11 research outputs found

    The number and length of bouts of REM sleep.

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    <p>Each number of REM bouts as a function of sleep period length (in seconds) is shown over the first 24h <b>(A)</b>; 2 days <b>(B)</b> and 3 days <b>(C)</b> after interventions; sleep deprivation (SD) and either ischemia and sham surgery and during the baseline time. The daily number of REM sleep bouts during baseline accounts for the control values (n = 6 baseline values belonging to each animal randomly assigned to the experimental groups were averaged for each condition). The figure represents the average (±SEM) number of sleep periods of a specific length in the following experimental groups: i. SD_IS (n = 6); ii. IS (n = 6); iii. SD_Sham (n = 4); and iv Sham (n = 6). Statistical analyses were performed by two-way ANOVA (factors: “group×length of the bout”) and post hoc analysis, with Tukey’s multiple comparison tests run afterward. a: p ≀ .01, IS group vs. baseline; SD_IS, SD_Sham and Sham groups. b: p< .0001, SD_IS group vs. baseline, IS and Sham groups.</p

    Changes in sleep EEG during the first 24h after interventions.

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    <p><b>(A)</b> The time line of the experiment. Sleep was analysed at the baseline before SD and after 24h from either ischemia or sham surgery; 12h dark,12h light periods. <b>(B)</b> The amount of total sleep (mean ± SEM) is represented by vertical bars. Dark bars indicate the baseline time, which was defined as the percentage of time spent in each state across 24h of recording baseline. White bars indicate post-surgery times across 24h after interventions. <b>(C)</b> Total, wake, non-REM and REM sleep (mean ± SEM) were analysed separately over the dark period. <b>(D)</b> Total, wake, non-REM and REM sleep (mean ± SEM) were analysed separately over the light period. Comparison with corresponding baselines was performed with paired t-tests (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0168430#pone.0168430.s006" target="_blank">S3</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0168430#pone.0168430.s007" target="_blank">S4</a> Tables for data set). Stars denote post-surgery times that differed significantly from baseline time and specific p values are shown. * P ≀ .05; **p ≀ .01; *** p ≀ .001; **** p ≀ .0001. Experimental groups: i. SD_IS (n = 6); ii. IS (n = 6); iii. SD_Sham (n = 4); and iv Sham (n = 6).</p

    Changes in sleep EEG during the 2 and 3 days after interventions.

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    <p><b>(A)</b> The timeline of the experiment. Sleep was analysed at the baseline and over the following 2 and 3 days. The baseline values was given by the percentage of time spent in each state across 24h of baseline recording. <b>(B)</b> The amount of total sleep (mean ± SEM) for each experimental group at the BL; 2 day and 3 day post-recovery (i. SD_IS (n = 6); ii. IS (n = 6); iii. SD_Sham (n = 4); and iv. Sham (n = 6)). Time (baseline, 2 and 3 days) is displayed in the x-axis. <b>(C)</b> Total, wake, non-REM and REM sleep (mean ± SEM) were analysed separately over the baseline and 2 and 3 days after interventions (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0168430#pone.0168430.s006" target="_blank">S3 Table</a> for data set). Statistical analyses were performed rANOVA (factors: group and time) and post hoc analysis, with Tukey’s multiple comparison tests run afterward. Asterisks (*) indicate a statistical difference between groups (*P ≀ .05), whereas dots (°) indicate a statistical difference between days within the same group (°°P ≀ .05).</p

    Schematic of the experiment design.

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    <p><b>(A)</b> Design for the sleep architecture analysis and for the time course of gene expression of MCH and OX systems. Ischemia surgery was performed on day 0, and then the rats were sacrificed at 4, 12 and 24 hours (acute phase) and 3, 4 and 7 days (chronic phase) following ischemic surgery. Baseline was recorded 2 days before ischemia for 24h; 12h dark and 12h light. Rats subjected to SD were also recorded over 6h of SD. The EEG/EMG recordings were stopped when animals were sacrificed; represented by each time point <b>(B)</b> Design for sleep architecture. Rats were implanted with EEG/EMG electrodes and then allowed to recover for 4 days, and then connected to a flexible cable and swivel and habituated for 3 days with a cable, before EEG/EMG recording. <b>C)</b> Design for SD interventions. SD was performed by gentle handling during the last 6 h of the light period; from 14:00 to 20:00. And ischemia/sham surgery was performed immediately after; at the beginning of the dark period, during either stroke or sham surgery EEG/EMG recordings were not performed <b>(D)</b> Not-to-scale representation of the placement of the screw electrodes over the parietal cortex and the cerebellar cortex (dark circles), Ref. = reference and Gnd = ground. EMG was bilaterally placed in the neck muscle using wire electrodes <b>(E)</b> An anesthetized rat fixed to the stereotaxic frame with EEG/EMG plug fixed to the skull with dental cement. Experimental groups: i. SD_IS (n = 6); ii. IS (n = 6); iii. SD_Sham (n = 4); and iv Sham (n = 6). Electroencephalogram (EEG); Electromyogram (EMG).</p

