Gold, Ralf

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","154"],["dc.contributor.author","Stasiolek, Mariusz"],["dc.contributor.author","Bayas, A."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Selmaj, K."],["dc.date.accessioned","2018-11-07T10:46:03Z"],["dc.date.available","2018-11-07T10:46:03Z"],["dc.date.issued","2004"],["dc.format.extent","158"],["dc.identifier.isi","000224003200531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47653"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","7th International Congress of the International-Society-of-Neuroimmunology"],["dc.relation.eventlocation","Venice, ITALY"],["dc.relation.issn","0165-5728"],["dc.title","Multiple sclerosis: impaired phenotype and maturation of plasmacytoid dendritic cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1170"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","1173"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Decard, Bernhard F."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Grunwald, Thomas"],["dc.contributor.author","Streit, Frank"],["dc.contributor.author","Stroet, Anke"],["dc.contributor.author","Niggemeier, Petra"],["dc.contributor.author","Schottstedt, Volkmar"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Chan, Andrew"],["dc.date.accessioned","2018-11-07T09:02:57Z"],["dc.date.available","2018-11-07T09:02:57Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective Vitamin D deficiency and Epstein-Barr virus (EBV) infection may be associated with the development of multiple sclerosis (MS). We investigated serum 25-hydroxyvitamin D (25-OH-D) levels and anti-EBV immunoreactivity in 25 individuals before the first clinical manifestation of MS. Patients and methods 56 serum samples of 25 individuals who had donated blood prior to the first clinical MS manifestation (clinically isolated syndrome (CIS)) (four male subjects, 21 female subjects, mean age 31.5 years at time of pre-CIS blood sampling; mean age at disease onset 33.4 years) were available, covering an interval of 7.3 years-2 months (mean 31.5 months) before CIS. In 18 of 25 patients serum samples were also obtained after established diagnosis of MS. Longitudinal age- and gender-matched healthy blood donors (four male subjects, 21 female subjects, 39 samples, mean age 32.5 years) served as controls. Serum 25-OH-D was measured by isotope dilution-liquid chromatography-tandem mass spectrometry. 25-OH-D levels were deconvoluted using published seasonal coefficients from a German population. Immunoglobulin G (IgG) against Epstein-Barr virus nuclear antigen-1 (EBNA1) were assessed using commercially available ELISA. Results Low 25-OH-D levels were observed during the 24-month pre-CIS interval (47.8 (32.5-77.2) nmol/l, median (IQR); healthy controls: 81.6 (57.7-98.5), p=0.004, however, still higher than after established diagnosis (24.5 (13.7-47.7), p<0.0001 compared with controls). IgG against EBNA1 during the 36-month pre-CIS interval was increased (185.9 (91.2-460.0) IU/ml, median (IQR); healthy controls 63.7 (29.5-121.6), p=0.002). Conclusions Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years."],["dc.identifier.doi","10.1136/jnnp-2012-303068"],["dc.identifier.isi","000311097700012"],["dc.identifier.pmid","22888143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24794"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","0022-3050"],["dc.title","Low vitamin D and elevated immunoreactivity against Epsteine-Barr virus before first clinical manifestation of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1009"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","1021"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Bayas, A."],["dc.contributor.author","Toyka, Klaus V."],["dc.date.accessioned","2018-11-07T11:12:22Z"],["dc.date.available","2018-11-07T11:12:22Z"],["dc.date.issued","2005"],["dc.description.abstract","The group of autoimmune neuropathies includes the Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuritis, multifocal motor neuropathy, neuropathies associated with monoclonal gammopathies, and vasculitic neuropathies. This educational review first addresses diagnostic pathways that facilitate more rational diagnostic decisions. Many therapies are effective for treating immune neuropathies. Unfortunately, none of the available therapies are specific. In the acute phase, glucocorticosteroids, plasmapheresis, and intravenous immunoglobulins play key roles. The list of long-term therapies includes azathioprine, cyclosporine, cyclophosphamide, and immunoglobulins. The therapeutic mechanisms involved are not clear for most of these compounds. Modem immunotherapy has to consider medical aspects, available