82 results on '"Dietel B"'
Search Results
2. Serum IL-6 concentration correlates with plaque vulnerability and rupture in patients with severe carotid stenosis
- Author
-
Dietel, B., primary, Urschel, K., additional, Tauchi, M., additional, and Achenbach, S., additional
- Published
- 2022
- Full Text
- View/download PDF
3. Alteration of connexin expression during early stage of atherosclerosis
- Author
-
Oshita, K., primary, Urschel, K., additional, Botos, B., additional, Achenbach, S., additional, Dietel, B., additional, and Tauchi, M., additional
- Published
- 2021
- Full Text
- View/download PDF
4. P572Granulocyte-colony-stimulating-factor attenuates the inflammatory response after experimental stroke by suppressing dendritic cell functions
- Author
-
Dietel, B., Altendorf, R., Daniel, W.G., Kollmar, R., and Garlichs, C.D.
- Published
- 2012
5. P351Prevention of t-cell specific immunosuppression after induced cerebral ischemia by the granulocyte-colony stimulating factor
- Author
-
Dietel, B., Altendorf, R., Daniel, W.G., Kollmar, R., and Garlichs, C.D.
- Published
- 2012
6. 11Dendritic cells affect plaque stability by the regulation of immunosuppressive processes in atherosclerosis
- Author
-
Dietel, B., Cicha, I., Altendorf, R., Daniel, W.G., and Garlichs, C.D.
- Published
- 2012
7. Impact of Litomosoides sigmodontis antigen on T cell differentiation and on the development of initial atherosclerotic lesions in APOE-knockout mice
- Author
-
Kühn, C., primary, Tauchi-Brück, M., additional, Ajendra, J., additional, Hörauf, A., additional, Stumpf, C., additional, Achenbach, S., additional, Hübner, M., additional, and Dietel, B., additional
- Published
- 2016
- Full Text
- View/download PDF
8. Phenotype of vulnerable atherosclerotic plaques shows strong association with single nucleotide polymorphism alleles of common risk variants for coronary artery disease
- Author
-
Furtmair, R., primary, Kuehn, C., additional, König, C., additional, Ekici, A., additional, Klinghammer, L., additional, Achenbach, S., additional, Reis, A., additional, Tauchi, M., additional, and Dietel, B., additional
- Published
- 2016
- Full Text
- View/download PDF
9. Impact of therapeutic treatment with MCS-18 on advanced murine atherosclerosis
- Author
-
Kuehn, C., primary, Kerek, F., additional, Steinkasserer, A., additional, Zinser, E., additional, Achenbach, S., additional, and Dietel, B., additional
- Published
- 2015
- Full Text
- View/download PDF
10. Effects of single nucleotid polymorphisms in VEGFR2 on shear stress activated endothelial cells
- Author
-
Urschel, K., primary, Schacher, N., additional, Winterpacht, A., additional, Pasutto, F., additional, Achenbach, S., additional, and Dietel, B., additional
- Published
- 2015
- Full Text
- View/download PDF
11. Genotoxicity of the neurotransmitter dopamine in vitro
- Author
-
Stopper, H, Schupp, N, Fazeli, G, Dietel, B, Queisser, N, Walitza, S, Gerlach, M, University of Zurich, and Stopper, H
- Subjects
3005 Toxicology ,610 Medicine & health ,10058 Department of Child and Adolescent Psychiatry - Published
- 2009
- Full Text
- View/download PDF
12. Dixon imaging allows quantification of murine plaque lipids by ex vivo MRI
- Author
-
Dietel, B., primary, Budinsky, L., additional, Garlichs, C., additional, Achenbach, S., additional, and Hess, A., additional
- Published
- 2014
- Full Text
- View/download PDF
13. Sodium potentiates proatherogenic effects of tnf-alpha under non-uniform shear stress in a tonebp-dependent manner
- Author
-
Wild, J., primary, Soehnlein, O., additional, Urschel, K., additional, Dietel, B., additional, Garlichs, C.D., additional, and Cicha, I., additional
- Published
- 2014
- Full Text
- View/download PDF
14. Maturation of dendritic cells is involved in the progression of atherosclerosis in ApoE-deficient mice
- Author
-
Dietel, B., primary, Muench, R., additional, Altendorf, R., additional, Cicha, I., additional, Steinkasserer, A., additional, Zinser, E., additional, Kerek, F., additional, Achenbach, S., additional, and Garlichs, C., additional
- Published
- 2013
- Full Text
- View/download PDF
15. Migration of regulatory T cells into human atherosclerotic lesions is associated with plaque stability and correlates inversely with infiltrated mature dendritic cells
- Author
-
Dietel, B., primary, Altendorf, R., additional, Cicha, I., additional, and Garlichs, C., additional
- Published
- 2013
- Full Text
- View/download PDF
16. Poster session 3
- Author
-
Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. L., additional, Cachofeiro, V., additional, Rochais, F., additional, Sturny, R., additional, Mesbah, K., additional, Miquerol, L., additional, Kelly, R. G., additional, Messaoudi, S., additional, Gravez, B., additional, Tarjus, A., additional, Pelloux, V., additional, Samuel, J. L., additional, Delcayre, C., additional, Launay, J. M., additional, Clement, K., additional, Farman, N., additional, Jaisser, F., additional, Hadyanto, L., additional, Castellani, C., additional, Vescovo, G., additional, Ravara, B., additional, Tavano, R., additional, Pozzobon, M., additional, De Coppi, P., additional, Papini, E., additional, Vettor, R., additional, Thiene, G., additional, Angelini, A., additional, Meloni, M., additional, Caporali, A., additional, Cesselli, D., additional, Fortunato, O., additional, Avolio, E., additional, Schindler, R., additional, Simrick, S., additional, Brand, T., additional, Smart, N. S., additional, Herman, A., additional, Roura Ferrer, S., additional, Rodriguez Bago, J., additional, Soler-Botija, C., additional, Pujal, J. M., additional, Galvez-Monton, C., additional, Prat-Vidal, C., additional, Llucia-Valldeperas, A., additional, Blanco, J., additional, Bayes-Genis, A., additional, Foldes, G., additional, Maxime, M., additional, Ali, N. N., additional, Schneider, M. D., additional, Harding, S. E., additional, Reni, C., additional, Mangialardi, G., additional, De Pauw, A., additional, Sekkali, B., additional, Friart, A., additional, Ding, H., additional, Graffeuil, A., additional, Catalucci, D., additional, Balligand, J. L., additional, Azibani, F., additional, Tournoux, F., additional, Schlossarek, S., additional, Polidano, E., additional, Fazal, L., additional, Merval, R., additional, Carrier, L., additional, Chatziantoniou, C., additional, Buyandelger, B., additional, Linke, W., additional, Zou, P., additional, Kostin, S., additional, Ku, C., additional, Felkin, L., additional, Birks, E., additional, Barton, P., additional, Sattler, M., additional, Knoell, R., additional, Schroder, K., additional, Benkhoff, S., additional, Shimokawa, H., additional, Grisk, O., additional, Brandes, R. P., additional, Parepa, I. R., additional, Mazilu, L., additional, Suceveanu, A. I., additional, Suceveanu, A., additional, Rusali, L., additional, Cojocaru, L., additional, Matei, L., additional, Toringhibel, M., additional, Craiu, E., additional, Pires, A. L., additional, Pinho, M., additional, Pinho, S., additional, Sena, C., additional, Seica, R., additional, Leite-Moreira, A., additional, Dabroi, F., additional, Schiaffino, S., additional, Kiseleva, E., additional, Krukov, N., additional, Nikitin, O., additional, Ardatova, L., additional, Mourouzis, I., additional, Pantos, C., additional, Kokkinos, A. D., additional, Cokkinos, D. V., additional, Scoditti, E., additional, Massaro, M., additional, Carluccio, M. A., additional, Pellegrino, M., additional, Calabriso, N., additional, Gastaldelli, A., additional, Storelli, C., additional, De Caterina, R., additional, Lindner, D., additional, Zietsch, C., additional, Schultheiss, H.-P., additional, Tschope, C., additional, Westermann, D., additional, Everaert, B. R., additional, Nijenhuis, V. J., additional, Reith, F. C. M., additional, Hoymans, V. Y., additional, Timmermans, J. P., additional, Vrints, C. J., additional, Simova, I., additional, Mateev, H., additional, Katova, T., additional, Haralanov, L., additional, Dimitrov, N., additional, Mironov, N., additional, Golitsyn, S. P., additional, Sokolov, S. F., additional, Yuricheva, Y. U. A., additional, Maikov, E. B., additional, Shlevkov, N. B., additional, Rosenstraukh, L. V., additional, Chazov, E. I., additional, Radosinska, J., additional, Knezl, V., additional, Benova, T., additional, Slezak, J., additional, Urban, L., additional, Tribulova, N., additional, Virag, L., additional, Kristof, A., additional, Kohajda, Z. S., additional, Szel, T., additional, Husti, Z., additional, Baczko, I., additional, Jost, N., additional, Varro, A., additional, Sarusi, A., additional, Farkas, A. S., additional, Orosz, S. Z., additional, Forster, T., additional, Farkas, A., additional, Zakhrabova-Zwiauer, O. M., additional, Hardziyenka, M., additional, Nieuwland, R., additional, Tan, H. L., additional, Raaijmakers, A. J. A., additional, Bourgonje, V. J. A., additional, Kok, G. J. M., additional, Van Veen, A. A. B., additional, Anderson, M. E., additional, Vos, M. A., additional, Bierhuizen, M. F. A., additional, Benes, J., additional, Sebestova, B., additional, Ghouri, I. A., additional, Kemi, O. J., additional, Kelly, A., additional, Burton, F. L., additional, Smith, G. L., additional, Ozdemir, S., additional, Acsai, K., additional, Doisne, N., additional, Van Der Nagel, R., additional, Beekman, H. D. M., additional, Van Veen, T. A. B., additional, Sipido, K. R., additional, Antoons, G., additional, Harmer, S. C., additional, Mohal, J. S., additional, Kemp, D., additional, Tinker, A., additional, Beech, D., additional, Burley, D. S., additional, Cox, C. D., additional, Wann, K. T., additional, Baxter, G. F., additional, Wilders, R., additional, Verkerk, A., additional, Fragkiadaki, P., additional, Germanakis, G., additional, Tsarouchas, K., additional, Tsitsimpikou, C., additional, Tsardi, M., additional, George, D., additional, Tsatsakis, A., additional, Rodrigues, P., additional, Barros, C., additional, Najmi, A. K., additional, Khan, V., additional, Akhtar, M., additional, Pillai, K. K., additional, Mujeeb, M., additional, Aqil, M., additional, Bayliss, C. R., additional, Messer, A. E., additional, Leung, M.-C., additional, Ward, D., additional, Van Der Velden, J., additional, Poggesi, C., additional, Redwood, C. S., additional, Marston, S., additional, Vite, A., additional, Gandjbakhch, E., additional, Gary, F., additional, Fressart, V., additional, Leprince, P., additional, Fontaine, G., additional, Komajda, M., additional, Charron, P., additional, Villard, E., additional, Falcao-Pires, I., additional, Gavina, C., additional, Hamdani, N., additional, Stienen, G. J. M., additional, Niessens, H. W. M., additional, Leite-Moreira, A. F., additional, Paulus, W. J., additional, Memo, M., additional, Marston, S. B., additional, Vafiadaki, E., additional, Qian, J., additional, Arvanitis, D. A., additional, Sanoudou, D., additional, Kranias, E. G., additional, Elmstedt, N., additional, Lind, B., additional, Ferm-Widlund, K., additional, Westgren, M., additional, Brodin, L.-A., additional, Mansfield, C., additional, West, T., additional, Ferenczi, M., additional, Wijnker, P. J. M., additional, Foster, D. B., additional, Coulter, A., additional, Frazier, A., additional, Murphy, A. M., additional, Shah, M., additional, Sikkel, M. B., additional, Desplantez, T., additional, Collins, T. P., additional, O' Gara, P., additional, Lyon, A. R., additional, Macleod, K. T., additional, Ottesen, A. H., additional, Louch, W. E., additional, Carlson, C., additional, Landsverk, O. J. B., additional, Stridsberg, M., additional, Sjaastad, I., additional, Oie, E., additional, Omland, T., additional, Christensen, G., additional, Rosjo, H., additional, Cartledge, J., additional, Clark, L. A., additional, Ibrahim, M., additional, Siedlecka, U., additional, Navaratnarajah, M., additional, Yacoub, M. H., additional, Camelliti, P., additional, Terracciano, C. M., additional, Chester, A., additional, Gonzalez-Tendero, A., additional, Torre, I., additional, Garcia-Garcia, F., additional, Dopazo, J., additional, Gratacos, E., additional, Taylor, D., additional, Bhandari, S., additional, Seymour, A.-M., additional, Fliegner, D., additional, Jost, J., additional, Bugger, H., additional, Ventura-Clapier, R., additional, Carpi, A., additional, Campesan, M., additional, Canton, M., additional, Menabo, R., additional, Pelicci, P. G., additional, Giorgio, M., additional, Di Lisa, F., additional, Hancock, M., additional, Venturini, A., additional, Al-Shanti, N., additional, Stewart, C., additional, Ascione, R., additional, Angelini, G., additional, Suleiman, M.-S., additional, Kravchuk, E., additional, Grineva, E., additional, Galagudza, M., additional, Kostareva, A., additional, Bairamov, A., additional, Krychtiuk, K. A., additional, Watzke, L., additional, Kaun, C., additional, Demyanets, S., additional, Pisoni, J., additional, Kastl, S. P., additional, Huber, K., additional, Maurer, G., additional, Wojta, J., additional, Speidl, W. S., additional, Varga, Z. V., additional, Farago, N., additional, Zvara, A., additional, Kocsis, G. F., additional, Pipicz, M., additional, Csonka, C., additional, Csont, T., additional, Puskas, G. L., additional, Ferdinandy, P., additional, Klevstigova, M., additional, Silhavy, J., additional, Manakov, D., additional, Papousek, F., additional, Novotny, J., additional, Pravenec, M., additional, Kolar, F., additional, Novakova, O., additional, Novak, F., additional, Neckar, J., additional, Barallobre-Barreiro, J., additional, Didangelos, A., additional, Yin, X., additional, Fernandez-Caggiano, M., additional, Drozdov, I., additional, Willeit, P., additional, Domenech, N., additional, Mayr, M., additional, Lemoine, S., additional, Allouche, S., additional, Coulbault, L., additional, Galera, P., additional, Gerard, J. L., additional, Hanouz, J. L., additional, Suveren, E., additional, Whiteman, M., additional, Studneva, I. M., additional, Pisarenko, O., additional, Shulzhenko, V., additional, Serebryakova, L., additional, Tskitishvili, O., additional, Timoshin, A., additional, Fauconnier, J., additional, Meli, A. C., additional, Thireau, J., additional, Roberge, S., additional, Lompre, A. M., additional, Jacotot, E., additional, Marks, A. M., additional, Lacampagne, A., additional, Dietel, B., additional, Altendorf, R., additional, Daniel, W. G., additional, Kollmar, R., additional, Garlichs, C. D., additional, Parente, V., additional, Balasso, S., additional, Pompilio, G., additional, Colombo, G., additional, Milano, G., additional, Squadroni, L., additional, Cotelli, F., additional, Pozzoli, O., additional, Capogrossi, M. C., additional, Ajiro, Y., additional, Saegusa, N., additional, Iwade, K., additional, Giles, W. R., additional, Stafforini, D. M., additional, Spitzer, K. W., additional, Sirohi, R., additional, Candilio, L., additional, Babu, G., additional, Roberts, N., additional, Lawrence, D., additional, Sheikh, A., additional, Kolvekar, S., additional, Yap, J., additional, Hausenloy, D. J., additional, Yellon, D. M., additional, Aslam, M., additional, Rohrbach, S., additional, Schlueter, K.