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1. Prevalence of lymphoplasmacytic synovitis in dogs with naturally occurring cranial cruciate ligament rupture

Author: Jay B. Erne, Robert L. Goring, Fidelma A Kennedy, and William C Schoenborn
Subjects: Male, Pathology, medicine.medical_specialty, Radiography, Lymphocytosis, Cruciate ligament, Dogs, Cytology, Synovitis, Synovial Fluid, Biopsy, Prevalence, medicine, Animals, Synovial fluid, Dog Diseases, Rupture, General Veterinary, medicine.diagnostic_test, business.industry, Anterior Cruciate Ligament Injuries, medicine.disease, Cross-Sectional Studies, medicine.anatomical_structure, Lameness, Female, lipids (amino acids, peptides, and proteins), business, Medial meniscus
Abstract: Objective—To determine the prevalence of lymphoplasmacytic synovitis (LPS) in dogs with naturally occurring cranial cruciate ligament (CCL) rupture and compare clinical, radiographic, cytologic, and histologic findings in dogs with and without LPS. Design—Cross-sectional study. Animals—110 dogs with naturally occurring CCL rupture. Procedures—Histologic examination of synovial biopsy specimens obtained at the time of surgical treatment was used to identify dogs with LPS. Clinical, radiographic, cytologic, and histologic findings were compared between dogs with and without LPS. Results—56 (51%) dogs had histologic evidence of LPS. There were no significant differences in age, body weight, duration of lameness, severity of lameness, severity of radiographic signs of degenerative joint disease, extent of CCL rupture (partial vs complete), or gross appearance of the medial meniscus between dogs with and without LPS. Mean tibial plateau angle was significantly lower in dogs with LPS than in dogs without LPS, and dogs with LPS were significantly more likely to have neutrophils in their synovial fluid. Lymphocytes were seen in synovial fluid from a single dog with LPS. Conclusions and Clinical Relevance—Results suggested that LPS was common in dogs with naturally occurring CCL rupture. However, only minor clinical, radiographic, cytologic, and histologic differences were identified between dogs with and without LPS.
Published: 2009
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2. Systemic infection with Geomyces organisms in a dog with lytic bone lesions

Author: A. Rick Alleman, Nicole I. Strik, Jay B. Erne, and Mark C. Walker
Subjects: Male, Sternum, Pathology, medicine.medical_specialty, Antifungal Agents, Microbiological culture, Itraconazole, Lethargy, Dogs, Geomyces, Oral administration, Cytology, medicine, Animals, Dog Diseases, Lymph node, General Veterinary, biology, business.industry, Onygenales, biology.organism_classification, Treatment Outcome, medicine.anatomical_structure, Mycoses, Lytic cycle, business, medicine.drug
Abstract: Case Description—A 5-year-old neutered male mixed-breed dog was evaluated by a veterinarian because of a 4-week history of progressive lethargy and poor appetite; the dog was then examined at a referral hospital. Clinical Findings—Hyperglobulinemia was identified via serum biochemical analyses performed before and after arrival at the hospital. Lysis of sternebrae 1 and 2 and sternal lymphadenopathy were detected radiographically. Fine-needle aspirates were collected from the affected sternebrae and lymph node for cytologic examination; findings were consistent with pyogranulomatous inflammation associated with fungal infiltrates. Geomyces organisms were identified via microbial culture of sternebral aspirates. Treatment and Outcome—Treatment consisted of oral administration of itraconazole. After 6 months, remodeling of the affected sternebrae and resolution of sternebral lysis were evident radiographically. Geomyces organisms and pyogranulomatous infiltrates persisted despite clinical improvement. Treatment with itraconazole was continued for an additional 3 months. Clinical Relevance—Infection with Geomyces organisms is typically localized to the skin and nail beds. In the dog of this report, systemic dissemination of Geomyces organisms resulted in lysis of the first 2 sternebrae. Cytologic examination of fine-needle aspirates and microbial culture of samples of the affected sternebrae were important diagnostic tests for successful identification of the organism. Despite 6 months of itraconazole administration and evidence of clinical improvement, fungal organisms persisted in the dog's affected sternebrae. Practitioners should include Geomyces infection among the differential diagnoses for suspected systemic mycosis and should perform cytologic examination and microbial culture of affected tissue throughout treatment of affected dogs.
Published: 2007
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3. Improved Muscle Function in Duchenne Muscular Dystrophy using a Combination of L-Arginine and Metformin

Author: O. Bieri, M. Sinnreich, A. Fischmann, S. Deuster, P. Hafner, U. Bonati, C. Hilker, E. Thomas, Stephan Frank, D. Fischer, B. Erne, E. Rutz, and Monika Gloor
Subjects: medicine.medical_specialty, Arginine, business.industry, Duchenne muscular dystrophy, General Medicine, medicine.disease, Metformin, Endocrinology, Internal medicine, Pediatrics, Perinatology and Child Health, medicine, Neurology (clinical), business, Function (biology), medicine.drug
Published: 2015
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4. Surface reactivity of InSb studied by cyclic voltammetry coupled to XPS

Author: B. Künstler-Hourriez, D. Lorans, B. Erne, F. Lefevre, B. Canava, M. Herlem, and A. Etcheberry
Subjects: Surface reactivity, X-ray photoelectron spectroscopy, Anodizing, Chemistry, Semiconductor materials, Inorganic chemistry, Analytical chemistry, General Physics and Astronomy, Cyclic voltammetry, Electrochemistry, Stoichiometry, Anode
Abstract: The surface chemistry of InSb was modified by anodic treatment at different pH. Using a coupled approach based on electrochemical and surface analysis techniques we determined different chemical configurations for the oxidized InSb surface. Sb-rich oxidized surfaces or stoichiometric ones have been obtained.
Published: 2006
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5. Can total and transition zone volume of the prostate determine whether to perform a repeat biopsy?

Author: Christian Seitz, Michael Marberger, B. Erne, Michael Dobrovits, M. Momeni, R. Wammack, S. Alavi, Mesut Remzi, and Bob Djavan
Subjects: Male, medicine.medical_specialty, Prostate biopsy, Urology, Prostate cancer, Prostate, Biopsy, Humans, Medicine, In patient, Aged, Probability, Ultrasonography, Models, Statistical, medicine.diagnostic_test, Repeat biopsy, business.industry, Biopsy, Needle, Prostatic Neoplasms, Middle Aged, Prostate-Specific Antigen, medicine.disease, Surgery, Prostate-specific antigen, medicine.anatomical_structure, Transrectal ultrasonography, business
Abstract: Objectives To compare the ability of total prostate (TP) and transition zone (TZ) volume to predict the outcome of a repeat prostate biopsy in patients with serum prostate-specific antigen (PSA) levels of 4 to 10 ng/mL. Methods A total of 1137 patients were included and underwent transrectal ultrasound-guided needle sextant and two transition zone biopsies of the prostate. All patients with a prior negative biopsy (benign prostatic tissue) underwent a repeat biopsy after 6 weeks. The TP and TZ volumes of the prostate were measured by transrectal ultrasonography. Results Of the 1137 patients, prostate cancer was diagnosed in 364 (32%), in 276 (24.2%) after the first biopsy and in 88 (7.7%) after the repeated biopsy. The TP and TZ volumes were larger in the patients with prostate cancer detected on the repeated biopsy ( P 3 and greater than 80 cm 3 and for TZ volume of less than 9 cm 3 and greater than 41 cm 3 would have spared 7.1% and 10% of repeated biopsies, respectively. Conclusions The probability for a positive repeat prostate biopsy increases in a logarithmic function for larger prostates, as well as for larger TP and, especially, for larger TZ volumes. The probability of finding prostate cancer on a repeat biopsy in prostates with small (less than 20 cm 3 ) and large (greater than 79 cm 3 ) TP, as well as in small (less than 9.3 cm 3 ) and large (greater than 41 cm 3 ) TZ volumes, was very low. Therefore, a repeat prostate biopsy within 6 weeks is unnecessary. These patients should be followed up by serial PSA determination.
Published: 2003
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6. VAMLA, TEMLA & Co

Author: B Erne and G Leschber
Subjects: Pulmonary and Respiratory Medicine
Published: 2015
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7. Einfluß der Lernphase auf Sicherheit und Effizienz der laparoskopischen Fundoplicatio

Author: Reinhold Függer, M. Remzi, B. Erne, F. Wrba, N. Bagmet, J. Lenglinger, G. Bischof, J. Miholic, and Raimund Jakesz
Subjects: Gynecology, medicine.medical_specialty, Transplant surgery, Cardiothoracic surgery, business.industry, medicine, Surgery, business, Abdominal surgery
Abstract: Bei der Einfuhrung der laparoskopischen Fundoplicatio wurden Patienten- und Operationsdaten, der postoperative Verlauf und die funktionellen Ergebnisse prospektiv dokumentiert. Innerhalb von 34 Monaten wurden 146 laparoskopische Nissen- (n = 102) oder Toupet-Fundoplicatio (n = 44) begonnen und in 139 Fallen auch laparoskopisch beendet (Konversionsrate = 5 %). Zweimal muste wegen postoperativer Komplikationen operativ revidiert werden (6. und 30. Operation). Die Operationsdauer betrug 75–375 (median: 165) min bei den ersten 40 Fallen und 50–235 (median: 105) min bei den spateren (p < 0,001). Alle 7 Konversionen und die 2 postoperativen Revisionen ereigneten sich wahrend der ersten 40 Operationen. Ubergewicht und fortgeschrittener Entzundungsgrad der Speiserohre verlangerten unabhangig von der Erfahrung des Operateurs die Dauer der Operation. 134 Patienten (92 %) konnten nach median 17 Monaten nachuntersucht werden. Bei 2 der ersten 40 Falle (5 %) kam es zu einem Wiederauftreten eines Refluxes sowie bei 7 von 94 (7,4 %) der spater Operierten.
Published: 2001
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8. Selective loss of myelin-associated glycoprotein from myelin correlates with anti-MAG antibody titre in demyelinating paraproteinaemic polyneuropathy

Author: S. L. Miller, Jean-Marc Gabriel, C. Vital, G. C. Miescher, Andreas J. Steck, B. Erne, and Anne Vital
Subjects: Male, Pathology, medicine.medical_specialty, Biopsy, Paraproteinemias, Fluorescent Antibody Technique, Myelin, CD57 Antigens, Antibody Specificity, Glial Fibrillary Acidic Protein, medicine, Humans, Myelin Sheath, Autoantibodies, Staining and Labeling, Myelin-associated glycoprotein, biology, Chemistry, Autoantibody, Peripheral Nervous System Diseases, Peroneal Nerve, medicine.disease, Immunohistochemistry, Myelin basic protein, Myelin-Associated Glycoprotein, medicine.anatomical_structure, Immunoglobulin M, nervous system, Immunology, biology.protein, Female, Neurology (clinical), Antibody, Polyneuropathy, Biomarkers, Myelin Proteins, Demyelinating Diseases
Abstract: Summary The IgM monoclonal autoantibodies of patients with demyelinating paraproteinaemic polyneuropathy recognize a carbohydrate structure present on both myelin-associated glycoprotein (MAG) and protein zero (Po). These autoantibodies are sufficient to cause the disease but the mechanism of demyelination remains unclear. We have analysed nerve biopsies from eight patients with polyneuropathy and anti-MAG antibodies by quantitative immunohistochemistry and find a concordant pattern of reduced expression of myelin markers with the loss of myelinated fibres. We report here novel features of this disease, in particular a selective lack of detectable MAG in a large proportion of myelinated fibres containing Po, myelin basic protein (MBP) and periaxin. There is also an inverse correlation of the distribution of MAG in peripheral never myelin with the serum anti-MAG antibody titres but no correlation of these titres with the loss of myelinated fibres. Double immunofluorescence staining of paraproteinaemic polyneuropathy (PPN) nerves shows anti-MAG IgM deposited on the periphery of myelinated fibres associated with or lacking MAG staining. These data suggest that the binding of anti-MAG antibodies to MAG and/or other myelin component(s) results in MAG downregulation and may have an essential role in the molecular mechanisms leading to demyelination and partial regeneration in this disease
Published: 1996
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9. 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. 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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
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10. What is your diagnosis? Urethral obstruction and fracture of os penis

