Background: While the exact mechanisms are not fully understood, there are significant links between sleep quality, anxiety, depressive symptoms, and cognitive emotion regulation. This research examines how sleep quality affects anxiety and depressive symptoms, as well as the potential of cognitive emotion regulation strategies (CERS) to moderate the impact of sleep quality on these symptoms. Methods: The Chinese version of the Pittsburgh Sleep Quality Index (CPSQI), the Cognitive Emotion Regulation Questionnaire (CERQ), the Patient Health Questionnaire-9 (PHQ-9), and the Generalized Anxiety Disorder Scale-7 (GAD-7) were all completed online by students from two colleges in China’s Xizang region. Results: The study included 4325 subjects. The prevalence of poor sleep quality, anxiety symptoms, and depression symptoms was 45.69%, 36.81%, and 51.86%, respectively. We observed significant direct effects on poor sleep and severity of anxiety/depression: c’1 = 0.586 (0. 544–0.628), and c’2 = 0.728 (0.683–0.773). Adaptive CERS only had a mediating effect on the relationship between sleep quality and depression symptoms, with a1b3 = −0.005 (−0.011–−0.001). The link between poor sleep quality and the intensity of anxiety and depression was significantly affected by the indirect effects of maladaptive CERS: effect a2b2 = 0.126 (0.106–0.147), and effect a2b4 = 0.145 (0.123–0.167). Conclusions: Individuals who experience poor sleep quality are more likely to have increased levels of anxiety and depression. However, enhancing sleep quality led to a decrease in anxiety and depression levels. Adaptive CERS did not predict anxiety, but they did predict depression. Multiple maladaptive CERS could increase levels of anxiety and depression. To prevent mental stress, it is crucial to examine sleep problems among college students, understand their cognitive strategies, promote the adoption of adaptive CERS, and reduce the reliance on maladaptive CERS.

Background/Objective: Sarcopenic obesity (SO), a pathological syndrome characterized by the co-existence of diminished muscle mass and excessive adipose accumulation, significantly compromises the quality of life in older adults. The purpose of this study was to systematically evaluate the efficacy of exercise, nutritional interventions, and neuromuscular electrical stimulation (NMES) in preventing and managing SO in middle-aged and older adults. Methods: A comprehensive search was conducted across PubMed, Web of Science, Embase, Cochrane Library, and CNKI for randomized controlled trials (RCTs) until January 2025. Meta-analyses were performed using the random-effects model and fixed-effects model based on the degree of heterogeneity and calculating the mean differences (MD) with 95% confidence intervals (CI). Subgroup analyses compared the intervention types. Results: Twenty-nine RCTs (1622 participants) were included. Exercise interventions significantly reduced the body fat percentage (MD = −2.79%, 95% CI: −3.94, −1.64, p < 0.001, I² = 74%), fat mass (MD = −6.77 kg, 95% CI: −11.48, −2.06, p = 0.005, I² = 98%), waist circumference (MD = −2.05 cm, 95% CI: −3.64, −0.46, p = 0.01, I² = 0%) and LDL-C (MD: −7.45 mg/dL, 95% CI: −13.82, −1.07, p = 0.02, I² = 0%), while improving handgrip strength (MD = 2.35 kg, 95% CI: 1.99, 2.70, p < 0.001, I² = 52%) and gait speed (MD = 0.19 m/s, 95% CI: 0.13, 0.24, p < 0.001, I² = 89%). Mixed training outperformed resistance-only regimens in reducing the body fat percentage and enhancing functional outcomes. NMES reduced the body fat percentage (MD = −2.01%, 95% CI: −3.54, −0.48, p = 0.01, I² = 93%) and waist circumference (MD = −1.72 cm, 95% CI: −2.35, −1.09, p < 0.001, I² = 0%) while increasing the Skeletal Muscle Index (MD = 0.26 kg/m², 95% CI: 0.22, 0.29, p < 0.001, I² = 38%). Synergy with nutritional supplementation amplified these effects. Nutritional interventions modestly improved total fat-free mass (MD = 0.77 kg, 95% CI: 0.04, 1.50, p = 0.04, I² = 0%) and handgrip strength (MD = 1.35 kg, 95% CI: 0.71, 2.00, p < 0.001, I² = 0%) but showed no significant impact on the metabolic markers (TG, TC, glucose, hemoglobin, and HOMA-IR). Conclusions: Exercise, particularly multimodal regimens combining aerobic and resistance training, is the cornerstone for improving body composition and physical function in SO. NMES serves as an effective adjunct for accelerating fat loss, while nutritional strategies require integration with exercise or prolonged implementation to yield clinically meaningful outcomes. Future research should prioritize standardized diagnostic criteria and long-term efficacy assessments of multimodal interventions.

