional, Hribova, P., additional, Skibova, J., additional, Zadrazil, J., additional, Maly, J., additional, and Viklicky, O., additional

Published
2010
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39. P446 Myocardial ischemic tolerance and expression of selected genes in spontaneously hypertensive rats adapted to chronic continuous hypoxia.

Author

Kolar, D, Brabcova, I, Zurmanova, J, Mandikova, P, Zajickova, P, Kalous, M, Pravenec, M, Novakova, O, Kolar, F, and Neckar, J

Subjects
*CORONARY disease, *GENE expression, *HYPERTENSION, *CHRONIC diseases, *HYPOXEMIA, *LABORATORY rats
Abstract

Purpose: Spontaneously hypertensive rats (SHR) are more susceptible to acute myocardial ischemia/ reperfusion injury than normotensive Brown Norway (BN) strain. It has been shown that the adaptation to chronic hypoxia improves ischemic tolerance in normotensive rats and the cardioprotective phenotype can be related to mitochondrial metabolism and signalling. Here we aimed at investigating effects of continuous normobaric hypoxia (CNH) on myocardial ischemic tolerance of SHR and conplastic strain SHR-mtBN (with mitochondrial genome from BN). We also analyzed the expression levels of selected genes of energy metabolism, antioxidant systems and signalling pathways.Methods: Rats were kept 21 days at CNH (inspired O2 fraction 0.1). Myocardial infarct size was determined after 20 min of ischemia and 2 h of reperfusion in open-chest rats (tetrazolium staining). In a separate group of animals, the total mRNA was isolated from left ventricles and gene expression was assessed by RT-PCR.Results: CNH reduced infarct size from 71 ± 4% of the area at risk in normoxic SHR to 49 ± 6% in hypoxic SHR. As compared to SHR, CNH induced more pronounced infarct size-limiting effect in SHR-mtBN. In both strains, CNH increased the mRNA expression of monoaminooxidase and β1-adrenoceptor, and decreased the expression of mitochondrial creatine kinase, superoxide dismutase, thioredoxin 2, thioredoxin-reductase 2 and peroxiredoxin 5. However, the expression of catalase, peroxiredoxin 3, mitochondrial hexokinase 2 and hypoxia-inducible factor 1α was markedly elevated in hypoxic SHR-mtBN as compared to hypoxic SHR.Conclusions: We demonstrate that CNH protects SHR hearts against acute ischemia/reperfusion injury with a possible involvement of mitochondrial genes.This work was supported by the Czech Science Foundation grant No. 13-10267S [ABSTRACT FROM PUBLISHER]

Published
2014
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40. P658 Adaptation to continuous normobaric hypoxia affects mitochondrial enzymes in spontaneously hypertensive rat hearts.

Author

Kalous, M, Weissova, R, Drahota, Z, Brabcova, I, Zurmanova, J, Novakova, O, Pravenec, M, Kolar, F, and Neckar, J

Subjects
ISCHEMIA, BIOLOGICAL adaptation, HYPOXIA-inducible factor 1, HYPERTENSION, MITOCHONDRIAL enzymes, LABORATORY rats, MESSENGER RNA
Abstract

