191 results on '"W. Solbach"'
Search Results
2. 微生物群对银屑病的作用:从疾病描述到治疗预测?
- Author
-
E.A. Langan, C.E.M. Griffiths, W. Solbach, J.K. Knobloch, D. Zillikens, and D. Thaҫi
- Subjects
Dermatology - Published
- 2018
- Full Text
- View/download PDF
3. The role of the microbiome in psoriasis: moving from disease description to treatment prediction?
- Author
-
E.A. Langan, C.E.M. Griffiths, W. Solbach, J.K. Knobloch, D. Zillikens, and D. Thaҫi
- Subjects
Dermatology - Published
- 2018
- Full Text
- View/download PDF
4. Tinea imbricata in Papua-Neuguinea: Behandlungsversuch mit Griseofulvin und Haloprogin bei einer Population des Gogol-Valley, Madang Province
- Author
-
J. Mattar and W. Solbach
- Subjects
Gynecology ,medicine.medical_specialty ,business.industry ,Complete remission ,New guinea ,Dermatology ,General Medicine ,medicine.disease ,Griseofulvin ,Skin symptoms ,Surgery ,chemistry.chemical_compound ,Infectious Diseases ,chemistry ,medicine ,Age distribution ,Tinea imbricata ,business ,Skin lesion ,Haloprogin ,medicine.drug - Abstract
Zusammenfassung: In zwei Dorfern des Gogol Valley (Papua-Neuguinea) wurden satliche 47 an Tinea imbricata erkrankten Personen erfas, wovon 39 einer Griseofuhin®- bzw. Mycan-den®-Therapie oder Kombination zugefuhrt wurden. Die Zuweisung zu den unterschiedlichen Behandlungsgruppen erfolgte anhand des Alters und des prozentualen Befalls der Korperoberflache. Die Therapiedauer betrug maximal 4 Wochen, der Beobachtungszeitraum insgesamt 6 Wochen. Eine Remission des Hautbefalls erfolgte fur beide Therapeutika von der 2. Behand-lungswoche an. Rezidive traten jedoch schon 1 Woche nach Therapieende auf. Es konnten Unterschiede in der Altersverteilung der Erkrankten in beiden Dorfern festgestellt werden; ein Unterschied im dorflichen Hygienestandard wird als Ursache diskutiert. Die Besonderheiten einer antimykotischen Therapie in einem Entwicklungsland werden beschrieben. Summary: In two villages of the Gogol Valley (Papua New Guinea) all residents suffering from tinea imbricata (n=47) were registered. Thirty-nine of these were treated with either griseofulvin (Grisovin®) or topically with haloprogin (mycanden®) or with a combination of both drugs. Patients were allocated to the different treatment groups according to age and the percentage of spreading of skin lesions on the body surface. Duration of therapy was four weeks at maximum, the total observation period was six weeks. Treatment with both drugs yielded in complete remission of skin symptoms starting with the second week of treatment. However, relapse occured one week after cessation of therapy in most of the cases. There were differences in the age distribution of the patients in both hamlets; in addition, a difference in hygienic standard was observed. The special quality of antimycotic treatment in a developing country is described.
- Published
- 2009
- Full Text
- View/download PDF
5. Effekt einer neuen Oberfl�chenbehandlung von Intraokularlinsen aus Silikon durch ein Fluoralkylsilan auf das Adh�renzverhalten Endophthalmitis-relevanter Bakterien in vitro
- Author
-
A. Bunse, H. Ohgke, A. Kienast, W. Solbach, Hans Hoerauf, H. Laqua, R. Kämmerer, M. Klinger, D.-H. Menz, and Joachim Dr. Dresp
- Subjects
Propionibacteriaceae ,Micrococcaceae ,biology ,business.industry ,medicine.medical_treatment ,Intraocular lens ,biology.organism_classification ,Microbiology ,Ophthalmology ,Propionibacterium acnes ,Intraocular lenses ,Staphylococcus epidermidis ,Medicine ,business - Abstract
Einleitung Dynasilan® ist ein Fluoralkylsilan, das an aktive OH-Molekulgruppen der Linsenoberflache gebunden werden kann und somit eine neue Moglichkeit der Oberflachenmodifikation von Intraokularlinsen (IOL) aus Silikon bietet. In der vorliegenden Untersuchung wurde der Effekt dieser neuen Oberflachenbehandlung an Silikon-IOL auf das Adharenzverhalten zweier Endophthalmitis-relevanter Keime, Staphylococcus epidermidis und Propionibacterium acnes, in vitro uberpruft.
- Published
- 2003
- Full Text
- View/download PDF
6. [Surveillance reports on pathogens and their antibiotic resistance patterns - a recommendation for standardization]
- Author
-
P, Warnke, M, Aepfelbacher, H, Fickenscher, W, Solbach, I, Steinmetz, and A, Podbielski
- Subjects
Bacteriological Techniques ,Germany ,Population Surveillance ,Drug Resistance, Bacterial ,Practice Guidelines as Topic ,Humans ,Bacterial Infections ,Disease Notification - Abstract
Surveillance reports on infectious agents and their antibiotic resistance patterns as well as on the usage of antibiotics are now enforced by law for many medical institutions in Germany. However, specific practice-oriented recommendations concerning the appropriate extent and informative mode of presentation are lacking. This consensus statement resulted from the experience from five German university hospitals in handling data from infection epidemiology and in the various possibilities for the presentation of surveillance reports. The consensus statement provides recommendations for the preparation of the legally demanded surveillance reports, extending the existing regulations. The relevance of statements on frequency and quality of microbiological tests is included. Furthermore, modes for the standardization of the data analysis are suggested in order to achieve a regional and national comparability of the results on a high quality level, similarly to the established standardized surveillance of nosocomial infections. This consensus statement describes the form in which the legally enforced reports can be presented in an informative and standardized way in order to facilitate the deduction and realization of preventive measurements.
- Published
- 2014
7. Control of Leishmania major infection in BALB/c mice by inhibition of early lymphocyte entry into peripheral lymph nodes
- Author
-
T Laskay, I Wittmann, A Diefenbach, M Röllinghoff, and W Solbach
- Subjects
Immunology ,Immunology and Allergy - Abstract
A single i.p. injection with the anti-CD62L (anti-L-selectin) mAb Mel-14 before parasite challenge protected BALB/c mice from the otherwise lethal infection with Leishmania major. The Mel-14 mAb treatment resulted in a significant (>90%) decrease in cellularity of the popliteal lymph node (PLN) with a decrease in the proportion of CD4+ cells and an increase of the proportion of B220+ cells. Furthermore, both activated cells (CD25+ and CD69+) and cells of the memory phenotype (CD45RBdull CD44high) were significantly enriched in PLN from Mel-14-treated BALB/c mice. After infection with L. major, the otherwise massive cellular infiltration in the draining PLN was completely blocked in the Mel-14-treated mice, and in these animals the high representation of both activated and memory cells in PLN remained characteristic for the first days of infection. The protective effect was found to be associated with a markedly increased production of IFN-gamma and with a decrease in IL-4 production upon restimulation of PLN and spleen cells with L. major Ag in vitro. The cured mice were found to be resistant against a secondary challenge with the parasites. These data suggest that the induction of a nonprotective Th2 response to L. major is associated with the entry of lymphocytes from the recirculating pool into the draining LN. The Mel-14-induced changes in the lymphoid microenvironment of the draining peripheral LN appear to favor the development of a protective Th1 cell-mediated immune response against the parasite.
- Published
- 1997
- Full Text
- View/download PDF
8. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain
- Author
-
H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. Zucconl, Javier Muruzabal, R. R. Allen, R. Rivolta, K. Haugaard, A. Nespolo, K. Hoang-Xuang, G. Bussone, T. Avramidis, E. Corsini, Christiana Franke, T. Vinogradova, H. Boot, K. Vestergaard, G. H. Jansen, N. Argentino, M. Raltzig, W. Linssen, Mark B. Pepys, P. Roblot, L. Lauritzen, E. Fainardi, D. Morin, T. X. Arbizu Urdiain, J. Wollenhaupt, S. Bostantjopoulou, G. Pavesi, A. D. Forman, Giovanni Fabbrini, D. Jean, J. J. Archelos, M. I. Blanchs, M. Del Gobbo, Anna Carla Turconi, Ch. Derouesné, Elio Scarpini, A. Visbeck, P. Castejon, J. P. Renou, F. Mounier-Vehier, G. Potagas, Ch. Duyckaerts, A. Filla, R. Schneider, G. Ronen, K. Nagata, J. P. Vedel, A. Henneberg, G. van Melle, C. Baratti, H. Knott, M. C. Prevett, A. Bes, B. Metin, Jos V. Reempts, L. Martorell, Mefkure Eraksoy, H. O. Handwerker, D. S. Younger, O. Oktem, D. Frongillo, C. Soriano-Soriano, L. Niehaus, F. Zipp, A. Tartaro, S Newman, R. H. Browne, P. Davous, R. Sanchez, M. Muros, M. E. Kornhuber, A. Lavarone, M. Mohr, M. R. Garcia, S. Russell, H. Kellar-Wood, M. R. Tola, B. Ostermeyer, Ch. Tzekov, K. Sartor, E. B. Ringelstein, P. P. Gazzaniga, Paul Krack, H. Fidaner, H. Rico, T. Dbaiss, F. Alameda, E. Torchiana, L. Rumbach, I. Charques, J. M. Bogaard, C. D. Frith, L. J. Rappelle, R. Brenner, A. Joutel, K. Fuxe, G. HÄcker, M. J. Blaser, J. Valls-SolÇ, G. Ulm, M. Alberdi, A. Bock, F. W. Bertelsmann, U. Wieshmann, J. Visa, J. R. Lupski, D. D'Amico, L. M. P. Ramos, A. A. Vanderbark, R. Horn, M. Warmuth, Dietmar Kühne, Mark S. Palmer, C. Ehrenheim, E. Canga, S. Viola, O. Scarpino, P. Naldi, R. Almeida, A. A. Raymond, J. Gamez, Stephan Arnold, A. DiGiovanni, J. Dalmau, C. C. Chari, H. F. Beer, J. C. Koetsier, J. Iriarte, E. Yunis, J. Casadevall, E. Le Guern, E. Stenager, S. R. Benbadis, J. M. Warter, F. Burklin, I. Theodorou, L. Johannesen, G. A. Graveland, X. Leclerc, I. Vecchio, L. Ozelius, G. Nicoletti, R. K. Gherardi, E. Esperet, M. L. Delodovici, F. Cattin, F. Paiau, Giorgio Sacilotto, C. A. J. Broere, D. Chavdarov, J. P. Willmer, C. H. Hawkes, Th. Naegele, E. Ellie, E. Dartigues, M. J. Guardiola, S. Hesse, Z. Levic, Marco Rovaris, P. Saugeir-Veber, B. A. Yaqub, H. F. Durwen, R. Larumbe, J. Ballabrina, M. Sendtner, J. Röther, M. Horstink, C. Kluglein, M.P. Montesi, H. Apaydin, J. Montoya, E. Waubant, Ch. Verellen-Dunoulin, A. Nicolai, J. Lopez-Delval, R. Lemon, G. Cantinho, E. Granieri, A. Zeviani, Wolfgang H. Oertel, U. Ficola, V. Di Piero, V. Fragola, K. Sabev, M. V. Guitera, I. Turki, F. Bolgert, P. Ingrand, J. M. Gobernado, L. M. E. Grimaldi, S. Baybas, B. Eymard, Y. Rolland, Y. Robitaille, Ta. Pampols, P. J. Koehler, A. Carroacedo, J. Vilchez, S. Di Vittorio, I. R. Rise, T. Nagy, M. Kuffner, E. Palazzini, A. Ott, J. Pruim, T. X. Arbizu, E. Manetti, C. Cervera, S. Felber, G. Gursoy, J. Scholz, G. A. Buscaino, M. S. Chen, A. Pascual, J. Hazan, J. U. Gajda, J. G. Cea, G. Bottini, G. Damalik, F. Le Doze, G. Bonaldi, J. M. Hew, C. Messina, A. M. Kennedy, J. M. Carney, N. M. F. Murray, M. Parent, M. Koepp, V. Dimova, D. De Leo, K. Jellinger, G. Salemi, S. Mientus, M. L. Hansen, F. Mazzucchelli, J. Vieth, M. Mauri, E. Bartels, L. Johannsen, C. Humphreys, J. Emile, D. N. Landon, E. Kansu, R. Sanchez-Pernaute, Rsj Frackowiak, M. Gonzalez Torres, L. Oller, C. Machedo, J. Kother, M. Billiard, H. Durak, T. Schindler, A. Frank, A. Uncini, A. Sbriccoli, C. Farinas, D. W. Paty, N. Fast, A. T. Zangaladze, A. Kerkhofs, J. M. Pino Garcia, I. De la Fuente, B. Marini, L. Gomez, I. Rubio, Alessandra Bardoni, C. Brodie, P. Acin, U. Sliwka, S. A. Hawkins, S. Tardieu, F. Vitullo, J. M. Pereira Monteino, R. Gagliardi, T. Jezewski, A. Cano, T. Lempert, F. Abad Alegria, G. Rotondo, D. Ince, C. Martinez Parra, Y. Huang, H. Luders, Y. Steinvil, F. G. A. Van Der Meche, R. Bianchi, A. Sanchez, T. Sevilla, J. M. Ketelslegers, A. Domzal-Stryga, M. Pandolfo, M. O. Josse, K. W. Neff, I. Blanco, G. W. Bruyn, O. W. Witte, J. L. Thibault, G. Andersen, J. Pariset, A. Marcone, R. J. M. Lane, A. Hofman, M. Verin, T. Matilla, P. Bedoucha, J. Roche, M. Lai, M. Collard, A. Ugarte, F. Gallecho, D. Silbersweig, C. Kennard, J. P. Azulay, T. W. Ho, P. L. I. Dellemijn, R. Girardello, F. Baas, B. Voss, F. Rozenberg, E. M. Brocker, V. Stanev, A. A. J. Soeterboek, A. Marra, A. Rey, E. Ertem, M. Sawradewicz-Rybak, J. De Keyser, P. Cavallari, F. Proust, Y. Chevalier, H. C. Hansen, D. Leys, C. A. Davie, K. Hoang-Xuan, C. Bairati, H. van Crevel, Thomas T. Warner, B. Bompais, A. Dobbeleir, T Campbell, C. Macko, C. J. M. Klijn, M. Dussallant, T. P. Berlit, W. Rozenbaum, M. J. van den Bent, W. A. Rocca, M. Muller, H. Hundemer, U. Zifko, M. Campera, F. Drislane, D. Ranoux, T. M. Kloss, Anil Kumar, I. Ruolt, C. Bargnani, B. Marescau, N. A. Losseff, S. Notermans, B. Kint, E. T. Burke, C. Aykut, J. Matias