Brück, Wolfgang

[["dc.bibliographiccitation.firstpage","245"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Expert Review of Clinical Pharmacology"],["dc.bibliographiccitation.lastpage","256"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Zamvil, Scott S"],["dc.date.accessioned","2021-06-01T10:48:27Z"],["dc.date.available","2021-06-01T10:48:27Z"],["dc.date.issued","2012"],["dc.description.abstract","Laquinimod is a novel, small, orally administered medication that has demonstrated efficacy in the treatment of multiple sclerosis, a chronic inflammatory demyelinating disease of the CNS. In preclinical testing, laquinimod inhibited the development of both acute and chronic paralysis in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Furthermore, laquinimod reduced inflammation, demyelination and axonal damage in experimental autoimmune encephalomyelitis in mice treated at disease induction or at clinical disease onset. Recent findings from the clinical trials indicate that laquinimod has significant effects in reducing relapse rate and has more pronounced effects in reducing sustained disability progression as well as brain atrophy, with a good safety profile. In conclusion, preclinical studies show that laquinimod's unique mechanisms of action, including its immunomodulatory and CNS-protective effects, translate into clinical benefits in relapsing-remitting multiple sclerosis patients."],["dc.identifier.doi","10.1586/ecp.12.12"],["dc.identifier.isi","000209288000009"],["dc.identifier.pmid","22697588"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85940"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.eissn","1751-2441"],["dc.relation.issn","1751-2433"],["dc.title","Laquinimod, a once-daily oral drug in development for the treatment of relapsing-remitting 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","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Jentoft, Mark E."],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Lennon, Vanda A."],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","Weinshenker, Brian G."],["dc.contributor.author","Wingerchuk, Dean M."],["dc.contributor.author","Giannini, Caterina"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Shuster, Elizabeth A."],["dc.contributor.author","Carter, Jonathan"],["dc.contributor.author","Boyd, Clara D."],["dc.contributor.author","Clardy, Stacey Lynn"],["dc.contributor.author","Cohen, Bruce A."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:02:13Z"],["dc.date.available","2018-11-07T10:02:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: To assess, in a surgical biopsy cohort of active demyelinating lesions, the diagnostic utility of aquaporin-4 (AQP4) immunohistochemistry in identifying neuromyelitis optica (NMO) or NMO spectrum disorder (NMOSD) and describe pathologic features that should prompt AQP4 immunohistochemical analysis and AQP4-immunoglobulin G (IgG) serologic testing. Methods: This was a neuropathologic cohort study of 20 surgical biopsies (19 patients; 11 cord/9 brain), performed because of diagnostic uncertainty, interpreted as active demyelinating disease and containing 2 or more of the following additional features: tissue vacuolation, granulocytic infiltrates, or astrocyte injury. Results: AQP4 immunoreactivity was lost in 18 biopsies and increased in 2. Immunopathologic features of the AQP4 loss cohort were myelin vacuolation (18), dystrophic astrocytes and granulocytes (17), vascular hyalinization (16), macrophages containing glial fibrillary acid protein (GFAP)-positive debris (14), and Creutzfeldt-Peters cells (0). All 14 cases with available serum tested positive for AQP4-IgG after biopsy. Diagnosis at last follow-up was NMO/NMOSD (15) and longitudinally extensive transverse myelitis (1 each relapsing and single). Immunopathologic features of the AQP4 increased cohort were macrophages containing GFAP-positive debris and granulocytes (2), myelin vacuolation (1), dystrophic astrocytes (1), Creutzfeldt-Peters cells (1), and vascular hyalinization (1). Diagnosis at last follow-up was multiple sclerosis (MS) and both tested AQP4-IgG seronegative after biopsy. Conclusions: AQP4 immunohistochemistry with subsequent AQP4-IgG testing has diagnostic utility in identifying cases of NMO/NMOSD. This study highlights the importance of considering NMOSD in the differential diagnosis of tumefactive brain or spinal cord lesions. AQP4-IgG testing may avert biopsy and avoid ineffective therapies if these patients are erroneously treated for MS."],["dc.identifier.isi","000347996400012"],["dc.identifier.pmid","25503621"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38185"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Diagnostic utility of aquaporin-4 in the analysis of active demyelinating lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1853-1857"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Oncology Letters"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Böhrnsen, Florian"],["dc.contributor.author","Enders, Christina"],["dc.contributor.author","Ludwig, Hans-Christoph"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Füzesi, Laszlo"],["dc.contributor.author","Gutenberg, Angelika"],["dc.date.accessioned","2018-06-26T08:12:45Z"],["dc.date.available","2018-06-26T08:12:45Z"],["dc.date.issued","2015-09"],["dc.description.abstract","Tumors of the pineal region (PR) are rare and can be subdivided into four main histomorphological groups: Pineal-parenchymal tumors (PPT), germ cell tumors (GCT), glial tumors and miscellaneous tumors. The appropriate pathological classification and grading of these malignancies is essential for determining the clinical management and prognosis. However, an early diagnosis is often delayed due to unspecific clinical