Sleep最新文献

Study objectives: To examine the unclear, inconsistent role of sleep architectural disruption in atrial fibrillation (AF) development.

Methods: Patients (age>18 years) who underwent in-laboratory sleep studies at Cleveland Clinic 2000-2015 were examined (follow-up: 7.8+3.5 years). Primary predictors were arousal index and total sleep time. Secondary predictors included sleep efficiency, wakefulness after sleep onset, sleep and REM latency, and percentage of each sleep stage. Predictors were fit to Cox proportional hazard models predicting time from sleep study to AF by diagnosis code. Covariates included demographics, anthropometrics, tobacco use, sleepiness, apnea hypopnea index, sleep apnea-specific hypoxic burden, cardiovascular risk factors and disease, mood disorders, medications, and positive airway pressure.

Results: In our cohort (n=27,232, age: 49.4±14.5 years, 43.7% male, 73.9% White), 2,077 (7.6%) developed incident AF. Arousal index was not associated with AF incidence. For every hour of decreased total sleep time, AF incidence increased 8% (HR=1.08, 95%CI=1.04-1.11). For every 10-unit decrease in sleep efficiency, AF incidence increased 6% (HR=1.06, 95%CI=1.04-1.09). For every hour of increased wakefulness after sleep onset, AF incidence increased 11% (HR=1.11, 95%CI=1.05-1.16). For every 10-unit increase in percent N1, AF incidence increased 6% (HR=1.06, 95%CI=1.01-1.10).

Conclusion: Less sleep time and greater sleep disruption were associated with increased incident AF in this large clinical cohort. These results suggest that sleep macro-architecture can influence AF development. Mechanistic and prospective studies are needed to verify whether sleep disruption is a novel target for AF prevention.

Study objectives: To investigate associations between adolescent sleep duration and timing, and blood leukocyte DNA methylation, one type of epigenetic modification that may respond to changes in sleep.

Methods: Cross-sectional epigenome-wide analysis of DNA methylation was conducted to identify sleep-related CpG sites in 269 females and 233 males (14.4±2.1 years on average) from the ELEMENT cohort study, in Mexico City. Sleep duration and midpoint on weekdays and weekends were assessed using 7-day wrist actigraphy (Actigraph GTX-BT), and DNA methylation in blood leukocytes was measured using the Illumina Infinium Methylation EPIC BeadChip. Linear regression was conducted to assess the relationship between sleep variables and DNA methylation at each array locus, adjusting for demographic confounders, batch effects, and cell types. Differentially methylated regions (DMRs) were assessed using ipDMR, and subsequent pathway analysis of relevant genes was conducted.

Results: At false discovery rate-adjusted p-value (Q)<0.05, there was one inverse site-specific association between sleep midpoint on weekends and cg04070324 (not annotated to a specific gene) among males only (Q=0.02). However, DMR analysis in the full sample revealed 1875 total significant DMRs at Q<0.05, and there was little overlap of DMRs associated with sleep duration versus midpoint. Sex-stratified analysis revealed more associations among males than females (e.g., 3284 DMRs compared to 1346). Based on pathway enrichment analysis, the male-specific pathways for sleep duration were related to DNA and metabolism, whereas for sleep midpoint they were related to developmental processes.

Conclusion: Epigenome-wide analysis identified distinct associations with sleep duration and timing, especially among male adolescents.

Study objectives: Insomnia, characterized by difficulty in initiating and sustaining sleep or waking prematurely without the ability to return to sleep, affects approximately 30% of the population. The underlying mechanisms of insomnia remain unclear and the objective diagnosic measures are scarce. It is an opportunity to explore the roles of peripheral blood exosomal miRNAs in insomnia patients. Methods: Exosomal miRNAs were isolated from 20 insomnia patients and an equal number of healthy individuals. A comprehensive genome-wide miRNA expression analysis was conducted to identify differential miRNAs between the two groups. To evaluate the diagnostic potential of these miRNAs, receiver operating characteristic (ROC) curves were employed. Furthermore, Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed on the target genes of differential exosome miRNA to explore their regulated signaling pathways and molecular functions.

