Now showing 1 - 10 of 23
  • 2016Journal Article
    [["dc.bibliographiccitation.firstpage","807"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","815"],["dc.bibliographiccitation.volume","139"],["dc.contributor.author","Haider, Lukas"],["dc.contributor.author","Zrzavy, Tobias"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Hoeftberger, Romana"],["dc.contributor.author","Bagnato, Francesca"],["dc.contributor.author","Grabner, Guenther"],["dc.contributor.author","Trattnig, Siegfried"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lassmann, Hans"],["dc.date.accessioned","2018-11-07T10:17:40Z"],["dc.date.available","2018-11-07T10:17:40Z"],["dc.date.issued","2016"],["dc.description.abstract","Multiple sclerosis is characterized by widespread primary demyelination and progressive degeneration, driven by heterogeneous mechanisms. Haider et al. provide a topographic map of the frequency with which different brain regions are affected by these processes, and show that demyelination and neurodegeneration involve inflammatory as well as vascular changes.Multiple sclerosis is characterized by widespread primary demyelination and progressive degeneration, driven by heterogeneous mechanisms. Haider et al. provide a topographic map of the frequency with which different brain regions are affected by these processes, and show that demyelination and neurodegeneration involve inflammatory as well as vascular changes.Multiple sclerosis is a chronic inflammatory disease with primary demyelination and neurodegeneration in the central nervous system. In our study we analysed demyelination and neurodegeneration in a large series of multiple sclerosis brains and provide a map that displays the frequency of different brain areas to be affected by these processes. Demyelination in the cerebral cortex was related to inflammatory infiltrates in the meninges, which was pronounced in invaginations of the brain surface (sulci) and possibly promoted by low flow of the cerebrospinal fluid in these areas. Focal demyelinated lesions in the white matter occurred at sites with high venous density and additionally accumulated in watershed areas of low arterial blood supply. Two different patterns of neurodegeneration in the cortex were identified: oxidative injury of cortical neurons and retrograde neurodegeneration due to axonal injury in the white matter. While oxidative injury was related to the inflammatory process in the meninges and pronounced in actively demyelinating cortical lesions, retrograde degeneration was mainly related to demyelinated lesions and axonal loss in the white matter. Our data show that accumulation of lesions and neurodegeneration in the multiple sclerosis brain does not affect all brain regions equally and provides the pathological basis for the selection of brain areas for monitoring regional injury and atrophy development in future magnetic resonance imaging studies."],["dc.identifier.doi","10.1093/brain/awv398"],["dc.identifier.isi","000371694600023"],["dc.identifier.pmid","26912645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41276"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","The topograpy of demyelination and neurodegeneration in the multiple sclerosis brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2014Conference Abstract
    [["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Kuhn, Susanne Antje"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Schirrmeister, Anne"],["dc.contributor.author","Kratzsch, Tobias"],["dc.contributor.author","Traeger, Uwe"],["dc.contributor.author","Hanlsch, Uwe Karsten"],["dc.contributor.author","Haberl, Hennes"],["dc.date.accessioned","2018-11-07T09:40:07Z"],["dc.date.available","2018-11-07T09:40:07Z"],["dc.date.issued","2014"],["dc.identifier.isi","000358613200183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33438"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","50th Annual Meeting of the American-Society-of-Clinical-Oncology"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","1527-7755"],["dc.relation.issn","0732-183X"],["dc.title","Proto-oncogene Ets-1 is pathologically expressed in low-grade astrocytomas and glioblastomas in a tissue and location specific pattern and correlates with patient survival"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2014Journal Article
    [["dc.bibliographiccitation.firstpage","202"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","World Neurosurgery"],["dc.bibliographiccitation.lastpage","206"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Allouch, Hassan"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Behnke-Mursch, Julianne"],["dc.contributor.author","Halatsch, Marc-Eric"],["dc.contributor.author","Mursch, Kay"],["dc.date.accessioned","2018-11-07T09:37:53Z"],["dc.date.available","2018-11-07T09:37:53Z"],["dc.date.issued","2014"],["dc.description.abstract","OBJECTIVE: Intraoperative ultrasound displays dynamic processes intraoperatively. Performing burr-hole biopsies under a real-time visual control is an interesting option for the neurosurgeon. However, the percentage of conclusive diagnoses obtained by this technique and the rate of complications must be evaluated in a larger series. METHODS: One hundred consecutive intracranial biopsies were analyzed. Through a burr hole, the lesion was localized by ultrasonography, and the planned needle trajectory was superimposed onto the image. Intracranial vessels were imaged by Doppler flow signals. Biopsies were taken in a mean depth of 41 mm (maximal 65 mm) from different parts of each tumor. RESULTS: Thirty-six lesions involved the corpus callosum, 16 lesions were located deeply within the white matter, five in the internal