Purpose: Adaptation to continuous normobaric hypoxia (CNH) increases cardiac ischemic tolerance. The protective role of cardiac mitochondria has been suggested in CNH. The present study investigated the effects of CNH on the expression and activity of selected mitochondrial proteins in spontaneously hypertensive rats (SHR), and in a novel conplastic strain SHR-mtBN. This strain is characterized with a selective replacement of the mitochondrial genome of SHR with more ischemic tolerant Brown Norway (BN) strain.Methods: Rats were kept 21 days at CNH (inspired O2 fraction 0.1). Left ventricular homogenate was used to assess the enzyme activity of malate dehydrogenase (MDH), citrate synthase (CS), NADH-cytochrome c oxidoreductase, succinate-cytochrome c oxidoreductase and cytochrome oxidase (COX). Protein and mRNA expression of the subunits of oxidative phosphorylation complexes (CI - Ndufa9, CII - Sdha, CIII- Uqcrc2, CIV - COX-4 and MTCO1, CV - Atp5a1) were evaluated using immunoblotting and RT-PCR.Results: Normoxic SHR-mtBN has by 14% lower amount of complex IV subunit MTCO1 (encoded by BN mitochondrial genome) compared to SHR. Adaptation to CNH resulted in raised content of complex IV subunits by 17% in both strains compared to normoxic controls. In addition, MDH activity decreased by 23% only in hypoxic SHR. These changes resulted in significant differences between SHR and SHR-mtBN after adaptation to CNH. As compared both hypoxic strains, SHR-mtBN demonstrated higher MDH activity and protein amount of Ndufa9 subunit of complex I, whereas the protein content of COX-4 and MTCO1 subunits of complex IV were lower compared to SHR. The expression on the mRNA level was decreased for CS (by 45%) as well as for cytochrome oxidase isoforms subunits COX 4.1 and COX 4.2 (by 22% and 23%, respectively) in the conplastic strain adapted to CNH compared to normoxic control. However, in the CNH adapted SHR strain, the decrease in mRNA level was found for COX 4.1 only (by 28%).Conclusions: Adaptation to CNH affected myocardial expression and activity of mitochondrial proteins in hypertensive strains, and replacement of the mitochondrial genome of SHR with BN modified the response to CNH.This work was supported by the Czech Science Foundation grant no. 13-10267S [ABSTRACT FROM PUBLISHER]

Published
2014
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41. Analysis of the fall-related risk of pharmacotherapy in Czech hospitals: A case control study.

Author

Maly J, Dosedel M, Kubena AA, Mala-Ladova K, Vosatka J, Brabcova I, Hajduchova H, Bartlova S, Tothova V, and Vlcek J

Subjects
Aged, 80 and over, Czech Republic epidemiology, Female, Humans, Male, Prospective Studies, Risk Factors, Hospitalization, Hospitals
Abstract

Rationale, Aims, and Objectives: Falls are among the major problems occurring in hospital setting, when drugs are viewed as important modifiable risk factor of falling. The aim was to analyse the effect of pharmacotherapy on the risk of falls in hospitalized patients., Methods: A multicentre prospective case-control study was conducted in 2017 retrieving data from four hospitals in South Bohemia, Czech Republic. An online database was constructed to collect patient and fall-related data. Each fall that occurred during hospitalization was assigned to appropriate controls (no fall during hospitalization) based on gender, age, length of hospitalization, and the number of drugs. Univariate and multivariate correlations were performed with a significance level of P < .05., Results: A total of 222 fall cases (107 males; median age, 81 y) and 1076 controls (516 males; median age, 80 y) were included. According to the first ATC level classification, drugs from groups S, N, and P were significantly associated with fall-related risk compared with controls (P < .05); further analysis of ATC levels showed that only psycholeptics (N05), antipsychotics (N05A), and tiapride were significantly associated with falls. Regression analysis revealed use of psycholeptics N05 (OR = 2.06; 95% CI, 1.56-2.76), or ophthalmologicals S01 (OR = 2.72; 95% CI, 1.37-5.41), as factors with the highest fall-related risk., Conclusions: Apart from the commonly considered fall-risk increasing drugs, other groups, such as ophthalmologicals, should also be considered; however, regarding clinical practice, it is difficult to evaluate the effects of individual drugs in the context of other risk factors of falls, due to the multifactorial nature of falls., (© 2019 John Wiley & Sons, Ltd.)

Published
2020
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42. Pharmacotherapy as major risk factor of falls - analysis of 12 months experience in hospitals in South Bohemia.