Results: We identified 51 differentially expressed miRNAs. Among these, miR-182-5p and miR-451a were markedly downregulated in patients as evidenced by their area under the curve (AUC) values. The areas under the ROC curves and 95% confidence intervals (Cl) of miR-182-5p and miR-451a in predicting the possibility of chronic insomnia patients were 0.863 (95% CI, 0.75-0.97) and 0.813 (95% CI, 0.68-0.95). Coexpression network analysis and enrichment analysis of miRNA target genes shed light on the molecular pathophysiology of insomnia, including autophagy and mitophagy.

Conclusion: These findings suggest that peripheral blood exosomal miRNAs may serve as potential non-invasive biomarkers for insomnia diagnosis and provide new insights into the molecular mechanisms underlying this sleep disorder.

Study objectives: To evaluate the impact of contextual stressors on postpartum sleep among Black mothers.

Methods: This prospective observational study examined associations of racial discrimination and financial strain (measured at 1 week postpartum) with self-reported maternal sleep difficulties at 1, 8, and 16 weeks postpartum and actigraph-estimated maternal sleep at 8 weeks postpartum.

Results: Mothers (N = 212) were Black/African American (100%) and non-Hispanic (98.6%) and averaged 22.7 (SD = 4.5) years of age. Multivariate regression models found unique associations between racial discrimination and financial strain and mothers' postpartum sleep, even after controlling for covariates expected to predict mothers' sleep (including infant sleep). Specifically, past year racial discrimination measured at 1 week postpartum was associated with poorer concurrent self-reported sleep (b = 1.24, p < .001) as well as greater actigraph-estimated night-to-night variability in total sleep time at 8 weeks postpartum (b = 12.89, p = .005). Financial strain reported at 1 week postpartum was prospectively associated with more self-reported sleep difficulties at 16 weeks postpartum (b = .52, p = .007) and with more actigraph-estimated sleep timing variability at 8 weeks postpartum (b = 9.77, p = .02).

Conclusion: Experiences of racial discrimination and financial strain may negatively impact Black mothers' sleep in the postpartum period, beyond the effects of their infant's sleep.

Study objectives: The manual annotation of polysomnography (PSG) hypnograms is difficult and time-consuming. U-Sleep is an alternative, fast and publicly available, automated sleep staging system evaluated in adult PSGs. In this study we compare the staging done by sleep experts and U-sleep in a pediatric sample.

Methods: PSGs from 56 children aged 6-17 years old (healthy or with a chronic disease) were compared manually annotated with the result of U-sleep. The two outcomes were compared using F1 overlap scores, accuracy, Cohen's kappa, and correlation coefficients. A qualitative analysis of the most significant systematic differences between the manual and automated scoring was performed.

Results: U-sleep matched the manually scored hypnograms with an overall mean F1 score (predicted performance) of 0.75 and reached an accuracy of 83.9% and an overall kappa value of 0.77. The stage-wise F1 scores, U-sleep achieved an F1 score of 0.79 in stage Wake, 0.40 in N1, 0.86 in N2, 0.84 in N3, and 0.86 in REM. The correlation between U-sleep and the manual scorer was moderately or very strong in all sleep stages (r = 0.57-0.81).

Conclusions: Overall, there is a high degree of agreement between manual and automatic scoring. This suggests that U-sleep is a valid and effective method for identifying sleep stages based on normal PSGs in a pediatric population. The disagreement was within what is expected for interscorer variation. Further evaluation needs of AI sleep scoring models includes analysis of outliers and pathological sleep staging - which is also a challenge in manual annotation.

