Neurobiology of Sleep and Circadian Rhythms最新文献_第2页

Sleep regularity and duration are associated with depression severity in a nationally representative United States sample 在具有全国代表性的美国样本中，睡眠规律和持续时间与抑郁症严重程度有关

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-07-17 DOI: 10.1016/j.nbscr.2025.100133

Katherine A. Maki, Li Yang, Nicole Farmer, Shreya Papneja, Gwenyth R. Wallen, Jennifer J. Barb

Background

Sleep hygiene is integral to health, and sleep regularity may be associated with mental health outcomes in addition to duration. Although sleep and depression relationships are well-studied, the relative impact of different sleep factors remains unclear. As patient-specific factors and health behaviors influence sleep and mental health, we investigated associations between sleep and depression severity considering such factors in a United States sample of adults.

Methods

Two cycles (2011–2012, 2013–2014) from the National Health and Nutritional Examination Survey were studied. Objective sleep duration (day and night), and the sleep regularity index (SRI) were calculated from physical activity monitors worn for seven days. Complex survey procedures with four-year weights were used, and backward selection was used to test relevant variables in the fully adjusted regression model.

Results

Among participants (n = 7297), we found associations between sleep-associated variables and SRI, with increased daytime sleep being the strongest correlate of decreased SRI. In the fully adjusted model, lower SRI scores and reduced subjective night sleep remained significantly associated with depression. Sex was an additional independent predictor, with females exhibiting higher depression scores, and a significant sex × SRI interaction revealed that the inverse relationship between SRI and depressive symptoms was stronger in females than in males. Health behaviors, including active tobacco and cannabis use, were also associated with increased depression severity in the adjusted model.

Conclusions

Daytime sleep may serve as an SRI proxy, although additional cohorts should confirm relationships. Higher depression severity was associated with different sleep components, emphasizing the importance of sleep hygiene in mental health. Behaviors like current smoking and cannabis use were also associated with increased depression. Research exploring the temporality and interactions between these factors may assist in non-pharmacologic depression treatment.

睡眠卫生是健康不可或缺的一部分，除了持续时间外，睡眠规律可能与心理健康结果有关。尽管睡眠和抑郁的关系已经得到了充分的研究，但不同睡眠因素的相对影响仍不清楚。由于患者特有的因素和健康行为影响睡眠和心理健康，我们在美国成年人样本中考虑了这些因素，调查了睡眠和抑郁严重程度之间的关系。方法对2011-2012年、2013-2014年两个周期的全国健康与营养检查调查进行分析。客观睡眠时间（白天和黑夜）和睡眠规律指数（SRI）由佩戴7天的身体活动监测仪计算。采用四年权的复杂调查程序，并采用逆向选择对完全调整回归模型中的相关变量进行检验。在参与者（n = 7297）中，我们发现睡眠相关变量与SRI之间存在关联，白天睡眠增加与SRI降低的相关性最强。在完全调整的模型中，较低的SRI得分和较少的主观夜间睡眠仍然与抑郁症显著相关。性别是另一个独立的预测因子，女性表现出更高的抑郁评分，显著的性别× SRI交互作用表明，女性的SRI与抑郁症状之间的负相关强于男性。在调整后的模型中，健康行为，包括积极使用烟草和大麻，也与抑郁症严重程度的增加有关。结论：白天睡眠可以作为SRI的替代指标，但需要更多的队列来证实两者之间的关系。较高的抑郁严重程度与不同的睡眠成分有关，强调了睡眠卫生对心理健康的重要性。目前吸烟和使用大麻等行为也与抑郁症的增加有关。探索这些因素之间的时间性和相互作用的研究可能有助于非药物治疗抑郁症。

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引用次数: 0

Loss of MeCP2 leads to sleep deficits that are time-of-day dependent and worsen with sleep deprivation MeCP2的缺失会导致睡眠不足，这种睡眠不足与时间有关，并随着睡眠剥夺而恶化

