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Metz, Imke
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Metz, Imke
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Metz, Imke
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Metz, I.
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2009Conference Paper [["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","91"],["dc.bibliographiccitation.volume","286"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Goldschmidt, Thomas"],["dc.contributor.author","Antel, Jack P."],["dc.contributor.author","Wegner, C."],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:22:05Z"],["dc.date.available","2018-11-07T11:22:05Z"],["dc.date.issued","2009"],["dc.description.abstract","Multiple sclerosis (MS) lesions are histopathologically characterized by inflammation, demyelination/remyelination, axonal damage and gliosis. Animal experimental and in vitro studies suggest that sex hormones influence the immune system and contribute to the increased likelihood in women of developing MS. However, a variety of studies have also shown that remyelination is more marked in female rodents or that female sex hormones are beneficial for myelin repair. To determine whether gender influences the histopathology of MS lesions, we compared the extent of inflammation, axonal damage and remyelination in MS lesions of female and male MS patients. We observed no differences in the composition of inflammatory infiltrates, axonal damage or cortical pathology. Similar numbers of oligodendroglial progenitor cells and mature oligodendrocytes were present in MS lesions. Remyelination is slightly, but not significantly, more extensive in women than men in early MS lesions. The absence of significant differences in lesion pathology between female and male MS patients might be explained by a lack of a gender influence, but also might be due to the limited number of tissue samples available for histopathological analysis. (C) 2009 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2009.07.014"],["dc.identifier.isi","000271621800020"],["dc.identifier.pmid","19674757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55923"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","14th European-Charcot-Foundation Symposium"],["dc.relation.eventlocation","Taormina, ITALY"],["dc.relation.issn","0022-510X"],["dc.title","Gender differences in the histopathology of MS?"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2010Journal Article [["dc.bibliographiccitation.firstpage","976"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","985"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Dziedzic, Tomasz"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Mueller, Sven"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:39:34Z"],["dc.date.available","2018-11-07T08:39:34Z"],["dc.date.issued","2010"],["dc.description.abstract","Axonal loss is a major component of the pathology of multiple sclerosis (MS) and the morphological basis of permanent clinical disability. It occurs in demyelinating plaques but also in the so-called normal-appearing white matter (NAWM). However, the contribution of Wallerian degeneration to axonal pathology is not known. Here, we analyzed the extent of Wallerian degeneration and axonal pathology in periplaque white matter (PPWM) and lesions in early multiple sclerosis biopsy tissue from 63 MS patients. Wallerian degeneration was visualized using an antibody against the neuropeptide Y receptor Y1 (NPY-Y1R). The number of SMI-32-positive axons with non-phosphorylated neurofilaments was significantly higher in both PPWM and plaques compared to control white matter. APP-positive, acutely damaged axons were found in significantly higher numbers in plaques compared to PPWM. Strikingly, the number of NPY-Y1R-positive axons undergoing Wallerian degeneration was significantly higher in PPWM and plaques than in control WM. NPY-Y1R-positive axons in PPWM were strongly correlated to those in the lesions. Our results show that Wallerian degeneration is a major component of axonal pathology in the periplaque white matter in early MS. It may contribute to radiological changes observed in early MS and most likely plays a major role in the development of disability."],["dc.identifier.doi","10.1111/j.1750-3639.2010.00401.x"],["dc.identifier.isi","000280629400010"],["dc.identifier.pmid","20477831"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19027"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1015-6305"],["dc.title","Wallerian Degeneration: A Major Component of Early Axonal Pathology in Multiple Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2006Conference Abstract [["dc.bibliographiccitation.firstpage","S225"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.lastpage","S226"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Kieseier, Bernd C."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Hartung, H.-P."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:22:40Z"],["dc.date.available","2018-11-07T09:22:40Z"],["dc.date.issued","2006"],["dc.identifier.isi","000241921400741"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29402"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","22nd Congress of the European-Committee-for-the-Treatment-and-Resarch-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","1352-4585"],["dc.title","Persistence of immunopathological and radiological homogeneity in a patient with relapsing-remitting multiple sclerosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2007Conference Abstract [["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Fischer, Ingo"],["dc.contributor.author","Guenther, A."