-D., additional, Piper, H. M., additional, Noll, T., additional, Guenduez, D., additional, Malinova, L., additional, Ryabukho, V. P., additional, Lyakin, D. V., additional, Denisova, T. P., additional, Montoro-Garcia, S., additional, Shantsila, E., additional, Lip, G. Y. H., additional, Kalaska, B., additional, Sokolowska, E., additional, Kaminski, K., additional, Szczubialka, K., additional, Kramkowski, K., additional, Mogielnicki, A., additional, Nowakowska, M., additional, Buczko, W., additional, Stancheva, N., additional, Mekenyan, E., additional, Gospodinov, K., additional, Tisheva, S., additional, Darago, A., additional, Rutkai, I., additional, Kalasz, J., additional, Czikora, A., additional, Orosz, P., additional, Bjornson, H. D., additional, Edes, I., additional, Papp, Z., additional, Toth, A., additional, Riches, K., additional, Warburton, P., additional, O'regan, D. J., additional, Ball, S. G., additional, Turner, N. A., additional, Wood, I. C., additional, Porter, K. E., additional, Kogaki, S., additional, Ishida, H., additional, Nawa, N., additional, Takahashi, K., additional, Baden, H., additional, Ichimori, H., additional, Uchikawa, T., additional, Mihara, S., additional, Miura, K., additional, Ozono, K., additional, Lugano, R., additional, Padro, T., additional, Garcia-Arguinzonis, M., additional, Badimon, L., additional, Ferraro, F., additional, Viner, R., additional, Ho, J., additional, Cutler, D., additional, Matchkov, V., additional, Aalkjaer, C., additional, Krijnen, P. A. J., additional, Hahn, N. E., additional, Kholova, I., additional, Sipkens, J. A., additional, Van Alphen, F. P., additional, Simsek, S., additional, Schalkwijk, C. G., additional, Van Buul, J. D., additional, Van Hinsbergh, V. W. M., additional, Niessen, H. W. M., additional, Caro, C. G., additional, Seneviratne, A., additional, Monaco, C., additional, Hou, D., additional, Singh, J., additional, Gilson, P., additional, Burke, M. G., additional, Heraty, K. B., additional, Krams, R., additional, Coppola, G., additional, Albrecht, K., additional, Schgoer, W., additional, Wiedemann, D., additional, Bonaros, N., additional, Steger, C., additional, Theurl, M., additional, Stanzl, U., additional, Kirchmair, R., additional, Amadesi, S., additional, Spinetti, G., additional, Cangiano, E., additional, Valgimigli, M., additional, Miller, A. M., additional, Cardinali, A., additional, Vierlinger, K., additional, Pagano, G., additional, Liccardo, D., additional, Zincarelli, C., additional, Femminella, G. D., additional, Lymperopoulos, A., additional, De Lucia, C., additional, Koch, W. J., additional, Leosco, D., additional, Rengo, G., additional, Hinkel, R., additional, Husada, W., additional, Trenkwalder, T., additional, Di, Q., additional, Lee, S., additional, Petersen, B., additional, Bock-Marquette, I., additional, Niemann, H., additional, Di Maio, M., additional, Kupatt, C., additional, Nourian, M., additional, Yassin, Z., additional, Kelishadi, R., additional, Memarian, S. H., additional, Heidari, A., additional, Leuner, A., additional, Poitz, D. M., additional, Brunssen, C., additional, Ravens, U., additional, Strasser, R. H., additional, Morawietz, H., additional, Vogt, F., additional, Grahl, A., additional, Flege, C., additional, Marx, N., additional, Borinski, M., additional, De Geest, B., additional, Jacobs, F., additional, Muthuramu, I., additional, Gordts, S. C., additional, Van Craeyveld, E., additional, Herijgers, P., additional, Weinert, S., additional, Medunjanin, S., additional, Herold, J., additional, Schmeisser, A., additional, Braun-Dullaeus, R. C., additional, Wagner, A. H., additional, Moeller, K., additional, Adolph, O., additional, Schwarz, M., additional, Schwale, C., additional, Bruehl, C., additional, Nobiling, R., additional, Wieland, T., additional, Schneider, S. W., additional, Hecker, M., additional, Cross, A., additional, Strom, A., additional, Cole, J., additional, Goddard, M., additional, Hultgardh-Nilsson, A., additional, Nilsson, J., additional, Mauri, C., additional, Mitkovskaya, N. P., additional, Kurak, T. A., additional, Oganova, E. G., additional, Shkrebneva, E. I., additional, Kot, Z. H. N., additional, Statkevich, T. V., additional, Molica, F., additional, Burger, F., additional, Matter, C. M., additional, Thomas, A., additional, Staub, C., additional, Zimmer, A., additional, Cravatt, B., additional, Pacher, P., additional, Steffens, S., additional, Blanco, R., additional, Sarmiento, R., additional, Parisi, C., additional, Fandino, S., additional, Blanco, F., additional, Gigena, G., additional, Szarfer, J., additional, Rodriguez, A., additional, Garcia Escudero, A., additional, Riccitelli, M. A., additional, Wantha, S., additional, Simsekyilmaz, S., additional, Megens, R. T., additional, Van Zandvoort, M. A., additional, Liehn, E., additional, Zernecke, A., additional, Klee, D., additional, Weber, C., additional, Soehnlein, O., additional, Lima, L. M., additional, Carvalho, M. G., additional, Gomes, K. B., additional, Santos, I. R., additional, Sousa, M. O., additional, Morais, C. A. S., additional, Oliveira, S. H. V., additional, Gomes, I. F., additional, Brandao, F. C., additional, Lamego, M. R. A., additional, Fornai, L., additional, Kiss, A., additional, Giskes, F., additional, Eijkel, G., additional, Fedrigo, M., additional, Valente, M. L., additional, Heeren, R. M. A., additional, Grdinic, A., additional, Vojvodic, D., additional, Djukanovic, N., additional, Grdinic, A. G., additional, Obradovic, S., additional, Majstorovic, I., additional, Rusovic, S., additional, Vucinic, Z., additional, Tavciovski, D., additional, Ostojic, M., additional, Lai, S.-C., additional, Chen, M.-Y., additional, Wu, H.-T., additional, Gouweleeuw, L., additional, Oberdorf-Maass, S. U., additional, De Boer, R. A., additional, Van Gilst, W. H., additional, Maass, A. H., additional, Van Gelder, I. C., additional, Benard, L., additional, Li, C., additional, Warren, D., additional, Shanahan, C. M., additional, Zhang, Q. P., additional, Bye, A., additional, Vettukattil, R., additional, Aspenes, S. T., additional, Giskeodegaard, G., additional, Gribbestad, I. S., additional, Wisloff, U., additional, Bathen, T. F., additional, Cubedo, J., additional, Alonso, R., additional, Mata, P., additional, Ivic, I., additional, Vamos, Z., additional, Cseplo, P., additional, Kosa, D., additional, Torok, O., additional, Hamar, J., additional, Koller, A., additional, Norita, K., additional, De Noronha, S. V., additional, Sheppard, M. N., additional, Amat-Roldan, I., additional, Iruretagoiena, I., additional, Psilodimitrakopoulos, S., additional, Crispi, F., additional, Artigas, D., additional, Loza-Alvarez, P., additional, Harrison, J. C., additional, Smart, S. D., additional, Besely, E. H., additional, Kelly, J. R., additional, Yao, Y., additional, Sammut, I. A., additional, Hoepfner, M., additional, Kuzyniak, W., additional, Sekhosana, E., additional, Hoffmann, B., additional, Litwinski, C., additional, Pries, A., additional, Ermilov, E., additional, Fontoura, D., additional, Lourenco, A. P., additional, Vasques-Novoa, F., additional, Pinto, J. P., additional, Roncon-Albuquerque, R., additional, Oyeyipo, I. P., additional, Olatunji, L. A., additional, Usman, T. O., additional, Olatunji, V. A., additional, Bacova, B., additional, Viczenczova, C., additional, Dosenko, V., additional, Goncalvesova, E., additional, Vanrooyen, J., additional, Maulik, S. K., additional, Seth, S., additional, Dinda, A. K., additional, Jaiswal, A., additional, Mearini, G., additional, Khajetoorians, D., additional, Kraemer, E., additional, Gedicke-Hornung, C., additional, Precigout, G., additional, Eschenhagen, T., additional, Voit, T., additional, Garcia, L., additional, Lorain, S., additional, Mendes-Ferreira, P., additional, Maia-Rocha, C., additional, Adao, R., additional, Cerqueira, R. J., additional, Mendes, M. J., additional, Castro-Chaves, P., additional, De Keulenaer, G. W., additional, Bras-Silva, C., additional, Ruiter, G., additional, Wong, Y. Y., additional, Lubberink, M., additional, Knaapen, P., additional, Raijmakers, P., additional, Lammertsma, A. A., additional, Marcus, J. T., additional, Westerhof, N., additional, Van Der Laarse, W. J., additional, Vonk-Noordegraaf, A., additional, Steinbronn, N., additional, Koch, E., additional, Steiner, G., additional, Berezin, A., additional, Lisovaya, O. A., additional, Soldatova, A. M., additional, Kuznetcov, V. A., additional, Yenina, T. N., additional, Rychkov, A. Y. U., additional, Shebeko, P. V., additional, Altara, R., additional, Hessel, M. H. M., additional, Hermans, J. J. R., additional, Blankesteijn, W. M., additional, Berezina, T. A., additional, Seden, V., additional, Bonanad, C., additional, Nunez, J., additional, Navarro, D., additional, Chilet, M. F., additional, Sanchis, F., additional, Bodi, V., additional, Minana, G., additional, Chaustre, F., additional, Forteza, M. J., additional, Llacer, A., additional, Galasso, G., additional, Ferrara, N., additional, Akhmedov, A., additional, Klingenberg, R., additional, Brokopp, C., additional, Hof, D., additional, Zoller, S., additional, Corti, R., additional, Gay, S., additional, Von Eckardstein, A., additional, Hoerstrup, S. P., additional, Luescher, T. F., additional, Heijman, J., additional, Zaza, A., additional, Johnson, D. M., additional, Rudy, Y., additional, Peeters, R. L. M., additional, Volders, P. G. A., additional, Westra, R. L., additional, Fujita, S., additional, Okamoto, R., additional, Taniguchi, M., additional, Konishi, K., additional, Goto, I., additional, Sugimoto, K., additional, Nakamura, M., additional, Shiraki, K., additional, Buechler, C., additional, and Ito, M., additional
- Published
- 2012
- Full Text
- View/download PDF
17. Poster session 2
- Author
-
Perez-Pomares, J. M., primary, Ruiz-Villalba, A., additional, Ziogas, A., additional, Segovia, J. C., additional, Ehrbar, M., additional, Munoz-Chapuli, R., additional, De La Rosa, A., additional, Dominguez, J. N., additional, Hove-Madsen, L., additional, Sankova, B., additional, Sedmera, D., additional, Franco, D., additional, Aranega Jimenez, A., additional, Babaeva, G., additional, Chizh, N., additional, Galchenko, S., additional, Sandomirsky, B., additional, Schwarzl, M., additional, Seiler, S., additional, Steendijk, P., additional, Huber, S., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Simrick, S., additional, Kreutzer, R., additional, Rao, C., additional, Terracciano, C. M., additional, Kirchhof, P., additional, Fabritz, L., additional, Brand, T., additional, Theveniau-Ruissy, M., additional, Parisot, P., additional, Francou, A., additional, Saint-Michel, E., additional, Mesbah, K., additional, Kelly, R. G., additional, Wu, H.-T., additional, Sie, S.-S., additional, Chen, C.-Y., additional, Kuan, T.