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-06-11 DOI: 10.1016/j.nbscr.2025.100132

Abrar Al Maghribi , Caitlin Ottaway , Michael Rempe , Elizabeth Medina , Kaitlyn Ford , Kristan Singletary , Lucia Peixoto

Rett syndrome (RTT) is a severe, progressive neurodevelopmental disorder caused by mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2). Sleep problems are frequently reported in Rett Syndrome, but the exact nature remains relatively unexplored. Currently there is limited understanding of MECP2's role in sleep architecture and regulation. In this study, we employed longitudinal electroencephalographic (EEG) and electromyographic (EMG) recordings to investigate sleep architecture during baseline conditions as well as the homeostatic response to sleep deprivation (SD) in Mecp2^-/y male mice. At baseline, Mecp2^-/y mice have more non-rapid-eye-movement (NREM) sleep and less rapid-eye-movement (REM) sleep than their wildtype littermates during the light period. However, Mecp2^-/y mice display altered sleep timing during the dark period, spending more time in both NREM and REM during the first half and less time during the second half. Mecp2^-/y mice also have lower EEG spectral power during wake and NREM at higher frequencies and higher power at lower frequencies during REM in compared to wildtype mice. In response to SD, Mecp2^-/y mice can accumulate and discharge sleep pressure normally and show a sleep rebound. However, baseline differences in sleep architecture are heightened after SD. Overall, our findings show that RTT mice exhibit distinct sleep patterns compared to wildtype mice, with time-of-day-dependent variations in NREM and REM sleep, as well as altered EEG spectral properties, that become more pronounced following SD. Future research should explore the molecular mechanisms through which MECP2 regulates sleep architecture to develop targeted therapeutics for sleep disturbances in RTT patients.

Rett综合征（RTT）是一种严重的进行性神经发育障碍，由编码甲基cpg结合蛋白2 （MECP2）的x连锁基因突变引起。睡眠问题经常在Rett综合征中被报道，但确切的性质仍然相对未知。目前对MECP2在睡眠结构和调节中的作用了解有限。在这项研究中，我们使用纵向脑电图（EEG）和肌电图（EMG）记录来研究基线条件下Mecp2-/y雄性小鼠的睡眠结构以及睡眠剥夺（SD）的稳态反应。在基线时，Mecp2-/y小鼠在光照期比野生型小鼠有更多的非快速眼动（NREM）睡眠和更少的快速眼动（REM）睡眠。然而，Mecp2-/y小鼠在黑暗期表现出睡眠时间的改变，在前半段的非快速眼动和快速眼动中花费更多的时间，在后半段花费更少的时间。与野生型小鼠相比，Mecp2-/y小鼠在较高频率的清醒和非快速眼动期间的脑电图频谱功率较低，而在较低频率的快速眼动期间的脑电图频谱功率较高。SD作用下，Mecp2-/y小鼠可正常积累和释放睡眠压力，出现睡眠反弹。然而，在SD后，睡眠结构的基线差异会加剧。总的来说，我们的研究结果表明，与野生型小鼠相比，RTT小鼠表现出不同的睡眠模式，NREM和REM睡眠的时间依赖性变化，以及脑电图频谱特性的改变，在SD后变得更加明显。未来的研究应探索MECP2调控睡眠结构的分子机制，以开发针对RTT患者睡眠障碍的靶向治疗方法。

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引用次数: 0

Neurobiology of the circadian clock and its role in cardiovascular disease: Mechanisms, biomarkers, and chronotherapy 生物钟的神经生物学及其在心血管疾病中的作用：机制、生物标志物和时间疗法

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-06-03 DOI: 10.1016/j.nbscr.2025.100131

Abhimanyu Thakur , Raj Kishore

Cardiovascular diseases are paramount cause of morbidity in aging population and aging disrupts normal circadian rhythm cycle. Circadian rhythms, regulated by the suprachiasmatic nucleus in the brain, profoundly influence cardiovascular health through intricate neurobiological mechanisms. These rhythms regulate gene expression in cardiomyocytes, modulate autonomic nervous system (ANS) activity, and synchronize cardiovascular functions with environmental cues, ultimately impacting heart rate, blood pressure, and susceptibility to cardiac events. The intricate relationship between circadian rhythms and cardiovascular health emphasizes the critical role of brain-heart communication in physiological processes.

