Stadelmann-Nessler, Christine

[["dc.bibliographiccitation.artnumber","andr.13292"],["dc.bibliographiccitation.firstpage","1660"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Andrology"],["dc.bibliographiccitation.lastpage","1672"],["dc.bibliographiccitation.volume","10"],["dc.contributor.affiliation","Pinkert‐Leetsch, Diana; 1\r\nDepartment of Diagnostic and Interventional Radiology\r\nUniversity Medical Center Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Rost, John Uwe; 1\r\nDepartment of Diagnostic and Interventional Radiology\r\nUniversity Medical Center Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Schmiedeknecht, Max Ulrich Heiner; 3\r\nDepartment of Neuropathology\r\nUniversity Medical Center Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Stadelmann, Christine; 3\r\nDepartment of Neuropathology\r\nUniversity Medical Center Goettingen\r\nGoettingen Germany"],["dc.contributor.affiliation","Alves, Frauke; 1\r\nDepartment of Diagnostic and Interventional Radiology\r\nUniversity Medical Center Goettingen\r\nGoettingen Germany"],["dc.contributor.author","Pinkert‐Leetsch, Diana"],["dc.contributor.author","Rost, John Uwe"],["dc.contributor.author","Schmiedeknecht, Max Ulrich Heiner"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Missbach‐Guentner, Jeannine"],["dc.date.accessioned","2022-11-28T08:48:04Z"],["dc.date.available","2022-11-28T08:48:04Z"],["dc.date.issued","2022-09-15"],["dc.date.updated","2022-11-27T10:10:46Z"],["dc.description.abstract","Abstract\r\n\r\nBackground\r\nThe unique anatomy of the male reproductive organ reflects its complex function from sperm maturation to their storage for months until emission. Since light microscopy in two dimensions (2d) cannot sufficiently demonstrate its complex morphology, a comprehensive visualization is required to identify pathologic alterations in its entire anatomical context.\r\n\r\n\r\nObjectives\r\nAim of this study was to use three‐dimensional (3d) light sheet fluorescence microscopy (LSFM) to visualize entire murine testes in 3d, label‐free and at subcellular resolution, and to assign local autofluorescence to testicular and deferent structures.\r\n\r\n\r\nMaterials and methods\r\nMurine testes were fixed with four different fixatives and subsequently cleared with benzoic acid/benzyl benzoate. Hereafter, complete murine testes were scanned with LSFM with different fluorescence filter sets and subsequently embedded in paraffin for further conventional planar histology.\r\n\r\n\r\nResults\r\nAutofluorescence signals of the murine reproductive organ allowed the unambiguous identification of the testicular anatomy from the seminiferous tubules to the vas deferens with their specific stratification independent of the used fixative. Blood vessels were visualized from the pampiniform plexus to the small capillaries of single tubules. Moreover, due to the specific intrinsic fluorescence properties of the efferent ducts and the epididymis, luminal caliber, the epithelial stratification and retronuclear cytoplasmic inclusions gave a unique insight into the interface of both morphological structures. Subsequent 2d histology confirmed the identified morphological structures.\r\n\r\n\r\nDiscussion\r\nLSFM analysis of the murine reproductive organ allows due to its intrinsic fluorescence a simple, label‐free 3d assessment of its entire duct morphology, the epithelial composition, and the associated blood supply in its anatomical relation.\r\n\r\n\r\nConclusion\r\nLSFM provides the technical basis for comprehensive analyses of pathologically altered murine testes in its entirety by depicting specific autofluorescence. Thereby it facilitates mouse studies of testicular disease or their drug‐related alterations in more detail potentially for clinical translation assessing human testicular biopsies."],["dc.description.sponsorship","Bundesministerium fuer Bildung und Forschung, Deutschland"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.identifier.doi","10.1111/andr.13292"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/117280"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","2047-2927"],["dc.relation.issn","2047-2919"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made."],["dc.title","The murine male reproductive organ at a glance: Three‐dimensional insights and virtual histology using label‐free light sheet microcopy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.journal","European Journal of