This study aims to elucidate the pathways through which Yiyin Anshen Granule (YA) exerts sedative-hypnotic effects in a mouse model of sleep deprivation. DL-4-chlorophenylalanine(PCPA)-treated mice received intragastric administration of YA and pentobarbital sodium-induced sleep tests were conducted on days 7, 14, and 29. The levels of key neurotransmitters, cytokines and receptor protein associated with insomnia were measured using enzyme-linked immunosorbent assay (ELISA) and Western blot. Additionally, 16S ribosomal DNA (rDNA) sequencing was performed to assess the impact of YA on gut microbiota, focusing on species abundance and diversity. YA significantly shortened sleep latency (P < 0.01) and prolonged sleep duration (P < 0.01) in sleep-deprived mice, effectively improving circadian rhythm disturbances compared to the model group (MOD). Biochemical analysis revealed that YA restored abnormal neurotransmitter levels in brain tissue, increasing 5-hydroxytryptamine (5-HT), γ-aminobutyric acid (GABA), and γ-aminobutyric acid type A receptor α-1 subunit (GABAARα1) expression (P < 0.01) and reducing the glutamate (Glu)/GABA ratio (P < 0.01). Additionally, the levels of B-cell lymphoma 2 (BCL-2) and interleukin-6 (IL-6) expression were significantly decreased (P < 0.05, 0.01), while interleukin-1 beta (IL-1β) expression increased (P < 0.01). YA treatment also significantly increased gut microbiota abundance and diversity, with microbiome profiles in the YA group being closer than those of diazepam group (DZP) to the control group (CON). Notably, YA reversed the dysbiosis of high-abundance gut microbiota species associated with insomnia at both the family and genus levels (P < 0.05, 0.01). The results of the present study indicated that YA alleviates insomnia symptoms by regulating neurotransmitter and inflammatory cytokines levels, and restoring gut microbia balance. These mechanisms collectively contribute to shortening sleep latency, prolonging sleep duration, and improving sleep quality in a mouse model of insomnia.

Postpartum sleep disorder and mental disorders are common unpleasant conditions faced by women after delivery, and they have many adverse effects on both mothers and infants. It is unclear whether breast milk composition is affected by maternal sleep, psychological state, diet and gut microbiome. This study aims to explore the effects of these key factors on the functional protein components of breast milk.

With a prospective design, this pilot study included a total of 41 postpartum women. Breast milk and maternal faecal samples collected at 42 days and 3 months postpartum were tested by liquid chromatography-mass spectrometry and 16S RNA sequencing, respectively. Sleep state, psychological state and dietary intake data were also collected from the mothers with validated questionnaires.

In the early postpartum period, sleep disorders and depression were associated with a decrease in the functional proteins in breast milk. Disordered sleep was significantly negatively correlated with α-lactalbumin (cor = -0.578, p < 0.001), osteopontin (cor = -0.522, p < 0.01) and κ-casein (cor = -0.451, p < 0.01). Depression was negatively correlated with αs1-casein (cor = -0.422, p < 0.01), β-casein (cor = -0.317, p < 0.05) and casein (cor = -0.318, p < 0.05). In 3 months postpartum, most associations were disappeared. But a positive correlation was observed between β-casein (cor = 0.414, p < 0.01), casein (cor = 0.372, p < 0.05), total protein (cor = 0.376, p < 0.05) and depression, while a positive correlation was found between total protein (cor = 0.357, p < 0.05) and disordered sleep at 3 months postpartum. Faecal microbiome data illustrated that changes in the gut microbiome at early postpartum were associated with sleep disorders/depression, but not with the diet. Furthermore, functional pathway analysis revealed metabolic regulation in the amino acid synthesis and metabolic pathways associated with specific microbes was involved in the reduction of breast milk protein.

Sleep disorders/depression could lead to significant changes in breast milk profiles at 42 days postpartum. Maternal gut microbiome might affect breast milk protein composition through regulating amino acid synthesis and metabolic pathways.

Adequate sleep is critical for nurses, affecting their physical, emotional, and occupational health. Nurses suffer from higher levels of sleep disorders than the national average, especially night-shift nurses, with rates as high as 61%. Irregular work/sleep patterns and occupational stress are the main contributors to inadequate sleep for nurses. Not only does this issue impact nurses, but insufficient sleep has been linked to billions of dollars lost due to decreased productivity and medical errors.

This integrative review explores and evaluates existing research on nonpharmacologic interventions designed to improve sleep function and quality for nurses.

A systematic search was performed to find research interventions that improved nurses' sleep. CINAHL, Scopus, and OVID Medline databases were searched using the terms (sleep OR circadian rhythm) AND (intervention OR sleep hygiene) AND (nurs*). After the initial search, reference lists and secondary sources were evaluated for potential articles for inclusion.

This review included 33 articles. Interventions included exercise, lighting manipulation, supplements, aromatherapy, education, music therapy, and mindfulness/meditation. All 7 exercise interventions included in this review improved participants' sleep length and quality. Nearly all mindfulness and aromatherapy interventions that promote relaxation and stress reduction were effective. Exposing nurses to bright light did not necessarily correlate with increased sleep but did improve fatigue levels at work.

Prioritizing sleep can ensure the health and safety of nurses, and further research is still needed. Health care organizations can positively impact this problem by implementing effective practices to improve the sleep health of nurses.

Parkinson's Disease (PD), a complex neurodegenerative disorder, is increasingly recognized as a systemic condition involving multi-organ interactions. Emerging evidence highlights roles of organ-brain axes (lung-, liver-, heart-, muscle-, bone-, and gut-brain) in PD pathogenesis. These axes communicate via neural, circulatory, endocrine, and inflammatory pathways, collectively driving neurodegeneration. For example, lung dysfunction in PD involves respiratory impairment and inflammatory signaling, while gut dysbiosis triggers α-synuclein aggregation via the vagus nerve. Such cross-organ interactions underscore PD's systemic nature, challenging traditional brain-centric models.

1. Decipher mechanisms linking peripheral organs (e.g., lung, gut) to PD via shared pathways. 2. Explore bidirectional organ-brain interactions (e.g., liver metabolism affecting neurotoxin clearance). 3. Propose multi-organ therapeutic strategies targeting integrated signaling networks. Key Scientific Concepts of Review. 1. Lung-Brain Axis: Respiratory dysfunction (motor impairment, inflammation) exacerbates neurodegeneration. 2. Liver-Brain Axis: Metabolic dysregulation alters neurotoxin clearance; drugs (e.g., levodopa) impact liver function. 3. Heart-Brain Axis: Autonomic dysfunction reduces cerebral blood flow; neuroendocrine changes promote α-synuclein pathology. 4. Muscle-Brain Axis: Neuromuscular/metabolic disruptions worsen motor symptoms. 5. Bone-Brain Axis: Bone-derived hormones (osteocalcin, OCN) and inflammation influence cognition. 6. Gut-Brain Axis: Dysbiosis drives α-synuclein misfolding; gut metabolites modulate neuroinflammation. Integrated Mechanisms: Shared pathways (neuroinflammation, oxidative stress) create a regulatory network, suggesting therapies targeting multi-organ crosstalk (e.g., probiotics, anti-inflammatory agents).

