8 research outputs found

    Patient characteristics, groups according to current episode.

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    <p>If not mentioned otherwise, values are number of patients, n (%).</p><p>**p≤0.01 chi-square test.</p

    MOESM1 of Actigraphy as an objective intra-individual marker of activity patterns in acute-phase bipolar disorder: a case series

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    Additional file 1: Table S1. Clinical data and activity variables for case 1. Table S2. Clinical data and activity variables for case 2. Table S3. Clinical data and activity variables for case 3

    Results from 64-minute period of continuous motor activity in the evening.

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    <p>All data are given as mean ± SD. p-values obtained in a one-way ANOVA. Post hoc Bonferroni test:</p><p>*p≤0.05, mania compared to healthy controls.</p

    Results from the 24-hour recording of motor activity.

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    <p>All data are given as mean ± SD. p-values obtained in a one-way ANOVA. Post hoc Bonferroni tests:</p><p>***p≤0.001, mania compared to healthy controls.</p>+<p>p≤0.05, depression compared to healthy controls.</p>+++<p>p≤0.001, depression compared to healthy controls.</p><p>(T): Tamhane’s T2 post hoc test was used when unequal variances were assumed.</p

    Results from the 64-minute period of continuous motor activity in the morning.

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    <p>All data are given as mean ± SD. p-values obtained in a one-way ANOVA. Post hoc Bonferroni tests:</p><p>*p≤0.05, mania compared to healthy controls.</p><p>**p≤0.01, mania compared to healthy controls.</p><p>***p≤0.001, mania compared to healthy controls.</p>+<p>p≤0.05, depression compared to healthy controls.</p>++<p>p≤0.01, depression compared to healthy controls.</p>#<p>p≤0.05, depression compared to mania.</p

    24-hour actigraphy recordings for all three groups.

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    <p>Activity counts from a patient with depression (A), a patient with mania (B) and a healthy control (C). The figure shows the activity counts in black during 24 hours from 12 h to 12 h the next day. The dark gray area at the end of recording A and the gray area at the beginning of recording B represent excluded periods, when the subject was not wearing the actigraph.</p

    Mapping genomic loci implicates genes and synaptic biology in schizophrenia

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    Schizophrenia has a heritability of 60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies
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