Neurology"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Schirmer, Lucas"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T08:39:40Z"],["dc.date.available","2018-11-07T08:39:40Z"],["dc.date.issued","2010"],["dc.format.extent","657"],["dc.identifier.isi","000293331101589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19052"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","Geneva, SWITZERLAND"],["dc.relation.issn","1351-5101"],["dc.title","Comparative study of neuronal and axonal pathology in early multiple sclerosis and CNS trauma lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","399"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Current Neurology and Neuroscience Reports"],["dc.bibliographiccitation.lastpage","404"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T11:24:39Z"],["dc.date.available","2018-11-07T11:24:39Z"],["dc.date.issued","2009"],["dc.description.abstract","Gray matter demyelination is frequent and extensive in most patients with multiple sclerosis (MS) and has recently received much attention in neuropathologic and imaging studies. Gray matter lesions show distinct pathologic features that make their detection difficult with conventional imaging techniques. Thus, despite their high prevalence, their impact on clinical symptoms has not been defined well so far. This review focuses on recent information from pathologic and imaging studies and summarizes our current knowledge on cortical pathology derived from human and experimental studies."],["dc.identifier.doi","10.1007/s11910-009-0058-x"],["dc.identifier.isi","000268572700008"],["dc.identifier.pmid","19664370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56452"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1528-4042"],["dc.title","Gray matter pathology and multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","768"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Annals of clinical and translational neurology"],["dc.bibliographiccitation.lastpage","783"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Malviya, Manish"],["dc.contributor.author","Barman, Sumanta"],["dc.contributor.author","Golombeck, Kristin S."],["dc.contributor.author","Planagumà, Jesús"],["dc.contributor.author","Mannara, Francesco"],["dc.contributor.author","Strutz-Seebohm, Nathalie"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Demir, Fatih"],["dc.contributor.author","Baksmeier, Christine"],["dc.contributor.author","Steckel, Julia"],["dc.contributor.author","Falk, Kim Kristin"],["dc.contributor.author","Gross, Catharina C."],["dc.contributor.author","Kovac, Stjepana"],["dc.contributor.author","Bönte, Kathrin"],["dc.contributor.author","Johnen, Andreas"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Martín-García, Elena"],["dc.contributor.author","Becker, Albert J."],["dc.contributor.author","Elger, Christian E."],["dc.contributor.author","Klöcker, Nikolaj"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Meuth, Sven G."],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Seebohm, Guiscard"],["dc.contributor.author","Leypoldt, Frank"],["dc.contributor.author","Maldonado, Rafael"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Dalmau, Josep"],["dc.contributor.author","Melzer, Nico"],["dc.contributor.author","Goebels, Norbert"],["dc.date.accessioned","2019-07-09T11:44:45Z"],["dc.date.available","2019-07-09T11:44:45Z"],["dc.date.issued","2017-11"],["dc.description.abstract","Objective: Autoimmune encephalitis is most frequently associated with anti-NMDAR autoantibodies. Their pathogenic relevance has been suggested by passive transfer of patients' cerebrospinal fluid (CSF) in mice in vivo. We aimed to analyze the intrathecal plasma cell repertoire, identify autoantibody-producing clones, and characterize their antibody signatures in recombinant form. Methods: Patients with recent onset typical anti-NMDAR encephalitis were subjected to flow cytometry analysis of the peripheral and intrathecal immune response before, during, and after immunotherapy. Recombinant human monoclonal antibodies (rhuMab) were cloned and expressed from matching immunoglobulin heavy- (IgH) and light-chain (IgL) amplicons of clonally expanded intrathecal plasma cells (cePc) and tested for their pathogenic relevance. Results: Intrathecal accumulation of B and plasma cells corresponded to the clinical course. The presence of cePc with hypermutated antigen receptors indicated an antigen-driven intrathecal immune response. Consistently, a single recombinant human GluN1-specific monoclonal antibody, rebuilt