Author: Jay B, Erne and W Thomas, McNicholas
Subjects: Diagnosis, Differential, Male, Fractures, Bone, Dogs, Treatment Outcome, Urethral Obstruction, Dysuria, Animals, Dog Diseases, Penis
Published: 2009

11. Characterization of human nerve basal lamina for their binding properties of anti-MAG antibodies

Author: M, Sollberger, B, Erne, S, Sansano, A J, Steck, and N, Schaeren-Wiemers
Subjects: Male, Myelin-Associated Glycoprotein, Nerve Fibers, Immunoglobulin M, Sural Nerve, Humans, Middle Aged, Basement Membrane, Myelin Sheath, Aged, Antibodies, Anti-Idiotypic, Protein Binding
Abstract: The functional importance of the basal lamina in Schwann cell development and in adult peripheral nerve fibers is well known. We have demonstrated previously by confocal microscopy that IgM deposits are present on the basal lamina of myelinating Schwann cells of nerve biopsies from patients with an anti-MAG IgM neuropathy. Therefore, the basal lamina was postulated to represent an early target for the uptake of autoantibodies on the surface of myelinated nerve fibers. In this study, the preparation of cell- and myelin-free basal lamina from human peripheral nerves, using a detergent-dependent method is described and characterized by immunohistochemical and biochemical analysis. Using these methods we demonstrated that an enrichment of basal lamina components of Schwann cells with extraction of myelin could be achieved. Western blot analysis and immunohistochemical characterization showed that anti-MAG IgM antibodies did not recognize an epitope on the basal lamina of normal nerves. The established method will allow in situ investigations of basal lamina components from human peripheral nerves in health and in disease, e.g. peripheral neuropathies of infectious or inflammatory origin.
Published: 2003

12. Rafts in adult peripheral nerve myelin contain major structural myelin proteins and myelin and lymphocyte protein (MAL) and CD59 as specific markers

Author: B, Erne, S, Sansano, M, Frank, and N, Schaeren-Wiemers
Subjects: Aged, 80 and over, Macromolecular Substances, Myelin and Lymphocyte-Associated Proteolipid Proteins, Proteolipids, Detergents, Membrane Transport Proteins, CD59 Antigens, Middle Aged, Cell Compartmentation, Rats, Membrane Microdomains, Solubility, Animals, Humans, Peripheral Nerves, Microscopy, Immunoelectron, Spinal Nerve Roots, Myelin P0 Protein, Biomarkers, Myelin Proteins, Myelin Sheath, Aged
Abstract: The myelin and lymphocyte protein (MAL) proteolipid is localized in central and peripheral compact myelin membranes, as well as in apical membranes of particular polarized cells. In this study, we addressed the question whether MAL and other peripheral myelin proteins are sorted and targeted to myelin membranes using mechanisms similar to those observed in polarized epithelial cells. To investigate the presence of raft-mediated sorting pathways in Schwann cells, we have isolated and analysed their composition in myelin membranes. Here, we show that rafts are present in adult human and rat peripheral compact myelin membranes and contain MAL, the GPI-anchored protein CD59, and substantial amounts of the PMP22 and P0. Colocalization studies show that CD59, and MAL have an almost identical expression pattern within compact myelin. Moreover, immuno-electron microscopy revealed that MAL, besides its localization in compact myelin, is also localized to Schmidt-Lanterman incisures. Taken together, our results demonstrate the presence of detergent-insoluble glycolipid-enriched complexes (DIGs) in different compartments of myelin membranes and indicate an important role for DIG-mediated transport mechanisms in the maintenance of the adult myelin sheath.
Published: 2002

13. O7: Successful pilot trial of L-arginine and metformin in Duchenne’s muscular dystrophy

Author: A. Fischmann, Stephan Frank, U. Bonati, E. Rutz, B. Erne, M. Sinnreich, Dirk Fischer, P. Hafner, Monika Gloor, and C. Neuhaus
Subjects: Neurology, Arginine, business.industry, Physiology (medical), Pilot trial, Duchenne's Muscular Dystrophy, Medicine, Neurology (clinical), Pharmacology, business, Sensory Systems, Metformin, medicine.drug
Published: 2014
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14. [Effect of the learning phase on safety and efficiency of laparoscopic fundoplication]

Author: M, Remzi, J, Lenglinger, B, Erne, N, Bagmet, R, Függer, G, Bischof, F, Wrba, R, Jakesz, and J, Miholic
Subjects: Adult, Aged, 80 and over, Male, Inservice Training, Fundoplication, Middle Aged, Hernia, Hiatal, Postoperative Complications, General Surgery, Humans, Education, Medical, Continuing, Female, Laparoscopy, Clinical Competence, Prospective Studies, Aged
Abstract: The introduction of laparoscopic techniques into surgical practice has required a learning process on the part of the surgeons involved. The duration, morbidity, and functional outcome of laparoscopic fundoplication were evaluated in our institution's first 146 cases. During a 34-month period the patients underwent laparoscopic Nissen (n = 102) or Toupet (n = 44) fundoplication. Conversion to open access was necessary in 7 cases, re-operation for complications in 2, all among the first 40 cases of the series. The median operating time was 165 min (range 75-375) in the first 40 cases, and 105 min (range 50-235) thereafter (P0.001). Body mass index, grade of esophagitis, and the surgeon's experience were independent predictors of the operating time. One hundred and thirty-four patients (92%) could be evaluated for recurrence of reflux, which was encountered in 2 (5%) of the first 40 cases and 8 (8%) of 94 patients in the later group.
Published: 2001

15. 158: Prevention of Primary Graft Dysfunction in Lung Transplantation by N-Acetylcysteine after Prolonged Cold Ischemia

Author: I. Inci, B. Erne, S. Arni, J. Wolfgang, S. Hillinger, B. Leskosek, and W. Weder
Subjects: Pulmonary and Respiratory Medicine, Transplantation, Surgery, Cardiology and Cardiovascular Medicine
Published: 2010
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16. Expression patterns of human PNS myelin proteins in neuropathies associated with anti-myelin antibodies

Author: J M, Gabriel, B, Erne, G C, Miescher, J, Ulrich, C, Vital, and A J, Steck
Subjects: Microscopy, Confocal, Biopsy, S100 Proteins, Paraproteinemias, Fluorescent Antibody Technique, Peripheral Nervous System Diseases, Myelin Basic Protein, Immunoenzyme Techniques, Epitopes, Myelin-Associated Glycoprotein, Polyneuropathies, Immunoglobulin M, Sural Nerve, Glial Fibrillary Acidic Protein, Humans, Peripheral Nerves, Myelin Proteins, Autoantibodies
Published: 1994

17. Ultrastructural analysis of rat articular cartilage following treatment with dexamethasone and glycosaminoglycan-peptide complex

Author: M, Annefeld, B, Erne, and Y, Rasser
Subjects: Cartilage, Articular, Male, Organelles, Microscopy, Electron, Tissue Extracts, Body Weight, Animals, Golgi Apparatus, Rats, Inbred Strains, Endoplasmic Reticulum, Dexamethasone, Rats
Abstract: This ultrastructural study describes a stereological analysis of rat articular cartilage, with and without exposure to dexamethasone and a chondroprotective drug used in the treatment of osteoarthritis. Normal rat cartilage was found to contain 27.6 x 10(4) chondrocytes/mm3 which occupied approximately 10% of the cartilage tissue, and the organelle content of each chondrocyte was calculated to be about 20% of the cytoplasmic volume. After 3 weeks of treatment with dexamethasone the chondrocytic volume was increased by 23% with a proportionate increase in the cellular volume of the whole cartilage, and in addition the organelle content was significantly reduced to about half that of the control chondrocytes. By contrast the administration of GP-C (RUMALON) to dexamethasone-treated animals reduced these steroid effects. No significant change was seen in the total chondrocyte numbers with either of the treatments. Whereas dexamethasone inhibits chondrocyte metabolism and produces concomitant ultrastructural changes, GP-C was found to counteract these effects, a result which supports the contention that GP-C helps to preserve chondrocyte function.
Published: 1990

18. Interferon- 1a in chronic inflammatory demyelinating polyneuropathy

Author: C. Naegeli, Thierry Kuntzer, R. Lettry-Trouillat, B. Erne, Julien Bogousslavsky, François Ochsner, Alexander J. Radziwill, and Andreas J. Steck
Subjects: Male, medicine.medical_specialty, Cyclophosphamide, medicine.medical_treatment, Chronic inflammatory demyelinating polyneuropathy, Azathioprine, Prednisone, Internal medicine, medicine, Humans, Chemotherapy, Interferon β1a, business.industry, Interferon beta-1a, Interferon-beta, Middle Aged, medicine.disease, Surgery, Monoclonal gammopathy, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating, Female, Neurology (clinical), medicine.symptom, business, medicine.drug
Abstract: Reported herein are the results of interferon-β1a (IFN-β1a) therapy in four patients with chronic inflammatory demyelinating polyneuropathy (CIDP) who failed to achieve a prolonged response to conventional therapy. Patients. Three women and one man with a mean age of 57.25 years (range, 52 to 64 years) and a mean duration of symptoms of 8.3 years (range, 1.5 to 13 years) participated in the study. All had a sensorimotor polyneuropathy that fulfilled clinical and electrodiagnostic criteria for CIDP. None had monoclonal gammopathy. All had a relapsing or progressive course after treatment with prednisone, plasma exchange (PE), IV immunoglobulin (IVIg), azathioprine, or cyclophosphamide. All required cyclic therapy, but after their initial response they no longer improved. None had been treated with prednisone, PE, or IVIg for at least 8 weeks before starting IFN-β1a. During this period, no one reported clinical deterioration. ### Study design. The study was planned to be a 6-month pilot, open-label therapeutic trial, with the right to …
Published: 1999
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19. IX Eular Workshop for Rheumatology Research