The gut-brain axis has emerged as a key player in the regulation of brain function and cognitive health. Gut microbiota dysbiosis has been observed in preclinical models of Alzheimer's disease and patients. Manipulating the composition of the gut microbiota enhances or delays neuropathology and cognitive deficits in mouse models. Accordingly, the health status of the animal facility may strongly influence these outcomes. In the present study, we longitudinally analyzed the fecal microbiota composition and amyloid pathology of 5XFAD mice housed in a specific opportunistic pathogen-free (SOPF) and a conventional facility. The composition of the microbiota of 5XFAD mice after aging in conventional facility showed marked differences compared to WT littermates that were not observed when the mice were bred in SOPF facility. The development of amyloid pathology was also enhanced by conventional housing. We then transplanted fecal microbiota (FMT) from both sources into wild-type (WT) mice and measured memory performance, assessed in the novel object recognition test, in transplanted animals. Mice transplanted with microbiota from conventionally bred 5XFAD mice showed impaired memory performance, whereas FMT from mice housed in SOPF facility did not induce memory deficits in transplanted mice. Finally, 18 weeks of housing SOPF-born animals in a conventional facility resulted in the reappearance of specific microbiota compositions in 5XFAD vs WT mice. In conclusion, these results show a strong impact of housing conditions on microbiota-associated phenotypes and question the relevance of breeding preclinical models in specific pathogen-free (SPF) facilities.

Housing conditions affect the composition of the gut microbiota. Gut microbiota of 6-month-old conventionally bred Alzheimer's mice is dysbiotic. Gut dysbiosis is absent in Alzheimer's mice housed in highly sanitized facilities. Transfer of fecal microbiota from conventionally bred mice affects cognition. Microbiota of mice housed in highly sanitized facilities has no effect on cognition.

Insomnia with objective short sleep duration is associated with increased hypertension risk. We aimed to explore the mechanism underlying the association between objective short sleep duration and hypertension in patients with chronic insomnia disorder (CID) by multi-omics.

CID was defined according to International Classification of Sleep Disorders-3, and objective short sleep duration was based on the median value of total sleep time of the overall subjects during an overnight polysomnography. We used the mean values of measured nighttime and morning systolic (SBP) and diastolic blood pressure (DBP) for analysis. Serum metabolomics and fecal 16S rDNA amplicon sequencing were used to explore characteristic metabolites and analyze gut microbiota distribution, respectively.

One hundred and three patients with CID and 70 normal sleepers were included. We found 52 objective short sleep duration insomnia phenotype (ISSD)-related serum metabolites. Among the 52 ISSD-related serum metabolites, indoxyl sulfate was positively correlated with BP after adjusting for confounding factors (SBP: β = 0.250, p = .028; DBP: β = 0.256, p = .030) in ISSD. In addition, the level of serum indoxyl sulfate was significantly correlated with the genera Prevotella 9 (r = .378, p = .027), CAG-56 (r = -.359, p = .037), Ruminiclostridium 9 (r = -.340, p = .049), and Ruminococcus 2 (r = -.356, p = .039) in ISSD.

Our study suggests that the ISSD phenotype is associated with significant changes in serum metabolic profile, including high levels of indoxyl sulfate. The latter molecule correlates both with BP and gut microbiota in patients with the ISSD phenotype, suggesting that indoxyl sulfate may be the molecular path resulting in increased hypertension risk in this phenotype.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex disorder characterized by persistent fatigue and cognitive impairments, with emerging evidence highlighting the role of gut health in its pathophysiology. The main objective of this review was to synthesize qualitative and quantitative data from research examining the gut microbiota composition, inflammatory markers, and therapeutic outcomes of interventions targeting the microbiome in the context of ME/CFS.

The data collection involved a detailed search of peer-reviewed English literature from January 1995 to January 2025, focusing on studies related to the microbiome and ME/CFS. This comprehensive search utilized databases such as PubMed, Scopus, and Web of Science, with keywords including "ME/CFS," "Gut-Brain Axis," "Gut Health," "Intestinal Dysbiosis," "Microbiome Dysbiosis," "Pathophysiology," and "Therapeutic Approaches." Where possible, insights from clinical trials and observational studies were included to enrich the findings. A narrative synthesis method was also employed to effectively organize and present these findings.

The study found notable changes in the gut microbiota diversity and composition in ME/CFS patients, contributing to systemic inflammation and worsening cognitive and physical impairments. As a result, various microbiome interventions like probiotics, prebiotics, specific diets, supplements, fecal microbiota transplantation, pharmacological interventions, improved sleep, and moderate exercise training are potential therapeutic strategies that merit further exploration.

Interventions focusing on the gut-brain axis may help reduce neuropsychiatric symptoms in ME/CFS by utilizing the benefits of the microbiome. Therefore, identifying beneficial microbiome elements and incorporating their assessments into clinical practice can enhance patient care through personalized treatments. Due to the complexity of ME/CFS, which involves genetic, environmental, and microbial factors, a multidisciplinary approach is also necessary. Since current research lacks comprehensive insights into how gut health might aid ME/CFS treatment, standardized diagnostics and longitudinal studies could foster innovative therapies, potentially improving quality of life and symptom management for those affected.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease worldwide, leading to substantial disease burden globally. Whether sleep duration is associated with the risk of MASLD, cirrhosis, hepatocellular carcinoma (HCC), and liver-related mortality remains underexplored.

A total of 489,261 middle-aged and older adults from the UK Biobank without prior liver diseases were included. The primary outcome was MASLD, with secondary outcomes, including cirrhosis, HCC, and liver-related mortality ascertained through linked hospital records and death registries. Sleep duration was self-reported at baseline survey and categorized into ≤ 5, 6, 7, 8 and ≥ 9 hours.

During a median (IQR) follow-up of 13.8 (1.5) years, 7,133 MASLD, 5,527 cirrhosis, 1,126 HCC, and 1,125 liver-related mortality cases were identified. After adjusting for potential confounders, the HRs [95% CIs] of MASLD were 1.44 [1.32;1.57], 1.17 [1.09;1.24], 1.00 (reference), 1.05 [0.99;1.11] and 1.35 [1.24;1.46] for ≤ 5, 6, 7, 8 and ≥ 9 hours of sleep duration, respectively. Similar trends were also observed for cirrhosis, HCC, and liver-related mortality. In addition, the U-shaped association between sleep duration and MASLD was more pronounced among participants without abnormal body mass index (overweight and obese), hypertension or insomnia (P for interaction <0.05).

Both short and long sleep duration are associated with an increased risk of MASLD, cirrhosis, HCC, and liver-related mortality. Maintaining a moderate sleep duration of 7 to 8 hours per day could be crucial to prevent against this escalating public health concern.

