👤 Ying-Pu Sun

Low physical activity (LPA) is associated with cardiovascular and cerebrovascular pathologies. This study aimed to assess the prevalence of several noncommunicable diseases relating to LPA. Using the 2021 Global Burden of Disease data set, we modelled LPA-related disease burdens across 204 countries and territories, quantifying mortality counts, age-standardised mortality rates, and disability-adjusted life years (DALYs) for five noncommunicable diseases. We conducted multivariable stratification analyses to assess variations by gender, age, and sociodemographic index (SDI) quintiles. We used age-period-cohort modelling to project burden trajectories, while applying counterfactual decomposition frameworks to delineate synergistic interactions between LPA and risk factors. We found that LPA accounted for 555 101 related deaths globally in 2021 across the five studied pathologies, mostly among individuals aged 60-94 years. Association between LPA-related disease burden and SDI followed a U-shaped distribution across regions and diseases. Among individuals aged 60-89 years, LPA-related deaths were significantly higher in women than in men, indicating a disproportionate burden on elderly females. Ischaemic heart disease (IHD) trends stabilised in low- and middle-SDI regions but declined significantly in high-SDI regions, underscoring global health disparities. From 2007 to 2011, LPA DALYs and mortality risk ratios for IHD, stroke, and lower extremity peripheral arterial disease declined from >1 to <1, whereas diabetes mellitus exhibited an opposite trend, highlighting LPA's persistent and significant impact on diabetes-related morbidity. Demographic shifts and epidemiological transitions were primary drivers of LPA-related disease burden across five pathologies. In high-SDI regions, epidemiological changes predominated, whereas population growth was a key factor in low- and middle-SDI regions. Synergistic interaction of these factors with LPA is projected to substantially amplify future disease burden. Physical activity should be increased among elderly women to address health risks associated with LPA. Likewise, urgent public health interventions are needed for LPA-related diabetes. As IHD burden rises in low- and middle-SDI regions, vascular disease care strategies require optimisation. Moreover, high-SDI regions should strengthen nationwide physical activity promotion, while low- and middle-SDI areas must enhance healthcare infrastructure and manage population growth to reduce LPA-related disease burdens. Show less

Cardiovascular-Kidney-Metabolic (CKM) syndrome is characterized by the interrelatedness of chronic kidney disease, cardiovascular disease, and metabolic disorders. Although physical activity is widely acknowledged as an effective intervention for improving the prognosis of chronic diseases, its impact on all-cause mortality among patients with CKM syndrome remains unclear. To investigate the impact of physical activity on all-cause mortality among patients with CKM syndrome. Data from the 2011 wave of the China Health and Retirement Longitudinal Study were used as the baseline, with follow-up conducted until 2013. According to the International Physical Activity Questionnaire criteria, weekly physical activity levels were divided into three categories: light-volume physical activity (LPA), moderate-volume physical activity (MPA), and vigorous-volume physical activity (VPA). Cox proportional hazards regression models were employed to assess the impact of varying levels of physical activity on all-cause mortality. Restricted cubic spline analysis was used to explore possible nonlinear relationships. A total of 3343 patients with CKM syndrome were enrolled in this study. During the 2-year follow-up period, 44 deaths were recorded. After adjusting for potential confounders, VPA was associated with a 54% lower risk of all-cause mortality (adjusted hazard ratios, 0.46; 95% confidence interval: 0.24-0.89). Dose-response relationships demonstrated that all-cause mortality decreased as physical activity increased, with a 5.8% reduction in all-cause mortality risk for every 1000 MET-min/week increment in physical activity levels. VPA was significantly associated with reduced all-cause mortality in patients with CKM syndrome. Encouraging patients with CKM syndrome to engage in increased physical activity may improve clinical outcomes. Key messages What is already known on this topic: Cardiovascular-Kidney-Metabolic (CKM) syndrome involves a complex interplay between cardiovascular disease, metabolic disorders, and chronic kidney disease. While prior studies have established that physical activity can decrease mortality risk in the general population as well as in patients with cardiovascular and metabolic syndromes, the evidence regarding its impact on individuals with CKM syndrome remains limited. Additionally, there is a lack of detailed dose-response analyses of physical activity specifically targeting this high-risk population. What this study adds: This study provides novel evidence indicating that vigorous-volume physical activity (>3000 MET-minutes/week) significantly decreases all-cause mortality by 54% among patients with CKM syndrome, whereas moderate-volume, and light-volume physical activities show no significant effects. Notably, a linear dose-response relationship was established, demonstrating that each 1000-MET increment corresponds to a 5.8% reduction in mortality risk. These findings address a critical knowledge gap by quantifying both the threshold and incremental benefits of physical activity specifically for individuals with CKM syndrome, a population characterized by unique multisystem pathophysiology. How this study might affect research, practice, or policy: The findings of this study have the potential to substantially impact clinical practice by offering evidence-based thresholds for physical activity recommendations in the management of CKM syndrome. The benefits associated with vigorous-volume physical activity (>3000 MET-minutes/week) may encourage guideline committees to formulate more precise exercise prescriptions tailored to this high-risk population. Additionally, these results can be incorporated into a multidisciplinary care framework designed for managing complex chronic conditions. Show less

