Quercetin (QR) has significant anti-respiratory syncytial virus (RSV) effects. However, its therapeutic mechanism has not been thoroughly explored. In this study, a lung inflammatory injury model caused by RSV was established in mice. Untargeted lung tissue metabolomics was used to identify differential metabolites and metabolic pathways. Network pharmacology was used to predict potential therapeutic targets of QR and analyze biological functions and pathways modulated by QR. By overlapping the results of the metabolomics and the network pharmacology analyses, the common targets of QR that were likely to be involved in the amelioration of RSV-induced lung inflammatory injury by QR were identified. Metabolomics analysis identified 52 differential metabolites and 244 corresponding targets, while network pharmacology analysis identified 126 potential targets of QR. By intersecting these 244 targets with the 126 targets, hypoxanthine–guanine phosphoribosyltransferase (HPRT1), thymidine phosphorylase (TYMP), lactoperoxidase (LPO), myeloperoxidase (MPO), and cytochrome P450 19A1 (CYP19A1) were identified as the common targets. The key targets, HPRT1, TYMP, LPO, and MPO, were components of purine metabolic pathways. The present study demonstrated that QR effectively ameliorated RSV-induced lung inflammatory injury in the established mouse model. Combining metabolomics and network pharmacology showed that the anti-RSV effect of QR was closely associated with purine metabolism pathways.

Sleep constitutes an essential physiological process that is vital for maintaining physical and mental wellbeing. However, the science of sleep focusing on basic questions such as “how” we sleep and “why” we sleep is still not clear. Over the past decade, substantial progress has also been made in elucidating the interactions between sleep and other biological processes, providing insights into the basic questions of sleep. Among these, emerging evidence highlights the microbiota-gut-brain axis (MGBA) as a pivotal bidirectional network that connects gut microorganisms with the central nervous system to regulate sleep architecture and homeostasis. This interaction is inherently bidirectional: sleep deprivation alters gut motility, mucosal integrity, and microbial composition, while microbial metabolites in turn influence neurotransmission ( γ -aminobutyric acid, serotonin), immune-endocrine balance, and inflammatory signaling. In this article, we will review recent studies about MGBA-targeted therapeutic strategies for sleep disorders, such as probiotics, prebiotics, and fecal microbiota transplantation, which aim to restore microbial homeostasis and improve sleep quality. Furthermore, we discuss emerging interventions that modulate microbial metabolites and neuroimmune-endocrine signaling, as well as innovative pharmacological approaches targeting MGBA dysfunction. Collectively, we hope this review will contribute to a deeper understanding of MGBA-mediated mechanisms in sleep disorders promises to inform novel preventive and therapeutic strategies, ultimately improving clinical outcomes and quality of life for affected individuals.

Major depressive disorder is a severe mental health condition characterized by persistent depressed mood and loss of interest. Current first-line pharmacotherapies often exhibit limited therapeutic performance and adverse side effects. Transcutaneous auricular vagus nerve stimulation (taVNS) is a promising, safe, and noninvasive alternative intervention with demonstrated neuromodulatory efficacy. Nevertheless, its mechanisms remain unclear. This study investigated whether the antidepressant properties of taVNS are associated with the microbiota-gut-brain axis, focusing on the potential crosstalk between differentially expressed hippocampal proteins and the gut microbiota. A chronic unpredictable mild stress (CUMS) rat model of depression was established, and taVNS was administered for 14 days. Hippocampal proteomic profiling was performed using data-independent acquisition. Fecal metagenomic sequencing was conducted to characterize alterations in gut microbial communities. Key signaling pathways were validated using Western blot, qRT-PCR, HE staining, and transmission electron microscopy, all of which were employed to systematically assess behavioral, proteomic, microbial, and molecular changes. Proteomics and molecular analyses revealed that taVNS upregulated hippocampal expression of glutamate ionotropic receptor N-methyl-D-aspartate type subunit 1 (GluN1) and brain-derived neurotrophic factor (BDNF), while simultaneously restoring mitogen-activated protein kinase (MAPK) signaling activity. Metagenomic profiling demonstrated that taVNS increased the abundance of Akkermansia muciniphila and reduced Ligilactobacillus reuteri. Ligilactobacillus levels were positively correlated with synaptogyrin-1 (Syngr1), indicating their potential association in enhancing the antidepressant effects mediated by the GluN1/MAPK/BDNF signaling cascade. TaVNS significantly alleviated depression-like behaviors in CUMS-exposed rats. The underlying mechanism may involve the restoration of synaptic function of glutamatergic neurons by regulating the GluN1/MAPK/BDNF signaling pathway. In addition, taVNS reshaped the gut microbiota, markedly increasing the abundance of Akkermansia muciniphila and Ligilactobacillus murinus while reducing Limosilactobacillus reuteri and Lactobacillus johnsonii. The positive correlation between Syngr1 protein level and Ligilactobacillus abundance in the hippocampus suggests that the microbiota-gut-brain axis may play a key role in the antidepressant effects of taVNS.