Over the past few decades, obesity has transitioned from a localized health concern to a pressing global public health crisis affecting over 650 million adults globally, as documented by WHO epidemiological surveys. As a chronic metabolic disorder characterized by pathological adipose tissue expansion, chronic inflammation, and neuroendocrine dysregulation that disrupts systemic homeostasis and impairs physiological functions, obesity is rarely an isolated condition; rather, it is frequently complicated by severe comorbidities that collectively elevate mortality risks. Despite advances in nutritional science and public health initiatives, sustained weight management success rates and prevention in obesity remain limited, underscoring its recognition as a multifactorial disease influenced by genetic, environmental, and behavioral determinants. Notably, the escalating prevalence of obesity and its earlier onset in younger populations have intensified the urgency to develop novel therapeutic agents that simultaneously ensure efficacy and safety. This review aims to elucidate the pathophysiological mechanisms underlying obesity, analyze its major complications-including type 2 diabetes mellitus (T2DM), cardiovascular diseases (CVD), non-alcoholic fatty liver disease (NAFLD), obesity-related respiratory disorders, obesity-related nephropathy (ORN), musculoskeletal impairments, malignancies, and psychological comorbidities-and critically evaluate current anti-obesity strategies. Particular emphasis is placed on emerging pharmacological interventions, exemplified by plant-derived natural compounds such as berberine (BBR), with a focus on their molecular mechanisms, clinical efficacy, and therapeutic advantages. By integrating mechanistic insights with clinical evidence, this review seeks to provide innovative perspectives for developing safe, accessible, and effective obesity treatments.

Sleep disorders have become a global social problem that increases the risk of developing mental illnesses and metabolic diseases. We aimed to identify biomarkers with which to non-invasively and objectively evaluate chronic sleep disorders. We used capillary electrophoresis-Fourier transform mass spectrometry (CE-FTMS) to analyze metabolomes in saliva collected from 50 persons each with good (≤ 2) and poor (≥ 6) sleep quality scored according to the Japanese version of the Pittsburgh Sleep Quality Index (PSQI-J) self-report questionnaire. The levels of five metabolites including glycerol and hippuric acid and eight including 2-hydroxybutyric acid (2HB), were respectively decreased and increased in participants with poor sleep quality. We established a random forest model consisting of six metabolites, including glycerol and hippuric acid, with a prediction accuracy of 0.866. Correlations between metabolites and sleep satisfaction were assessed using the Oguri-Shirakawa-Azumi sleep inventory, middle-age and aged version (OSA-MA) questionnaire. The results showed that 2'-deoxyguanosine, N1-acetylspermine, and 2,4-dihydroxybenzoic acid correlated positively, whereas glucosamine 6-phosphate and trimethylamine N-oxide correlated negatively with sleep quality. These findings suggested that changes in salivary metabolites reflect pathophysiological mechanisms of chronic sleep disorders, and that saliva samples could serve as non-invasive and objective diagnostic targets for predicting habitual sleep quality.

This study investigated the longitudinal effects of acute (7-day) and prolonged (3-month) high-altitude exposure on gut microbiota in healthy adult males, addressing the limited data available in human populations. A cohort of 406 healthy adult males was followed, and fecal samples were collected at three time points: baseline at 800 m (406 samples), 7 days after ascending to 4,500 m (406 samples), and 2 weeks post-return to 800 m following 3 months at high altitude (186 samples). High-throughput 16S ribosomal DNA sequencing was employed to analyze microbiota composition and diversity. Results revealed significant changes in alpha- and beta-diversity, with acute high-altitude exposure inducing more pronounced effects compared to prolonged exposure. Specifically, acute exposure increased opportunistic pathogens (Ruminococcus and Oscillibacter) but decreased beneficial short-chain fatty acid producers (Faecalibacterium and Bifidobacterium). Notably, these changes in microbiota persisted even after returning to low altitude, indicating long-term remodeling. Functional analyses revealed substantial changes in metabolic pathways, suggesting microbiota-driven adaptations to energy utilization under high-altitude hypoxic conditions. In summary, acute high-altitude exposure caused dramatic changes in gut microbiota, while prolonged exposure led to structural and functional reshaping. These findings enhance our understanding of how high-altitude environments reshape gut microbiota.

This study is the first to investigate the impact of high-altitude exposure on gut microbiota adaptation in a large-scale longitudinal cohort. It seeks to enhance understanding of how high-altitude environments reshape gut microbiota. Acute exposure to high altitude significantly affected both α-diversity and β-diversity of gut microbiota, with acute exposure causing more pronounced changes than prolonged adaptation, indicating temporary disruptions in microbial communities. Notable shifts in microbial abundance were observed, including increased levels of genera linked to hypoxic stress (e.g., Gemmiger, Ruminococcus, and Parabacteroides) and decreased levels of beneficial bacteria (e.g., Faecalibacterium, Roseburia, and Bifidobacterium), suggesting possible adverse health effects. Functional analysis indicated changes in metabolism-related pathways post-exposure, supporting the idea that high-altitude adaptations involve metabolic adjustments for energy management. These findings enhance understanding of high-altitude physiology, illustrating the role of gut microbiota in hypoxic health.

Insomnia, a prevalent sleep disorder, significantly impacts global health. While Western medications provide temporary relief, their risks of dependency and cognitive impairment have spurred the search for safer alternatives. Traditional Chinese Medicine (TCM) offers a promising approach to treating insomnia by focusing on harmonizing the balance of Yin and Yang and the functions of internal organs. This review explores recent research advances in TCM for insomnia treatment, integrating classical theories with modern scientific understanding of key pathological mechanisms, including neurotransmitter regulation (GABA, monoamines), immune-inflammatory responses, the HPA axis, and interactions with the gut microbiota. Growing clinical evidence supports the effectiveness of classical TCM prescriptions and treatments like acupuncture in improving sleep quality, particularly when combined with Western medications to enhance efficacy and reduce dependency. However, TCM also has its limitations. Future research directions should focus on modernizing TCM applications, addressing comorbidities associated with insomnia, exploring the role of gut microbiota, and optimizing medicinal and edible homologous products. By integrating traditional knowledge with cutting-edge technologies, TCM holds great potential for advancing personalized and effective insomnia treatments globally.

Ultra-processed food (UPF) consumption has been linked to adverse metabolic outcomes, potentially mediated by alterations in gut microbiota and metabolite production.

This study aims to explore the cross-sectional and longitudinal associations between NOVA-classified UPF consumption, fecal microbiota, and fecal metabolome in a population of Mediterranean older adults at high cardiovascular risk.

A total of 385 individuals, aged between 55 and 75 years, were included in the study. Dietary and lifestyle information, anthropometric measurements, and stool samples were collected at baseline and after 1-year follow-up. Fecal microbiota and metabolome were assessed using 16 S rRNA sequencing and liquid chromatography-tandem mass spectrometry, respectively.

At baseline, higher UPF consumption was associated with lower abundance of Ruminococcaceae incertae sedis (β = - 0.275, P = 0.047) and lower concentrations of the metabolites propionylcarnitine (β = - 0.0003, P = 0.013) and pipecolic acid (β = - 0.0003, P = 0.040) in feces. Longitudinally, increased UPF consumption was linked to reduced abundance of Parabacteroides spp. after a 1-year follow-up (β = - 0.278, P = 0.002).

High UPF consumption was associated with less favorable gut microbiota and metabolite profiles, suggesting a possible link to reduced short-chain fatty acid (SCFA) production, altered mitochondrial energy metabolism, and impaired amino acid metabolism. These findings support the reduction of UPF consumption and the promotion of dietary patterns rich in fiber for better gut health. Further research is needed to confirm these associations and clarify the underlying mechanisms.

ISRCTN89898870 ( https://doi.org/10.1186/ISRCTN89898870 ).