-C., additional, Lin, C. S., additional, Ismailoglu, Z., additional, Guven, M., additional, Yakici, A., additional, Ata, Y., additional, Ozcan, S., additional, Yildirim, E., additional, Ongen, Z., additional, Miroshnikova, V., additional, Demina, E., additional, Rodygina, T., additional, Kurjanov, P., additional, Denisenko, A., additional, Schwarzman, A., additional, Rubanenko, A., additional, Shchukin, Y., additional, Germanov, A., additional, Goldbergova, M., additional, Parenica, J., additional, Lipkova, J., additional, Pavek, N., additional, Kala, P., additional, Poloczek, M., additional, Vasku, A., additional, Parenicova, I., additional, Spinar, J., additional, Gambacciani, C., additional, Chiavacci, E., additional, Evangelista, M., additional, Vesentini, N., additional, Kusmic, C., additional, Pitto, L., additional, Chernova, A., additional, Nikulina, S. U. Y., additional, Arvanitis, D. A., additional, Mourouzis, I., additional, Pantos, C., additional, Kranias, E. G., additional, Cokkinos, D. V., additional, Sanoudou, D., additional, Vladimirskaya, T. E., additional, Shved, I. A., additional, Kryvorot, S. G., additional, Schirmer, I. M., additional, Appukuttan, A., additional, Pott, L., additional, Jaquet, K., additional, Ladilov, Y., additional, Archer, C. R., additional, Bootman, M. D., additional, Roderick, H. L., additional, Fusco, A., additional, Sorriento, D., additional, Santulli, G., additional, Trimarco, B., additional, Iaccarino, G., additional, Hagenmueller, M., additional, Riffel, J., additional, Bernhold, E., additional, Katus, H. A., additional, Hardt, S. E., additional, Maqsood, A., additional, Zi, M., additional, Prehar, S., additional, Neyses, L., additional, Ray, S., additional, Oceandy, D., additional, Khatami, N., additional, Wadowski, P., additional, Wagh, V., additional, Hescheler, J., additional, Sachinidis, A., additional, Mohl, W., additional, Chaudhry, B., additional, Burns, D., additional, Henderson, D. J., additional, Bax, N. A. M., additional, Van Marion, M. H., additional, Shah, B., additional, Goumans, M. J., additional, Bouten, C. V. C., additional, Van Der Schaft, D. W. J., additional, Van Oorschot, A. A. M., additional, Maas, S., additional, Braun, J., additional, Van Tuyn, J., additional, De Vries, A. A. F., additional, Gittenberger-De Groot, A. C., additional, Bageghni, S., additional, Drinkhill, M. J., additional, Batten, T. F. C., additional, Ainscough, J. F. X., additional, Onate, B., additional, Vilahur, G., additional, Ferrer-Lorente, R., additional, Ybarra, J., additional, Diez-Caballero, A., additional, Ballesta-Lopez, C., additional, Moscatiello, F., additional, Herrero, J., additional, Badimon, L., additional, Martin-Rendon, E., additional, Clifford, D. M., additional, Fisher, S. A., additional, Brusnkill, S. J., additional, Doree, C., additional, Mathur, A., additional, Clarke, M., additional, Watt, S. M., additional, Hernandez-Vera, R., additional, Kavanagh, D., additional, Yemm, A. I., additional, Frampton, J., additional, Kalia, N., additional, Terajima, Y., additional, Shimizu, T., additional, Tsuruyama, S., additional, Ishii, H., additional, Sekine, H., additional, Hagiwara, N., additional, Okano, T., additional, Vrijsen, K. R., additional, Chamuleau, S. A. J., additional, Sluijter, J. P. G., additional, Doevendans, P. F. M., additional, Madonna, R., additional, Delli Pizzi, S., additional, Di Donato, L., additional, Mariotti, A., additional, Di Carlo, L., additional, D'ugo, E., additional, Teberino, M. A., additional, Merla, A., additional, T, A., additional, De Caterina, R., additional, Kolker, L., additional, Ali, N. N., additional, Maclellan, K., additional, Moore, M., additional, Wheeler, J., additional, Harding, S. E., additional, Fleck, R. A., additional, Rowlinson, J. M., additional, Kraenkel, N., additional, Ascione, R., additional, Madeddu, P., additional, O'sullivan, J. F., additional, Leblond, A. L., additional, Kelly, G., additional, Kumar, A. H. S., additional, Metharom, P., additional, Buneker, C. K., additional, Alizadeh-Vikali, N., additional, Hynes, B. G., additional, O'connor, R., additional, Caplice, N. M., additional, Noseda, M., additional, De Smith, A. J., additional, Leja, T., additional, Rao, P. H., additional, Al-Beidh, F., additional, Abreu Pavia, M. S., additional, Blakemore, A. I., additional, Schneider, M. D., additional, Stathopoulou, K., additional, Cuello, F., additional, Ehler, E., additional, Haworth, R. S., additional, Avkiran, M., additional, Morawietz, H., additional, Eickholt, C., additional, Langbein, H., additional, Brux, M., additional, Goettsch, C., additional, Goettsch, W., additional, Arsov, A., additional, Brunssen, C., additional, Mazilu, L., additional, Parepa, I. R., additional, Suceveanu, A. I., additional, Suceveanu, A. P., additional, De Man, F. S., additional, Guignabert, C., additional, Tu, L., additional, Handoko, M. L., additional, Schalij, I., additional, Fadel, E., additional, Postmus, P. E., additional, Vonk-Noordegraaf, A., additional, Humbert, M., additional, Eddahibi, S., additional, Del Giudice, C., additional, Anastasio, A., additional, Fazal, L., additional, Azibani, F., additional, Bihry, N., additional, Merval, R., additional, Polidano, E., additional, Samuel, J.-L., additional, Delcayre, C., additional, Zhang, Y., additional, Mi, Y. M., additional, Ren, L. L., additional, Cheng, Y. P., additional, Guo, R., additional, Liu, Y., additional, Jiang, Y. N., additional, Kokkinos, A. D., additional, Tretjakovs, P., additional, Jurka, A., additional, Bormane, I., additional, Mikelsone, I., additional, Reihmane, D., additional, Elksne, K., additional, Krievina, G., additional, Verbovenko, J., additional, Bahs, G., additional, Lopez-Andres, N., additional, Rousseau, A., additional, Calvier, L., additional, Akhtar, R., additional, Labat, C., additional, Cruickshank, K., additional, Diez, J., additional, Zannad, F., additional, Lacolley, P., additional, Rossignol, P., additional, Hamesch, K., additional, Subramanian, P., additional, Li, X., additional, Thiemann, A., additional, Heyll, K., additional, Dembowsky, K., additional, Chevalier, E., additional, Weber, C., additional, Schober, A., additional, Yang, L., additional, Kim, G., additional, Gardner, B., additional, Earley, J., additional, Hofmann-Bowman, M., additional, Cheng, C.-F., additional, Lian, W.-S., additional, Lin, H., additional, Jinjolia, N. J., additional, Abuladze, G. A., additional, Tvalchrelidze, S. H. T., additional, Khamnagadaev, I., additional, Shkolnikova, M., additional, Kokov, L., additional, Miklashevich, I., additional, Drozdov, I., additional, Ilyich, I., additional, Bingen, B. O., additional, Askar, S. F. A., additional, Ypey, D. L., additional, Van Der Laarse, A., additional, Schalij, M. J., additional, Pijnappels, D. A., additional, Roney, C. H., additional, Ng, F. S., additional, Chowdhury, R. A., additional, Chang, E. T. Y., additional, Patel, P. M., additional, Lyon, A. R., additional, Siggers, J. H., additional, Peters, N. S., additional, Obergrussberger, A., additional, Stoelzle, S., additional, Bruggemann, A., additional, Haarmann, C., additional, George, M., additional, Fertig, N., additional, Moreira, D., additional, Souza, A., additional, Valente, P., additional, Kornej, J., additional, Reihardt, C., additional, Kosiuk, J., additional, Arya, A., additional, Hindricks, G., additional, Adams, V., additional, Husser, D., additional, Bollmann, A., additional, Camelliti, P., additional, Dudhia, J., additional, Dias, P., additional, Cartledge, J., additional, Connolly, D. J., additional, Nobles, M., additional, Sebastian, S., additional, Tinker, A., additional, Opel, A., additional, Daimi, H., additional, Haj Khelil, A., additional, Be Chibani, J., additional, Barana, A., additional, Amoros, I., additional, Gonzalez De La Fuente, M., additional, Caballero, R., additional, Aranega, A., additional, Kelly, A., additional, Bernus, O., additional, Kemi, O. J., additional, Myles, R. C., additional, Ghouri, I. A., additional, Burton, F. L., additional, Smith, G. L., additional, Del Lungo, M., additional, Sartiani, L., additional, Spinelli, V., additional, Baruscotti, M., additional, Difrancesco, D., additional, Mugelli, A., additional, Cerbai, E., additional, Thomas, A. M., additional, Aziz, Q., additional, Khambra, T., additional, Addlestone, J. M. A., additional, Cartwright, E. J., additional, Wilkinson, R., additional, Song, W., additional, Marston, S., additional, Jacquet, A., additional, Mougenot, N. M., additional, Lipskaia, A. J., additional, Paalberends, E. R., additional, Stam, K., additional, Van Dijk, S. J., additional, Van Slegtenhorst, M., additional, Dos Remedios, C., additional, Ten Cate, F. J., additional, Michels, M., additional, Niessen, H. W. M., additional, Stienen, G. J. M., additional, Van Der Velden, J., additional, Read, M. I., additional, Andreianova, A. A., additional, Harrison, J. C., additional, Goulton, C. S., additional, Kerr, D. S., additional, Sammut, I. A., additional, Wallner, M., additional, Von Lewinski, D., additional, Kindsvater, D., additional, Saes, M., additional, Morano, I., additional, Muegge, A., additional, Buyandelger, B., additional, Kostin, S., additional, Gunkel, S., additional, Vouffo, J., additional, Ng, K., additional, Chen, J., additional, Eilers, M., additional, Isaacson, R., additional, Milting, H., additional, Knoell, R., additional, Cattin, M.-E., additional, Crocini, C., additional, Schlossarek, S., additional, Maron, S., additional, Hansen, A., additional, Eschenhagen, T., additional, Carrier, L., additional, Bonne, G., additional, Coppini, R., additional, Ferrantini, C., additional, Olivotto, I., additional, Belardinelli, L., additional, Poggesi, C., additional, Leung, M. C., additional, Messer, A. E., additional, Copeland, O., additional, Marston, S. B., additional, Mills, A. M., additional, Collins, T., additional, O'gara, P., additional, Thum, T., additional, Regalla, K., additional, Macleod, K. T., additional, Prodromakis, T., additional, Chaudhry, U., additional, Darzi, A., additional, Yacoub, M. H., additional, Athanasiou, T., additional, Bogdanova, A., additional, Makhro, A., additional, Hoydal, M., additional, Stolen, T. O., additional, Johnssen, A. B., additional, Alves, M., additional, Catalucci, D., additional, Condorelli, G., additional, Koch, L. G., additional, Britton, S. L., additional, Wisloff, U., additional, Bito, V., additional, Claus, P., additional, Vermeulen, K., additional, Huysmans, C., additional, Ventura-Clapier, R., additional, Sipido, K. R., additional, Seliuk, M. N., additional, Burlaka, A. P., additional, Sidorik, E. P., additional, Khaitovych, N. V., additional, Kozachok, M. M., additional, Potaskalova, V. S., additional, Driesen, R. B., additional, Galan, D. T., additional, De Paulis, D., additional, Arnoux, T., additional, Schaller, S., additional, Pruss, R. M., additional, Poitz, D. M., additional, Augstein, A., additional, Braun-Dullaeus, R. C., additional, Schmeisser, A., additional, Strasser, R. H., additional, Micova, P., additional, Balkova, P., additional, Hlavackova, M., additional, Zurmanova, J., additional, Kasparova, D., additional, Kolar, F., additional, Neckar, J., additional, Novak, F., additional, Novakova, O., additional, Pollard, S., additional, Babba, M., additional, Hussain, A., additional, James, R., additional, Maddock, H., additional, Alshehri, A. S., additional, Baxter, G. F., additional, Dietel, B., additional, Altendorf, R., additional, Daniel, W. G., additional, Kollmar, R., additional, Garlichs, C. D., additional, Sirohi, R., additional, Roberts, N., additional, Lawrence, D., additional, Sheikh, A., additional, Kolvekar, S., additional, Yap, J., additional, Arend, M., additional, Walkinshaw, G., additional, Hausenloy, D. J., additional, Yellon, D. M., additional, Posa, A., additional, Szabo, R., additional, Szalai, Z., additional, Szablics, P., additional, Berko, M. A., additional, Orban, K., additional, Murlasits, Z. S., additional, Balogh, L., additional, Varga, C., additional, Ku, H. C., additional, Su, M. J., additional, Chreih, R.-M., additional, Ginghina, C., additional, Deleanu, D., additional, Ferreira, A. L. B. J., additional, Belal, A., additional, Ali, M. A., additional, Fan, X., additional, Holt, A., additional, Campbell, R., additional, Schulz, R., additional, Bonanad, C., additional, Bodi, V., additional, Sanchis, J., additional, Morales, J. M., additional, Marrachelli, V., additional, Nunez, J., additional, Forteza, M. J., additional, Chaustre, F., additional, Gomez, C., additional, Chorro, F. J., additional, Csont, T., additional, Fekete, V., additional, Murlasits, Z., additional, Aypar, E., additional, Bencsik, P., additional, Sarkozy, M., additional, Varga, Z. V., additional, Ferdinandy, P., additional, Duerr, G. D., additional, Zoerlein, M., additional, Dewald, D., additional, Mesenholl, B., additional, Schneider, P., additional, Ghanem, A., additional, Rittling, S., additional, Welz, A., additional, Dewald, O., additional, Becker, E., additional, Peigney, C., additional, Bouleti, C., additional, Galaup, A., additional, Monnot, C., additional, Ghaleh, B., additional, Germain, S., additional, Timmermans, A., additional, Ginion, A., additional, De Meester, C., additional, Sakamoto, K., additional, Vanoverschelde, J.-L., additional, Horman, S., additional, Beauloye, C., additional, Bertrand, L., additional, Maroz-Vadalazhskaya, N., additional, Drozd, E., additional, Kukharenko, L., additional, Russkich, I., additional, Krachak, D., additional, Seljun, Y., additional, Ostrovski, Y., additional, Martin, A.-C., additional, Le Bonniec, B., additional, Lecompte, T., additional, Dizier, B., additional, Emmerich, J., additional, Fischer, A.-M., additional, Samama, C.