15 results on '"Jirak P"'
Search Results
2. Rotationsstabilität und der Visus-Ergebnisse einer 1-teiligen, hydrophilen torischen Acryl IOL über einen Zeitraum von 1,5 Jahren (K)
- Author
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Jirak, P, Gyoengyoessy, B, Schönherr, U, Jirak, P, Gyoengyoessy, B, and Schönherr, U
- Published
- 2016
3. Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes.
- Author
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IMPROVE-IT Investigators, Musliner, T., Tershakovec, A., Gurfinkel, E., Aylward, P., Tonkin, A., Maurer, G., Van de Werf, F., Nicolau, J.C., Theroux, P., Genest, J., Armstrong, P., Corbalan, R., Isaza, D., Spinar, J., Grande, P., Voitk, J., Kesaniemi, A., Bassand, J.P., Farnier, M., Darius, H., Keltai, M., Mathur, A., Mittal, S., Reddy, K., Lewis, B., De Ferrari, G.M., Ophuis, T.O., Jukema, J., White, H., Pedersen, T., Britto, F., Ruzyllo, W., Carrageta, M., Duris, T., Dalby, A., Seung, K.B., Lopez-Sendon, J., Dellborg, M., Mach, F., Guneri, S., Parkhomenko, A., Brady, A., Cannon, C., Blazing, M., Ballantyne, C., de Lemos, J., Kleiman, N., McGuire, D.K., Centeno, E., Casalins, M., Cartasegna, L., Beltrano, M.C., Guerrero, R., Fanuele, M., Berra, F., Egido, J., Colombo, H., Dellatorre, M., Terns, P., Blumberg, E., Reges, P., Azize, G., Ramos, H., Fernandez, R., Carlessi, C., Milesi, R., Schmuck, R., Duronto, E., Procopio, G., Carlevaro, O., Maffeo, H., Beloscar, J., Viso, M., Hominal, M., Castoldi, M., Bluguermann, J., Mauro, D., Macin, S., Cocco, N., Ruiz, N., Ricart, J., Lozada, A., Nani, S., Turri, D., Fernandez, H., Caruso, O., Zarandon, R., Bono, J., Arias, V., Allall, O., Marino, J., Cusimano, S., Schygiel, P., Buzetti, C., Penaloza, N., Berli, M., Worthley, S., Roach, A., Chew, D., Wright, T., Leitch, J., Hicks, E., Rankin, J., Venn-Edmonds, C., Lehman, R., Morrison, H., Shaw, J., Mak, V., Hii, C., Smith, K., Cross, D., Lilwall, L., Nelson, G., Loxton, A., Horowitz, J., Rose, J., Steinwender, C., Leisch, F., Kammler, J., Brussee, H., Zweiker, R., Niederl, E., Weihs, W., Giorgio, G., Lang, I., Drexel, H., Zanolin, D., Hoppe, U., Atzenhofer-Baumgartner, K., Pichler, M., Hainzer, D., Eber, B., Pichler, F., Foeger, B., Wechselberger, T., Mayr, H., Hofer, J., Stockenhuber, F., Warlits, B., Huber, K., Egger, F., Weidinger, F., Ziegler, B., Jirak, P., Metzler, B., Pachinger, O., Wanitschek, M., Auer, J., Grabscheit, G., Podczeck-Schweighofer, A., Priesnitz, T., Frank, H., El Allaf, D., Marechal, P., Roosen, J., Joly, E., Lefebvre, P., Arend, C., Sinnaeve, P., De Velder, L., Hellemans, S., Vanhauwaert, B., Van Dorpe, A., Heyse, A., Vantomme, C., Striekwold, H., Van Den Broeck, D., Lancellotti, P., Schoors, D., Lemoine, I., Taeymans, Y., De Wolf, L., Brike, C., Vercauteren, S., Tahon, S., Vervoort, G., Mestdagh, I., Pirenne, B., Cardinal, F., Lips, S., Dujardin, K., Debrouwer, K., Dhooghe, G., Holvoet, G., van de Borne, P., Renard, M., De Clippel, M., Lesseliers, H., Van Miert, N., Saraiva, J., Vicente, C., Rossi, P., Dos Santos, L.B., Duda, N., Tognon, A.P., Serrano, C., Gomes, F.L., Manenti, E.R., Silveira, D.S., Maia, L., Mouco, O.M., Paiva, M., Antonangelo, A., de Souza, J., Lino, E.A., Leães, P., Blacher, M.G., Kormann, A., Ultramari, F.T., Dutra, O., Mendelski, A.M., Morgado, S., Ardito, W., Greque, G., Ardito, R.V., Pimentel Filho, P., Zucchetti, C., Alves, A., Seabra, A.M., Mattos, M., Miranda, L.F., Silva, D., Uehara, R.M., Marin Neto, J., Schmidt, A., Braga, J., Rodrigues, A., Abrantes, J., Pinheiro, L., Bodanese, L., Magedanz, É.H., Piegas, L., Dos Santos, E.S., Wainstein, M., Ribeiro, J., Stein, R., Marino, R., Machado, V.M., Moraes Junior, J., Guimarães, S., da Costa, F.A., Ferraz, R.F., Albuquerque, D., Rocha, R.M., de Carvalho Moreira, R., Dohmann, H., Costantini, C., Tarastchuk, J.C., Coelho, O., Cirillo, W., Sousa, A., Almeira, A.S., Stefanini, E., Silva, F., Teixeira, M., da Cunha, C., Précoma, D., Facchi, T.L., Rupka, D., Thiessen, S., Warnica, J., Smith, B., Della Siega, A., Klinke, P., Nelson, S., Dion, D., Gilbert, N., Hui, W., Kvill, L., Sussex, B., Luther, A., Dupuis, R., Ouimet, F., Pandey, A., Clarus, S., Senaratne, M., Ferdinandis, H., Mukherjee, A., Bozek, B., Vizel, S., Markov, G., Zimmermann, R., Stephens, W., Tremblay, B., Wong, G., Uchida, N., Brossoit, R., Peck, C., Van Kieu, C., Forgione, M., Bata, I., Cossett, J., Kostuk, W., Arnold, M., Bone, C., Grondin, F., Bilodeau, N., Gosselin, G., David, M., Giannoccaro, J., Beresford, P., Polasek, P., Roberts, P., Doucet, M., Beaudry, M., Cheung, S., Cleveland, T., Bhargava, R., McCallum, A., Ma, P., Morrissette, J., Cleveland, D., Chadwyn, D., Nigro, F., Weeks, A., Cryderman, C., Leader, R., Houde, G., Rousseau, S., Pearce, M., Radyk, M., Lonn, E., Magi, A., Lefkowitz, C., Sandrin, F., Coffin, N., Lubelsky, B., Coldwell, J., Habot, J., McPherson, C., De Larochelliere, R., Roy, M., Haichin, R., Barber, C., Bhesania, T., Kitagawa, H., To, T., Donnelly, B., Tymchak, W., Harris, L., Kouz, S., Huynh, T., St Jacques, B., Lamy, A., Rizzo, A., Stein, J., Childs, C., Wong, B., Poirier, R., Gupta, M., Dela