Short sleep duration and poor sleep quality have been associated with obesity. Asian populations report shorter sleep duration compared to other groups. We therefore aimed to explore the relationships between sleep duration, sleep quality, dozing, daytime napping, snoring, insomnia and adiposity in a multi-ethnic Asian population, and investigate the potential contribution of disturbed sleep to the risk of obesity amongst Asian populations.

We studied 8876 participants of the HELIOS study, a multi-ethnic population-based cohort comprising Chinese, Malay, and Indian Asian men and women living in Singapore. Sleep traits and psychological symptoms were assessed using validated tools which included the Pittsburg Sleep Quality Index, Generalised Anxiety Disorder-7, and Patient Health Questionnaire-9. We employed multivariable regression models to examine the associations between sleep and adiposity, while also conducting sub-group and sensitivity analyses to strengthen the reliability of our results.

The 8876 participants were 69.3% Chinese, 12.5% Malays, and 18.2% Indians, with mean age: 51.7 ± 11.8 years (standard deviation). Malays had the shortest sleep duration, while Chinese had the best sleep quality. Short sleep duration, poor sleep quality, and snoring were associated with higher BMI and waist circumference, independent of age, sex, ethnicity, and various confounding factors (education, household income, current smoking, regular alcohol drinking status, presence of diabetes and hypertension, and markers for anxiety and depression; P < 0.005). The estimated population attributable fraction for short sleep and snoring as contributors to obesity were 6.6% (95% CI: 2.5-10.6%) and 18.6% (95% CI: 17.0-20.2%), respectively.

Sleep duration, sleep quality, and snoring are associated with adiposity in a multi-ethnic Asian population of Chinese, Malays, and Indians. Our findings suggest that a substantial portion of obesity in Asian populations could be averted through public health interventions aimed at improving sleep duration and quality.

The interplay between Parkinson's disease (PD) and sleep disturbances suggests that sleep problems constitute a risk factor for PD progression, but the underlying mechanisms remain unclear. Microglial activation and oxidative stress are considered to play an important role in the pathogenesis of aging and neurodegenerative diseases. We hypothesized that sleep deprivation (SD) could exacerbate PD progression via modulating microglial activation and oxidative stress. To test this hypothesis, we established a PD mouse model using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), then subjected the mice to SD. A battery of behavioral tests, including rotarod, pole, adhesive removal, and open field tests, were used to assess motor function. Our study showed that SD exacerbated motor deficits, loss of tyrosine hydroxylase (TH), microglial activation and oxidative stress damage in PD model mice. Fecal microbiota transplantation experiments revealed that SD mediated PD progression, microglial activation and oxidative stress via the gut microbiota. 16S rRNA sequencing analysis indicated that SD increased the abundances of bacteria such as Bacteroidaceae, while decreasing the abundances of bacteria including Lactobacillus. Non-targeted metabolomic analysis of gut microbiota-derived metabolites revealed that SD significantly increased the production of adenosine (ADO), a purine metabolite. Probiotic supplementation reversed the effects of SD on motor deficits, dopaminergic neuron loss, microglial activation and oxidative stress damage in PD mice; it also decreased SD-induced ADO production. Administration of Adenosine A2A receptor (A2AR) inhibitors, Istradefylline (Ist), attenuated the roles of SD and ADO in promoting microglial activation, oxidative stress and PD progression. Taken together, our findings indicate that SD accelerates PD progression via regulating microbiota associated microglial activation and oxidative stress, suggesting that efforts to improve sleep quality can be used to prevent and treat PD.

Redox imbalance induced by the accumulation of reactive oxygen species (ROS) accelerates age-related processes, often accompanied by a decrease in circadian rhythm amplitude. However, the underlying mechanisms by which ROS modulate circadian rhythms remain poorly understood. In this study, we found that ROS disrupt circadian rhythms in both zebrafish, as indicated by changes in diurnal behavior and clock gene expression, and in a human cell model. Using weighted gene co-expression network analysis (WGCNA) and machine learning approaches (RF, LASSO, SVM), EZH2 was identified as a key gene involved in regulating circadian rhythms under oxidative stress conditions. To further investigate the role of EZH2, we employed ezh2-/- mutants, Morpholino injection, and overexpression treatment and discovered that EZH2 is crucial in mediating the effect of ROS on circadian rhythms. Furthermore, EZH2 interacts with the CLOCK-BMAL1 complex to regulate the transcription of clock genes, as demonstrated through co-immunoprecipitation (co-IP), chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays. Our study revealed that ROS disrupt circadian rhythms by regulating the interaction between EZH2 and the CLOCK-BMAL1 complex, shedding light on the molecular mechanisms of circadian rhythm disruption under oxidative stress and suggesting potential targets for age-related and circadian disorders.

Sleep is an essential homeostatic process that undergoes dynamic changes throughout the lifespan, with distinct life stages predisposed to specific sleep pathologies. Similarly, the gut microbiome also varies with age, with different signatures associated with health and disease in the latest decades of life. Emerging research has shown significant cross-talk between the gut microbiota and the brain through several pathways, suggesting the microbiota may influence sleep, though the specific mechanisms remain to be elucidated. Here, we critically examine the existing literature on the potential impacts of the gut microbiome on sleep and how this relationship varies across adulthood. We suggest that age-related shifts in gut microbiome composition and immune function may, in part, drive age-related changes in sleep. We conclude with an outlook on the therapeutic potential of microbiome-targeted interventions aimed at improving sleep across adulthood, particularly for individuals experiencing high stress or with sleep complaints.

Microglia, the brain's resident macrophages, are key mediators of neuroinflammation, responding to immune pathogens and toxins. They play a crucial role in clearing cellular debris, regulating synaptic plasticity, and phagocytosing amyloid-β (Aβ) plaques in Alzheimer's disease (AD). Recent studies indicate that microglia not only exhibit intrinsic circadian rhythms but are also regulated by circadian clock genes, influencing specific functions such as phagocytosis and the modulation of neuroinflammation. Disruption of the circadian rhythm is closely associated with AD pathology. In this review, we will provide an overview of how circadian rhythms regulate microglia-mediated neuroinflammation in the progression of AD, focusing on the pathway from the central nervous system (CNS) and the peripheral immune system. We also discuss potential therapeutic targets, including hormone modulation, lifestyle interventions, and anti-inflammatory therapies, aimed at maintaining brain health in AD. This will shed light on the involvement of circadian rhythm in AD and explore new avenues for AD treatment.

Neurodegenerative diseases (NDs), including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS), arise from complex interactions between genetic factors, environmental exposures, and aging. Additionally, gut dysbiosis has been linked to systemic inflammation and neurodegeneration. Advances in microbiome and metabolome profiling techniques have provided deeper insights into how alterations in gut microbiota and dietary patterns affect metabolic pathways and contribute to the progression of NDs. This review explores the profiles of gut microbiome and metabolome derived biomarkers and their roles in NDs. Across phyla, families, and genera, we identified 55 microbial alterations in PD, 24 in AD, 4 in ALS, and 17 in MS. Some notable results include an increase in Akkermansia in PD, AD, and MS and a decrease in short-chain fatty acids (SCFAs) in PD and AD. We examined the effects of probiotics, prebiotics, fecal microbiota transplants (FMT), sleep, exercise, and diet on the microbiota, all of which contributed to delayed onset and alleviation of symptoms. Further, artificial intelligence (AI) and machine learning (ML) algorithms applied to omics data have been crucial in identifying novel therapeutic targets, diagnosing and predicting prognosis, and enabling personalized medicine using microbiota-modulating therapies in NDs patients.

