Figure 1 Within-groups sum of squares vs number of clusters Within-groups sum of squares vs number of clusters to determine the number needed for k-means.

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Figure Pedigrees of the SCA42 families identified in this study
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Figure 3 Pedigree of familial idiopathic transverse myelitis
Figure 1 Percentages of patients with first seizure experiencing a recurrent seizure over time This graph is based on a fixed-effect pooled percentage.
Figure 2 Needle biopsy of the left vastus lateralis
Figure 2. Change in total PSPRS score from baseline to each study visit for all participants Change in total PSPRS score from baseline to each study visit.
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Figure Pedigree of the family
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Figure 1 Genetic profile of 90 patients with dysferlin deficiency
Figure 1 Dominant and recessive missense and nonsense variants in neurofilament light (NEFL)‏ Dominant and recessive missense and nonsense variants in.
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Table 4 Associations in SNP array data between the Braak stage and previously known AD risk loci (341 variants) comparing participants with Braak stage.
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Figure 3 qRT-PCR fold change comparison, disease vs CON, of splice vs no-splice primer sites qRT-PCR fold change comparison, disease vs CON, of splice.
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Figure 2 Linkage analysis of chromosome 19
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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.
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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.
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Figure 1 Histamine flare in patients and controls
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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.
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Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial.
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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 CD56bright natural killer (NK) cell counts in daclizumab high-yield process (DAC HYP)-treated patientsData are medians with 25th and 75th percentiles.
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Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.
Figure 2 Neuroimaging characteristics of TARDBP carriers
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Figure 1 bvFTD PINBPA network
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Figure 1 Within-groups sum of squares vs number of clusters Within-groups sum of squares vs number of clusters to determine the number needed for k-means cluster analysis. Within-groups sum of squares vs number of clusters Within-groups sum of squares vs number of clusters to determine the number needed for k-means cluster analysis. The cluster algorithm assumes a given number of clusters to determine the grouping of patients. Figure 1 shows 15 separate cluster algorithms with 1–15 clusters assumed and the within-groups sum of squares calculated for each. Optimally, one would like to select a small number of clusters for ease of interpretation but with a small within-groups sum of squares. When there is a bend (like an elbow), it provides evidence that the gain is large (i.e., reducing the sum of squares) in identifying a fixed number of clusters with decreased evidence to increase the number of clusters. Our analysis showed no evidence of a bend, so we chose 2 clusters for convenience of interpretation. Hiroshi Mitsumoto et al. Neurol Genet 2015;1:e3 © 2015 American Academy of Neurology