Guiu, P. Maquet, T. Drogendijk, M. Leone, K. von Ammon, M. Pepeliarska, C. Prados, L. DiGiamberardino, T. Logtenberg, G. Lenoir, I. Castaldo, Damhaut, M. Radionova, G. Sirabian, R. Navon, Giovanni Antonini, K. Al Moutaery, E. Chamas, R. Schönhuber, M. Giannini, B. Debilly, I. Labatut, H. Henon, J. A. Egido, M. Baudrimont, J. N. Lorenzo, J. E. C. Bromberg, R. Antonacci, J. J. Vilchez, T. Moulin, B. Rautenstrauss, Giovanni Meola, J. Noth, S Mammi, P. Laforet, F. Lopez, C. Gehring, S. Bort, G. Rancurel, D. Decamps, S. Kostadinova, Y. Shapira, B. Neundoerfer, D. Chavrot, M. Solimena, J. P. Salier, W. Deberdt, R. Hoff-Jörgensen, A. Messina, S. Meairs, G. Rosoklija, E. Nelis, I. Bertran, C. Ertekin, J. Lohmeyer, Mitermayer Galvao dos Reis, L. Calo, E. Maccagnano, A. P. Hays, J. Verlooy, M. G. Forno, T. Blanco, L. Bail, Gabriella Silvestri, J. Montero, F. Bertrand, R. T. Ghnassia, C. Besses, T. Sereghy, F. Shalit, G. Bogliun, S. Braghi, St. Baykouchev, C. Franke, A. Lasa, L. C. Archard, J. Kriebel, S. Shaunak, M. Nocito, Alexander Tsiskaridze, E. Manfredini, T. Seigal, David G. Gadian, M. Barlas, J. D. Degos, C. Seeber, J. Caemert, J. L. Mas, R. B. Pepinsky, M. G. D'Angelo, N. Baumann, S. Yorifuji, H. P. Endtz, M. A. Cassatella, R. A. C. Hughes, V. Golzi, A. Bittencourt, A. Ferreira, M. Sanson, C. Alper, M. Vermeulen, M. A. A. van Walderveen, E. Alexiou, C. H. Lucas, M. Fiorelli, Y. N. Debbink, R. Gil, S. Congia, T. Banerjee, J. M. Bouchard, A. N. Pinto, A. Ceballos-Baumann, G. Grollier, P. I. M. Schmitz, M. D. Catata, N. Lahat, N. S. Rao, P. Papathanasopoulos, J. Valls-Solé, D. Claus, G. Schroter, A. Castro, C. Videbaek, R. Martinez Dreke, A. D. Platts, M. Hermesl, A. C. PeÇanha-Martins, M. Cardoso Silva, P. Masnou, M. J. A. Tanner, Ch. Confavreux, B. Mishu, H. Rasmussen, L. Valenciano, Carlo Pozzilli, S. W. Li, V. Salzman, Y. Vashtang, Massimo Franceschi, M. Severo, G. Deuschl, S. Setien, G. Mariani, A. Protti, J. Castillo, M. J. B. Taphoorn, M. Frontali, I. Milonas, D. Decoq, J. A. Navarro, S. Castellvi-Pel, C. Ertikin, M. Urtasun, Y. Lajat, B. E. Kendall, E. Verdu, B. Gueguen, E. Boisen, R. Couderc, A Danek, JM Stevens, F. Nicoli, L. Feltri, M. L. Vazquez-Andre, J. A. Morgan-Hughes, L. D'Angelo, F. Y. Liew, L. F. Pascual, J. Patrignani Ochoa, Vittorio Martinelli, J. Cophignon, L. Zhang, S. Martin, J. F. Meder, H. C. Buschmann, L. Bertin, J. van Gijn, A. Barreiro, A. Cools, C. Leon, A. Berod, E. A. Anllo, E. Zanette, L. Petrov, R. Barona, B. Gallicchio, P. J. Cozzone, N. Diederich, G. Cancel, L. Schelosky, P. Orizaola, K. Yulug, S. Ozer, Valeria A. Sansone, B. Guiraud-Chaumeil, K. Voigt, P. Labauge, M. Eoli, J. Zhu, J. Aguirre, M. Ferrarini, B. Zyluk, E. Planas, A. Cadilha, C. Tortorella, H. Bismuth, C. E. Counsell, A. Laun, A. Ferlini, Rio J. Montalban, N. Biary, L. Becker, M. Fardeau, M. Poloni, V. M. S. de Bruin, C. Fornada, J. Barros, E. Ganzmann, E. Touze, D. Wallach, J. Peila, H. Fujimura, M. T. Iba-Zizen, G. Macchi, C. Villoslada, R. Gouider, Ph. Rondepierre, P. Grummich, P. Chiodi, C. Conte, M. Michels, P. Annunziata, G. Semana, C. Sommer, J. Vajsar, D. Zekin, J. Kulisevsky, David G. Munoz, B. Jacotot, M. Magoni, A. Luxen, T. Garcia-Silva, S. Di Cesare, Christophe Tzourio, M. Gomori, I. Picomell, L. Santoro, F. Villa, Giovanni Pennisi, T. Ribalta, J. M. Molto, L. Marzorati, P. Loiseau, F. Gemignani, A. Gironell, J. Wissel, A. Prusinski, F. Cailloux, P. Villanueva-Hemandez, P. Cozzone, T. Del Ser, J. Sans-Sabrafen, M. Zappia, P. W. A. Willems, G. Tchernia, D. Gardeur, R. Bauer, F. Palomo, H. Metz, S. Lamoureux, C. Chastang, I. Reinhard, A. Goldfarb, S. Harder, Jordi Río, C. Ozkara, E. Tekinsoy, P. Vontobell, J. De Recondo, M. Rabasa, L. Lacomblez, F. Boon, Dgt Thomas, V. Palma, Renato Mantegazza, A. Dervis, M. Nueckel, B. YalÇinerner, I. Duran, G. Dalla Volta, A. Zubimendi, J. Pinheiro, A. Marbini, Xavier Montalban, H. Wekerle, X. Pereira Monteino, F. Crespo, F. Koskas, N. Battistini, C. Ruiz, H. Offner, J. de Pommery, P. Kanovsky, J. Y. Barnett, J. Pardo, G. Tomei, R. Rene, H. M. Lokhorst, P. Thajeb, H. Bilgin, D. McGehee, R. Fahsold, L. Morgante, Katie Sidle, C. Delwaide, M. N. Diaye, P. H. Rice, A. Creange, C. Sabev, K. Stephan, K. WeilBenborn, G. Magnani, L. Grymonprez, F. Cardellach, M. Kaps, N. G. Meco, F. Vega, V. Bonifati, A. Desomer, M. Baldy-Moulinier, G. Kvale, F. J. Authier, B. Yegen, T. Ho, J. M. Rozet, E. A. Cabanis, L. Bruce, L. Ambrosoli, M. A. Petrella, M. Hernandez, P. Timmings, H. B. van der Worp, F. Mahieux, A. Urbano-Marquez, D. A. Krendel, A. A. Garcia, R. Divari, R. Michalowicz, M. R. Piedmonte, M. Bondavalli, M. Zanca, P. F. Ippel, Onofre Combarros, B. Tavitian, E. Hirsch, I. Anastasopoulos, A. Roses, A. Köhler, P. Vienna, V. Timmerman, P. Sergi, F. Cornelio, A. Di Pasquale, R. Verleger, S. Castellvirel, J. Proano, B. van Moll, F. Rubio, W. Hacke, I. Lavenu, L. Zetta, M. W. Tas, N. Bittmann, M. Bonamini, O. R. Hommes, V. Dousset, N. Afsar, S. Belal, R. R. Myers, J. Goes, Giuseppe Vita, E. Clementi, V. G. Karepov, M. Jueptner, A Vincent, P. Emmrich, Th. Heb, A. Caballo, J. Gallego, T. Mokrusch, C. Perla, L. Gebuhrer, O. Titlbach, Alessandro Prelle, A. Czlonkowska, M. Russo, D. Hadjiev, T. S. Chkhikvishvili, M. Oehlschlager, G. Becker, I. Günther, E. N. Stenager, J. Garcia Agundez, J. Casademont, J. Batlle, S. Podobnik-Sarkanji, C. Alonso-Villaverde, B. Delaguillaume, B. Genc, B. Mazoyer, A. Rodriguez-Al-barino, Ch. Hilger, B. Ferrero, R. Price, W. Grisold, L. Fuhry, D. Oulbani, D. Ewing, A. Petkov, W. Walther, A. Gokyigit, John Newsom-Davis, J. Tayot, D. Seliak, G. Pelliccioni, D. Campagne, K. Kessler, F. Boureau, D. Perani, J. P. N'Guyen, N. Tchalucova, B. A. Antin-Ozerkis, C. Lacroix, B. D. Aronovich, I. H. Jenkins, E. A. dos Reis, M. Hortells, H. M. Meinck, H. Ch. Buschmann, S. C. J. M. Jacobs, T. Wetter, P. Creissard, N. Martinez, J. Weidenfeldl, H. J. Sturenburg, G. Damlacik, V. Gracia, J. C. Turpin, A. Pou-Serradell, J. P. Vincent, T. Gagoshidze, U. Ozkutlu, M. McLeod, K. Siegfried, I. Tchaoussoglou, J. Hildebrand, S. Kowalska, M. C. Picot, G. Galardin, L. Crevits, F. Andreetta, S. Larumbe-Lobalde, G. de la Sierra, J. C. Alvarez-Cermeno, R. J. Seitz, P. L. Oey, L. Ptacek, A. M. J. Paans, A. Wirrwar, A. Schmied, J. Uilchez, H. Tounsi, D. Hipola, V. Avoledo, Y. Hirata, P. Vermersch, T. M. Aisonobe, J. Valls-SoIè, H. Staunton, J. Dichgans, R. Karabudak, I. Dones, G. Porta, E. Janssens, Maria Martinez, J. M. Fernandez-Real, R. Villagra, Y. Yoshino, C. Kabus, K. Schimrigk, I. Girard-Buttaz, F. Piccoli, F. Aichner, P. Zuchegna, S. M. Al Deeb, F. Bono, N. Busquets, A. Jobert, Patrizia Ciscato, M. Martin, L. Polman, S. Darbra, V. Le Cam-Duchez, F. Baldissera, B. Baykan-Kurt, D. Guez, M. Bratoeva, H. Matsui, M. Mila, H. Perron, L. Bjorge, G. Husby, Steven T. DeKosky, D. R. Cornblath, J. M. Gabriel, J. J. Poza, Y. Wu, A. Toscano, R. P. Kleyweg, J. Kuhnen, S. O. Confort-Gouny, A. Barcelo, A. M. Conti, C. Fiol, C. Steichen-Wiehn, J. Rodes, M. Cavenaile, C. Vedeler, M. Drlicek, C. Argentino, M. L. Peris, A. Cervello, A. Z. GinaÏ, S. Yancheva, D. Passingham, S. Aoba, D. L. Lopez, T. Rechlin, K. Sonka, L. Grazzi, V. Folnegovic-Smalc, Maurizio Moggio, S. Rivaud, F. G. I. Jennekens, C. H. Hartard, H. Meierkord, G. Stocklin, M. D. Catala, W. C. McKay, E. Salmon, C. Navarro, I. Pastor, L. Canafoglia, M. De Braekeleer, P. K. Thomas, C. Mocellini, C. Pierre-Jerome, M. C. Dalakas, P. Pollak, M. Levivier, Niall Quinn, G. E. Rivolta, Z. Tunca, H. Zeumer, J. Garcia Tena, St. Guily, P. Gaudray, Johannes Kornhuber, V. Petrunjashev, R. Montesanti, R. J. Abbott, H. Petit, G. Kiteva-Trencevska, F. Carletto, C. Ramo, I. M. Pino, P. Beau, G. F. Mennuni, F. Moschian, F. Meneghini, B. Zdziarska, B. Fontaine, C. Stephens, G. Meco, K. Reiners, G. Badlan, M. Sessa, I. Degaey, S. M. Hassan, C. Albani, F. Caroeller, M. Schroeder, G. Savettieri, A. Novelletto, R. Kurita, P. Oschmann, I. Plaza, M. Oliveres, Simone Spuler, A. Molins, M. Schwab, J. R. Kalden, C. P. Gennaula, Y. Baklan, O. Picard, J. M. Léger, B. Mokri, E. Ghidoni, M. Jacob, D. Deplanque, W. JÄnisch, C. De Andres, P. De Deyn, G. Guomundsson, B. Herron, J. Barado, J. L. Gastaut, Guglielmo Scarlato, F. Poron, Nicola Jones, H. Teisserenc, C. P. Hawkins, A. J. Steck, H. C. Chandler, S. Blanc, J. H. Faiss, Jm. Soler Insa, I. Sarova-Ponchas, M. Malberin, A. Sackmann, G. De Vuono, K. Kaiser-Rub, K. Badhia, E. Szwabowska-Orzeszko, S. Ramm, C. Jodice, G. Franck, J. Marta-Moreno, R. Sciolla, C. Fritz, A. Attaccalite, F. Weber, E. Neuman, M. Cannata, A. Rodriguez, I. Nachainkin, R. Raffaele, T. S. Yu, N. Losseff, E. Fabrizio, C. Khati, M. Keipes, M. P. Ortega, M. Ramos-Alvarez, E. Brambilla, A. Tarasov, K. H. Wollinsky, O. B. Paulson, F. Boller, G. Bozzato, H. Wagnur, R. Canton, D. Testa, E. Kutluaye, M. Calopa, D. Smadja, G. Malatesta, F. Baggi, A. Stracciari, G. Daral, G. Avanzini, J. Perret, J. Arenas, P. Boon, I. Gomes, A. Vortmeyer, P. Cesaro, S. Venz, E. Bernd Ringelstein, N. Milani, D. Laplane, P. Seibel, E. Tournier-Lasserve, Alexis Brice, L. Motti, E. Wascher, R. J. Abbot, F. Miralles, A. Turon, P. De Camilli, G. Luz, G. C. Guazzi, S. Tekin, F. Lesoin, T. Kryst, N. Lannoy, F. Gerstenbrand, S. Ballivet, H. A. M. van Diemen, J. Lopez-ArLandis, P. Bell, A. Silvani, M. A. Garcia, S. Vorstrup, D. Langdon, S. Ueno, B. Sander, V. Ozurk, C. Gurses, P. Berlit, J. M. Martinez-Lage, M. Treacy, S. O. Rodiek, S. Cherninkova, J. Grimaud, P. Marozzi, K. Hasert, S. Goldman, S. H. Ingwersen, A. Taghavy, T. Roig, R. Harper, I. Sarova-Pinchas, Anthony H.V. Schapira, R. Lebtahi, A. Vidaller, B. Stankov, D. Link, J. p. Malin, V. Petrova, Ludwig Kappos, J. L. Ochoa, T. Torbergsen, M. Carpo, M. Donato, Simon Shorvon, J. Mieszkowski, J. Perez-Serra, Raymond Voltz, G. Comi, S. Rafique, A. Perez-Sempere, N. Khalfallah, S. Bailleul, M. Borgers, S. Banfi, S. Mossman, A. Laihinen, G. Filippini, R. A. Grunewald, E. Stern, H. D. Herrmann, A. G. Droogan, P. Xue, A. Grilo, L. La Mantia, J. H. J. Wokke, S. Pizzul, Kie Kian Ang, S. Rapaport, W. Szaplyko, B. Romero, P. Brunet, A. Albanese, C. Davie, V. Crespi, F. Birklein, H. Sharif, L. Jose, D. Auer, N. Heye, Martin N. Rossor, C. E. Henderson, M. J. Koepp, J. Rubio, P. L. Baron, S. Mahal, Juha O. Rinne, J. I. Emparanza, S. E. C. Davies, Frederik Barkhof, M. Riva, R. E. Brenner, B. A. Pope, Lemaire, E. Dupont, D. Ulbricht, G. C. Pastorino, R. Retska, E. Chroni, A. Danielli, V. Malashkhia, T. Canet, J. C. Garcia-Valdecasas, J. Serena, R. A. Pfeiffer, B. Wirk, B. Muzzetto, V. Caruso, M. L. Giros, A. Ming Wang, E. L. E. Guern, F. Bille-Turg, Y. Satoh, C. H. Franke, M. Ait-Kaci-Ahmed, D. Genis, T. Pasierski, D. Riva, M. Panisset, A. Chamorro, P.A. van Doorn, S. Schellong, H. Hamer, F. Durif, P. Krauseneck, Y. Bahou, B. A. Pickut, M. Rijnites, H. Nyland, G. Jager, L. L. Serra, A. Rohl, X. P. Li, O. Arena, Hubert Kwieciński, N. Milpied, M. C. Bourdel, S. Assami, L. Law, J. Moszkowski, J. W. Thorpe, M. Aguennouz, R. Martin, D. Hoffmann, P. Morris, A. Destée, D. J. Charron, U. Senin, A. P. SempereE, M. Dreyfus, A. L. Benabid, M. Gomez, S. Heindle, M. C. Morel-Kopp, M. Hennerici, A. I. Santos, M. Djannelidze, N. Artemis, John Collinge, T. Rundek, M. Y. Voloshin, P. de Castro, Th. Wiethege, D. A. S. Compston, D. Schiffer, A. J. Hughes, D. Jimenez, V. Parlato, A. Papadimitriou, J. M. Gergaud, R. Sterzi, J. Arpa, G. de Pinieux, F. Buggle, P. Gimbergues, H. Ruottinen, R. Marzella, W. Koehler, Y. Yurekli, A. Haase, Z. Privorkin, G. K. Harvey, B. Chave, A. J. Grau, E. M. Stadlan, J. List, C. Zorzi, B.W. van Oosten, P. Derkinderen, B. Casati, J. M. Maloteaux, K. Vahedi, W. L. J. van Putten, J. C. Sabourin, D. Lorenzetti, Plenevaux, J. W. B. Moll, A. Morento Fernandez, M. Lema, M. A. Horsfleld, P. De Jongh, S. Gikova, K. Kutluk, Monique M.B. Breteler, P. Saddier, A. Berbinschi, R. E. Cull, P. Echaniz, H. Kober, C. Minault, V. Kramer, A. L. Edal, S. Passero, T. Eckardt, K. E. Davies, A. Salmaggi, R. Kaiser, A. A. Grasso, Claudio Mariani, G. Egersbach, Hakan Gurvit, O. Dereeper, C. Vital, L. Wrabetz, A. Vecino, M. Aguilar, G. Bielicki, H. Becher, J. Castro, S. Iotti, M. G. Natali-Sora, E. Berta, S. Carlomagno, L. Ayuso-Peralta, P. H. Rondepierre, I. Bonaventura, B. V. Deuren, N. Van Blercom, M. Sciaky, J. Faber, M. Alberoni, M. Nieto, F. Sellal, C. Stelmasiak, M. Takao, J. Bradley, D. Zegers de Beyl, H. Porsche, G. Goi, H. Pongratz, F. Chapon, S. Happe, Robin S. Howard, B. Weder, S. Vlaski-Jekic, J. M. Ferro, R. Nemni, A. Daif, Herbert