There is growing evidence that sleep deprivation promotes cancer progression. In addition, colon cancer patients often experience sleep deprivation due to factors such as cancer pain and side effects of treatment. The occurrence of liver metastases is an important factor in the mortality of colon cancer patients. However, the relationship between sleep deprivation and liver metastases from colon cancer has not been elucidated.

A sleep deprivation liver metastasis model was constructed to evaluate the effect of sleep deprivation on liver metastasis of colon cancer. Subsequently, mice feces were collected for untargeted metabolomics to screen and identify the key mediator, Kynurenic acid (KynA). Furthermore, HILPDA was screened by transcriptomics, and its potential mechanism was explored through ChIP, co-IP, ubiquitination experiments, phenotyping experiments, etc. RESULTS: Sleep deprivation promotes liver metastases in colon cancer. Functionally, sleep deprivation aggravates lipid accumulation and decreases the production of the microbiota metabolite KynA. In contrast, KynA inhibited colon cancer progression in vitro. In vivo, KynA supplementation reversed the promoting effects of sleep deprivation on liver metastases from colon cancer. Mechanistically, KynA downregulates the expression of P4HA2 to promote the ubiquitination and degradation of HIF-1α, which leads to a decrease in the transcription of HILPDA, and ultimately leads to an increase in lipolysis of colon cancer cells.

Our findings reveal that sleep deprivation impairs intracellular lipolysis by KynA, leading to lipid droplets accumulation in colon cancer cells. This process ultimately promotes colon cancer liver metastasis. This suggests a promising strategy for colon cancer treatment.

Sleep is one of the basic physiological needs of human beings. Preoperative sleep disorders are associated with poor prognosis in surgical patients, and sleep disorders have been shown to be one of the risk factors for gastrointestinal dysfunction. However, there are now few studies to investigate whether improving preoperative sleep disorders can promote the recovery of postoperative gastrointestinal function. This study aimed to investigate the effects and significance of improving preoperative sleep quality with zolpidem on postoperative gastrointestinal function.

In this prospective, randomized, double-blind clinical trial, 76 patients undergoing elective laparoscopic partial colorectal resection and with a Pittsburgh Sleep Quality Index (PSQI) score > 5, were randomly divided into two groups. The zolpidem group (Group Z, n = 38) was given a capsule containing 10 mg of zolpidem the night before the operation, and the control group (Group C, n = 38) was given an empty capsule the night before the operation. Follow-up visits were performed on the 1st, 3rd, and 7th postoperative days, respectively. The primary outcome of this study was the I-FEED (Intake, Feeling nauseated, Emesis, Physical Exam, and Duration of symptoms) score on the third postoperative day (POD3). Secondary outcomes included time to postoperative first flatus, first feces, and first food intake (semi-liquid diet), I-FEED scores, visual analog scores (VAS) during coughing and at rest, times of patient-controlled intravenous analgesia (PCIA) effective presses, sufentanil dosage, number of remedial analgesia in the 24-hour postoperative period, and changes in inflammatory markers (TNF-α).

Compared with Group C, Group Z had a lower I-FEED score on POD1 (P < 0.05) and shorter time to first flatus and first food intake (P < 0.05); there were significant differences between the two groups in VAS scores during coughing and at rest on POD1, VAS score during coughing on POD3, times of PCIA effective presses and sufentanil dosage in the 24-hour postoperative period, and patient satisfaction (P < 0.05).

For patients with sleep disorders, the use of zolpidem to improve sleep the night before surgery is beneficial in partially improving postoperative gastrointestinal function, relieving postoperative pain, and increasing patient satisfaction.

ChiCTR2300077566 November 13, 2023.

This review aims to examine the effects of the photoperiod on farm animals and to provide insights into how lighting management can optimize production performance, reproduction, and welfare. The production performance of farm animals is influenced by a variety of factors, such as diet, breed, and environment. Among these, lighting is a crucial component of the feeding environment. With the advancement of intensive farming, lighting measures are increasingly receiving attention. The photoperiod regulates the biological rhythms of animals and affects the secretion of hormones within the animal's body, particularly melatonin. Melatonin regulates the secretion and release of several other hormones through various pathways, such as growth hormone, prolactin, and gonadotropins. Therefore, the environmental light cycle participates in a variety of physiological activities within animals. An appropriate photoperiod can enhance the production performance, reproduction performance, and welfare conditions of farm animals. Choosing the appropriate lighting duration based on different animals, physiological stages, and production purposes can enhance the economic benefits of farms. In this review, we summarized the recent findings on the impact of photoperiods in different farm animal feeding environments on animal husbandry, although research on the suitable photoperiod for some animals might be outdated and is also discussed in this article. For lactating dairy cows, calves, poultry, pigs (excluding boars), and rabbits, continuous light exposure exceeding 12 h per day can be implemented to enhance growth and production performance. In contrast, for boars and goats, daily light exposure should be limited to less than 10 h to optimize reproductive and productive efficiency. Overall, this review aimed to provide theoretical support for research on the optimal photoperiod for farm animals.

The Mendelian randomization approach has emerged as a powerful tool, leveraging genetic variations as natural random experiments to minimize confounding and infer causality with unique advantages. Previous research has highlighted the crucial roles of gut microbiotas and inflammatory factors in mental-behavioral disorders, albeit to varying degrees. However, the precise causal relationship between gut microbiotas and mental-behavioral disorders remains elusive, and the potential role of inflammatory factors as mediators in this process is unclear.

To investigate the associations between gut microbiotas, inflammatory factors, and mental-behavioral disorders, we pooled data from large-scale genome-wide association studies (GWAS). Our study screened 27 diseases, encompassing nine subtypes of mental-behavioral disorders: neurodevelopmental disorders, eating disorders, sleep disorders, schizophrenia spectrum disorders, stress- and trauma-related disorders, mood and affective disorders, cognitive and executive function disorders, personality and somatization disorders, and addiction disorders. Mendelian randomization(MR) was employed to assess causal relationships between gut microbiotas, inflammatory factors, and these mental-behavioral disorders, with inverse variance weighting (IVW) as the primary statistical method. Furthermore, we explored whether inflammatory factors mediate the relationship between gut microbiotas and mental-behavioral disorders.

Having investigated the intricate interplay among gut microbiota, inflammatory factors, and mental-behavioral disorders, we have identified nine pivotal inflammatory factors that intricately regulate the progression of eight distinct disease subtypes. Noteworthy among these findings, levels of CC motif chemokine ligand 28 (CCL28) and CC motif chemokine ligand 25 (CCL25) are associated with the progression of attention-deficit/hyperactivity disorder (ADHD), interleukin-18 (IL-18) levels are linked to anorexia, IL-12β levels are related to schizophrenia (SZ) progression, IL-8 levels are associated with manic episodes, and IL-10 and monocyte chemoattractant protein-2 (MCP-2) levels are closely related to enduring personality changes(EPC). Additionally, fibroblast growth factor 19 (FGF19) levels are associated with cognitive disorders, while C-X-C motif chemokine ligand 1 (CXCL1) levels are related to executive functioning.

