Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.

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Teaching NeuroImages Neurology Resident and Fellow Section © 2013 American Academy of Neurology A 51-year-old woman with triplegia and blindness.

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Date of download: 6/30/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Quantification and Functional Characterization of.

Harry Irving, Hung Jiew Lee, John Parratt

Copyright © 2010 American Medical Association. All rights reserved.

Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein MRI features of patients with MS who had antibodies.

Volume 18, Issue 1, Pages (February 2011)

Figure Model contrasting the potential role of antibodies to myelin oligodendrocyte glycoprotein (MOG) or aquaporin-4 (AQP4) in opticospinal inflammationMOG-specific.

Figure 3 Brain MRI findings in patients with MOG-Ab Extensive brain lesions with large diameter (A and B), posterior reversible encephalopathy–like lesions.

Figure 4 Neuromyelitis optica spectrum disorder brain lesions

Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.

Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.

Figure 1 Percent positivity by clinical feature Overall, 6

Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum.

Figure 3 JCV index changes in JCV+ patients

Figure 3 Multifocal visual-evoked potentials in optic neuritis Figure shows the visual-evoked potentials (VEPs) in 52 sectors of the retina. Multifocal.

Figure 2 NMDAR-Ab levels, clinical syndromes, and therapy in 8 informative patients with white matter syndromes in association with NMDAR-Ab NMDAR-Ab levels,

Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.

Figure 1 Neuromyelitis optica spectrum disorder (NMOSD) subgroups and patients with relapsing-remitting multiple sclerosis (RRMS) show different antibody.

Figure 1 Biomarkers associated with different clinical phases in MS

Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.

Figure 2 Elevated antibody reactivities against myelin and Epstein-Barr virus (EBV) peptides in relapsing-remitting multiple sclerosis (RRMS) and higher.

Figure 2 APCs from laquinimod-treated mice inhibit differentiation of Tfh cells APCs from laquinimod-treated mice inhibit differentiation of Tfh cells.

Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure 1 8-Iso-PGF2α levels in CSF of patients with MS and controlsCSF 8-iso-prostaglandin F2α (8-iso-PGF2α) levels were estimated using an ELISA. (A)

Figure 2. ROC curves for different group comparisons

Figure 4 Neuropathology of MOG and AQP4 antibody–associated demyelinating lesions in the brain The biopsy specimen revealed a small actively demyelinating.

Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.

Figure 2 Concordance of results for commercial cell-based assay (CBA) and fluorescence-activated cell sorting (FACS) assays, FACS titers, and disease activity.

Figure 2 JCV index JCV index (A) Fifty samples of natalizumab-treated patients with multiple sclerosis were assessed twice for their anti-JCV antibody.

Figure 2 Representative brain MRIs from patients with neuromyelitis optica Lesions are localized at sites of high aquaporin-4 expression (white dots).

Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.

Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,

Figure 4 Aquaporin-4 immunoglobulin G (AQP4-IgG) index in time-matched paired serum-CSF specimens: 3 attack/preattack pairs and 7 bridge/remission pairs.

Figure 1 JCV serostatus JCV serostatus (A) Serostatus of 1,921 natalizumab-treated patients with multiple sclerosis, with JCV− patients shown in black.

Figure 5 Pairwise correlations between selected patient-reported outcomes and performance tests in patients with MS (A) The number of pairwise correlations.

Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.

Figure Clinical and radiologic course(A) The T2 contrast-enhanced sequence on day 3 shows an extensive central cord lesion extending from C2 to T7. Clinical.

Figure 1 Kaplan-Meier estimation of time to neuromyelitis optica (NMO) conversion and development of motor disability Kaplan-Meier estimation of time to.

Figure 1. Antibodies to MOG in a proportion of adult patients with MS

Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases Distribution of MOG IgG antibody in pediatric demyelinating diseases (A)

Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.

Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.

Figure 1 Anti-Epstein-Barr virus nuclear antigen-1 IgG quartile antibody status differences in MRI measures Anti-Epstein-Barr virus nuclear antigen-1 IgG.