    Effects of sleep deprivation (SD) pre-ischemia on the infarct volume.

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    <p>Lesion volumes corrected for edema were calculated by cresyl violet staining at 12 and 24 hours and 3, 5 and 7 days after ischemic surgery are displayed on the x-axis (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0168430#pone.0168430.s002" target="_blank">S2 Fig</a> for infarct volume assessed without edema correction and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0168430#pone.0168430.s004" target="_blank">S1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0168430#pone.0168430.s005" target="_blank">S2</a> Tables for data set). <b>(A)</b> Representative sets of brain sections from a rat subjected to 6h of SD pre-ischemia (left panel), and rats subjected to ischemia without SD (right panel). The infarct areas are delineated by a thin black line. L1 is at 2.7 mm anterior to bregma, and the interval between each level is 1 mm (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0168430#sec007" target="_blank">methods</a>). <b>(B)</b> Infarct volume (mean ± SEM) assessed at 12 and 24 hours and 3, 5 and 7 days after interventions (n = 6 per group) were analysed by unpaired t-test. Dots represent infarct volume of each animal during each time points. Asterisks (*) indicate a statistical difference between groups, **p ≀ .01; *** p ≀ .001.</p

    sj-docx-1-eso-10.1177_23969873241227751 – Supplemental material for Trajectories of self-reported daytime sleepiness post-ischemic stroke and transient ischemic attack: A propensity score matching study versus non-stroke patients

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    Supplemental material, sj-docx-1-eso-10.1177_23969873241227751 for Trajectories of self-reported daytime sleepiness post-ischemic stroke and transient ischemic attack: A propensity score matching study versus non-stroke patients by SĂ©bastien Baillieul, Renaud Tamisier, Bastien GĂ©vaudan, Sarah Alexandre, Olivier Detante, Yves Dauvilliers, Claudio Bassetti, Jean-Louis PĂ©pin and SĂ©bastien Bailly in European Stroke Journal</p

    Association signal at the mapping intervals flanking rs34593439 and rs7553711.

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    <p>Association scores at 15q25.1 (panel A) and 1q25.1 (panel B). Genotyped (diamonds) and imputed (circles) SNPs are indicated and the top genotyped SNP in the interval is outlined in orange. A SNP in 15q25.1 previously associated with Diabetes is outlined in blue. The degree of red color in each diamond or circle indicates the strength of LD with the top SNP (on a scale shown in the legend at the upper left hand corner of the plot). The X-axis shows the chromosome and physical distance (kb) from the human genome reference sequence (hg19), the left Y-axis shows the negative base ten logarithm of the p-value and the right Y-axis shows recombination rate (cM/Mb) as a navy line. The genome-wide significance threshold (P<5×10<sup>−8</sup>) is given by the dashed grey line. Genes in the regions are annotated at the bottom as green arrows. Also indicated in 1q25.1 is a ∌130 kb region with no SNPs on the ImmunoChip.</p

    Non-HLA narcolepsy risk variant loci reaching genome-wide significance.

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    <p>Chr.: Chromosome; BP: position according to NCBI build 36 (Hg18) coordinates; MAF_N: minor allele frequency in narcolepsy (_N) and controls (_C); P: P value according to variance component model (EMMAX). EMMAX does not provide OR (Odds Ratio) or adjusted allele frequencies, therefore MAF, OR, and 95% confidence intervals (CI) were calculated with Plink on subset of 8,474 samples with the greatest PCA homogeneity (see Figure S2; EV 11.21<0.004, EV 4.12<0.01).</p

    Sample collections.

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    *<p>Numbers of samples by country of origin are listed in the <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003270#s3" target="_blank">Methods</a> section.</p><p>Case cohort names represent location of genotyping, and do not reflect country of origin of samples.</p
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