Figure 2 Between-group comparisons

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Figure Pedigrees of the SCA42 families identified in this study

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Figure EDSS, FS scores, and Modified MSFC scores

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 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 1 Linear relationship between CSF inflammation and glucose in meningitis; analysis stratified by diagnostic category (aseptic, n = 115 and microbial,

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 3 sVEGF concentrations in anemia and hypoxemic diseases

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

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 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 Correlation between the Kurtzke Expanded Disability Status Scale and the relative expression of hsa-miR-337-3p Correlation between the Kurtzke Expanded.

Figure 1 Histamine flare in patients and controls

Figure 2 Changes in fatigue under treatment

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 3 Genotype-phenotype correlation in SPG7 mutations and age at onset of symptoms Genotype-phenotype correlation in SPG7 mutations and age at onset.

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

Figure 1 (A–D) Nuclear factor (erythroid-derived 2)-like 2–related transcripts are increased 6 weeks after treatment in responders but not in nonresponders.

Figure 1 bvFTD PINBPA network

Figure 2 Seizure outcomes

Figure 2 Overview of apheresis therapies

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 Lysosome dysfunction observed in patient-derived fibroblasts with the TMEM106B p.Asp252Asn substitution Lysosome dysfunction observed in patient-derived.

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 Within-group comparisons (before–after)‏

Figure 5 C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo C5B3 inhibited inflammatory infiltration in an NMOSD mouse model in vivo.

Figure 1 Toxic factors are enriched in Ex-En fractions prepared from MS B-cell Sup by water exclusion precipitation Toxic factors are enriched in Ex-En.

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 Prevalence for MS cumulated over 10 years in the United States per 100,000 population by age and sex 2010 Prevalence for MS cumulated over.

Figure 2 Toxic factors are enriched in exosome-enriched fractions prepared from MS B-cell Sup by ultracentrifugation Toxic factors are enriched in exosome-enriched.

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

Figure 1 Glutamine antagonist JHU083 inhibits T-cell proliferation in vitro Glutamine antagonist JHU083 inhibits T-cell proliferation in vitro T-cell proliferation.

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Figure 2 Between-group comparisons Between-group comparisons Effects of vitamin D3 supplementation on serum levels of proinflammatory and anti-inflammatory markers (n = 25 per group). (A–F) IL-6, IL-17A, and IL-10 mRNA expression levels of healthy controls (HCs), multiple sclerosis participants (MSPs), and first-degree relative participants (FDRPs). HPs (A), MSPs (B), and FDRPs (C). One-way analysis of variance, followed by the post hoc Tukey test, was used. Data were expressed as mean ± SD, and 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.