This review explores the neurobiology of circadian clock in cardiovascular disease, exploring how peripheral clocks in cardiovascular tissues influence organ physiology and how their disruption contributes to pathogenesis. The examination of neurobiological pathways linking circadian clock to cardiovascular disease, including ANS function, neuroendocrine signaling, and inflammatory responses, highlights the interplay between brain and heart. By probing environmental and lifestyle factors that modulate the circadian clock, as well as sex-specific variations in circadian rhythms, the review provides a comprehensive understanding of how these factors impact cardiovascular health. The discussion of emerging concepts, such as exosome-mediated intracellular communication in circadian physiology, offers new insights into the molecular mechanisms underlying brain-heart interactions. Furthermore, the exploration of diagnostic potential and therapeutic strategies, particularly chronotherapy, emphasizes the importance of targeting the circadian clock for disease prevention and treatment in cardiovascular medicine. This comprehensive assessment not only advances our understanding about circadian clock's role in cardiovascular health but also paves the way for innovative approaches in theranostic, ultimately improving patient outcomes.

心血管疾病是老年人发病的首要原因，老龄化破坏了正常的昼夜节律周期。昼夜节律由大脑视交叉上核调节，通过复杂的神经生物学机制深刻影响心血管健康。这些节律调节心肌细胞的基因表达，调节自主神经系统（ANS）的活动，并使心血管功能与环境信号同步，最终影响心率、血压和对心脏事件的易感性。昼夜节律与心血管健康之间的复杂关系强调了脑-心通讯在生理过程中的关键作用。本文综述了心血管疾病中生物钟的神经生物学，探讨了心血管组织中的外周时钟如何影响器官生理以及它们的破坏如何导致发病。研究将生物钟与心血管疾病联系起来的神经生物学途径，包括ANS功能、神经内分泌信号和炎症反应，强调了大脑和心脏之间的相互作用。通过探索调节生物钟的环境和生活方式因素，以及昼夜节律的性别差异，该综述提供了对这些因素如何影响心血管健康的全面理解。对新兴概念的讨论，如昼夜生理学中外泌体介导的细胞内通讯，为脑-心相互作用的分子机制提供了新的见解。此外，对诊断潜力和治疗策略的探索，特别是时间疗法，强调了在心血管医学中以生物钟为目标预防和治疗疾病的重要性。这项全面的评估不仅促进了我们对生物钟在心血管健康中的作用的理解，而且为创新的治疗方法铺平了道路，最终改善了患者的预后。

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引用次数: 0

Sleep and immune health: How dogs, goats and ‘factor S’ shaped a field 睡眠和免疫健康：狗、山羊和“S因素”如何塑造一个领域

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100118

Mark R. Opp , Luca Imeri

Chronic insufficient sleep kills! Although this statement has high ‘face validity’, it is only recently that empirical evidence existed to support it. There are now sufficient data for numerous meta-analyses and systematic reviews to demonstrate that chronic insufficient sleep is associated with many inflammatory pathologies that are a public health burden. As a result, it is now well accepted that sleep is important for physical and mental health. This awareness derives from research that began in the late 19th and early 20th centuries and continues to the present day. In this narrative review we trace this rich history within the context of the research contributions of Professor James Krueger and his colleagues. The historic and current research by Professor Krueger and colleagues is fundamental to the many ongoing pre-clinical and clinical research programs focused on all aspects of sleep and immune health.

长期睡眠不足会致命！虽然这种说法具有很高的“表面效度”，但直到最近才有经验证据支持它。现在有足够的数据进行大量的荟萃分析和系统综述，以证明慢性睡眠不足与许多炎症病理有关，这些炎症病理是公共卫生负担。因此，人们普遍认为睡眠对身心健康都很重要。这种意识源于始于19世纪末和20世纪初并持续至今的研究。在这篇叙述性评论中，我们在詹姆斯·克鲁格教授和他的同事的研究贡献的背景下追溯了这段丰富的历史。克鲁格教授及其同事的历史和当前研究是许多正在进行的临床前和临床研究项目的基础，这些研究项目专注于睡眠和免疫健康的各个方面。

引用次数: 0

Sleep and circadian disorders as risk factors for autoimmune disease: A population-based study 睡眠和昼夜节律紊乱是自身免疫性疾病的危险因素：一项基于人群的研究

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100129

Amber R. Li , Bhaavyaa Shah , Michael L. Thomas , Michael J. McCarthy , Alejandro D. Meruelo

Background

Sleep and circadian disruption have been increasingly linked to immune dysregulation, yet population-level associations with autoimmune disease remain underexplored. We examined whether delayed sleep phase disorder (DSPD), obstructive sleep apnea (OSA), primary insomnia, and hypersomnia were associated with autoimmune conditions in a large, diverse U.S. cohort.

Methods

Data were drawn from the All of Us Research Program Registered Tier Dataset v8. Participants were categorized into sleep disorder groups based on clinical diagnoses, with regular sleepers serving as controls. Autoimmune disease was defined using SNOMED-coded records. DSPD and primary insomnia were analyzed using rare disease logistic regression; OSA and hypersomnia were analyzed using 1:5 propensity score matching. Adjusted logistic regression models included age, sex at birth, race, ethnicity, income, BMI, and chronic inflammatory diagnosis. E-values assessed robustness to unmeasured confounding.

Results

All four sleep disorder groups showed significantly higher odds of autoimmune diagnosis relative to regular sleepers (p < 2.2 × 10⁻¹⁶). Adjusted odds ratios were: DSPD (OR = 0.26; 95 % CI: 0.15–0.45), OSA (OR = 0.46; 95 % CI: 0.41–0.52), primary insomnia (OR = 0.46; 95 % CI: 0.41–0.52), and hypersomnia (OR = 0.48; 95 % CI: 0.46–0.50). Older age, female sex, and chronic inflammation were associated with higher autoimmune prevalence. Asian race and BMI were inversely associated with autoimmune risk; higher income was unexpectedly associated with greater autoimmune diagnosis.

Conclusions

Distinct sleep phenotypes were associated with autoimmune conditions. These associations may reflect shared or bidirectional links between sleep disruption and immune dysregulation.

背景：睡眠和昼夜节律紊乱与免疫失调的联系越来越紧密，但在人群水平上与自身免疫性疾病的关联仍未得到充分探讨。我们研究了延迟睡眠阶段障碍（DSPD）、阻塞性睡眠呼吸暂停（OSA）、原发性失眠和嗜睡是否与自身免疫性疾病有关。方法数据来自All of Us Research Program注册Tier Dataset v8。根据临床诊断，参与者被分为睡眠障碍组，正常睡眠者作为对照组。自身免疫性疾病的定义使用snomed编码记录。采用罕见病logistic回归分析DSPD与原发性失眠症；采用1:5倾向评分匹配法对OSA和嗜睡症进行分析。调整后的logistic回归模型包括年龄、出生性别、种族、民族、收入、BMI和慢性炎症诊断。e值评估了对未测量混杂的稳健性。结果4个睡眠障碍组的自身免疫诊断率均高于正常睡眠组(p <；2.2 × 10−16)。调整后的优势比为：DSPD (OR = 0.26；95% ci: 0.15-0.45), osa (or = 0.46；95% CI: 0.41-0.52)，原发性失眠(OR = 0.46；95% CI: 0.41-0.52)和嗜睡症(OR = 0.48；95% ci: 0.46-0.50)。年龄较大、女性和慢性炎症与较高的自身免疫性患病率相关。亚洲人种和BMI与自身免疫风险呈负相关；高收入出乎意料地与更高的自身免疫诊断相关。结论不同的睡眠表型与自身免疫性疾病相关。这些关联可能反映了睡眠中断和免疫失调之间的共享或双向联系。

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引用次数: 0

The cell-intrinsic circadian clock is dispensable for lateral posterior clock neuron regulation of Drosophila rest-activity rhythms 果蝇休息-活动节律的外侧后时钟神经元调节，离不开细胞内的生物钟

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100124

Charlene Y.P. Guerrero, Madelyn R. Cusick, Amanda J. Samaras, Natalie S. Shamon, Daniel J. Cavanaugh

Circadian control of behavior arises from intercommunication among a distributed network of circadian clock neurons in the brain. Single-cell sequencing and brain connectome data support the division of the ∼240 brain clock neurons in Drosophila into ∼20 subclusters, and functional studies demonstrate that these populations differentially contribute to behavioral outputs. Here, we have used genetic tools that enable highly selective, cell-specific manipulations to investigate the role of molecular clock function and neuronal activity within the lateral posterior clock neurons (LPNs) in the regulation of rest-activity rhythms. We find that genetic silencing of these neurons, which compromises signaling with downstream neuronal targets, substantially reduces the strength of free-running rest-activity rhythms. In contrast, locomotor activity patterns are robust to CRISPR-mediated disruption of molecular clock cycling within the LPNs. We conclude that the LPNs act as driven oscillators that retain the capacity to transmit circadian information in the absence of cell-intrinsic molecular clocks.

行为的昼夜节律控制源于大脑中分布的昼夜节律时钟神经元网络之间的相互交流。单细胞测序和脑连接组数据支持果蝇约240个脑时钟神经元分为约20个亚簇，功能研究表明，这些群体对行为输出的贡献是不同的。在这里，我们使用了遗传工具，使高选择性，细胞特异性操作，以研究分子钟功能和神经元活动在外侧后时钟神经元（lpn）内调节休息-活动节律中的作用。我们发现，这些神经元的基因沉默会损害下游神经元目标的信号，从而大大降低自由运行的休息-活动节律的强度。相反，运动活动模式对crispr介导的lpn内分子时钟循环的破坏是稳健的。我们得出结论，lpn作为驱动振荡器，在缺乏细胞固有分子钟的情况下保留了传递昼夜节律信息的能力。

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引用次数: 0

Synergies from a distance: Inspirations from the struggles of Dr James M Krueger 远距离协同效应：来自詹姆斯·克鲁格博士奋斗的启示

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100114

William A. Banks

In this article for Dr Krueger's Festschrift, I trace how his early career influenced many aspects in the fields of sleep, neuroimmunology, and the microbiome. Mostly, however, I trace how his career and interests intertwined with those of Abba J. Kastin and mine and how he exerted a profound influence on the direction of our studies. Dr. Krueger, while developing his career as a sleep researcher, encountered resistance to his work that required two major paradigm shifts: 1) that bacterial products could affect sleep and 2) that small peptides can cross the blood-brain barrier (BBB) in sufficient amounts to affect brain functioning. Dr Kastin had also shown that small peptides administered peripherally could affect brain function and postulated that this was because they could cross the BBB. Our efforts to determine whether peptides could or could not cross the BBB were bolstered by Dr Krueger's exemplary struggles.

在这篇为克鲁格博士撰写的文章中，我追溯了他早期的职业生涯如何影响了睡眠、神经免疫学和微生物组等领域的许多方面。然而，我主要是追溯他的事业和兴趣是如何与阿巴·j·卡斯汀和我的事业和兴趣交织在一起的，以及他是如何对我们的研究方向产生深远影响的。克鲁格博士在发展自己的睡眠研究事业时，遇到了对他的工作的阻力，这需要他进行两个主要的范式转变：1)细菌产物可能影响睡眠；2)小肽可以通过血脑屏障（BBB），数量足够多，从而影响大脑功能。卡斯汀博士还指出，在外围注射小肽可以影响大脑功能，并推测这是因为它们可以穿过血脑屏障。我们努力确定肽是否能或不能通过血脑屏障是由克鲁格博士的示范斗争支持。

引用次数: 0

Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection 感染的先天免疫机制：我们所知道的和感染期间影响睡眠的潜在保守机制

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100121

Mark R. Zielinski , Sean D. Carey , John A. Craig

Evidence indicates relationships between sleep and the innate immune system during homeostatic sleep and sleep responses after infection. The innate immune system and sleep-like states are highly conserved between simple species and more complex species such as humans. A wide variety of bacteria, viruses, and parasites change sleep patterns in the host during infection. The effects of infection on sleep can occur, in part, due to the bolus and route of infection, prior exposure, immune status of the individual/organism, and the type of pathogen. In addition, elements of circadian patterns and sleep prior to and after infection can modulate the infection pathology and resolution. Innate immune molecules, such as the cytokines interleukin-1 beta and tumor necrosis factor-alpha, fluctuate with the time of day of increased activity and sleep propensity, increase in response to increased waking activity from sleep loss, and are altered from infection by bacteria and viruses to alter sleep and the electroencephalogram. This review focuses innate immune mechanisms of how pathogen recognition receptors, pathogen-associated molecular patterns and danger-associated molecular patterns, energy-related molecules, oxidative stress, and inflammasomes are activated with infection to potentially affect sleep.

有证据表明，在体内平衡睡眠和感染后的睡眠反应期间，睡眠与先天免疫系统之间存在关系。先天免疫系统和睡眠状态在简单物种和更复杂的物种（如人类）之间是高度保守的。在感染期间，各种各样的细菌、病毒和寄生虫会改变宿主的睡眠模式。感染对睡眠的影响部分是由于感染的剂量和途径、先前的暴露、个体/生物体的免疫状态以及病原体的类型。此外，感染前后的昼夜节律模式和睡眠因素可以调节感染的病理和解决。先天免疫分子，如细胞因子白细胞介素-1 β和肿瘤坏死因子α，随着一天中活动增加和睡眠倾向的时间而波动，对睡眠不足引起的清醒活动增加的反应增加，并因细菌和病毒感染而改变，从而改变睡眠和脑电图。本文综述了病原体识别受体、病原体相关分子模式和危险相关分子模式、能量相关分子、氧化应激和炎症小体在感染时激活的先天免疫机制，以潜在地影响睡眠。

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引用次数: 0

No association between chronotype and cardiovascular response to a cognitive challenge in the morning using a Bayesian approach 使用贝叶斯方法，睡眠类型与心血管对早晨认知挑战的反应之间没有关联

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100125

Larissa N. Wüst , Christian Cajochen , Ruta Lasauskaite

A chronotype is defined as a preference for certain behaviours (e.g., sleep and wake) to occur at specific times of day. It is therefore also temporally linked with cognitive performance across the day. In an exploratory analysis, we sought to find associations between chronotypes determined from self-reported habitual sleep timing and from salivary melatonin onset with mental effort during a 2-back working memory task. Mental effort was operationalized as sympathetic beta-adrenergic impact on the heart, which is best reflected by the cardiac pre-ejection period (PEP) and also influences systolic blood pressure (SBP). Each participant underwent two experimental sessions in the morning: once after sleeping for 8 h and once after sleeping for 5 h the night before. To determine the timing of evening melatonin onset, participants took saliva samples at hourly intervals at home in the evening, prior to their experimental sessions. Chronotypes were determined using reported sleep times from the Munich Chronotype Questionnaire and average melatonin onset during both sleep conditions. Based on this, participants were grouped into early, intermediate, or late types. Neither alertness (BF₁₀ = 0.019), perceived task demand (BF₁₀ = 0.008), nor SBP response (BF₁₀ = 0.268) were credibly impacted by sleep-time derived chronotype, while the association with PEP response (BF₁₀ = 0.631) during a cognitive challenge in the morning was inconclusive. Similarly, the timing of evening melatonin onset did not affect alertness (BF₁₀ = 0.003), perceived task demand (BF₁₀ = 0.006), or PEP or SBP response (PEP: BF₁₀ = 0.232, SBP: BF₁₀ = 0.263) during the cognitive challenge. Our data shows no impact of chronotypes on effort-related cardiovascular response during a cognitive challenge in the morning, which was scheduled according to habitual sleep times.

时间类型被定义为对特定行为（例如，睡眠和醒来）在一天中特定时间发生的偏好。因此，它也与一天中的认知表现有暂时的联系。在一项探索性分析中，我们试图发现自我报告的习惯性睡眠时间和唾液褪黑素在两回工作记忆任务中与精神努力之间的联系。精神努力被运作为对心脏的交感-肾上腺素能影响，这在心脏射血前期（PEP）中得到最好的反映，也影响收缩压（SBP）。每个参与者在早上进行两次实验：一次是在睡了8小时后，一次是在前一天晚上睡了5小时后。为了确定褪黑素在晚上起作用的时间，参与者在实验开始之前，每隔一小时在家里采集一次唾液样本。根据慕尼黑睡眠类型问卷报告的睡眠时间和两种睡眠状态下褪黑素的平均分泌量来确定睡眠类型。在此基础上，参与者被分为早期、中期和晚期。警觉性（BF10 = 0.019）、感知任务需求（BF10 = 0.008）和收缩压反应（BF10 = 0.268）均不受睡眠时间衍生时型的影响，而与早晨认知挑战时PEP反应（BF10 = 0.631）的关系尚无定论。同样，在认知挑战期间，夜间褪黑激素的发作时间并不影响警觉性（BF10 = 0.003）、感知任务需求（BF10 = 0.006）或PEP或SBP反应（PEP: BF10 = 0.232, SBP: BF10 = 0.263）。我们的数据显示，在早晨的认知挑战中，生物钟类型对与努力相关的心血管反应没有影响，这是根据习惯睡眠时间安排的。

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引用次数: 0

Sleep in disease: inflammation and chronic rhinosinusitis 睡眠中的疾病：炎症和慢性鼻窦炎

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100120

Vivek C. Pandrangi , Jeremiah A. Alt

Chronic rhinosinusitis (CRS) is a common inflammatory disorder that is associated with significant quality of life (QOL) impairment, including sleep dysfunction. There are multiple factors that have been independently associated with poor sleep among this population including alterations in inflammatory mediators, rhinologic symptom interference such as nasal discharge, obstruction, and facial pain, and co-morbid conditions including asthma. While there is a high prevalence of sleep dysfunction among this population, treatment with both medical and surgical options may lead to sustained improvements in sleep. This review aims to highlight the burden of sleep dysfunction, discuss common theories regarding the etiology, and evaluate strategies that may facilitate improvement in sleep dysfunction among patients with CRS.

慢性鼻窦炎（CRS）是一种常见的炎症性疾病，与显著的生活质量（QOL）损害相关，包括睡眠障碍。在这一人群中，有多种因素与睡眠不良独立相关，包括炎症介质的改变、鼻症状的干扰，如鼻溢液、梗阻和面部疼痛，以及包括哮喘在内的合并症。虽然这一人群中睡眠障碍的患病率很高，但药物和手术治疗可能会导致睡眠的持续改善。本综述旨在强调睡眠功能障碍的负担，讨论有关病因的常见理论，并评估可能有助于改善CRS患者睡眠功能障碍的策略。

引用次数: 0