therapeutic evidence, and long-term economic burden."],["dc.identifier.doi","10.1007/s00115-005-1942-5"],["dc.identifier.isi","000231649800014"],["dc.identifier.pmid","16080020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53648"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0028-2804"],["dc.title","Autoimmune neuropathien - Current aspects of immunopathologic diagnostics and therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","271"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Astrophysical Journal"],["dc.bibliographiccitation.lastpage","276"],["dc.bibliographiccitation.volume","545"],["dc.contributor.author","Klose, S."],["dc.contributor.author","Stecklum, B."],["dc.contributor.author","Masetti, N."],["dc.contributor.author","Pian, E."],["dc.contributor.author","Palazzi, E."],["dc.contributor.author","Henden, A. A."],["dc.contributor.author","Hartmann, D. H."],["dc.contributor.author","Fischer, O."],["dc.contributor.author","Gorosabel, J."],["dc.contributor.author","Sanchez-Fernandez, C."],["dc.contributor.author","Butler, D."],["dc.contributor.author","Ott, T."],["dc.contributor.author","Hippler, S."],["dc.contributor.author","Kasper, M."],["dc.contributor.author","Weiss, R."],["dc.contributor.author","Castro-Tirado, A."],["dc.contributor.author","Greiner, J."],["dc.contributor.author","Bartolini, C."],["dc.contributor.author","Guarnieri, A."],["dc.contributor.author","Piccioni, A."],["dc.contributor.author","Benetti, S."],["dc.contributor.author","Ghinassi, F."],["dc.contributor.author","Magazzu, A."],["dc.contributor.author","Hurley, K."],["dc.contributor.author","Cline, T."],["dc.contributor.author","Trombka, J."],["dc.contributor.author","McClanahan, T."],["dc.contributor.author","Starr, R."],["dc.contributor.author","Goldstein, J."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Mazets, E."],["dc.contributor.author","Golenetskii, S."],["dc.contributor.author","Noeske, K."],["dc.contributor.author","Papaderos, P."],["dc.contributor.author","Vreeswijk, P. M."],["dc.contributor.author","Tanvir, N."],["dc.contributor.author","Oscoz, A."],["dc.contributor.author","Munoz, J. A."],["dc.contributor.author","Ceron, JMC"],["dc.date.accessioned","2018-11-07T08:29:13Z"],["dc.date.available","2018-11-07T08:29:13Z"],["dc.date.issued","2000"],["dc.description.abstract","We report near-infrared and optical follow-up observations of the afterglow of the GRB 000418 starting 2.5 days after the occurrence of the burst and extending over nearly 7 weeks. GRB 000418 represents the second case for which the afterglow was initially identified by observations in the near-infrared. During the first 10 days its R-band afterglow was well characterized by a single power-law decay with a slope of 0.86. However, at later times the temporal evolution of the afterglow flattens with respect to a simple power-law decay. Attributing this to an underlying host galaxy, we find its magnitude to be R = 23.9 and an intrinsic afterglow decay slope of 1.22. The afterglow was very red with R-K approximate to 4 mag. The observations can be explained by an adiabatic, spherical fireball solution and a heavy reddening due to dust extinction in the host galaxy. This supports the picture that (long) bursts are associated with events in star-forming regions."],["dc.identifier.doi","10.1086/317816"],["dc.identifier.isi","000166018300026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16599"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Univ Chicago Press"],["dc.relation.issn","0004-637X"],["dc.title","The very red afterglow of GRB 000418: Further evidence for dust extinction in a gamma-ray burst host galaxy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1236"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1237"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Schneider-Gold, Christiane"],["dc.contributor.author","Wessig, Carsten"],["dc.contributor.author","Hoepker, Martin"],["dc.contributor.author","Erdlenbruch, Bernhard"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Toyka, Klaus V."],["dc.date.accessioned","2018-11-07T09:21:23Z"],["dc.date.available","2018-11-07T09:21:23Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1007/s00415-006-0150-y"],["dc.identifier.isi","000241113100021"],["dc.identifier.pmid","16598612"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29091"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Pregnancy and delivery of a healthy baby in autoimmune Lambert-Eaton myasthenic syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Stasiolek, Mariusz"],["dc.contributor.author","Bayas, A."],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Selmaj, K."],["dc.date.accessioned","2018-11-07T10:56:30Z"],["dc.date.available","2018-11-07T10:56:30Z"],["dc.date.issued","2005"],["dc.format.extent","S121"],["dc.identifier.isi","000232249900443"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50026"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Hodder Arnold, Hodder Headline Plc"],["dc.publisher.place","London"],["dc.relation.conference","21st Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis/10th Annual Meeting of Rehabilitation in MS"],["dc.relation.eventlocation","Thessaloniki, GREECE"],["dc.relation.issn","1352-4585"],["dc.title","Impaired reaction of plasmacytoid dendritic cells to toll-like receptor 7 and 9 ligands in MS patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","2"],["dc.bibliographiccitation.volume","192"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:48:55Z"],["dc.date.available","2018-11-07T10:48:55Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1016/j.jneuroim.2007.10.011"],["dc.identifier.isi","000252163200001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48312"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Many roads lead to Rome: Heterogeneity among encephalitogenic T cell clones"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical & Experimental Immunology"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Hofstetter, Harald H."],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Lesch, K. P."],["dc.contributor.author","Linker, Ralf Andreas"],["dc.contributor.author","Toyka, Klaus V."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T10:55:12Z"],["dc.date.available","2018-11-07T10:55:12Z"],["dc.date.issued","2005"],["dc.description.abstract","Serotonin (5-hydroxytryptamine, 5-HT) is one of the most extensively studied neurotransmitters of the central nervous system. It also has been identified in constituents of the immune system. Therefore serotonin has been suggested to serve as a mediator of bidirectional interactions between the nervous system and the immune system. We investigated this interaction in experimental autoimmune encephalomyelitis (EAE), a well-defined animal model of autoimmune disease of the central nervous system (CNS) mimicking features of the human disease multiple sclerosis. EAE was induced by immunization with the autoantigens myelin basic protein (MBP) or the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) spanning amino acids 35-55 (MOGp 35-55). We studied EAE in knockout (KO) mice lacking the 5-HT transporter (5-HTT) on a C57.BL/6 background, in comparison with wild-type C57.BL/6 animals. After immunization with MOGp 35-55, or with rat MBP, the disease courses of the 5-HTT knockout mice were attenuated as compared to wildtype control mice. This difference was more pronounced in female animals. To dissect potential immune mechanisms underlying this phenomenon, histological studies of the CNS and cytokine measurements in mononuclear cells from the spleens of 5-HTT KO mice and wild-type controls were performed. We found a reduction of the inflammatory infiltrate in the CNS and of the neuroantigen-specific production of IFN-gamma in splenocytes, again accompanied by a gender difference. These findings suggest a potential role of extracellular 5-HT homeostasis in the fine-tuning of neuroantigen-specific immune responses."],["dc.identifier.doi","10.1111/j.1365-2249.2005.02901.X"],["dc.identifier.isi","000231824900005"],["dc.identifier.pmid","16178854"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49732"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0009-9104"],["dc.title","Absence of reuptake of serotonin influences susceptibility to clinical autoimmune disease and neuroantigen-specific interferon-gamma production in mouse EAE"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","397"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","406"],["dc.bibliographiccitation.volume","211"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Weller, Charlotte"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Schmidt, Jens"],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Metselaar, Josbert M."],["dc.contributor.author","Gold, Ralf"],["dc.date.accessioned","2018-11-07T11:14:26Z"],["dc.date.available","2018-11-07T11:14:26Z"],["dc.date.issued","2008"],["dc.description.abstract","Liposomal encapsulation leads to enhanced efficacy of glucocorticosteroids (GS) in treatment of autoimmune diseases. Here we compare liposomal prednisolone (PL) to liposomal methylprednisolone (MPL) in chronic-relapsing myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE), a model closely reflecting aspects of multiple sclerosis (MS). At the maximum of the first relapse, a single dose of PL or MPL was applied at 10 mg/kg