from intrathecal cePc, was sufficient to reproduce NMDAR epitope specificity in vitro. After intraventricular infusion in mice, it accumulated in the hippocampus, decreased synaptic NMDAR density, and caused severe reversible memory impairment, a key pathogenic feature of the human disease, in vivo. Interpretation: A CNS-specific humoral immune response is present in anti-NMDAR encephalitis specifically targeting the GluN1 subunit of the NMDAR. Using reverse genetics, we recovered the typical intrathecal antibody signature in recombinant form, and proved its pathogenic relevance by passive transfer of disease symptoms from man to mouse, providing the critical link between intrathecal immune response and the pathogenesis of anti-NMDAR encephalitis as a humorally mediated autoimmune disease."],["dc.identifier.doi","10.1002/acn3.444"],["dc.identifier.pmid","29159189"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14885"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59083"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2328-9503"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","NMDAR encephalitis: passive transfer from man to mouse by a recombinant antibody."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","793"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","796"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Lucchinetti, C."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T08:59:26Z"],["dc.date.available","2018-11-07T08:59:26Z"],["dc.date.issued","2001"],["dc.description.abstract","Severe tissue destruction is the presumed histopathological correlate of hypointense multiple sclerosis (MS) lesions. In this study we correlated changes of lesion hypointensity over time with initial histopathological features in 14 biopsied MS lesions. The extent of hypointensity increased in initially demyelinated plaques and decreased in remyelinating lesions. The initial axonal loss determined the increase of hypointensity over time. In conclusion, both axonal loss and demyelinating activity determine the evolution of hypointensity over time."],["dc.identifier.doi","10.1002/ana.1053"],["dc.identifier.isi","000169091400016"],["dc.identifier.pmid","11409432"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23896"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","A longitudinal MRI study of histopathologically defined hypointense multiple sclerosis lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","856"],["dc.bibliographiccitation.issue","6518"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","860"],["dc.bibliographiccitation.volume","370"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Ojha, Ravi"],["dc.contributor.author","Pedro, Liliana D."],["dc.contributor.author","Djannatian, Minou"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Kuivanen, Suvi"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Kallio, Katri"],["dc.contributor.author","Kaya, Tuğberk"],["dc.contributor.author","Anastasina, Maria"],["dc.contributor.author","Smura, Teemu"],["dc.contributor.author","Levanov, Lev"],["dc.contributor.author","Szirovicza, Leonora"],["dc.contributor.author","Tobi, Allan"],["dc.contributor.author","Kallio-Kokko, Hannimari"],["dc.contributor.author","Österlund, Pamela"],["dc.contributor.author","Joensuu, Merja"],["dc.contributor.author","Meunier, Frédéric A."],["dc.contributor.author","Butcher, Sarah J."],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Helenius, Ari"],["dc.contributor.author","Gokce, Ozgun"],["dc.contributor.author","Teesalu, Tambet"],["dc.contributor.author","Hepojoki, Jussi"],["dc.contributor.author","Vapalahti, Olli"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Balistreri, Giuseppe"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2021-04-14T08:31:26Z"],["dc.date.available","2021-04-14T08:31:26Z"],["dc.date.issued","2020"],["dc.description.abstract","The causative agent of coronavirus disease 2019 (COVID-19) is the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). For many viruses, tissue tropism is determined by the availability of virus receptors and entry cofactors on the surface of host cells. In this study, we found that neuropilin-1 (NRP1), known to bind furin-cleaved substrates, significantly potentiates SARS-CoV-2 infectivity, an effect blocked by a monoclonal blocking antibody against NRP1. A SARS-CoV-2 mutant with an altered furin cleavage site did not depend on NRP1 for infectivity. Pathological analysis of olfactory epithelium obtained