Figure 1 Patterns of study retention The proportion of individuals actively participating in the study is displayed over the course of the study. Patterns.

Figure 3 Pedigrees of 3 multiplex families with NLRP3 mutations and MS The patient numbers refer to the patients listed in table 1. Pedigrees of 3 multiplex.

Figure Overview of patients with demyelinating diseases, presence of clinical symptoms frequently associated with NMDAR encephalitis, and antibody status.

Figure 2 Summary of the utility of MOG-Abs and OCB testing in predicting pediatric disease course at onset compared to clinical follow-up at 1 yearFollowing.

Figure 1 Representative spinal cord MRIs from patients with neuromyelitis optica Longitudinally extensive transverse myelitis of the cervical (A) and cervicothoracic.

Figure 2 Correlation between wGRS and age at onset The figure shows the correlation between weighted genetic risk score (wGRS) and age at onset in all.

Figure 2. Detection of KIR4.1 autoantibodies using LIPS

Figure 1 Full-length MOG cell-based assay using a serum dilution of 1:160 as a cutoff for positivity (red line in both plots)(A) Myelin olidgodendrocyte.

Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.

Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.

Figure 2 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG binding to AQP4 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG.

Figure 2 Assessment of fluctuation in fatigue scores using environmental data The relationship between fatigue (as measured by the Modified Fatigue Impact.

Figure 3 Fluorescence-activated cell sorting (FACS) employing cells singly transfected with M1-AQP4 or M23-AQP4 or cotransfected with both AQP4 isoforms.

Figure 1. MBP-specific IFN-γ+ but not IL-17+ frequencies are significantly different between patients with MS and HCs MBP-specific IFN-γ+ but not IL-17+

Figure 2 Overview of apheresis therapies

Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF and.

Figure 6 Multiple target epitopes exist in the N-terminal domains of Caspr2 (A) Multidomain deletion constructs of Caspr2 were generated to determine which.

Figure 2 Cell-based assay demonstrating differential binding of AChR antibodies to the adult and fetal receptorsThe fetal (gamma subunit specific) and.

Figure 1 Cell gating and binding curve from FACS experiments and M23 and M1 antibody titers during relapses and remission Cell gating for fluorescence-activated.

Figure 3 C5B3 blocked MAC formation

Figure 2 Antibodies to MOG detected with anti-human IgG (H + L) as the secondary antibody(A) Schematic of the human MOG proteins tested. Antibodies to.

Figure 2 Time from incident ADS event to MS diagnosis

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 4 C5B3 decreased NMOSD mouse model lesions in vivo

Figure 4 Illustration of a practice effect by examining longitudinal performance measures in patients with MS and cohabitants (A) Response time for each.

Figure (A and B) Effect of canakinumab in muscle strength measured in each patient as mean bilateral GF (A) and TMS (B) during the mean study period of.

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Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis optica (NMO) service were negative for IgG1 antibodies to myelin oligodendrocyte glycoprotein (MOG); however, 23 AQP4-seronegative patients were identified as MOG-IgG1 seropositive (red). Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis optica (NMO) service were negative for IgG1 antibodies to myelin oligodendrocyte glycoprotein (MOG); however, 23 AQP4-seronegative patients were identified as MOG-IgG1 seropositive (red). Of the 58 patients with NMO, 37 (63.4%) were AQP4 seropositive, 8 (13.8%) were MOG-IgG1 seropositive, and 13 (22%) were double seronegative. (B) A second cohort from Japan was screened blinded to clinical information. None of the 49 AQP4-seropositive patients (blue) or 27 patients with multiple sclerosis (MS) were positive for MOG antibodies, but 6/25 patients with acute disseminated encephalomyelitis (ADEM), transverse myelitis (TM), optic neuritis (ON), or AQP4-seronegative NMO were MOG antibody positive (red). CBA = cell-based assay. Patrick Waters et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e89 © 2015 American Academy of Neurology