Cruz, C., Constance, C., Gauthier, M., Ervin, F., Ouellette, M., Kokis, A., Lemay, C., Kwok, K., Leung, C., Lee, D., Nesmith, J., Renton, J., Syan, G., Turek, M., Hogan, D., Griffin, P., Lipson, A., Winestock, J., Abramson, B., Fogel, A., Gagne, C., Bergeron, J., Clarke, A., Slipp, S., Darcel, I., Carling-Chambers, L., Kannampuzha, P., Pallie, S., Krekorian, S., Vertes, G., Roth, S., Lai, K., Heath, J., Perez, L., Arriagada, G., Castro, P., Villa, F., Rodríguez, M., Ramos, G., Baraona, F., Núñez, A., García, M., Jofre, C., Silva, P., Lamich, R., Yovaniniz, P., Escobar, E., Dussaubat, A., Segura, E., Ramirez, M., Lapostol, C., Palma, A., Encina, L., Zapata, M., Baeza, N., Varela, P., Pérez, L., Jaramillo, C., Ruiz, S., Sanchez, G., Perdomo, I., Manzur, F., Cohen, L.E., Velasquez, J., Arana, C., Alvarez, Y., Triana, M., Balaguera, J., de Salazar, D., Rendon, N., Botero, R., Ruiz, A., Saaibi, J., Medina, J., Jaramillo, M., Calderón, M.J., Delgado, J., Bohorquez, R., Medina, M.F., Herrera, M., Rosales, D., Mendoza, F., Martinez, S., Ternera, A., Castro, R., Baiz, A., Martinez, M., Orozco, A., Suarez, M., Fonseca, Y., Beltran, R., Cepeda, M., Jaramillo, N., Valenzuela, C., Gutierrez, M., Sanchez, A., Vitovec, J., Hlinomaz, O., Poloczek, M., Mayer, O., Veselka, J., Vejvoda, J., Soucek, M., Spac, J., Novobilsky, K., Srp, V., Francek, L., Branny, M., Sknouril, L., Motovska, Z., Rohac, F., Stankova, A., Fiala, T., Holub, M., Zeman, K., Pohludkova, L., Pospisilova, E., Tuma, P., Cihalik, C., Oral, I., Podpera, I., Stepanovova, R., Uricar, M., Solar, M., Pelouch, R., Porzer, M., Grussmannova, K., Stipal, R., Reichert, P., Hradec, J., Kral, J., Sejkova, B., Janek, B., Pitha, J., Linhart, A., Polacek, P., Koeber, L., Clemmensen, P., Hebin, C.H., Schmidt, E., Pedersen, M.S., Roseva-Nielsen, N., Kristensen, K., Bang-Hansen, T., Jensen, J., Laage-Petersen, J., Nielsen, H., Stokholm, E., Thayssen, P., Cappelen, H., Jensen, T., Winther-Friis, B., Klausen, I., Hedegaard, B., May, O., Andersen, M., Bottzauw, J., Lush, A., Markenvard, J., Vestager, K.M., Bronnum-Schou, J., Hempel, H., Petersen, J., Nielsen, A.J., Thomsen, K., Nielsen, T., Nygaard, A., Sykulski, R., Jensen, B.S., Ralfkiaer, N., Gottschalck, H., Rasmussen, S., Pedersen, L.R., Dodt, K., Skovsbøl, M., Andersen, O., Tuxen, C., Meier, A.W., Kristensen, T., Rasmussen, O., Lopez, J., Salazar, D., Sanchez, L., Rosero, F., Penaherrera, E., Duarte, Y.C., Marmol, R., Andrade, G., Guzman, E., Morillo, A., Aug, L., Loogna, I., Laanmets, P., Mustonen, J., Mäntylä, P., Kesäniemi, A., Ukkola, O., Kervinen, H., Juhela, S., Juvonen, J., Toppinen, A., Jarvenpaa, J., Syvanne, M., Svahn, T., Voutilainen, S., Huotari, A., Nikkila, M., Raiskinmäki, S., Kotila, M., Rajala, A., Laukkanen, J., Hiltunen, P., Melin, J., Nyman, K., Luukkonen, J., Kosonen, P., Huttunen, M., Seppänen, V., Airaksinen, J., Juonala, M., Lehto, S., Savolainen, K., Halkosaari, M., Sia, J., Palomaki, A., Luoma, J., Utriainen, S., Valpas, S., Tiensuu, T., Lilleberg, J., Kainulainen, R., Schiele, F., Bassand, J., Meneveau, N., Galinier, M., Jean, M., Martelet, M., Mouallem, J., Elbaz, M., Puel, J., Carrié, D., Coisne, D., Varroud-Vial, N., Jaboureck, O., Dujardin, J., Leroy, F., Mansourati, J., Funck, F., Jourdain, P., Guillard, N., Coviaux, F., Gay, A., Dourmap-Collas, C., Froger-Bompas, C., Paillard, F., Tricot, O., Maquin-Mavier, I., Dubois-Rande, J.L., Pongas, D., Paris, A.P., Delahaye, F., Ovize, M., Benyahya, L., Bonnet, J., Belle, L., Mangin, L., Lafitte, B., Zemour, G., Doux, N., Agraou, B., El Mansour, N., Traisnel, G., El Jarroudi, M., Ohlmann, P., Diadema, B., Escande, M., Legros, G., Demarcq, J.M., Haftel, Y., Alsagheer, S., Dambrine, P., Cottin, Y., Ghostine, S., Caussin, C., Gacem, A., Bouvier, J.M., Poulard, J., Davy, J., Furber, A., Prunier, F., Muenzel, T., Genth-Zotz, S., Appel, K., Kretzschmar, D., Ferrari, M., Terres, W., Uher, T., Schulze, H., Ochs, H., Morbach, S., Duengen, H., Gross, M., Oezcelik, C., Tahirovic, E., Heuer, H., Laschewski, B., Kadel, C., Rahn, G., Steiner, S., Kreuzer, J., Tsoy, I., Zeiher, A., Muegge, A., Hanefeld, C., Boehm, S., Boudriot, E., Hodenberg, E., Lippe, B., Hausdorf, C., Sydow, K., Baldus, S., Schlesner, C., Tiroch, K., Haltern, G., Guelker, H., Wilhelm, J., Dietz, S., Ebelt, H., Buerke, M., Rupprecht, H., Rittgen, J., Schaeufele, T., Meinhardt, G., Schieber, M., Honold, M., Sieprath, S., Nienaber, C., Hacker, J., Butter, C., Lapp, H., Hirn, S., Pauschinger, M., Zahn, R., Scheffler, U., Schaefer, A., Schieffer, B., Tebbe, U., Kriete, M., Mudra, H., Raeder, T., Braun, P., Zeymer, U., Kouraki, K., Reppel, M., Schunkert, H., Weil, J., Olbrich, H., Schwaiger, P., Mueller, O., Blessing, E., Buss, I., Bohlscheid, V., Kaddatz, J., Skowasch, D., Nickenig, G., Twelker, K., Osterhues, H., Varghese, T., Burghard, S., Kaeaeb, S., Klauss, V., Sohn, H.Y., Hauptmann, K., Schulze, M., Gall, K., Felix, S., Doerr, M., Mante, J., Gulba, D., Freick, M., Werner, G., Kleinertz, K., Hobbach, H.P., Halbach, M., Mueller-Ehmsen, J., Mueller, M.E., Mitrovic, V., Peil, A., Laufs, U., vom Dahl, J., Baumanns, S., Scholtz, W., Wiemer, M., Haude, M., Van de