Gut microbiotas and mental-behavioral disorders have causal relationships, with inflammatory factors mediating the pathway from gut microbiotas to these disorders.

Metabolic Syndrome (MS) is a cluster of metabolic abnormalities closely associated with hypertension, diabetes, hyperlipidemia, obesity, etc. Our previous research indicated that fecal microbiota transplantation (FMT) could improve MS, but the factors influencing the efficacy of washed microbiota transplantation (WMT) in treating MS patients remain unclear. The objective of this study is to analyze the influencing factors of WMT in treating MS patients.

The clinical data and influencing factors related to MS patients were collected retrospectively. Not only the changes in body mass index [BMI = weight (kg)/height (m)2], blood glucose, blood lipids, and blood pressure were analyzed, but also the influencing factors of WMT in treating MS patients were carried out based on Logistic Regression. The 16S rRNA gene amplicon sequencing was performed on fecal samples before and after WMT treatment.

A total of 210 patients were included, including 68 patients in the WMT group and 142 patients in the drug treatment (DT) group. WMT had a significant improvement and ASCVD downregulation effect on MS patients, and 42.65% of MS patients removed the label of MS after WMT treatment. Independent influencing factors for treating MS patients through WMT include age < 60 years old, high smoking index, infection, single donor selection, single-course WMT treatment, and having hypertension, diabetes, or obesity. WMT treated MS patients by maintaining the balance of gut microbiota.

WMT has a significant effect in improving MS and downregulating ASCVD risk stratification. The therapeutic effect of WMT on MS patients is closely related to their age, smoking index, infection, chronic disease status, donor type, and WMT courses. Therefore, we can improve the efficacy of WMT by reducing independent influencing factors that affect gut microbiota homeostasis.

Nurses who work during the global pandemic are known to experience physical and psychological exhaustion, as well as severe anxiety and depression symptoms. This study aimed to explore the relationships between sleep duration, sleep quality, and depression symptoms among nurses during the outbreak of the Omicron variant.

A cross-sectional study was conducted between August 2022 and September 2022. Participants (N = 2140) were evaluated for depression symptoms via the Hospital Anxiety and Depression Scale (HADS), and sleep was evaluated via the Pittsburgh Sleep Quality Index (PSQI), and "short sleep duration" was defined as ≤ 5 h per day. Demographic information was also collected. Binary and multivariate logistic regression was performed to assess the relationships between sleep duration, sleep quality, and depression symptoms.

In total, 2140 nurses were included in this study; 1481 (69.2%) had poor sleep quality, while 866 (40.4%) had depression symptom scores > 7 according to the HADS criteria. Both duration and quality of sleep were significantly correlated with depression symptoms among nurses (P < 0.001). In multivariable analyses adjusted for potential confounders, short sleep duration (≤ 5 h) was associated with an odds ratio (OR) of 2.26 (95% confidence interval [CI] 1.25-4.07), whereas poorer sleep quality was associated with an OR of 1.97 (95% CI 1.32-2.94) for experiencing depression symptoms.

Following the COVID-19 pandemic, there was a strong association between the sleep quality, sleep duration and depression symptoms among nurses. We recommend the development of targeted interventions to increase sleep duration, enhance sleep quality and alleviate depression symptoms.

The microbiome, comprising the diverse microbial communities inhabiting the human body, has emerged as a critical factor in regulating immune function and inflammation. The relationship between the microbiome and uveitis represents a promising frontier in ophthalmological research, with the microbiome increasingly implicated in disease onset and progression. Research has predominantly focused on the gut microbiome, with animal studies providing evidence that dysbiosis is a key factor in autoimmunity. As the understanding of the microbiome increases, so does the potential for developing innovative treatments that leverage the microbiome's impact on immune and inflammatory processes. Future research will be crucial for deciphering the complexities of the interaction between the microbiome and immune system and for creating effective microbiome-based therapies for those with uveitis. Incorporating microbiome research into clinical practice could transform how uveitis is managed, leading to better and more individualized approaches for management. This review discusses the current understanding of the microbiome-uveitis axis, the promise of microbiome-based diagnostics and therapeutics, and the critical need for large-scale, longitudinal studies. Unlocking the potential of microbiome-targeted approaches may revolutionize the management of uveitis and other inflammatory diseases.

Alzheimer's disease (AD) is a prevalent neurodegenerative disease (ND). In recent years, multiple clinical and animal studies have shown that mitochondrial dysfunction may be involved in the pathogenesis of AD. In addition, short-chain fatty acids (SCFA) produced by intestinal microbiota metabolism have been considered to be important factors affecting central nervous system (CNS) homeostasis. Among the main mediators of host-microbe interactions, volatile fatty acids play a crucial role. Nevertheless, the influence and pathways of microorganisms and their metabolites on Alzheimer's disease (AD) remain uncertain.

In this study, we present distinctions in blood and fecal SCFA levels and microbiota composition between healthy individuals and those diagnosed with AD. We found that AD patients showed a decrease in the abundance of Akkermansia muciniphila and a decrease in propionic acid both in fecal and in blood. In order to further reveal the effects and the mechanisms of propionic acid on AD prevention, we systematically explored the effects of propionic acid administration on AD model mice and cultured hippocampal neuronal cells. Results showed that oral propionate supplementation ameliorated cognitive impairment in AD mice. Propionate downregulated mitochondrial fission protein (DRP1) via G-protein coupled receptor 41 (GPR41) and enhanced PINK1/PARKIN-mediated mitophagy via G-protein coupled receptor 43 (GPR43) in AD pathophysiology which contribute to maintaining mitochondrial homeostasis both in vivo and in vitro. Administered A. muciniphila to AD mice before disease onset showed improved cognition, mitochondrial division and mitophagy in AD mice.

Taken together, our results demonstrate that A. muciniphila and its metabolite propionate protect against AD-like pathological events in AD mouse models by targeting mitochondrial homeostasis, making them promising therapeutic candidates for the prevention and treatment of AD. Video Abstract.

Gut microbes have been used to predict CRC risk. Fecal occult blood test (FOBT) has been recommended for population screening of CRC.

To analyze the effects of fecal occult blood test (FOBT) on gut microbes.

Fecal samples from 107 healthy individuals (FOBT-negative) and 111 CRC patients (39 FOBT-negative and 72 FOBT-positive) were included for 16 S ribosomal RNA sequencing. Based on the results of different FOBT, the community structure and diversity of intestinal bacteria in healthy individuals and CRC patients were analyzed. Characteristic gut bacteria were screened, and various machine learning algorithms were applied to construct CRC risk prediction models.

The gut microbiota of healthy people and CRC patients with different fecal occult blood were mapped. There was no statistical difference in diversity between CRC patients with negative FOBT and positive FOBT. Bacteroides, Blautia and Escherichia-Shigella were more correlated to healthy individuals, while Streptococcus showed higher correlation with CRC patients with negative FOBT. The accuracy of CRC risk prediction model based on the support vector machines (SVM) algorithm was the highest (89.71%). Subsequently, FOBT was included as a characteristic element in the model construction, and the prediction accuracy of the model was all increased. Similarly, the CRC risk prediction model based on SVM algorithm had the highest accuracy (92%).

