Gene expression biomarkers for neurobehavioral impairment from total sleep deprivation microarray data [D9]
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE98566 | GEO | 2018/04/10
REPOSITORIES: GEO
Similar Datasets
Project description:Healthy human adults were recruited to a sleep lab at Washington State University and remained there 7 consecutive days. Six received a well-rested Control condition of 10 h Time-In-Bed (TIB) nightly. Another 11 subjects underwent Sleep Deprivation. They had a Baseline with 10 h TIB, followed by an Experimental phase of 62 h continued wakefulness, and finally two nights of 10 h TIB before dismissal. Blood draws on one Baseline day, one Experimental day, and one Recovery day were used for gene expression microarrays.
2018-04-10 | GSE98565 | GEO
Project description:Healthy human adults were recruited to a sleep lab at Washington State University and remained there 7 consecutive days. Six received a well-rested Control condition of 10 h Time-In-Bed (TIB) nightly. Another 11 subjects underwent Sleep Deprivation. They had a Baseline with 10 h TIB, followed by an Experimental phase of 62 h continued wakefulness, and finally two nights of 10 h TIB before dismissal. Blood draws on one Baseline day, one Experimental day, and one Recovery day were used for gene expression microarrays.
2018-04-10 | GSE98564 | GEO
Project description:Healthy young males (n=13) attended in this controlled laboratory experiment stimulating a workin week with reduced sleep. After baseline, the experimental group (n=9) were partially sleep deprived for 5 nights (time in bed 4 h/night) and had a recovery period of two nights (8 h/night). The control group (n= 4) spent the time in the same laboratory conditions but sleeping normally (8 h/night). RNA expression was detected in peripheral blood mononuclear cells (PBMC) taken in the morning after baseline (BL), sleep restriction (SR), and recovery (REC) periods.
2013-12-12 | E-MEXP-3936 | biostudies-arrayexpress
Project description:In a cross balanced design human subjects were given one week of sufficient sleep and insufficient sleep (6 h per day). Following each of these conditions they were then kept awake for a day, a night and the subsequent day. During each of these periods of extended wakefulness 10 blood samples were taken, RNA was extracted from leukocytes, labelled and hybridised to human whole-genome microarrays
2013-02-27 | GSE39445 | GEO
Project description:In a cross balanced design human subjects were given one week of sufficient sleep and insufficient sleep (6 h per day). Following each of these conditions they were then kept awake for a day, a night and the subsequent day. During each of these periods of extended wakefulness 10 blood samples were taken, RNA was extracted from leukocytes, labelled and hybridised to human whole-genome microarrays
2017-02-08 | GSE82114 | GEO
Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Blood draws were done every 4 hours during a 3-day (+1 baseline day) study: 24-hour normal baseline (6 time points: day 1 8hr, 12hr, 16hr, 20hr, day 2 0hr, 4hr), 38 hours of continuous wakefulness (10 time points: day 2 8hr, 12hr, 16hr, 20hr, day 3 0hr, 4hr, 8hr, 12hr, 16hr, 20hr) and subsequent recovery sleep (3 time points: day 4 0hr, 4hr, 8hr), for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. The missing/failed samples were as following: Resistant subjects (total 10 samples): BH006 day 2 20hr, 12hr, BH003 day 2 12hr, 4hr, BH003 day 3 4hr, BH008 day 4 0hr, BH008 day 1 16hr, BH008 day 3 16hr 20hr, BH010 day 4 0hr; Sensitive subjects (total 7 samples): BH004 day 2 12hr and 1 more missing sample, BH026 day 2 4hr, BH007 day 2 20hr and 1 more missing sample, BH016 day 2 4hr, BH015 day 3 0hr.
2014-10-02 | E-GEOD-56931 | biostudies-arrayexpress
Project description:Although the specific functions of sleep have not been completely elucidated, the literature has suggested that sleep is essential for proper homeostasis. Sleep loss is associated with changes in behavioral, neurochemical, cellular, and metabolic functions as well as impaired immune response. We evaluated the gene expression profiles of healthy volunteers submitted to 48 hours of prolonged wakefulness (PW) followed by 12 hours of sleep recovery (SR) using high-resolution microarrays. Peripheral whole blood was collected in the morning before the initiation of sleep deprivation (baseline), after the second night of PW, and one night after SR. the identified differentially expressed genes were related to immune response, DNA damage and repair as well as inflammation. Examples of these include: killer cell lectin-like receptors family granzymes and T-cell receptors, which play important roles in host defense. These results support the idea that sleep loss can lead to alteration of molecular processes that drive perturbation of cellular immunity, induction of inflammatory response and homeostatic imbalance. Moreover, down-regulation of multiple genes after prolonged wakefulness (in comparison with baseline condition) and up-regulated after sleep recovery (in comparison with prolonged wakefulness condition) were observed, suggesting an attempt of the body to re-establish internal homeostasis. In silico validation of alterations in the expression of CETN3, DNAJC, IGFR2B and CEACAM genes, confirmed the previous findings related to the molecular effects of sleep deprivation. It is clear that confirmatory studies will be necessary to fully validate the potential candidate genes and functional networks identified. Nevertheless, the present findings confirm that the effects of sleep deprivation are not restricted to the brain and can occur intensely in peripheral tissues. The peripheral blood from each volunteer (nine individuals) were collected in the baseline night and every morning after PW and after the night of SR.