-M., additional, Godier, A., additional, Mogensen, S., additional, Furchtbauer, E. M., additional, Aalkjaer, C., additional, Choong, W. L., additional, Jovanovic, A., additional, Khan, F., additional, Daniel, J. M., additional, Dutzmann, J. M., additional, Widmer-Teske, R., additional, Guenduez, D., additional, Sedding, D., additional, Castro, M. M., additional, Cena, J. J. C., additional, Cho, W. J. C., additional, Goobie, G. G., additional, Walsh, M. P. W., additional, Schulz, R. S., additional, Dutzmann, J., additional, Preissner, K. T., additional, Sones, W., additional, Kotlikoff, M., additional, Serizawa, K., additional, Yogo, K., additional, Aizawa, K., additional, Hirata, M., additional, Tashiro, Y., additional, Ishizuka, N., additional, Varela, A., additional, Katsiboulas, M., additional, Tousoulis, D., additional, Papaioannou, T. G., additional, Vaina, S., additional, Davos, C. H., additional, Piperi, C., additional, Stefanadis, C., additional, Basdra, E. K., additional, Papavassiliou, A. G., additional, Hermenegildo, C., additional, Lazaro-Franco, M., additional, Sobrino, A., additional, Bueno-Beti, C., additional, Martinez-Gil, N., additional, Walther, T., additional, Peiro, C., additional, Sanchez-Ferrer, C. F., additional, Novella, S., additional, Ciccarelli, M., additional, Franco, A., additional, Dorn, G. W., additional, Cseplo, P., additional, Torok, O., additional, Springo, Z. S., additional, Vamos, Z., additional, Kosa, D., additional, Hamar, J., additional, Koller, A., additional, Bubb, K. J., additional, Ahluwalia, A., additional, Stepien, E. L., additional, Gruca, A., additional, Grzybowska, J., additional, Goralska, J., additional, Dembinska-Kiec, A., additional, Stolinski, J., additional, Partyka, L., additional, Zhang, H., additional, Sweeney, D., additional, Thomas, G. N., additional, Fish, P. V., additional, Taggart, D. P., additional, Cioffi, S., additional, Bilio, M., additional, Martucciello, S., additional, Illingworth, E., additional, Caporali, A., additional, Shantikumar, S., additional, Marchetti, M., additional, Martelli, F., additional, Emanueli, C., additional, Meloni, M., additional, Al Haj Zen, A., additional, Sala-Newby, G., additional, Del Turco, S., additional, Saponaro, C., additional, Dario, B., additional, Sartini, S., additional, Menciassi, A., additional, Dario, P., additional, La Motta, C., additional, Basta, G., additional, Santiemma, V., additional, Bertone, C., additional, Rossi, F., additional, Michelon, E., additional, Bianco, M. J., additional, Castelli, A., additional, Shin, D. I., additional, Seung, K. B., additional, Seo, S. M., additional, Park, H. J., additional, Kim, P. J., additional, Baek, S. H., additional, Choi, Y. S., additional, Her, S. H., additional, Kim, D. B., additional, Lee, J. M., additional, Park, C. S., additional, Rocchiccioli, S., additional, Cecchettini, A., additional, Pelosi, G., additional, Citti, L., additional, Parodi, O., additional, Trivella, M. G., additional, Michel-Monigadon, D., additional, Burger, F., additional, Dunoyer-Geindre, S., additional, Pelli, G., additional, Cravatt, B., additional, Steffens, S., additional, Didangelos, A., additional, Mayr, U., additional, Yin, X., additional, Stegemann, C., additional, Shalhoub, J., additional, Davies, A. H., additional, Monaco, C., additional, Mayr, M., additional, Lypovetska, S., additional, Grytsenko, S., additional, Njerve, I. U., additional, Pettersen, A. A., additional, Opstad, T. B., additional, Bratseth, V., additional, Arnesen, H., additional, Seljeflot, I., additional, Dumitriu, I. E., additional, Baruah, P., additional, Antunes, R. F., additional, Kaski, J. C., additional, Trapero, I., additional, Benet, I., additional, Alguero, C., additional, Chaustre, F. J., additional, Mangold, A., additional, Puthenkalam, S., additional, Distelmaier, K., additional, Adlbrecht, C., additional, Lang, I. M., additional, Koizumi, T., additional, Inoue, I., additional, Komiyama, N., additional, Nishimura, S., additional, Korneeva, O. N., additional, Drapkina, O. M., additional, Fornai, L., additional, Angelini, A., additional, Kiss, A., additional, Giskes, F., additional, Eijkel, G., additional, Fedrigo, M., additional, Valente, M. L., additional, Thiene, G., additional, Heeren, R. M. A., additional, Padro, T., additional, Casani, L., additional, Suades, R., additional, Bertoni, B., additional, Carminati, R., additional, Carlini, V., additional, Pettinari, L., additional, Martinelli, C., additional, Gagliano, N., additional, Noppe, G., additional, Buchlin, P., additional, Marquet, N., additional, Baeyens, N., additional, Morel, N., additional, Baysa, A., additional, Sagave, J., additional, Dahl, C. P., additional, Gullestad, L., additional, Carpi, A., additional, Di Lisa, F., additional, Giorgio, M., additional, Vaage, J., additional, Valen, G., additional, Vafiadaki, E., additional, Papalouka, V., additional, Terzis, G., additional, Spengos, K., additional, Manta, P., additional, Gales, C., additional, Genet, G., additional, Dague, E., additional, Cazorla, O., additional, Payre, B., additional, Mias, C., additional, Ouille, A., additional, Lacampagne, A., additional, Pathak, A., additional, Senard, J. M., additional, Abonnenc, M., additional, Da Costa Martins, P., additional, Srivastava, S., additional, Gautel, M., additional, De Windt, L., additional, Comelli, L., additional, Lande, C., additional, Ucciferri, N., additional, Ikonen, L., additional, Vuorenpaa, H., additional, Kujala, K., additional, Sarkanen, J.-R., additional, Heinonen, T., additional, Ylikomi, T., additional, Aalto-Setala, K., additional, Capros, H., additional, Sprincean, N., additional, Usurelu, N., additional, Egorov, V., additional, Stratu, N., additional, Matchkov, V., additional, Bouzinova, E., additional, Moeller-Nielsen, N., additional, Wiborg, O., additional, Gutierrez, P. S., additional, Aparecida-Silva, R., additional, Borges, L. F., additional, Moreira, L. F. P., additional, Dias, R. R., additional, Kalil, J., additional, Stolf, N. A. G., additional, Zhou, W., additional, Suntharalingam, K., additional, Brand, N., additional, Vilar Compte, R., additional, Ying, L., additional, Bicknell, K., additional, Dannoura, A., additional, Dash, P., additional, Brooks, G., additional, Tsimafeyeu, I., additional, Tishova, Y., additional, Wynn, N., additional, Oyeyipo, I. P., additional, Olatunji, L. A., additional, Maegdefessel, L., additional, Azuma, J., additional, Toh, R., additional, Raaz, U., additional, Merk, D. R., additional, Deng, A., additional, Spin, J. M., additional, Tsao, P. S., additional, Tedeschi, L., additional, Taranta, M., additional, Naldi, I., additional, Grimaldi, S., additional, Cinti, C., additional, Bousquenaud, M., additional, Maskali, F., additional, Poussier, S., additional, Marie, P. Y., additional, Boutley, H., additional, Karcher, G., additional, Wagner, D. R., additional, Devaux, Y., additional, Torre, I., additional, Psilodimitrakopoulos, S., additional, Iruretagoiena, I., additional, Gonzalez-Tendero, A., additional, Artigas, D., additional, Loza-Alvarez, P., additional, Gratacos, E., additional, Amat-Roldan, I., additional, Murray, L., additional, Carberry, D. M., additional, Dunton, P., additional, Miles, M. J., additional, Suleiman, M.-S., additional, Kanesalingam, K., additional, Taylor, R., additional, Mc Collum, C. N., additional, Parniczky, A., additional, Solymar, M., additional, Porpaczy, A., additional, Miseta, A., additional, Lenkey, Z. S., additional, Szabados, S., additional, Cziraki, A., additional, Garai, J., additional, Myloslavska, I., additional, Menazza, S. M., additional, Canton, M. C., additional, Di Lisa, F. D. L., additional, Oliveira, S. H. V., additional, Morais, C. A. S., additional, Miranda, M. R., additional, Oliveira, T. T., additional, Lamego, M. R. A., additional, Lima, L. M., additional, Goncharova, N. S., additional, Naymushin, A. V., additional, Kazimli, A. V., additional, Moiseeva, O. M., additional, Carvalho, M. G., additional, Sabino, A. P., additional, Mota, A. P. L., additional, Sousa, M. O., additional, Niessner, A., additional, Richter, B., additional, Hohensinner, P. J., additional, Rychli, K., additional, Zorn, G., additional, Berger, R., additional, Moertl, D., additional, Pacher, R., additional, Wojta, J., additional, Huelsmann, M., additional, Kukharchik, G., additional, Nesterova, N., additional, Pavlova, A., additional, Gaykovaya, L., additional, Krapivka, N., additional, Konstantinova, I., additional, Sichinava, L., additional, Prapa, S., additional, Mccarthy, K. P., additional, Kilner, P. J., additional, Xu, X. Y., additional, Johnson, M. R., additional, Ho, S. Y., additional, Gatzoulis, M. A., additional, Stoupel, E. G., additional, Garcia, R., additional, Merino, D., additional, Montalvo, C., additional, Hurle, M. A., additional, Nistal, J. F., additional, Villar, A. V., additional, Perez-Moreno, A., additional, Gilabert, R., additional, and Ros, E., additional
- Published
- 2012
- Full Text
- View/download PDF
18. Oral abstract presentations
- Author
-
Pereira, L., primary, Ruiz-Hurtado, G., additional, Morel, E., additional, Dominguez, A., additional, Benitah, J. P., additional, Bers, D. M., additional, Lezoualc'h, F., additional, Gomez, A., additional, Collins, T. P., additional, Sikkel, M. B., additional, O' Gara, P., additional, Lyon, A. R., additional, Harding, S. E., additional, Macleod, K. T., additional, Wantha, S., additional, Alard, J. E., additional, Doering, Y., additional, Drechsler, M., additional, Megens, R. T., additional, Hackeng, T., additional, Weber, C., additional, Soehnlein, O., additional, Dietel, B., additional, Cicha, I., additional, Altendorf, R., additional, Daniel, W. G., additional, Garlichs, C. D., additional, Mukherjee, U., additional, Ong, S. B., additional, Davidson, S. M., additional, Szabadkai, G., additional, Yellon, D. M., additional, Hausenloy, D. J., additional, Neary, M. T., additional, Hall, A. R., additional, Hirst, E., additional, Mohun, T. J., additional, Breckenridge, R. A., additional, Akhmedov, A., additional, Camici, G. G., additional, Stivala, S., additional, Holy, E. W., additional, Breitenstein, A., additional, Lohmann, C., additional, Beer, J.-H., additional, Tanner, F. C., additional, Matter, C. M., additional, Luescher, T. F., additional, Hulsmans, M., additional, Geeraert, B., additional, Arnould, T., additional, Tsatsanis, C., additional, Holvoet, P., additional, Hermida, N., additional, Markl, A., additional, Hamelet, J., additional, Herijgers, P., additional, Horman, S., additional, Noppe, G., additional, Beauloye, C., additional, Van Bilsen, M., additional, Dessy, C., additional, Balligand, J.-L., additional, Del Giorno, R., additional, Moreno Velasquez, I., additional, Leander, K., additional, Frumento, P., additional, Vikstrom, M., additional, Pirro, M., additional, Mannarino, M. R., additional, Mannarino, E., additional, De Faire, U., additional, Gigante, B., additional, Chaudhry, B., additional, Chrystal, P., additional, Henderson, D. J., additional, Fulcoli, F. G., additional, Chen, L., additional, Martucciello, S., additional, Illingworth, E., additional, Baldini, A., additional, Mavroidis, M., additional, Davos, C., additional, Psarras, S., additional, Varela, A., additional, Kostavasili, I., additional, Capetanaki, Y., additional, Engstrom Klarstrom, K., additional, Skoglund, C., additional, Kalvegren, H., additional, Bengtsson, T., additional, Drawnel, F., additional, Wachten, D., additional, Molkentin, J. D., additional, Sjaastad, I., additional, Liu, N., additional, Mikoshiba, K., additional, Bootman, M. D., additional, Roderick, H. L., additional, Di Gregoli, K., additional, Salter, R., additional, and Johnson, J. L., additional
- Published
- 2012
- Full Text
- View/download PDF
19. Überlegungen zu einem allgemeinen Strategiebegriff
- Author
-
Ringlstetter, Max, Henzler, Herbert, Mirow, Michael, Ringlstetter, M ( Max ), Henzler, H ( Herbert ), Mirow, M ( Michael ), Dietel, B, Seidl, David; https://orcid.org/0000-0002-0368-196X, Ringlstetter, Max, Henzler, Herbert, Mirow, Michael, Ringlstetter, M ( Max ), Henzler, H ( Herbert ), Mirow, M ( Michael ), Dietel, B, and Seidl, David; https://orcid.org/0000-0002-0368-196X
- Published
- 2003
20. Einige Eigenschaften einer Mutante des menschlichen Leber-Epithelstammes Chang
- Author
-
Dietel, B. and Edlinger, E.
- Published
- 1959
- Full Text
- View/download PDF
21. Über die Wirkung von Schlangengift auf in vitro gezüchtete Säugetierzellen
- Author
-
Edlinger, E. and Dietel, B.
- Published
- 1959
- Full Text
- View/download PDF
22. Emergence of dendritic cells in the myocardium after acute myocardial infarction - implications for inflammatory myocardial damage
- Author
-
Yilmaz, A., Dietel, B., Iwona Cicha, Schubert, K., Hausmann, R., Daniel, W. G., Garlichs, C. D., and Stumpf, C.
23. ATP citrate lyase (ACLY)-dependent immunometabolism in mucosal T cells drives experimental colitis in vivo.
- Author
-
Schulz-Kuhnt A, Rühle K, Javidmehr A, Döbrönti M, Biwank J, Knittel S, Neidlinger P, Leupold J, Liu LJ, Dedden M, Taudte RV, Gessner A, Fromm MF, Mielenz D, Kreiss L, Waldner MJ, Schürmann S, Friedrich O, Dietel B, López-Posadas R, Plattner C, Zundler S, Becker C, Atreya R, Neurath MF, and Atreya I
- Subjects
- Humans, Animals, ATP Citrate (pro-S)-Lyase metabolism, CD8-Positive T-Lymphocytes metabolism, Inflammation metabolism, Butyrates, Intestinal Mucosa metabolism, Dextran Sulfate, Disease Models, Animal, Intraepithelial Lymphocytes metabolism, Colitis metabolism, Inflammatory Bowel Diseases
- Abstract
Objective: Mucosal T cells play a major role in inflammatory bowel disease (IBD). However, their immunometabolism during intestinal inflammation is poorly understood. Due to its impact on cellular metabolism and proinflammatory immune cell function, we here focus on the enzyme ATP citrate lyase (ACLY) in mucosal T cell immunometabolism and its relevance for IBD., Design: ACLY expression and its immunometabolic impact on colitogenic T cell function were analysed in mucosal T cells from patients with IBD and in two experimental colitis models., Results: ACLY was markedly expressed in colon tissue under steady-state conditions but was significantly downregulated in lamina propria mononuclear cells in experimental dextran sodium sulfate-induced colitis and in CD4
+ and to a lesser extent in CD8+ T cells infiltrating the inflamed gut in patients with IBD. ACLY-deficient CD4+ T cells showed an impaired capacity to induce intestinal inflammation in a transfer colitis model as compared with wild-type T cells. Assessment of T cell immunometabolism revealed that ACLY deficiency dampened the production of IBD-relevant cytokines and impaired glycolytic ATP production but enriched metabolites involved in the biosynthesis of phospholipids and phosphatidylcholine. Interestingly, the short-chain fatty acid butyrate was identified as a potent suppressor of ACLY expression in T cells, while IL-36α and resolvin E1 induced ACLY levels. In a translational approach, in vivo administration of the butyrate prodrug tributyrin downregulated mucosal infiltration of ACLYhigh CD4+ T cells and ameliorated chronic colitis., Conclusion: ACLY controls mucosal T cell immunometabolism and experimental colitis. Therapeutic modulation of ACLY expression in T cells emerges as a novel strategy to promote the resolution of intestinal inflammation., Competing Interests: Competing interests: MFN has served as an advisor for Pentax, Giuliani, MSD, Abbvie, Janssen, Takeda and Boehringer. Moreover, MFN serves as an associated editor of the journal Gut. The remaining authors disclose no conflicts., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ.)- Published
- 2024
- Full Text
- View/download PDF
24. The Shear Stress-Regulated Expression of Glypican-4 in Endothelial Dysfunction In Vitro and Its Clinical Significance in Atherosclerosis.
