Figure 3 Within-group comparisons (before–after)‏

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Figure Pedigrees of the SCA42 families identified in this study

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Figure 2 ERG amplitude reduction in the follow-up study

Figure 2 Sanger sequencing, conservation, and summary of known ACO2 mutations Sanger sequencing, conservation, and summary of known ACO2 mutations (A)

Figure 1 Summary of prior diagnostic workup in neuromuscular disorder cases Summary of prior diagnostic workup in neuromuscular disorder cases Percentage.

Figure 3 Pedigree of familial idiopathic transverse myelitis

Figure 1 Box plot of the venous diameter in lesions

Figure 2 Needle biopsy of the left vastus lateralis

Figure 1 Stiff-person syndrome spectrum patient serum bound to membranes of live GlyRα1-transfected HEK293 cells Stiff-person syndrome spectrum patient.

Figure 4 Correlation of age with [11C](R)-PK11195 binding in the normal-appearing white matter (NAWM) and thalami Correlation of age with [11C](R)-PK11195.

Figure 1 Hierarchical clustering (HCL) outcome of all tested samples with the expression profile of the case report set as unknown Hierarchical clustering.

Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production

Figure 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.

Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.

Figure 1 Comparison of miR-150-5p (log scale), prednisone dose (mg), and QMG score between the thymectomy (ETTX) and prednisone groups Comparison of miR-150-5p.

Figure 4 Mitochondrial respiration is affected in lymphoblastoid cell lines (LCLs) of ACO2 mutation carriers Mitochondrial respiration is affected in lymphoblastoid.

Figure Pedigree of the family

Figure 4 Abundance of cytokines which showed significant difference in expression in the plasma and the cultured PBMC of patients with RRMS Abundance of.

Figure 2 Luciferase assays of transiently transfected HEK 293 cells with reporter constructs containing the 766-bp wild-type KCNJ18 or c.-542 T/A mutant.

Figure 3 Gene expression in CSF cell pellets

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

Figure 1 Dominant and recessive missense and nonsense variants in neurofilament light (NEFL)‏ Dominant and recessive missense and nonsense variants in.

Figure 3 Temporal trends in FALS incidence

Table 4 Associations in SNP array data between the Braak stage and previously known AD risk loci (341 variants) comparing participants with Braak stage.

Figure 1 All patients with pediatric genetic movement disorders, their genetic diagnoses, and type of genetic investigations All patients with pediatric.

Figure 5 Neurite structure is not disrupted by the lack of neurofilament light (NEFL)‏ Neurite structure is not disrupted by the lack of neurofilament.

Figure 2 Linkage analysis of chromosome 19

Figure 1 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.

Figure 3 Mutation carrier–derived lymphoblastoid cell lines (LCLs) show decreased aconitase 2 activity and mitochondrial respiration deficiency compared.

Figure Family tree with the HLA haplotyping of 6 members of the family

Figure 4 Relative abundances of the order Clostridiales and its family members are differentially changed by therapy Relative abundances of the order Clostridiales.

Figure 3 Analysis of the prognostic value of IL-10–producing B cells or IL-6/IL-10–B-cell ratio measurements in patients with RIS/CIS MS Analysis of the.

Figure Comparison between minutes of MVPA/day and nDGv in patients with MS (green) or monoADS (blue)‏ Comparison between minutes of MVPA/day and nDGv in.

Figure 2 Functionally significant genes

Table 2 Rs number, gene, OR, 95% CI, and permutation p value for the statistical significant variants resulted from allelic association analysis association.

Figure 1 Family pedigree and DNA sequencing results

Figure 4 Voltage-clamp recordings of KCNJ18 carrying the patient's SNVs expressed in Xenopus laevis oocytes under control conditions and after application.

Figure 1 [18F]florbetapir standardized uptake value ratio analytical method [18F]florbetapir standardized uptake value ratio analytical method Flowchart.

Figure Alluvial plot of modified Rankin Scale (mRS) scores during and at the end of hospital stay Alluvial plot of modified Rankin Scale (mRS) scores during.

Figure 3 Voltage-clamp recording of the wild-type KCNJ18 (left) and the KCNJ18 carrying the patient's SNVs (right) expressed in Xenopus laevis oocytes.

Figure 1 Phenotype and functional properties of B cells in MS and HCs at baseline Phenotype and functional properties of B cells in MS and HCs at baseline.

Figure 1 Flowchart of patient inclusion

Figure 1 Histamine flare in patients and controls

Figure 1 Considerations for concussed athletes leading to medical care or return to sport (RTS)‏ Considerations for concussed athletes leading to medical.

Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.

Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial.

Figure 2 Kaplan-Meier survival graphs for 10-year risks of overall and post-90-day recurrent ischemic stroke (IS) and death Kaplan-Meier survival graphs.

Figure 1 Annualized percentage brain volume change

Figure 2 BVL according to on-study disability worsening

Figure 2 Repopulation of CD19+ cells in low and high BSA patients and calculation of the BSA Repopulation of CD19+ cells in low and high BSA patients and.

Figure 2 Frequency of the proportion of total WMLs with central veins in PPMS, RRMS, and SVD Frequency of the proportion of total WMLs with central veins.

Figure 2 Natalizumab increases expression of proinflammatory genes and cytokines by CD49d+ memory CD4 cells Natalizumab increases expression of proinflammatory.

Figure 4 CHCHD2 but not TOP1MT expression rescues molecular defects

Figure 3 DMF promotes an anti-inflammatory cytokine B-cell profile

Figure 1 bvFTD PINBPA network

Figure 2 Seizure outcomes

Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521

Ingo Kleiter et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e504

Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453

Figure 2 Pedigrees of families and segregation analysis of variants c

Figure 3 C5B3 blocked MAC formation

Figure 2 LMNB1 mRNA expression

Figure 1 ASO functions ASO functions Target mRNA fates depending on ASO mechanism of action that is determined by where the ASO is targeted and by ASO.

Figure 3 Changing appearance of the frontal cortex with age associated with increasing myelination Changing appearance of the frontal cortex with age associated.

Figure 2 Between-group comparisons

Figure 2 Time from incident ADS event to MS diagnosis

Figure 2 Nonhuman primate brain immunohistochemistry

Figure 4 Venn diagram for B-cell Sup proteins compared with proteins from exosome-enriched fractions from a human B-cell line Venn diagram for B-cell Sup.

Figure 3 A receiver operating characteristic curve of days to IVMP as a predictor of failure to regain 0.2 logMAR (20/30) vision (AUC 0.84, p < 0.001)‏

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.

Figure 4 Western blotting

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Figure 3 Within-group comparisons (before–after)‏ Within-group comparisons (before–after) Effects of vitamin D3 on serum levels of proinflammatory and anti-inflammatory markers (n = 25 per group) (A–C) and the ratio of pro-to anti-inflammatory cytokines (D and E). IL-6, IL-17A, and IL-10 mRNA expression levels of healthy participants, patients with MS, and first-degree relatives. Paired t test analysis was used. Data were expressed as mean ± SD. *p < 0.05 was regarded as statistically significant. Reza Hashemi et al. Neurol Genet 2018;4:e278 Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.