Budka, W. Van Paesschen, B. Waldecker, F. Carceller, J. Lacau, F. Soga, J. Peres Serra, E. Timmerman, A. M. vd Vliet, J. L. Emparanza, N. Vanacore, A. Pizzuti, N. Marti, A. Davalos, N. Ayraud, U. Zettl, J. Vivancos, Z. Katsarou, H. M. Mehdorn, G. Geraud, M. Merlini, M. Schröter, A. Ebner, M. Lanteri-Minet, R. Soler, G. P. Anzola, S. L. Hauser, L. Cahalon, S. DiDonato, R. Cantello, M. Marchau, J. Gioanni, F. Heidenreich, J. Manuel Martinez Lage, P. Descoins, F. Woimant, J. F. Campo, M. H. Verdier-taillefer, M. S. F. Barkhof, G. J. Kemp, A. O. Ceballos-Baumann, J. Berciano, M. Guidi, Tarek A. Yousry, B. Chandra, A. Rapoport, P. Canhao, A. Spitzer, T. Maeda, J. M. Pereira Monteiro, V. Paquis, Th. Mokrusch, F. J. Arrieta, I. Sangla, F. Canizares-Liebana, Lang Chr, André Delacourte, V. Fetoni, P. Kovachev, D. Kidd, L. Ferini-Strambi, E. Donati, E. Idman, A. Chio, C. Queiros, D. Michaelis, S. Boyacigil, A. Rodrigo, S. M. Yelamos, B. Chassande, P. Louwen, C. Tranchant, E. Ciafalon, A. Lombardo, A. Twijnstra, A. L. Fernandez, H. Kott, A. Cannas, N. Zsurger, T. Zileli, E. Metin, P. C. Bain, G. Fromont, B. Tedesi, A. Liberani, X. Navarro, M. C. Rowbotham, V. Hachinski, F. Cavalcanti, W. Rostene, R. M. Gardiner, F. Gonzalez, B. Köster, E. A. van der Veen, J. P. Lefaucheur, C. Marescaux, D. Boucquey, E. Parati, S. Yamaguchi, A. S. Orb, R. Grant, G. D. P. Smith, P. Goethals, M. Haguenau, G. Georgiev, I. N. van Schaik, Guy A. Rouleau, E. Iceman, G. Fayet, M. G. Kaplitt, C. Baracchini, H. Magnusson, G. Meneghetti, N. Malichard, M. L. Subira, D. Mancia, A. Berenguer, D. Navarrete Palau, H. Franssen, G. Kiziltan, M. P. Lopez, J. Montalt, S. Norby, R. Piedra Crespo, T. L. Rothstein, R. Falip, B. YalÇiner, F. Chedru, I. W. Thorpe, F. W. Heatley, D. S. C. Ochoa, C. Labaune, M. Devoti, O. Lider, Jakob Korf, N. Suzuki, E. A. Maguire, A. Moulignier, J. C. van Swieten, F. Monaco, J. Cartron, A. Steck, B. Uludag, M. Alexandra, H. Reichmann, T. Rossi, L. E. Claveria, A. M. Crouzel, M. A. Mena, J. Gasnault, J. W. Kowalski, S. I. Mellgren, V. Feigin, L. Demisch, J. Montalban, J. Renato, J. Mathieu, N. Goebels, L. Bava, K. Kunre, M. Pulik, S. Di Donato, C. Tzekov, H. Veldman, S. Giménez-Roldan, B. Lechevalier, L. Redondo, B. Pillon, M. Gugenheim, E. Roullet, J. M. Valdueza, C. Gori, H. J. Friedrich, L. de Saint Martin, F. Block, E. Basart, M. Heilmann, B. Becq Giraudon, C. Rodolico, G. Stevanin, Elizabeth K. Warrington, A. T. M. Willemsen, K. Kunze, C. Ben Hamida, M. Alam, J. R. ùther, A. Battistel, G. Della Marca, Richard S. J. Frackowiak, F. Palau, T. Brandt, Chicoutimi, L. Bove, L. Callea, A. Jaspert, T. Klopstock, K. Fassbender, Alan J. Thomas, A. Ferbert, V. Nunes, Douglas Russell, P. Garancini, C. Sanz-Sebastian, O. Santiag, G. Dhaenens, G. Seidel, I. Savic, A. Florea-Strat, M. Rousseaux, N. Catala, E. O'Sullivan, M. J. Manifacier, H. Kurtel, T. Mendel, P. Chariot, M. Salas, D. Brenton, R. Lopez, J. Thorpe, Jimmy D. Bell, E. Hofmann, E. Botia, J. Pacquereau, A. Struppler, C. d'Aniello, D. Conway, A. Garcia-Merino, K. Toyooka, S. Hodgkinson, E. Ciusani, Stefano Bastianello, A. Andrade Filho, M. Zaffaroni, G. Pleiffer, F. Coria, A. Schwartz, D. Baltadjiev, I. Rother, K. Joussen, J. Touchon, K. Kutlul, P. Praamstra, H. Sirin, S. Richard, C. Mariottu, L. Frattola, S. T. Dekesky, G. Wieneke, M. Chatel, O. Godefroy, C. Desnuelle, S. OzckmekÇi, C. H. Zielinski, P. van Deventer, S. Jozwiak, I. Galan, J. M. Grau, V. Vieira, T. A. Treves, S. Ertan, A. Pujol, S. Blecic, E. M. Zanette, F. Ceriani, W. Camu, L. Aquilone, A. Benomar, F. Greco, A. Pascual-Leone Pascual, T. Yanagihara, F. A. Delfino, R. Damels, S. Merkelbach, J. Beltran, A. Barrientos, S. Brugge, B. Hildebrandt-Müller, M. H. Nascimento, M. Rocchi, F. Cervantes, E. Castelli, R. M. Pressler, S. Yeil, A. del Olmo, J. L. Herranz, L. J. Kappelle, Y. Demir, N. Inoue, R. Hershkoviz, A. Luengo, S. Bien, F. Viallet, P. Malaspina, G. De Michele, G. Nolfe, P. Adeleine, T. Liehr, G. Fenelon, H. Masson, Kailash P. Bhatia, W. Haberbosch, S. Mederer, R. S. J. Frackowiak, Tanya Stojkovic, S. Previtali, A. E. Harding, W. Kohler, N. P. Quin, T. R. Marra, J. P. Moisan, A. Melchor, M. L. Viguera, Mary G. Sweeney, G. L. Romani, J. Hezel, R. A. Dierckx, R. Torta, A. Kratzer, T. Pauwels, D. Decoo, Adriana Campi, Neil Kitchen, J. Haas, U. Neubauer, J. J. Merland, A. Yagiz, A. Antonuzzo, A. Zangaladze, J. Parra, Pablo Martinez-Lage, D. J. Brooks, S. Hauser, R. Di Pierri, M. Campero, R. Caldarelli-Stefano, A. M. Colangelo, J. L. Pozo, C. Estol, F. Picard, A. Palmieri, J. Massons, JT Phillips, G. B. Groozman, R. Pentore, L. M. Ossege, C. Bayon, Hans-Peter Hartung, R. Konyalioglu, R. Lampis, D. Ancri, M. Miletta, F. J. Claramonte, W. Retz, F. Hentges, JM Cooper, M. Cordes, M. Limburg, M. Brock, G. R. Coulton, K. Helmke, Rosa Larumbe, A. Ohly, F. Landgraf, A. M. Drewes, Claudia Trenkwalder, M. Keidel, T. Segura, C. Scholz, J. HÄgele, D. Baudoin-Martin, P. Manganelli, J. Valdueza, M. Farinotti, U. Zwiener, M. P. Schiavalla, Y. P. Young, O. Barlas, G. Hertel, E. H. Weiss, M. Eiselt, A. Lossos, M. Bartoli, L. Krolicki, W. Villafana, W. Peterson, Nicoletta Meucci, C. Agbo, R. Luksch, F. Fiacco, G. Ponsot, M. Lopez, Howard L. Weiner, M. D. Alonso, K. Petry, Sanjay M. Sisodiya, P. Giustini, S. Tyrdal, R. Poupon, J. Blanke, P. Oubary, A. A. Kruize, H. Trabucchi, R. R. C. Stewart, H. Grehl, B. M. Kulig, V. Vinhas, D. Spagnoli, B. Mahe, J. Tatay, C. Hess, M. D. Albadalejo, G. Birbamer, M. Alonso, F. Valldeoriola, J. Figols, I. Wirguin, E. Diez Tejedor, C. S. Weiller, L.H. van den Berg, P. Barreiro, L. Pianese, S. Cocozza, R. Kohnen, E. Redolfi, F. Faralli, G. Gosztonyl, A. J. Gur, A. Keyser, V. Fichter-Gagnepain, B. Wildemann, E. Omodeo-Zorini, Gregoire, J. Schopohl, F. Fraschini, G. Wunderlich, B. Jakubowska, F. P. Serra, N. B. Jensen, O. Delattre, C. Leno, A. Dario, P. Grafe, F. Graus, M. C. Vigliani, J. L. Dobato, Philip N. Hawkins, R. Marés, A. Rimola, N. Meussi, G. Aimard, W. Hospers, A. M. Robertson, C. Kaplan, W. Lamadé, Karen E. Morrison, Amadio, E. Kieffer, F. Dromer, P. Bernasconi, M. Repeto, Davide Pareyson, Jeremy Rees, A. Guarneri, P. Odin, P. Bouche, L. Nogueira, J. Munoz, L. Leocani, M. J. Arcusa, R. S. J. Frackowiack, John S. Duncan, D. Karacostas, D. Edwin, I. Costa, M. Menetrey, P. Grieb, A. M. Salvan, S. Cunha, P. Merel, P. Pfeiffer, A. Astier, F. Federico, A. Mrabet, M. G. Buzzi, L. Knudsen, I. F. Pye, L. Falqui, C. R. Hornig, C. E. Shaw, C. Brigel, T. C. Britton, R. Codoceo, T. Pampols, Vincent J. Cunningham, N. Archidiacono, G. Chazot, J. B. Posner, L. L. O. Befalo, M. Monclus, C. Cabezas, H. Moser, H. Stodal, J. Ley-Pozo, L. Brusa, R. Di Mascio, P. Giannini, J. Fernandez, R. Santiago Luis, J. Garcia Tigera, J. Wilmink, P. Pignatelli, M. El Amrani, V. Lucivero, M. Baiget, R. Lodi, P. H. Cabre, L. Grande, A. Korczyn, R. Fahlbusch, C. Milanese, W. Huber, J. Susseve, H. C. Nahser, K. Mondrup, X. O. Breakefield, J. Sarria, T. H. Vogt, A. Alessandri, M. Daffertshofer, I. Nelson, M. L. Monticelli, O. Dammann, G. G. Farnarier, G. Felisari, A. Quattrini, A. Boiardi, P. Mazetti, H. Liu, J. Duarte, M. E. Gaunt, H. Strik, N. Yulug, A. Urman, J. Posner, Aida Suarez Gonzalez, Ma. L. Giros, Z. Matkovic, D. Kompf, A. D. Korczyn, A. Steinbrecher, R. Wenzel, M. C. de Rijk, R. Doronzo, J. Julien, O. Hasegawa, M. Kramer, V. Collado-Scidel, M. Alonso de Lecinana, L. Dell'Arciprete, S. Rapuzzi, S. Bahar, H. Willison, M. T. Ramacci, J.J. Martin, Lopez-Bresnahan, C. Malapani, R. Haaxma, T. Rosenberg, J. Patrignani, R. Vichi, Martin R. Farlow, J. Roquer, L. Krols, M. Pimenta, C. Bucka, U. Klose, M. Roberts, J. Salas-Puig, R. Ghnassia, A. Mercuri, C. Maltempo, I. Tournev, P. Homeyer, D. Caparros-Lefevre, E. P. O. Sullivan, T. Vashadze, Ph. Lyrer, A. Deltoro, H. Kondo, M. Steinling, A. Graham, G. C. Miescher, A. Pace, D. Branca, G. Avello, H. H. Kornhuber, D. Fernandes, H. Friedrich, R. Chorao, H. O. Lüders, R. T. Bax, J. A. Macias, N. Yilmaz, J. Veroust, M. Miller, S. Confort-Gouny, J. L. Sastre, D. Servello, G. Boysen, S. Koeppen, V. Planté-Bordeneuve, H. Albrecht, R. H. M. King, G. Orkodashili, R. Doornbos, H. Toyooka, V. Larrue, M. Sabatelli, K. Williams, M. Stevens, V. Maria, M. Comabella, C. Lammers, R. M. L. Poublon, E. Tizzano, P. Pazzaglia, F. Zoeller, M. B. Delisle, J. P. Goument, J. M. Minderhoud, A. Sghirlanzoni, V. Meininger, M. Al Deeb, C. Bertelt, A. Cagni, A. Algra, F. Morales, K. A. Flugel, M. Maidani, M. Noya, Z. Seidl, U. Roelcke, D. Cannata, E. Katiane EmbiruÇu, E. M. Wicklein, K. Willmes, L. Hanoglu, J. F. Pellissier, Yves Agid, E. Cuadrado, S. Brock, D. Maimone, Z. G. Nadareishvili, E. Matta, S. Hilmi, V. Assuerus, F. Lomena, R. Springer, F. Cabrera-Valdivia, Oscar L. Lopez, M. Casazza, F. Vivancos, Ralf Gold, T. Crawford, B. Moulard, M. Poisson, W. l. McDonald, D. E. Grobbe, Alan Connelly, H. Ozcan, S. Abeta, H. Severo Ochoa, A. C. van Loenen, E. Libson, M. J. Marti, B. George, C. Ferrarese, B. Jacobs, L. Divano, T. Ben-Hur, A. L. Bootsma, V. Martinez, A. Conti, R. P. Maguire, B. Schmidt, D. M. Campos, D. A. Guzman, E. Meary, C. Richart, P. B. Christensen, T. Schroeder, Massimo Zeviani, K. Jensen, R. Aliaga, S. Seitz-Dertinger, J. W. Griffin, C. Fryze, H. Baas, S. Braun, A. M. Porrini, B. Yemez, M. J. Sedano, C. Creisson, A. Del Santo, A. Mainz, R. Kay, S. Livraghi, R. de Waal, D. Macgregor, H. Hefter, R. Garghentino, U. Ruotsalainen, M. Matsumoto, M. G. Beaudry, P. M. Morrison, J. C. Petit, C. Walon, Ph. Chemouilli, F. Henderson, R. Massa, A. Cruz Martinez, U. Liska, F. Hecht, Ernst Holler, V. S. de Bruin, B. B. Sheitman, S. M. Bentzen, C. Bayindir, F. Pallesta, P. E. Roland, J. Parrilla, P. Zunker, L. F. Burchinskaya, G. Mellino, S. Ben Ayed, D. Bonneau, P. Nowacki, M. Goncalves, P. Riederer, N. Mavroudakis, J. Togores, L. Rozewicz, S. Robeck, Y. Perez Gilabert, L. Rampello, A. Rogopoulos, S. Martinez, F. Schildermans, C. Radder, P. B. Hedlund, J. Cambier, M. Aabed, G. D. Jackson, P. Gasparini, P. Santacruz, J. Vandevivere, H. Dural, A. Mantel, W. Dorndorf, N. Ediboglu, A. Lofgren, J. Bogousslavsky, P. Thierauf, L. Goullard, R. Maserati, B. Moering, M. Ryba, J. Serra, G. G. Govan, A. Pascual-Leone, S. Schaeffer, M. R. Rosenfeld, A. P. Correia, K. Ray Chaudhuri, L. Campbell, R. Spreafico, B. Genetet, A. M. Tantot, R. A. G. Hughes, J. A. Vidal, G. Erkol, J. Y. Delattre, B. Yaqub, B. K. Hecht, E. Mayayo, Ph. Scheltens, J. Corral, M. Calaf, L. Henderson, C. Y. Li, U. Bogdahn, R. Sanchez-Roy, M. Navasa, J. Ballabriga, G. Broggi, T. Gudeva, C. Rose, J. Vion-Dury, J. A. Gastaut, J. Pniewski, Nicola J. Robertson, G. Kohncke, M. Billot, S. Gok, E. Castellli, F. Denktas, P. Bazzi, F. Spinelli, I. F. Moseley, C. D. Mardsen, B. Barbiroli, O. M. Koriech, A. Miller, Hiroaki Yoshikawa, F. X. Borruat, J. Zielasek, P. Le Coz, J. Pascual, A. Drouet, L. T. Giron, F. Schondube, R. Midgard, M. Alizadeh, M. Liguori, Lionel Ginsberg, L. Harms, C. Tilgner, G. Tognoni, F. Molteni, Mar Tintoré, M. Psylla, C. Goulon-Goeau, M. V. Aguilar, Massimo Filippi, K. H. Mauritz, Thomas V. Fernandez, C. Basset, S. Rossi, P. Meneses, B. Jandolo, T. Locatelli, D. Shechtcr, C. Magnani, R. Ferri, Bruno Dubois, J. M. Warier, S. Berges, F. Idiman, M. Schabet, R. R. Diehl, P. D'aurelio, M. Musior, Reinhard Hohlfeld, P. Smeyers, M. Olivé, A. Riva, C. A. Broere, N. Egund, S. Franceschetti, V. Bonavita, Nicola Canal, E. Timmermans, M. Ruiz, S. Barrandon, G. Vasilaski, B. Deweer, L. Galiano, S. F. T. M. de Bruijn, L. Masana, A. Goossens, B. Heye, K. Lauer, Heinz Gregor Wieser, Stephen R. Williams, B. Garavaglia, A. P. Sempere, F. Grigoletto, P. Poindron, R. Lopez-Pajares, I. Leite, T. A. McNell, C. Caucheteur, J. M. Giron, A. D. Collins, P. Freger, J. Sanhez Del Rio, D. A. Harn, K. Lindner, S. S. Scherer, G. Serve, M. Juncadella, X. Estivill, R. Binkhorst, M. Anderson, B. Tekinsoy, C. Sagan, T. Anastopoulos, G. Japaridze, S. Guillou, F. Erminio, Jon Sussman, P. G. Oomes, D. S. Rust, S. Mascheroni, O. Berger, M. Peresson, K. V. Toyka, T. W. Polder, M. Huberman, B. Arpaci, H. Ramtami, I. Martinez, Ph. Violon, P. P. Gazzaniga Pozzill, R. Ruda, P. Auzou, J. Parker, S. P. Morrissey, Jiahong Zhu, F. Rotondi, P. Baron, W. Schmid, P. Doneda, M. Spadaro, M. C. Nargeot, I. Banchs, J.S.P. van den Berg, R. Ferrai, M. Robotti, M. Fredj, Pedro M. Rodríguez