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Background Neuroinflammation-induced injury is intimately associated with poor prognosis in patients with cerebral venous sinus thrombosis (CVST). The cyclic GMP-AMP synthase–stimulator of interferon gene (cGAS–STING) axis is a cytoplasmic double-stranded DNA (dsDNA) sensing pathway has recently emerged as a crucial mediator of neuroinflammation in ischemic stroke. However, the role of the cGAS–STING pathway in modulating post-CVST inflammation and the underlying mechanisms involved remain unclear. Methods A CVST model was induced by ferric chloride in male C57BL/6J mice. The selective cGAS inhibitor RU.521, STING agonist 2′3′-cGAMP, and STING siRNA were delivered by intranasal administration or intraventricular injection. Post-CVST assessments included rotarod test, TUNEL staining, Fluoro-Jade C staining, dihydroethidium staining, western blotting, qPCR, immunofluorescence, immunohistochemistry, ELISA and flow cytometry. Results cGAS, STING, NLRP3 and GSDMD were significantly upregulated after CVST and mostly in the microglia of the mouse brain. CVST triggered the release of dsDNA into the cytoplasm and elicited an inflammatory response via activating the cGAS–STING axis. RU.521 decreased the levels of 2′3′-cGAMP, STING and downstream inflammatory cytokines, and suppressed the expressions of NLRP3 inflammasome and pyroptosis-pertinent components containing cleaved caspase-1, GSDMD, GSDMD-C, pro- and cleaved IL-1β, and cleaved IL-1β/pro-IL-1β. Besides, RU.521 treatment also reduced oxidative stress, lessened the numbers of microglia and neutrophils, and ameliorated neuronal apoptosis, degeneration along with neurological deficits post-CVST. 2′3'-cGAMP delivery enhanced the expressions of STING and related inflammatory mediators, NLRP3 inflammasome and pyroptosis-relevant proteins, whereas these alterations were significantly abrogated by the silencing of STING by siRNA. Conclusions Our data demonstrate that repression of the cGAS–STING pathway diminishes the neuroinflammatory burden of CVST and highlight this approach as a potential therapeutic tactic in CVST-mediated pathologies.

In this study, silver nanoparticles (Ag NPs) coated with catechol-conjugated chitosan (CSS) were prepared using green methods. Interestingly, we uncovered that CSS-coated Ag NPs (CSS-Ag NPs) exhibited a higher toxicity against gram-negative Escherichia coli ( E. coli ) bacteria than against gram-positive Staphylococcus aureus (S. aureus) bacteria. The differences revealed that the CSS-Ag NPs killed gram bacteria with distinct, species-specific mechanisms. The aim of this study is to further investigate these underlying mechanisms through a series of analyses. The ultrastructure and morphology of the bacteria before and after treatment with CSS-Ag NPs were observed. The results demonstrated the CSS-Ag NPs killed gram-positive bacteria through a disorganization of the cell wall and leakage of cytoplasmic content. In contrast, the primary mechanism of action on gram-negative bacteria was a change in membrane permeability, induced by adsorption of CSS-Ag NPs. The species-specific mechanisms are caused by structural differences in the cell walls of gram bacteria. Gram-positive bacteria are protected from CSS-Ag NPs by a thicker cell wall, while gram-negatives are more easily killed due to an interaction between a special outer membrane and the nanoparticles. Our study offers an in-depth understanding of the antibacterial behaviors of CSS-Ag NPs and provides insights into ultimately optimizing the design of Ag NPs for treatment of bacterial infections.

Periodontitis, a bacterium-induced inflammatory disease that is characterized by alveolar bone loss, is highly prevalent worldwide. Elucidating the underlying mechanisms of alveolar bone loss in periodontitis is crucial for understanding its pathogenesis. Classically, bone cells, such as osteoclasts, osteoblasts and bone marrow stromal cells, are thought to dominate the development of bone destruction in periodontitis. Recently, osteocytes, the cells embedded in the mineral matrix, have gained attention. This review demonstrates the key contributing role of osteocytes in periodontitis, especially in alveolar bone loss. Osteocytes not only initiate physiological bone remodeling but also assist in inflammation-related changes in bone remodeling. The latest evidence suggests that osteocytes are involved in regulating bone anabolism and catabolism in the progression of periodontitis. The altered secretion of receptor activator of NF-κB ligand (RANKL), sclerostin and Dickkopf-related protein 1 (DKK1) by osteocytes affects the balance of bone resorption and formation and promotes bone loss. In addition, the accumulation of prematurely senescent and apoptotic osteocytes observed in alveolar bone may exacerbate local destruction. Based on their communication with the bloodstream, it is noteworthy that osteocytes may participate in the interaction between local periodontitis lesions and systemic diseases. Overall, further investigations of osteocytes may provide vital insights that improve our understanding of the pathophysiology of periodontitis.