- Author
-
Urschel K, Hug KP, Zuo H, Büttner M, Furtmair R, Kuehn C, Stumpfe FM, Botos B, Achenbach S, Yuan Y, Dietel B, and Tauchi M
- Subjects
- Humans, Cells, Cultured, Clinical Relevance, Glypicans genetics, Glypicans metabolism, Heparan Sulfate Proteoglycans metabolism, Human Umbilical Vein Endothelial Cells metabolism, Atherosclerosis genetics, Atherosclerosis metabolism, Plaque, Atherosclerotic genetics, Plaque, Atherosclerotic metabolism
- Abstract
Retention of circulating lipoproteins by their interaction with extracellular matrix molecules has been suggested as an underlying mechanism for atherosclerosis. We investigated the role of glypican-4 (GPC4), a heparan sulfate (HS) proteoglycan, in the development of endothelial dysfunction and plaque progression; Expression of GPC4 and HS was investigated in human umbilical vein/artery endothelial cells (HUVECs/HUAECs) using flow cytometry, qPCR, and immunofluorescent staining. Leukocyte adhesion was determined in HUVECs in bifurcation chamber slides under dynamic flow. The association between the degree of inflammation and GPC4, HS, and syndecan-4 expressions was analyzed in human carotid plaques; GPC4 was expressed in HUVECs/HUAECs. In HUVECs, GPC4 protein expression was higher in laminar than in non-uniform shear stress regions after a 1-day or 10-day flow ( p < 0.01 each). The HS expression was higher under laminar flow after a 1 day ( p < 0.001). Monocytic THP-1 cell adhesion to HUVECs was facilitated by GPC4 knock-down ( p < 0.001) without affecting adhesion molecule expression. GPC4 and HS expression was lower in more-inflamed than in less-inflamed plaque shoulders ( p < 0.05, each), especially in vulnerable plaque sections; Reduced expression of GPC4 was associated with atherogenic conditions, suggesting the involvement of GPC4 in both early and advanced stages of atherosclerosis.
- Published
- 2023
- Full Text
- View/download PDF
25. The presence of cerebellar B cell aggregates is associated with a specific chemokine profile in the cerebrospinal fluid in a mouse model of multiple sclerosis.
- Author
-
Schropp V, Chunder R, Dietel B, Tacke S, and Kuerten S
- Subjects
- Mice, Animals, Ligands, Chemokines, Cytokines, Chemokines, CXC, Receptors, Chemokine, Multiple Sclerosis pathology, Encephalomyelitis, Autoimmune, Experimental pathology
- Abstract
Background: The presence of meningeal ectopic lymphoid structures (ELS) in a subgroup of patients diagnosed with secondary progressive multiple sclerosis (SPMS) corresponds to a pronounced cortical inflammation and an aggravated disease course. In MP4-induced experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS), B cell aggregates develop in the central nervous system (CNS) in the chronic stage of the disease. Therefore, the model is suitable for studying key molecules of ELS development and maintenance. Here, we investigated whether there is a specific cytokine and chemokine signature in paired cerebrospinal fluid (CSF) and serum samples associated with the presence of cerebellar B cell and T cell pathology and B cell aggregates of MP4-immunized mice., Methods: Paired CSF and serum samples were collected from the cisterna magna and periphery of MP4-immunized mice at the chronic stage of disease. A control group with mice immunized only with the adjuvant (vehicle) was included in the study. A selected panel of 34 cytokines and chemokines were measured by MAGPIX® for both cohorts. For the assessment of B cell and T cell infiltration, immunohistochemical staining was performed and analyzed using light microscopy. To detect specific chemokine receptors additional staining was conducted., Results: While we detected several upregulated cytokines and chemokines in the CSF of MP4-immunized mice independent of the extent of B cell and T cell pathology compared to vehicle-immunized mice, C-C motif chemokine ligand (CCL)-1 was associated with high B cell and T cell infiltration. Furthermore, the level of certain chemokines, including CCL1, CCL5, CCL7, CCL12, CCL22 and C-X-C motif chemokine ligand (CXCL)-13, was significantly increased (p < 0.05) in MP4-immunized mice showing a high number of B cell aggregates. While C-C motif chemokine receptor (CCR)5 had a ubiquitous expression independent of the extent of B cell and T cell pathology, C-X-C motif chemokine receptor (CXCR)-5 and CXCR6 expression was specifically associated with high B cell and T cell pathology., Conclusion: Our data suggest that multiple cytokines and chemokines are involved in the pathophysiology of MP4-induced EAE. Furthermore, the presence of B cell aggregates was associated with a specific chemokine profile in the CSF, which might be useful for predicting the presence of these aggregates without the necessity to histologically screen the CNS tissue., (© 2023. The Author(s).)
- Published
- 2023
- Full Text
- View/download PDF
26. The Involvement of Cx43 in JNK1/2-Mediated Endothelial Mechanotransduction and Human Plaque Progression.
- Author
-
Tauchi M, Oshita K, Urschel K, Furtmair R, Kühn C, Stumpfe FM, Botos B, Achenbach S, and Dietel B
- Subjects
- Humans, Mechanotransduction, Cellular, Cells, Cultured, Human Umbilical Vein Endothelial Cells metabolism, Extracellular Signal-Regulated MAP Kinases metabolism, JNK Mitogen-Activated Protein Kinases metabolism, Connexins metabolism, Connexin 43 genetics, Connexin 43 metabolism, Plaque, Atherosclerotic metabolism
- Abstract
Atherosclerotic lesions preferentially develop at bifurcations, characterized by non-uniform shear stress (SS). The aim of this study was to investigate SS-induced endothelial activation, focusing on stress-regulated mitogen-activated protein kinases (MAPK) and downstream signaling, and its relation to gap junction proteins, Connexins (Cxs). Human umbilical vein endothelial cells were exposed to flow ("mechanical stimulation") and stimulated with TNF-α ("inflammatory stimulation"). Phosphorylated levels of MAPKs (c-Jun N-terminal kinase (JNK1/2), extracellular signal-regulated kinase (ERK), and p38 kinase (p38K)) were quantified by flow cytometry, showing the activation of JNK1/2 and ERK. THP-1 cell adhesion under non-uniform SS was suppressed by the inhibition of JNK1/2, not of ERK. Immunofluorescence staining and quantitative real-time PCR demonstrated an induction of c-Jun and c-Fos and of Cx43 in endothelial cells by non-uniform SS, and the latter was abolished by JNK1/2 inhibition. Furthermore, plaque inflammation was analyzed in human carotid plaques ( n = 40) using immunohistochemistry and quanti-gene RNA-assays, revealing elevated Cx43
+ cell counts in vulnerable compared to stable plaques. Cx43+ cell burden in the plaque shoulder correlated with intraplaque neovascularization and lipid core size, while an inverse correlation was observed with fibrous cap thickness. Our results constitute the first report that JNK1/2 mediates Cx43 mechanoinduction in endothelial cells by atheroprone shear stress and that Cx43 is expressed in human carotid plaques. The correlation of Cx43+ cell counts with markers of plaque vulnerability implies its contribution to plaque progression.- Published
- 2023
- Full Text
- View/download PDF
27. Bone marrow stroma cells promote induction of a chemoresistant and prognostic unfavorable S100A8/A9high AML cell subset.
- Author
-
Böttcher M, Panagiotidis K, Bruns H, Stumpf M, Völkl S, Geyh S, Dietel B, Schroeder T, Mackensen A, and Mougiakakos D
- Subjects
- Humans, Bone Marrow metabolism, Calgranulin A genetics, Calgranulin A metabolism, Prognosis, Interleukin-6, Leukemia, Myeloid, Acute metabolism
- Abstract
The bone marrow (BM) stroma represents a protective niche for acute myeloid leukemia (AML) cells. However, the complex underlying mechanisms remain to be fully elucidated. We found 2 small, intracellular, calcium-sensing molecules, S100A8 and S100A9, among the top genes being upregulated in primary AML blasts upon stromal contact. As members of the S100 protein family, they can modulate such cellular processes as proliferation, migration, and differentiation. Dysregulation of S100 proteins is described as a predictor of poor survival in different human cancers, including increased S100A8 expression in de novo AML. Thus, we wanted to decipher the underlying pathways of stroma-mediated S100A8/A9 induction, as well as its functional consequences. Upregulation of S100A8/A9 after stromal cross talk was validated in AML cell lines, was contact independent and reversible and resulted in accumulation of S100A8/A9high cells. Accordingly, frequency of S100A8/A9high AML blasts was higher in the patients' BM than in peripheral blood. The S100A8/A9high AML cell population displayed enhanced utilization of free fatty acids, features of a more mature myeloid phenotype, and increased resilience toward chemotherapeutics and BCL2 inhibition. We identified stromal cell-derived interleukin-6 (IL-6) as the trigger for a Jak/STAT3 signaling-mediated S100A8/A9 induction. Interfering with fatty acid uptake and the IL-6-Jak/STAT3 pathway antagonized formation of S100A8/A9high cells and therapeutic resistance, which could have therapeutic implications as a strategy to interfere with the AML-niche dynamics., (© 2022 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)
- Published
- 2022
- Full Text
- View/download PDF
28. Accuracy of BIS monitoring using a novel interface device connecting conventional needle-electrodes and BIS sensors during frontal neurosurgical procedures.
- Author
-
Harada H, Muta S, Kakuma T, Ukeda M, Ota S, Hirata M, Fujioka H, Nakashima O, Dietel B, and Tauchi M
- Subjects
- Adult, Aged, Female, Humans, Male, Middle Aged, Anesthesia, General methods, Biosensing Techniques methods, Electrodes, Electroencephalography drug effects, Electroencephalography instrumentation, Monitoring, Intraoperative methods, Neurosurgical Procedures methods
- Abstract
Background: Bispectral index (BIS) monitoring is a widely used non-invasive method to monitor the depth of anesthesia. However, in the event of surgeries requiring a frontal approach, placement of the electrode may be impossible at the designated area to achieve a proper BIS measurement., Methods: We developed an investigational interface device to connect needle-electrodes to BIS sensors. The safety and clinical performance were investigated in patients who underwent surgery. Direct BIS values from a disposable BIS electrode and indirect values via the interface device were simultaneously recorded from the same areas of electrode placement in a single patient. The agreement between the direct and indirect BIS values was statistically analyzed., Results: The interface device with a silver electrode demonstrated sufficient electric conduction to transmit electroencephalogram signals. The overall BIS curves were similar to those of direct BIS monitoring. Direct and indirect BIS values from 18 patients were statistically analyzed using a linear mixed model and a significant concordance was confirmed (indirect BIS = 7.0405 + 0.8286 * direct BIS, p<0.0001). Most observed data (2582/2787 data points, 92.64%) had BIS unit differences of 10 or less., Conclusions: The interface device provides an opportunity for intraoperative BIS monitoring of patients, whose clinical situation does not permit the placement of conventional adhesive sensors at the standard location., Competing Interests: The authors have declared that no competing interests exist.
- Published
- 2021
- Full Text
- View/download PDF
29. Investigation of Wall Shear Stress in Cardiovascular Research and in Clinical Practice-From Bench to Bedside.
- Author
-
Urschel K, Tauchi M, Achenbach S, and Dietel B
- Subjects
- Humans, Coronary Artery Disease metabolism, Coronary Artery Disease pathology, Coronary Artery Disease physiopathology, Coronary Circulation, Endothelial Cells metabolism, Endothelial Cells pathology, Plaque, Atherosclerotic metabolism, Plaque, Atherosclerotic pathology, Plaque, Atherosclerotic physiopathology, Plaque, Atherosclerotic therapy, Shear Strength, Stress, Mechanical
- Abstract
In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyperlipidemia. A tremendous amount of studies has demonstrated that hemodynamic forces modify endothelial athero-susceptibility phenotypes. Endothelial cells possess mechanosensors on the apical surface to detect a blood stream-induced force on the vessel wall, known as "wall shear stress (WSS)", and induce cellular and molecular responses. Investigations to elucidate the mechanisms of this process are on-going: on the one hand, hemodynamics in complex vessel systems have been described in detail, owing to the recent progress in imaging and computational techniques. On the other hand, investigations using unique in vitro chamber systems with various flow applications have enhanced the understanding of WSS-induced changes in endothelial cell function and the involvement of the glycocalyx, the apical surface layer of endothelial cells, in this process. In the clinical setting, attempts have been made to measure WSS and/or glycocalyx degradation non-invasively, for the purpose of their diagnostic utilization. An increasing body of evidence shows that WSS, as well as serum glycocalyx components, can serve as a predicting factor for atherosclerosis development and, most importantly, for the rupture of plaques in patients with high risk of coronary heart disease.