Author: C. Fournier, B. Texier, G. Chiocchia, M. C. Boissier, D. Herbage, C. M. S. Brown, C. Plater Zyberk, R. N. Maini, A. Palacios, J. Sieper, D. Heinegard, G. S. Panayi, A. Gentric, L. Mackenzie, P. M. Lydyard, P. Youinou, E. J. Menzel, B. Kaik, Yu. K. Sykulev, A. Je. Guschin, V. I. Vasiljev, K. K. Ostreiko, T. V. Yeronina, I. A. Tumanova, M. Moynier, M. Abderrazik, B. Combe, M. Rucheton, J. Brochier, T. Tuomi, T. Palosuo, M. Heliövaara, K. Aho, N. J. McHugh, I. E. James, C. G. M. Kallenberg, J. W. Cohen Tervaert, R. Goldschmeding, A. E. G. K. R. Von Dem Borne, M. Bouanani, M. Piechaczyk, B. Pau, M. Bastide, S. Le Page, W. Williams, D. Parkhouse, G. Cambridge, D. A. Isenberg, J. Nimmegeers, F. De Keyser, G. Verbruggen, E. M. Veys, M. J. F. Walravens, I. Verdeyen, B. Vandepol, W. Cortens, L. Schatteman, K. Goethals, D. -H. Wu, A. Tavoni, R. Neri, C. Garzelli, C. Vitali, S. Bombardieri, D. Logar, T. Kveder, J. Dobovisek, B. Rozman, H. A. Menard, G. Boire, F. J. Lopez-Longo, Ch. Masson, S. Lapointe, E. W. St. Clair, L. Zerva, H. M. Moutsopoulos, J. D. Keene, D. S. Pisetsky, A. P. Van Dam, H. T. M. Cuypers, I. Winkel, R. J. T. Smeenk, D. Taylor, E. Valente, J. P. Foster, D. G. Williams, M. R. Stocks, R. Caporali, F. De Gennaro, A. Cerino, F. Cobianchi, G. C. B. Astaldi-Ricotti, C. Montecucco, W. Habets, P. T. G. Sillekens, M. H. Hoet, G. McAllister, M. R. Lerner, W. J. Van Venrooij, W. J. Habets, A. Van Der Kemp, B. De Jong, R. Scarpa, A. Pucino, C. Di Girolamo, G. della Valle, G. Larizza, D. Casiere, P. Oriente, L. Paimela, J. Palvimo, P. Kurki, W. Hassfeld, G. Steiner, W. Graninger, J. S. Smolen, E. J. Lopez-Longo, A. Larose, R. Hoet, R. Zewald, R. Smeenk, K. Brinkman, H. Van Den Brink, A. Westgeest, R. Huss, E. F. Krapf, M. Herrmann, W. Leitmann, J. R. Kalden, K. Merétey, L. Cebecauer, U. Böhm, D. Kozakova, M. Brózik, P. Temesvári, L. Nagy, B. Bozic, M. Stegnar, N. Vene, P. Peternel, C. Giuggioli, P. Monti, G. Rossi, C. Ferri, S. Chiellini, C. Baboonian, P. J. W. Venables, L. Roffe, J. Booth, F. Krapf, I. Abuljadayel, A. Ebringer, N. L. Cox, S. R. Brand, D. P. McIntosh, R. M. Bernstein, M. F. Van Den Broek, M. C. J. Van Bruggen, T. Smetsers, P. Kuyer, L. Van De Putte, W. B. Van Den Berg, A. Toivanen, S. Jalkanen, R. Lahesmaa-Rantala, O. Isomäki, K. Pekkola-Heino, R. Merilahti-Palo Saario, R. Von Essen, H. Isomäki, K. Granfors, J. S. H. Gaston, P. F. Life, L. Bailey, P. A. Bacon, S. Khalafpour, C. Wilson, J. Awad, P. Toivanen, R. Saario, M. Skurnik, C. Van Der Straeten, H. Mielants, M. Gazic, K. Hartung, T. Riedel, S. Stannat, Ch. Specker, E. Röther, K. Pirner, D. Schendel, M. Baur, A. Corvetta, H. H. Peter, H. J. Lakomek, H. Deicher, A. P. Andonopoulos, C. A. Papasteriades, A. A. Drosos, G. S. Dimou, W. Shattles, P. Venables, P. J. Charles, J. R. Markwick, P. J. Venables, M. Galeazzi, P. Lulli, T. Tuzi, S. Cappellacci, M. Morellini, S. Trabace, F. Cutrupi, R. Sorrentino, S. Botti, C. Iannicola, S. Costanzi, R. Tosi, A. Gospodinoff, J. F. Eliaou, H. Humbert, P. Balaguer, J. C. Nicolas, J. Sany, J. Clot, L. I. Sakkas, H. Bird, K. I. Welsh, C. Pitzalis, G. Kingsley, D. Haskard, T. L. Vischer, S. Bas, C. Werner-Favre, D. Wohlwend, R. H. Zubler, A. Afeltra, O. De Pita, P. Basso, A. Pietrucci, G. M. Ferri, L. Bonomo, R. Gerli, C. Cernetti, A. Bertotto, E. Agea, C. Arcangeli, L. Lanfrancone, P. Rambotti, S. Crupi, A. Baglioni, F. Spinozzi, S. Papazoglou, D. Skoumi, P. Athanasiou, A. Iliopoulos, A. Stavropoulou, T. Kontomerkos, G. Hendrich, J. G. Kuipers, M. Hammer, R. E. Schmidt, M. N. Manoussakis, G. Germandis, L. V. Zerva, H. J. Siouna-Fatourou, P. D. Katsikis, A. Mavridis, A. Toubert, M. Sadouk, B. de la Tour, C. Vaquero, B. Amor, P. Miossec, M. Naviliat, I. Cretien, J. Banchereau, P. Graninger, B. Aschauer, A. Sinski, J. Smolen, J. Krutmann, R. Kirnbauer, A. Köck, T. Schwarz, L. T. May, P. B. Sehgal, T. A. Luger, M. Field, C. Q. Chu, M. Feldmann, B. Wilbrink, J. J. Nietfeld, M. Helle, L. C. M. Boeije, J. L. A. M. Van Roy, W. Den Otter, L. A. Aarden, O. Huber-Bruning, J. Malejczyk, A. Urbanski, M. Malejczyk, A. Karbowski, W. Völker, U. Feige, A. M. Malfait, N. Wieme, L. Gyselbrecht, A. A. J. Van de Loo, P. L. E. M. Van Lent, D. O. Haskard, S. Wellicome, J. Lanchbury, M. Thornhill, K. Krutmann, F. Gschnait, M. Yaron, I. Yaron, J. -M. Dayer, I. Bleiberg, F. -A. Meyer, C. P. J. Maury, A. -M. Teppo, E. Salo, P. Pelkonen, A. Malfait, Ph. Cochez, M. Gruschwitz, P. U. Müller, G. Wick, R. Madhok, R. Wilson, M. Frame, J. Thompson, R. D. Sturrock, G. Partsch, M. Matucci-Cerinic, S. Marabini, S. Jantsch, J. Neumüller, R. Eberl, H. M. van Beuningen, O. J. Arntz, G. J. Zlabinger, C. Steffen, H. S. Brand, G. P. J. Van Kampen, M. H. M. T. De Koning, E. Kiljan, J. K. Van Der Korst, C. G. Gemmell, A. J. G. Swaak, A. Van Rooyen, N. D. Hall, A. D. Woolf, B. Kantharia, J. Maymo, D. R. Blake, N. J. Goulding, P. J. Maddison, E. Munthe, H. B. Berntzen, M. Fagerhol, A. Mathieu, R. Pala, L. Contu, R. Cirillo, P. Garau, P. Nurchis, G. C. Viberti, O. Meyer, C. Zenklusen, Z. Le Thi Huong Du, C. Gaudouen, J. Ph. Mery, P. Ronco, M. F. Kahn, N. Rasmussen, W. Szpirt, B. Thomsen, R. L. Humbel, E. J. Ter Borg, G. Horst, E. Hummel, P. C. Limburg, A. Aeschilmann, P. Bourgeois, D. J. De Rooij, L. B. A. Van de Putte, L. Verbeek, C. Farinaro, E. Infranzi, M. Couret, C. Ackerman, K. De Vlam, V. Carapic, D. Carapic, M. Annefeld, B. Erne, L. J. Rosenwasser, C. J. Pazoles, I. G. Otterness, D. C. Hanson, B. McDonald, L. D. Loose, M. Dougados, K. P. Machold, I. Wiesenberg-Böttcher, K. Wanner, W. Pignat, H. Altmann, H. Tuschl, H. Bröll, G. Balestrieri, A. Tincani, R. Cattaneo, M. T. Bertoli, M. Martinelli, F. Allegro, P. L. Meroni, G. Balesini, G. Aichinger, E. Schlögl, Ch. Huber, Y. Shoenfeld, E. Fleishmaker, S. Mendlovic, E. Mozes, M. Blank, N. Talal, E. J. M. Hogervorst, W. Van Eden, R. Van Der Zee, D. Psychos, G. Dimou, S. Stefanaki-Nikou, C. S. Papadimitriou, L. Settas, P. Alexiou, G. Dimitriadis, E. Mataftsi, E. Soliou, A. Tourkantonis, M. Babic, M. E. C. Jeurissen, and A. MTh Boerbooms
Subjects: 030203 arthritis & rheumatology, medicine.medical_specialty, business.industry, Public health, General Medicine, Rheumatology, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Family medicine, medicine, 030212 general & internal medicine, business
Published: 1989
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20. The mode of action of a glycosaminoglycan-peptide-complex (Rumalon®) on articular cartilage of the rat in vivo

Author: M. Annefeld and B. Erne
Subjects: Cartilage, Articular, Male, Pathology, medicine.medical_specialty, Dexamethasone, Glycosaminoglycan, symbols.namesake, Rheumatology, Bone Marrow, In vivo, Internal medicine, medicine, Animals, Tissue Extracts, business.industry, Endoplasmic reticulum, Cartilage, Anti-Inflammatory Agents, Non-Steroidal, Rats, Inbred Strains, General Medicine, Golgi apparatus, Rats, medicine.anatomical_structure, Endocrinology, Ultrastructure, symbols, Autoradiography, Bone marrow, business, medicine.drug
Abstract: Quantitative ultrastructural morphometry and autoradiography of articular cartilage were used to assess in 3 months old rats the effects of in vivo administration of dexamethasone alone or in combination with a glycosaminglycan-peptide-complex (GAGPC). Dexamethasone treatment (3 mg/kg week for three weeks) induced a decrease of 35S-sulphate incorporation in cartilage and ultrastructural changes of articular chondrocytes, mainly characterized by an increase in cell mortality rate, a decrease in length of endoplasmic reticulum, in the number of Golgi bodies and in mitochondrial pool and size. These autoradiographic and ultrastructural changes were reversed or prevented when GAGPC was administered concomitantly with dexamethasone. These results show that the modifications measured by quantitative ultrastructural morphometry of chondrocytes are consistent with changes in biosynthetic functions and that the GAGPC protects cartilage from the inhibitory effects of corticoids.
Published: 1987
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21. The Effect of Dexamethasone on Cartilage and Bone of Rats

Author: B. Erne and M. Annefeld
Subjects: Chemistry, Molecular biology
Abstract: Die Effekte von Dexamethason auf den Gelenkknorpel der Ratte wurden in einem ultrastrukturellen Chondrozyten-Testsystem (Annefeld 1985) gepruft. Die morphometrische Analyse der Chondrozytenultrastruktur im Kniegelenk der Ratte nach Dexamethasongabe (3 mg/kg Dexamethason dreimal in wochentlichen Abstanden intramuskular injiziert) ergibt, das die Zellorganellen, die fur die Synthese und Sekretion der Knorpelmatrixsubstanzen verantwortlich sind, um etwa die Halfte reduziert sind. Das Zytoplasma enthalt vorwiegend massive Einlagerungen von Glykogen und Mikrofilamenten. Die durch Dexamethason induzierten regressiven Veranderungen konnen durch zusatzliche Behandlung mit einer Glykosaminoglykan-Peptid-Komplex-haltigen Substanz (GP-C) uber 5 Wochen dosisabhangig reduziert werden. Die ultrastrukturell quantitativ ermittelten Veranderungen korrelieren in idealer Weise mit dem radioaktiv markierten Sulfateinbau in den Gelenkknorpel, der das Mas der Proteoglykansynthese und damit die Aktivitat und Funktionsfahigkeit dieses Gewebes reflektiert. Bei gleicher Versuchsanordnung wurde anhand elektronenmikroskopischer Ubersichtsaufnahmen die Zelldichte, die Zell/Matrix-Relation und die Dicke des verkalkten und unverkalkten Knorpels ermittelt. Histologisch morphometrisch wurde zusatzlich das subchondrale Knochengewebe untersucht. Die wesentlichen Veranderungen im Knochengewebe nach Dexamethason-Behandlung waren: 1. Abnahme der trabekularen Knochenmasse im subchondralen Knochen, 2. Abnahme der Mineralisationsfront an den Knochentrabekeln, 3. Reduktion der Osteoblasten und des Osteoids, 4. Abnahme der Knochenzuwachsrate. Die durch Dexamethason induzierten degenerativen Knochenveranderungen konnen partiell durch Gabe eines Ossein-Hydroxyapatit-Komplexes (OHC) reduziert werden.
Published: 1989
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22. The Effect of Up and Down Regulators on Growth Plate Chondrocyte Metabolism

Author: M. Annefeld, Y. Rasser, and B. Erne
Subjects: Growth plate chondrocyte, Chemistry, Molecular biology
Abstract: Im Tierexperiment lassen sich mit systemischer Gabe von Glukokortikosteroiden regressive Veranderungen im Epiphysenfugenknorpel junger Ratten erzeugen. Die negativen Effekte von Dexamethason auf den Wachstumsknorpel 300 g schwerer Ratten dokumentieren sich in einer Verschmalerung der Epiphysenfuge als Resultat einer gehemmten Chondrozytenproliferation und Knorpelmatrixproduktion. Die Inhibition der Chondrozytenproliferation wird histologisch morphometrisch anhand der Epiphysenfugendicke, der Anzahl von Zellsaulen und dem Verhaltnis proliferierter zu hypertrophierter Chondrozyten ermittelt. Die verminderte Knorpelmatrixproduktion wird autoradiographisch mit radioaktiv markiertem 35S-Sulfateinbau gemessen. Gleichzeitige Behandlung mit dem Glycosaminoglykan-Peptid-Complex (GP-C = RUMALON) wirkt dem negativen Effekt von Dexamethason entgegen. Die Werte in der De-xamethason + GP-C-Gruppe erreichen annahernd diejenigen der Kontroll-Gruppe, unterscheiden sich aber signifikant von der Dexamethason-Gruppe ohne Therapie.
Published: 1989
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23. Happy to breed in the city? Urban food resources limit reproductive output in Western Jackdaws.