Atherosclerosis (AS), one of the most common types of cardiovascular disease, has initially been attributed to the accumulation of fats and fibrous materials. However, more and more researchers regarded it as a chronic inflammatory disease nowadays. Infective disease, such as periodontitis, is related to the risk of atherosclerosis. Porphyromonas gingivalis ( P. gingivalis ), one of the most common bacteria in stomatology, is usually discovered in atherosclerotic plaque in patients. Furthermore, it was reported that P. gingivalis can promote the progression of atherosclerosis. Elucidating the underlying mechanisms of P. gingivalis in atherosclerosis attracted attention, which is thought to be crucial to the therapy of atherosclerosis. Nevertheless, the pathogenesis of atherosclerosis is much complicated, and many kinds of cells participate in it. By summarizing existing studies, we find that P. gingivalis can influence the function of many cells in atherosclerosis. It can induce the dysfunction of endothelium, promote the formation of foam cells as well as the proliferation and calcification of vascular smooth muscle cells, and lead to the imbalance of regulatory T cells (Tregs) and T helper (Th) cells, ultimately promoting the occurrence and development of atherosclerosis. This article summarizes the specific mechanism of atherosclerosis caused by P. gingivalis . It sorts out the interaction between P. gingivalis and AS-related cells, which provides a new perspective for us to prevent or slow down the occurrence and development of AS by inhibiting periodontal pathogens.

The highlighted energy consumption of Internet data center (IDC) in China has become a pressing issue with the implementation of the Chinese dual carbon strategic goal. This paper provides a comprehensive review of cooling technologies for IDC, including air cooling, free cooling, liquid cooling, thermal energy storage cooling and building envelope. Firstly, the environmental requirements for the computer room and the main energy consumption items for IDC are analyzed. The evaluation indicators and government policies for promoting green IDC are also summarized. Next, the traditional cooling technology is compared to four new cooling technologies to find effective methods to maximize energy efficiency in IDC. The results show that traditional cooling consumes a significant amount of energy and has low energy efficiency. The application of free cooling can greatly improve the energy efficiency of IDC, but its actual implementation is highly dependent on geographical and climatic conditions. Liquid cooling, on the other hand, has higher energy efficiency and lower PUE compared to other cooling technologies, especially for high heat density servers. However, it is not yet mature and its engineering application is not widespread. In addition, thermal energy storage (TES) based cooling offers higher energy efficiency but must be coupled with other cooling technologies. Energy savings can also be achieved through building envelope improvements. Considering the investment and recovery period for IDC, it is essential to seek efficient cooling solutions that are suitable for IDC and take into account factors such as IDC scale, climate conditions, maintenance requirements, etc. This paper serves as a reference for the construction and development of green IDC in China.

The relationship between periodontitis and systemic diseases, notably including atherosclerosis and diabetes, has been studied for several years. Porphyromonas gingivalis, a prominent component of oral microorganism communities, is the main pathogen that causes periodontitis. As a result of the extensive analysis of this organism, the evidence of its connection to systemic diseases has become more apparent over the last decade. A significant amount of research has explored the role of Porphyromonas gingivalis in atherosclerosis, Alzheimer’s disease, rheumatoid arthritis, diabetes, and adverse pregnancy outcomes, while relatively few studies have examined its contribution to respiratory diseases, nonalcoholic fatty liver disease, and depression. Here, we provide an overview of the current state of knowledge about Porphyromonas gingivalis and its systemic impact in an aim to inform readers of the existing epidemiological evidence and the most recent preclinical studies. Additionally, the possible mechanisms by which Porphyromonas gingivalis is involved in the onset or exacerbation of diseases, together with its effects on systemic health, are covered. Although a few results remain controversial, it is now evident that Porphyromonas gingivalis should be regarded as a modifiable factor for several diseases.