Loo, A., Pistorius, K., Schaefer, J., Schwinger, R., Goeing, O., Jung, W., Birkemeyer, R., Lee, W., Kong, S., Yu, C., Chui, K., Merkely, B., Szelényi, Z., Polgár, P., Svab, S., Herczeg, B., Bajcsi, É., Vértes, A., Davidovits, S., Nagy, A., Király, C., Lupkovics, G., Kenéz, A., Poór, F., Takács, J., Kirschner, R., Simonyi, G., Koncz, J., Édes, I., Gergely, S., Katona, A., Nagy, E., Kovács, Z., Gyetvai, I., Salamon, C., Kolman, É., Sitkei, É., Csapó, K., Molnar, K., Mező, I., Sereg, M., Reddy, P., Manjunath, C., Narayanappa, S., Kumar, S., Sinha, N., Kapoor, A., Christopher, J., Reddy, G., Rani, M., Oomman, A., Ramamurthee, K., Kumar, N., Pasha, S.S., Rao, C., Murty, G.S., Chopra, A., Kapila, D., Bali, H., Chattree, K., Hasan, O., Suryaprakash, G., Rao, D., Babu, R., Bhargavi, M., Naik, S., Khan, S., Chopra, V., Sapra, R., Kaul, U., Ghose, T., Menon, R., Battikadi, S., Mullasari, A., Subban, V.K., Dani, S., Iby, M., Chandra, P., Sethi, S., Bhargava, M., Arora, P., Tyagi, G., Padmanabhan, T., Malhotra, S., Talwar, K., Shafiq, N., Kasliwal, R., Bansal, M., Eldar, M., Berger, M., Shechter, M., Atar, S., Roguin, N., Kilimnik, M., Hayek, T., Hamoud, S., Katz, A., Plaev, T., Shotan, A., Vazan, A., Weiss, A., Leibowitz, D., Zimlichman, R., Ben-Aharon, J., Hammerman, H., Dragu, R., Rozenman, Y., Witzling, V., Tzivoni, D., Moriel, M., Halkin, A., Sheps, D., Bogomolny, N., Mosseri, M., Khudyak, Y., Halabi, S., Uziel-Iunger, K., Yuval, R., Shimoni, S., Caspi, A., Botwin, S., Gavish, D., Sandler, A., Pollak, A., Kreisberg, B., Hussein, O., Jabal, K., Henkin, Y., Grosbard, A., Rosenschein, U., Rivlin, E., Zeltser, D., Platner, N., Porter, A., Harel, N., Lishner, M., Elis, A., Karny, M., Fuchs, S., Stein, G., Grossman, E., Gealel, Z., Schlaeffer, F., Liberty, I., Golik, A., Tzuman, O., De Ferrari, G., Pavesi, C., Poggio, L., Damiano, S., Pazzano, A.S., Mennuni, M., Paloscia, L., Mascellanti, M., Piovaccari, G., Grosseto, D., Mascia, F., Vetrano, A., Zingarelli, A., Mazzantini, S., Visconti, L., Terzi, G., Senni, M., Gavazzi, A., Scuri, P., Carmelo, M., De Caterina, R., Conti, M., Novo, S., Graceffa, A., Arvigo, L., Lunetta, M., Filardi, P., Chiariello, M., Scala, O., Pirozzi, E., Musella, F., Moretti, L., Testa, M., Vicentini, A., De Feo, S., Biasucci, L., Cardillo, M.T., Puccioni, E., Galli, M., Menegato, A., Margheri, M., Maresta, A., Gatti, C., Guarini, P., Damiano, M., Golino, P., Porcu, M., Fele, N., Gensini, G., Lombardi, A., Ciuti, G., Bernardi, D., Mariani, P., Paolini, E., Marenzi, G., Moltrasio, M., Terrosu, P., Chessa, P., Guglielmino, G., Miccoli, F., Oldoino, E., Ragni, M., Poli, M., Basso, V., Rapezzi, C., Branzi, A., Gallelli, I., Perna, G., Guazzarotti, F., Marra, S., Usmiani, T., Olivari, Z., Calzolari, D., Santoro, G., Minneci, C., Achilli, A., Nassiacos, D., Sommariva, L., Romeo, F., Fedele, F., Foschi, M.L., Bruno, N., Centurion, C., Patrizi, G., De Maria, E., Gonnelli, S., Vichi, V., Cassadonte, F., Rotella, G., Capucci, A., Villani, G., Gaspardone, A., Ferrante, R., Scollo, V., Pancaldi, L., Saccà, S., Gabrielli, D., Ciliberti, D., Savini, E., Binaghi, G., Di Biase, M., Ieva, R., Fattore, L., Cicia, G., Cavallini, C., Tamburino, C., Sacco, A., Mafrici, A., Di Pasquale, G., Pavesi, P.C., Scioli, R., Lioy, E., Occhiuzzi, E., Matino, M.G., Russo, V., Moscogiuri, M.G., Cuccia, C., Forgione, C., Volpe, M., Palano, F., Branca, G., Rossi, R., Modena, M., Olaru, I.A., Zanini, R., Cianflone, D., Cristell, N., Pantaleoni, M., Guiducci, U., Menozzi, C., Gaddi, O., Fasulo, A., Indolfi, C., Emanuele, V., Guerra, F., Iliceto, S., Marotta, C., Morocutti, G., Presbitero, P., Rossi, M., Bonatti, S., Grieco, A., Chiodi, L., Betti, I., Zuppiroli, A., Fanelli, R., Stanco, G., Azzolini, P., Ruggieri, C., Bocconcelli, P., Airoldi, F., Tavano, D., Brunelli, C., Caso, P., Scalzone, A., Ghigliotti, G., Facciorusso, A., Sim, K., Kiam, O., Chee, K., Bin Ismail, O., Zambahari, R., Ophuis, T., van Nes, E., Werter, C.J., Ophuis, A.J., Troquay, R.P., Hamer, B.J., Lenderink, T., Feld, R.J., van Hessen, M.W., Viergever, E.P., van der Sluis, A., Lok, D.J., Badings, E.A., Nierop, P.R., Danse, I.Y., Hermans, W.R., Holwerda, N.J., Thijssen, H.J., Theunissen, L.J., van der Zwaan, C., Van Den Berg, B.J., Hendriks, I.H., Ronner, E., Withagen, A.J., Dijkshoorn-Giesen, A.H., Ezechiels, J.P., Kuijper, A.F., Den Hartog, F.R., Van Kalmthout, P.M., Buijs, E.M., van der Zeijst, M., Zwart, P.A., Zuidgeest, J.A., van Eck, M., Daniels, M.C., van der Ven-Elzebroek, N., Van 't Hof, A., van Boven, A.J., van der Weerdt, A., Dunselman, P.H., Alings, M.A., van Es, R.F., The, S.H., Gurlek, C., Liem, A.H., van Lennep, H.W., Van Vlies, B., Kalkman, C., Swart, H.P., van der Bij, P., Taverne, R., Ciampricotti, R., van Dam, C., Spierenburg, H., van Ruijven, I., van Kempen, L.H., Willems, F.F., Dirkali, A., Stoel, I., Plomp, J., Veldmeijer, S., Tjeerdsma, G., Nijmeijer, R., Van Hal, J.M., Bartels, G.L., Posma, J.L., Linssen, G.C., Fauser, C.G., Waalewijn, R.A., Groenemeijer, B.E., Pos, L., Fast, J.H., Droste, H.T., Westenburg, J., Veenstra, W., Koolen, J., van Loo, L.W., Smits, W., Milhous, J.G., van