Cruz, B. Erne, D. G. Piepgras, M. C. Arne-Bes, J. Escudero, C. Goetz, A. R. Naylor, M. Hallett, O. Abramsky, E. Bonifacio, L. E. Larsson, R. Pellikka, P. Valalentino, D. Guidetti, B. Buchwald, C. H. Lücking, D. Gauvreau, F. Pfaff, A. Ben Younes-Chennoufi, R. Kiefer, R. Massot, K. A. Hossmann, L. Werdelin, P. J. Baxter, U. Ziflo, S. Allaria, C. D. Marsden, M. Cabaret, S. P. Mueller, E. Calabrese, R. Colao, S. I. Bekkelund, M. Yilmaz, O. Oktem-Tanor, R. Gine, M. E. Scheulen, J. Beuuer, A. Melo, Z. Gulay, M. D. Have, C. Frith, D. Liberati, J. Gozlan, P. Rondot, Ch. Brunholzl, M. Pocchiari, J. Pena, L. Moiola, C. Salvadori, A. Cabello, T. Catarci, S. Webb, C. Dettmers, N. A. Gregson, Alexandra Durr, F. Iglesias, U. Knorr, L. Ferrini-Strambi, F. Kruggel, P. Allard, A. Coquerel, P. Genet, F. Vinuels, C. Oberwittler, A. Torbicki, P. Leffers, B. Renault, B. Fauser, C. Ciano, G. Uziel, J. M. Gibson, F. Anaya, C. Derouesné, C. N. Anagnostou, M. Kaido, W. Eickhoff, G. Talerico, M. L. Berthier, A. Capdevila, M. Alons, D. Rezek, E. Wondrusch, U. Kauerz, D. Mateo, M. A. Chornet, Holon, N. Pinsard, I. Doganer, E. Paoino, H. Strenge, C. Diaz, J. R. Brasic, W. Heide, I. Santilli, W. M. Korn, D. Selcuki, M. J. Barrett, D. Krieger, T. Leon, T. Houallah, M. Tournilhac, C. Nos, D. Chavot, F. Barbieri, F. J. Jimenez-Jimenez, J. Muruzabal, K. Poeck, A. Sennlaub, L. M. Iriarte, L. G. Lazzarino, C. Sanz, P. A. Fischer, S. D. Shorvon, R. Hoermann, F. Delecluse, M. Krams, O. Corabianu, F. H. Hochberg, Christopher J. Mathias, B. Debachy, C. M. Poser, L. Delodovici, A. Jimenez-Escrig, F. Baruzzi, F. Godenberg, D. Cucinotta, P. J. Garcia Ruiz, K. Maier-Hauff, P. R. Bar, R. Mezt, R. Jochens, S. Karakaneva, C. Roberti, E. Caballero, Joseph E. Parisi, M. Zamboni, T. Lacasa, B. Baklan, J. C. Gautier, J. A. Martinez-Matos, W. Pollmann, G. Thomas, L. Verze, E. Chleide, R. Alvarez Sala, I. Noel, E. Albuisson, O. Kastrup, S. I. Rapoport, H. J. Braune, H. Lörler, M. Le Merrer, A. Biraben, S. Soler, S. J. Taagholt, U. Meyding-Lamadé, K. Bleasdale-Barr, Isabella Moroni, Y. Campos, J. Matias-Guiu, G. Edan, M. G. Bousser, John B. Clark, J. Garcia de Yebenes, N. K. Olsen, P. Hitzenberger, S. Einius, Aj Thompson, Ch. J. Vecht, T. Crepin-Leblond, Klaus L. Leenders, A. Di Muzio, L. Georgieva, René Spiegel, K. Sabey, D. Ménégalli, J. Meulstee, U. Liszka, P. Giral, C. Sunol, J. M. Espadaler, A. D. Crockar, K. Varli, G. Giraud, P. J. Hülser, A. Benazzouz, A. Reggio, M. Salvatore, K. Genc, M. Kushnir, S. Barbieri, J. Ph. Azulay, M. Gianelli, N. Bathien, A. AlMemar, F. Hentati, I. Ragueneau, F. Chiarotti, R. C. F. Smits, A. K. Asbury, F. Lacruz, B. Muller, Alan J. Thompson, Gordon Smith, K. Schmidt, C. Daems Monpeun, Juergen Weber, A. Arboix, G. R. Fink, A. M. Cobo, M. Ait Kaci Ahmed, E. Gencheva, Israel-Biet, G. Schlaug, P. De Jonghe, Philip Scheltens, K. Toyka, P. Gonzalez-Porque, A. Cila, J. M. Fernandez, P. Augustin, J. Siclia, S. Medaglini, D. E. Ziogas, A. Feve, L. Kater, G. J. E. Rinkel, D. Leppert, Rüdiger J. Seitz, S. Ried, C. Turc-Carel, G. Smeyers, F. Godinho, M. Czygan, M. Rijntjes, E. Aversa, M. Frigo, Leif Østergaard, J. L. Munoz Blanco, A. Cruz-Matinez, J. De Reuck, C. Theillet, T. Barroso, V. Oikonen, Florence Lebert, M. Kilinc, C. Cordon-Cardon, G. Stoll, E. Thiery, F. Pulcinelli, J. Solski, M. Schmiegelow, L. J. Polman, P. Fernandez-Calle, C. Wikkelso, M. Ben Hamida, M. Laska, E. Kott, W. Sulkowski, C. Lucas, N. M. Bornstein, D. Schmitz, M. W. Lammers, A. de Louw, R. J. S. Wise, P. A. van Darn, C. Antozzi, P. Villanueva, P. H. E. Hilkens, C. Constantin, W. Ricart, A. Wolf, M. Gamba, P. Maguire, Alessandro Padovani, B. M. Patten, Marie Sarazin, H. Ackermann, L. Durelli, S. Timsit, Sebastian Jander, B. W. Scheithauer, G. Demir, J. P. Neau, P. Barbanti, A. Brand, N. AraÇ, V. Fischer-Gagnepain, R. Marchioli, G. Serratrice, C. Maugard-Louboutin, G. T. Spencer, D. Lücke, G. Mainardi, K. Harmant Van Rijckevorsel, G. B. Creel, R. Manzanares, Francesco Fortunato, A. May, J. Workman, K. Johkura, E. Fernandez, Carlo Colosimo, L. Calliauw, L. Bet, Félix F. Cruz-Sánchez, M. Dhib, H. Meinardi, F. Carrara, J. Kuehnen, C. Peiro, H. Lassmann, K. Skovgaard Olsen, A. McDonald, L. Sciulli, A. Cobo, A. Monticelli, B. Conrad, J. Bagunya, J. Benitez, V. Desnizza, B. Dupont, O. Delrieu, D. Moraes, J. J. Heimans, F. Garcia Rio, M. Matsumto, A. Fernandez, R. Nermni, R. Chalmers, M. J. Marchau, F. Aguado, P. Velupillai, P. J. Martin, P. Tassan, V. Demarin, A. Engelien, T. Gerriets, Comar, J. L. Carrasco, J. P. Pruvo, A. Lopez de Munain, D. Pavitt, J. Alarcon, Chris H. Polman, B. Guldin, N. Yeni, Hartmut Brückmann, N. Wilczak, H. Szwed, R. Causaran, G. Kyriazis, M. E. Westarp, M. Gasparini, N. Pecora, J. M. Roda, E. Lang, V. Scaioli, David R. Fish, D. Caputo, O. Gratzl, R. Mercelis, A. Perretti, G. Steimetz, I. Link, C. Rigoletto, A. Catafau, G. Lucotte, M. Buti, G. Fagiolari, A. Piqueras, C. Godinot, J. C. Meurice, Erodriguez J. Dominigo, F. Lionnet, H. Grzelec, David J. Brooks, P. M. G. Munro, F. X. Weilbach, M. Maiwald, W. Split, B. Widjaja-Cramer, V. Ozturk, J. Colas, E. Brizioli, J. Calleja, L. Publio, M. Desi, R. Soffietti, P. Cortinovis-Tourniaire, E. F. Gonano, G. Cavaletti, S. Uselli, K. Westerlind, H. Betuel, C. O. Dhiver, H. Guggenheim, M. Hamon, R. Fazio, P. Lehikoinen, A. Esser, B. Sadzot, G. Fink, Angelo Antonini, D. Bendahan, V. Di Carlo, G. Galardi, A. F. Boller, M. Aksenova, Del Fiore, V. de la Sayette, H. Chabriat, A. Nicoletti, A. Dilouya, M. L. Harpin, E. Rouillet, J. Stam, A. Wolters, M. R. Delgado, Eduardo Tolosa, G. Said, A. J. Lees, L. Rinaldi, A. Schulze-Bonhage, MA Ron, C. Lefebvre, E. W. Radü, R. Alvarez, M. L. Bots, P. Reganati, S. Palazzi, A. Poggi, N. J. Scolding, V. Sazdovitch, T. Moreau, E. Maes, M. A. Estelies, P. Petkova, Jose-Felix Marti-Masso, G De La Meilleure, N. Mullatti, M. Rodegher, N. C. Notermans, T. A. T. Warner, S. Aktan, J. P. Louboutin, L. Volpe, C. Scheidt, W. Aust, C. M. Wiles, U. Schneider, S. K. Braekken, W. R. Willems, K. Usuku, Peter M. Rothwell, C. Talamon, M. L. Sacchetti, A. Codina, M. H. Marion, A. Santoro, J. Roda, A. Bordoni, D. J. Taylor, S. Ertas, H. H. Emmen, J. Vichez, V. BesanÇon, R. E. Passingham, M. L. Malosio, A. Vérier, M. Bamberg, A. W. Hansen, E. Mostacero, G. Gaudriault, Marie Vidailhet, B. Birebent, K. Strijckmans, F. Giannini, T. Kammer, I. Araujo, J. Nowicki, E. Nikolov, A. Hutzelmann, R. Gherardi, J. Verroust, L. Austoni, A. Scheller, A. Vazquez, S. Matheron, H. Holthausen, J. M. Gerard, M. Bataillard, S. Dethy, V. H. Patterson, V. Ivanez, N. P. Hirsch, F. Ozer, M. Sutter, C. Jacomet, M. Mora, Bruno Colombo, A. Sarropoulos, T. H. Papapetropoulos, M. Schwarz, D. S. Dinner, N. Acarin, B. Iandolo, J. O. Riis, P. R. J. Barnes, F. Taroni, J. Kazenwadel, L. Torre, A. Lugaresi, I. L. Henriques, S. Pauli, S. Alfonso, Pedro Quesada, A. S. T. Planting, J. M. Castilla, Thomas Gasser, M. Van der Linden, A. Alfaro, E. Nobile-Orazio, G. Popova, W. Vaalburg, F. G. A. van der Mech, L. Williams, F. Medina, J. P. Vernant, J. Yaouanq, B. Storch-Hagenlocher, A. Potemkowski, R. Riva, M. H. Mahagne, M. Ozturk, Ve. Drory, N. Konic, C. Jungreis, A. Pou Serradell, J. L. Gauvrit, G. J. Chelune, S. Hermandez, T. Dingus, L. Hewer, Ch. Koch, M. N. Metz-Lutz, G. Parlato, M. Sinaki, Charles Pierrot-Deseilligny, H. C. Diener, J. Broeckx, J. Weill-Fulazza, M. L. Villar, M. Rizzo, O. Ganslandt, C. Duran, N. A. Fletcher, G. Di Giovacchino, Susan T. Iannaccone, C. Kolig, N. Fabre, H. A. Crockard, Rita Bella, M. Tazir, E. Papagiannuli, K. Overgaard, Emma Ciafaloni, I. Lorenzetti, F. Viader, P. A. H. Millac, I. Montiel, L. H. Visser, M. Palomar, P. L. Murgia, H. Pedersen, Rafael Blesa, S. Seddigh, W. O. Renier, I. Lemahieu, H. M. L. Jansen, L. Rosin, J. Galofre, K. Mattos, M. Pondal, G. M. Hadjigeorgiou, D. Francis, L. Cantin, D. Stegeman, M. Rango, A. B. M. F. Karim, S. Schraff, B. Castellotti, I. Iriarte, E. Laborde, T. J. Tjan, R. Mutani, D. Toni, B. Bergaasco, J. G. Young, C. Klotzsch, A. Zincone, X. Ducrocq, M. Uchuya, O. J. Kolar, A. Quattrone, T. Bauermann, Nereo Bresolin, J. Vallée, B. C. Jacobs, A. Campos, Werner Poewe, J. A. Villanueva, A. W. Kornhuber, A. Malafosse, E. Diez-Tejedor, G. Jungreia, M. J. A. Puchner, A. Komiyama, O. Saribas, V. Volpini, L. Geremia, S. Bressi, A. Nibbio, Timothy E. Bates, T. z. Tzonev, E. Ideman, G. A. Damlacik, G. Martino, G. Crepaldi, T. Martino, Kjell Någren, E. Idiman, D. Samuel, J. M. Perez Trullen, Y. van der Graaf, J. O. Thorell, M. J. M. Dupuis, E. Sieber, R. D'Alessandro, C. Cazzaniga, J. Faiss, A. Tanguy, A. Schick, I. Hoksergen, A. Cardozo, R. Shakarishvili, G. K. Wennlng, J. L. Marti-Vilalta, J. Weissenbach, I. L. Simone, Amalia C. Bruni, Darius J. Adams, C. Weiller, A. Pietrangeli, F. Croria, C. Vigo-Pelfrey, Patricia Limousin, A. Ducros, G. Conti, O. Lindvall, E. Richter, M. Zuffi, A. Nappo, T. Riise, J. Wijdenes, M. J. Fernandez, J. Rosell, P. Vermersh, S. Servidei, M. S. C. Verdugo, F. Gouttiere, W. Solbach, M. Malbezin, I. S. Watanabe, A. Tumac, W. I. McDonald, D. A. Butterfield, P. P. Costa, F. deRino, F. Bamonti, J. M. Cesar, C. H. Lahoz, I. Mosely, M. Starck, M. H. Lemaitre, K. M. Stephan, S. Tex, R. Bokonjic, I. Mollee, L. Pastena, M. Gutierrez, F. Boiler, M. C. Martinez-Para, M. Velicogna, O. Obuz, A. Grinspan, M. Guarino, L. M. Cartier, E. Ruiz, D. Gambi, S. Messina, M. Villa, Michael G. Hanna, J. Valk, Leone Pascual, M. Clanet, Z. Argov, B. Ryniewicz, E. Magni, B. Berlanga, K. S. Wong, C. Gellera, C. Prevost, F. Gonzalez-Huix, R. Petraroli, J. E. G. Benedikz, I. Kojder, C. Bommelaer, L. Perusse, M. R. Bangioanni, Guy M. McKhann, A. Molina, C. Fresquet, E. Sindern, Florence Pasquier, M. J. Rosas, M. Altieri, O. Simoncini, M. Koutroumanidis, C. A. F. Tulleken, M. Dary-Auriol, S. Oueslati, H. Kruyer, I. Nishisho, C. R. Horning, A. Vital, G. V. Czettritz, J. Ph. Neau, B. Mihout, A. Ameri, M. Francis, S. Quasthoff, D. Taussig, S. Blunt, P. Valentin, C. Y. Gao, O. Heinzlef, H. d'Allens, C. Coudero, M. Erfas, G. Borghero, P. J. Modrego Pardo, M. C. Patrosso, N. L. Gershfeld, P. A. J. M. Boon, O. Sabouraud, M. Lara, J. Svennevig, G. L. Lenzi, A. Barrio, H. Villaroya, JosÇ M. Manubens, O. Boespflug-Tanguy, M. Carreras, D. A. Costiga, J. P. Breux, S. Lynn, C. Oliveras Ley, A. G. Herbaut, J. Nos, C. Tornali, Y. A. Hekster, J. L. Chopard, J. M. Manubens, P. Chemouilli, A. Jovicic, F. Dworzak, S. Smirne, S. E. Soudain, B. Gallano, D. Lubach, G. Masullo, G. Izquierdo, A. Pascual Leone Pascual, A. Sessa, V. Freitas, O. Crambes, L. Ouss, G. W. Van Dijk, P. Marchettini, P. Confalonieri, M. Donaghy, A. Munnich, M. Corbo, and M. E. L. van der Burg
- Subjects
Neurology ,business.industry ,Media studies ,Library science ,Medicine ,Neurology (clinical) ,business - Published
- 1994
- Full Text
- View/download PDF
9. Aminoglykoside bei Patienten mit Mukoviszidose und pulmonaler Exazerbation: Vergleich von Einmal- und Dreimalgabe
- Author
-
Ulrich Heininger, W. Solbach, Klemens Stehr, and B. Böwing
- Subjects
Chemotherapy ,medicine.medical_specialty ,Exacerbation ,medicine.drug_class ,business.industry ,medicine.medical_treatment ,Antibiotics ,Respiratory disease ,Aminoglycoside ,medicine.disease ,Cystic fibrosis ,Gastroenterology ,Surgery ,Internal medicine ,Pediatrics, Perinatology and Child Health ,medicine ,Tobramycin ,Netilmicin ,business ,medicine.drug - Abstract
Twenty-six patients with cystic fibrosis and pulmonary exacerbations were enrolled in a prospective randomized study to compare the efficacy of aminoglycosides (tobramycin or netilmicin) administered once daily (21 episodes, 5 with netilmicin, 16 with tobramycin) and thrice daily (23 episodes, 2 with netilmicin, 21 with tobramycin), respectively. In addition, the patients received an anti-pseudomonal beta-lactam antibiotic. In the single-dose group the total daily dosage was 4.97 +/- 1.12 mg/kg (total dosage per exacerbation: 74.55 mg/kg), compared to 9.60 +/- 2.70 mg/kg in the triple-dose group (total dosage per exacerbation: 165.12 mg/kg). The mean peak and trough serum levels of the aminoglycoside were 8.31 +/- 1.76 mg/l and 0.18 +/- 0.10 mg/l, respectively in the single dose group compared to 6.12 +/- 1.30 mg/l and 0.58 +/- 0.31 mg/l in the triple dose group. Success of treatment, defined as decrease in leucocyte counts, normalization of elevated CRP-values, number of days in hospital and interval until next admission to hospital, was not different between both groups. We conclude that single daily dose of aminoglycosides was as efficacious as triple dose in our patients.