from human COVID-19 autopsies revealed that SARS-CoV-2 infected NRP1-positive cells facing the nasal cavity. Our data provide insight into SARS-CoV-2 cell infectivity and define a potential target for antiviral intervention."],["dc.identifier.doi","10.1126/science.abd2985"],["dc.identifier.pmid","33082293"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83594"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/73"],["dc.identifier.url","https://rdp.sfb274.de/literature/publications/8"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","TRR 274: Checkpoints of Central Nervous System Recovery"],["dc.relation","TRR 274 | A06: The role of lipid-sensing nuclear receptors as checkpoints in regulating phagocyte function during recovery from demyelinating injury"],["dc.relation.eissn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.relation.workinggroup","RG Stadelmann-Nessler"],["dc.relation.workinggroup","RG Cantuti"],["dc.relation.workinggroup","RG Gokce (Systems Neuroscience – Cell Diversity)"],["dc.relation.workinggroup","RG Simons (The Biology of Glia in Development and Disease)"],["dc.rights","CC BY 4.0"],["dc.title","Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6940"],["dc.bibliographiccitation.issue","27"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","6945"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Töpperwien, Mareike"],["dc.contributor.author","Meer, Franziska van der"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","Salditt, Tim"],["dc.date.accessioned","2020-03-11T09:06:18Z"],["dc.date.available","2020-03-11T09:06:18Z"],["dc.date.issued","2018"],["dc.description.abstract","To quantitatively evaluate brain tissue and its corresponding function, knowledge of the 3D cellular distribution is essential. The gold standard to obtain this information is histology, a destructive and labor-intensive technique where the specimen is sliced and examined under a light microscope, providing 3D information at nonisotropic resolution. To overcome the limitations of conventional histology, we use phase-contrast X-ray tomography with optimized optics, reconstruction, and image analysis, both at a dedicated synchrotron radiation endstation, which we have equipped with X-ray waveguide optics for coherence and wavefront filtering, and at a compact laboratory source. As a proof-of-concept demonstration we probe the 3D cytoarchitecture in millimeter-sized punches of unstained human cerebellum embedded in paraffin and show that isotropic subcellular resolution can be reached at both setups throughout the specimen. To enable a quantitative analysis of the reconstructed data, we demonstrate automatic cell segmentation and localization of over 1 million neurons within the cerebellar cortex. This allows for the analysis of the spatial organization and correlation of cells in all dimensions by borrowing concepts from condensed-matter physics, indicating a strong short-range order and local clustering of the cells in the granular layer. By quantification of 3D neuronal \"packing,\" we can hence shed light on how the human cerebellum accommodates 80% of the total neurons in the brain in only 10% of its volume. In addition, we show that the distribution of neighboring neurons in the granular layer is anisotropic with respect to the Purkinje cell dendrites."],["dc.identifier.doi","10.1073/pnas.1801678115"],["dc.identifier.pmid","29915047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/63291"],["dc.language.iso","en"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.relation.orgunit","Institut für Röntgenphysik"],["dc.relation.workinggroup","RG Salditt (Structure of Biomolecular Assemblies and X-Ray Physics)"],["dc.rights","CC BY-NC-ND 4.0"],["dc.subject.gro","x-ray imaging"],["dc.subject.gro","biomedical tomography"],["dc.title","Three-dimensional virtual histology of human cerebellum by X-ray phase-contrast tomography"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","19057"],["dc.bibliographiccitation.issue","50"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","19062"],["dc.bibliographiccitation.volume","103"],["dc.contributor.author","Zhou, D."],["dc.contributor.author","Srivastava, Rajneesh"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Grummel, Verena"],["dc.contributor.author","Sommer, Norbert"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hemmer, Bernhard"],["dc.date.accessioned","2018-11-07T08:51:00Z"],["dc.date.available","2018-11-07T08:51:00Z"],["dc.date.issued","2006"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Although