Rossum, P., Stuij, S., Scott, R., Richards, A.M., Morrison, Z., Devlin, G., Fisher, R., Stewart, R., Benetar, J., Voss, J., Wong, S., Scott, D., Luke, R., Tang, E., Davidson, L., Hamer, A., Wilson, S., Price, R., Hart, H., Turner, A., Jortveit, J., Calic, S., Gundersen, T., Brunvand, H., Fosse, L., Nygaard, O., Gjellefall, B., Gravdal, S.A., Ringstad, R., Atar, D., Clausen, H., Hysing, J., Arvesen, K., Topper, M., Flagstad, E., Graven, T., Haug, H.H., Dalin, L., Al-Ani, R., Otterstad, J., Ausen, K., Aaser, E., Olufsen, M., Halvorsen, S., Gullestad, L., Stueflotten, W., Waage, K., Stødle, R.M., Hall, C., Aase, O., Nordeng, J., Soyland, E., Fageraas, E.R., Lied, A., Aske, R., Raouf, N., Johansson, J., Herrscher, T., Skogrand, E., Bjornstad, H., Aagnes, I., Arntsen, B.I., Vegsundvaag, J., Skjold, M.E., Velle, H., Aambakk, M.B., Skjetne, O., Byfuglien, A., Rodriguez, J., Galvez, D., Medina, F., Hernandez, H.A., Chavez, V., Morales, R., Huapalla, E., Velasquez, D., Torres, F., Aguirre, O., Yanez, L., Andrade, M., Campos, C., Arce, R., Mogrovejo, W., Osores, F., Bustamante, G., Rodriguez, M., Berrospi, P., Garcia, C., Talledo, M., Navarro, P., Horna, M., Herrera, V., Kadziela, J., Rybicka-Musialik, A., Trusz-Gluza, M., Berger-Kucza, A., Musial, W., Tycinska, A., Gil, R., Gziut, A., Gorny, J., Tyllo, M., Reszka, Z., Mickiewicz-Pawlowska, M., Wrzosek, B., Kosior, J., Staneta, P., Korzeniak, R., Kalarus, Z., Markowicz, E., Miekus, P., Konarzewski, M., Kleinrok, A., Puzniak, M., Grajek, S., Janus, M., Krzyzanowski, M., Hoffmann, A., Muzalewski, P., Polonski, L., Kazik, A., Nowalany-Kozielska, E., Wojciechowska, C., Ponikowski, P., Nawrocka, S., Filipiak, K., Serafin, A., Dubiel, J., Mielecki, W., Ogorek, M., Kopcik, D., Jaworska, K., Skonieczny, G., Kawecka-Jaszcz, K., Bryniarski, L., Tracz, W., Lesniak-Sobelga, A., Jankielewicz, J., Zaluska, R., Trojnar, R., Kawalek, P., Gaciong, Z., Pulkowski, G., Anaszewicz, M., Samul, W., Adamus, J., Cholewa, M., Kubik, L., Szczechowicz, R., Rekosz, J., Kwiatkowska, D., Gajek, J., Mazurek, W., Kominek, M., Siminiak, T., Guzniczak, E., Monteiro, P., Providencia, L., Monteiro, S., Pinho, T., Gavina, C., Sousa, C., Loureiro, J., Ferreira, A.R., Cardoso, A., Araujo, J., Rebolo, I., Catarino, C., Santos, J., Nunes, L.P., Mimoso, J., Marques, N., Leitao, M., Pais, J., Fernandes, A., Diogo, A., Nóbrega, J., Moreira, J.I., Mateus, P., Oliveira, J., Selas, M., Ribeiro, V., Albuquerque, A., Reis, R., Ramos, A., Salazar, F., Nair, D., Ng, C.K., Yeo, D., Wong, A., Funiak, S., Belicova, M., Striezova, I., Krajci, P., Sojka, G., Herman, O., Zemberova, A., Pella, D., Fedacko, J., Banikova, A., Micko, K., Macek, V., Moscovic, M., Vahala, P., Vykoukalova, T., Dzupina, A., Marusakova, M., Stevlik, J., Akubzanova, E., Hatalova, K., Burgess, L., Coetzee, C., Mabin, T., Roos, J., Mohamed, Z., Pillay, T., Corbett, C., Bodenstein, W., Tayob, F., Ebrahim, I., Bolsman, C., Horak, A., Lloyd, E., Pretorius, M., Commerford, P., De 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H., Kelley, M., Diffenback, M., Friedman, B., Zirkle, J., Severa, L., Sample, S., Dignen, K., Raisinghani, A., Ben-Yehuda, O., Ghannadian, B., Moscoso, R., Mankowski, J., Boliek, W., Rukavina, M., Davis, W., Ledbetter, S., Handel, F., Mastouri, R., Mahenthiran, J., Foltz, J., Malhotra, V., Jonas, J., Berk, M., Singh, V., Nelson, M., Elsner, G., Gall, J., Kondo, N., Frank, S., Chandraratna, P., Ranasinghe, S., Ebrahimi, R., Treadwell, M., Walters, B., Hughes, L., Kramer, J., Kumar, K., Mente, T., Lachterman, B., Schifferdecker, B., Munshi, K., Sease, D., Waldo, D., Chandler, G., Manns, D., Nahhas, A., Kamalesh, M., Williams, V., Reich, D., Desalca, M., Sharma, S., Liston, M., Gupta, K., Costa, M., Altschuller, A., Lemmertz, K., Shanes, J., Hansen, C., Therrien, M., Mendelson, R., Ramnarine, R., Myers, G., Donovan, C., Klein, M., Fine, D., Owens, S., Murray, C., Ketroser, R., Heifetz, S., Darnell, Z., Touchon, R., Taghizadeh, B., Bohle, D., Norwood, D., Forrest, T., Jackson, S., Shumate, 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IMPROVE-IT Investigators, Musliner, T., Tershakovec, A., Gurfinkel, E., Aylward, P., Tonkin, A., Maurer, G., Van de Werf, F., Nicolau, J.C., Theroux, P., Genest, J., Armstrong, P., Corbalan, R., Isaza, D., Spinar, J., Grande, P., Voitk, J., Kesaniemi, A., Bassand, J.P., Farnier, M., Darius, H., Keltai, M., Mathur, A., Mittal, S., Reddy, K., Lewis, B., De Ferrari, G.M., Ophuis, T.O., Jukema, J., White, H., Pedersen, T., Britto, F., Ruzyllo, W., Carrageta, M., Duris, T., Dalby, A., Seung, K.B., Lopez-Sendon, J., Dellborg, M., Mach, F., Guneri, S., Parkhomenko, A., Brady, A., Cannon, C., Blazing, M., Ballantyne, C., de Lemos, J., Kleiman, N., McGuire, D.K., Centeno, E., Casalins, M., Cartasegna, L., Beltrano, M.C., Guerrero, R., Fanuele, M., Berra, F., Egido, J., Colombo, H., Dellatorre, M., Terns, P., Blumberg, E., Reges, P., Azize, G., Ramos, H., Fernandez, R., Carlessi, C., Milesi, R., Schmuck, R., Duronto, E., Procopio, G., Carlevaro, O., Maffeo, H., Beloscar, J., Viso, M., Hominal, M., Castoldi, M., Bluguermann, J., Mauro, D., Macin, S., Cocco, N., Ruiz, N., Ricart, J., Lozada, A., Nani, S., Turri, D., Fernandez, H., Caruso, O., Zarandon, R., Bono, J., Arias, V., Allall, O., Marino, J., Cusimano, S., Schygiel, P., Buzetti, C., Penaloza, N., Berli, M., Worthley, S., Roach, A., Chew, D., Wright, T., Leitch, J., Hicks, E., Rankin, J., Venn-Edmonds, C., Lehman, R., Morrison, H., Shaw, J., Mak, V., Hii, C., Smith, K., Cross, D., Lilwall, L., Nelson, G., Loxton, A., Horowitz, J., Rose, J., Steinwender, C., Leisch, F., Kammler, J., Brussee, H., Zweiker, R., Niederl, E., Weihs, W., Giorgio, G., Lang, I., Drexel, H., Zanolin, D., Hoppe, U., Atzenhofer-Baumgartner, K., Pichler, M., Hainzer, D., Eber, B., Pichler, F., Foeger, B., Wechselberger, T., Mayr, H., Hofer, J., Stockenhuber, F., Warlits, B., Huber, K., Egger, F., Weidinger, F., Ziegler, B., Jirak, P., Metzler, B., Pachinger, O., Wanitschek, M., Auer, J., Grabscheit, G., Podczeck-Schweighofer, A., Priesnitz, T., Frank, H., El