- Published
- 1993
- Full Text
- View/download PDF
10. Infektionen mit respiratorischen Bakterien verändern die Anpassung von Lungengewebszellen an Hypoxie
- Author
-
T. Hellwig-Bürgel, Jan Rupp, J. Deiwick, Klaus Dalhoff, and W. Solbach
- Subjects
Pulmonary and Respiratory Medicine - Published
- 2008
- Full Text
- View/download PDF
11. M. genavense: zu langsam für die Diagnose?
- Author
-
W. Solbach, Klaus Dalhoff, Jan Rupp, E. Kramme, and B. Schaaf
- Subjects
Pulmonary and Respiratory Medicine - Published
- 2008
- Full Text
- View/download PDF
12. Apoptosis driven infection
- Author
-
G, van Zandbergen, W, Solbach, and T, Laskay
- Subjects
Macrophages ,Cell Membrane ,Animals ,Humans ,Leishmaniasis, Cutaneous ,Phosphatidylserines ,Leishmania major ,Signal Transduction - Abstract
Professional phagocytes like polymorphonuclear neutrophil granulocytes (PMN) and macrophages (MF) kill pathogens as the first line of defense. These cells possess numerous effector mechanisms to eliminate a threat at first contact. However, several microorganisms still manage to evade phagocytic killing, survive and retain infectivity. Some pathogens have developed strategies to silently infect their preferred host phagocytes. The best example of an immune silencing phagocytosis process is the uptake of apoptotic cells. Immune responses are suppressed by the recognition of phosphatidylserine (PS) on the outer leaflet of their plasma membrane. Taking Leishmania major as a prototypic intracellular pathogen, we showed that these organisms can use the apoptotic "eat me" signal PS to silently enter PMN. PS-positive and apoptotic parasites, in an altruistic way, enable the intracellular survival of the viable parasites. Subsequently these pathogens again use PS exposition, now on infected PMN, to silently invade their definitive host cells, the MF. In this review, we will focus on L. major evasion strategies and discuss other pathogens and their use of the apoptotic "eat me" signal PS to establish infection.
- Published
- 2007
13. [The influence of a new surface treatment of silicone intracoular lenses with fluoralkylsitan on the adherence of endophthalmitic bacteria in vitro]]
- Author
-
A, Kienast, D-H, Menz, J, Dresp, M, Klinger, A, Bunse, H, Ohgke, W, Solbach, H, Laqua, R, Kämmerer, and H, Hoerauf
- Subjects
Lenses, Intraocular ,Endophthalmitis ,Prosthesis-Related Infections ,Coated Materials, Biocompatible ,Surface Properties ,Colony Count, Microbial ,Staphylococcus epidermidis ,Humans ,Bisphenol A-Glycidyl Methacrylate ,Propionibacterium acnes ,Bacterial Adhesion - Abstract
Dynasilan is a fluoroalkylsilan which is able to bind to surface active molecules of intraocular lenses (IOLs), thereby offering a new option for surface modification of silicone lenses. The purpose of this in vitro study was to investigate the influence of this new surface treatment on the adherence of two typical endophthalmitis-inducing bacteria ( Staphylococcus epidermidis, Propionibacterium acnes).A total of 14 Dynasilan-treated and 14 untreated silicone lenses were incubated at 37 degrees C for 24 h in brain heart infusion broth (10(8) CFU/ml) either with Staphylococcus epidermidis or with Propionibacterium acnes for 1 h. Subsequently, the adherent bacteria were resuspended using ultrasonification at 35 kHz for 3 x 45 s. After a dilution series and incubation at 37 degrees C for 24 h or 3 days the colonies were counted.On untreated IOLs incubated with Staphylococcus epidermidis the average number of bacteria was 3.6 x 10(7)/ml, and on treated IOLs the number of counted colonies was reduced to 1.09 x 10(7)/ml. Incubated with Propionibacterium acnes the average number of adherent bacteria on untreated IOLs was 4.75 x 10(4)/ml and on modified IOLs the number was reduced to 2.94 x 10(4)/ml.Dynasilan surface treatment may reduce the adherence of Staphylococcus epidermidis and Propionibacterium acnes on silicone intraocular lenses. Further studies regarding the stability of this treatment, its biocompatibility and influence on lens epithelial cell adhesion are in progress.
- Published
- 2003
14. In vitro susceptibility and eradication of Chlamydia pneumoniae cardiovascular strains from coronary artery endothelium and smooth muscle cells
- Author
-
J, Gieffers, W, Solbach, and M, Maass
- Subjects
Humans ,Endothelium, Vascular ,Chlamydophila pneumoniae ,In Vitro Techniques ,Chlamydophila Infections ,Anti-Bacterial Agents - Abstract
Recovery of viable Chlamydia pneumoniae from atheromas of coronary heart diseases patients has initiated pilot studies to eradicate C. pneumoniae from vascular tissue by antibiotic treatment. To provide data for the selection of effective antibiotics, we investigated the in vitro activity of anti-chlamydial antibiotics to eliminate vascular strains of C. pneumoniae from coronary endothelial and smooth muscle cells, celltypes that are involved in the pathogenesis of atherosclerosis.The susceptibility of the obligate intracellular chlamydiae was studied in primary coronary endothelial cells, smooth muscle cells and immortalized epithelial cells. Minimal inhibitory concentrations (MICs) were determined for ofloxacin, levofloxacin, trovafloxacin, moxifloxacin, erythromycin, azithromycin, roxithromycin, rifapentin and rifampin.In vitro, rifampin was the most effective drug overall. Moxifloxacin and trovafloxacin were as effective as the macrolides of which roxithromycin was the most active one.Actively replicating C. pneumoniae can be eliminated in vitro from cell types, involved in the pathogenesis of atherosclerosis by various antibiotics. These data provide an experimental background for the selection of antibiotics in clinical eradication studies and will help to assess the potential success of prevention and eradication therapies.
- Published
- 2001
15. [Mitral valve endocarditis caused by Erysipelothrix rhusiopathiae]
- Author
-
J P, Heidrich, M, Stahl, R, Dittmann, M, Maass, and W, Solbach
- Subjects
Heart Valve Prosthesis Implantation ,Electrocardiography ,Erysipelothrix Infections ,Time Factors ,Echocardiography ,Injections, Intravenous ,Humans ,Mitral Valve Insufficiency ,Ampicillin ,Female ,Endocarditis, Bacterial ,Penicillins ,Aged - Abstract
A 67 year-old country woman was admitted to the hospital because of a four weeks history of continuous catarrh, arthralgia and fever. Recently, she had also developed upper abdominal pain after oral ibuprofen treatment. The clinical examination showed a patient of impaired general condition. The heart and lungs were auscultatory normal and there were no signs of dyspnea, cyanosis or inflammatory skin lesions.Physical examination of heart and lung, electrocardiography and transthoracic echocardiography were without pathological findings.Gastroscopy revealed acute antral gastritis and duodenitis with presence of Helicobacter pylori. Eradication therapy resolved the abdominal symptoms but fever returned after the antibiotic therapy was stopped. The patient developed a severe endocarditis with progressive mitral regurgitation within a few days. Erysipelothrix rhusiopathiae was isolated from blood cultures and identified by conventional and molecular methods. The patient was treated successfully with 3 x 2 g ampicillin daily, applied parenterally for six weeks, and a mitral valve replacement.This was an unusual manifestation of systemic Erysipelothrix rhusiopathiae infection. The bacterium Erysipelothrix rhusiopathiae has still to be considered in the diagnosis and treatment of endocarditis in patients with increased risk of exposure (e.g. farmers, butchers and fishermen).
- Published
- 2001
16. Klinik, Verlauf und Prävention von Patienten mit MRSA-Kolonisation und Infektion / Results of Clinical Course and Prevention in Patients with MRSA Colonisation and Infection
- Author
-
W. Solbach, C. Eckmann, H. Braasch, P. Kujath, and H.-P. Bruch
- Subjects
Gynecology ,medicine.medical_specialty ,business.industry ,Clinical course ,Medicine ,In patient ,business - Abstract
In einer retrospektiven Analyse wurden alle Falle von MRSA zwischen 1994 und 1999 ausgewertet. Seit dem 01.01.1996 wurden die Patienten isoliert und lokal mit Chlorhexidin und Muciprocin behandelt. Nur bei einer manifesten Infektion wurde Vancomycin appliziert. In 98 Fallen wurde MRSA nachgewiesen (Durchschnittsalter 66,7 Jahre). Die haufigsten assoziierten Faktoren waren vorherige Antibiotikagabe (n=95), stationarer Aufenthalt uber 28 Tage (n=78) sowie Malignitat (n=36). Nach Einfuhrung standardisierter Isolationsmasnahmen und strikter Kriterien der Antibiotikagabe sank die Inzidenz von n=31 (1996) auf n= 13 (1999). 39 Patienten wurden eradiziert, 34 mit MRSA-Besiedelung entlassen. 25 Patienten verstarben, davon n=7 an einer MRSA-Infektion.
- Published
- 2001
- Full Text
- View/download PDF
17. The host response to Leishmania infection
- Author
-
W, Solbach and T, Laskay
- Subjects
Antibodies, Protozoan ,Antigens, Protozoan ,Mice, Inbred Strains ,Nitric Oxide ,Host-Parasite Interactions ,Mice ,CD28 Antigens ,Antigens, CD ,Superoxides ,Cell Adhesion ,Animals ,Humans ,Genetic Predisposition to Disease ,Saliva ,Leishmaniasis ,Inflammation ,Leishmania ,Mice, Knockout ,Antigen Presentation ,Membrane Glycoproteins ,Macrophages ,Immunity, Innate ,Lymphocyte Subsets ,Insect Vectors ,Killer Cells, Natural ,Oxidative Stress ,B7-1 Antigen ,Cytokines ,B7-2 Antigen ,Lymph Nodes ,Psychodidae - Published
- 1999
18. P916 Treponema pallidum in the vitreous tap
- Author
-
H. Hagedorn, F. Hansmann, H. Hoerauf, Johann Roider, H. Laqua, W. Solbach, C. Tiemann, I. Ewert, and M. Müller
- Subjects
Microbiology (medical) ,Infectious Diseases ,Treponema ,biology ,Chemistry ,Vitreous tap ,Pharmacology (medical) ,General Medicine ,biology.organism_classification ,Microbiology - Published
- 2007
- Full Text
- View/download PDF
19. Effect of IL-7 treatment on Leishmania major-infected BALB.Xid mice: enhanced lymphopoiesis with sustained lack of B1 cells and clinical aggravation of disease
- Author
-
A, Hoerauf, W, Solbach, M, Röllinghoff, and A, Gessner
- Subjects
B-Lymphocytes ,Mice ,Mice, Inbred BALB C ,X Chromosome ,Interleukin-7 ,Lymphopenia ,Immunologic Deficiency Syndromes ,Animals ,Leishmaniasis, Cutaneous ,Disease Susceptibility ,Mice, SCID ,Hematopoiesis ,Leishmania major - Abstract
The Xid immunodeficiency was characterized by a total lack of B1 cells and reduced numbers and functions of B2 cells. In BALB.Xid mice, this defect results in an reduced susceptibility against infections with parasites such as Trypanosoma cruzi and Leishmania major. Since IL-7 acts on the B cell compartment by stimulation of pre-B cell proliferation, we analyzed the effect of recombinant IL-7 on L. major infection in BALB.Xid mice. After application of a single dose of IL-7 simultaneously with the infection, the clinical course in BALB.Xid mice was markedly aggravated, resembling that of normal BALB/c mice. IL-7-induced disease promotion was accompanied by an up to 100-fold higher parasite load in several tissues of these mice. When cytokine production of purified, L. major-specific CD4+ T cells from lesion-draining lymph nodes was examined, the IFN-gamma production seen in untreated BALB.Xid mice was suppressed in IL-7-treated animals. One of the major effects of IL-7 treatment in the lymphoid organs of BALB.Xid mice was the increase of the total number of B220, sIgM and MHC II-positive cells. These cells belonged to the B2 subset, since cells expressing surface molecules characteristic for B1 cells (Mac-1 and Ly-1) remained absent in spleens, lymph nodes and the peritoneum. In conclusion, selective up-regulation of B2 cells by IL-7 in the absence of B1 cells is associated with disease aggravation in L. major-infected BALB.Xid mice.
- Published
- 1995
20. [Aminoglycosides in patients with mucoviscidosis and pulmonary exacerbation. Comparison of once or three times daily administration]
- Author
-
U, Heininger, B, Böwing, K, Stehr, and W, Solbach
- Subjects
Adult ,Male ,Adolescent ,Cystic Fibrosis ,Dose-Response Relationship, Drug ,Tobramycin ,Humans ,Female ,Pseudomonas Infections ,Netilmicin ,Pneumonia ,Drug Administration Schedule - Abstract
Twenty-six patients with cystic fibrosis and pulmonary exacerbations were enrolled in a prospective randomized study to compare the efficacy of aminoglycosides (tobramycin or netilmicin) administered once daily (21 episodes, 5 with netilmicin, 16 with tobramycin) and thrice daily (23 episodes, 2 with netilmicin, 21 with tobramycin), respectively. In addition, the patients received an anti-pseudomonal beta-lactam antibiotic. In the single-dose group the total daily dosage was 4.97 +/- 1.12 mg/kg (total dosage per exacerbation: 74.55 mg/kg), compared to 9.60 +/- 2.70 mg/kg in the triple-dose group (total dosage per exacerbation: 165.12 mg/kg). The mean peak and trough serum levels of the aminoglycoside were 8.31 +/- 1.76 mg/l and 0.18 +/- 0.10 mg/l, respectively in the single dose group compared to 6.12 +/- 1.30 mg/l and 0.58 +/- 0.31 mg/l in the triple dose group. Success of treatment, defined as decrease in leucocyte counts, normalization of elevated CRP-values, number of days in hospital and interval until next admission to hospital, was not different between both groups. We conclude that single daily dose of aminoglycosides was as efficacious as triple dose in our patients.