or at 4 mg/kg and compared to classical methylprednisolone (MP) pulse therapy. PL at 10 mg/kg was superior to free MP with long-term efficacy and a sustained protection even during the second and third relapse. At the same time, in vivo magnetic resonance imaging of rat brains revealed a significant reduction of T2-lesions after PL application. Comparison of PL and MPL at 10 mg/kg disclosed superior effects for MPL with an enhanced reduction of inflammatory infiltration as well as preservation of myelin and axons. Dose titration experiments underscored a dose-dependent efficacy of liposomal GS with a sustained efficacy especially of the higher dosage. In histological analyses, PL10 was superior in reducing macrophage and T cell infiltration as well as demyelination and axonal loss while the lower dosages were still at least as effective as free MP. FACS analyses revealed an effect of liposome formulations on T cell numbers, the CD4/CD8 ratio, frequencies of regulatory T cells and adhesion molecule expression. In summary, liposomal GS and especially methylprednisolone formulations display an enhanced efficacy not only in acute inflammatory, but also in chronic demyelinating models of MS and confer long-term protection from relapses. These findings lay the groundwork for applying liposomal GS in clinical MS trials in the near future. (c) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2008.02.005"],["dc.identifier.isi","000256272800012"],["dc.identifier.pmid","18394606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54122"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0014-4886"],["dc.title","Liposomal glucocorticosteroids in treatment of chronic autoimmune demyelination: Long-term protective effects and enhanced efficacy of methylprednisolone formulations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","894"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY"],["dc.bibliographiccitation.lastpage","905"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Belharazem, Djeda"],["dc.contributor.author","Schalke, Berthold"],["dc.contributor.author","Gold, Ralf"],["dc.contributor.author","Nix, Wilfred"],["dc.contributor.author","Vitacolonna, Mario"],["dc.contributor.author","Hohenberger, Peter"],["dc.contributor.author","Roessner, Eric"],["dc.contributor.author","Schulze, Torsten J."],["dc.contributor.author","Saruhan-Direskeneli, Gueher"],["dc.contributor.author","Yilmaz, Vuslat"],["dc.contributor.author","Ott, German"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Marx, Alexander"],["dc.date.accessioned","2018-11-07T09:51:57Z"],["dc.date.available","2018-11-07T09:51:57Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: The capacity of thymomas to generate mature CD4+ effector T cells from immature precursors inside the tumor and export them to the blood is associated with thymoma-associated myasthenia gravis (TAMG). Why TAMG (+) thymomas generate and export more mature CD4+ T cells than MG(-) thymomas is unknown. Methods: Unfixed thymoma tissue, thymocytes derived thereof, peripheral blood mononuclear cells (PBMCs), T-cell subsets and B cells were analysed using qRT-PCR and western blotting. Survival of PBMCs was measured by MTT assay. FAS-mediated apoptosis in PBMCs was quantified by flow cytometry. NF-kappa B in PBMCs was inhibited by the NF-kappa B-Inhibitor, EF24 prior to FAS-Ligand (FASLG) treatment for apoptosis induction. Results: Expression levels of the apoptosis inhibitor cellular FLICE-like inhibitory protein (c-FLIP) in blood T cells and intratumorous thymocytes were higher in TAMG(+) than in MG(-) thymomas and non-neoplastic thymic remnants. Thymocytes and PBMCs of TAMG patients showed nuclear NF-kappa B accumulation and apoptosis resistance to FASLG stimulation that was sensitive to NF-kappa B blockade. Thymoma removal reduced cFLIP expression in PBMCs. Interpretation: We conclude that thymomas induce cFLIP overexpression in thymocytes and their progeny, blood T cells. We suggest that the stronger cFLIP overexpression in TAMG(+) compared to MG(-) thymomas allows for the more efficient generation of mature CD4+ T cells in TAMG(+) thymomas. cFLIP overexpression in thymocytes and exported CD4+ T cells of patients with TAMG might contribute to the pathogenesis of TAMG by impairing central and peripheral T-cell tolerance."],["dc.identifier.doi","10.1002/acn3.210"],["dc.identifier.isi","000367238200003"],["dc.identifier.pmid","26401511"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36014"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2328-9503"],["dc.title","cFLIP overexpression in T cells in thymoma-associated myasthenia gravis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]