FOB affects the community composition of gut microbes. When predicting CRC risk based on gut microbiome, considering the influence of FOBT is expected to improve the accuracy of CRC risk prediction.

Iraq and Afghanistan War-era Veterans are at elevated risk for physical injuries and psychiatric illnesses, in particular the polytrauma triad of mild traumatic brain injury (mTBI), post-traumatic stress disorder (PTSD), and chronic pain. The gut microbiome has been implicated in modulation of critical processes beyond digestion, including immune system functioning and stress responsivity, and may be an important factor in understanding physical and mental health outcomes following deployment and trauma exposure. However, minimal research to date has sought to characterize gut microbiome composition in this population. Male Veterans of the conflicts in Iraq and Afghanistan who previously completed a Veterans Affairs' comprehensive TBI evaluation were enrolled in the current study. Participants completed self-report measures of PTSD symptom severity, pain intensity and interference, fatigue, cognitive symptoms, substance use, and sleep quality. They also submitted fecal samples, and metagenomic sequencing was used to calculate alpha and beta diversity and taxonomic microbial composition. Associations between microbiome data and clinical variables were then examined. Alpha and beta diversity measures were not significantly correlated with clinical outcomes. Fatigue, post-concussive symptoms, executive function symptoms, and cannabis use were associated with differences in gut microbial composition, specifically Verrucomicrobiota. Together, results suggest that altered gut microbiome composition is associated with psychiatric and cognitive symptoms in Veterans and highlight a potential new therapeutic target of interest. Future research is needed to examine whether probiotic treatment is effective for reducing symptoms common in this clinical population.

Recent research has suggested imbalances in gut microbiota composition as contributors to cardiac aging. An individual's physical condition, along with lifestyle-associated factors, including diet and medication, are significant determinants of gut microbiota composition. This review discusses evidence of bidirectional associations between aging and gut microbiota, identifying gut microbiota-derived metabolites as potential regulators of cardiac aging. It summarizes the effects of gut microbiota on cardiac aging diseases, including cardiac hypertrophy and fibrosis, heart failure, and atrial fibrillation. Furthermore, this review discusses the potential anti-aging effects of modifying gut microbiota composition through dietary and pharmacological interventions. Lastly, it underscores critical knowledge gaps and outlines future research directions. Given the current limited understanding of the direct relationship between gut microbiota and cardiac aging, there is an urgent need for preclinical and clinical investigations into the mechanistic interactions between gut microbiota and cardiac aging. Such endeavors hold promise for shedding light on the pathophysiology of cardiac aging and uncovering new therapeutic targets for cardiac aging diseases.

Sleep disturbances are increasingly prevalent, significantly impacting physical and mental health. Recent research reveals a bidirectional relationship between gut microbiota and sleep, mediated through the microbiota-gut-brain axis. This review examines the role of gut microbiota in sleep physiology and explores how biotics, including probiotics, prebiotics, synbiotics, postbiotics, and fermented foods, can enhance sleep quality. Drawing from animal and human studies, we discuss neurobiological mechanisms by which biotics may influence sleep, including modulation of neurotransmitters, immune responses, and hormonal regulation. Key microbial metabolites, such as short-chain fatty acids, are highlighted for their role in supporting sleep-related neurochemical processes. Additionally, this review presents dietary strategies and food processing technologies, like fermentation, as innovative approaches for sleep enhancement. Although promising, the available research has limitations, including small sample sizes, variability in biotic strains and dosages, and reliance on subjective sleep assessments. This review underscores the need for standardized protocols, objective assessments such as polysomnography, and personalized biotic interventions. Emerging findings highlight the therapeutic potential of gut microbiota modulation for sleep improvement, though further large-scale human trials are essential to refine strain selection, dosage, and formulation. This interdisciplinary exploration seeks to advance food-based interventions and holistic strategies for managing sleep disorders and improving quality of life.

Perfluorooctanoic acid (PFOA) has been widely documented to affect various aspects of health, including development, metabolism and neuronal function in a variety of organisms. Despite numerous reports detailing these effects, a comprehensive mechanistic model remains elusive, especially with regard to the long-term effects of PFOA, as it bioaccumulates in food chains with a long half-life. In this study, we evaluated the impact of PFOA on several critical physiological states of Drosophila melanogaster. Our findings indicate that PFOA exposure significantly decreases reproductive capacity and induces alterations in starvation resistance and feeding behavior in flies. Interestingly, PFOA exposure also caused changes in locomotor activity and sleep patterns compared with flies receiving a standard diet. Notably, compared with controls, the F2 generation showed increased locomotion and shorter sleep duration during the dark phase, even without direct exposure to PFOA, indicating possible transgenerational effects. Transcriptomic analysis revealed that PFOA also disrupts fatty acid metabolism and alters the expression of immune-responsive genes in Drosophila. In the U-2 OS human osteosarcoma cell line, we examined the impact of PFOA on circadian rhythm regulatory proteins and discovered that, compared with controls, BMAL1 levels increased at concentrations from 10 nM to 10 μM. In summary, this research highlights the influence of PFOA on diverse biological processes, including reproduction, feeding behavior, starvation resistance, locomotion, and sleep activity in Drosophila. It also highlights the ability of PFOA to alter BMAL1 expression patterns in human osteosarcoma cells with deleterious effects.

Alzheimer's disease (AD) is a common type of dementia due to neuronal impairment. In addition, psychobehavioral symptoms including severe sleep disorders, depression and anxiety can occur in most patients with AD.

We report a case of a 68-year-old woman with a 2-year history of AD. She initially presented with memory loss, progressively more severe, leading to a depressive and anxious status. The clinical symptoms also included severe sleep disturbances. Considering the age and health state of the patient, a non-pharmacological treatment of bright light therapy was used to improve her sleep quality. The treatment was provided for 30 minutes twice a day, during 8:30 am to 9:00 am and 16:30 pm to 17:00 pm. After 4 weeks of therapy, the sleep quality notably improved, with a marked decrease in daytime sleep, increase in nighttime sleep, and disappearance of nocturnal activity. The depression and anxiety were also suppressed significantly.

This case report suggested that bright light therapy can have a positive effect on sleep quality in elderly patients with AD and can be used as an effective and safe non-pharmacological treatment.

Livestock may respond differently to circadian rhythms, leading to differences in the composition of the animal products. Nevertheless, the circadian effects on rumen microorganisms and animal products are poorly understood. In the study, it was found that dairy cows exhibited increased milk fat levels, decreased acetic acid concentrations in the rumen fluid, and elevated acetic acid levels in the blood during the night compared to those of the day. Correlational analyses suggested a high association between Succiniclasticum, Lactobacillus, Prevotellacene NK3B31_group, Muribaculaceae_unclassified, etc., which were significantly enriched in rumen fluid at night, and milk fat levels. The differential metabolite Vitamin B6, significantly elevated at night, promoted the translocation of acetic acid into the circulation by increasing the level of rumen epithelial MCT1 protein expression. In addition, we found that both acetic acid treatment time and dose modulated the expression of lipid metabolism transcription factors (PPARγ, PPARα, and SREBP1c) and downstream genes (FASN, SCD1, ACCα, and CPT1A). Additionally, the mTORC1 and AMPK pathways were responsible for the effects of acetic acid on transcription factors and genes involved in lipid metabolism. Differences in rumen microbial taxa were observed between the day and night. Microbial metabolite (acetic acid) was found to be absorbed into the bloodstream and entered the mammary gland at night at a significantly elevated level. This regulation impacted the expression of lipid metabolism-related transcription factors (PPARγ, PPARα, and SREBP1c), as well as downstream genes through the mTORC1 and AMPK signaling pathways, ultimately affecting milk fat synthesis. These findings provide a new perspective for the microbial regulation of milk synthesis.

