TY - JOUR A1 - Edgecock, T. R. A1 - Caretta, O. A1 - Davenne, T. A1 - Densam, C. A1 - Fitton, M. A1 - Kelliher, D. A1 - Loveridge, P. A1 - Machida, S. A1 - Prior, C. A1 - Rogers, C. A1 - Rooney, M. A1 - Thomason, J. A1 - Wilcox, D. A1 - Wildner, E. A1 - Efthymiopoulos, I. A1 - Garoby, R. A1 - Gilardoni, S. A1 - Hansen, C. A1 - Benedetto, E. A1 - Jensen, E. A1 - Kosmicki, A. A1 - Martini, M. A1 - Osborne, J. A1 - Prior, G. A1 - Stora, T. A1 - Melo Mendonca, T. A1 - Vlachoudis, V. A1 - Waaijer, C. A1 - Cupial, P. A1 - Chancé, A. A1 - Longhin, A. A1 - Payet, J. A1 - Zito, M. A1 - Baussan, E. A1 - Bobeth, C. A1 - Bouquerel, E. A1 - Dracos, M. A1 - Gaudiot, G. A1 - Lepers, B. A1 - Osswald, F. A1 - Poussot, P. A1 - Vassilopoulos, N. A1 - Wurtz, J. A1 - Zeter, V. A1 - Bielski, J. A1 - Kozien, M. A1 - Lacny, L. A1 - Skoczen, B. A1 - Szybinski, B. A1 - Ustrycka, A. A1 - Wroblewski, A. A1 - Marie-Jeanne, M. A1 - Balint, P. A1 - Fourel, C. A1 - Giraud, J. A1 - Jacob, J. A1 - Lamy, T. A1 - Latrasse, L. A1 - Sortais, P. A1 - Thuillier, T. A1 - Mitrofanov, S. A1 - Loiselet, M. A1 - Keutgen, Th. A1 - Delbar, Th. A1 - Debray, F. A1 - Trophine, C. A1 - Veys, S. A1 - Daversin, C. A1 - Zorin, V. A1 - Izotov, I. A1 - Skalyga, V. A1 - Burt, G. A1 - Dexter, A. C. A1 - Kravchuk, V. L. A1 - Marchi, T. A1 - Cinausero, M. A1 - Gramegna, F. A1 - De Angelis, G. A1 - Prete, G. A1 - Collazuol, G. A1 - Laveder, M. A1 - Mazzocco, M. A1 - Mezzetto, M. A1 - Signorini, C. A1 - Vardaci, E. A1 - Di Nitto, A. A1 - Brondi, A. A1 - La Rana, G. A1 - Migliozzi, P. A1 - Moro, R. A1 - Palladino, V. A1 - Gelli, N. A1 - Berkovits, D. A1 - Hass, M. A1 - Hirsh, T. Y. A1 - Schuhmann, M. A1 - Stahl, A. A1 - Wehner, J. A1 - Bross, A. A1 - Kopp, J. A1 - Neuffer, D. A1 - Wands, R. A1 - Bayes, R. A1 - Laing, A. A1 - Soler, P. A1 - Agarwalla, S. K. A1 - Cervera Villanueva, A. A1 - Donini, A. A1 - Ghosh, T. A1 - Gómez Cadenas, J. J. A1 - Hernández, P. A1 - Martín-Albo, J. A1 - Mena, O. A1 - Burguet-Castell, J. A1 - Agostino, L. A1 - Buizza-Avanzini, M. A1 - Marafini, M. A1 - Patzak, T. A1 - Tonazzo, A. A1 - Duchesneau, D. A1 - Mosca, L. A1 - Bogomilov, M. A1 - Karadzhov, Y. A1 - Matev, R. A1 - Tsenov, R. A1 - Akhmedov, E. A1 - Blennow, M. A1 - Lindner, M. A1 - Schwetz, T. A1 - Fernández Martinez, E. A1 - Maltoni, M. A1 - Menéndez, J. A1 - Giunti, C. A1 - González García, M. C. A1 - Salvado, J. A1 - Coloma, P. A1 - Huber, P. A1 - Li, T. A1 - López Pavón, J. A1 - Orme, C. A1 - Pascoli, S. A1 - Meloni, D. A1 - Tang, J. A1 - Winter, W. A1 - Ohlsson, T. A1 - Zhang, H. A1 - Scotto-Lavina, L. A1 - Terranova, F. A1 - Bonesini, M. A1 - Tortora, L. A1 - Alekou, A. A1 - Aslaninejad, M. A1 - Bontoiu, C. A1 - Kurup, A. A1 - Jenner, L. J. A1 - Long, K. A1 - Pasternak, J. A1 - Pozimski, J. A1 - Back, J. J. A1 - Harrison, P. A1 - Beard, K. A1 - Bogacz, A. A1 - Berg, J. S. A1 - Stratakis, D. A1 - Witte, H. A1 - Snopok, P. A1 - Bliss, N. A1 - Cordwell, M. A1 - Moss, A. A1 - Pattalwar, S. A1 - Apollonio, M. T1 - High intensity neutrino oscillation facilities in Europe JF - Physical Review Special Topics-Accelerators and Beams N2 - The EUROnu project has studied three possible options for future, high intensity neutrino oscillation facilities in Europe. The first is a Super Beam, in which the neutrinos come from the decay of pions created by bombarding targets with a 4 MW proton beam from the CERN High Power Superconducting Proton Linac. The far detector for this facility is the 500 kt MEMPHYS water Cherenkov, located in the Frejus tunnel. The second facility is the Neutrino Factory, in which the neutrinos come from the decay of mu(+) and mu(-) beams in a storage ring. The far detector in this case is a 100 kt magnetized iron neutrino detector at a baseline of 2000 km. The third option is a Beta Beam, in which the neutrinos come from the decay of beta emitting isotopes, in particular He-6 and Ne-18, also stored in a ring. The far detector is also the MEMPHYS detector in the Frejus tunnel. EUROnu has undertaken conceptual designs of these facilities and studied the performance of the detectors. Based on this, it has determined the physics reach of each facility, in particular for the measurement of CP violation in the lepton sector, and estimated the cost of construction. These have demonstrated that the best facility to build is the Neutrino Factory. However, if a powerful proton driver is constructed for another purpose or if the MEMPHYS detector is built for astroparticle physics, the Super Beam also becomes very attractive. KW - EMMA KW - beta-beam Y1 - 2013 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-126611 VL - 16 IS - 2 ER - TY - JOUR A1 - Kleinschnitz, Christoph A1 - Grund, Henrike A1 - Wingler, Kirstin A1 - Armitage, Melanie E. A1 - Jones, Emma A1 - Mittal, Manish A1 - Barit, David A1 - Schwarz, Tobias A1 - Geis, Christian A1 - Kraft, Peter A1 - Barthel, Konstanze A1 - Schuhmann, Michael K. A1 - Herrmann, Alexander M. A1 - Meuth, Sven G. A1 - Stoll, Guido A1 - Meurer, Sabine A1 - Schrewe, Anja A1 - Becker, Lore A1 - Gailus-Durner, Valerie A1 - Fuchs, Helmut A1 - Klopstock, Thomas A1 - de Angelis, Martin Hrabe A1 - Jandeleit-Dahm, Karin A1 - Shah, Ajay M. A1 - Weissmann, Norbert A1 - Schmidt, Harald H. H. W. T1 - Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration N2 - Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox42/2) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox42/2 mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy. KW - Schlaganfall Y1 - 2010 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-68416 ER -