- Published
- 1993
21. Hit and run, hit and hide or permanent hit: why it is premature to dump Koch's postulates in rheumatic diseases
- Author
-
G R, Burmester and W, Solbach
- Subjects
Antigens, Bacterial ,Rheumatic Diseases ,Humans ,Cross Reactions ,Autoantibodies - Published
- 1992
22. [Untitled]
- Author
-
W. Solbach
- Subjects
media_common.quotation_subject ,Stuttgart ,General Medicine ,Art ,Anatomy ,Humanities ,Developmental Biology ,media_common - Published
- 2009
- Full Text
- View/download PDF
23. Different patterns of the L-histidine decarboxylase (HDC) gene expression in mice resistant and susceptible to experimental cutaneous leishmaniasis.
- Author
-
Z. Pós, K. Müller, I. Novak, E. Buzás, W. Solbach, A. Falus, and T. Laskay
- Subjects
LEISHMANIA ,HISTAMINE ,LEISHMANIASIS ,LYMPH nodes - Abstract
Objective and design: In the present study the experimental murine Leishmania major ( L. major) infection model was used to investigate the role of histamine biosynthesis in cutaneous leishmaniasis. Subjects, treatment and methods: A novel RNase Protection Assay (RPA) was developed and applied for the assessment of L-histidine decarboxylase (HDC) gene expression in organs of resistant C57BL/6 and susceptible BALB/c mice after infection with L. major. Results: In the acute phase of infection a rapid but transient induction of HDC expression was observed in the infected lymph nodes of both strains correlating both temporally and spatially with parasite spread. The signal was present in the draining popliteal lymph nodes of both hosts, however, only susceptible mice known to be unable to control parasite dissemination showed induction of HDC in their distant periaortic lymph nodes as well. During the chronic phase of infection only the heavily parasitized organs of BALB/c mice showed high HDC gene expression. Conclusions: These data suggest that expression of the histamine-producing enzyme HDC in the decisive acute phase of leishmaniasis is not coupled with development of either appropriate Th1 or inadequate Th2 responses to L. major. We hypothesize however, that during the chronic phase of infection elevated HDC levels, possibly of mast cell origin, are associated with Th2-dominated responses and serious disease development. [ABSTRACT FROM AUTHOR]
- Published
- 2004
24. Interactions of human T cell subsets during the induction of cytotoxic T lymphocytes: the role of interleukins.
- Author
-
Sabent, W. Solbach, Röllinghoff, Barth M., and Wagner, H.
- Subjects
- *
T cells , *LYMPHOCYTES , *INTERLEUKINS , *MONOCLONAL antibodies , *KILLER cells , *MITOGENS , *LECTINS - Abstract
In this work we study the role of subsets of human I cells, detectable by the OKT series of monoclonal antibodies, in the production of and the response to the lymphokine interleukin-2 (11-2) during the course of an allogeneic cytotoxic T lymphocyte response in vitro. The results obtained establish that the 11-2 producer cells reside within the OKT4 positive T cell subset. Once produced. 11-2 mediates the clonal expansion of alloantigen- activated cytotoxic T killer cells which reside in the OKT8 positive I cell subset. 11-2 appears to have no mitogenic activity on the activated OKT4 positive T cells which produce the lymphokine. In order to release 11-2, the OKT4 positive T cell requires a stimulus, such as allogeneic cells or the lectin phytohaemagglutinin A (PHA). Macro- phages are also required for 11-2 production, but the macrophage requirement can be bypassed by a soluble macrophage product as found in supernatants of lymphocyte cultures stimulated with lipopolysaccharide (LPS), the biological activity presumably representing Interleukin-l (11-1). [ABSTRACT FROM AUTHOR]
- Published
- 1982
25. Expression and Characterization of Leucocyte Antigens
- Author
-
R. Allen, S. Ferrone, J. Hoch, A. Bankhurst, J. Spellmann, G. R. Burmester, A. Dimitriu-Bona, P. Gregersen, S. J. Waters, R. J. Winchester, O. R. Burrone, F. Calabi, D. Gilmore, B. Wright, C. Milstein, E. Clark, P. Martin, J. Hansen, J. Ledbetter, L. de Leij, S. Poppema, T. H. The, J. E. De Vries, R. Vaessen, P. Janssens, B. Tan, A. Heiman, C. G. Figdor, B. Dörken, M. Pfreundschuh, G. Moldenhauer, E. Schwarz, G. Hämmerling, D. Frisman, S. Baird, E. Gazit, Y. Gothelf, R. Gil, S. Orgad, E. J. Yunis, Ch. Girardet, D. Heumann, J.-P. Mach, V. von Fliedner, S. Carrel, S. M. Goyert, J. Silver, N. Hogg, P. Hokland, S. F. Schlossman, J. Ritz, J. Kalil, J. P. Abita, C. Chomienne, O. Poirier, D. Besluau, H. Dastot, M. Reboul, M. Fellous, J. Colombani, L. Kater, P. Brekelmans, T. Daemen, H. J. Schuurman, F. Katz, S. Povey, K. Stanley, C. Schneider, M. Greaves, F. A. Lemonnier, P. P. Le Bouteiller, B. Malissen, P. Golstein, M. Malissen, Z. Mishal, D. H. Caillol, B. R. Jordan, F. Kourilsky, K. Lennert, H. Stein, H. K. Miiller-Hermelink, R. Vollenweider, R. A. Karol, J. Eng, D. Dennison, E. Faris, D. M. Marcus, D. Piatier-Tonneau, B. Boyer, P. Debre, D. Charron, J. M. Reuben, E. M. Hersh, P. W. A. Mansell, G. Newell, A. Rios, H. Rumpold, D. Kraft, O. Förster, T. F. Schulz, J. Alsenz, O. Scheiner, J. Lambris, M. P. Dierich, J. P. R. M. Van Laarhoven, R. Broekhuizen, G. Th. Spierenburg, C. H. M. M. De Bruyn, W. Solbach, M. Röllinghoff, H. Wagner, I. S. Szer, A. Irani, W. J. M. Tax, G. Janossy, M. Jonker, R. Willems, J. Leeuwenberg, P. J. A. Capel, R. A. P. Koene, H. F. M. Leeuwenberg, H. M. Willems, P. A. T. Tetteroo, F. Visser, P. Landsdorp, A. E. G. Kr. von dem Borne, J. S. Thompson, N. E. Goeken, S. A. Brown, J. R. Rhoades, K. Yamamoto, H. Nakauchi, H. Karasuyama, K. Kitamura, K. Tanimoto, and K. Okumura
- Subjects
Antiserum ,Gel electrophoresis ,Messenger RNA ,Antigen ,Immunoprecipitation ,Chemistry ,Translation (biology) ,Pan-T antigens ,Molecular biology ,Raji cell - Abstract
In vitro translation and immunoprecipitation were used to identify messenger RNAs (mRNAs) coding for lymphocyte surface antigens. The mRNAs were extracted from human lymphoblastoid cell lines of B-cell or T-cell origin. Messenger RNA was also extracted from fibroblastoid lines as non-lymphoid control. Translation products were reacted with a xenoantiserum raised against human lymphoid surface antigens. Products immunoprecipitated with antiserum were analyzed by SDS-polyacrylamide gel electrophoresis and fluorography.
- Published
- 1984
- Full Text
- View/download PDF
26. Kinetics of cell-mediated immunity developing during the course of Leishmania major infection in 'healer' and 'non-healer' mice: progressive impairment of response to and generation of interleukin-2
- Author
-
W, Solbach, M, Lohoff, H, Streck, P, Rohwer, and M, Röllinghoff
- Subjects
Immunity, Cellular ,Mice, Inbred BALB C ,T-Lymphocytes ,education ,Antigens, Protozoan ,Lymphocyte Activation ,Mice, Inbred C57BL ,Mice ,Animals ,Interleukin-2 ,Female ,Lymph Nodes ,Leishmaniasis ,Research Article - Abstract
Leishmania major (L. major)-infected mice of 'non-healer' (BALB/c) and 'healer' (C57BL/6) mouse-strain origin were studied with regard to the kinetics of cell-mediated immunity developing during the course of the disease. Cells obtained from lymph nodes draining L. major-infected footpads were comparatively analysed for their representation in the respective L3T4+, Lyt-2+ and sIg+ lymphocyte subsets; they were studied for their capacity to release interleukin-2 and to proliferate in response to L. major antigen and concanavalin A, including the determination of the frequencies of T cells proliferating antigen-specifically with or without an exogenous source of IL-2. The data obtained indicate L. major infection-induced long-lasting alterations in the cellular composition of the lymph node in both 'healer' and 'non-healer' mice. Moreover, they suggest that the inability of 'non-healer' mice to recover from L. major infection is associated with a progressive impairment of their lymph node T cells to release interleukin-2 in the culture supernatant and to respond to this lymphokine in vitro.
- Published
- 1987
27. Lymphokines in Human Lymphomas: Evidence for Malignant Proliferation of T Cells Producing Interleukin-2 in Sézary-Syndrome
- Author
-
M. Rollinghoff, S. Barth, W. Solbach, and H. Wagner
- Subjects
Interleukin 2 ,Mycosis fungoides ,business.industry ,Lymphoblastic Leukemia ,Chronic lymphocytic leukemia ,Lymphokine ,Phorbol Myristate Acetate ,medicine.disease ,hemic and lymphatic diseases ,medicine ,Cancer research ,Hairy cell leukemia ,business ,medicine.drug - Abstract
In man there are various clinical forms of T-lymphocytic neoplasia, including approximately 25% of acute lymphoblastic leukemia [6], a small percentage of chronic lymphocytic leukemia [5], rare cases of hairy cell leukemia [19], and all patients with cutaneous lymphomas, i.e., with mycosis fungoides, nodular papulosis, and Sezary-syndrome [14].
- Published
- 1982
- Full Text
- View/download PDF
28. Murine T cell subsets and interleukins: relationships between cytotoxic T cells, helper T cells and accessory cells
- Author
-
H, Wagner, M, Kronke, W, Solbach, P, Scheurich, M, Röllinghoff, and K, Pfizenmaier
- Subjects
Major Histocompatibility Complex ,Mice ,T-Lymphocytes ,Histocompatibility Antigens Class II ,Animals ,Humans ,Mice, Nude ,Cell Communication ,T-Lymphocytes, Helper-Inducer ,Thymus Gland ,Interleukin-1 ,T-Lymphocytes, Cytotoxic - Published
- 1982
29. [A classification system for HTLV-III infected patients]
- Author
-
W, Solbach
- Subjects
Acquired Immunodeficiency Syndrome ,AIDS-Related Complex ,HIV ,Humans - Published
- 1986
30. Interleukin-2 production in peripheral blood mononuclear cells of patients with gastrointestinal tumors
- Author
-
B, Koch, W, Regnat, W, Solbach, R, Lanz, P, Hermanek, and J R, Kalden
- Subjects
Adult ,Male ,Adolescent ,Prostaglandins E ,Age Factors ,Antibodies, Monoclonal ,Middle Aged ,Dinoprostone ,Monocytes ,Carcinoembryonic Antigen ,Crohn Disease ,Humans ,Interleukin-2 ,Female ,Lymphocytes ,Mitogens ,Child ,Cell Division ,Aged ,Gastrointestinal Neoplasms - Abstract
Peripheral blood mononuclear cells of patients with different tumors of the gastrointestinal tract (esophagus, stomach, colon, rectum), with Crohn's disease and healthy controls were analyzed for their capacity to produce mitogen induced interleukin-2 (I1-2). Tumor patients could be divided into two groups, one group exhibiting a nearly normal and a second group showing a significantly decreased production of I1-2. Most of the patients with a carcinoma of the colon were found in the low-producer group. Patients with Crohn's disease did not significantly differ from the relevant controls. Tumor patients with proven metastasis produced less I1-2 as compared to those with localized disease although the differences are not significant. When I1-2 containing supernatants of patients with tumors were additionally analyzed for the presence of prostaglandin E2, an inverse relationship could be demonstrated. Supernatants showing a suppressed activity of I1-2 exhibited increased amounts of PGE2, indicating a modulation of I1-2 production by prostaglandin E2.
- Published
- 1984
31. [Tinea imbricata in Papua-New Guinea. Treatment with griseofulvin and haloprogine in a population of the Gogol-Valley, Madang province]
- Author
-
J, Mattar and W, Solbach
- Subjects
Male ,Papua New Guinea ,Tinea ,Phenyl Ethers ,Humans ,Drug Therapy, Combination ,Female ,Griseofulvin - Published
- 1982
32. Chronic Inflammation Disrupts Circadian Rhythms in Splenic CD4+ and CD8+ T Cells in Mice.
- Author
-
Hirose M, Leliavski A, de Assis LVM, Matveeva O, Skrum L, Solbach W, Oster H, and Heyde I
- Subjects
- Animals, Mice, Inflammation, Circadian Rhythm, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Encephalomyelitis, Autoimmune, Experimental
- Abstract
Internal circadian clocks coordinate 24 h rhythms in behavior and physiology. Many immune functions show daily oscillations, and cellular circadian clocks can impact immune functions and disease outcome. Inflammation may disrupt circadian clocks in peripheral tissues and innate immune cells. However, it remains elusive if chronic inflammation impacts adaptive immune cell clock, e.g., in CD4+ and CD8+ T lymphocytes. We studied this in the experimental autoimmune encephalomyelitis (EAE), a mouse model for multiple sclerosis, as an established experimental paradigm for chronic inflammation. We analyzed splenic T cell circadian clock and immune gene expression rhythms in mice with late-stage EAE, CFA/PTx-treated, and untreated mice. In both treatment groups, clock gene expression rhythms were altered with differential effects for baseline expression and peak phase compared with control mice. Most immune cell marker genes tested in this study did not show circadian oscillations in either of the three groups, but time-of-day- independent alterations were observed in EAE and CFA/PTx compared to control mice. Notably, T cell effects were likely independent of central clock function as circadian behavioral rhythms in EAE mice remained intact. Together, chronic inflammation induced by CFA/PTx treatment and EAE immunization has lasting effects on circadian rhythms in peripheral immune cells.
- Published
- 2024
- Full Text
- View/download PDF
33. Dynamics of immunity over time: decline of anti-SARS-CoV-2 IgG antibodies and T-cell responses after mRNA vaccination in residents and health care workers in nursing homes and homes with assisted living support.
- Author
-
Schiffner J, Eisemann N, Baltus H, Jensen S, Wunderlich K, Schuesseler S, Eicker C, Teegen B, Boniakowsky D, Solbach W, and Mischnik A
- Abstract
Background: In the present study, we investigated the dynamics of immunity over time by measuring anti SARS-CoV-2 IgG antibodies and SARS-CoV-2 specific T-cell responses (interferon-gamma release assay) after two doses of vaccines in residents and health care workers (HCW). Mostly, 224 (98%) residents and 244 (89%) HCW received two doses of mRNA vaccine (BNT162b2, Pfizer-BioNTech); the rest of the participants received heterologous vaccinations with mRNA and vector vaccines. The study was conducted at the time when the Delta variant of SARS-CoV-2 prevailed., Methods: We analyzed blood samples of 228 residents (median age 83.8 years) and of 273 HCW (median age 49.7 years) from five nursing homes and one home for the elderly with assisted living support at one specific time point. Participants received two vaccinations. The blood samples were analyzed for SARS-CoV-2 specific IgG antibody and T-cell responses., Results: The initial immune responses in the younger participants were about 30% higher than in the older age group. Over time the estimated mean of the parameters (estimated from the study sample for the total population) decreased in all groups within the maximum observation period of 232 days. Comorbidities such as coronary heart disease or diabetes mellitus reduced the initial immune responses regardless of age. With regard to measured IgG antibody levels, absolute values decreased over time, whereas the interferon-gamma response remained at a constant level between day 120 and 180 and seemed to be less dependent on the time elapsed after vaccination., Conclusions: Based on our data, it does not seem possible to determine a reliable threshold of robust immunity, but we suggest that high titres of neutralizing capacity and interferon-gamma response might be an indicator of protection against severe COVID-19 courses., Competing Interests: The authors declare that they have no competing interests., (Copyright © 2023 Schiffner et al.)