Author

Maly J, Dosedel M, Vosatka J, Mala-Ladova K, Kubena AA, Brabcova I, Hajduchova H, Bartlova S, Tothova V, and Vlcek J

Abstract

This study aimed to analyze the effect of fall risk-increasing drugs (FRIDs) and drug-related factors relative to falls through clinical pharmacy service in hospitalized patients, focusing on the relevance of clinical pharmacist evaluation in the context of physician assessment. A prospective study of inpatient falls was conducted in 2017 retrieving data from 4 hospitals in South Bohemia, Czech Republic. An online database was developed to collect patient and fall-related data, and fall evaluation records. Healthcare professionals classified the overall effect of drugs on falls using Likert scale. Univariate and multivariate correlations were performed with a significance level of p < 0.05. Out of the total 280 falls (mean age of patients 77.0 years), a mean of 2.8 diagnoses with fall-related risk, 8.8 drugs, and 4.1 FRIDs per fall were identified. Incidence of falls decreased quarterly (p < 0.001). Use of FRIDs were positively associated with increasing age (p = 0.007). Clinical pharmacists were more likely to identify pharmacotherapy as the relevant fall-related risk, compared to physicians evaluation (p < 0.001). An increasing total number of prescribed drugs as well as higher number of FRIDs increased the suspicion in both professionals in the context of drug-related causes of falls., Competing Interests: The authors report no conflicts of interest in this work.

Published
2019
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43. β-Adrenergic signaling, monoamine oxidase A and antioxidant defence in the myocardium of SHR and SHR-mtBN conplastic rat strains: the effect of chronic hypoxia.

Author

Hahnova K, Brabcova I, Neckar J, Weissova R, Svatonova A, Novakova O, Zurmanova J, Kalous M, Silhavy J, Pravenec M, Kolar F, and Novotny J

Subjects
Adenylyl Cyclases metabolism, Animals, Male, Malondialdehyde metabolism, Rats, Rats, Inbred SHR, Signal Transduction physiology, Hypoxia metabolism, Monoamine Oxidase metabolism, Myocardium metabolism, Receptors, Adrenergic, beta metabolism
Abstract

The β-adrenergic signaling pathways and antioxidant defence mechanisms play important roles in maintaining proper heart function. Here, we examined the effect of chronic normobaric hypoxia (CNH, 10% O 2 , 3 weeks) on myocardial β-adrenergic signaling and selected components of the antioxidant system in spontaneously hypertensive rats (SHR) and in a conplastic SHR-mtBN strain characterized by the selective replacement of the mitochondrial genome of SHR with that of the more ischemia-resistant Brown Norway strain. Our investigations revealed some intriguing differences between the two strains at the level of β-adrenergic receptors (β-ARs), activity of adenylyl cyclase (AC) and monoamine oxidase A (MAO-A), as well as distinct changes after CNH exposure. The β 2 -AR/β 1 -AR ratio was significantly higher in SHR-mtBN than in SHR, apparently due to increased expression of β 2 -ARs. Adaptation to hypoxia elevated β 2 -ARs in SHR and decreased the total number of β-ARs in SHR-mtBN. In parallel, the ability of isoprenaline to stimulate AC activity was found to be higher in SHR-mtBN than that in SHR. Interestingly, the activity of MAO-A was notably lower in SHR-mtBN than in SHR, and it was markedly elevated in both strains after exposure to hypoxia. In addition to that, CNH markedly enhanced the expression of catalase and aldehyde dehydrogenase-2 in both strains, and decreased the expression of Cu/Zn superoxide dismutase in SHR. Adaptation to CNH intensified oxidative stress to a similar extent in both strains and elevated the IL-10/TNF-α ratio in SHR-mtBN only. These data indicate that alterations in the mitochondrial genome can result in peculiar changes in myocardial β-adrenergic signaling, MAO-A activity and antioxidant defence and may, thus, affect the adaptive responses to hypoxia.

Published
2018
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44. Identification of Gene Transcripts Implicated in Peritoneal Membrane Alterations.

Author

Parikova A, Vlijm A, Brabcova I, de Graaff M, Struijk DG, Viklicky O, and Krediet RT

Subjects
Animals, Biopsy, Needle, Confidence Intervals, Dialysis Solutions pharmacology, Disease Models, Animal, Immunohistochemistry, Male, Nephrectomy methods, Peritoneal Dialysis adverse effects, Peritoneal Fibrosis pathology, Random Allocation, Rats, Rats, Wistar, Real-Time Polymerase Chain Reaction, Kidney Failure, Chronic therapy, Neovascularization, Pathologic genetics, Peritoneal Dialysis methods, Peritoneal Fibrosis genetics, Transcription, Genetic
Abstract

♦ BACKGROUND: Permanent stimulation of the peritoneum during peritoneal dialysis (PD) is likely to result in increased expression of genes encoding proteins involved in inflammation and tissue remodeling. Peritoneal fibrosis and neoangiogenesis may develop. ♦ OBJECTIVE: To assess highly expressed genes potentially in volved in peritoneal alterations during PD treatment using an animal model. ♦ METHODS: A PD catheter was implanted in 36 male Wistar rats after 70% nephrectomy. The rats were divided into 3 groups, exposed to dialysis solution for 8 weeks, and sacrificed 2 weeks later. Group B was exposed to a buffer, group D was exposed to a 3.86% glucose-based dialysis solution, and in group D+H, a second hit of intraperitoneal blood on top of the dialysis solution was given to induce the development of peritoneal sclerosis. Before sacrifice, peritoneal function was assessed. Omental tissue was obtained for analysis of gene expression using RT-qPCR. ♦ RESULTS: Fibrosis scores, vessel counts, and peritoneal function parameters were not different between the groups. Genes involved in the transforming growth factor beta signaling pathway, cell proliferation, angiogenesis, and inflammation were more expressed (p < 0.05) in the D+H group. Almost no differences were found between the control groups. We identified 4 genes that were related to peritoneal transport. ♦ CONCLUSION: Already a mid-term peritoneal exposure, when no microscopical and functional alterations are present, provokes activation of gene pathways of cell proliferation, fibrosis, neoangiogenesis, and inflammation., (Copyright © 2016 International Society for Peritoneal Dialysis.)

Published
2016
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45. Tubular atrophy and low netrin-1 gene expression are associated with delayed kidney allograft function.

Author

Wohlfahrtova M, Brabcova I, Zelezny F, Balaz P, Janousek L, Honsova E, Lodererova A, Wohlfahrt P, and Viklicky O

Subjects
Atrophy, Biopsy, Delayed Graft Function metabolism, Delayed Graft Function pathology, Gene Expression Regulation, Humans, Immunohistochemistry, Logistic Models, Nerve Growth Factors analysis, Netrin-1, Principal Component Analysis, Prospective Studies, Reperfusion Injury complications, Tumor Suppressor Proteins analysis, Delayed Graft Function etiology, Kidney Transplantation adverse effects, Kidney Tubules pathology, Nerve Growth Factors genetics, Tumor Suppressor Proteins genetics
Abstract

Background: Delayed graft function (DGF) caused by ischemia/reperfusion injury (I/RI) negatively influences the outcome of kidney transplantation. This prospective single-center study characterized the intrarenal transcriptome during I/RI as a means of identifying genes associated with DGF development., Methods: Characterization of the intrarenal transcription profile associated with I/RI was carried out on three sequential graft biopsies from respective allografts before and during transplantation. The intragraft expression of 92 candidate genes was measured using quantitative real-time reverse transcriptase polymerase chain reaction (2) in delayed (n=9) and primary function allografts (n=26)., Results: Cold storage was not associated with significant changes to the expression profile of the target gene transcripts; however, up-regulation of 16 genes associated with enhanced activation of innate and adaptive immune responses and apoptosis was observed after reperfusion. Multivariate logistic regression analysis revealed that higher tubular atrophy scores (ct) together with a lower expression of Netrin-1 might predict DGF development (training area under the receiver operating curve=0.89, cross-validated area under the receiver operating curve=0.81)., Conclusions: Poor baseline tubular cell quality (defined by a higher rate of tubular atrophy) combined with the reduced potential of apoptotic survival factors represented by decreased Netrin-1 gene expression were associated with delayed kidney graft function.

Published
2014
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46. Transgenic rescue of defective Cd36 enhances myocardial adenylyl cyclase signaling in spontaneously hypertensive rats.