symptoms, and histological support is not always decisive to identify the diversity of tumors of the PR. The present study aimed to characterize 18 tumors of the PR using comparative genomic hybridization. All the tumors were primarily surgically resected without any previous irradiation or chemotherapy. In addition to chromosomal aberrations in PPT and different GCTs of the PR, the present study described, for the first time, the chromosomal changes in a few rare entities (solitary-fibrous and neuroendocrine tumors) of the PR. The tumors in the study, regardless of histology and World Health Organization grade, were characterized by frequent gains at 7, 9q, 12q, 16p, 17 and 22q, and losses at 13q. While the detection of chromosomal aberrations in these tumors appears not to be indicative enough of histological entities and their grade of malignancy, the present data may be of use to select genes of interest for higher resolution genomic analyses."],["dc.identifier.doi","10.3892/ol.2015.3383"],["dc.identifier.pmid","26622764"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15149"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.title","Common molecularcytogenetic alterations in tumors originating from the pineal region"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e1906"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e1913"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Tobin, W. Oliver"],["dc.contributor.author","Kalinowska-Lyszczarz, Alicja"],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Tosakulwong, Nirubol"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2021-12-01T09:22:30Z"],["dc.date.available","2021-12-01T09:22:30Z"],["dc.date.issued","2021"],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.identifier.doi","10.1212/WNL.0000000000012782"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94416"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Clinical Correlation of Multiple Sclerosis Immunopathologic Subtypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","194"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","CANCER GENETICS AND CYTOGENETICS"],["dc.bibliographiccitation.lastpage","197"],["dc.bibliographiccitation.volume","200"],["dc.contributor.author","Schaefer, Inga-Marie"],["dc.contributor.author","Martinez, Ramon"],["dc.contributor.author","Enders, Christina"],["dc.contributor.author","Loertzer, Hagen"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Fuezesi, Laszlo"],["dc.contributor.author","Gutenberg, Angelika"],["dc.date.accessioned","2018-11-07T08:41:20Z"],["dc.date.available","2018-11-07T08:41:20Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/j.cancergencyto.2010.04.013"],["dc.identifier.isi","000279373500019"],["dc.identifier.pmid","20620607"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19445"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0165-4608"],["dc.title","Molecular cytogenetics of malignant pheochromocytoma with cerebral metastasis"],["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.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Schmidt, H."],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T09:16:23Z"],["dc.date.available","2018-11-07T09:16:23Z"],["dc.date.issued","2006"],["dc.format.extent","359"],["dc.identifier.isi","000240061000029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27924"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","51st Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Mannheim, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","The presence of the chemokine receptor CCR2 on specific myeloid cells determines the outcome of autoimmune encephalomyelitis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2487"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2500"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Schmidt, Hauke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Zabel, Mark D."],["dc.contributor.author","Hille, Andrea"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Prinz, Marco R."],["dc.date.accessioned","2018-11-07T11:24:34Z"],["dc.date.available","2018-11-07T11:24:34Z"],["dc.date.issued","2009"],["dc.description.abstract","The chemokine receptor CCR2 plays a vital role for the induction of autoimmunity in the central nervous system. However, it remains unclear how the pathogenic response is mediated by CCR2-bearing cells. By combining bone marrow chimerism with gene targeting we detected a mild disease-modulating role of CCR2 during experimental autoimmune encephalomyelitis, a model for central nervous system autoimmunity, on radio-resistant cells that was independent from targeted CCR2 expression on endothelia. Interestingly, absence of CCR2 on lymphocytes did not influence autoimmune demyelination. In contrast, engagement of CCR2 on accessory cells was required for experimental autoimmune encephalomyelitis induction. CCR2Ly-6C(hi) monocytes were rapidly recruited to the inflamed central nervous system and were crucial for the effector phase of disease. Selective depletion of this specific monocyte subpopulation through engagement of CCR2 strongly reduced central nervous system autoimmunity. Collectively, these data indicate a disease-promoting role of CCR2Ly-6C(hi) monocytes during autoimmune inflammation of the central nervous system."