2012-05-01 | E-GEOD-37667 | biostudies-arrayexpress
Project description:In a cross balanced design human subjects were given one week of sufficient sleep and insufficient sleep (6 h per day). Following each of these conditions they were then kept awake for a day, a night and the subsequent day. During each of these periods of extended wakefulness 10 blood samples were taken, RNA was extracted from leukocytes, labelled and hybridised to human whole-genome microarrays A total of 427 samples comprising 26 human subjects, for which 20 samples across multiple time-points/sleep condition were collected. We have focussed on two genotypes related to the variable number tandem repeat (VNTR) polymorphism of the circadian gene PERIOD3 (PER3): a 4-repeat VNTR allele of PER3 (PER3(4/4)) and a 5-repeat VNTR allele of PER3 (PER3(5/5)).
2013-02-27 | E-GEOD-39445 | biostudies-arrayexpress
Project description:Sleep is a conserved physiological process, and sleep loss typically imposes negative effects on animal health. However, natural short sleepers, who sleep less without the usual negative effects of sleep deprivation, exist in the human population. One example are individuals that possess rare genetic mutations in the human dec2 gene; these individuals sleep on average ~6hrs/day rather than the typical 8hrs/day. Like many natural short sleepers, humans harboring the dec2P384R mutation do not exhibit any obvious adverse phenotypes typically associated with sleep loss, suggesting that these individuals may require less total sleep/day to achieve the same physiological outcomes. Potentially, the dec2P384R mutation could activate compensatory mechanisms that allow these individuals to thrive with less sleep. To test this directly, we used a dec2P384R short sleep Drosophila model to understand the effects of the dec2P384R mutation on animal health and dissect the genetic mechanisms that might drive these physiological changes. We found that expression of the mammalian dec2P384R mutation in fly sleep neurons was sufficient to mimic the short sleep phenotype observed in mammals. Remarkably, dec2P384R lived significantly longer with improved health and memory despite having a short sleep phenotype. The improved physiological effects in dec2P384R mutants were enabled, in part, by enhanced mitochondrial fitness and upregulation of multiple stress response pathways. Moreover, we provide evidence that the improved health in dec2P384R mutants may also contribute to the short sleep phenotype, and this may extend to other pro-longevity mutants.
2023-04-26 | GSE230462 | GEO
Project description:Introduction: Sleep deprivation is associated with increased cardiovascular risk, which is more pronounced in women than men; however, causal evidence is lacking and the underlying mechanisms are unclear. We used randomized crossover design of prolonged sleep deprivation that mimics “life-like conditions” and endothelial cells (ECs) harvested from healthy women to investigate directly whether sleep deprivation impairs endothelial function and to identify underlying mechanisms. Methods: Healthy women with normal habitual sleep (7-9 h/day) were randomly allocated to 6-weeks of adequate sleep (7-9 h/day) or sleep deprivation (1.5 h less than habitual sleep) in a crossover design. Sleep duration was monitored objectively by actigraphy. EC harvesting and brachial artery flow-mediated dilation (FMD) were performed at baseline and the end of adequate sleep and sleep deprivation period. Results: Twenty-eight healthy women (mean [SE] age 35±13 years; BMI 25±3 kg/m2) participated. Compared with adequate sleep, sleep deprivation reduced FMD (mean±SE 8.65±0.48 vs. 7.35±0.39, p=0.02) and increased EC inflammation (nuclear factor-κB nuclear fluorescence area mean±SE 1.36±0.24 vs. 2.04±0.38 μm2, p=0.03 and mRNA expression of vascular cell adhesion molecule-1 mean±SE 1.00±0.19 vs. 2.31±0.72, p=0.04) compared with adequate sleep. Sleep deprivation increased EC oxidative stress by 67% compared with adequate sleep (redox sensitive fluorogenic probe fluorescence intensity, p=0.002) without upregulating antioxidant response. Using RNA-seq and a predicted protein-protein interaction algorithm, we identified reduced expression of serum response factor, a transcription factor that primes cortical response to sleep deprivation, and its endothelial target Defective in Cullin Neddylation-1 Domain Containing 3 as novel mediators of impaired nuclear factor (erythroid-derived 2)-like 2-mediated antioxidant responses in ECs in sleep deprivation. Conclusion: Sleep deprivation impairs clearance of endothelial oxidant stress accumulated during wakefulness leading to endothelial dysfunction and potentially increased cardiovascular risk in women. Trial Registration Number: ClinicalTrials.gov NCT02835261
2024-04-05 | GSE171831 | GEO