Author

Klevstig M, Manakov D, Kasparova D, Brabcova I, Papousek F, Zurmanova J, Zidek V, Silhavy J, Neckar J, Pravenec M, Kolar F, Novakova O, and Novotny J

Subjects
Adenylyl Cyclases genetics, Adrenergic beta-1 Receptor Agonists pharmacology, Animals, CD36 Antigens metabolism, Cyclic AMP-Dependent Protein Kinases metabolism, Dobutamine pharmacology, GTP-Binding Proteins metabolism, Myocardial Contraction, Rats, Rats, Inbred SHR, Rats, Transgenic, Receptors, Adrenergic, beta metabolism, Adenylyl Cyclases metabolism, CD36 Antigens genetics, Myocardium metabolism, Signal Transduction
Abstract

Dysfunction or abnormalities in the regulation of fatty acid translocase Cd36, a multifunctional membrane protein participating in uptake of long-chain fatty acids, has been linked to the development of heart diseases both in animals and humans. We have previously shown that the Cd36 transgenic spontaneously hypertensive rat (SHR-Cd36), with a wild type Cd36, has higher susceptibility to ischemic ventricular arrhythmias when compared to spontaneously hypertensive rat (SHR) carrying a mutant Cd36 gene, which may have been related to increased β-adrenergic responsiveness of these animals (Neckar et al., 2012 Physiol. Genomics 44:173-182). The present study aimed to determine whether the insertion of the wild type Cd36 into SHR would affect the function of myocardial G protein-regulated adenylyl cyclase (AC) signaling. β-Adrenergic receptors (β-ARs) were characterized by radioligand-binding experiments and the expression of selected G protein subunits, AC, and protein kinase A (PKA) was determined by RT-PCR and Western blot analyses. There was no significant difference in the amount of trimeric G proteins, but the number of β-ARs was higher (by about 35 %) in myocardial preparations from SHR-Cd36 as compared to SHR. Besides that, transgenic rats expressed increased amount (by about 20 %) of the dominant myocardial isoforms AC5/6 and contained higher levels of both nonphosphorylated (by 11 %) and phosphorylated (by 45 %) PKA. Differently stimulated AC activity in SHR-Cd36 significantly exceeded (by about 18-30 %) the enzyme activity in SHR. Changes at the molecular level were reflected by higher contractile responses to stimulation by the adrenergic agonist dobutamine. In summary, it can be concluded that the increased susceptibility to ischemic arrhythmias of SHR-Cd36 is attributable to upregulation of some components of the β-AR signaling pathway, which leads to enhanced sensitization of AC and increased cardiac adrenergic responsiveness.

Published
2013
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47. B-cell-related biomarkers of tolerance are up-regulated in rejection-free kidney transplant recipients.

Author

Viklicky O, Krystufkova E, Brabcova I, Sekerkova A, Wohlfahrt P, Hribova P, Wohlfahrtova M, Sawitzki B, Slatinska J, Striz I, Volk HD, and Reinke P

Subjects
Adult, Aged, Biomarkers, Female, Forkhead Transcription Factors analysis, Gene Expression Profiling, Humans, Male, Middle Aged, Prospective Studies, Proto-Oncogene Proteins genetics, Up-Regulation, B-Lymphocytes immunology, Graft Rejection, Immune Tolerance, Kidney Transplantation immunology
Abstract