capsule, and one in the upper brainstem. There were three cerebellar and 17 temporal lesions. Ten tumors did not exceed a diameter of 15 mm in any plane. The mean time interval from skin incision to the end of suturing was 45 minutes, and the mean time from the surgeons entering the operating theater to leaving the theater was 63 minutes. In 95% of the lesions, a diagnosis could be established. Transient neurologic deficits occurred in five patients, which were permanent in three. In 42 patients without postoperative neurological symptoms, postoperative computed tomography scans were obtained within 24 hours; a visible hemorrhage occurred in eight (19%), six of which were seen intraoperatively. CONCLUSION: When intraoperative ultrasound-navigated biopsies were used they obtained a similar percentage of conclusive diagnoses as stereotactic biopsies. The complication rate is comparable as well. Emerging intracranial complications such as hemorrhages can be observed. However, their incidence cannot be decreased."],["dc.identifier.doi","10.1016/j.wneu.2013.01.019"],["dc.identifier.isi","000342911400139"],["dc.identifier.pmid","23313261"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32944"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1878-8769"],["dc.relation.issn","1878-8750"],["dc.title","Real-Time Ultrasound Monitoring During Intracranial Needle Biopsies: Operative Results and Detection of Complications in 100 Cases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2012Journal Article Discussion
    [["dc.bibliographiccitation.firstpage","753"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","755"],["dc.bibliographiccitation.volume","259"],["dc.contributor.author","Schirmer, Lucas"],["dc.contributor.author","Seifert, Christian L."],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Wunderlich, Silke"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T09:11:41Z"],["dc.date.available","2018-11-07T09:11:41Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1007/s00415-011-6231-6"],["dc.identifier.isi","000302489400021"],["dc.identifier.pmid","21901482"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26778"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.title","Clinicopathological considerations in acute disseminated encephalomyelitis (ADEM): a fulminant case with favorable outcome"],["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"]]
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  • 2013Conference Abstract
    [["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Wimmer, Isabella"],["dc.contributor.author","Haider, L."],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lassmann, Hans"],["dc.date.accessioned","2018-11-07T09:18:49Z"],["dc.date.available","2018-11-07T09:18:49Z"],["dc.date.issued","2013"],["dc.format.extent","9"],["dc.identifier.isi","000328751400004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28488"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","29th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis / 18th Annual Conference of Rehabilitation in MS"],["dc.relation.eventlocation","Copenhagen, DENMARK"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Iron and oxidative damage in the multiple sclerosis brain"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2011Journal Article
    [["dc.bibliographiccitation.firstpage","1554"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Brain Behavior and Immunity"],["dc.bibliographiccitation.lastpage","1568"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Kipp, Markus"],["dc.contributor.author","Gingele, S."],["dc.contributor.author","Pott, F."],["dc.contributor.author","Clarner, T."],["dc.contributor.author","van der Valk, Paul"],["dc.contributor.author","Denecke, Bernd"],["dc.contributor.author","Gan, Lin"],["dc.contributor.author","Siffrin, Volker"],["dc.contributor.author","Zipp, Frauke"],["dc.contributor.author","Dreher, W."],["dc.contributor.author","Baumgartner, W."],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Godbout, R."],["dc.contributor.author","Amor, Sandra"],["dc.contributor.author","Beyer, Cordian"],["dc.date.accessioned","2018-11-07T08:50:28Z"],["dc.date.available","2018-11-07T08:50:28Z"],["dc.date.issued","2011"],["dc.description.abstract","Several lines of evidence indicate that remyelination represents one of the most effective mechanisms to achieve axonal protection. For reasons that are not yet understood, this process is often incomplete or fails in multiple sclerosis (MS). Activated astrocytes appear to be able to boost or inhibit endogenous repair processes. A better understanding of remyelination in MS and possible reasons for its failure is needed. Using the well-established toxic demyelination cuprizone model, we created lesions with either robust or impaired endogenous remyelination capacity. Lesions were analyzed for mRNA expression levels by Affymetrix GeneChip (R) arrays. One finding was the predominance of immune and stress response factors in the group of genes which were classified as remyelination-supporting factors. We further demonstrate that lesions with impaired remyelination capacity show weak expression of the radial-glia cell marker brain lipid binding protein (BLBP, also called B-FABP or FABP7). The expression of BLBP in activated astrocytes correlates with the presence of oligodendrocyte progenitor cells. BLBP-expressing astrocytes are also detected in experimental autoimmune encephalomyelitis during the remission phase. Furthermore, highest numbers of BLBP-expressing astrocytes were evident in lesions of early MS, whereas significantly less are present at the rim of (chronic)-active lesions from patients with long disease duration. Transfection experiments show that BLBP regulates growth factor expression in U87 astrocytoma cells. In conclusion, we provide evidence that expression of BLBP in activated astrocytes negatively correlates with disease duration and in parallel with remyelination failure. (C) 2011 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Medical Faculty, RWTH Aachen; Hertie-Foundation; DFG"],["dc.identifier.doi","10.1016/j.bbi.2011.05.003"],["dc.identifier.isi","000296124700007"],["dc.identifier.pmid","21620951"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21700"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0889-1591"],["dc.title","BLBP-expression in astrocytes during experimental demyelination and in human multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2019Journal Article