Darkness is equated with sadness. This study explored how light that differentially impacts non-visual photoreception (blue-enriched vs blue-depleted light) affects how we feel about ourselves. In a repeated-measured design, thirty-five participants (22 female participants, 13 male participants, Mage = 20.29, SD = 2.09) completed the Self-Referential Encoding Task (SRET) under both blue-enriched or blue-depleted light conditions, with light conditions randomised and counterbalanced between sessions. The SRET involved participants deciding whether positive (e.g., "good") and negative (e.g., "terrible") words were self-descriptive. Trial-by-trial performance analysis using logistic mixed effects models revealed that blue-enriched light significantly increased the likelihood of rejecting negative words as self-descriptive. A Hierarchical Drift Diffusion Model (HDDM) further examined latent decision-making processes and found evidence accumulation to be faster under blue-enriched light when rejecting negative descriptors, suggesting rejecting negative self-descriptors was easier under blue-enriched light. We find light can acutely influence self-perception, with blue-enriched light decreasing negative self-thoughts.

Obstructive sleep apnea (OSA) exerts pathogenic effects through a combination of sleep fragmentation (SF) and intermittent hypoxia (IH). The mechanisms through which sleep disruption impacts memory might arise by investigating disruption of specific sleep stages and, when such disruption occurs through OSA, by evaluating the individual contributions of SF and IH. Given region-specific EEG slow activity during non-REM sleep has been associated with overnight declarative, motor and spatial memory formation, we investigated the effects of disrupting slow wave sleep (SWS) on a virtual maze navigation task. Thirty three participants (24 male, 56 years old [range 28-68 years] with OSA (baseline AHI4%>20/hour) who were habitually well-treated and adherent to CPAP completed 3 timed trials on a 3D spatial maze before and after polysomnographically (PSG) recorded sleep. We restricted CPAP withdrawal to SWS through real-time monitoring of the PSG under three conditions: 1) stable-SWS on therapeutic CPAP, 2) SWS-CPAP withdrawal containing SF and IH, and 3) SWS-CPAP withdrawal with supplemental oxygen containing SF with reduced IH. SWS-specific CPAP withdrawal (with or without supplemental oxygen) did not significantly impact EEG slow oscillation or spatial navigational memory, despite effectively reducing %SWS and SWS bout length. Greater regional EEG slow oscillation (0.6-1Hz), but not delta (1-4Hz) activity, was associated with improvements in overnight memory during stable SWS in the CPAP condition. These observations suggest that slow oscillations may be important for overnight memory processing, and sleep disruptions of sufficient magnitude to reduce slow oscillations may be required to capture demonstrable change in spatial navigation performance.

Studies in rats indicate that oscillatory signatures of memory processing during sleep, and specifically hippocampal sharp wave-ripples, also regulate peripheral glucose concentration. Here, we examined whether there is a similar link between such signatures of memory processing and glucose regulation during sleep in healthy humans. We obtained polysomnographic recordings and continuous recordings of peripheral interstitial glucose levels (1 sample/min) from 10 participants (5 females) during two consecutive nights. Temporal relationships between EEG events of interest and glucose levels were examined using cross-correlation functions and time-event histograms. Confirming the findings in rats, we find that sleep spindles, a core signature of sleep-dependent memory processing, are followed within 1-6 min by a robust decrease in glucose concentrations. By contrast, slow oscillation events hallmarking slow wave sleep (SWS) were followed, with a lag of 5-11 min, by an increase in glucose levels. Transitions into rapid eye movement (REM) sleep were followed by a glucose decrease after 10-14 min, whereas awakenings and microarousals were linked to immediate glucose increases. These temporal relationships indicate a sleep-specific regulation of peripheral glucose concentrations that is linked to both signatures of sleep-dependent memory processing as well as the macro-architecture of sleep. They possibly reflect noradrenergic regulation of sympathetic activity via the brainstem locus coeruleus, and may be of relevance in clinical conditions with concurrent disturbances of sleep and glucose regulation.