Background: Molecular signatures have recently been identified in operationally tolerant long-term kidney transplant patients; however, their expression in patients on immunosuppression remains unclear., Methods: In this prospective study, the gene expression profiles of eight selected tolerance-associated genes (MS4A1, CD79B, TCL1A, TMEM176B, FOXP3, TOAG-1, MAN1A1, and TLR5) in the peripheral blood of 67 kidney transplant recipients at days 0, 7, 14, 21, 28, 60, 90, and at 6 and 12 months, and in graft biopsies were measured. Similarly, using flow cytometry, CD45CD19CD3 B-cell counts were evaluated in the follow-up. Expression patterns were compared among patients with biopsy-proven acute rejection, borderline changes, and in rejection-free patients. A generalized linear mixed model with gamma distribution for repeated measures adjusted for induction therapy was used for statistical analysis of longitudinal data and Kruskal-Wallis test for case biopsy data., Results: Compared to patients with rejection, a significantly higher number of peripheral B cells were observed during follow-up in rejection-free patients and in patients with borderline changes. Gene expression patterns of MS4A1 (CD20), TCL1A, CD79B, TOAG-1, and FOXP3 genes were significantly higher in rejection-free patients as compared to rejection group with the highest differences during the first 3 months. In contrast, TMEM176B (TORID) was up-regulated in the rejection group. Similar trends were also observed between patients with borderline changes and acute rejection. Higher intragraft expression of TOAG-1 was observed in rejection-free patients., Conclusions: These observations suggest an association of B-cell signatures, seen also in drug-free tolerant patients, with controlled alloimmune response.

Published
2013
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48. Cytokine gene expression profile in monocytic cells after a co-culture with epithelial cells.

Author

Kolesar L, Brabcova E, Thorburn E, Sekerkova A, Brabcova I, Jaresova M, Viklicky O, and Striz I

Subjects
Cell Line, Coculture Techniques, Cytokines biosynthesis, Epithelial Cells cytology, Epithelial Cells metabolism, Gene Expression Profiling, Humans, Monocytes cytology, Monocytes metabolism, RNA, Messenger biosynthesis, RNA, Messenger immunology, Time Factors, Cytokines immunology, Epithelial Cells immunology, Gene Expression Regulation immunology, Monocytes immunology
Abstract

Epithelial cells represent an important source of cytokines that may modulate the influx and functions of mononuclear phagocytes. The aim of our study was to characterize changes in the gene expression of selected cytokines in human macrophages co-cultured with respiratory epithelial cells. The A549 alveolar type II-like cell line was co-cultured with THP-1 cells (monocyte/macrophage cell line) in filter-separated mode to avoid their cell-cell contact. At different time-points (0, 4, 8, 12 and 24 h), the cells were harvested separately to evaluate their gene and protein expression (IL-1 beta, IL-6, IL-8, IL-10 and GM-CSF). Quantitative RT-PCR analysis showed prominent changes in the THP-1 cytokine gene expression induced by a co-culture with A549 cells. Fourfold upregulation of mRNA expression has been found in 12 genes and 4-fold downregulation in 5 genes as compared to the unstimulated control sample with a p value smaller than 0.05. The induction of inhibin beta A and IL-1 beta mRNA after 12 h and the expression of IL-1 alpha and GM-CSF mRNA after 24 h were the most prominent. When looking at the cytokine levels in culture supernatants, IL-1 beta and IL-8 were induced early (at 8 h) as compared to the release of IL-6 and GM-CSF (at 24 h). We conclude that respiratory epithelial cells constitutively regulate the cytokine gene expression of macrophages located in their environment and might further modulate the release of cytokines by posttranslational pathways.

Published
2012
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49. Regulatory T cells in kidney transplant recipients: the effect of induction immunosuppression therapy.

Author

Krystufkova E, Sekerkova A, Striz I, Brabcova I, Girmanova E, and Viklicky O

Subjects
Adolescent, Adult, Aged, Antilymphocyte Serum therapeutic use, Basiliximab, Female, Flow Cytometry, Follow-Up Studies, Humans, Immune Tolerance, Immunosuppression Therapy, Interleukin-2 Receptor alpha Subunit immunology, Male, Middle Aged, Prognosis, Prospective Studies, Recombinant Fusion Proteins therapeutic use, Young Adult, Antibodies, Monoclonal therapeutic use, Graft Rejection immunology, Immunosuppressive Agents therapeutic use, Kidney Transplantation immunology, T-Lymphocytes, Regulatory drug effects, T-Lymphocytes, Regulatory immunology
Abstract