Obesity has become a growing public health problem worldwide, especially in children and adolescents. The ultrasensitive C-reactive protein (hs-CRP)/high-density lipoprotein cholesterol (HDL-C) index is a widely recognized marker of metabolic disorders and inflammatory responses. However, its connection to overweight or obesity in children and adolescents remains unclear. This study aimed to examine the association between the hs-CRP/HDL-C index and overweight or obesity, to identify its possible threshold effect, and to offer a new theoretical basis for prevention and control among youth. This study investigated the relationship between hs-CRP/HDL-C index and overweight and obesity in children and adolescents aged 6–19 years, utilizing data from the 2015–2020 National Health and Nutrition Examination Survey (NHANES). This analysis employed t tests, Chi-square tests, multiple logistic regression, restricted cubic spline regression (RCS), and piecewise regression methods to validate the association between the hs-CRP/HDL-C index and overweight/obesity, and to explore potential nonlinear patterns and key thresholds between the two. This study included 3853 children and adolescents. Multivariate logistic regression analysis revealed a significant positive relationship between the log-transformed indicator and overweight/obesity (OR = 5.81; 95% CI 5.02–6.75; P < 0.001). Furthermore, smoothed curve fitting revealed a nonlinear S-shaped dose–response relationship between the two variables. In addition, segmented regression analysis of hs-CRP/HDL-C identified two inflection points (0.653 and 1.593). Notably, except for household income, interaction p values across subgroups were all greater than 0.05, indicating high stability and consistency among subgroups. However, household income exerted a significant modifying effect. This study finds that the hs-CRP/HDL-C index is associated with overweight and obesity in children and adolescents in a manner that is not linear. There is a critical range (0.653–1.593) where higher values of the index are related to lower rates of overweight and obesity. Based on these results, it is recommended that pediatric healthcare providers use hs-CRP/HDL-C testing routinely, which may help identify children at risk and support early obesity prevention. Future studies should confirm these findings in additional groups and develop more effective interventions.

Background: Respiratory syncytial virus (RSV) is a leading cause of acute lower respiratory infections in humans, contributing to a substantial burden on both families and society. To date, no bibliometric studies have specifically addressed RSV pneumonia. We therefore employed bibliometric methods to analyze the top 100 most-cited articles in this field, aiming to construct a visual knowledge map and quantitatively identify current research hotspots and emerging trends. Methods: We retrieved relevant publications from the Web of Science Core Collection (WoSCC) database. Using Microsoft Excel 2019, CiteSpace 6.2.R4, and VOSviewer 1.6.18, we performed a visual analysis of annual publication trends, countries, institutions, authors, journals, and keywords. Results: The 100 most-cited articles received a total of 15,949 citations, with individual citation counts ranging from 46 to 2846 and a median of 74. The United States contributed the most publications, and the Centers for Disease Control and Prevention (CDC) was the most productive institution. The most prolific authors were Cohen, Cheryl; Graham, Barney S; Anderson, LJ; and Ramilo, O. The Pediatric Infectious Disease Journal published and received the most citations in this domain. “Bronchiolitis” was identified as the keyword with the strongest citation burst. Conclusion: Current research on RSV pneumonia remains focused on pathogenesis, treatment, and prognosis. The development of new antiviral drugs and immunoprophylaxis strategies continues to be a central direction for future studies.