Background Despite global progress, infectious diarrhea remains a leading cause of under‐five mortality, with burdens unevenly distributed across ages and regions. Moving beyond traditional epidemiology, there is an urgent need to translate population‐level trends into actionable, biologically informed strategies. This study analyzes the global burden to identify high‐risk populations and define age‐specific etiological profiles, thereby creating a foundational map for targeted multiomics research and biomarker‐driven interventions. Methods Utilizing Global Burden of Disease (GBD) 2021 data from 204 countries and territories, we assessed the incidence, mortality, and death probability of infectious diarrhea in children under five, stratified by age, region, and sociodemographic index (SDI). Temporal trends from 1990 to 2021 were analyzed using estimated annual percentage change (EAPC) and joinpoint regression. A detailed pathogen‐attributable burden analysis was performed, elucidating age‐varying etiologies. These epidemiological patterns were framed to highlight critical gaps where multiomics approaches (e.g., gut microbiome, host immune response profiling) and subsequent biomarker discovery could elucidate underlying biological mechanisms of age‐specific susceptibility and pathogen dominance. Results In 2021, neonates (< 28 days) bore the highest burden. Mortality declined slowest among children aged 6–11 months (EAPC = −4.2%). Rotavirus persisted as the primary lethal pathogen. A critical transition was observed: The second‐leading cause of death shifted from adenovirus in infants (before 6–11 months) to Shigella in older children (after 12–23 months), with the proportional mortality attributable to Shigella, norovirus, and cholera increasing markedly after 12 months of age. This precise etiological mapping identifies distinct biological and immunological epochs in early childhood, each presenting unique targets for biomarker identification and mechanism‐based intervention. Conclusion This analysis clarifies the global and age‐stratified burden of pediatric infectious diarrhea, moving from descriptive statistics toward a framework for precision public health. The defined age–etiology transitions provide a direct rationale for applying multiomics technologies to discover the host and microbial biomarkers underlying these patterns. Integrating such biomarkers with demographic data can transform current “age‐tailored” guidelines into truly individualized risk prediction, vaccine strategy optimization, and targeted antimicrobial stewardship. Concurrently, our age‐specific characterization of pathogen transitions provides epidemiological evidence to optimize age‐specific management of childhood infectious diarrhea and to identify priority populations for intervention in resource‐limited settings, ultimately advancing more effective and personalized clinical and preventive care for vulnerable children.

Background Ischemic stroke presents a significant threat to human health due to its high disability rate and mortality. Currently, the clinical treatment drug, rt-PA, has a narrow therapeutic window and carries a high risk of bleeding. There is an urgent need to find new effective therapeutic drugs for ischemic stroke. Icariin (ICA), a key ingredient in the traditional Chinese medicine Epimedium, undergoes metabolism in vivo to produce Icaritin (ICT). While ICA has been reported to inhibit neuronal apoptosis after cerebral ischemia-reperfusion (I/R), yet its underlying mechanism remains unclear. Methods PC-12 cells were treated with 200 µM H 2 O 2 for 8 h to establish a vitro model of oxidative damage. After administration of ICT, cell viability was detected by Thiazolyl blue tetrazolium Bromide (MTT) assay, reactive oxygen species (ROS) and apoptosis level, mPTP status and mitochondrial membrane potential (MMP) were detected by flow cytometry and immunofluorescence. Apoptosis and mitochondrial permeability transition pore (mPTP) related proteins were assessed by Western blotting. Middle cerebral artery occlusion (MCAO) model was used to establish I/R injury in vivo. After the treatment of ICA, the neurological function was scored by ZeaLonga socres; the infarct volume was observed by 2,3,5-Triphenyltetrazolium chloride (TTC) staining; HE and Nissl staining were used to detect the pathological state of the ischemic cortex; the expression changes of mPTP and apoptosis related proteins were detected by Western blotting. Results In vitro: ICT effectively improved H 2 O 2 -induced oxidative injury through decreasing the ROS level, inhibiting mPTP opening and apoptosis. In addition, the protective effects of ICT were not enhanced when it was co-treated with mPTP inhibitor Cyclosporin A (CsA), but reversed when combined with mPTP activator Lonidamine (LND). In vivo: Rats after MCAO shown cortical infarct volume of 32–40%, severe neurological impairment, while mPTP opening and apoptosis were obviously increased. Those damage caused was improved by the administration of ICA and CsA. Conclusions ICA improves cerebral ischemia-reperfusion injury by inhibiting mPTP opening, making it a potential candidate drug for the treatment of ischemic stroke. Graphical Abstract