- Published
- 2023
- Full Text
- View/download PDF
34. Long-Term Course of Humoral and Cellular Immune Responses in Outpatients After SARS-CoV-2 Infection.
- Author
-
Schiffner J, Backhaus I, Rimmele J, Schulz S, Möhlenkamp T, Klemens JM, Zapf D, Solbach W, and Mischnik A
- Subjects
- Antibodies, Viral, Cross-Sectional Studies, Humans, Immunity, Cellular, Immunoglobulin G, Outpatients, Prospective Studies, COVID-19, SARS-CoV-2
- Abstract
Characterization of the naturally acquired B and T cell immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is important for the development of public health and vaccination strategies to manage the burden of COVID-19 disease. We conducted a prospective, cross-sectional analysis in COVID-19 recovered patients at various time points over a 10-month period in order to investigate how circulating antibody levels and interferon-gamma (IFN-γ) release by peripheral blood cells change over time following natural infection. From March 2020 till January 2021, we enrolled 412 adults mostly with mild or moderate disease course. At each study visit, subjects donated peripheral blood for testing of anti-SARS-CoV-2 IgG antibodies and IFN-γ release after SARS-CoV-2 S-protein stimulation. Anti-SARS-CoV-2 immunoglobulin G (IgG) antibodies were positive in 316 of 412 (76.7%) and borderline in 31 of 412 (7.5%) patients. Our confirmation assay for the presence of neutralizing antibodies was positive in 215 of 412 (52.2%) and borderline in 88 of 412 (21.4%) patients. Likewise, in 274 of 412 (66.5%) positive IFN-γ release and IgG antibodies were detected. With respect to time after infection, both IgG antibody levels and IFN-γ concentrations decreased by about half within 300 days. Statistically, production of IgG and IFN-γ were closely associated, but on an individual basis, we observed patients with high-antibody titres but low IFN-γ levels and vice versa. Our data suggest that immunological reaction is acquired in most individuals after natural infection with SARS-CoV-2 and is sustained in the majority of patients for at least 10 months after infection after a mild or moderate disease course. Since, so far, no robust marker for protection against COVID-19 exists, we recommend utilizing both, IgG and IFN-γ release for an individual assessment of the immunity status., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Schiffner, Backhaus, Rimmele, Schulz, Möhlenkamp, Klemens, Zapf, Solbach and Mischnik.)
- Published
- 2021
- Full Text
- View/download PDF
35. Antibody Profiling of COVID-19 Patients in an Urban Low-Incidence Region in Northern Germany.
- Author
-
Solbach W, Schiffner J, Backhaus I, Burger D, Staiger R, Tiemer B, Bobrowski A, Hutchings T, and Mischnik A
- Subjects
- Antibodies, Viral, Germany epidemiology, Humans, Incidence, SARS-CoV-2, COVID-19
- Abstract
A vast majority of COVID-19 cases present with mild or moderate symptoms. The study region is in an urban and well-defined environment in a low-incidence region in Northern Germany. In the present study, we explored the dynamics of the antibody response with respect to onset, level and duration in patients with confirmed SARS-CoV-2 infection. Anti-SARS-CoV-2 IgG and IgA were detected by automated enzyme-linked immunosorbent assay (ELISA) of SARS-CoV-2 infected patients monitored by the Health Protection Authority. This explorative monocentric study shows IgA and IgG antibody profiles from 118 patients with self-reported mild to moderate, or no COVID-19 related symptoms after laboratory-confirmed infection with SARS-CoV-2. We found that 21.7% and 18.1% of patients were seronegative for IgA or IgG, respectively. Clinically, most of the seronegative patients showed no to only moderate symptoms. With regard to antibody profiling 82% of all patients developed sustainable antibodies (IgG) and 78% (IgA) 3 weeks or later after the infection. Our data indicate that antibody-positivity is a useful indicator of a previous SARS-CoV-2 infection. Negative antibodies do not rule out SARS-CoV-2 infection. Future studies are needed to determine the functionality of the antibodies in terms of neutralization capacity leading to personal protection and prevention ability to transmit the virus as well as to protect after vaccination., (Copyright © 2020 Solbach, Schiffner, Backhaus, Burger, Staiger, Tiemer, Bobrowski, Hutchings and Mischnik.)
- Published
- 2020
- Full Text
- View/download PDF
36. Combined culture and metagenomic analyses reveal significant shifts in the composition of the cutaneous microbiome in psoriasis.
- Author
-
Langan EA, Künstner A, Miodovnik M, Zillikens D, Thaçi D, Baines JF, Ibrahim SM, Solbach W, and Knobloch JK
- Subjects
- Adult, Bacteria genetics, Bacteria immunology, Bacteriological Techniques, DNA, Bacterial genetics, DNA, Bacterial isolation & purification, Female, Humans, Male, Metagenomics, Microbiota genetics, Middle Aged, Prospective Studies, Psoriasis immunology, RNA, Ribosomal, 16S genetics, Skin immunology, Bacteria isolation & purification, Microbiota immunology, Psoriasis microbiology, Skin microbiology
- Abstract
Background: The treatment of psoriasis has been revolutionized by the development of biologic therapies. However, the pathogenesis of psoriasis, in particular the role of the cutaneous microbiome, remains incompletely understood. Moreover, skin microbiome studies have relied heavily on 16S rRNA sequencing data in the absence of bacterial culture., Objectives: To characterize and compare the cutaneous microbiome in 20 healthy controls and 23 patients with psoriasis using metagenomic analyses and to determine changes in the microbiome during treatment., Methods: Swabs from lesional and nonlesional skin from patients with psoriasis, and from controls matched for site and skin microenvironment, were analysed using both 16S rRNA sequencing and traditional culture combined with mass spectrometry (MALDI-TOF) in a prospective study., Results: Psoriasis was associated with an increased abundance of Firmicutes and a corresponding reduction in Actinobacteria, most marked in lesional skin, and at least partially reversed during systemic treatment. Shifts in bacterial community composition in lesional sites were reflected in similar changes in culturable bacteria, although changes in the microbiota over repeated swabbing were detectable only with sequencing. The composition of the microbial communities varied by skin site and microenvironment. Prevotella and Staphylococcus were significantly associated with lesional skin, and Anaerococcus and Propionibacterium with nonlesional skin. There were no significant differences in the amount of bacteria cultured from the skin of healthy controls and patients with psoriasis., Conclusions: Shifts in the cutaneous microbiome in psoriasis, particularly during treatment, may shed new light on the pathogenesis of the disease and may be clinically exploited to predict treatment response. What's already known about this topic? Alterations in the composition of the cutaneous microbiome have been described in psoriasis, although methodological differences in study design prevent direct comparison of results. To date, most cutaneous microbiome studies have focused on 16S rRNA sequencing data, including both living and dead bacteria. What does this study add? This prospective observational study confirms that changes in the composition of the cutaneous microbiome, detected by 16S rRNA sequencing, are consistent with those identified by bacterial culture and mass spectrometry. The changes in the microbiome during antipsoriasis therapy should be further investigated to determine whether these represent potential novel biomarkers of treatment response. What is the translational message? Characterization of cutaneous microbiota may ultimately move into the clinic to help facilitate treatment selection, not only by optimizing currently available treatments, but also by identifying new therapeutic targets., (© 2019 British Association of Dermatologists.)
- Published
- 2019
- Full Text
- View/download PDF
37. Type-1 interferons prolong the lifespan of neutrophils by interfering with members of the apoptotic cascade.
- Author
-
Aga E, Mukherjee A, Rane D, More V, Patil T, van Zandbergen G, Solbach W, Dandapat J, Tackenberg H, Ohms M, Sarkar A, and Laskay T
- Subjects
- Caspase 3 metabolism, Cells, Cultured, Coculture Techniques methods, Cytokines metabolism, Humans, Inflammation metabolism, Interferon-beta metabolism, Signal Transduction physiology, Apoptosis physiology, Interferon Type I metabolism, Longevity physiology, Neutrophils metabolism
- Abstract
Polymorphonuclear Neutrophils (PMNs) are metabolically highly active phagocytes, present in abundant numbers in the circulation. These active cells take the onus of clearing invading pathogens by crowding at inflammatory sites in huge numbers. Though PMNs are extremely short living and die upon spontaneous apoptosis, extended lifespan has been observed among those cells arrive at the inflammation sites or tackle intracellular infections or face any microbial challenges. The delay/inhibition of spontaneous apoptosis of these short-living cells at the inflammatory core rather helps in combating pathogens. Like many candidates, type-1 interferons (type-1 IFNs) is a group of cytokines predominant at the inflammation site. Although there are some isolated reports, a systematic study is still lacking which addresses the impact of the predominant type of interferon on the spontaneous apoptosis of neutrophils. Here in, we have observed that exposure of these IFNs (IFN-β, IFN-α & IFN-ω etc) on human neutrophils prevents the degradation of the Bfl1, an important anti-apoptotic partner in the apoptotic cascade. Treatment showed a significant reduction in the release of cytochrome-C in the cytosol, a critical regulator in the intrinsic apoptotic pathway. We also noticed a reduction in the conversion of procaspase -3 to active caspase-3, a crucial executioner caspase towards initiation of apoptosis. Taken together our results show that exposure to interferon interferes with apoptotic pathways of neutrophils and thereby delay its spontaneous apoptosis. These findings would help us further deciphering specific roles if these inflammatory agents are causing any immune-metabolomic changes on PMNs at the inflammatory and infection core., (Copyright © 2018. Published by Elsevier Ltd.)
- Published
- 2018
- Full Text
- View/download PDF
38. The role of the microbiome in psoriasis: moving from disease description to treatment selection?
- Author
-
Langan EA, Griffiths CEM, Solbach W, Knobloch JK, Zillikens D, and Thaçi D
- Subjects
- Host-Pathogen Interactions physiology, Humans, Psoriasis therapy, RNA, Ribosomal, 16S genetics, Sequence Analysis, RNA, Skin Diseases, Bacterial complications, Streptococcal Infections complications, Microbiota physiology, Psoriasis microbiology, Skin microbiology
- Abstract
Background: With several million microbes per square centimetre of skin, the task of mapping the physiological cutaneous microbiome is enormous. Indeed, the reliance on bacterial culture to identify cutaneous bacterial communities has led to a systematic underappreciation of cutaneous microbial diversity, potentially limiting our understanding of common inflammatory skin diseases, including psoriasis. However, based heavily on developments in molecular biology and bioinformatics, including next-generation sequencing, the last decade has witnessed a marked increase in our understanding of the extent and composition of the cutaneous microbiome. It is already clear that skin-specific (skin site and skin microenvironment), individual-specific (hygiene, sex, age and hormonal status), disease-specific (atopic eczema, acne) and genetic factors can all influence the cutaneous microbiome, albeit to varying and, as yet, ill-defined extents., Objectives: To investigate the role of the microbiome in psoriasis and to outline how microbiome studies can be harnessed to provide new insights into disease pathogenesis and treatment selection., Methods: This review briefly describes the process of 16S ribosomal RNA sequencing and then charts our current understanding of the cutaneous microbiome in health and the alterations (dysbiosis) associated with chronic inflammatory diseases, with particular reference to psoriasis., Results: The possibility and clinical relevance of intraindividual cross-talk between the various microbiomes is discussed and potential mechanisms underpinning the interactions between resident skin flora and the immune system are highlighted., Conclusions: Ultimately, in the age of personalized medicine, the integration of cutaneous microbiome signatures and comprehensive disease and drug response endotypes will herald a novel approach in the clinical management of chronic multisystem inflammatory diseases., (© 2017 British Association of Dermatologists.)
- Published
- 2018
- Full Text
- View/download PDF
39. "Life-like" assessment of antimicrobial surfaces by a new touch transfer assay displays strong superiority of a copper alloy compared to silver containing surfaces.
- Author
-
Knobloch JK, Tofern S, Kunz W, Schütze S, Riecke M, Solbach W, and Wuske T
- Subjects
- Reproducibility of Results, Surface Properties, Alloys pharmacology, Anti-Infective Agents pharmacology, Copper pharmacology, Silver pharmacology
- Abstract
Transmission of bacteria from inanimate surfaces in healthcare associated environments is an important source of hospital acquired infections. A number of commercially available medical devices promise to fulfill antibacterial activity to reduce environmental contamination. In this study we developed a touch transfer assay modeling fingerprint transmission to investigate the antibacterial activity of surfaces, with confirmed antibacterial activity by a modified ISO 22196 (JIS Z 2801) assay to test such surfaces under more realistic conditions. Bacteria were taken up from a dry standardized primary contaminated surface (PCS) with disinfected fingers or fingers covered with sterile and moistened cotton gloves. Subsequently, bacteria were transferred by pressing on secondary contaminated surfaces (SCS) with or without potential antibacterial activity and the relative reduction rate was determined after 24 h. A stable transmission rate between PCS and SCS was observed using moistened sterile gloves. A copper containing alloy displayed at least a tenfold reduction of the bacterial load consistently reaching less than 2.5 cfu/cm2. In contrast, no significant reduction of bacterial contamination by silver containing surfaces and matured pure silver was observed in the touch transfer assay. With the touch transfer assay we successfully established a new reproducible method modeling cross contamination. Using the new method we were able to demonstrate that several surfaces with confirmed antimicrobial activity in a modified ISO 22196 (JIS Z 2801) assay lacked effectiveness under defined ambient conditions. This data indicate that liquid based assays like the ISO 22196 should be critically reviewed before claiming antibacterial activity for surfaces in the setting of contamination of dry surfaces by contact to the human skin. We suggest the newly developed touch transfer assay as a new additional tool for the assessment of potential antimicrobial surfaces prior utilization in hospital environments.
- Published
- 2017
- Full Text
- View/download PDF
40. Lymphocyte Circadian Clocks Control Lymph Node Trafficking and Adaptive Immune Responses.
- Author
-
Druzd D, Matveeva O, Ince L, Harrison U, He W, Schmal C, Herzel H, Tsang AH, Kawakami N, Leliavski A, Uhl O, Yao L, Sander LE, Chen CS, Kraus K, de Juan A, Hergenhan SM, Ehlers M, Koletzko B, Haas R, Solbach W, Oster H, and Scheiermann C
- Subjects
- Adoptive Transfer, Animals, Encephalomyelitis, Autoimmune, Experimental immunology, Flow Cytometry, Fluorescent Antibody Technique, Lymph Nodes immunology, Mice, Mice, Inbred C57BL, Mice, Transgenic, Real-Time Polymerase Chain Reaction, Adaptive Immunity immunology, Chemotaxis, Leukocyte immunology, Circadian Clocks immunology, Immunologic Surveillance immunology, Lymphocytes immunology
- Abstract
Lymphocytes circulate through lymph nodes (LN) in search for antigen in what is believed to be a continuous process. Here, we show that lymphocyte migration through lymph nodes and lymph occurred in a non-continuous, circadian manner. Lymphocyte homing to lymph nodes peaked at night onset, with cells leaving the tissue during the day. This resulted in strong oscillations in lymphocyte cellularity in lymph nodes and efferent lymphatic fluid. Using lineage-specific genetic ablation of circadian clock function, we demonstrated this to be dependent on rhythmic expression of promigratory factors on lymphocytes. Dendritic cell numbers peaked in phase with lymphocytes, with diurnal oscillations being present in disease severity after immunization to induce experimental autoimmune encephalomyelitis (EAE). These rhythms were abolished by genetic disruption of T cell clocks, demonstrating a circadian regulation of lymphocyte migration through lymph nodes with time-of-day of immunization being critical for adaptive immune responses weeks later., (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.)
- Published
- 2017
- Full Text
- View/download PDF
41. IL-16 and MIF: messengers beyond neutrophil cell death.
- Author
-
Roth S, Solbach W, and Laskay T
- Subjects
- Cell Death physiology, Humans, Signal Transduction, Interleukin-16 metabolism, Macrophage Migration-Inhibitory Factors metabolism, Neutrophils metabolism
- Published
- 2016
- Full Text
- View/download PDF
42. Transcription regulates HIF-1α expression in CD4(+) T cells.
- Author
-
Bollinger T, Bollinger A, Gies S, Feldhoff L, Solbach W, and Rupp J
- Subjects
- CD4-Positive T-Lymphocytes immunology, Female, Humans, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Lymphocyte Activation immunology, Male, Protein Stability, RNA, Messenger genetics, RNA, Messenger metabolism, CD4-Positive T-Lymphocytes metabolism, Gene Expression Regulation, Hypoxia-Inducible Factor 1, alpha Subunit genetics, Transcription, Genetic
- Abstract
The transcription factor hypoxia inducible factor-1α (HIF-1α) mediates the metabolic adaptation of cells to hypoxia and T-helper cell fate. However, HIF-1α regulation in CD4(+) T cells (T cells) remains elusive. Here we observed that depletion of oxygen (O2⩽2%) alone was not sufficient to induce HIF-1α expression in T cells. However, when hypoxic T cells were stimulated, HIF-1α was expressed and this was dependent on nuclear factor-κB- and nuclear factor of activated T cell (NFAT)-mediated transcriptional upregulation of Hif-1α mRNA. HIF-1α upregulation could be blocked by drugs inhibiting NF-κB, NFAT or mammalian target of rapamycin precluding CD4(+) T-cell stimulation or translation in T cells, as well as by blocking transcription. CD3, CD28, phorbol-12-myristat-13-acetat (PMA) or ionomycin-stimulated T cells did not express HIF-1α under normoxic conditions. In conclusion, regulation of HIF-1α expression in CD4(+) T cells in hypoxia gravely relies on its transcriptional upregulation and subsequent enhanced protein stabilization.