Background/Objectives: Moschus (musk) has long been used in traditional Tibetan medicine to prevent and treat epidemic febrile illnesses. However, its antiviral mechanisms remain poorly understood. Given the urgent need for effective treatments against viral respiratory tract infections (VRTIs), this study aimed to systematically investigate the molecular targets and pharmacological pathways through which Moschus may exert therapeutic effects. Methods: Based on the identification of bioactive compounds with favorable pharmacokinetics, we applied integrated network pharmacology and multi-omics analyses to systematically identify key therapeutic targets involved in VRTIs. Gene Set Enrichment Analysis (GSEA) and immune infiltration further revealed strong associations with multiple immune cell subsets, reflecting their pivotal roles in immunomodulatory mechanisms during viral infections. Molecular docking confirmed the strong binding affinities between Moschus compounds and these key targets. Results: Notably, testosterone exhibited the strongest and most consistent binding across key targets, suggesting its potential as a pivotal bioactive compound. Importantly, the antiviral effects of Moschus may be mediated in part by the downregulation of the key genes MCL1, MAPK3, and CDK2, which are involved in the regulation of viral replication, apoptosis, and host immune responses. Conclusions: This study provides a comprehensive mechanistic framework supporting the multi-target antiviral potential of Moschus, offering a scientific basis for its further development as a therapeutic agent against VRTIs.

Body image plays a significant role in emotional and behavioral health. This study examined the short-term longitudinal association between body image sati

Depression is a significant global health concern, particularly prevalent among college students, and can be exacerbated by negative parenting styles. This study investigates the impact of such parenting on depressive symptoms among college students and explores the mediating role of eating disorders (EDs) and the moderating roles of ethnicity and maladaptive Cognitive Emotion Regulation Strategies (CERS). The longitudinal study was conducted from June to December 2021 and involved 2,993 enrolled students at two Tibetan universities. Data were collected at three time points using validated instruments including the Patient Health Questionnaire-9 for measuring depressive symptoms, the Short Egna Minnen av Barndoms Uppfostran (s-EMBU) for measuring negative parenting styles, the Eating Attitude Test-26 for measuring EDs, and the Cognitive Emotion Regulation Questionnaire for measuring maladaptive CERS. Statistical analyses, including Pearson correlation and moderated mediation models, were conducted using SPSS software. The average age of the participants in the study was 19.8 (SD = 1.3) years, with males accounting for 34.4%, Tibetans and other ethnic groups accounting for 56.8%, and urban students accounting for 29.0%. Negative parenting styles were associated with higher levels of EDs and depressive symptoms. A longitudinal moderated mediation model revealed that EDs significantly mediated the relationship between negative parenting styles and depressive symptoms. Additionally, the impact of EDs on depressive symptoms was moderated by maladaptive CERS, where higher levels of these strategies intensified the relationship, while lower levels mitigated it. Ethnicity had no moderating effect on direct and indirect paths. The study indicates that negative parenting styles contribute to depressive symptoms among college students through EDs. Maladaptive CERS amplify the impact of EDs on depressive symptoms, suggesting the importance of addressing these strategies in preventive and therapeutic settings. This research underscores the need for interventions targeting family dynamics and emotional regulation to mitigate depressive symptoms in vulnerable populations.

Background/Objectives: Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, is implicated in the pathogenesis of ulcerative colitis (UC). Tryptophan metabolism and its interaction with the aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2–related factor 2 (Nrf2) axis represent a crucial regulatory network in intestinal homeostasis. This study aimed to investigate whether the probiotic fermentation product postbiotic Nagqu4580 alleviates UC by modulating this network to inhibit intestinal epithelial ferroptosis. Methods: An acute UC model was induced in mice using 4% dextran sodium sulfate (DSS). The therapeutic effects of postbiotic Nagqu4580 were evaluated through disease activity index (DAI), colon length, histopathology, inflammatory cytokines, and intestinal barrier function. Ferroptosis was assessed by measuring lipid peroxidation (MDA, 4-HNE), antioxidant capacity (GSH/GSSG), and expression levels of GPX4 and ACSL4. Serum tryptophan metabolites were profiled using targeted metabolomics, the activation of the AhR/Nrf2 pathway was examined by Western blot, immunofluorescence, and qPCR, and gut microbiota composition was analyzed by 16S rRNA sequencing. Results: Postbiotic Nagqu4580 dose-dependently ameliorated DSS-induced UC in mice, as evidenced by reduced DAI scores, mitigated colon shortening and histological damage, decreased inflammatory cytokines (TNF-α, IL-1β, IL-6), and restored intestinal barrier function by upregulating tight junction proteins (Claudin-1, ZO-1, Occludin). Mechanistically, postbiotic Nagqu4580 inhibited intestinal epithelial ferroptosis by reducing MDA and 4-HNE levels, restoring the GSH/GSSG balance, downregulating ACSL4, and upregulating GPX4. Serum metabolomics revealed that postbiotic Nagqu4580 reshaped tryptophan metabolism, increasing beneficial metabolites such as 5-hydroxyindoleacetic acid (5-HIAA) and decreasing potentially harmful metabolites such as 3-indoxyl sulfate (3-IS). 16S rRNA sequencing further revealed that the postbiotic Nagqu4580 partially reversed DSS-induced gut microbiota dysbiosis, with a slight increase in the abundance of beneficial genera and a significant reduction in the abundance of pro-inflammatory genera. Furthermore, postbiotic Nagqu4580 significantly activated the AhR/Nrf2 signaling pathway, enhancing the expression of AhR, Nrf2, and their downstream antioxidant genes HO-1 and GPX4. Conclusions: Postbiotic Nagqu4580 alleviates UC by inhibiting intestinal epithelial ferroptosis. Our data suggest that this protective effect is associated with the remodeling of gut microbiota-related tryptophan metabolism and subsequent activation of the AhR/Nrf2 antioxidant axis. Our findings highlight the therapeutic potential of postbiotic Nagqu4580 as a postbiotic agent for UC.