Allaf, D., Marechal, P., Roosen, J., Joly, E., Lefebvre, P., Arend, C., Sinnaeve, P., De Velder, L., Hellemans, S., Vanhauwaert, B., Van Dorpe, A., Heyse, A., Vantomme, C., Striekwold, H., Van Den Broeck, D., Lancellotti, P., Schoors, D., Lemoine, I., Taeymans, Y., De Wolf, L., Brike, C., Vercauteren, S., Tahon, S., Vervoort, G., Mestdagh, I., Pirenne, B., Cardinal, F., Lips, S., Dujardin, K., Debrouwer, K., Dhooghe, G., Holvoet, G., van de Borne, P., Renard, M., De Clippel, M., Lesseliers, H., Van Miert, N., Saraiva, J., Vicente, C., Rossi, P., Dos Santos, L.B., Duda, N., Tognon, A.P., Serrano, C., Gomes, F.L., Manenti, E.R., Silveira, D.S., Maia, L., Mouco, O.M., Paiva, M., Antonangelo, A., de Souza, J., Lino, E.A., Leães, P., Blacher, M.G., Kormann, A., Ultramari, F.T., Dutra, O., Mendelski, A.M., Morgado, S., Ardito, W., Greque, G., Ardito, R.V., Pimentel Filho, P., Zucchetti, C., Alves, A., Seabra, A.M., Mattos, M., Miranda, L.F., Silva, D., Uehara, R.M., Marin Neto, 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Ieva, R., Fattore, L., Cicia, G., Cavallini, C., Tamburino, C., Sacco, A., Mafrici, A., Di Pasquale, G., Pavesi, P.C., Scioli, R., Lioy, E., Occhiuzzi, E., Matino, M.G., Russo, V., Moscogiuri, M.G., Cuccia, C., Forgione, C., Volpe, M., Palano, F., Branca, G., Rossi, R., Modena, M., Olaru, I.A., Zanini, R., Cianflone, D., Cristell, N., Pantaleoni, M., Guiducci, U., Menozzi, C., Gaddi, O., Fasulo, A., Indolfi, C., Emanuele, V., Guerra, F., Iliceto, S., Marotta, C., Morocutti, G., Presbitero, P., Rossi, M., Bonatti, S., Grieco, A., Chiodi, L., Betti, I., Zuppiroli, A., Fanelli, R., Stanco, G., Azzolini, P., Ruggieri, C., Bocconcelli, P., Airoldi, F., Tavano, D., Brunelli, C., Caso, P., Scalzone, A., Ghigliotti, G., Facciorusso, A., Sim, K., Kiam, O., Chee, K., Bin Ismail, O., Zambahari, R., Ophuis, T., van Nes, E., Werter, C.J., Ophuis, A.J., Troquay, R.P., Hamer, B.J., Lenderink, T., Feld, R.J., van Hessen, M.W., Viergever, E.P., van der Sluis, A., Lok, D.J., Badings, E.A., Nierop, P.R., 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Andrade, M., Roux, J., Murray, A., Soma, P., Delport, E., Cassel, G., Van Zyl, L., Cronje, T., Sarvan, M., Moodley, R., Guerra, M., Swanepoel, N., Bayat, J., Klug, E., Hellig, S., Yoon, J., Kim, J., Chung, W., Choi, Y., Cho, M., Lee, S., Kwon, H., Hong, B., Seung, K., Chang, K., Rha, S., Jeong, M.H., Hong, Y., Lee, C., Seong, I., Jeong, J., Tahk, S., Yoon, M., Chae, S.C., Kim, H., Lopez, V., Roldan, J.M., Mancisidor, P., Froufe, J., López, A., Franco, S., Molina, A., Soriano, F., Cobos, M., Mejía, H.D., Sanz, R., Vazquez, A., Garri, F., Esteban, I., Marco, P., Artaecheverria, J., Cequier, A., Esplugas, E., Gonzalez, J., de Sa, E., Armada, E., Worner, F., Hernández, I., Roncales, F., Gomollon, J., del Rio, A., Alameda, J., Basilio, E., Rafols, M., Ferres, R., Molla, C., Pascual, J., Cortada, J., García, C., Iglesias, G., Villa, E., Aros, F., Goya, I., Bueno, M., Pereira, R.V., Clavero, X., Pasaron, C.D., Jorda, R., Pereira, R., Perez, O., de Teresa, E., Navarro, M., de la Guia, F., 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B., Gruberg, L., Singer, A., Ramgadoo, M., Lalonde, T., Morin, R., French, W., Barillas, O., Gradner, G., Kahn, Z., Gress, J., Rocco, D., Thew, S., Stifter, W., Fisher, M., McNamara, J., Kupfer, J., Agocha, A., Cush, S., Jones, S., Whitaker, T., Stover, T., Kumkumian, G., Kent, K., Greenberg, A., Pandey, P., Pytlewski, G., Matsumura, M., Kai, W., Sameshima, S., Thomas, J., MacNicholas, D., Pillai, K., Jones, D., Navas, J.P., Laskoe, B., Patel, P., Fini, G., Minor, S., Shipwash, T., Cabrera-Santamaria, A., Rivera, E., Mincher, L., Jafar, M., Yen, M., Finkle, C., Rahimtoola, A., Severson, L., Labroo, A., Jinich, D., Tam, K., Vogel, C., Aggarwal, R., Zakhary, B., Curtis, S., Lyster, M., Humphrey, K., Lavine, P., Fujise, K., Birnbaum, Y., Allen, J., Kesselbrenner, M., Michel, K., Staniloae, C., Liu, M., Sonel, A., Macioce-Caffas, A., Amidon, T., Leggett, J., Yedinak, S., Gudmundsson, G., Sabharwal, J., Dagefoerde, N., Wu, W., Meyerrose, G., Roongsritong, C., Jenkins, L., Lieberman, S., 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H., Kelley, M., Diffenback, M., Friedman, B., Zirkle, J., Severa, L., Sample, S., Dignen, K., Raisinghani, A., Ben-Yehuda, O., Ghannadian, B., Moscoso, R., Mankowski, J., Boliek, W., Rukavina, M., Davis, W., Ledbetter, S., Handel, F., Mastouri, R., Mahenthiran, J., Foltz, J., Malhotra, V., Jonas, J., Berk, M., Singh, V., Nelson, M., Elsner, G., Gall, J., Kondo, N., Frank, S., Chandraratna, P., Ranasinghe, S., Ebrahimi, R., Treadwell, M., Walters, B., Hughes, L., Kramer, J., Kumar, K., Mente, T., Lachterman, B., Schifferdecker, B., Munshi, K., Sease, D., Waldo, D., Chandler, G., Manns, D., Nahhas, A., Kamalesh, M., Williams, V., Reich, D., Desalca, M., Sharma, S., Liston, M., Gupta, K., Costa, M., Altschuller, A., Lemmertz, K., Shanes, J., Hansen, C., Therrien, M., Mendelson, R., Ramnarine, R., Myers, G., Donovan, C., Klein, M., Fine, D., Owens, S., Murray, C., Ketroser, R., Heifetz, S., Darnell, Z., Touchon, R., Taghizadeh, B., Bohle, D., Norwood, D., Forrest, T., Jackson, S., Shumate, 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- Abstract