- Published
- 2016
- Full Text
- View/download PDF
43. Dimethylfumarate Impairs Neutrophil Functions.
- Author
-
Müller S, Behnen M, Bieber K, Möller S, Hellberg L, Witte M, Hänsel M, Zillikens D, Solbach W, Laskay T, and Ludwig RJ
- Subjects
- Animals, Blotting, Western, Cell Movement drug effects, Cells, Cultured, Confidence Intervals, Disease Models, Animal, Epidermolysis Bullosa Acquisita pathology, Humans, Mice, Mice, Inbred C57BL, Reactive Oxygen Species metabolism, Dimethyl Fumarate pharmacology, Epidermolysis Bullosa Acquisita immunology, Neutrophils cytology, Neutrophils drug effects
- Abstract
Host defense against pathogens relies on neutrophil activation. Inadequate neutrophil activation is often associated with chronic inflammatory diseases. Neutrophils also constitute a significant portion of infiltrating cells in chronic inflammatory diseases, for example, psoriasis and multiple sclerosis. Fumarates improve the latter diseases, which so far has been attributed to the effects on lymphocytes and dendritic cells. Here, we focused on the effects of dimethylfumarate (DMF) on neutrophils. In vitro, DMF inhibited neutrophil activation, including changes in surface marker expression, reactive oxygen species production, formation of neutrophil extracellular traps, and migration. Phagocytic ability and autoantibody-induced, neutrophil-dependent tissue injury ex vivo was also impaired by DMF. Regarding the mode of action, DMF modulates-in a stimulus-dependent manner-neutrophil activation using the phosphoinositide 3-kinase/Akt-p38 mitogen-activated protein kinase and extracellular signal-regulated kinase 1/2 pathways. For in vivo validation, mouse models of epidermolysis bullosa acquisita, an organ-specific autoimmune disease caused by autoantibodies to type VII collagen, were employed. In the presence of DMF, blistering induced by injection of anti-type VII collagen antibodies into mice was significantly impaired. DMF treatment of mice with clinically already-manifested epidermolysis bullosa acquisita led to disease improvement. Collectively, we demonstrate a profound inhibitory activity of DMF on neutrophil functions. These findings encourage wider use of DMF in patients with neutrophil-mediated diseases., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
44. Hypertension and mild chronic kidney disease persist following severe haemolytic uraemic syndrome caused by Shiga toxin-producing Escherichia coli O104:H4 in adults.
- Author
-
Derad I, Obermann B, Katalinic A, Eisemann N, Knobloch JK, Sayk F, Wellhöner P, Lehnert H, Solbach W, Süfke S, Steinhoff J, and Nitschke M
- Subjects
- Adult, Anti-Bacterial Agents therapeutic use, Antibodies, Monoclonal, Humanized therapeutic use, Azithromycin therapeutic use, Complement Inactivating Agents therapeutic use, Drug Therapy, Combination, Escherichia coli Infections drug therapy, Escherichia coli Infections microbiology, Female, Follow-Up Studies, Glomerular Filtration Rate, Hemolytic-Uremic Syndrome drug therapy, Hemolytic-Uremic Syndrome microbiology, Humans, Hypertension prevention & control, Male, Middle Aged, Prospective Studies, Renal Insufficiency, Chronic prevention & control, Treatment Outcome, Enterohemorrhagic Escherichia coli, Escherichia coli Infections complications, Hemolytic-Uremic Syndrome complications, Hypertension microbiology, Renal Insufficiency, Chronic microbiology
- Abstract
Background: Shiga toxin-producing, enteroaggregative Escherichia coli was responsible for the 2011 outbreak of haemolytic uraemic syndrome (HUS). The present single-centre, observational study describes the 1-year course of the disease with an emphasis on kidney function. Outcome data after 1 year are associated with treatment and patient characteristics at onset of HUS., Methods: Patients were treated according to a standardized approach of supportive care, including a limited number of plasmapheresis. On top of this treatment, patients with severe HUS (n = 35) received eculizumab, a humanized anti-C5 monoclonal antibody inhibiting terminal complement activation. The per-protocol decision--to start or omit an extended therapy with eculizumab accompanied by azithromycin--separated the patients into two groups and marked Day 0 of the prospective study. Standardized visits assessed the patients' well-being, kidney function, neurological symptoms, haematological changes and blood pressure., Results: Fifty-six patients were regularly seen during the follow-up. All patients had survived without end-stage renal disease. Young(er) age alleviated restoring kidney function after acute kidney injury even in severe HUS. After 1 year, kidney function was affected with proteinuria [26.7%; 95% confidence interval (CI) 13.8-39.6], increased serum creatinine (4.4%, CI 0.0-10.4), increased cystatin C (46.7%, CI 32.1-61.3) and reduced (<90 mL/min) estimated glomerular filtration rate (46.7%, CI 32.1-61.3). Nine of the 36 patients without previous hypertension developed de novo hypertension (25%, CI 10.9-39.1). All these patients had severe HUS., Conclusions: Although shiga toxin-producing Escherichia coli (STEC)-HUS induced by O104:H4 was a life-threatening acute disease, follow-up showed a good recovery of organ function in all patients. Whereas kidney function recovered even after longer duration of dialysis, chronic hypertension developed after severe HUS with neurological symptoms and could not be prevented by the extended therapy., (© The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
45. Production, crystallization and X-ray diffraction analysis of the protease CT441 from Chlamydia trachomatis.
- Author
-
Kohlmann F, Shima K, Rupp J, Solbach W, Hilgenfeld R, and Hansen G
- Subjects
- Amino Acid Sequence, Bacterial Proteins isolation & purification, Crystallization, Molecular Sequence Data, Bacterial Proteins chemistry, Chlamydia trachomatis metabolism, X-Ray Diffraction
- Abstract
The prokaryotic obligate intracellular pathogen Chlamydia trachomatis is the most prevalent cause of preventable blindness, affecting approximately six million people worldwide. In addition, C. trachomatis is the most commonly reported sexually transmitted pathogen in Europe and the US, causing pelvic inflammation, ectopic pregnancy and infertility. As in other intracellular pathogens, proteases play crucial roles during most stages of the complex life cycle of Chlamydia. CT441 is a chlamydial protease that has been reported to interfere with oestrogen signalling of the host cell. Here, the recombinant production, purification and crystallization of an inactive variant of CT441, designated CT441° (active-site Ser455 replaced by Ala), are described. CT441° was crystallized in space group P22121, with unit-cell parameters a = 86.7, b = 184.0, c = 209.6 Å. A complete diffraction data set was collected to a resolution of 2.95 Å.
- Published
- 2015
- Full Text
- View/download PDF
46. Secondary necrotic neutrophils release interleukin-16C and macrophage migration inhibitory factor from stores in the cytosol.
- Author
-
Roth S, Agthe M, Eickhoff S, Möller S, Karsten CM, Borregaard N, Solbach W, and Laskay T
- Abstract
Neutrophils harbor a number of preformed effector proteins that allow for immediate antimicrobial functions without the need for time-consuming de novo synthesis. Evidence indicates that neutrophils also contain preformed cytokines, including interleukin (IL)-1ra, CXCL8 and CXCL2. In the search for additional preformed cytokines, a cytokine array analysis identified IL-16 and macrophage migration inhibitory factor (MIF) as preformed cytokines in lysates from human primary neutrophils. Both IL-16 and MIF are unconventional cytokines because they lack a signal sequence. Using confocal immunofluorescence microscopy as well as western blot analysis of subcellular fractions, IL-16 and MIF were found to be stored in the cytosol rather than in the granules of human neutrophils, which implies an unconventional secretion mechanism for both cytokines. IL-16 is synthesized and stored as a precursor (pre-IL-16). We present evidence that the processing of pre-IL-16 to the biologically active IL-16C is mediated by caspase-3 and occurs during both spontaneous and UV-induced apoptosis of human neutrophils. Although IL-16 processing occurs during apoptosis, IL-16C and MIF release was observed only during secondary necrosis of neutrophils. Screening a panel of microbial substances and proinflammatory cytokines did not identify a stimulus that induced the release of IL-16C and MIF independent of secondary necrosis. The data presented here suggest that IL-16 and MIF are neutrophil-derived inflammatory mediators released under conditions of insufficient clearance of apoptotic neutrophils, as typically occurs at sites of infection and autoimmunity.
- Published
- 2015
- Full Text
- View/download PDF
47. Mechanisms of apoptosis inhibition in Chlamydia pneumoniae-infected neutrophils.
- Author
-
Sarkar A, Möller S, Bhattacharyya A, Behnen M, Rupp J, van Zandbergen G, Solbach W, and Laskay T
- Subjects
- Gene Expression Regulation, Humans, Interleukin-8 metabolism, MAP Kinase Signaling System, Myeloid Cell Leukemia Sequence 1 Protein genetics, Myeloid Cell Leukemia Sequence 1 Protein metabolism, NF-kappa B metabolism, Phosphatidylinositol 3-Kinases genetics, Phosphatidylinositol 3-Kinases metabolism, Phosphorylation, Signal Transduction, p38 Mitogen-Activated Protein Kinases genetics, p38 Mitogen-Activated Protein Kinases metabolism, Apoptosis, Chlamydophila pneumoniae growth & development, Neutrophils microbiology
- Abstract
The obligatory intracellular bacterium Chlamydia pneumoniae (C. pneumoniae) can survive and multiply in neutrophil granulocytes. Since neutrophils are short living cells, inhibition of neutrophil apoptosis appears to play a major role in the productive infection of neutrophils by C. pneumoniae. In the present study, we have investigated which survival pathways and which events of the apoptotic process are modulated in C. pneumoniae-infected neutrophils. All infection experiments were carried out using primary human neutrophils in vitro. We show that infection with C. pneumoniae activates PI3K/Akt as well as the ERK1/2 and p38 MAP kinases and present evidence that activation of the PI3K/Akt and ERK1/2 pathways are essential to initiate the apoptosis delay in C. pneumoniae-infected neutrophils. Both the PI3K/Akt and ERK1/2 pathways are involved in the maintained expression of the anti-apoptotic protein Mcl-1. In addition, we also showed that the PI3K/Akt pathway leads to the activation of NF-κB-dependent release of IL-8 by infected neutrophils. Infection with C. pneumoniae activates the PI3K/Akt and ERK1/2 MAPK survival pathways in neutrophils, induces the NF-κB dependent release of IL-8 and leads to the maintenance of Mcl-1 expression in neutrophils., (Copyright © 2015 Elsevier GmbH. All rights reserved.)
- Published
- 2015
- Full Text
- View/download PDF
48. The role of endoplasmic reticulum-related BiP/GRP78 in interferon gamma-induced persistent Chlamydia pneumoniae infection.
- Author
-
Shima K, Klinger M, Schütze S, Kaufhold I, Solbach W, Reiling N, and Rupp J
- Subjects
- Endoplasmic Reticulum Chaperone BiP, Hep G2 Cells, Hepatocytes immunology, Hepatocytes microbiology, Humans, Chlamydophila Infections immunology, Chlamydophila pneumoniae immunology, Heat-Shock Proteins metabolism, Host-Pathogen Interactions, Interferon-gamma metabolism
- Abstract
Direct interaction of Chlamydiae with the endoplasmic reticulum (ER) is essential in intracellular productive infection. However, little is known about the interplay between Chlamydiae and the ER under cellular stress conditions that are observed in interferon gamma (IFN-γ) induced chlamydial persistent infection. ER stress responses are centrally regulated by the unfolded protein response (UPR) under the control of the ER chaperone BiP/GRP78 to maintain cellular homeostasis. In this study, we could show that the ER directly contacted with productive and IFN-γ-induced persistent inclusions of Chlamydia pneumoniae (Cpn). BiP/GRP78 induction was observed in the early phase but not in the late phase of IFN-γ-induced persistent infection. Enhanced BiP/GRP78 expression in the early phase of IFN-γ-induced persistent Cpn infection was accompanied by phosphorylation of the eukaryotic initiation factor-2α (eIF2α) and down-regulation of the vesicle-associated membrane protein-associated protein B. Loss of BiP/GRP78 function resulted in enhanced phosphorylation of eIF2α and increased host cell apoptosis. In contrast, enhanced BiP/GRP78 expression in IFN-γ-induced persistent Cpn infection attenuated phosphorylation of eIF2α upon an exogenous ER stress inducer. In conclusion, ER-related BiP/GRP78 plays a key role to restore cells from stress conditions that are observed in the early phase of IFN-γ-induced persistent infection., (© 2015 John Wiley & Sons Ltd.)
- Published
- 2015
- Full Text
- View/download PDF
49. Structural basis of the proteolytic and chaperone activity of Chlamydia trachomatis CT441.
- Author
-
Kohlmann F, Shima K, Hilgenfeld R, Solbach W, Rupp J, and Hansen G
- Subjects
- Bacterial Proteins genetics, Chlamydia trachomatis genetics, Crystallography, X-Ray, Models, Molecular, Molecular Chaperones genetics, Protein Binding, Protein Conformation, Protein Structure, Tertiary, Proteolysis, Recombinant Proteins, Bacterial Proteins metabolism, Chlamydia trachomatis metabolism, Gene Expression Regulation, Bacterial physiology, Molecular Chaperones metabolism
- Abstract
Chlamydia trachomatis is the most prevalent cause of preventable blindness worldwide and a major reason for infectious infertility in females. Several bacterial factors have been implicated in the pathogenesis of C. trachomatis. Combining structural and mutational analysis, we have shown that the proteolytic function of CT441 depends on a conserved Ser/Lys/Gln catalytic triad and a functional substrate-binding site within a flexible PDZ (postsynaptic density of 95 kDa, discs large, and zonula occludens) domain. Previously, it has been suggested that CT441 is involved in modulating estrogen signaling responses of the host cell. Our results show that although in vitro CT441 exhibits proteolytic activity against SRAP1, a coactivator of estrogen receptor α, CT441-mediated SRAP1 degradation is not observed during the intracellular developmental cycle before host cells are lysed and infectious chlamydiae are released. Most compellingly, we have newly identified a chaperone activity of CT441, indicating a role of CT441 in prokaryotic protein quality control processes., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)
- Published
- 2015
- Full Text
- View/download PDF
50. Immobilized immune complexes induce neutrophil extracellular trap release by human neutrophil granulocytes via FcγRIIIB and Mac-1.
- Author
-
Behnen M, Leschczyk C, Möller S, Batel T, Klinger M, Solbach W, and Laskay T
- Subjects
- Aminopyrine pharmacology, Antioxidants pharmacology, Ascorbic Acid pharmacology, Autoimmune Diseases immunology, Butadienes pharmacology, CD11a Antigen metabolism, CD18 Antigens metabolism, Cell Degranulation, Cells, Cultured, Extracellular Signal-Regulated MAP Kinases antagonists & inhibitors, GPI-Linked Proteins immunology, Humans, Imidazoles pharmacology, Inflammation immunology, Intracellular Signaling Peptides and Proteins antagonists & inhibitors, Intracellular Signaling Peptides and Proteins immunology, Lymphocyte Function-Associated Antigen-1 immunology, Macrophage-1 Antigen metabolism, Mesalamine pharmacology, Nitriles pharmacology, Onium Compounds pharmacology, Phosphoinositide-3 Kinase Inhibitors, Protein-Tyrosine Kinases antagonists & inhibitors, Protein-Tyrosine Kinases immunology, Proto-Oncogene Proteins c-akt antagonists & inhibitors, Pyridines pharmacology, Pyrimidines pharmacology, Reactive Oxygen Species metabolism, Receptors, IgG antagonists & inhibitors, Syk Kinase, p38 Mitogen-Activated Protein Kinases antagonists & inhibitors, src-Family Kinases antagonists & inhibitors, src-Family Kinases immunology, Antigen-Antibody Complex immunology, Macrophage-1 Antigen immunology, Neutrophil Activation immunology, Neutrophils immunology, Receptors, IgG immunology
- Abstract
Canonical neutrophil antimicrobial effector mechanisms, such as degranulation, production of reactive oxygen species, and release of neutrophil extracellular traps (NETs), can result in severe pathology. Activation of neutrophils through immune complexes (ICs) plays a central role in the pathogenesis of many autoimmune inflammatory diseases. In this study, we report that immobilized ICs (iICs), which are hallmarks of several autoimmune diseases, induce the release of NETs from primary human neutrophils. The iIC-induced NET formation was found to require production of reactive oxygen species by NADPH oxidase and myeloperoxidase and to be mediated by FcγRIIIb. Blocking of the β2 integrin macrophage-1 Ag but not lymphocyte function-associated Ag-1 abolished iIC-induced NET formation. This suggests that FcγRIIIb signals in association with macrophage-1 Ag. As intracellular signaling pathways involved in iIC-induced NET formation we identified the tyrosine kinase Src/Syk pathway, which downstream regulates the PI3K/Akt, p38 MAPK, and ERK1/2 pathways. To our knowledge, the present study shows for the first time that iICs induce NET formation. Thus, we conclude that NETs contribute to pathology in autoimmune inflammatory disorders associated with surface-bound ICs., (Copyright © 2014 by The American Association of Immunologists, Inc.)
- Published
- 2014
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.