Author: Meyrier E, Jenni L, Bötsch Y, Strebel S, Erne B, and Tablado Z
Abstract: Urban areas expand worldwide, transforming landscapes and creating new challenging habitats. Some bird species, mainly omnivorous feeding on human waste and cavity nesters, commonly breed in these habitats and are, therefore, regarded as urban-adapted. Although urban areas may provide new nesting sites and abundant human waste, the low breeding success found in some of these species suggests that the poor protein content in human waste might limit breeding parameters. We investigated whether the breeding success of a cavity nester and omnivorous species commonly breeding in urban areas, the Western Jackdaw ( Corvus monedula ), depended on the availability of good-quality non-urban food. We approached the objective by combining a literature review and experiments in the field. With the literature review, we compared jackdaw populations in different habitats across Europe and found that clutch size and number of fledglings per pair decreased with distance to non-urban foraging grounds, even after controlling for the effect of colony size, latitude, and climate. In two experiments, we tested whether the breeding success of urban pairs could be increased by supplementing high-quality food, first only during egg formation and second also until chick fledging. Food supplementation during egg formation led to larger eggs and higher hatching success than in urban control nests, but this did not result in higher chick survival. However, when food supplementation was prolonged until fledging in the second experiment, we observed a significant increase of nestling survival. These findings highlight that research and management actions should not only focus on species displaced by urbanization, but also on "urban-adapted" species, as they might be suffering from a mismatch between availability of nesting sites in buildings and adequate non-urban food resources. In these cases, nest sites should be provided in or close to adequate food resources.
Published: 2017
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24. Targeting deregulated AMPK/mTORC1 pathways improves muscle function in myotonic dystrophy type I.

Author: Brockhoff M, Rion N, Chojnowska K, Wiktorowicz T, Eickhorst C, Erne B, Frank S, Angelini C, Furling D, Rüegg MA, Sinnreich M, and Castets P
Subjects: AMP-Activated Protein Kinases genetics, Adult, Aminoimidazole Carboxamide pharmacology, Animals, Disease Models, Animal, Female, Humans, Male, Mechanistic Target of Rapamycin Complex 1, Mice, Mice, Mutant Strains, Middle Aged, Multiprotein Complexes genetics, Multiprotein Complexes metabolism, Muscle Relaxation drug effects, Muscle Relaxation genetics, Myotonic Dystrophy genetics, Myotonic Dystrophy physiopathology, Myotonin-Protein Kinase genetics, Myotonin-Protein Kinase metabolism, Signal Transduction genetics, Sirolimus pharmacokinetics, TOR Serine-Threonine Kinases genetics, TOR Serine-Threonine Kinases metabolism, AMP-Activated Protein Kinases metabolism, Aminoimidazole Carboxamide analogs & derivatives, Multiprotein Complexes antagonists & inhibitors, Muscle Fibers, Skeletal enzymology, Myotonic Dystrophy drug therapy, Myotonic Dystrophy enzymology, Ribonucleotides pharmacology, Signal Transduction drug effects, Sirolimus pharmacology, TOR Serine-Threonine Kinases antagonists & inhibitors
Abstract: Myotonic dystrophy type I (DM1) is a disabling multisystemic disease that predominantly affects skeletal muscle. It is caused by expanded CTG repeats in the 3'-UTR of the dystrophia myotonica protein kinase (DMPK) gene. RNA hairpins formed by elongated DMPK transcripts sequester RNA-binding proteins, leading to mis-splicing of numerous pre-mRNAs. Here, we have investigated whether DM1-associated muscle pathology is related to deregulation of central metabolic pathways, which may identify potential therapeutic targets for the disease. In a well-characterized mouse model for DM1 (HSALR mice), activation of AMPK signaling in muscle was impaired under starved conditions, while mTORC1 signaling remained active. In parallel, autophagic flux was perturbed in HSALR muscle and in cultured human DM1 myotubes. Pharmacological approaches targeting AMPK/mTORC1 signaling greatly ameliorated muscle function in HSALR mice. AICAR, an AMPK activator, led to a strong reduction of myotonia, which was accompanied by partial correction of misregulated alternative splicing. Rapamycin, an mTORC1 inhibitor, improved muscle relaxation and increased muscle force in HSALR mice without affecting splicing. These findings highlight the involvement of AMPK/mTORC1 deregulation in DM1 muscle pathophysiology and may open potential avenues for the treatment of this disease., Competing Interests: M. Sinnreich owns shares of Novartis and is coinventor on a patent application for drug discovery in DM1 (EP 16/166212.7). M. Sinnreich’s institution (University Hospital Basel) has received research support from CSL Behring and Roche, not in relation to this study. C. Angelini is part of the European Board of Genzyme-Sanofi.
Published: 2017
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25. Identification of Plant-derived Alkaloids with Therapeutic Potential for Myotonic Dystrophy Type I.

Author: Herrendorff R, Faleschini MT, Stiefvater A, Erne B, Wiktorowicz T, Kern F, Hamburger M, Potterat O, Kinter J, and Sinnreich M
Subjects: Alkaloids chemistry, Alkaloids isolation & purification, Alternative Splicing drug effects, Animals, Cell Line, Drug Evaluation, Preclinical methods, Humans, Mice, Myotonic Dystrophy genetics, Myotonic Dystrophy metabolism, Myotonic Dystrophy pathology, 3' Untranslated Regions, Alkaloids pharmacology, DNA-Binding Proteins genetics, DNA-Binding Proteins metabolism, Models, Biological, Myotonic Dystrophy drug therapy, RNA-Binding Proteins genetics, RNA-Binding Proteins metabolism, Trinucleotide Repeat Expansion
Abstract: Myotonic dystrophy type I (DM1) is a disabling neuromuscular disease with no causal treatment available. This disease is caused by expanded CTG trinucleotide repeats in the 3' UTR of the dystrophia myotonica protein kinase gene. On the RNA level, expanded (CUG)n repeats form hairpin structures that sequester splicing factors such as muscleblind-like 1 (MBNL1). Lack of available MBNL1 leads to misregulated alternative splicing of many target pre-mRNAs, leading to the multisystemic symptoms in DM1. Many studies aiming to identify small molecules that target the (CUG)n-MBNL1 complex focused on synthetic molecules. In an effort to identify new small molecules that liberate sequestered MBNL1 from (CUG)n RNA, we focused specifically on small molecules of natural origin. Natural products remain an important source for drugs and play a significant role in providing novel leads and pharmacophores for medicinal chemistry. In a new DM1 mechanism-based biochemical assay, we screened a collection of isolated natural compounds and a library of over 2100 extracts from plants and fungal strains. HPLC-based activity profiling in combination with spectroscopic methods were used to identify the active principles in the extracts. The bioactivity of the identified compounds was investigated in a human cell model and in a mouse model of DM1. We identified several alkaloids, including the β-carboline harmine and the isoquinoline berberine, that ameliorated certain aspects of the DM1 pathology in these models. Alkaloids as a compound class may have potential for drug discovery in other RNA-mediated diseases., (© 2016 by The American Society for Biochemistry and Molecular Biology, Inc.)
Published: 2016
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26. Improved Muscle Function in Duchenne Muscular Dystrophy through L-Arginine and Metformin: An Investigator-Initiated, Open-Label, Single-Center, Proof-Of-Concept-Study.

Author: Hafner P, Bonati U, Erne B, Schmid M, Rubino D, Pohlman U, Peters T, Rutz E, Frank S, Neuhaus C, Deuster S, Gloor M, Bieri O, Fischmann A, Sinnreich M, Gueven N, and Fischer D
Subjects: Arginine administration & dosage, Biopsy, Child, Drug Therapy, Combination, Humans, Magnetic Resonance Imaging, Metformin administration & dosage, Muscle, Skeletal pathology, Muscle, Skeletal physiopathology, Nitric Oxide Synthase Type I drug effects, Pilot Projects, Arginine therapeutic use, Metformin therapeutic use, Muscle, Skeletal drug effects, Muscular Dystrophy, Duchenne drug therapy
Abstract: Unlabelled: Altered neuronal nitric oxide synthase function in Duchenne muscular dystrophy leads to impaired mitochondrial function which is thought to be one cause of muscle damage in this disease. The study tested if increased intramuscular nitric oxide concentration can improve mitochondrial energy metabolism in Duchenne muscular dystrophy using a novel therapeutic approach through the combination of L-arginine with metformin. Five ambulatory, genetically confirmed Duchenne muscular dystrophy patients aged between 7–10 years were treated with L-arginine (3 x 2.5 g/d) and metformin (2 x 250 mg/d) for 16 weeks. Treatment effects were assessed using mitochondrial protein expression analysis in muscular biopsies, indirect calorimetry, Dual-Energy X-Ray Absorptiometry, quantitative thigh muscle MRI, and clinical scores of muscle performance. There were no serious side effects and no patient dropped out. Muscle biopsy results showed pre-treatment a significantly reduced mitochondrial protein expression and increased oxidative stress in Duchenne muscular dystrophy patients compared to controls. Post-treatment a significant elevation of proteins of the mitochondrial electron transport chain was observed as well as a reduction in oxidative stress. Treatment also decreased resting energy expenditure rates and energy substrate use shifted from carbohydrates to fatty acids. These changes were associated with improved clinical scores. In conclusion pharmacological stimulation of the nitric oxide pathway leads to improved mitochondria function and clinically a slowing of disease progression in Duchenne muscular dystrophy. This study shall lead to further development of this novel therapeutic approach into a real alternative for Duchenne muscular dystrophy patients., Trial Registration: ClinicalTrials.gov NCT02516085.
Published: 2016
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27. Proteasome inhibitors increase missense mutated dysferlin in patients with muscular dystrophy.