Insufficient nocturnal sleep was associated with a higher risk of fibrosis in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). Dietary fiber intake may improve the stimulate the secretion of sleep cytokines, inhibit the inflammatory pathway, contribute to regulating sleep disorders and alleviate liver fibrosis. The associations of dietary fiber intake, sleep patterns, with liver fibrosis remain unclear. The study aimed to explore the associations between dietary fiber, sleep, and liver fibrosis, as well as the moderating effect of dietary fiber intake between sleep patterns and liver fibrosis in MASLD patients.

Using data from the National Health and Nutrition Examination Survey (NHANES) database spanning from 2017 to 2020, a cross-sectional study included participants with MASLD was performed to assess the relationship between sleep patterns, dietary fiber intake, and liver fibrosis. Weighted univariate and multivariate logistic regression models were used to examine the linear connection between sleep pattern, dietary fiber intake, and liver fibrosis. Restricted cubic spline (RCS) method was also performed to describe the nonlinear relationship. A two-part linear regression model was also used to estimate threshold effects. The moderating effect of dietary fiber intake was further investigated in different subgroups. All results were presented as odds ratios (ORs) and 95% confidence intervals (CIs).

Totally, 1343 MASLD patients were included for final analysis. Among them, 207 (15.41%) have liver fibrosis. Dietary fiber intake did not correlate significantly with sleep pattern in patients with MASLD (Spearman's r = -0.028, P = 0.1678). Poor sleep pattern was related to higher odds of liver fibrosis (OR = 3.23, 95%CI: 1.05-9.90), while dietary fiber intake ≥ 15 gm/day was associated with lower liver fibrosis risk (OR = 0.51, 95%CI: 0.32-0.83). On the association between sleep pattern and liver fibrosis stratified by dietary fiber intake revealed that poor sleep patterns (OR = 15.13, 95%CI: 4.40-52.01) remained associated with increased liver fibrosis risk among individuals with dietary fiber intake < 15 gm/day. No connection was observed between poor sleep patterns and liver fibrosis in MASLD patients with higher dietary fiber intake, with moderate dietary fiber supplementation beneficial in mitigating poor sleep patterns associated with liver fibrosis. The similar findings were also found in patients aged < 50 years old, ≥ 50 years old, females, those with and without CVD groups, hypertension, and dyslipidemia. Particularly, dietary fiber intake also moderates the relationship between sleep patterns and liver fibrosis in the F4 stage (OR = 13.26, 95%CI: 4.08-43.11).

Dietary fiber intake affects the relationship between sleep patterns and liver fibrosis in MASLD patients.

To investigate whether self-reported symptoms of obstructive sleep apnea (OSA), including snoring, snorting/stopping breathing, and sleepiness, are associated with increased risk of kidney stones.

This cross-sectional study was conducted based on the 2015-2020 National Health and Nutrition Examination Survey (NHANES). Self-reported symptoms of OSA and history of kidney stones were diagnosed via questionnaires. Multivariable logistic regression was used to determine the associations between self-reported symptoms of OSA and kidney stones. Subgroup analyses and interaction tests were performed to address this issue further.

A total of 9,973 participants were enrolled, and the prevalence of kidney stones was 10.76%. Although no significant association was observed between frequent snoring and kidney stones after covariate adjustments (OR 1.033, 95% CI 0.726, 1.469 p = 0.850), frequent snorting/stopping breathing was associated with a greater risk of kidney stones after covariate adjustments (OR 1.655, 95% CI 1.262, 2.172, p = 0.002). Participants who often or almost always felt sleepy also had a greater risk of kidney stones after covariate adjustment (OR 1.651, 95% CI 1.222, 2.229; p = 0.004). The interaction tests suggested that marital status (p = 0.015) and smoking status (p < 0.001) significantly interacted with the association between snorting/stopping breathing and kidney stones.

Self-reported frequent snorting/stopping breathing and sleepiness may be associated with increased risk of kidney stones. Although these findings may emphasize prevention of kidney stones in these people, further research was still needed to verify our results.

To investigate the relationship between biological, psychological, and social factors underlying Burning Mouth Syndrome (BMS).

A case (n = 40) and control (n = 42) study containing 80 variables was examined using two network models based on regularized partial correlations (n = 82).

The structure of the associative pathways with the BMS was revealed. Direct associations involved Gastrointestinal Alterations (0.23), Vitamin D Deficiency (0.29), Musculoskeletal Alterations (0.29), Symptom Severity Score 2 (SSS2) (0.22), Cortisol Variation (0.10), Interpersonal Sensitivity (0.04), Hostility (0.03). Global Severity Index, Symptom Severity Score 1, Psychoticism, Obsession-Compulsion, Depression, Anxiety, and Somatization were indirectly related. The SSS2 was the most influential on BMS accuracy.

Gastrointestinal alterations and vitamin D deficiency show a significant influence on BMS while cortisol mediates in multiple associative pathways between musculoskeletal alterations, gastrointestinal alterations, vitamin D deficiency, non-restorative sleep, fatigue, and cognitive problems. In addition to anxiety and depression, psychoticism, interpersonal sensitivity, and hostility stand out as psychological factors that seem to be related to a lack of vitamin D. None of the factors studied seem to have a relevant predictive potential for BMS, except for nonspecific symptoms of central sensitization.

Despite recent findings suggesting an altered gut microbiota in those suffering from insomnia disorder (ID), research into the gut microbiota, oral microbiota, serum metabolites, and their interactions in patients with ID is sparse.

We collected a total of 114 fecal samples, 133 oral cavity samples and 20 serum samples to characterize the gut microbiota, oral microbiota and serum metabolites in a cohort of 76 ID patients (IDs) and 59 well-matched healthy controls (HCs). We assessed the microbiota as potentially biomarkers for ID for ID by 16S rDNA sequencing and elucidated the interactions involving gut microbiota, oral microbiota and serum metabolites in ID in conjunction with untargeted metabolomics.

Gut and oral microbiota of IDs were dysbiotic. Gut and oral microbial biomarkers could be used to differentiate IDs from HCs. Eleven significantly altered serum metabolites, including adenosine, phenol, and phenol sulfate, differed significantly between groups. In multi-omics analyses, adenosine showed a positive correlation with genus_Lachnospira (p=0.029) and total sleep time (p=0.016). Additionally, phenol and phenol sulphate had a negative correlation with genus_Coprococcus (p=0.0059; p=0.0059) and a positive correlation with Pittsburgh Sleep Quality Index (p=0.006; p=0.006) and Insomnia Severity Index (p=0.021; p=0.021).

Microbiota and serum metabolite changes in IDs are strongly correlated with clinical parameters, implying mechanistic links between altered bacteria, serum metabolites and ID. This study offers novel perspective into the interaction among gut microbiota, oral microbiota, and serum metabolites for ID.