Background: Regulatory T cells have been suggested to down-regulate the alloimmune response. The aim of this prospective open study was to evaluate the effects of different inductive agents on peripheral blood regulatory T cells in kidney transplant patients and to analyse their association with short-term graft outcome., Methods: Regulatory and effector T cell numbers in peripheral blood were determined by flow cytometry in 71 prospectively followed kidney transplant recipients at postoperative day 0, 7, 14, 21, 28, 60 and 90. Patients were treated with a calcineurin inhibitor-based triple immunosuppression with polyclonal rabbit anti-thymocyte globulin (rATG, n = 28), basiliximab, the anti-CD25 monoclonal antibody (n = 18) or without induction (controls, n = 25). Flow cytometry data were correlated to rejection incidence., Results: Compared to controls, CD4(+)CD25(+)FoxP3(+) regulatory T-cell expansion among CD4(+) T cells was noticed in the rATG group at all post-transplant time-points by Day 14 (P < 0.001). A significant decrease in Treg frequency (P < 0.001) and concurrently a transient increase of CD4(+)CD25(low/-)FoxP3(+) population were observed in basiliximab-treated patients 7-60 days post-transplantation. Biopsy-proven acute rejection occurred in 16.7% of controls, 10.7% of the rATG group and in 11.1% of the basiliximab group. Higher CD4(+)FoxP3(+)/CD8(+)CD45RA(+)CD62L(-) ratios were observed repeatedly in those patients after basiliximab induction who were rejection free (P < 0.01)., Conclusions: In this study, the rATG induction therapy was associated with an expansion of regulatory cells. Sustained high CD4(+)FoxP3(+)/Teff ratios were associated with the absence of rejection after basiliximab induction.

Published
2012
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50. Differential regulation of the nuclear factor-κB pathway by rabbit antithymocyte globulins in kidney transplantation.

Author

Urbanova M, Brabcova I, Girmanova E, Zelezny F, and Viklicky O

Subjects
Adult, Aged, Animals, Apoptosis, Biopsy, Down-Regulation drug effects, Down-Regulation immunology, Down-Regulation physiology, Female, Follow-Up Studies, Gene Expression Profiling, Graft Rejection immunology, Graft Rejection pathology, Graft Rejection prevention & control, Humans, Kidney metabolism, Kidney pathology, Kidney Transplantation pathology, Male, Middle Aged, NF-kappa B genetics, RNA, Messenger metabolism, Rabbits, Signal Transduction immunology, Antilymphocyte Serum pharmacology, Immunosuppression Therapy methods, Kidney Transplantation immunology, Kidney Transplantation physiology, NF-kappa B metabolism, Signal Transduction drug effects, Signal Transduction physiology
Abstract

Background: Induction therapy is associated with excellent short-term kidney graft outcome. The aim of this study was to evaluate differences in the intragraft transcriptome after successful induction therapy using two rabbit antithymocyte globulins., Methods: The expression of 376 target genes involved in tolerance, inflammation, T- and B-cell immune response, and apoptosis was evaluated using the quantitative real-time reverse-transcriptase polymerase chain reaction (2(-ΔΔCt)) method in kidney graft biopsies with normal histological findings and stable renal function, 3 months posttransplantation after induction therapy with Thymoglobulin, ATG-Fresenius S (ATG-F), and a control group without induction therapy., Results: The transcriptional pattern induced by Thymoglobulin differed from ATG-F in 18 differentially expressed genes. Down-regulation of genes involved in the nuclear factor-κB pathway (TLR4, MYD88, and CD209), costimulation (CD80 and CTLA4), apoptosis (NLRP1), chemoattraction (CCR10), and dendritic cell function (CLEC4C) was observed in the biopsies from patients treated with Thymoglobulin. A hierarchical clustering analysis clearly separated the Thymoglobulin group from the ATG-F group, while the control group had a similar profile as the Thymoglobulin group., Conclusions: Despite normal morphology in graft biopsy taken 3 months posttransplantation, the intrarenal transcriptome differed in patients treated with induction therapy using different rATGs. In the Thymoglobulin high-risk group, the transcriptome profile was identical to the low-risk group. Therefore, the down-regulation of the nuclear factor-κB pathway after Thymoglobulin induction in vivo is likely to explain the clinical success of this biologic.

Published
2012
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