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T10:58:41Z"],["dc.date.available","2018-11-07T10:58:41Z"],["dc.date.issued","2007"],["dc.format.extent","316"],["dc.identifier.isi","000249149200047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50520"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","Joint Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy (DGNN)/Polish-Associatin-of-Neuropathologists"],["dc.relation.eventlocation","Greifswald, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Macrophage activation patterns in active multiple sclerosis lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2008Review [["dc.bibliographiccitation.firstpage","1759"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1775"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Gavrilova, R. H."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Scheithauer, Bernd W."],["dc.contributor.author","Weigand, S."],["dc.contributor.author","Thomsen, K."],["dc.contributor.author","Mandrekar, Jay"],["dc.contributor.author","Altintas, A."],["dc.contributor.author","Erickson, Bradley J."],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Giannini, Caterina"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Linbo, L."],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:13:15Z"],["dc.date.available","2018-11-07T11:13:15Z"],["dc.date.issued","2008"],["dc.description.abstract","Atypical imaging features of multiple sclerosis lesions include size > 2 cm, mass effect, oedema and/or ring enhancement. This constellation is often referred to as 'tumefactive multiple sclerosis'. Previous series emphasize their unifocal and clinically isolated nature, however, evolution of these lesions is not well defined. Biopsy may be required for diagnosis. We describe clinical and radiographic features in 168 patients with biopsy confirmed CNS inflammatory demyelinating disease (IDD). Lesions were analysed on pre- and post-biopsy magnetic resonance imaging (MRI) for location, size, mass effect/oedema, enhancement, multifocality and fulfilment of Barkhof criteria. Clinical data were correlated to MRI. Female to male ratio was 1.2 : 1, median age at onset, 37 years, duration between symptom onset and biopsy, 7.1 weeks and total disease duration, 3.9 years. Clinical course prior to biopsy was a first neurological event in 61%, relapsing-remitting in 29% and progressive in 4%. Presentations were typically polysymptomatic, with motor, cognitive and sensory symptoms predominating. Aphasia, agnosia, seizures and visual field defects were observed. At follow-up, 70% developed definite multiple sclerosis, and 14% had an isolated demyelinating syndrome. Median time to second attack was 4.8 years, and median EDSS at follow-up was 3.0. Multiple lesions were present in 70% on pre- biopsy MRI, and in 83% by last MRI, with Barkhof criteria fulfilled in 46% prior to biopsy and 55% by follow-up. Only 17% of cases remained unifocal. Median largest lesion size on T2-weighted images was 4 cm ( range 0.5-12), with a discernible size of 2.1cm( range 0.5-7.5). Biopsied lesions demonstrated mass effect in 45% and oedema in 77%. A strong association was found between lesion size, and presence of mass effect and/or oedema (P < 0.001). Ring enhancement was frequent. Most tumefactive features did not correlate with gender, course or diagnosis. Although lesion size > 5 cm was associated with a slightly higher EDSS at last follow-up, long-term prognosis in patients with disease duration > 10 years was better ( EDSS 1.5) compared with a population-based multiple sclerosis cohort matched for disease duration ( EDSS 3.5; P < 0.001). Given the retrospective nature of the study, the precise reason for biopsy could not always be determined. This study underscores the diagnostically challenging nature of CNS IDDs that present with atypical clinical or radiographic features. Most have multifocal disease at onset, and develop RRMS by follow-up. Although increased awareness of this broad spectrum may obviate need for biopsy in many circumstances, an important role for diagnostic brain biopsy may be required in some cases."],["dc.description.sponsorship","NCRR NIH HHS [UL 1 RR24150-01]; NINDS NIH HHS [R01 NS049577, NS049577]"],["dc.identifier.doi","10.1093/brain/awn098"],["dc.identifier.isi","000257397100010"],["dc.identifier.pmid","18535080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53846"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical and radiographic spectrum of pathologically confirmed tumefactive multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Journal Article [["dc.bibliographiccitation.firstpage","1541"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","1549"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Wildemann, Brigitte"],["dc.date.accessioned","2018-11-07T10:07:21Z"],["dc.date.available","2018-11-07T10:07:21Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Histopathological studies have revealed four different immunopathological patterns of lesion pathology in early multiple sclerosis (MS). Pattern II MS is characterised by immunoglobulin and complement deposition in addition to T-cell and macrophage infiltration and is more likely to respond to plasma exchange therapy, suggesting a contribution of autoantibodies. Objective: To assess the frequency of anti-myelin oligodendrocyte glycoprotein (MOG), anti-M1-aquaporin-4 (AQP4), anti-M23-AQP4, anti-N-methyl-d-aspartate-type glutamate receptors (NMDAR) and 25 other anti-neural antibodies in pattern II MS. Methods: Thirty-nine serum samples from patients with MS who had undergone brain biopsy (n = 24; including 13 from patients with pattern II MS) and from histopathologically non-classified MS patients (n = 15) were tested for anti-MOG, anti-M1-AQP4, anti-M23-AQP4, anti-NMDAR, anti-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-type glutamate receptors (AMPAR), anti-gamma-aminobutyric acid receptors (GABABR), anti-leucine-rich, glioma-activated protein 1 (LGI1), anti-contactin-associated protein 2 (CASPR2), anti-dipeptidyl-peptidase-like protein-6 (DPPX), anti-Tr/Delta/notch-like epidermal growth factor-related receptor (DNER), anti-Hu, anti-Yo, anti-Ri, anti-Ma1/Ma2, anti-CV2/collapsin response mediator protein 5 (CRMP5), anti-glutamic acid decarboxylase (GAD), anti-amphiphysin, anti-Ca/RhoGTPase-activating protein 26 (ARHGAP26), anti-Sj/inositol-1,4,5-trisphosphate receptor 1 (ITPR1), anti-Homer3, anti-carbonic anhydrase-related protein (CARPVIII), antiprotein kinase gamma (PKCgamma), anti-glutamate receptor delta 2 (GluRdelta2), anti-metabotropic glutamate receptor 1 (mGluR1) and anti-mGluR5, as well as for anti-glial nuclei antibodies (AGNA) and Purkinje cell antibody 2 (PCA2). Results: Antibodies to MOG belonging to the complement-activating immunoglobulin G1 (IgG1) subclass were detected in a patient with pattern II MS. Detailed brain biopsy findings are shown. Conclusion: This is the largest study on established anti-neural antibodies performed in MS so far. MOG-IgG may play a role in a small percentage of patients diagnosed with pattern II MS."],["dc.identifier.doi","10.1177/1352458515622986"],["dc.identifier.isi","000390575300013"],["dc.identifier.pmid","26869529"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39258"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Screening for MOG-IgG and 27 other anti-glial and anti-neuronal autoantibodies in 'pattern II multiple sclerosis' and brain biopsy findings in a MOG-IgG-positive case"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2008Conference Abstract [["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:11:46Z"],["dc.date.available","2018-11-07T11:11:46Z"],["dc.date.issued","2008"],["dc.format.extent","S273"],["dc.identifier.isi","000259675700901"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53506"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","13th Annual Meeting of the Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/24th Congress of the European-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis/5th Congress of the Latin-Amer-Comm-for-Treatment-and-Res-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Montreal, CANADA"],["dc.relation.issn","1352-4585"],["dc.title","T cell- and macrophage-associated pathology correlates with response to corticosteroids"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2009Conference Abstract [["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Loescher, A."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Mueller, S."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:24:24Z"],["dc.date.available","2018-11-07T11:24:24Z"],["dc.date.issued","2009"],["dc.format.extent","447"],["dc.identifier.isi","000268421800064"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56398"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","54th Annual Meeting of the German-Society-of-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Astroglia Pathology in Early Multiple Sclerosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2009Conference Abstract [["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.volume","256"],["dc.contributor.author","Dziedzic, Tomasz"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Mueller, S."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T08:29:27Z"],["dc.date.available","2018-11-07T08:29:27Z"],["dc.date.issued","2009"],["dc.format.extent","S36"],["dc.identifier.isi","000268248700095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16655"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.publisher.place","Heidelberg"],["dc.relation.conference","19th Meeting of the European-Neurological-Society"],["dc.relation.eventlocation","Milan, ITALY"],["dc.relation.issn","0340-5354"],["dc.title","Wallerian degeneration contributes to axonal damage in plaques and periplaque white matter in patients with multiple sclerosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2008Journal Article [["dc.bibliographiccitation.firstpage","1527"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","ARCHIVES OF NEUROLOGY"],["dc.bibliographiccitation.lastpage","1532"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Nessler, Stefan"],["dc.contributor.author","Zhou, D."],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Kieseier, Bernd C."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:09:15Z"],["dc.date.available","2018-11-07T11:09:15Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Multiple sclerosis (MS) is a heterogeneous autoimmune disease of the central nervous system. The identification of 4 different immunopathological subtypes of MS raises the question of whether these subtypes represent different patient subgroups that can be distinguished according to their leading mechanism of myelin destruction or whether this is a stage-dependent process in the development of lesions in a given patient. Objective: To document intraindividual immunopathological and radiological homogeneity of 2 different lesions in a single patient with relapsing-remitting MS over time. Design: Case report. Setting: A neuropathological referral center for inflammatory demyelinating diseases of the central nervous system. Patient: A 49-year-old woman with clinically definite relapsing-remitting MS. Main Outcome Measures: Radiological and immunopathological analysis of MS lesions. Results: Identical pathological findings in 2 different MS lesions separated by more than 2 years were identified. These lesions displayed similar and distinct radiological features on cranial imaging. Conclusions: In this patient we were able to show the same antibody/complement-mediated lesion pathological findings with compatible identical ring enhancement on T1-weighted magnetic resonance images and hypointense rims on T2-weighted images after an interval of 26 months. Our observations support the concept of intraindividual homogeneity of a given immunopathological MS subtype."],["dc.identifier.doi","10.1001/archneur.65.11.1527"],["dc.identifier.isi","000260797200018"],["dc.identifier.pmid","19001173"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52968"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","Persistence of Immunopathological and Radiological Traits in Multiple Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS