Changes in athletes' brain network connections during isometric muscle contractions after sleep restriction.

Paeoniflorin alleviates anxiety-like behaviors in sleep-deprived male mice by suppressing inflammation of the paraventricular nucleus of the hypothalamus.

Sleep disturbance is thought to impair immune regulation and reduce the effectiveness of cancer immunotherapies such as immune checkpoint blockade, but the mechanisms in colorectal cancer are not well defined. This study investigated how recurrent sleep deprivation influences colon cancer progression and immune responses, with particular attention to the role of Galectin-9. A murine CT26 colon carcinoma model was established to examine tumor growth dynamics and host immune responses under scheduled cycles of sleep deprivation. For tumor implantation, mice were injected with CT26 cells stably transduced to overexpress Galectin-9 (Gal-9 OE) or with vector-transduced wild-type control CT26 cells. Immune phenotyping was conducted using flow cytometry, and chromatin immunoprecipitation assays were employed to assess regulatory mechanisms at the Gal-9 promoter. To further evaluate therapeutic potential, a bispecific CD3/Gal-9 antibody was administered to determine its capacity to restore immune activity and restrain tumor growth under sleep-disrupted conditions. Sleep deprivation significantly increased tumor burden and induced immune suppression, characterized by elevated Gal-9 expression, increased regulatory T cell infiltration, and diminished cytotoxic T cell activity. Treatment with the bispecific CD3/Gal-9 antibody reversed these effects, reducing tumor growth and enhancing antitumor immune responses in Gal-9-overexpressing tumors. Sleep deprivation promotes immune evasion and reduces ICB efficacy in colorectal cancer through Gal-9-mediated pathways. Targeting Gal-9 with bispecific antibodies may represent a viable approach to restore immune competence in sleep-disrupted conditions. These findings highlight the importance of sleep quality in cancer progression and suggest that integrating lifestyle interventions with immunotherapy may improve clinical outcomes.

High-resolution mapping reveals frequency-specific alterations in phase amplitude coupling after sleep deprivation.

Sleep deprivation (SD) and excessive light exposure (LD) are increasingly prevalent stressors in modern life, yet their combined impact on retinal integrity remains unclear. This study investigates how SD amplifies LD-induced retinal injury and explores the mechanistic role of ferroptosis-a regulated, iron-dependent form of lipid peroxidation-driven cell death. We established a dual-stressor mouse model with four groups: control, SD, LD, and SD+LD. Retinal structure and function were evaluated via OCT, ERG, histology, and behavioral tests. Mechanistic insights were obtained from transcriptomic profiling, immunostaining, electron microscopy, and pharmacological inhibition using Liproxstatin-1 (Lip-1). While SD alone caused no overt damage, SD+LD synergistically exacerbated retinal degeneration. Transcriptomic and molecular analyses revealed pronounced ferroptosis activation in the SD+LD group-marked by reduced antioxidant defenses (↓GPX4, xCT, GCH1, FSP1), elevated lipid peroxidation (↑4-HNE, MDA, ALOX15, ACSL4), disrupted iron homeostasis (↑HO-1, ↓FPN, ↓FTH1), and mitochondrial shrinkage. Lip-1 treatment reversed these changes and preserved retinal function. Short-term sleep deprivation exacerbated light-induced retinal injury by promoting ferroptosis, as indicated by disrupted antioxidant capacity, enhanced lipid peroxidation, and disturbed iron homeostasis. Treatment with Lip-1 substantially attenuated these changes.

Gut-derived IL-17A via STAT3/RORγt signaling underlies sleep disruption-induced depression: Targeting effects of Schisandrin B therapy.

A Rhodiola-derived acidic glycopeptide maintains sleep homeostasis by regulating brain lipid metabolism in Drosophila.

Weight self-stigma and associated factors among primary school students in Linhai, China: a cross-sectional study.

Studies in mammal models show that reduced sleep is associated with increased food intake. Zebrafish (Danio rerio) is emerging as a promising model for studying sleep and feeding behaviour due to its similarities with mammals. Our goal was to investigate whether sleep restriction increases food intake in zebrafish, its potential effects on central regulation of feeding, and whether effects are similar in both sexes. Individually housed male and female adult zebrafish were exposed to nighttime (ND) or daytime (DD) vibrations and compared to a control group without vibration (n = 30 males and n = 27 females). ND, but not DD, reduced sleep during the disturbance period, with males showing a significant effect and females exhibiting an altered sleep pattern without a statistically significant reduction. ND also significantly increased food intake in males, as measured by daily milligrammes and number of pellets consumed. In contrast, ND females exhibited a decrease in the time spent feeding, suggesting a sex-specific response to sleep disruption. The whole brain expression of neuropeptide Y (npy), proopiomelanocortin (pomc), and its receptor melanocortin-4 (mc4r) were analysed by RT-qPCR. Males from ND exhibited significantly reduced pomc mRNA levels. Grouped-housed (three male and two female) zebrafish exposed to ND also exhibited increased food intake. In conclusion, sleep restriction affected food intake behaviour and the central regulation in zebrafish, with distinct sex-specific effects.

Cognitive performance is significantly affected by sleep, but mild chronic sleep deprivation in daily life remains difficult to measure. Laboratory-enforced sleep restriction may not fully replicate real-life conditions. This study investigates whether Social Jet Lag (SJL), an indicator of misalignment between biological and social time, can used as a proxy for mild chronic sleep deprivation and its impact on cognitive function. Participants leading typical social lives were selected based on their SJL scores, and cognitive performance was assessed using an online experiment incorporating a Psychomotor Vigilance Task (PVT) and a Sustained Attention to Response Task (SART) at different times (post-wake and pre-sleep) and across multiple days (Sunday, Monday, and Friday). Generalised linear modelling (GLM) revealed that SJL was consistently the most explanatory factor for cognitive performance, while test timing also had a significant impact. Cognitive performance impairments due to SJL remained stable across days, suggesting a stable influence of sleep timing irregularity. Additionally, SJL was associated with increased false-positive rates in the SART, indicating reduced response inhibition ability. While SJL proved to be a useful measure compared to average sleep duration and the Sleep Regularity Index (SRI), its effectiveness may be specific to populations following structured work schedules.

Sequential associations among perceived heat-related symptoms, fatigue, and performance-related behavior during summer training.

In combat and sport, there is an urgent need to identify readiness for performance to decide on removal from and return to activity. Cognitive readiness, including attention, can be impaired for many potentially coexisting reasons, including concussive or subconcussive injury, insufficient sleep/fatigue, and intoxication. Standard tests of concussion, sleep deprivation, and intoxication are often lengthy or require specialized skill or equipment to conduct. The ideal readiness screen should predict readiness or be associated with surrogate measures of readiness, be sensitive to multiple conditions that may impair readiness, and be reliable and rapid. This study outlines the methodology for an evidence-based process to develop multimodal rapid screening tests for readiness that are applicable across a broad range of environments, including military far-forward/sports sideline, garrison, and clinic.

Sleep is a fundamental process supporting the dynamic regulation of neural function. Emerging methods have proposed that the aperiodic components of brain signals (such as the spectral slope, spectral intercept, and spectral knee), in addition to entropy-based measures, offer robust empirical markers of neural states. The present study investigates the sensitivity of these broadband spectral metrics in comparison to classical band-limited measures, specifically slow wave activity (SWA; 0.75-4.5 Hz), in a 9-day mouse sleep deprivation paradigm involving baseline, sleep restriction, and recovery phases (open-source database). Spectral parameters were computed using the FOOOF algorithm. Results indicate that SWA differentiates between baseline and rebound sleep only during NREM episodes. In contrast, both the spectral slope and spectral intercept capture sleep deprivation-related changes during both REM and NREM sleep, suggesting these fractal measures reflect sleep homeostasis across stages. Given the shift of the spectral knee towards higher frequencies in mice (~8-10 Hz) as compared to humans (generally around 1 Hz), eliminating the overlap of the spectral slope with the traditional SWA range in these rodents, homeostatic regulation appears to be not strictly bounded to the lower frequencies (0.75-4.5 Hz). Normalised spectral entropy did not differentiate between baseline and recovery sleep, potentially due to its sample size sensitivity. These findings support the empirical utility of broadband spectral parameters in assessing sleep-wake dynamics and highlight their potential to complement or surpass traditional band-limited metrics.

Cognition in the time of dysbiosis: Sleep disruption and the gut-brain dialogue.

This review describes the evaluation, diagnosis, and management of less-common etiologies of postpartum headache, and offers a systematic approach to the evaluation, diagnosis, and treatment of the parturient with this very common complaint. Approximately 40% of parturients develop a headache in the immediate postpartum period, with roughly half of these attributable to an underlying etiology or disorder. Unfortunately, the confounding nature of the postpartum state, with attendant fatigue, stress, sleep deprivation, and other derangements of normal physiology, and the heterogeneity of postpartum disorders leading to headache, often delay diagnosis of these rare forms of headache. Although postdural puncture headache and headache as a symptom of preeclampsia comprise the majority of "secondary" postpartum headaches, other less-common causes of postpartum headache include headaches caused by cerebral vascular abnormalities, hemorrhagic processes, or mass effects/space-occupying lesions. Many of these less-common headaches herald serious underlying disorders that present a significant threat to patient health and require prompt diagnosis and treatment.

Why do we sleepwalk? A noradrenergic hypothesis of NREM sleep parasomnias.

Sleep quality and social isolation are two of the numerous environmental, social and health-related factors that contribute to major depressive disorder (MDD). In human studies, a strong association has been found between sleep quality and perceived loneliness, with each potentially exacerbating the other. In mouse studies, sleep deprivation is performed on either group-housed or individually housed mice, depending on the protocol, but the effect of social isolation is often not assessed. Here, we aimed to investigate the potential synergistic effects of sleep disturbances and social isolation in adolescent (Postnatal day 36) and young adult (9 weeks old) female mice. The mice were subjected to sleep disturbances for 7 days, consisting of 4 h of sleep restriction during the light phase, while group- or single-housed for 7 days. Both the individual and combined effects of sleep disturbance and social isolation were assessed. Our findings reveal significantly longer immobility in the tail suspension test in young adult mice after 7 days of sleep disturbance + social isolation compared to those in the sleep disturbance + socially housed group. The same effect was not seen with adolescent mice. This interaction between sleep disturbance and social isolation in the young adult group suggests a synergistic effect. In conclusion, single housing of mice can change the behavioural outcome of a sleep disturbance protocol. Further, adolescent mice appeared more resilient to the adverse behavioural effects of sleep disturbance in combination with social isolation than young adult mice.

Effects of Dendrobium officinale on chronic fatigue in rats: Modulation of tryptophan metabolism.

Poor sleep health is common among university students, but there are diverging viewpoints on whether their sleep loss helps, harms, or has no impact on academic performance. We investigated whether sleep health markers in first-year university students predicted longitudinal academic outcomes when accounting for key variables. First-year university students who were pursuing a science, technology, engineering, and mathematics (STEM) career pathway (n = 489) were recruited to complete a baseline session that included measures of global sleep quality, chronotype, daytime sleepiness, social jetlag (change in sleep timing from weekdays to weekends), demographics, mental health, and fluid intelligence (reasoning). At the end of year 1 and year 2, we extracted data on cumulative grade-point average (GPA), academic major change, STEM pathway change, and institutional withdrawal. After adjusting for demographic, mental health, and fluid intelligence factors, we observed that worse global sleep quality, evening chronotype, and worse social jetlag independently predicted year 1 GPA. Global sleep quality also predicted year 2 GPA, even when accounting for prior academic performance. Students with shorter sleep durations were more likely to switch from their STEM career pathway, even when accounting for academic performance, demographics, mental health, and fluid intelligence. In conclusion, sleep health markers are predictive of better future academic performance and retention in STEM pathways. There is a need for individual and environmental interventions to improve sleep health in first-year students and to determine causal direction.NEW & NOTEWORTHY Many believe that science, technology, engineering, and mathematics (STEM) students must sacrifice their sleep to achieve academic success. In striking contrast, the current research demonstrates that better sleep health in freshmen STEM majors predicted better academic success, even after accounting for mental health, fluid intelligence, and prior academic performance. The current work was the first to document that sleep health predicted better persistence in a STEM track across 2 yr.

Sleep serves as a fundamental regulator of brain functions, integrating processes of neuroplasticity, metabolic homeostasis, and immune surveillance. Among the diverse immune constituents implicated in these dynamics, microglia and T cells have emerged as pivotal effectors, whose activities are finely tuned to sleep-wake rhythms. These cell populations exert significant regulatory influence over neuronal excitability, synaptic integrity, and behavioral expression. Their functional states are governed by intrinsic circadian mechanisms as well as extrinsic environmental cues, while their transcriptional and phenotypic landscapes are modulated by epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. Perturbations in sleep architecture due to chronic sleep deprivation, circadian disruption or neuroinflammatory conditions can induce epigenetic reprogramming in both microglia and T cells leading to aberrant immune activation, defective synaptic maintenance, and cognitive impairment. This review synthesizes emerging evidence that delineates the intricate connections between sleep dynamics and the epigenetic regulation of neuroimmune function, with particular emphasis on the coordinated roles of microglia and T cells in maintaining central nervous system (CNS) homeostasis. A deeper mechanistic understanding of these regulatory networks is indispensable for developing targeted therapeutic interventions that modulate neuroimmune interactions in sleep-associated neurological and psychiatric disorders.