Statin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular events, but whether the addition of ezetimibe, a nonstatin drug that reduces intestinal cholesterol absorption, can reduce the rate of cardiovascular events further is not known. We conducted a double-blind, randomized trial involving 18,144 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and had LDL cholesterol levels of 50 to 100 mg per deciliter (1.3 to 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.3 to 3.2 mmol per liter) if they were not receiving lipid-lowering therapy. The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy). The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization (≥30 days after randomization), or nonfatal stroke. The median follow-up was 6 years. The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001). The Kaplan-Meier event rate for the primary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference, 2.0 percentage points; hazard ratio, 0.936; 95% confidence interval, 0.89 to 0.99; P=0.016). Rates of prespecified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups. When added to statin therapy, ezetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outcomes. Moreover, lowering LDL cholesterol to levels below previous targets provided additional benef
- Published
- 2015
4. Rotationsstabilität und Patientenzufriedenheit nach Implantation einer neuen torischen Intraokularlinse (K)
- Author
-
Jirak, P, Gyoengyoessy, B, Schönherr, U, Jirak, P, Gyoengyoessy, B, and Schönherr, U
- Published
- 2014
5. Rotationsstabilität und Patientenzufriedenheit nach Implantation einer neuen torischen Intraokularlinse (K)
- Author
-
Jirak, P, Gyoengyoessy, B, Schönherr, U, Jirak, P, Gyoengyoessy, B, and Schönherr, U
- Published
- 2014
6. Proximal tubular cells contain a phenotypically distinct, scattered cell population involved in tubular regeneration
- Author
-
Smeets, B., Boor, P., Dijkman, H.B., Sharma, S.V., Jirak, P., Mooren, F., Berger, K., Bornemann, J., Gelman, I.H., Floege, J., Vlag, J. van der, Wetzels, J.F.M., Moeller, M.J., Smeets, B., Boor, P., Dijkman, H.B., Sharma, S.V., Jirak, P., Mooren, F., Berger, K., Bornemann, J., Gelman, I.H., Floege, J., Vlag, J. van der, Wetzels, J.F.M., and Moeller, M.J.
- Abstract
Item does not contain fulltext, Regeneration of injured tubular cells occurs after acute tubular necrosis primarily from intrinsic renal cells. This may occur from a pre-existing intratubular stem/progenitor cell population or from any surviving proximal tubular cell. In this study, we characterize a CD24-, CD133-, and vimentin-positive subpopulation of cells scattered throughout the proximal tubule in normal human kidney. Compared to adjacent 'normal' proximal tubular cells, these CD24-positive cells contained less cytoplasm, fewer mitochondria, and no brush border. In addition, 49 marker proteins are described that are expressed within the proximal tubules in a similar scattered pattern. For eight of these markers, we confirmed co-localization with CD24. In human biopsies of patients with acute tubular necrosis (ATN), the number of CD24-positive tubular cells was increased. In both normal human kidneys and the ATN biopsies, around 85% of proliferating cells were CD24-positive - indicating that this cell population participates in tubular regeneration. In healthy rat kidneys, the novel cell subpopulation was absent. However, upon unilateral ureteral obstruction (UUO), the novel cell population was detected in significant amounts in the injured kidney. In summary, in human renal biopsies, the CD24-positive cells represent tubular cells with a deviant phenotype, characterized by a distinct morphology and marker expression. After acute tubular injury, these cells become more numerous. In healthy rat kidneys, these cells are not detectable, whereas after UUO, they appeared de novo - arguing against the notion that these cells represent a pre-existing progenitor cell population. Our data indicate rather that these cells represent transiently dedifferentiated tubular cells involved in regeneration. Copyright (c) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
- Published
- 2013
7. Proximal tubular cells contain a phenotypically distinct, scattered cell population involved in tubular regeneration
- Author
-
Smeets, B., Boor, P., Dijkman, H.B., Sharma, S.V., Jirak, P., Mooren, F., Berger, K., Bornemann, J., Gelman, I.H., Floege, J., Vlag, J. van der, Wetzels, J.F.M., Moeller, M.J., Smeets, B., Boor, P., Dijkman, H.B., Sharma, S.V., Jirak, P., Mooren, F., Berger, K., Bornemann, J., Gelman, I.H., Floege, J., Vlag, J. van der, Wetzels, J.F.M., and Moeller, M.J.