Author: Azakir BA, Erne B, Di Fulvio S, Stirnimann G, and Sinnreich M
Subjects: Administration, Intravenous, Adult, Alleles, Boronic Acids pharmacology, Boronic Acids therapeutic use, Bortezomib, Cell Membrane drug effects, Cell Membrane metabolism, Cells, Cultured, Dysferlin, Humans, Male, Monocytes drug effects, Monocytes metabolism, Myoblasts drug effects, Myoblasts metabolism, Proteasome Inhibitors pharmacology, Pyrazines pharmacology, Pyrazines therapeutic use, Membrane Proteins genetics, Muscle Proteins genetics, Muscular Dystrophies drug therapy, Muscular Dystrophies genetics, Mutation, Missense genetics, Proteasome Inhibitors therapeutic use
Abstract: No treatment is available for patients affected by the recessively inherited, progressive muscular dystrophies caused by a deficiency in the muscle membrane repair protein dysferlin. A marked reduction in dysferlin in patients harboring missense mutations in at least one of the two pathogenic DYSF alleles encoding dysferlin implies that dysferlin is degraded by the cell's quality control machinery. In vitro evidence suggests that missense mutated dysferlin might be functional if salvaged from degradation by the proteasome. We treated three patients with muscular dystrophy due to a homozygous Arg555Trp mutation in dysferlin with the proteasome inhibitor bortezomib and monitored dysferlin expression in monocytes and in skeletal muscle by repeated percutaneous muscle biopsy. Expression of missense mutated dysferlin in the skeletal muscle and monocytes of the three patients increased markedly, and dysferlin was correctly localized to the sarcolemma of muscle fibers on histological sections. Salvaged missense mutated dysferlin was functional in a membrane resealing assay in patient-derived muscle cells treated with three different proteasome inhibitors. We conclude that interference with the proteasomal system increases expression of missense mutated dysferlin, suggesting that this therapeutic strategy may benefit patients with dysferlinopathies and possibly other genetic diseases., (Copyright © 2014, American Association for the Advancement of Science.)
Published: 2014
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28. An essential role of MAG in mediating axon-myelin attachment in Charcot-Marie-Tooth 1A disease.

Author: Kinter J, Lazzati T, Schmid D, Zeis T, Erne B, Lützelschwab R, Steck AJ, Pareyson D, Peles E, and Schaeren-Wiemers N
Subjects: Adult, Aged, 80 and over, Animals, Axons pathology, Cell Adhesion Molecules metabolism, Charcot-Marie-Tooth Disease pathology, Disease Models, Animal, Female, Humans, Immunoglobulins metabolism, Male, Mice, Knockout, Mice, Transgenic, Middle Aged, Myelin Proteins genetics, Myelin Proteins metabolism, Myelin Sheath pathology, Myelin-Associated Glycoprotein genetics, Sural Nerve pathology, Young Adult, Axons metabolism, Charcot-Marie-Tooth Disease metabolism, Myelin Sheath metabolism, Myelin-Associated Glycoprotein metabolism, Sural Nerve metabolism
Abstract: Charcot-Marie-Tooth disease type 1A (CMT1A) is a hereditary demyelinating peripheral neuropathy caused by the duplication of the PMP22 gene. Demyelination precedes the occurrence of clinical symptoms that correlate with axonal degeneration. It was postulated that a disturbed axon-glia interface contributes to altered myelination consequently leading to axonal degeneration. In this study, we examined the expression of MAG and Necl4, two critical adhesion molecules that are present at the axon-glia interface, in sural nerve biopsies of CMT1A patients and in peripheral nerves of mice overexpressing human PMP22, an animal model for CMT1A. We show an increase in the expression of MAG and a strong decrease of Necl4 in biopsies of CMT1A patients as well as in CMT1A mice. Expression analysis revealed that MAG is strongly upregulated during peripheral nerve maturation, whereas Necl4 expression remains very low. Ablating MAG in CMT1A mice results in separation of axons from their myelin sheath. Our data show that MAG is important for axon-glia contact in a model for CMT1A, and suggest that its increased expression in CMT1A disease has a compensatory role in the pathology of the disease. Thus, we demonstrate that MAG together with other adhesion molecules such as Necl4 is important in sustaining axonal integrity., (Copyright © 2012 Elsevier Inc. All rights reserved.)
Published: 2013
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29. Prevention of primary graft dysfunction in lung transplantation by N-acetylcysteine after prolonged cold ischemia.

Author: Inci I, Erne B, Arni S, Jungraithmayr W, Inci D, Hillinger S, Vogt P, Leskosek B, and Weder W
Subjects: Animals, Glutathione metabolism, Graft Survival physiology, Lung metabolism, Lung surgery, Models, Animal, NF-kappa B metabolism, Nitric Oxide metabolism, Primary Graft Dysfunction metabolism, Swine, Acetylcysteine therapeutic use, Cold Ischemia adverse effects, Free Radical Scavengers therapeutic use, Lung Transplantation, Primary Graft Dysfunction prevention & control
Abstract: Background: N-Acetylcysteine (NAC), a thiol-containing compound that has been used as an anti-oxidant, may also lead to an increased glutathione synthesis. This study assessed the protective effect of NAC on primary graft dysfunction after lung transplantation., Methods: Porcine single left-lung transplantation was performed in 2 experimental groups after 24 hours of cold storage. Donor and recipient animals were treated with intravenous injection of 150 mg/kg NAC 60 minutes before harvest and reperfusion, followed by 12.5 mg/kg/hour continuous perfusion during the 8-hour observation period (NAC). Control animals did not receive any treatment. Hemodynamic and respiratory parameters were recorded throughout the observation period. Bronchoalveolar lavage (BAL) nitrite, neutrophil elastase (NE), protein accumulation, interleukin (IL)-8, nuclear factor-κB (p50 sub-unit), and reduced glutathione (GSH) in lung tissue and red blood were measured., Results: During the observation period, the mean pulmonary artery pressure, oxygenation, airway pressure, and static lung compliance were significantly better in NAC animals compared with controls (p < 0.05). Extravascular lung water index was higher at points during the reperfusion in the control group. BAL protein, nitrite, NE, and IL-8 cytokine levels at the end of the experiment were significantly higher in the controls than in the NAC group (p < 0.05). Lung tissue reduced GSH levels were significantly higher in the NAC group than in the control group. Red blood cell GSH levels were always higher in the NAC group during the reperfusion period. Reverse transcription polymerase chain reaction for IL-8 messenger RNA was significantly higher in controls during the reperfusion period than in the NAC group (p = 0.001). The amount of lung tissue nuclear NF-κB (p50 sub-unit) was significantly higher in controls than in NAC pigs (p = 0.03)., Conclusion: In this model, donor and recipient treatment with NAC effectively protected the lung from primary graft dysfunction after prolonged cold ischemia., (Copyright © 2010 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.)
Published: 2010
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30. Global deprivation of brain-derived neurotrophic factor in the CNS reveals an area-specific requirement for dendritic growth.

Author: Rauskolb S, Zagrebelsky M, Dreznjak A, Deogracias R, Matsumoto T, Wiese S, Erne B, Sendtner M, Schaeren-Wiemers N, Korte M, and Barde YA
Subjects: Animals, Cell Count, Cells, Cultured, Dendrites metabolism, Dendrites ultrastructure, Female, Hippocampus cytology, Immunohistochemistry, Male, Mice, Mice, Knockout, Neostriatum ultrastructure, Neurons cytology, Neurons ultrastructure, Oligodendroglia cytology, Oligodendroglia ultrastructure, Optic Nerve growth & development, Optic Nerve ultrastructure, tau Proteins metabolism, Brain-Derived Neurotrophic Factor metabolism, Hippocampus growth & development, Neostriatum growth & development
Abstract: Although brain-derived neurotrophic factor (BDNF) is linked with an increasing number of conditions causing brain dysfunction, its role in the postnatal CNS has remained difficult to assess. This is because the bdnf-null mutation causes the death of the animals before BDNF levels have reached adult levels. In addition, the anterograde axonal transport of BDNF complicates the interpretation of area-specific gene deletion. The present study describes the generation of a new conditional mouse mutant essentially lacking BDNF throughout the CNS. It shows that BDNF is not essential for prolonged postnatal survival, but that the behavior of such mutant animals is markedly altered. It also reveals that BDNF is not a major survival factor for most CNS neurons and for myelination of their axons. However, it is required for the postnatal growth of the striatum, and single-cell analyses revealed a marked decreased in dendritic complexity and spine density. In contrast, BDNF is dispensable for the growth of the hippocampus and only minimal changes were observed in the dendrites of CA1 pyramidal neurons in mutant animals. Spine density remained unchanged, whereas the proportion of the mushroom-type spine was moderately decreased. In line with these in vivo observations, we found that BDNF markedly promotes the growth of cultured striatal neurons and of their dendrites, but not of those of hippocampal neurons, suggesting that the differential responsiveness to BDNF is part of a neuron-intrinsic program.
Published: 2010
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31. The myelin protein MAL affects peripheral nerve myelination: a new player influencing p75 neurotrophin receptor expression.

Author: Buser AM, Schmid D, Kern F, Erne B, Lazzati T, and Schaeren-Wiemers N
Subjects: Animals, Cell Communication physiology, Cell Differentiation physiology, Membrane Microdomains metabolism, Membrane Transport Proteins genetics, Mice, Mice, Transgenic, Myelin Proteins genetics, Myelin Sheath ultrastructure, Myelin and Lymphocyte-Associated Proteolipid Proteins, Nerve Fibers, Myelinated ultrastructure, Peripheral Nerves growth & development, Peripheral Nerves ultrastructure, Proteolipids genetics, RNA, Messenger metabolism, Receptor, Nerve Growth Factor genetics, Schwann Cells metabolism, Membrane Transport Proteins metabolism, Myelin Proteins metabolism, Myelin Sheath metabolism, Nerve Fibers, Myelinated metabolism, Peripheral Nerves metabolism, Proteolipids metabolism, Receptor, Nerve Growth Factor metabolism
Abstract: The myelin and lymphocyte protein (MAL) is a raft-associated membrane protein predominantly expressed by oligodendrocytes and Schwann cells. Here we show that MAL regulates myelination in the peripheral nervous system. In mice overexpressing MAL, myelination was retarded and fibers were hypomyelinated, whereas myelination in MAL knockout mice was accelerated. This was not due to impaired Schwann cell proliferation, differentiation or axonal sorting. We found that the expression level of p75 neurotrophin receptor mRNA and protein was strongly reduced in developing sciatic nerves in MAL-overexpressing mice. This reduction is well correlated with the observed alterations in myelination initiation, speed of myelination and alterations in Remak bundle development. Our results suggest a functional role for MAL in peripheral myelination by influencing the expression of membrane components that mediate axon-glia interaction during ensheathment and myelin wrapping.
Published: 2009
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32. Immunoglobulin M deposition in cutaneous nerves of anti-myelin-associated glycoprotein polyneuropathy patients correlates with axonal degeneration.

Author: Stalder AK, Erne B, Reimann R, Renaud S, Fuhr P, Thomann S, Arnold A, Probst A, Schaeren-Wiemers N, and Steck AJ
Subjects: Aged, Biopsy, Female, Humans, Immunoglobulin M analysis, Lectins, Male, Microscopy, Confocal, Microscopy, Electron, Transmission, Middle Aged, Myelin Sheath immunology, Myelin-Associated Glycoprotein, Nerve Fibers, Myelinated immunology, Nerve Fibers, Myelinated metabolism, Nerve Fibers, Myelinated pathology, Neurofilament Proteins metabolism, Peripheral Nerves immunology, Peripheral Nerves pathology, Peripheral Nerves physiopathology, Polyneuropathies immunology, Polyneuropathies physiopathology, Schwann Cells immunology, Schwann Cells pathology, Sensory Receptor Cells immunology, Skin innervation, Wallerian Degeneration immunology, Wallerian Degeneration physiopathology, Immunoglobulin M blood, Myelin Sheath pathology, Neoplasm Proteins immunology, Polyneuropathies pathology, Sensory Receptor Cells pathology, Wallerian Degeneration pathology
Abstract: Anti-myelin-associated glycoprotein (MAG) neuropathy is an antibody-mediated polyneuropathy. We correlated clinical features, immunoglobulin (Ig) M blood levels, IgM deposition and axonal degeneration in skin biopsies of anti-MAG neuropathy patients. By confocal microscopy, IgM deposits were found exclusively within perineurium-enclosed nerves; they were not found on single, non-perineurium-ensheathed myelinated axons. There was a linear correlation between IgM accumulation in nerve fascicles with IgM blood levels but not with anti-MAG antibody titer or disease duration. Axons with specific IgM deposits had signs of axonal damage, including neurofilament disintegration. Nodal structures were intact even at sites where the axons showed pathologic changes. Ultrastructural analysis revealed degeneration of myelinating Schwann cells. Taken together, these findings suggest that in anti-MAG neuropathy patients, IgM deposits are entrapped within cutaneous perineurium-ensheathed nerve bundles where they accumulate in the endoneurial space. High local IgM levels in the endoneurium may be required for IgM deposition on myelin and subsequent axonal injury and degeneration. This study underlines the importance of early, effective anti-B-cell treatments for preventing progression of this neuropathy.
Published: 2009
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33. The septin cytoskeleton in myelinating glia.