- Published
- 2021
- Full Text
- View/download PDF
30. Differential Responses to Bioink-Induced Oxidative Stress in Endothelial Cells and Fibroblasts.
- Author
-
Genç H, Hazur J, Karakaya E, Dietel B, Bider F, Groll J, Alexiou C, Boccaccini AR, Detsch R, and Cicha I
- Subjects
- Alginates toxicity, Animals, Biocompatible Materials toxicity, Cell Line, Cell Survival drug effects, Endothelial Cells cytology, Fibroblasts cytology, Gelatin toxicity, Humans, Mice, NIH 3T3 Cells, Tissue Scaffolds chemistry, Alginates chemistry, Biocompatible Materials chemistry, Endothelial Cells drug effects, Fibroblasts drug effects, Gelatin chemistry, Oxidative Stress drug effects
- Abstract
A hydrogel system based on oxidized alginate covalently crosslinked with gelatin (ADA-GEL) has been utilized for different biofabrication approaches to design constructs, in which cell growth, proliferation and migration have been observed. However, cell-bioink interactions are not completely understood and the potential effects of free aldehyde groups on the living cells have not been investigated. In this study, alginate, ADA and ADA-GEL were characterized via FTIR and NMR, and their effect on cell viability was investigated. In the tested cell lines, there was a concentration-dependent effect of oxidation degree on cell viability, with the strongest cytotoxicity observed after 72 h of culture. Subsequently, primary human cells, namely fibroblasts and endothelial cells (ECs) were grown in ADA and ADA-GEL hydrogels to investigate the molecular effects of oxidized material. In ADA, an extremely strong ROS generation resulting in a rapid depletion of cellular thiols was observed in ECs, leading to rapid necrotic cell death. In contrast, less pronounced cytotoxic effects of ADA were noted on human fibroblasts. Human fibroblasts had higher cellular thiol content than primary ECs and entered apoptosis under strong oxidative stress. The presence of gelatin in the hydrogel improved the primary cell survival, likely by reducing the oxidative stress via binding to the CHO groups. Consequently, ADA-GEL was better tolerated than ADA alone. Fibroblasts were able to survive the oxidative stress in ADA-GEL and re-entered the proliferative phase. To the best of our knowledge, this is the first report that shows in detail the relationship between oxidative stress-induced intracellular processes and alginate di-aldehyde-based bioinks.
- Published
- 2021
- Full Text
- View/download PDF
31. Formation of atherosclerotic lesions is independent of eosinophils in male mice.
- Author
-
Hofheinz K, Seibert F, Ackermann JA, Dietel B, Tauchi M, Oszvar-Kozma M, Kühn H, Schett G, Binder CJ, and Krönke G
- Subjects
- Animals, Biomarkers, Eosinophils, Lipoproteins, LDL metabolism, Male, Mice, Oxidation-Reduction, Arteriosclerosis, Atherosclerosis
- Abstract
Background and Aims: Oxidation of low-density lipoprotein (LDL) and oxidized LDL-mediated activation of the innate immune system have been recognized as early key events during the pathogenesis of atherosclerosis. Recent evidence identified eosinophils as a major source of enzymatic lipid oxidation and suggested a potential role of type 2 immunity in atherogenesis. However, the involvement of individual type 2 immune cell subsets involved in this process has been incompletely defined. We therefore sought to determine the role of eosinophils during LDL oxidation and the pathogenesis of this disease., Methods: Using eosinophil-deficient dblGATA1 mice, we studied the role of eosinophils in two established mouse models of atherosclerosis., Results: These experiments revealed that the presence of eosinophils did neither affect biomarkers of LDL oxidation nor atherosclerotic lesion development., Conclusions: The obtained results show that LDL oxidation and development of atherosclerosis are largely independent of eosinophils or eosinophil-mediated LDL oxidation., (Copyright © 2020 Elsevier B.V. All rights reserved.)
- Published
- 2020
- Full Text
- View/download PDF
32. A Single Injection of N -Oleoyldopamine, an Endogenous Agonist for Transient Receptor Potential Vanilloid-1, Induced Brain Hypothermia, but No Neuroprotective Effects in Experimentally Induced Cerebral Ischemia in Rats.
- Author
-
Tejada de Rink MM, Naumann U, Kollmar R, Schwab S, Dietel B, Harada H, and Tauchi M
- Subjects
- Animals, Brain metabolism, Dopamine analogs & derivatives, Male, Rats, Rats, Wistar, TRPV Cation Channels metabolism, Brain Ischemia therapy, Hypothermia, Hypothermia, Induced, Neuroprotective Agents pharmacology
- Abstract
Targeted temperature management, or therapeutic hypothermia, is a potent neuroprotective approach after ischemic brain injury. Hypothermia should be induced as soon as possible after the onset of acute stroke to assure better outcomes. Accordingly, drugs with a fast-acting hypothermic effect sustainable through the period of emergency transportation to hospital would have clinical advantages. Activation of the transient receptor potential vanilloid-1 (TRPV1) can induce hypothermia. Our immunohistochemical investigations confirmed that TRPV1 was distributed to perivascular and periventricular regions of the rat brain, where TRPV1 can be easily detected by TRPV1 agonists. An endogenous TRPV1 selective agonist, N -oleoyldopamine (OLDA), and a synthetic antagonist, AMG 9810, were injected intraperitoneally into healthy adult male Wister rats, and brain and core temperatures and gross motor activities were monitored. Comparison with baseline temperatures showed that TRPV1 injection immediately induced mild hypothermia ( p < 0.05 in brain and p < 0.01 in body), and AMG 9810 induced immediate mild hyperthermia (not significant). However, the OLDA-induced hypothermia did not decrease lesion volume after middle carotid artery occlusion in rats. Relative to vehicle, OLDA yielded poorer outcomes and AMG 9810 yielded better outcomes in neurological scores and lesion size. Our study showed that, as an agonist of TRPV1, OLDA has suitable hypothermia-inducing properties, but did not decrease lesion volume. Therefore, the search for novel TRPV1 agonists and/or antagonists providing hypothermia and neuroprotection should continue. Further investigations should also target OLDA-induced transient hypothermia combined with long-term hypothermia maintenance with surface cooling, which mimics the anticipated clinical use of this class of drug.
- Published
- 2020
- Full Text
- View/download PDF
33. Impact of single nucleotide polymorphisms in the VEGFR2 gene on endothelial cell activation under non‑uniform shear stress.
- Author
-
Schacher NM, Raaz-Schrauder D, Pasutto F, Stumpfe FM, Tauchi M, Dietel B, Achenbach S, and Urschel K
- Subjects
- Alleles, Biomarkers, Cell Adhesion, Cells, Cultured, Gene Expression, Genotype, Human Umbilical Vein Endothelial Cells, Humans, Immunohistochemistry, Vascular Cell Adhesion Molecule-1 genetics, Vascular Cell Adhesion Molecule-1 metabolism, Biomechanical Phenomena genetics, Endothelial Cells metabolism, Polymorphism, Single Nucleotide, Vascular Endothelial Growth Factor Receptor-2 genetics
- Abstract
Single nucleotide polymorphisms (SNPs) in vascular endothelial growth factor receptor 2 (VEGFR2) are associated with coronary artery disease, hypertension and myocardial infarction. However, their association with atherosclerosis remains to be fully elucidated. The purpose of the present study was to determine whether SNPs are involved in atherogenesis, by analyzing their impact on human umbilical vein endothelial cells (HUVECs) under laminar and non‑uniform shear stress in a well‑established in vitro model that simulates shear stress‑induced proatherogenic processes at vessel bifurcations. All experiments were performed using freshly isolated HUVECs. Three SNPs in the VEGFR2 gene (rs1870377 T>A, rs2071559 A>G and rs2305948 C>T) were genotyped and the expression levels of VEGFR2 were semi‑quantitatively determined using western blotting. Subsequently, the HUVECs were seeded in bifurcating flow‑through cell culture slides and flow (9.6 ml/min) was applied for 19 h, including tumor necrosis factor‑α stimulation during the final 2 h of flow. The protein expression levels of VCAM‑1, E‑selectin and VEGFR2 and the adhesion of THP‑1 cells were analyzed in laminar and non‑uniform shear stress regions. Data were analyzed for associations with the respective SNPs. The total expression of VEGFR2 was significantly lower under non‑uniform shear stress than under laminar shear stress conditions, independent of the genotype. The expression of VEGFR2 between the different shear stress patterns was not significantly altered by the different SNPs. The expression levels of VCAM‑1 and E‑selectin were lower in the A/A genotype compared with those in other genotypes in rs1870377 T>A and rs2071559 A>G. In conclusion, the results suggested that SNPs within the VEGFR2 gene have a significant impact on shear stress‑related endothelial activation.
- Published
- 2019
- Full Text
- View/download PDF
34. Filarial extract of Litomosoides sigmodontis induces a type 2 immune response and attenuates plaque development in hyperlipidemic ApoE-knockout mice.
- Author
-
Kuehn C, Tauchi M, Furtmair R, Urschel K, Raaz-Schrauder D, Neumann AL, Frohberger SJ, Hoerauf A, Regus S, Lang W, Sagban TA, Stumpfe FM, Achenbach S, Hübner MP, and Dietel B
- Subjects
- Animals, Atherosclerosis chemically induced, Atherosclerosis genetics, Atherosclerosis immunology, Dietary Fats adverse effects, Dietary Fats pharmacology, Hyperlipidemias chemically induced, Hyperlipidemias genetics, Hyperlipidemias immunology, Mice, Mice, Knockout, ApoE, Plaque, Atherosclerotic chemically induced, Plaque, Atherosclerotic immunology, Th1 Cells immunology, Th1 Cells pathology, Atherosclerosis drug therapy, Complex Mixtures chemistry, Complex Mixtures pharmacology, Filarioidea chemistry, Hyperlipidemias drug therapy, Plaque, Atherosclerotic drug therapy, Th2 Cells immunology
- Abstract
A type 1 immune response is involved in atherosclerosis progression, whereas the role of a type 2 polarization, especially with regard to an enhanced T helper (T
h )2 cell differentiation, is still unclear. Helminths trigger type 2 immune responses, protecting the host from inflammatory disorders. We investigated whether an increased type 2 polarization by administration of Litomosoides sigmodontis adult worm extract (LsAg) affects atherosclerosis in apolipoprotein E-deficient (ApoE-/- ) mice. Injections of 50 µg LsAg, i.p. into ApoE-/- mice induced a type 2 immune response shown by increased frequencies of peritoneal eosinophils and alternatively activated macrophages. To analyze the effect of LsAg on atherosclerosis initiation, ApoE-/- mice received a high-fat diet for 12 wk and weekly injections of 50 µg LsAg from wk 5 to 12. Therapeutic effects on advanced atherosclerosis were analyzed in mice that were fed a high-fat diet for 12 wk followed by 12 wk of normal chow and weekly LsAg injections. Both preventive and therapeutic LsAg application significantly decreased plaque size. Therapeutic treatment even caused regression of plaque size and macrophage density in the aortic root and reduced Th 1-specific gene expression and intraplaque inflammation. In addition, plaque size after therapeutic treatment was inversely correlated with plaque-infiltrated alternatively activated macrophages. In vitro , LsAg treatment of HUVECs reduced intracellular levels of phosphorylated NF-κB-p65, IκB-α, and JNK1/2. In bifurcation flow-through slides, THP-1 cell adhesion to a HUVEC monolayer was decreased by LsAg in regions of nonuniform shear stress. Applying inhibitors of the respective kinases suggests JNK1/2 inhibition is involved in the suppressed cell adhesion. A switch to an enhanced type 2 immune response by LsAg exerts antiatherogenic effects on murine plaque development, indicating a protective role of a hampered type 1 polarization. In vitro , LsAg affects endothelial signaling pathways, among which JNK1/2 inhibition seems to be involved in the suppression of monocytic cell adhesion under proatherogenic shear stress.-Constanze, K., Tauchi, M., Furtmair, R., Urschel, K., Raaz-Schrauder, D., Neumann, A.-L., Frohberger, S. J., Hoerauf, A., Regus, S., Lang, W., Sagban, T. A., Stumpfe, F. M., Achenbach, S., Hübner, M. P., Dietel, B. Filarial extract of Litomosoides sigmodontis induces a type 2 immune response and attenuates plaque development in hyperlipidemic ApoE-knockout mice.- Published
- 2019
- Full Text
- View/download PDF
35. Targeted Temperature Management: Peltier's Element-Based Focal Brain Cooling Protects Penumbra Neurons from Progressive Damage in Experimental Cerebral Ischemia.
- Author
-
Tauchi M, Tejada de Rink MM, Fujioka H, Okayama S, Nakamura KI, Dietel B, Achenbach S, Kollmar R, Schwab S, Ushijima K, and Harada H
- Subjects
- Animals, Brain pathology, Infarction, Middle Cerebral Artery pathology, Male, Rats, Sprague-Dawley, Hypothermia, Induced methods, Infarction, Middle Cerebral Artery therapy
- Abstract
Targeted temperature management (TTM), or therapeutic hypothermia, is one of the most potent neuroprotective approaches after ischemic and traumatic brain injuries. TTM has been applied clinically with various methods, but effective achievement and maintenance of the target temperature remain challenging. Furthermore, timing of cooling and target body and brain temperature to optimize effectiveness for neuroprotection and to minimize side effects are yet to be standardized. Focal brain cooling is a potential strategy to minimize adverse effects of systemic TTM. In this study, we report on a focal brain cooling device for animals and its effectiveness of focal cooling in several animal models of ischemic cerebral stroke. A focal brain cooling device was constructed using a Peltier's element, a thermoelectric heat pump. The device was validated for its cooling ability, and optimal settings to induce an effective intracranial temperature were determined using male Sprague-Dawley rats. Transient and permanent middle cerebral artery occlusions were experimentally induced, and focal brain cooling was applied using the device varying the timing and duration of cooling. The stroke-induced infarct and edema volumes were evaluated from Nissl-stained cryosections. The focal brain cooling device was able to decrease and subsequently maintained cerebral hypothermia in free-moving rats without altering the core temperature. The device with validated intracranial temperatures produced neuroprotective effects in the acute phase of ischemic neural death, reperfusion injury, progressing damage to the penumbra, and edema formation. In conclusion, our validated focal cooling device enabled rapid and accurate cerebral TTM in rats. Using this device, we were able to test the neuroprotective effect of focal TTM in several pathological stages of cerebral ischemia, which warrants further studies to develop clinically feasible TTM procedures for patients with cerebral stroke.
- Published
- 2018
- Full Text
- View/download PDF
36. Correction: Enzymatic lipid oxidation by eosinophils propagates coagulation, hemostasis, and thrombotic disease.
- Author
-
Uderhardt S, Ackermann JA, Fillep T, Hammond VJ, Willeit J, Santer P, Mayr M, Biburger M, Miller M, Zellner KR, Stark K, Zarbock A, Rossaint J, Schubert I, Mielenz D, Dietel B, Raaz-Schrauder D, Ay C, Gremmel T, Thaler J, Heim C, Herrmann M, Collins PW, Schabbauer G, Mackman N, Voehringer D, Nadler JL, Lee JJ, Massberg S, Rauh M, Kiechl S, Schett G, O'Donnell VB, and Krönke G
- Published
- 2018
- Full Text
- View/download PDF
37. Plasma levels of sRANKL and OPG are associated with atherogenic cytokines in patients with intermediate cardiovascular risk.