- Abstract
Item does not contain fulltext, Regeneration of injured tubular cells occurs after acute tubular necrosis primarily from intrinsic renal cells. This may occur from a pre-existing intratubular stem/progenitor cell population or from any surviving proximal tubular cell. In this study, we characterize a CD24-, CD133-, and vimentin-positive subpopulation of cells scattered throughout the proximal tubule in normal human kidney. Compared to adjacent 'normal' proximal tubular cells, these CD24-positive cells contained less cytoplasm, fewer mitochondria, and no brush border. In addition, 49 marker proteins are described that are expressed within the proximal tubules in a similar scattered pattern. For eight of these markers, we confirmed co-localization with CD24. In human biopsies of patients with acute tubular necrosis (ATN), the number of CD24-positive tubular cells was increased. In both normal human kidneys and the ATN biopsies, around 85% of proliferating cells were CD24-positive - indicating that this cell population participates in tubular regeneration. In healthy rat kidneys, the novel cell subpopulation was absent. However, upon unilateral ureteral obstruction (UUO), the novel cell population was detected in significant amounts in the injured kidney. In summary, in human renal biopsies, the CD24-positive cells represent tubular cells with a deviant phenotype, characterized by a distinct morphology and marker expression. After acute tubular injury, these cells become more numerous. In healthy rat kidneys, these cells are not detectable, whereas after UUO, they appeared de novo - arguing against the notion that these cells represent a pre-existing progenitor cell population. Our data indicate rather that these cells represent transiently dedifferentiated tubular cells involved in regeneration. Copyright (c) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
- Published
- 2013
8. Subtotal ablation of parietal epithelial cells induces crescent formation.
- Author
-
Sicking, E.M., Fuss, A., Uhlig, S., Jirak, P., Dijkman, H., Wetzels, J., Engel, D.R., Urzynicok, T., Heidenreich, S., Kriz, W., Kurts, C., Ostendorf, T., Floege, J., Smeets, B., Moeller, M.J., Sicking, E.M., Fuss, A., Uhlig, S., Jirak, P., Dijkman, H., Wetzels, J., Engel, D.R., Urzynicok, T., Heidenreich, S., Kriz, W., Kurts, C., Ostendorf, T., Floege, J., Smeets, B., and Moeller, M.J.
- Abstract
01 april 2012, Item does not contain fulltext, Parietal epithelial cells (PECs) of the renal glomerulus contribute to the formation of both cellular crescents in rapidly progressive GN and sclerotic lesions in FSGS. Subtotal transgenic ablation of podocytes induces FSGS but the effect of specific ablation of PECs is unknown. Here, we established an inducible transgenic mouse to allow subtotal ablation of PECs. Proteinuria developed during doxycycline-induced cellular ablation but fully reversed 26 days after termination of doxycycline administration. The ablation of PECs was focal, with only 30% of glomeruli exhibiting histologic changes; however, the number of PECs was reduced up to 90% within affected glomeruli. Ultrastructural analysis revealed disruption of PEC plasma membranes with cytoplasm shedding into Bowman's space. Podocytes showed focal foot process effacement, which was the most likely cause for transient proteinuria. After >9 days of cellular ablation, the remaining PECs formed cellular extensions to cover the denuded Bowman's capsule and expressed the activation marker CD44 de novo. The induced proliferation of PECs persisted throughout the observation period, resulting in the formation of typical cellular crescents with periglomerular infiltrate, albeit without accompanying proteinuria. In summary, subtotal ablation of PECs leads the remaining PECs to react with cellular activation and proliferation, which ultimately forms cellular crescents.
- Published
- 2012
9. Subtotal ablation of parietal epithelial cells induces crescent formation.
- Author
-
Sicking, E.M., Fuss, A., Uhlig, S., Jirak, P., Dijkman, H., Wetzels, J., Engel, D.R., Urzynicok, T., Heidenreich, S., Kriz, W., Kurts, C., Ostendorf, T., Floege, J., Smeets, B., Moeller, M.J., Sicking, E.M., Fuss, A., Uhlig, S., Jirak, P., Dijkman, H., Wetzels, J., Engel, D.R., Urzynicok, T., Heidenreich, S., Kriz, W., Kurts, C., Ostendorf, T., Floege, J., Smeets, B., and Moeller, M.J.
- Abstract
01 april 2012, Item does not contain fulltext, Parietal epithelial cells (PECs) of the renal glomerulus contribute to the formation of both cellular crescents in rapidly progressive GN and sclerotic lesions in FSGS. Subtotal transgenic ablation of podocytes induces FSGS but the effect of specific ablation of PECs is unknown. Here, we established an inducible transgenic mouse to allow subtotal ablation of PECs. Proteinuria developed during doxycycline-induced cellular ablation but fully reversed 26 days after termination of doxycycline administration. The ablation of PECs was focal, with only 30% of glomeruli exhibiting histologic changes; however, the number of PECs was reduced up to 90% within affected glomeruli. Ultrastructural analysis revealed disruption of PEC plasma membranes with cytoplasm shedding into Bowman's space. Podocytes showed focal foot process effacement, which was the most likely cause for transient proteinuria. After >9 days of cellular ablation, the remaining PECs formed cellular extensions to cover the denuded Bowman's capsule and expressed the activation marker CD44 de novo. The induced proliferation of PECs persisted throughout the observation period, resulting in the formation of typical cellular crescents with periglomerular infiltrate, albeit without accompanying proteinuria. In summary, subtotal ablation of PECs leads the remaining PECs to react with cellular activation and proliferation, which ultimately forms cellular crescents.
- Published
- 2012
10. Subtotal ablation of parietal epithelial cells induces crescent formation.
- Author
-
Sicking, E.M., Fuss, A., Uhlig, S., Jirak, P., Dijkman, H., Wetzels, J., Engel, D.R., Urzynicok, T., Heidenreich, S., Kriz, W., Kurts, C., Ostendorf, T., Floege, J., Smeets, B., Moeller, M.J., Sicking, E.M., Fuss, A., Uhlig, S., Jirak, P., Dijkman, H., Wetzels, J., Engel, D.R., Urzynicok, T., Heidenreich, S., Kriz, W., Kurts, C., Ostendorf, T., Floege, J., Smeets, B., and Moeller, M.J.
