Sleep最新文献

Study objectives: Obstructive sleep apnea (OSA) is associated with a significant welfare burden. Little information is available about long-term welfare consequences for women and men. Here we evaluated the long-term gender-associated welfare of patients with OSA.

Methods: Using data from the Danish National Patient Registry and other public databases, all patients aged 20-64 years with a diagnosis of OSA were included. They were compared with citizens matched by age, sex, marital status, and community location, in a ratio of 1:4. All health and social costs were included from public registries.

Results: A total of 55,783 men and 19,241 women with OSA were compared with 223,783 and 76,961 controls, respectively. As a group, people with OSA had significantly higher morbidity, mortality, health costs, transfer incomes, sickness benefits, whereas their educational level, and professional affiliation were lower, and patients retired earlier than their corresponding controls. These patterns could be identified as much as 15 years before diagnosis, with changes becoming more pronounced after diagnosis and management. There was a significant gender difference, whereby women had higher morbidity and mortality rates and social welfare social costs than men in all domains, before and after diagnosis. The total case patient net costs for men/women were 4217/8259 €/year before diagnosis and 8749/13730 €/year after diagnosis.

Conclusions: OSA is associated with a significant welfare burden (morbidity, mortality, healthcare cost, social impact). These effects are present years before diagnosis and increase thereafter. There are significant gender differences, whereby women tend to experience a significantly higher health and welfare burden than men before and after diagnosis. The study highlights a need to pay closer attention to OSA, particularly in women, in whom the disease is probably underdiagnosed.

Study objectives: Sleep disruption is common in people with cancer and survivors, but understanding the mechanisms driving these problems is difficult due to heterogeneity among cancers, patients, and treatment modalities. We investigated whether the common antifolate chemotherapeutic agent methotrexate (MTX) promotes changes in sleep independent of cancer in adult mice.

Methods: Adult mice (> 7 weeks old, both sexes, n=13) were exposed to either a clinically relevant chemotherapy regimen with methotrexate (n=7) or saline (control, n=6) accompanied by continuous EEG/EMG telemetry recording. Sleep states were scored as either wake, NREM sleep, or REM sleep in 5-second epochs weekly during MTX or saline treatment and then two weeks following the last injection to examine enduring changes in sleep/wake cycles.

Results: MTX exposure caused NREM sleep fragmentation, indicated by (1) shorter and more frequent NREM sleep bouts, (2) more transitions between wake & NREM sleep, and (3) more accumulated NREM sleep bouts over time. These effects were first detected after the second MTX injection and lasted into the two-week follow-up recording. MTX did not alter delta power in NREM sleep, indicating no changes to sleep quality. The total time spent in each vigilance state remained unaffected by MTX use. Finally, when given MTX, male mice displayed more fragmented sleep compared to female mice.

Conclusions: Methotrexate promotes NREM sleep fragmentation, without affecting sleep quality or time spent asleep. This effect is stronger in males. These data suggest that chemotherapy can cause long-term sleep disruption independent of cancer presence.

Study objectives: Racial and ethnic sleep disparities have been documented; however, the mechanisms are unclear. In a cross-sectional analysis, we examined the contribution of features of the physical environment to sleep disparities among Black, Chinese, Hispanic, and White adults (N=1945, average age:68.5+9.1).

Methods: Physical environment measures were self-reported (aesthetic quality, walking environment) and objectively-measured via Geographic Information Systems (walking destination density, proportion of land dedicated to retail space, overall built environment score). Sleep duration (short:<6 hours) and sleep efficiency were measured via 7-day actigraphy. Multi-level linear and Poisson regression models with robust variance were fit to examine associations with adjustment for covariates. Direct and indirect mediation was tested via path models.

Results: Insufficient sleep was highest for minoritized individuals (short sleep: 32.5-44.1%, <85% sleep efficiency: 9.3-10.5%). Living in neighborhoods with higher aesthetic quality scores was associated with sleeping 5.8 minutes (0.67, 10.85) longer on average. Higher walking destination density, proportion retail, and built environment scores were associated with shorter sleep duration and higher prevalence of short sleep (adjusted prevalence ratio: 1.0001 [1.0005,1.0016], 1.02 [1.01,1.04], and 1.06 [1.02,1.09], respectively). Proportion retail partially explained the Black-White (2.8%) and Chinese-White (11.3%) difference in sleep duration. The Hispanic-White difference in sleep duration was partially (5.8-26.5%) explained by differences in aesthetic quality, walking destination density, proportion retail, and built environment score. There were no associations between features of the physical environment and sleep efficiency.

Conclusions: Features of the physical environment partially contributed to racial disparities in sleep duration and is a likely target for intervention.

Study objectives: The alignment between greater sleep demands and heightened neuroplasticity in childhood suggests that sleep plays a key role in brain maturation. While sleep duration is commonly accepted as a marker for adequate sleep, this indicator overlooks differences in individual sleep needs. Subjective perception of sleepiness may offer additional insight into sleep insufficiency relative to individual needs. This study aimed to investigate the associations between sleep duration and brain morphology in typically developing children, and the moderating effect of subjective sleepiness in these associations.

Methods: In 81 children (45 boys, 10.53 years old), actigraphy-derived estimates of sleep duration were obtained over 5 to 7 days and subjective daytime sleepiness was self-reported. Gray matter volume (GMV) was estimated for 11 brain regions. Linear associations between sleep duration and regional GMV were tested, along with the interaction between sleepiness and sleep duration in relation to regional GMV.

Results: Sleep duration negatively correlated with GMV in the insula at the group level. Subjective sleepiness moderated the relationship between sleep duration and GMV, with associations found in the hippocampus and middle temporal gyrus for children prone to sleepiness, and in the precuneus for those without sleepiness.

Conclusion: The current results suggest that normative variations in sleep duration may bear on child brain morphology, with distinct associations at varying levels of subjective daytime sleepiness in regions subsuming executive functioning and memory consolidation. These findings highlight the importance of incorporating both objective and subjective aspects of sleep in future research on sleep health and neurodevelopment.

Study objectives: Brief sleep loss alters cognition and synaptic structures of principal neurons in hippocampus and neocortex. However, while in vivo recording and bioinformatic data suggest that inhibitory interneurons are more strongly affected by sleep loss, it is unclear how sleep and sleep deprivation affect interneurons' synapses. Disruption of the SST+ interneuron population seems to be a critical early sign of neuropathology in Alzheimer's dementia, schizophrenia, and bipolar disorder - and the risk of developing all three is increased by habitual sleep loss. We aimed to test how the synaptic structures of SST+ interneurons in various brain regions are affected by brief sleep disruption.

Methods: We used Brainbow 3.0 to label SST+ interneurons in the dorsal hippocampus, prefrontal cortex, and visual cortex of male SST-CRE transgenic mice, then compared synaptic structures in labeled neurons after a 6-h period of ad lib sleep, or gentle handling sleep deprivation (SD) starting at lights on.

Results: Dendritic spine density among SST+ interneurons in both hippocampus and neocortex was altered in a subregion-specific manner, with increased overall and thin spine density in CA1, dramatic increases in spine volume and surface area in CA3, and small but significant changes (primarily decreases) in spine size in CA1, PFC and V1.

Conclusions: Our suggest that the synaptic connectivity of SST+ interneurons is significantly altered in a brain region-specific manner by a few hours of sleep loss. This suggests a cell type-specific mechanism by which sleep loss disrupts cognition and alters excitatory-inhibitory balance in brain networks.