- Author
-
Raaz-Schrauder D, Schrauder MG, Stumpf C, Lewczuk P, Kilian T, Dietel B, Garlichs CD, Schlundt C, Achenbach S, and Klinghammer L
- Subjects
- Adult, Aged, Aged, 80 and over, Atherosclerosis epidemiology, Biomarkers blood, Coronary Artery Disease epidemiology, Enzyme-Linked Immunosorbent Assay, Female, Germany epidemiology, Humans, Male, Middle Aged, Morbidity trends, Risk Factors, Young Adult, Atherosclerosis blood, Coronary Artery Disease blood, Cytokines blood, Osteoprotegerin blood, RANK Ligand blood, Risk Assessment
- Abstract
Osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) are regulators of bone remodeling, but are also considered to play important roles in coronary artery disease (CAD). This study evaluated potential associations of soluble (s) RANKL and OPG with atherosclerosis-relevant cytokines. Blood was collected from 414 individuals who presented to our hospital with intermediate likelihood for CAD for further examination. Plasma concentrations of total sRANKL, OPG, and 20 cytokines were measured using sandwich-type enzyme-linked immunoassays (ELISAs; OPG and sRANKL) and Luminex laser-based fluorescence analysis and correlated with each other. The plasma levels of interferon-γ (IFN-γ) and the T-helper cell 2 cytokines interleukin-4 (IL-4) and IL-13 showed a positive correlation with sRANKL. The association with sRANKL levels was negative for IFN-γ-induced protein-10 (IP-10) and monocyte chemotactic protein-1 (MCP-1). The strongest independent association with sRANKL in multivariable analyses was found for IFN-γ (positive) and IP-10 (negative), while IL-13 showed a positive and independent association with OPG plasma levels. OPG and sRANKL plasma levels correlate strongly and independently with specific circulating atherosclerosis-related cytokines in patients with intermediate cardiovascular risk.
- Published
- 2017
- Full Text
- View/download PDF
38. Cell specificity of magnetic cell seeding approach to hydrogel colonization.
- Author
-
Singh R, Wieser A, Reakasame S, Detsch R, Dietel B, Alexiou C, Boccaccini AR, and Cicha I
- Subjects
- Animals, Biocompatible Materials chemistry, Bombyx, Cell Adhesion, Cell Line, Cell Proliferation, Cells, Cultured, Fibroins chemistry, Glucuronic Acid chemistry, Hexuronic Acids chemistry, Humans, Tissue Engineering methods, Alginates chemistry, Endothelial Cells cytology, Fibroblasts cytology, Hydrogel, Polyethylene Glycol Dimethacrylate chemistry, Magnetite Nanoparticles chemistry, Tissue Scaffolds chemistry
- Abstract
Tissue-engineered scaffolds require an effective colonization with cells. Superparamagnetic iron oxide nanoparticles (SPIONs) can enhance cell adhesion to matrices by magnetic cell seeding. We investigated the possibility of improving cell attachment and growth on different alginate-based hydrogels using fibroblasts and endothelial cells (ECs) loaded with SPIONs. Hydrogels containing pure alginate (Alg), alginate dialdehyde crosslinked with gelatin (ADA-G) and Alg blended with G or silk fibroin (SF) were prepared. Endothelial cells and fibroblasts loaded with SPIONs were seeded and grown on hydrogels for up to 7 days, in the presence of magnetic field during the first 24 h. Cell morphology (fluorescent staining) and metabolic activity (WST-8 assay) of magnetically-seeded versus conventionally seeded cells were compared. Magnetic seeding of ECs improved their initial attachment and further growth on Alg/G hydrogel surfaces. However, we did not achieve an efficient and stable colonization of ADA-G films with ECs even with magnetic cell seeding. Fibroblast showed good initial colonization and growth on ADA-G and on Alg/SF. This effect was further significantly enhanced by magnetic cell seeding. On pure Alg, initial attachment and spreading of magnetically-seeded cells was dramatically improved compared to conventionally-seeded cells, but the effect was transient and diminished gradually with the cessation of magnetic force. Our results demonstrate that magnetic seeding improves the strength and uniformity of initial cell attachment to hydrogel surface in cell-specific manner, which may play a decisive role for the outcome in tissue engineering applications. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2948-2956, 2017., (© 2017 Wiley Periodicals, Inc.)
- Published
- 2017
- Full Text
- View/download PDF
39. Hypoxia-inducible protein 2 Hig2/Hilpda mediates neutral lipid accumulation in macrophages and contributes to atherosclerosis in apolipoprotein E-deficient mice.
- Author
-
Maier A, Wu H, Cordasic N, Oefner P, Dietel B, Thiele C, Weidemann A, Eckardt KU, and Warnecke C
- Subjects
- Animals, Apolipoproteins E deficiency, Atherosclerosis genetics, Atherosclerosis pathology, Dinoprostone genetics, Dinoprostone metabolism, Disease Models, Animal, Female, Foam Cells pathology, Humans, Male, Mice, Mice, Knockout, Neoplasm Proteins genetics, Perilipin-2 genetics, Perilipin-2 metabolism, Plaque, Atherosclerotic genetics, Plaque, Atherosclerotic pathology, Vascular Endothelial Growth Factor A biosynthesis, Vascular Endothelial Growth Factor A genetics, Atherosclerosis metabolism, Foam Cells metabolism, Lipid Metabolism, Neoplasm Proteins metabolism, Plaque, Atherosclerotic metabolism
- Abstract
Recently we identified hypoxia-inducible protein 2 (HIG2)/hypoxia-inducible lipid droplet-associated (HILPDA) as lipid droplet (LD) protein. Because HILPDA is highly expressed in atherosclerotic plaques, we examined its regulation and function in murine macrophages, compared it to the LD adipose differentiation-related protein (Adrp)/perilipin 2 (Plin2), and investigated its effects on atherogenesis in apolipoprotein E-deficient ( ApoE
-/- ) mice. Tie2 -Cre-driven Hilpda conditional knockout (cKO) did not affect viability, proliferation, and ATP levels in macrophages. Hilpda proved to be a target of hypoxia-inducible factor 1 (Hif-1) and peroxisome proliferator-activated receptors. In contrast, Adrp/Plin2 was not induced by Hif-1. Hilpda localized to the endoplasmic reticulum-LD interface, the site of LD formation. Hypoxic lipid accumulation and storage of oxidized LDL, cholesteryl esters and triglycerides were abolished in Hilpda cKO macrophages, independent of the glycolytic switch, fatty acid or lipoprotein uptake. Hilpda depletion reduced resistance against lipid overload and increased production of reactive oxygen species after reoxygenation. LPS-stimulated prostaglandin-E2 production was dysregulated in macrophages, demonstrating the substrate buffer and reservoir function of LDs for eicosanoid production. In ApoE-/- Hilpda expression were reduced. Thus, macrophage Hilpda is crucial to foam-cell formation and lipid deposition, and to controlled prostaglandin-E2 production. By these means Hilpda promotes lesion formation and progression of atherosclerosis.-Maier, A., Wu, H., Cordasic, N., Oefner, P., Dietel, B., Thiele, C., Weidemann, A., Eckardt, K.-U., Warnecke, C. Hypoxia-inducible protein 2 Hig2/Hilpda mediates neutral lipid accumulation in macrophages and contributes to atherosclerosis in apolipoprotein E-deficient mice.Vegf expression were reduced. Thus, macrophage Hilpda is crucial to foam-cell formation and lipid deposition, and to controlled prostaglandin-E2 production. By these means Hilpda promotes lesion formation and progression of atherosclerosis.-Maier, A., Wu, H., Cordasic, N., Oefner, P., Dietel, B., Thiele, C., Weidemann, A., Eckardt, K.-U., Warnecke, C. Hypoxia-inducible protein 2 Hig2/Hilpda mediates neutral lipid accumulation in macrophages and contributes to atherosclerosis in apolipoprotein E-deficient mice., (© FASEB.)- Published
- 2017
- Full Text
- View/download PDF
40. Enzymatic lipid oxidation by eosinophils propagates coagulation, hemostasis, and thrombotic disease.
- Author
-
Uderhardt S, Ackermann JA, Fillep T, Hammond VJ, Willeit J, Santer P, Mayr M, Biburger M, Miller M, Zellner KR, Stark K, Zarbock A, Rossaint J, Schubert I, Mielenz D, Dietel B, Raaz-Schrauder D, Ay C, Gremmel T, Thaler J, Heim C, Herrmann M, Collins PW, Schabbauer G, Mackman N, Voehringer D, Nadler JL, Lee JJ, Massberg S, Rauh M, Kiechl S, Schett G, O'Donnell VB, and Krönke G
- Subjects
- Adult, Aged, Animals, Arachidonate 12-Lipoxygenase genetics, Arachidonate 15-Lipoxygenase genetics, Atherosclerosis diagnosis, Atherosclerosis metabolism, Blotting, Western, Cells, Cultured, Eosinophil Cationic Protein metabolism, Humans, Hydroxyeicosatetraenoic Acids metabolism, Logistic Models, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, Oxidation-Reduction, Phosphatidylethanolamines metabolism, Prospective Studies, Reverse Transcriptase Polymerase Chain Reaction, Risk Factors, Thrombin metabolism, Arachidonate 12-Lipoxygenase metabolism, Arachidonate 15-Lipoxygenase metabolism, Blood Coagulation, Eosinophils metabolism, Hemostasis, Lipids analysis, Thrombosis metabolism
- Abstract
Blood coagulation is essential for physiological hemostasis but simultaneously contributes to thrombotic disease. However, molecular and cellular events controlling initiation and propagation of coagulation are still incompletely understood. In this study, we demonstrate an unexpected role of eosinophils during plasmatic coagulation, hemostasis, and thrombosis. Using a large-scale epidemiological approach, we identified eosinophil cationic protein as an independent and predictive risk factor for thrombotic events in humans. Concurrent experiments showed that eosinophils contributed to intravascular thrombosis by exhibiting a strong endogenous thrombin-generation capacity that relied on the enzymatic generation and active provision of a procoagulant phospholipid surface enriched in 12/15-lipoxygenase-derived hydroxyeicosatetraenoic acid-phosphatidylethanolamines. Our findings reveal a previously unrecognized role of eosinophils and enzymatic lipid oxidation as regulatory elements that facilitate both hemostasis and thrombosis in response to vascular injury, thus identifying promising new targets for the treatment of thrombotic disease., (© 2017 Uderhardt et al.)
- Published
- 2017
- Full Text
- View/download PDF
41. Matricellular protein SPARCL1 regulates tumor microenvironment-dependent endothelial cell heterogeneity in colorectal carcinoma.
- Author
-
Naschberger E, Liebl A, Schellerer VS, Schütz M, Britzen-Laurent N, Kölbel P, Schaal U, Haep L, Regensburger D, Wittmann T, Klein-Hitpass L, Rau TT, Dietel B, Méniel VS, Clarke AR, Merkel S, Croner RS, Hohenberger W, and Stürzl M
- Subjects
- Animals, Colorectal Neoplasms pathology, Human Umbilical Vein Endothelial Cells pathology, Humans, Jurkat Cells, Mice, Neovascularization, Pathologic pathology, Calcium-Binding Proteins metabolism, Colorectal Neoplasms blood supply, Colorectal Neoplasms metabolism, Extracellular Matrix Proteins metabolism, Human Umbilical Vein Endothelial Cells metabolism, Neoplasm Proteins metabolism, Neovascularization, Pathologic metabolism, Tumor Microenvironment
- Abstract
Different tumor microenvironments (TMEs) induce stromal cell plasticity that affects tumorigenesis. The impact of TME-dependent heterogeneity of tumor endothelial cells (TECs) on tumorigenesis is unclear. Here, we isolated pure TECs from human colorectal carcinomas (CRCs) that exhibited TMEs with either improved (Th1-TME CRCs) or worse clinical prognosis (control-TME CRCs). Transcriptome analyses identified markedly different gene clusters that reflected the tumorigenic and angiogenic activities of the respective TMEs. The gene encoding the matricellular protein SPARCL1 was most strongly upregulated in Th1-TME TECs. It was also highly expressed in ECs in healthy colon tissues and Th1-TME CRCs but low in control-TME CRCs. In vitro, SPARCL1 expression was induced in confluent, quiescent ECs and functionally contributed to EC quiescence by inhibiting proliferation, migration, and sprouting, whereas siRNA-mediated knockdown increased sprouting. In human CRC tissues and mouse models, vessels with SPARCL1 expression were larger and more densely covered by mural cells. SPARCL1 secretion from quiescent ECs inhibited mural cell migration, which likely led to stabilized mural cell coverage of mature vessels. Together, these findings demonstrate TME-dependent intertumoral TEC heterogeneity in CRC. They further indicate that TEC heterogeneity is regulated by SPARCL1, which promotes the cell quiescence and vessel homeostasis contributing to the favorable prognoses associated with Th1-TME CRCs.
- Published
- 2016
- Full Text
- View/download PDF
42. Corrigendum: Identification of two novel Chlorotoxin derivatives CA4 and CTX-23 with chemotherapeutic and anti-angiogenic potential.
- Author
-
Xu T, Fan Z, Li W, Dietel B, Wu Y, Beckmann MW, Wrosch JK, Buchfelder M, Eyupoglu IY, Cao Z, and Savaskan NE
- Published
- 2016
- Full Text
- View/download PDF
43. Oxalate-induced chronic kidney disease with its uremic and cardiovascular complications in C57BL/6 mice.
- Author
-
Mulay SR, Eberhard JN, Pfann V, Marschner JA, Darisipudi MN, Daniel C, Romoli S, Desai J, Grigorescu M, Kumar SV, Rathkolb B, Wolf E, Hrabě de Angelis M, Bäuerle T, Dietel B, Wagner CA, Amann K, Eckardt KU, Aronson PS, Anders HJ, and Knauf F
- Subjects
- Animals, Fibroblast Growth Factor-23, Fibrosis, Hypertension pathology, Mice, Mice, Inbred C57BL, Myocardium pathology, Renal Insufficiency, Chronic chemically induced, Renal Insufficiency, Chronic pathology, Uremia pathology, Disease Models, Animal, Hypertension etiology, Oxalic Acid, Renal Insufficiency, Chronic complications, Uremia etiology
- Abstract
Chronic kidney disease (CKD) research is limited by the lack of convenient inducible models mimicking human CKD and its complications in experimental animals. We demonstrate that a soluble oxalate-rich diet induces stable stages of CKD in male and female C57BL/6 mice. Renal histology is characterized by tubular damage, remnant atubular glomeruli, interstitial inflammation, and fibrosis, with the extent of tissue involvement depending on the duration of oxalate feeding. Expression profiling of markers and magnetic resonance imaging findings established to reflect inflammation and fibrosis parallel the histological changes. Within 3 wk, the mice reproducibly develop normochromic anemia, metabolic acidosis, hyperkalemia, FGF23 activation, hyperphosphatemia, and hyperparathyroidism. In addition, the model is characterized by profound arterial hypertension as well as cardiac fibrosis that persist following the switch to a control diet. Together, this new model of inducible CKD overcomes a number of previous experimental limitations and should serve useful in research related to CKD and its complications., (Copyright © 2016 the American Physiological Society.)
