Figure Pedigree of the family

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Figure Pedigrees of the SCA42 families identified in this study

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Figure 1 Phenotype and genotype of an undiagnosed family with autosomal recessive spastic ataxia Phenotype and genotype of an undiagnosed family with autosomal.

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 Family pedigree and clinical improvement with riboflavin treatment Family pedigree and clinical improvement with riboflavin treatment (A) The proband.

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 2 Spinal cord lesions

Figure 3 Immunohistochemical analyses of positive and negative Epstein-Barr virus (EBV) control tissues using immunostaining Immunohistochemical analyses.

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

Figure Sural nerve electron microscopy

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 2 Neurochemical profiles for each neurocognitive trajectory

Figure 1 Quantitative spinal cord MRI maps and segmentations

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

Figure Association of hippocampal subfield volumes to cognition by neopterin level, volumes, and cognition adjusted for age, education, race, sex, and.

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

Figure WDR45 sequence changes in patients A and B

Figure 3 Effects of RTX on specific anti-pathogen IgGs

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 3 Transport activity of human SLC25A4 and SLC25A4 p.Lys33Gln

Figure 2 Schematic displaying the 3 described CHT mutant proteins alongside wild type molecule (Adapted from reference 2, using Microsoft Powerpoint Software)‏

Figure 3 Receiver operating characteristics for CSF glucose (n = 225) and serum/CSF glucose ratio (n = 156) as predictors for microbial meningitis Receiver.

Figure 1 Characteristics of the German National MS Cohort

Figure 2 Linkage analysis of chromosome 19

Figure 3 Clinical outcome of apheresis therapies for NMOSD attacks

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 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 1 Family pedigree and MRI

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 1 Responder rates of patients at 4 weeks compared with prevaccinated levels Responder rates of patients at 4 weeks compared with prevaccinated levels.

Figure 6 Cellular composition after tissue dissociation

Figure 1 Pedigree and genetic findings

Figure 1 Histamine flare in patients and controls

Figure 2 Changes in fatigue under treatment

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 1 Family pedigrees, clinical photographs, and multispecies alignment showing the effect of the 3 reported mutations Family pedigrees, clinical photographs,

Figure 1 Annualized percentage brain volume change

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 Pathogenic deletions upstream of LMNB1

Figure 4 CHCHD2 but not TOP1MT expression rescues molecular defects

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 Unique second neurofibromatosis type 1 (NF1) gene mutations in multiple café-au-lait macules (CALMs) from an individual with segmental NF1 Unique.

Figure 3 Within-group comparisons (before–after)‏

Figure Pedigree, neuroimaging, and gene analysis

Figure 2 Time from incident ADS event to MS diagnosis

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.

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Figure Pedigree of the family Pedigree of the family “−” indicates the presence of VPS13A p.(Thr186_Leu232del). “+” indicates no deletion. Individuals without genotypes shown were not available for analysis. Black shapes indicate individuals affected with the primary disorder, and gray shapes indicate individuals affected with the second, separate phenotype. Individual V:7 died at the age of 10 years before the typical age at onset; thus, the affection status could not be determined. Numbers inside circles indicate more than 1 individual in the family. The index case is denoted by an arrow. Susan Walker et al. Neurol Genet 2018;4:e242 Copyright © 2018 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.