the cause of MS is still uncertain, many findings point toward an ongoing autoimmune response to myelin antigens. Because of its location on the outer surface of the myelin sheath and its pathogenicity in the experimental autoimmune encephalomyelitis model, myelin oligodendrocyte glycoprotein (MOG) is one of the potential disease-causing self antigens in MS. However, the role of MOG in the pathogenesis of MS has remained controversial. In this study we addressed the occurrence of autoantibodies to native MOG and its implication for demyelination and axonal loss in MS. We applied a high-sensitivity bioassay, which allowed detecting autoantibodies that bind to the extracellular part of native MOG. Antibodies, mostly IgG, were found in sera that bound with high affinity to strictly conformational epitopes of the extracellular domain of MOG. IgG but not IgM antibody titers to native MOG were significantly higher in MS patients compared with different control groups with the highest prevalence in primary progressive MS patients. Serum autoantibodies to native MOG induced death of MOG-expressing target cells in vitro. Serum from MS patients with high anti-MOG antibody titers stained white matter myelin in rat brain and enhanced demyelination and axonal damage when transferred to autoimmune encephalomyelitis animals. Overall these findings suggest a pathogenic antibody response to native MOG in a subgroup of MS patients."],["dc.identifier.doi","10.1073/pnas.0607242103"],["dc.identifier.isi","000242884200034"],["dc.identifier.pmid","17142321"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein in 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","471"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical & Experimental Metastasis"],["dc.bibliographiccitation.lastpage","482"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Rietkoetter, Eva"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Kramer, Franz-Josef"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Stadelmann, Chr."],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T09:26:31Z"],["dc.date.available","2018-11-07T09:26:31Z"],["dc.date.issued","2013"],["dc.description.abstract","An essential function of the transcription factors LEF1/TCF4 in cerebral metastases of lung adenocarcinomas has been described in mouse models, suggesting a WNT/beta-catenin effect as potential mechanism. Their role in humans is still unclear, thus we analyzed LEF1, TCF4, beta-catenin, and early stage prognostic markers in 25 adenocarcinoma brain metastases using immunohistochemistry (IHC). IHC revealed nuclear TCF4 in all adenocarcinoma samples, whereas only 36 % depicted nuclear LEF1 and nuclear beta-catenin signals. Samples with nuclear LEF1 as well as high TCF4 (++++) expression were associated with a shorter survival (p = 0.01, HR = 6.68), while nuclear beta-catenin had no significant impact on prognosis and did not significantly correlate with nuclear LEF1. High proliferation index Ki67 was associated with shorter survival in late-stage disease (p = 0.03, HR 3.27). Additionally, we generated a LEF1/TCF4 as well as an AXIN2 signature, the latter as representative of WNT/beta-catenin activity, following a bioinformatics approach with a gene expression dataset of cerebral metastases in lung adenocarcinoma. To analyze the prognostic relevance in primary lung adenocarcinomas, we applied both signatures to a microarray dataset of 58 primary lung adenocarcinomas. Only the LEF1/TCF4 signature was able to separate clusters with impact on survival (p = 0.01, HR = 0.32). These clusters displayed diverging enrichment patterns of the cell cycle pathway. In conclusion, our data show that LEF1/TCF4, but not beta-catenin, have prognostic relevance in primary and cerebrally metastasized human lung adenocarcinomas. In contrast to the previous in vivo findings, these results indicate that LEF1/TCF4 act independently of beta-catenin in this setting."],["dc.identifier.doi","10.1007/s10585-012-9552-7"],["dc.identifier.isi","000317297400011"],["dc.identifier.pmid","23224985"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30319"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1573-7276"],["dc.relation.issn","0262-0898"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Nuclear LEF1/TCF4 correlate with poor prognosis but not with nuclear beta-catenin in cerebral metastasis of lung adenocarcinomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]