•MRI-derived ALPS index and normalized choroid plexus volume (NCPV) were evaluated as biomarkers of glymphatic function in Parkinson’s disease (PD).•PD patients exhibited significantly lower ALPS and higher NCPV compared with healthy controls.•NCPV was independently associated with global cognition and predicted cognitive decline.•Lower ALPS and higher NCPV at baseline predicted steeper longitudinal decline in cognition and memory in the PPMI cohort.•Higher baseline NCPV was linked to increased risk of cognitive conversion in PD.•ALPS index and NCPV may serve as exploratory MRI markers to identify PD patients at risk for cognitive deterioration. Emerging evidence suggests that dysfunction of the brain’s glymphatic system may be relevant to cognitive decline in Parkinson’s disease (PD). However, in vivo indirect imaging correlates and predictive value for disease progression remain unclear. We evaluated whether two MRI-derived indices, diffusion tensor image analysis along the perivascular space (ALPS) and normalized choroid plexus volume (NCPV), are associated with cognitive status and subsequent cognitive decline in PD. This study analyzed a self-collected cohort and the PPMI cohort. ALPS and NCPV were extracted from diffusion tensor imaging and T1-weighted images, respectively. Cross-sectional group comparisons were performed using analysis of covariance. Associations with clinical and cognitive measures were assessed using Spearman correlation and multivariate linear regression. To address stage heterogeneity, we added an early-duration subgroup analysis (PD < 1 year vs healthy controls) in the self-collected cohort. Longitudinal cognitive trajectories were evaluated using linear mixed-effects models, and cognitive conversion was assessed using Kaplan-Meier survival analysis and Cox proportional hazards regression. In the self-collected cohort, PD patients showed significantly lower ALPS and higher NCPV than healthy controls. NCPV was significantly associated with MMSE and showed independent predictive value in regression analysis. In the PD <1 year subgroup, no significant PD-HCs differences were detected for ALPS or NCPV, similar to the early, drug-naïve PPMI cohort where cross-sectional differences were not observed. In the PPMI cohort, lower ALPS and higher NCPV at baseline predicted steeper decline in global cognition and verbal memory over time. Higher baseline NCPV was also associated with increased risk of cognitive conversion. MRI-derived ALPS index and NCPV, while indirect and potentially influenced by multiple factors, were associated with cognitive status and progression in PD. These exploratory markers may aid in identifying individuals at higher risk for cognitive deterioration.

White button mushrooms ( Agaricus bisporus ) were treated with 5 μl L −1 , 10 μl L −1 , 20 μl L −1 , and 50 μl L −1 peppermint oil and then stored at 4 °C for 8 days to investigate with respect to browning and postharvest qualities. It was found that 20 μl L −1 peppermint oil treatment could provide the best effect on inhibiting browning of fruit bodies. Our results indicated 20 μl L −1 peppermint oil fumigation restrains browning development and alleviated membrane lipid peroxidation, as reflected by lower electrolyte leakage (17.42%), malondialdehyde (MDA) content (21.95%), and weight loss (1.69%) compared with those of the control mushrooms at 8 days, respectively. In addition, the 20 μl L −1 peppermint oil fumigation had 1.49-fold and 1.24-fold higher phenolics and flavonoids accumulation respectively than those in control and retained high levels of soluble protein and total sugar at the end of the storage time. Furthermore, peppermint oil treatment significantly improved the antioxidant system, which increased the activity of superoxide dismutase (SOD) and phenylalnine ammonia lyase (PAL), and inhibited the activity of polyphenol oxidase (PPO) and peroxidase (POD), as well as regulated the relative expression levels of genes encoding polyphenol oxidase ( AbPPO1, AbPPO2, AbPPO5, AbPPO6 ) and phenylalanine ammonia lyase ( AbPAL1, AbPAL2 ) during the storage period. These findings suggest that peppermint oil fumigation is a promising method to control browning and improve the quality of button mushrooms.