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dc.contributor.authorBirisik, Omer
dc.contributor.authorIcoz, Sema
dc.contributor.authorAkman-Demir, Gulsen
dc.contributor.authorEraksoy, Mefkure
dc.contributor.authorTuzun, Erdem
dc.contributor.authorKurtuncu, Murat
dc.contributor.authorTURKOGLU, Recai
dc.contributor.authorPehlivan, Munevver
dc.date.accessioned2021-03-06T08:33:39Z
dc.date.available2021-03-06T08:33:39Z
dc.identifier.citationTuzun E., Kurtuncu M., TURKOGLU R., Icoz S., Pehlivan M., Birisik O., Eraksoy M., Akman-Demir G., "Enhanced complement consumption in neuromyelitis optica and Behcet's disease patients", JOURNAL OF NEUROIMMUNOLOGY, cilt.233, ss.211-215, 2011
dc.identifier.issn0165-5728
dc.identifier.othervv_1032021
dc.identifier.otherav_e18c419c-fe1d-48a4-b1d4-cb7dcd62157d
dc.identifier.urihttp://hdl.handle.net/20.500.12627/148482
dc.identifier.urihttps://doi.org/10.1016/j.jneuroim.2010.11.010
dc.description.abstractThe complement system is essential in the pathogenesis of inflammatory central nervous system disorders. To investigate the involvement of complement pathways in neuromyelitis optica (NMO), levels of breakdown products for classical (C4d), alternative (FBb) and common (sC5b-9) pathways were measured in the sera of 28 NMO and control patients (30 Behcet's disease (BD), 29 multiple sclerosis (MS)) and 31 healthy controls by ELISA. Classical and/or alternative pathway consumption was enhanced in NMO and BD patients as compared to MS patients and healthy controls. Our results suggest that NBD and NMO differ from MS by the predominance of complement system involvement. (C) 2010 Elsevier B.V. All rights reserved.
dc.language.isoeng
dc.subjectSinirbilim ve Davranış
dc.subjectYaşam Bilimleri
dc.subjectTemel Bilimler
dc.subjectNEUROSCIENCES
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectİmmünoloji
dc.titleEnhanced complement consumption in neuromyelitis optica and Behcet's disease patients
dc.typeMakale
dc.relation.journalJOURNAL OF NEUROIMMUNOLOGY
dc.contributor.departmentAcıbadem Mehmet Ali Aydınlar Üniversitesi , ,
dc.identifier.volume233
dc.identifier.startpage211
dc.identifier.endpage215
dc.contributor.firstauthorID2043


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