Author: Buser AM, Erne B, Werner HB, Nave KA, and Schaeren-Wiemers N
Subjects: Animals, Biomarkers metabolism, Cell Differentiation physiology, Cell Line, Cytoskeletal Proteins genetics, Cytoskeletal Proteins metabolism, GTP Phosphohydrolases genetics, GTP Phosphohydrolases metabolism, GTP-Binding Proteins genetics, Humans, Membrane Transport Proteins genetics, Membrane Transport Proteins metabolism, Mice, Myelin Proteins genetics, Myelin Proteins metabolism, Myelin and Lymphocyte-Associated Proteolipid Proteins, Neuroglia cytology, Peripheral Nervous System metabolism, Protein Binding, Protein Isoforms genetics, Protein Isoforms metabolism, Proteolipids genetics, Proteolipids metabolism, Rats, Septins, Two-Hybrid System Techniques, Cytoskeleton metabolism, GTP-Binding Proteins metabolism, Myelin Sheath metabolism, Neuroglia physiology
Abstract: Myelin is organized in subdomains with distinct protein and lipid composition. How these domains are established and maintained is currently unknown. Cytoskeletal elements interacting with membrane components could generate and sustain such structural domains. Here, we demonstrate that the transmembrane myelin protein MAL interacts with the cytoskeleton protein septin 6. Septins represent a fourth filamentous system involved in membrane compartmentalization, vesicle transport and scaffold formation. We report that multiple septin complexes are associated with myelin, and that they display an overlapping but non-identical composition in the central and peripheral nervous system. The expression of distinct subsets of septins was upregulated during myelin formation in peripheral nerves and oligodendrocytes. In the PNS, septins were highly enriched in non-compact myelin compartments, particularly in the paranodal loops and the microvilli at the node of Ranvier. Importantly in myelin lacking Septin 6, the abundance of its closest homolog Sept11 was increased, suggesting a functional compensatory role. Our data demonstrate that the septin cytoskeleton is an integral component of the myelin sheath and interacts with distinct myelin constituents such as MAL. We suggest that septins are intriguing candidates for membrane compartmentalization in myelin internodes.
Published: 2009
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34. Allograft inflammatory factor-1: a pathogenetic factor for vasculitic neuropathy.

Author: Broglio L, Erne B, Tolnay M, Schaeren-Wiemers N, Fuhr P, Steck AJ, and Renaud S
Subjects: Adult, Aged, Arteries metabolism, Arteries pathology, Arteries physiopathology, Biomarkers analysis, Biomarkers metabolism, Biopsy, Calcium-Binding Proteins, Chemotaxis, Leukocyte immunology, DNA-Binding Proteins analysis, Female, Humans, Immunohistochemistry, Male, Microfilament Proteins, Middle Aged, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular pathology, Muscle, Smooth, Vascular physiopathology, Peripheral Nerves pathology, Peripheral Nerves physiopathology, Peripheral Nervous System Diseases pathology, Peripheral Nervous System Diseases physiopathology, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating pathology, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating physiopathology, Sural Nerve metabolism, Sural Nerve pathology, Sural Nerve physiopathology, Up-Regulation physiology, Vasculitis pathology, Vasculitis physiopathology, DNA-Binding Proteins metabolism, Peripheral Nerves metabolism, Peripheral Nervous System Diseases metabolism, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating metabolism, Vasculitis metabolism
Abstract: Allograft inflammatory factor-1 (AIF-1) is a cytokine that plays a major role in the immune response and proliferative vasculopathy that occur during chronic allograft rejection. The purpose of this study was to characterize the cellular expression pattern and pathogenetic role of AIF-1 in nerve biopsies from patients with vasculitic neuropathy. We performed immunohistochemistry in human nerve biopsies of 10 patients with vasculitic neuropathies (VASs), 6 with chronic inflammatory demyelinating polyneuropathies (CIDPs), 5 with noninflammatory axonal neuropathies (NIANs), and 3 control nerves (CNs). In the CIDP and VAS nerves, AIF-1 expression was higher than in CN and NIAN nerves (P < 0.05). AIF-1 was increased in the arterial walls of VAS compared with CIDP nerves (P < 0.05). Vascular smooth muscle cells in vasculitic nerve express AIF-1 at a higher level compared with CIDP and NIAN. AIF-1 plays a role in inflammatory nerve disease and vascular smooth muscle cell proliferation and may be a new molecular target for treatment.
Published: 2008
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35. Ibutilide and sinus arrest.

Author: Neumayr G, Gatterer H, and Erne B
Subjects: Aged, 80 and over, Anti-Arrhythmia Agents adverse effects, Anti-Arrhythmia Agents therapeutic use, Arrhythmias, Cardiac prevention & control, Female, Heart Arrest prevention & control, Humans, Sulfonamides therapeutic use, Heart Arrest chemically induced, Heart Arrest diagnosis, Sulfonamides adverse effects
Published: 2007
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36. Laparoscopic gastric re-banding versus laparoscopic gastric bypass as a rescue operation for patients with pouch dilatation.

Author: Lanthaler M, Mittermair R, Erne B, Weiss H, Aigner F, and Nehoda H
Subjects: Dilatation, Pathologic, Humans, Laparoscopy, Patient Satisfaction, Postoperative Complications surgery, Reoperation, Retrospective Studies, Treatment Failure, Gastric Bypass methods, Gastroplasty, Stomach pathology
Abstract: Background: The authors assessed whether laparoscopic rebanding or laparoscopic Roux-en-Y gastric bypass (LRYGBP) is the best approach for failed gastric banding after pouch dilatation., Methods: Between January 2000 and June 2005, 489 patients underwent laparoscopic gastric banding, and of these, 33 (6.7%) required rescue procedures for pouch dilatation. Each reoperated patient was contacted to obtain information about their postoperative course. Additionally, preoperative weight and BMI, weight loss at 1 year postoperatively, weight at time of pouch dilatation and the time-period between the primary operation and pouch dilatation were analyzed., Results: The most common operation for pouch dilatation was band repositioning or rebanding (16 patients). Band removal without replacement was performed in 7 patients. 8 patients underwent conversion to a LRYGBP. 1 patient underwent laparoscopic gastric sleeve resection and 1 patient received an intragastric balloon. Patients who underwent conversion to LRYGBP are very content and, although weight loss has been nearly the same as after gastric banding, they would prefer the gastric bypass operation to the gastric banding., Conclusion: Conversion to LRYGBP appears to offer significant advantages, and appears to be the rescue therapy of choice after failed laparoscopic gastric banding.
Published: 2006
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37. Unraveling the differential expression of the two isoforms of myelin-associated glycoprotein in a mouse expressing GFP-tagged S-MAG specifically regulated and targeted into the different myelin compartments.

Author: Erb M, Flueck B, Kern F, Erne B, Steck AJ, and Schaeren-Wiemers N
Subjects: Animals, Axons metabolism, Axons ultrastructure, Brain cytology, Brain metabolism, Gene Expression Regulation, Developmental, Green Fluorescent Proteins genetics, Green Fluorescent Proteins metabolism, Mice, Mice, Inbred C57BL, Mice, Transgenic, Models, Biological, Myelin Sheath ultrastructure, Myelin-Associated Glycoprotein genetics, Peripheral Nerves cytology, Peripheral Nerves metabolism, Protein Isoforms genetics, RNA, Messenger metabolism, Recombinant Fusion Proteins genetics, Sciatic Nerve cytology, Sciatic Nerve metabolism, Myelin Sheath metabolism, Myelin-Associated Glycoprotein metabolism, Protein Isoforms metabolism, Recombinant Fusion Proteins metabolism
Abstract: The two myelin-associated glycoprotein (MAG) isoforms are cell adhesion molecules that differ only in their cytoplasmic domains, but their specific roles are not well understood. In this study, we present a transgenic mouse line that specifically expresses GFP-tagged S-MAG correctly regulated and targeted into the myelin sheath allowing the specific discrimination of L- and S-MAG on the subcellular level. Here, we describe the differential expression pattern and spatial distribution of L- and S-MAG during development as well as in the adult central and peripheral nervous system. In peripheral nerves, where S-MAG is the sole isoform, we observed S-MAG concentrated in different ring-like structures such as periaxonal and abaxonal rings, and discs spanning through the compact myelin sheath perpendicular to the axon. In summary, our data provide new insight in the subcellular distribution of the two isoforms fundamental for the understanding of their specific functions in myelin formation and maintenance.
Published: 2006
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38. Normal expression of myelin protein zero with frame-shift mutation correlates with mild phenotype.

Author: Steck AJ, Erne B, Pareyson D, Sghirlanzoni A, Taroni F, and Schaeren-Wiemers N
Subjects: Adult, Biopsy, Blotting, Western, Demyelinating Diseases pathology, Female, Frameshift Mutation, Humans, Immunohistochemistry, Myelin Proteins biosynthesis, Pedigree, Phenotype, Sural Nerve chemistry, Sural Nerve pathology, Demyelinating Diseases genetics, Demyelinating Diseases metabolism, Myelin P0 Protein biosynthesis, Myelin P0 Protein genetics, Sural Nerve metabolism
Abstract: Mutations in the gene encoding for myelin protein zero (MPZ) cause inherited demyelinating peripheral neuropathies of different severity. The molecular and cellular mechanisms by which the MPZ mutations cause neuropathy are incompletely understood. We investigated MPZ, myelin basic protein, and peripheral myelin protein 22 (PMP22) protein expression levels in a nerve biopsy of a Charcot-Marie-Tooth type 1B patient heterozygous for the Val 102 frame-shift mutation. We demonstrate by quantitative immunohistochemical as well as by Western blot analyses that MPZ expression levels were not reduced in myelin membranes, a finding that is in accordance with the mild phenotype of this patient. Our data show that heterozygous 'loss-of-function' of MPZ may not necessarily lead to reduced protein levels. In conclusion, we demonstrate that careful analysis of protein expression levels in peripheral nerve tissues provides important information with respect to the understanding of the molecular basis of these neuropathies.
Published: 2006
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39. IgM deposits on skin nerves in anti-myelin-associated glycoprotein neuropathy.

Author: Lombardi R, Erne B, Lauria G, Pareyson D, Borgna M, Morbin M, Arnold A, Czaplinski A, Fuhr P, Schaeren-Wiemers N, and Steck AJ
Subjects: Biopsy, Humans, Microscopy, Confocal, Polyradiculoneuropathy immunology, Skin immunology, Immunoglobulin M immunology, Myelin-Associated Glycoprotein immunology, Nerve Fibers, Myelinated immunology, Polyradiculoneuropathy diagnosis, Skin innervation
Abstract: Anti-myelin-associated glycoprotein (anti-MAG) neuropathy is a chronic demyelinating neuropathy with predominant involvement of large sensory fibers and deposits of IgM and complement on sural nerve myelinated fibers. We assessed the presence of IgM deposits on skin myelinated nerve fibers and the involvement of unmyelinated axons in anti-MAG neuropathy. Skin biopsies were performed in 14 patients with anti-MAG neuropathy, in 8 patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and in 2 patients with IgM paraproteinemic neuropathy. Biopsies were taken at the proximal thigh in 20 patients, at the distal leg in 21 patients, at the proximal arm in 13 patients, and at the hand or fingertip in 10 patients. We found IgM deposits on dermal myelinated fibers in all anti-MAG neuropathy patients, with a greater prevalence at the distal site of the extremities. Deposits were located throughout the length of the fibers and at the paranodal loops. CIDP and IgM paraproteinemic neuropathies did not show any deposit of IgM. Anti-MAG neuropathy and CIPD patients showed a decrease in epidermal nerve fiber density reflecting an associated axonal loss. In anti-MAG neuropathy, both large- and small-diameter nerve fibers are affected, and specific deposits of IgM are found on skin myelinated nerve fibers.
Published: 2005
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40. The raft-associated protein MAL is required for maintenance of proper axon--glia interactions in the central nervous system.

Author: Schaeren-Wiemers N, Bonnet A, Erb M, Erne B, Bartsch U, Kern F, Mantei N, Sherman D, and Suter U
Subjects: Animals, Axons pathology, Axons ultrastructure, Cell Adhesion Molecules metabolism, Cell Communication genetics, Central Nervous System ultrastructure, Down-Regulation genetics, Kv1.2 Potassium Channel, Membrane Microdomains ultrastructure, Membrane Transport Proteins genetics, Mice, Mice, Knockout, Microscopy, Electron, Myelin Basic Protein metabolism, Myelin Proteins genetics, Myelin Sheath pathology, Myelin Sheath ultrastructure, Myelin and Lymphocyte-Associated Proteolipid Proteins, Myelin-Associated Glycoprotein metabolism, Nerve Growth Factors metabolism, Neural Conduction genetics, Oligodendroglia ultrastructure, Optic Nerve metabolism, Optic Nerve pathology, Optic Nerve ultrastructure, Potassium Channels genetics, Potassium Channels metabolism, Protein Transport genetics, Proteolipids genetics, Ranvier's Nodes metabolism, Ranvier's Nodes pathology, Ranvier's Nodes ultrastructure, Sciatic Nerve metabolism, Sciatic Nerve pathology, Sciatic Nerve ultrastructure, Axons metabolism, Central Nervous System metabolism, Membrane Microdomains metabolism, Membrane Transport Proteins metabolism, Myelin Proteins metabolism, Myelin Sheath metabolism, Oligodendroglia metabolism, Potassium Channels, Voltage-Gated, Proteolipids metabolism
Abstract: The myelin and lymphocyte protein (MAL) is a tetraspan raft-associated proteolipid predominantly expressed by oligodendrocytes and Schwann cells. We show that genetic ablation of mal resulted in cytoplasmic inclusions within compact myelin, paranodal loops that are everted away from the axon, and disorganized transverse bands at the paranode--axon interface in the adult central nervous system. These structural changes were accompanied by a marked reduction of contactin-associated protein/paranodin, neurofascin 155 (NF155), and the potassium channel Kv1.2, whereas nodal clusters of sodium channels were unaltered. Initial formation of paranodal regions appeared normal, but abnormalities became detectable when MAL started to be expressed. Biochemical analysis revealed reduced myelin-associated glycoprotein, myelin basic protein, and NF155 protein levels in myelin and myelin-derived rafts. Our results demonstrate a critical role for MAL in the maintenance of central nervous system paranodes, likely by controlling the trafficking and/or sorting of NF155 and other membrane components in oligodendrocytes.
Published: 2004
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41. Microheterogeneity of anti-myelin-associated glycoprotein antibodies.

Author: Fluri F, Ferracin F, Erne B, and Steck AJ
Subjects: Adult, Aged, Aged, 80 and over, Autoantibodies blood, Central Nervous System Diseases immunology, Electrophysiology, Enzyme-Linked Immunosorbent Assay, Female, Humans, Immunoglobulin M blood, Male, Middle Aged, Myelin-Associated Glycoprotein blood, Paraproteinemias immunology, Autoantibodies metabolism, Immunoglobulin M metabolism, Myelin-Associated Glycoprotein immunology, Myelin-Associated Glycoprotein metabolism
Abstract: Antibodies to the myelin-associated glycoprotein (MAG) are implicated in the pathogenesis of an acquired demyelinating polyneuropathy. We studied IgM affinity to MAG in 18 patients with anti-MAG antibodies. Binding of sera was tested for anti-MAG immunoreactivity in central nervous system (CNS) by ELISA and in CNS and peripheral nervous system (PNS) by Western blot analysis. Furthermore, immunohistochemical characterization of IgM binding on sural nerve tissue was investigated using the indirect peroxidase method. Western blot analysis revealed that all sera detected MAG in central myelin, but only eight in peripheral myelin. Anti-MAG-IgM-ELISA-titers correlated significantly (p<0.0001) with PNS-Western blot results. By indirect immunoperoxidase immunohistochemistry, 12 sera stained myelin sheaths, while 6 sera showed no staining. These results demonstrate considerable variations in antibody binding strength to MAG between PNS myelin and CNS myelin. The relevance of these differences for the pathogenesis of the neuropathy and clinical impairment remains to be demonstrated.
Published: 2003
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42. Matrix metalloproteinases-9 and -2 in secondary vasculitic neuropathies.

Author: Renaud S, Erne B, Fuhr P, Said G, Lacroix C, Steck AJ, and Leppert D
Subjects: Adult, Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Nerve Tissue enzymology, Tissue Distribution, Demyelinating Diseases enzymology, Matrix Metalloproteinase 2 metabolism, Matrix Metalloproteinase 9 metabolism, Polyneuropathies enzymology, Vasculitis enzymology
Abstract: Matrix metalloproteinases (MMPs) are a family of zinc-dependent endoproteinases that play an important role in inflammation and tissue degradation. MMP-9 and MMP-2 are gelatinases that have been implicated in the degradation of the blood-brain or blood-nerve barrier. We present an immunohistochemical study on 11 nerve biopsy samples of inflammatory and non-inflammatory polyneuropathies. Perineurium and endothelium were positive for MMP-2 in all tissue sections. In addition, there was a specific up-regulation of MMP-2 in stromal cells of chronic inflammatory demyelinating polyneuropathy (CIDP) and even more in vasculitic neuropathies. MMP-9-positive cells were detected in vessel walls, infiltrates, epineurium and endoneurium of vasculitic neuropathies. In CIDP, MMP-9-positive cells were prominent in vessel walls. Only a few MMP-9-positive cells were detected in noninflammatory controls in blood vessels and adhering to vessel walls. Double staining indicated that the infiltrating cells were T cells and macrophages. Our findings suggest that MMP-9 plays an important role in inflammatory peripheral neuropathy probably as means for inflammatory cell invasion.
Published: 2003
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43. The pathophysiology of benign prostatic hyperplasia.

Author: Djavan B, Remzi M, Erne B, and Marberger M
Subjects: Aging pathology, Androgens blood, Androgens genetics, Apoptosis, Epithelial Cells pathology, Estrogens physiology, Growth Substances metabolism, Humans, Male, Prostate metabolism, Prostate pathology, Prostatic Hyperplasia epidemiology, Prostatic Hyperplasia therapy, Stem Cells pathology, Stromal Cells pathology, Prostatic Hyperplasia pathology
Abstract: The development of human benign prostatic hyperplasia and its related signs and symptoms clearly requires a combination of testicular androgens and aging. Although the role of androgens as a causative factor for human benign prostatic hyperplasia is debated, they undoubtedly play at least a permissive role. The principle prostatic androgen is dihydrotestosterone. Two isoenzymes of 5-alpha reductase have been discovered. Type 2 is dominant in the genital issue. Testosterone is reduced by the 5-a reductase to dihydrotestosterone. Benign prostatic hyperplasia is predominantly due to stromal hyperplasia of the gland and affects more than 70% of men of 70 years or older with or without obstruction. Recent studies identified transforming growth factor-b, fibroblast growth factor and insulin-like growth factor family members as key regulators of cell proliferation and extracellular matrix turnover with interrelated activities. Furthermore, estrogens, andenergic signaling and inflammatory processes have been shown to have an impact. Without a solid understanding of the physiology and pathophysiology of benign prostatic hyperplasia it can be difficult to interpret the results of clinical trials and symptoms., ((c) 2002 Prous Science. All rights reserved.)
Published: 2002
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44. Rafts in adult peripheral nerve myelin contain major structural myelin proteins and myelin and lymphocyte protein (MAL) and CD59 as specific markers.

Author: Erne B, Sansano S, Frank M, and Schaeren-Wiemers N
Subjects: Aged, Aged, 80 and over, Animals, Biomarkers analysis, CD59 Antigens biosynthesis, Cell Compartmentation, Detergents chemistry, Humans, Macromolecular Substances, Membrane Microdomains metabolism, Microscopy, Immunoelectron, Middle Aged, Myelin P0 Protein analysis, Myelin P0 Protein biosynthesis, Myelin Proteins biosynthesis, Myelin Sheath metabolism, Myelin Sheath ultrastructure, Myelin and Lymphocyte-Associated Proteolipid Proteins, Peripheral Nerves metabolism, Peripheral Nerves ultrastructure, Proteolipids biosynthesis, Proteolipids ultrastructure, Rats, Solubility, Spinal Nerve Roots metabolism, Spinal Nerve Roots ultrastructure, CD59 Antigens analysis, Membrane Microdomains chemistry, Membrane Transport Proteins, Myelin Proteins analysis, Myelin Sheath chemistry, Peripheral Nerves chemistry, Proteolipids analysis
Abstract: The myelin and lymphocyte protein (MAL) proteolipid is localized in central and peripheral compact myelin membranes, as well as in apical membranes of particular polarized cells. In this study, we addressed the question whether MAL and other peripheral myelin proteins are sorted and targeted to myelin membranes using mechanisms similar to those observed in polarized epithelial cells. To investigate the presence of raft-mediated sorting pathways in Schwann cells, we have isolated and analysed their composition in myelin membranes. Here, we show that rafts are present in adult human and rat peripheral compact myelin membranes and contain MAL, the GPI-anchored protein CD59, and substantial amounts of the PMP22 and P0. Colocalization studies show that CD59, and MAL have an almost identical expression pattern within compact myelin. Moreover, immuno-electron microscopy revealed that MAL, besides its localization in compact myelin, is also localized to Schmidt-Lanterman incisures. Taken together, our results demonstrate the presence of detergent-insoluble glycolipid-enriched complexes (DIGs) in different compartments of myelin membranes and indicate an important role for DIG-mediated transport mechanisms in the maintenance of the adult myelin sheath.
Published: 2002
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45. Caspr3 and caspr4, two novel members of the caspr family are expressed in the nervous system and interact with PDZ domains.

Author: Spiegel I, Salomon D, Erne B, Schaeren-Wiemers N, and Peles E
Subjects: Adult, Aged, Animals, Cell Membrane ultrastructure, Cells, Cultured, Chromosomes, Human, Pair 16 genetics, Chromosomes, Human, Pair 9 genetics, DNA, Complementary analysis, Humans, Immunohistochemistry, Macromolecular Substances, Membrane Proteins genetics, Mice, Middle Aged, Molecular Sequence Data, Nerve Tissue Proteins genetics, Nervous System cytology, Neuroglia cytology, Neurons cytology, Protein Binding physiology, Protein Structure, Tertiary genetics, RNA, Messenger metabolism, Rats, Receptors, Cell Surface genetics, Sequence Homology, Amino Acid, Sequence Homology, Nucleic Acid, Cell Adhesion Molecules, Neuronal, Cell Membrane metabolism, Drosophila Proteins, Membrane Proteins isolation & purification, Nerve Tissue Proteins isolation & purification, Nervous System metabolism, Neuroglia metabolism, Neurons metabolism, Receptors, Cell Surface isolation & purification
Abstract: The NCP family of cell-recognition molecules represents a distinct subgroup of the neurexins that includes Caspr and Caspr2, as well as Drosophila Neurexin-IV and axotactin. Here, we report the identification of Caspr3 and Caspr4, two new NCPs expressed in nervous system. Caspr3 was detected along axons in the corpus callosum, spinal cord, basket cells in the cerebellum and in peripheral nerves, as well as in oligodendrocytes. In contrast, expression of Caspr4 was more restricted to specific neuronal subpopulations in the olfactory bulb, hippocampus, deep cerebellar nuclei, and the substantia nigra. Similar to the neurexins, the cytoplasmic tails of Caspr3 and Caspr4 interacted differentially with PDZ domain-containing proteins of the CASK/Lin2-Veli/Lin7-Mint1/Lin10 complex. The structural organization and distinct cellular distribution of Caspr3 and Caspr4 suggest a potential role of these proteins in cell recognition within the nervous system., ((c) 2002 Elsevier Science (USA).)
Published: 2002
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46. Characterization of human nerve basal lamina for their binding properties of anti-MAG antibodies.