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; Gemeinnutzige Hertie-Stiftung"],["dc.identifier.doi","10.1093/brain/awp144"],["dc.identifier.isi","000269963600019"],["dc.identifier.pmid","19531531"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56435"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","CCR2Ly-6C(hi) monocytes are crucial for the effector phase of autoimmunity in the central nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","923"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","936"],["dc.bibliographiccitation.volume","142"],["dc.contributor.author","Schwabenland, Marius"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Prinz, Marco"],["dc.date.accessioned","2021-12-01T09:23:07Z"],["dc.date.available","2021-12-01T09:23:07Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract As extremely sensitive immune cells, microglia act as versatile watchdogs of the central nervous system (CNS) that tightly control tissue homeostasis. Therefore, microglial activation is an early and easily detectable hallmark of virtually all neuropsychiatric, neuro-oncological, neurodevelopmental, neurodegenerative and neuroinflammatory diseases. The recent introduction of novel high-throughput technologies and several single-cell methodologies as well as advances in epigenetic analyses helped to identify new microglia expression profiles, enhancer-landscapes and local signaling cues that defined diverse previously unappreciated microglia states in the healthy and diseased CNS. Here, we give an overview on the recent developments in the field of microglia biology and provide a practical guide to analyze disease-associated microglia phenotypes in both the murine and human CNS, on several morphological and molecular levels. Finally, technical limitations, potential pitfalls and data misinterpretations are discussed as well."],["dc.description.abstract","Abstract As extremely sensitive immune cells, microglia act as versatile watchdogs of the central nervous system (CNS) that tightly control tissue homeostasis. Therefore, microglial activation is an early and easily detectable hallmark of virtually all neuropsychiatric, neuro-oncological, neurodevelopmental, neurodegenerative and neuroinflammatory diseases. The recent introduction of novel high-throughput technologies and several single-cell methodologies as well as advances in epigenetic analyses helped to identify new microglia expression profiles, enhancer-landscapes and local signaling cues that defined diverse previously unappreciated microglia states in the healthy and diseased CNS. Here, we give an overview on the recent developments in the field of microglia biology and provide a practical guide to analyze disease-associated microglia phenotypes in both the murine and human CNS, on several morphological and molecular levels. Finally, technical limitations, potential pitfalls and data misinterpretations are discussed as well."],["dc.identifier.doi","10.1007/s00401-021-02370-8"],["dc.identifier.pii","2370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94564"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Analyzing microglial phenotypes across neuropathologies: a practical guide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1797"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Leukemia"],["dc.bibliographiccitation.lastpage","1807"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Deckert, M."],["dc.contributor.author","Engert, Andreas"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Ferreri, Andres J. M."],["dc.contributor.author","Finke, Juergen"],["dc.contributor.author","Illerhaus, Gerald"],["dc.contributor.author","Klapper, Wolfram"],["dc.contributor.author","Korfel, A."],["dc.contributor.author","Kueppers, Ralf"],["dc.contributor.author","Maarouf, M."],["dc.contributor.author","Montesinos-Rongen, Manuel"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Schlegel, Uwe"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Wiestler, Otmar D."],["dc.contributor.author","Siebert, Reiner"],["dc.contributor.author","DeAngelis, L. M."],["dc.date.accessioned","2018-11-07T08:49:14Z"],["dc.date.available","2018-11-07T08:49:14Z"],["dc.date.issued","2011"],["dc.description.abstract","Recent studies addressing the molecular characteristics of PCNSL, which is defined as malignant B-cell lymphoma with morphological features of DLBCL, have significantly improved our understanding of the pathogenesis of this lymphoma entity, which is associated with an inferior prognosis as compared with DLBCL outside the CNS. This unfavorable prognosis stimulated intense efforts to improve therapy and induced recent series of clinical studies, which addressed the role of radiotherapy and various chemotherapeutic regimens. This review combines the discussion of diagnosis, differential diagnosis and recent progress in studies addressing the molecular pathogenesis as well as therapeutic options in PCNSL. Leukemia (2011) 25, 1797-1807; doi:10.1038/leu.2011.169; published online 5 August 2011"],["dc.identifier.doi","10.1038/leu.2011.169"],["dc.identifier.isi","000298405500002"],["dc.identifier.pmid","21818113"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21408"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0887-6924"],["dc.title","Modern concepts in the biology, diagnosis, differential diagnosis and treatment of primary central nervous system lymphoma"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Kantorova, Ema"],["dc.contributor.author","Michalik, Jozef"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Slavik, Pavol"],["dc.contributor.author","Sivak, Stefan"],["dc.contributor.author","Kurca, Egon"],["dc.date.accessioned","2018-11-07T10:18:32Z"],["dc.date.available","2018-11-07T10:18:32Z"],["dc.date.issued","2016"],["dc.format.extent","21"],["dc.identifier.isi","000371657100048"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41465"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","ACTRIMS Forum"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Anaplastic astrocytoma mimicking progressive multifocal leucoencephalopathy in patient with active relapsing-remitting multiple sclerosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]