    [["dc.bibliographiccitation.firstpage","1196"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1209"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Bergner, Caroline G."],["dc.contributor.author","Meer, Franziska"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Türkmen, Mevlude"],["dc.contributor.author","Valizada, Emil"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2022-03-01T11:45:41Z"],["dc.date.available","2022-03-01T11:45:41Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/glia.23598"],["dc.identifier.eissn","1098-1136"],["dc.identifier.issn","0894-1491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103412"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Microglia damage precedes major myelin breakdown in X‐linked adrenoleukodystrophy and metachromatic leukodystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2013Journal Article
    [["dc.bibliographiccitation.firstpage","848"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","861"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Wimmer, Isabella"],["dc.contributor.author","Haider, Lukas"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lassmann, Hans"],["dc.date.accessioned","2018-11-07T09:16:47Z"],["dc.date.available","2018-11-07T09:16:47Z"],["dc.date.issued","2013"],["dc.description.abstract","ObjectiveIron may contribute to the pathogenesis and progression of multiple sclerosis (MS) due to its accumulation in the human brain with age. Our study focused on nonheme iron distribution and the expression of the iron-related proteins ferritin, hephaestin, and ceruloplasmin in relation to oxidative damage in the brain tissue of 33 MS and 30 control cases. MethodsWe performed (1) whole-genome microarrays including 4 MS and 3 control cases to analyze the expression of iron-related genes, (2) nonheme iron histochemistry, (3) immunohistochemistry for proteins of iron metabolism, and (4) quantitative analysis by digital densitometry and cell counting in regions representing different stages of lesion maturation. ResultsWe found an age-related increase of iron in the white matter of controls as well as in patients with short disease duration. In chronic MS, however, there was a significant decrease of iron in the normal-appearing white matter (NAWM) corresponding with disease duration, when corrected for age. This decrease of iron in oligodendrocytes and myelin was associated with an upregulation of iron-exporting ferroxidases. In active MS lesions, iron was apparently released from dying oligodendrocytes, resulting in extracellular accumulation of iron and uptake into microglia and macrophages. Iron-containing microglia showed signs of cell degeneration. At lesion edges and within centers of lesions, iron accumulated in astrocytes and axons. InterpretationIron decreases in the NAWM of MS patients with increasing disease duration. Cellular degeneration in MS lesions leads to waves of iron liberation, which may propagate neurodegeneration together with inflammatory oxidative burst. Ann Neurol 2013;74:848-861"],["dc.description.sponsorship","Austrian Science Fund [P24245-B19]"],["dc.identifier.doi","10.1002/ana.23974"],["dc.identifier.isi","000329891100015"],["dc.identifier.pmid","23868451"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28011"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.title","Iron and Neurodegeneration in the Multiple Sclerosis Brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2012Conference Abstract
    [["dc.bibliographiccitation.firstpage","12"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Bunyan, Reem F."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:05:35Z"],["dc.date.available","2018-11-07T09:05:35Z"],["dc.date.issued","2012"],["dc.identifier.isi","000328702200008"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25356"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","28th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Lyon, FRANCE"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Axonal damage in inflammatory demyelinating lesions of paediatric patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2016Conference Abstract
    [["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Pfeifenbring, Sabine"],["dc.contributor.author","Bunyan, Reem F."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Gaertner, J."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T10:08:45Z"],["dc.date.available","2018-11-07T10:08:45Z"],["dc.date.issued","2016"],["dc.format.extent","67"],["dc.identifier.isi","000383267200107"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39527"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","London, ENGLAND"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Oligodendroglial damage and remyelination in paediatric multiple sclerosis lesions."],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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