- Published
- 2016
- Full Text
- View/download PDF
44. Erratum: Identification of two novel Chlorotoxin derivatives CA4 and CTX-23 with chemotherapeutic and anti-angiogenic potential.
- Author
-
Xu T, Fan Z, Li W, Dietel B, Wu Y, Beckmann MW, Wrosch JK, Buchfelder M, Eyupoglu IY, Cao Z, and Savaskan NE
- Published
- 2016
- Full Text
- View/download PDF
45. Evaluation of hydrogel matrices for vessel bioplotting: Vascular cell growth and viability.
- Author
-
Singh R, Sarker B, Silva R, Detsch R, Dietel B, Alexiou C, Boccaccini AR, and Cicha I
- Subjects
- Alginates pharmacology, Animals, Biocompatible Materials pharmacology, Blood Vessels drug effects, Cell Proliferation drug effects, Cell Shape drug effects, Cell Survival drug effects, Fibroblasts cytology, Fibroblasts drug effects, Glucuronic Acid pharmacology, Hexuronic Acids pharmacology, Human Umbilical Vein Endothelial Cells cytology, Human Umbilical Vein Endothelial Cells drug effects, Humans, Mitochondria drug effects, Mitochondria metabolism, Myocytes, Smooth Muscle cytology, Myocytes, Smooth Muscle drug effects, Myocytes, Smooth Muscle metabolism, Sus scrofa, Blood Vessels cytology, Blood Vessels growth & development, Hydrogel, Polyethylene Glycol Dimethacrylate pharmacology, Tissue Engineering methods
- Abstract
Developing matrices biocompatible with vascular cells is one of the most challenging tasks in tissue engineering. Here, we compared the growth of vascular cells on different hydrogels as potential materials for bioplotting of vascular tissue. Formulations containing alginate solution (Alg, 2%, w/v) blended with protein solutions (silk fibroin, gelatin, keratin, or elastin) at 1% w/v were prepared. Human umbilical vein endothelial cells (ECs), smooth muscle cells (SMCs), and fibroblasts were cultivated on hydrogels for 7 days. Cell number and morphology was visualised using fluorescent staining at day 3 and 7. Cell metabolic activity was analysed using WST assay. Compared to pure Alg, Alg/keratin, Alg/gelatin and Alg/silk fibroin provided superb surfaces for ECs, supporting their attachment, growth, spreading and metabolic activity. SMCs showed best colonization and growth on Alg/silk fibroin and Alg/keratin hydrogels, whereas on elastin-containing hydrogels, cell clustering was observed. Fibroblasts growth was enhanced on Alg/elastin, and strongly improved on silk fibroin- and keratin-containing hydrogels. In contrast to the previous studies with alginate dialdehyde-gelatin crosslinked gels, Alg/gelatin blend hydrogels provided a less favourable scaffold for fibroblasts. Taken together, the most promising results were obtained with silk fibroin- and keratin-containing hydrogels, which supported the growth of all types of vascular cells. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 577-585, 2016., (© 2015 Wiley Periodicals, Inc.)
- Published
- 2016
- Full Text
- View/download PDF
46. Identification of two novel Chlorotoxin derivatives CA4 and CTX-23 with chemotherapeutic and anti-angiogenic potential.
- Author
-
Xu T, Fan Z, Li W, Dietel B, Wu Y, Beckmann MW, Wrosch JK, Buchfelder M, Eyupoglu IY, Cao Z, and Savaskan NE
- Subjects
- Angiogenesis Inhibitors chemistry, Animals, Antineoplastic Agents chemistry, Cell Line, Tumor, Humans, Rats, Scorpion Venoms chemistry, Angiogenesis Inhibitors pharmacology, Antineoplastic Agents pharmacology, Brain Neoplasms blood supply, Brain Neoplasms drug therapy, Brain Neoplasms metabolism, Brain Neoplasms pathology, Cell Proliferation drug effects, Glioma blood supply, Glioma drug therapy, Glioma metabolism, Glioma pathology, Neovascularization, Pathologic drug therapy, Neovascularization, Pathologic metabolism, Neovascularization, Pathologic pathology, Scorpion Venoms pharmacology
- Abstract
Brain tumors are fast proliferating and destructive within the brain microenvironment. Effective chemotherapeutic strategies are currently lacking which combat this deadly disease curatively. The glioma-specific chloride ion channel represents a specific target for therapy. Chlorotoxin (CTX), a peptide derived from scorpion venom, has been shown to be specific and efficacious in blocking glioma Cl(-) channel activity. Here, we report on two new derivatives (termed CA4 and CTX-23) designed and generated on the basis of the peptide sequence alignments of CTX and BmKCT. The novel peptides CA4 and CTX-23 are both effective in reducing glioma cell proliferation. In addition, CTX, CA4 and CTX-23 impact on cell migration and spheroid migration. These effects are accompanied by diminished cell extensions and increased nuclear sizes. Furthermore, we found that CA4 and CTX-23 are selective with low toxicity against primary neurons and astrocytes. In the ex vivo VOGiM, which maintain the entire brain tumor microenvironment, both CTX and CA4 display anti-tumor activity and reduce tumor volume. Hence, CTX and CA4 reveal anti-angiogenic properties with endothelial and angiogenic hotspots disrupting activities. These data report on the identification of two novel CTX derivatives with multiple anti-glioma properties including anti-angiogenesis.
- Published
- 2016
- Full Text
- View/download PDF
47. Suppression of proatherogenic leukocyte interactions by MCS-18--Impact on advanced atherosclerosis in ApoE-deficient mice.
- Author
-
Kuehn C, Tauchi M, Stumpf C, Daniel C, Bäuerle T, Schwarz M, Kerek F, Steinkasserer A, Zinser E, Achenbach S, and Dietel B
- Subjects
- Animals, Apolipoproteins E deficiency, Atherosclerosis drug therapy, Atherosclerosis pathology, Disease Models, Animal, Human Umbilical Vein Endothelial Cells drug effects, Human Umbilical Vein Endothelial Cells metabolism, Human Umbilical Vein Endothelial Cells pathology, Humans, Intercellular Adhesion Molecule-1 biosynthesis, Intercellular Adhesion Molecule-1 drug effects, Leukocytes drug effects, Leukocytes pathology, Mice, Mice, Knockout, NF-kappa B biosynthesis, NF-kappa B drug effects, NF-kappa B genetics, Atherosclerosis genetics, Biological Products pharmacology, Intercellular Adhesion Molecule-1 genetics, Leukocytes metabolism
- Abstract
Objective: Atherosclerosis is associated with chronic inflammatory responses of the arterial blood vessels. The previously observed protective effect of the MCS-18 substance against the initiation of atherosclerosis in a murine model was explained by its pronounced anti-inflammatory activity. Here, we investigated its impact on murine plaque progression in advanced atherosclerosis and on proatherogenic processes., Approach & Results: ApoE-deficient mice were fed a high-fat diet for 12 weeks to induce atherosclerosis, followed by normal chow and intraperitoneal injections of either MCS-18 (500 μg, n = 10) or saline (n = 10) twice a week for another 12 weeks. Plaque size was reduced in MCS-18 treated mice compared to controls (p = 0.001), which was associated with a reduced size of the lipid core (p = 0.01). There was a decrease in apoptotic cells (p = 0.02), endothelial ICAM-1 expression (p < 0.001), and macrophage density (p = 0.01) in the MCS-18 group. In addition, human and murine dendritic cells (DCs) and human umbilical vein endothelial cells (HUVECs) were treated with MCS-18 (50-200 μg/ml) to analyze cell migration and adhesion under flow conditions. MCS-18 reduced human (p = 0.01) and murine (p = 0.006) DC migration. Furthermore, adhesion of MCS-18-treated DCs to a HUVEC monolayer was decreased (p < 0.001). Compared to controls, CD209 (p < 0.001) and CCR7 (p = 0.003) expression was decreased in MCS-18-treated DCs, while in HUVECs lower levels of ICAM-1 (p < 0.001) and of phosphorylated NF-κB-p65 (p = 0.002) were observed. Blocking of ICAM-1 reduced DC adhesion (p < 0.001)., Conclusions: MCS-18 exhibits interesting therapeutic effects when applied in advanced murine atherosclerosis. Its antiatherogenic impact might be associated with a suppressed adhesion to the endothelium due to down-regulation of endothelial ICAM-1 expression., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
48. A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder.
- Author
-
Simpson TL, Malte CA, Dietel B, Tell D, Pocock I, Lyons R, Varon D, Raskind M, and Saxon AJ
- Subjects
- Adrenergic alpha-1 Receptor Antagonists adverse effects, Adult, Craving drug effects, Double-Blind Method, Female, Humans, Male, Middle Aged, Pilot Projects, Prazosin adverse effects, Sleep Stages drug effects, Treatment Outcome, Young Adult, Adrenergic alpha-1 Receptor Antagonists therapeutic use, Alcoholism complications, Alcoholism drug therapy, Prazosin therapeutic use, Stress Disorders, Post-Traumatic complications, Stress Disorders, Post-Traumatic drug therapy
- Abstract
Background: Posttraumatic stress disorder (PTSD) and alcohol dependence (AD) commonly co-occur and are associated with greater symptom severity and costs than either disorder alone. No pharmacologic interventions have been found to decrease both alcohol use and PTSD symptom severity relative to matched placebo. Prazosin, an alpha-1 adrenoreceptor antagonist, has demonstrated the efficacy of reducing PTSD and AD symptoms among individuals with one or the other disorder and may be useful in addressing comorbid PTSD/AD., Methods: Prazosin and matched placebo were compared in the context of an outpatient 6-week double-blind randomized controlled pilot trial involving 30 individuals with comorbid PTSD/AD. Medication was titrated to 4 mg q am, 4 mg q pm and 8 mg qhs by the end of week 2. Participants in both conditions received 5 medical management sessions. Information regarding alcohol use, craving, and PTSD was gathered daily using a telephone interactive voice response system., Results: Participants randomized to prazosin had a greater reduction in percent days drinking per week and percent days heavy drinking per week between baseline and week 6 than did placebo participants. No significant differences were detected within or between groups in change from weeks 1 to 6 in total PTSD symptoms. Participants in the prazosin condition reported drowsiness on significantly more days than those in the placebo condition., Conclusions: Consistent with the extant research evaluating medications for comorbid PTSD/AD, the current evaluation of prazosin also found decreased alcohol consumption but no medication effect on PTSD symptomatology., (Copyright © 2015 by the Research Society on Alcoholism.)
- Published
- 2015
- Full Text
- View/download PDF
49. Quantification of plaque lipids in the aortic root of ApoE-deficient mice by 3D DIXON magnetic resonance imaging in an ex vivo model.
- Author
-
Dietel B, Budinsky L, Kuehn C, Uder M, Achenbach S, and Hess A
- Subjects
- Animals, Aorta pathology, Disease Models, Animal, Imaging, Three-Dimensional, Lipids chemistry, Magnetic Resonance Imaging methods, Male, Mice, Aortic Diseases pathology, Apolipoproteins E deficiency, Plaque, Atherosclerotic pathology
- Abstract
Objectives: To establish a dedicated protocol for the three-dimensional (3D) quantification of plaque lipids in apolipoprotein E-deficient (apoE(-/-)) mice using ex vivo MRI., Methods: ApoE(-/-) mice were fed a high-fat diet (n = 10) or normal food (n = 10) for 3 months. Subsequently, a 3D FLASH MRI sequence was used to view the anatomy of the aortic root in the isolated hearts, where a 3D double-echo two-excitation pulse sequence (DIXON sequence) was used to selectively image plaque lipids. The vessel wall, lumen and plaque lipid volumes were quantified by MRI and histology for correlation analysis., Results: DIXON MRI allowed visualisation and accurate quantification of plaque lipids. When comparing the vessel wall, lumen and plaque lipid sizes in the aortic root, Bland-Altman and linear regression analysis revealed a close correlation between MRI results and the histological data both on a slice-by-slice basis and of the volumetric measurements (vessel wall: r (2) = 0.775, p < 0.001; vessel lumen: r (2) = 0.875; p = 0.002; plaque lipid: r (2) = 0.819, p = 0.003)., Conclusions: The combination of 3D FLASH and DIXON-sequence MRI permits an accurate ex vivo assessment of the investigated plaque parameters in the aortic root of mice, particularly the lipid content.
- Published
- 2015
- Full Text
- View/download PDF
50. Shell matters: Magnetic targeting of SPIONs and in vitro effects on endothelial and monocytic cell function.
- Author
-
Matuszak J, Dörfler P, Zaloga J, Unterweger H, Lyer S, Dietel B, Alexiou C, and Cicha I
- Subjects
- Cell Survival, Cells, Cultured, Ferric Compounds, Humans, Magnetics, Ferrosoferric Oxide, Human Umbilical Vein Endothelial Cells cytology, Metal Nanoparticles, Monocytes cytology
- Abstract
Superparamagnetic iron oxide nanoparticles (SPIONs) are versatile and easily functionalized agents with high potential for diagnostic and therapeutic intravascular applications. In this study, we analyzed the responses of endothelial (ECs) and monocytic cells to three different types of SPIONs, in order to assess the influence of physico-chemical properties on the biological reactions to SPIONs. The following formulations were used: (1) Lauric acid-coated and BSA-stabilized SPION-1,(2) Lauric acid/BSA-coated SPION-2 and (3) dextran-coated SPION-3. SPION-1 were strongly internalized by ECs and reduced their viability in static conditions. Additionally, they had a dose-dependent inhibitory effect on monocytic cell chemotaxis to MCP-1, but did not affect monocytic cell recruitment by ECs. SPION-2 uptake was less pronounced, both in ECs and monocytic cells, and these particles were better tolerated by the vascular cells. Not being internalized by endothelial or monocytic cells, SPION-3 did not induce relevant effects on cell viability, motility or endothelial-monocytic cell interactions.Taken together, localized accumulation of circulating SPION under physiologic-like flow conditions and their cellular uptake depends on the physicochemical characteristics. Our findings suggest that SPION-2 are suitable for magnetic targeting of atherosclerotic plaques. Due to their excellent biocompatibility and low internalization, SPION-3 may represent a suitable imaging agent for intravascular applications.
- Published
- 2015
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.