Author: Sollberger M, Erne B, Sansano S, Steck AJ, and Schaeren-Wiemers N
Subjects: Aged, Basement Membrane metabolism, Basement Membrane ultrastructure, Humans, Male, Middle Aged, Myelin Sheath metabolism, Myelin Sheath ultrastructure, Protein Binding physiology, Sural Nerve metabolism, Sural Nerve ultrastructure, Antibodies, Anti-Idiotypic metabolism, Immunoglobulin M metabolism, Myelin-Associated Glycoprotein metabolism, Nerve Fibers metabolism, Nerve Fibers ultrastructure
Abstract: The functional importance of the basal lamina in Schwann cell development and in adult peripheral nerve fibers is well known. We have demonstrated previously by confocal microscopy that IgM deposits are present on the basal lamina of myelinating Schwann cells of nerve biopsies from patients with an anti-MAG IgM neuropathy. Therefore, the basal lamina was postulated to represent an early target for the uptake of autoantibodies on the surface of myelinated nerve fibers. In this study, the preparation of cell- and myelin-free basal lamina from human peripheral nerves, using a detergent-dependent method is described and characterized by immunohistochemical and biochemical analysis. Using these methods we demonstrated that an enrichment of basal lamina components of Schwann cells with extraction of myelin could be achieved. Western blot analysis and immunohistochemical characterization showed that anti-MAG IgM antibodies did not recognize an epitope on the basal lamina of normal nerves. The established method will allow in situ investigations of basal lamina components from human peripheral nerves in health and in disease, e.g. peripheral neuropathies of infectious or inflammatory origin.
Published: 2002
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47. TNF-alpha expression in painful and nonpainful neuropathies.

Author: Empl M, Renaud S, Erne B, Fuhr P, Straube A, Schaeren-Wiemers N, and Steck AJ
Subjects: Adult, Aged, Aged, 80 and over, Biopsy, Blood Proteins metabolism, Female, Humans, Immunohistochemistry, Inflammation blood, Inflammation pathology, Inflammation physiopathology, Lymphocytes pathology, Macrophages pathology, Male, Middle Aged, Pain pathology, Peripheral Nervous System Diseases pathology, Sural Nerve metabolism, Sural Nerve pathology, Sural Nerve physiopathology, Biomarkers blood, Pain blood, Pain physiopathology, Peripheral Nervous System Diseases blood, Peripheral Nervous System Diseases physiopathology, Tumor Necrosis Factor-alpha metabolism
Abstract: Objective: To determine whether the cytokine tumor necrosis factor alpha (TNF-alpha) acts as a pain mediator in neuropathic pain in humans., Background: In animal models, inflammatory cytokines such as TNF-alpha have been shown to facilitate neuropathic pain., Methods: The expression of TNF-alpha was analyzed immunohistochemically in 20 human nerve biopsy specimens of patients with painful (n = 10) and nonpainful (n = 10) neuropathies. Additionally, serum soluble TNF-alpha receptor I (sTNF-RI) levels were determined in 24 patients with neuropathies, 16 of which were painful and 8 that were painless., Results: Colocalization studies by confocal fluorescence microscopy for S-100 and TNF-alpha showed expression of TNF-alpha in human Schwann cells. Patients with painful neuropathies showed a stronger TNF-alpha immunoreactivity in myelinating Schwann cells relative to the epineurial background staining compared with patients with nonpainful neuropathy (0.949 +/- 0.047 vs 1.010 +/- 0.053, p < 0.05). Although there was no difference in sTNF-RI levels between painful (n = 16) and nonpainful (n = 8) neuropathies (sTNF-RI: 1412 +/- 545 pg/mL vs 1,318 +/- 175 pg/mL), patients with a mechanical allodynia (n = 9) had elevated serum sTNF-RI (1627 +/- 645 pg/mL vs 1233 +/- 192 pg/mL, p < 0.05) compared with patients without allodynia (n = 15)., Conclusions: TNF-alpha expression of human Schwann cells may be up-regulated in painful neuropathies. The elevation of sTNF-RI in patients with centrally mediated mechanical allodynia suggests that systemic sTNF-RI levels may influence central pain processing mechanisms.
Published: 2001
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48. Characterisation of autoantibodies to peripheral myelin protein 22 in patients with hereditary and acquired neuropathies.

Author: Ritz MF, Lechner-Scott J, Scott RJ, Fuhr P, Malik N, Erne B, Taylor V, Suter U, Schaeren-Wiemers N, and Steck AJ
Subjects: Adult, Aged, Blotting, Western, Case-Control Studies, Diabetic Neuropathies immunology, Female, Humans, Male, Middle Aged, Miller Fisher Syndrome immunology, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating immunology, Recombinant Proteins immunology, Autoantibodies blood, Charcot-Marie-Tooth Disease immunology, Myelin Proteins immunology, Polyneuropathies immunology
Abstract: To investigate the possibility that an autoimmune mechanism may play a role in the hereditary neuropathy Charcot-Marie-Tooth type 1A (CMT1A), sera were analysed by Western blot for anti-peripheral myelin protein 22 (PMP22) autoantibodies. These sera were compared with sera from patients with CMT type 2 (CMT2), acquired peripheral neuropathies such as chronic inflammatory demyelinating neuropathy (CIDP), anti-MAG IgM neuropathy, Miller-Fisher syndrome (MFS), diabetic neuropathy and with control blood donors. Anti-PMP22 positive sera were detected in 70% of patients with CMT1 and unexpectedly in 60% of patients with CMT2. Interestingly, 44% of the patients with other peripheral neuropathies and 23% of the apparently healthy controls showed also anti-PMP22 antibody reactivity. Immunohistochemical analysis of the human anti-PMP22 antisera on healthy sural nerve sections and on PMP22-expressing COS cells revealed that these sera did not recognise endogenous PMP22. Our results indicate that anti-PMP22 autoantibodies are found in sera of patients with different types of peripheral neuropathies, but their role in the pathogenesis of these diseases remains to be determined.
Published: 2000
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49. Anti-MAG IgM penetration into myelinated fibers correlates with the extent of myelin widening.

Author: Ritz MF, Erne B, Ferracin F, Vital A, Vital C, and Steck AJ
Subjects: Fluorescent Antibody Technique, Humans, Microscopy, Electron, Myelin Sheath ultrastructure, Peroneal Nerve ultrastructure, Sural Nerve ultrastructure, Immunoglobulin M analysis, Immunoglobulin M immunology, Myelin Sheath immunology, Myelin Sheath pathology, Paraproteinemias immunology, Paraproteinemias pathology, Peroneal Nerve pathology, Sural Nerve pathology
Abstract: The purpose of this study was to evaluate the relationship between immunoglobulin M (IgM) antibodies penetration into myelinated peripheral nerve fibers and the widening of the peripheral myelin sheaths in anti-myelin-associated glycoprotein (anti-MAG) demyelinating IgM monoclonal polyneuropathy. Demyelinating polyneuropathy with monoclonal IgM is often associated with anti-MAG autoantibodies, which are thought to initiate the disease with IgM deposits usually present on the myelin sheaths. We analyzed nerve biopsies from 12 patients with an anti-MAG demyelinating neuropathy by confocal and electron microscopy. The total number of nerve fibers and the proportion of IgM-associated fibers were quantified after immunohistochemical staining. The affinities of IgM were examined by analyzing the binding pattern of serum IgM on normal peripheral nerve sections. Ultrastructural examinations of the biopsies showed a good correlation between in situ widened myelin sheaths and the IgM penetration level into myelinated fibers. The terminal complement complex appears not be involved in the penetration of IgM into the myelinated fibers. Our findings suggest a causative role of the IgM anti-MAG antibodies in the ultrastructural modifications of the myelin sheaths. The basement membrane and myelin components appear to be the major targets of the IgM monoclonal antibodies. However, the pathogenic mechanism whereby IgM antibodies reach their targets and induce nerve damage are still unclear., (Copyright 1999 John Wiley & Sons, Inc.)
Published: 1999
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50. Matrix metalloproteinase upregulation in chronic inflammatory demyelinating polyneuropathy and nonsystemic vasculitic neuropathy.

Author: Leppert D, Hughes P, Huber S, Erne B, Grygar C, Said G, Miller KM, Steck AJ, Probst A, and Fuhr P
Subjects: Adult, Aged, Chronic Disease, Collagenases metabolism, Demyelinating Diseases pathology, Demyelinating Diseases physiopathology, Female, Gelatinases metabolism, Gene Expression Regulation, Enzymologic, Humans, Inflammation, Macrophages enzymology, Male, Matrix Metalloproteinase 2, Matrix Metalloproteinase 3 metabolism, Matrix Metalloproteinase 7, Matrix Metalloproteinase 9, Middle Aged, Peripheral Nervous System Diseases pathology, Peripheral Nervous System Diseases physiopathology, Polyradiculoneuropathy pathology, Polyradiculoneuropathy physiopathology, Stromal Cells enzymology, Sural Nerve enzymology, Sural Nerve pathology, T-Lymphocytes enzymology, Vasculitis pathology, Vasculitis physiopathology, Demyelinating Diseases enzymology, Metalloendopeptidases genetics, Metalloendopeptidases metabolism, Peripheral Nervous System Diseases enzymology, Polyradiculoneuropathy enzymology, Vasculitis enzymology
Abstract: Objective: To determine the expression pattern and cellular source of matrix metalloproteinases (MMPs) in chronic inflammatory demyelinating polyneuropathy (CIDP) and nonsystemic vasculitic neuropathy (NSVN)., Background: MMPs are endopeptidases involved in tissue destruction and infiltration by immune cells in multiple sclerosis and Guillain-Barré syndrome. Enzyme inhibitors of MMPs attenuate clinical symptoms in corresponding animal models of these diseases. MMP inhibition may therefore be a novel approach for the treatment of CIDP and NSVN. However, the spectrum of MMPs expressed in chronic inflammatory neuropathies has not been established., Methods: The expression of MMP-2, MMP-3, MMP-7, and MMP-9 in T cells, macrophages, and stromal cells in CIDP, NSVN, and noninflammatory neuropathies (NIN) was quantitated by immunohistochemistry. Results were correlated with clinical and electrophysiologic findings., Results: The production of MMP-2 and MMP-9 is increased in nerve tissue in CIDP and NSVN compared with NIN. T cells are the predominant source of MMP-2 and MMP-9 in CIDP and NSVN, whereas macrophages contribute only to a minor extent. Stromal cells of the perineurium/epineurium are an additional source of MMP-2 in NSVN, but not in CIDP. Expression of MMP-3 and MMP-7 was not detectable in CIDP or NSVN. Expression of MMP-2 and MMP-9 did not correlate with clinical disease activity and electrophysiologic measurements., Conclusions: The upregulation of MMP-2 and MMP-9 is a specific feature of CIDP and NSVN, and selective inhibitors of these enzymes could be used to prevent inflammatory tissue damage. The similar increase of MMP-2 and MMP-9 in both demyelinating (CIDP) and nondemyelinating (NSVN) neuropathies raises doubts about whether MMPs play a primary role in demyelination.
Published: 1999
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