- Abstract
01 april 2012, Item does not contain fulltext, Parietal epithelial cells (PECs) of the renal glomerulus contribute to the formation of both cellular crescents in rapidly progressive GN and sclerotic lesions in FSGS. Subtotal transgenic ablation of podocytes induces FSGS but the effect of specific ablation of PECs is unknown. Here, we established an inducible transgenic mouse to allow subtotal ablation of PECs. Proteinuria developed during doxycycline-induced cellular ablation but fully reversed 26 days after termination of doxycycline administration. The ablation of PECs was focal, with only 30% of glomeruli exhibiting histologic changes; however, the number of PECs was reduced up to 90% within affected glomeruli. Ultrastructural analysis revealed disruption of PEC plasma membranes with cytoplasm shedding into Bowman's space. Podocytes showed focal foot process effacement, which was the most likely cause for transient proteinuria. After >9 days of cellular ablation, the remaining PECs formed cellular extensions to cover the denuded Bowman's capsule and expressed the activation marker CD44 de novo. The induced proliferation of PECs persisted throughout the observation period, resulting in the formation of typical cellular crescents with periglomerular infiltrate, albeit without accompanying proteinuria. In summary, subtotal ablation of PECs leads the remaining PECs to react with cellular activation and proliferation, which ultimately forms cellular crescents.
- Published
- 2012
11. Parietal epithelial cells participate in the formation of sclerotic lesions in focal segmental glomerulosclerosis
- Author
-
Smeets, B., Kuppe, C., Sicking, E.M., Fuss, A., Jirak, P., Kuppevelt, A.H.M.S.M. van, Endlich, K., Wetzels, J.F.M., Grone, H.J., Floege, J., Moeller, M.J., Smeets, B., Kuppe, C., Sicking, E.M., Fuss, A., Jirak, P., Kuppevelt, A.H.M.S.M. van, Endlich, K., Wetzels, J.F.M., Grone, H.J., Floege, J., and Moeller, M.J.
- Abstract
Item does not contain fulltext, The pathogenesis of the development of sclerotic lesions in focal segmental glomerulosclerosis (FSGS) remains unknown. Here, we selectively tagged podocytes or parietal epithelial cells (PECs) to determine whether PECs contribute to sclerosis. In three distinct models of FSGS (5/6-nephrectomy + DOCA-salt; the murine transgenic chronic Thy1.1 model; or the MWF rat) and in human biopsies, the primary injury to induce FSGS associated with focal activation of PECs and the formation of cellular adhesions to the capillary tuft. From this entry site, activated PECs invaded the affected segment of the glomerular tuft and deposited extracellular matrix. Within the affected segment, podocytes were lost and mesangial sclerosis developed within the endocapillary compartment. In conclusion, these results demonstrate that PECs contribute to the development and progression of the sclerotic lesions that define FSGS, but this pathogenesis may be relevant to all etiologies of glomerulosclerosis.
- Published
- 2011
12. Parietal epithelial cells participate in the formation of sclerotic lesions in focal segmental glomerulosclerosis
- Author
-
Smeets, B., Kuppe, C., Sicking, E.M., Fuss, A., Jirak, P., Kuppevelt, A.H.M.S.M. van, Endlich, K., Wetzels, J.F.M., Grone, H.J., Floege, J., Moeller, M.J., Smeets, B., Kuppe, C., Sicking, E.M., Fuss, A., Jirak, P., Kuppevelt, A.H.M.S.M. van, Endlich, K., Wetzels, J.F.M., Grone, H.J., Floege, J., and Moeller, M.J.
- Abstract
Item does not contain fulltext, The pathogenesis of the development of sclerotic lesions in focal segmental glomerulosclerosis (FSGS) remains unknown. Here, we selectively tagged podocytes or parietal epithelial cells (PECs) to determine whether PECs contribute to sclerosis. In three distinct models of FSGS (5/6-nephrectomy + DOCA-salt; the murine transgenic chronic Thy1.1 model; or the MWF rat) and in human biopsies, the primary injury to induce FSGS associated with focal activation of PECs and the formation of cellular adhesions to the capillary tuft. From this entry site, activated PECs invaded the affected segment of the glomerular tuft and deposited extracellular matrix. Within the affected segment, podocytes were lost and mesangial sclerosis developed within the endocapillary compartment. In conclusion, these results demonstrate that PECs contribute to the development and progression of the sclerotic lesions that define FSGS, but this pathogenesis may be relevant to all etiologies of glomerulosclerosis.
- Published
- 2011
13. Parietal epithelial cells participate in the formation of sclerotic lesions in focal segmental glomerulosclerosis
- Author
-
Smeets, B., Kuppe, C., Sicking, E.M., Fuss, A., Jirak, P., Kuppevelt, A.H.M.S.M. van, Endlich, K., Wetzels, J.F.M., Grone, H.J., Floege, J., Moeller, M.J., Smeets, B., Kuppe, C., Sicking, E.M., Fuss, A., Jirak, P., Kuppevelt, A.H.M.S.M. van, Endlich, K., Wetzels, J.F.M., Grone, H.J., Floege, J., and Moeller, M.J.
- Abstract
Item does not contain fulltext, The pathogenesis of the development of sclerotic lesions in focal segmental glomerulosclerosis (FSGS) remains unknown. Here, we selectively tagged podocytes or parietal epithelial cells (PECs) to determine whether PECs contribute to sclerosis. In three distinct models of FSGS (5/6-nephrectomy + DOCA-salt; the murine transgenic chronic Thy1.1 model; or the MWF rat) and in human biopsies, the primary injury to induce FSGS associated with focal activation of PECs and the formation of cellular adhesions to the capillary tuft. From this entry site, activated PECs invaded the affected segment of the glomerular tuft and deposited extracellular matrix. Within the affected segment, podocytes were lost and mesangial sclerosis developed within the endocapillary compartment. In conclusion, these results demonstrate that PECs contribute to the development and progression of the sclerotic lesions that define FSGS, but this pathogenesis may be relevant to all etiologies of glomerulosclerosis.
- Published
- 2011
14. Fungale Keratitis durch Fusarien - ein diagnostisches und therapeutisches Problem
- Author
-
Jirak, P, Viestenz, A, Hammer, P, Schönherr, U, Jirak, P, Viestenz, A, Hammer, P, and Schönherr, U
- Published
- 2006
15. Fungale Keratitis durch Fusarien - ein diagnostisches und therapeutisches Problem
- Author
-
Jirak, P, Viestenz, A, Hammer, P, Schönherr, U, Jirak, P, Viestenz, A, Hammer, P, and Schönherr, U
- Published
- 2006
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