Gestational exposure to micro- and/or nanoparticles (M/NPs) may be closely associated with adverse maternal and offspring outcomes involving multiple organ dysfunctions. Organ functional change is achieved through metabolic adaptation in response to changes in the external environment; yet, intricacies of these organ dysfunctions and underlying metabolic changes remain poorly understood, particularly at spatial suborgan level. Using a pregnant mouse model exposed to polystyrene (PS)-M/NPs (sizes: 100 nm, 5 μm, 10 mg/L in drinking water) from gestation day 1 to 18, we construct a comprehensive multisub-organ lipid metabolic landscape. This analysis integrates MALDI-mass spectrometry imaging with histological assessment to monitor changes in maternal suborgans-placenta-fetus unit. Our findings reveal distinct metabolic responses between maternal and fetal organs to gestational PS-M/NPs exposure. We identify potential targeted suborgans and spatial biomarkers associated with PS-M/NPs exposure according to histological damage and metabolic remodeling, including placental junctional and labyrinth zone (e.g., phosphatidylserine, phosphatidylethanolamine [PE]), renal cortex of maternal kidney (e.g., ceramide [Cer], PE, sphingomyelin [SM], phosphatidylglycerol [PG], phosphatidylserine), ventricular muscular layer and interventricular septum of maternal heart (e.g., PE, lysophosphatidylethanolamine [LPE], lysophosphatidic acid [LPA]), fetal brain and spinal cord (e.g., Cer), and fetal liver (e.g., Cer). Furthermore, phosphatidylserine synthesis and glycolipid metabolism pathways are found to be exclusively enriched following PS-NP and PS-MP exposure in the multiorgan network, respectively. We propose an M/NPs scale-exposed suborgan effect framework, which provides a molecular foundation and potential spatial biomarkers for elucidating intersub-organ interactions in response to M/NPs exposure and their role in mediating pregnancy state. Show less

Assessing white matter hyperintensity (WMH) is essential for the diagnosis, treatment, and prognosis of multiple sclerosis (MS) and neuromyelitis optical spectrum disorder (NMOSD). MS and NMOSD present dispersed small lesions alongside larger aggregated lesions that are irregularly shaped, posing challenges for the automatic segmentation of WMH on magnetic resonance images. Furthermore, research on NMOSD brain WMH segmentation is limited due to the rare nature of the disease. This study aims to propose a deep learning method for MS and NMOSD brain WMH segmentation. In this study, we propose a 2.5D Fourier Convolutional ResUnet (FrC-ResUnet). It utilizes a spectral encoder to extract global information, enabling accurate segmentation of scattered lesions. Additionally, the model incorporates the selective features module (SFM) and the convolutional block attention module (CBAM) to enhance lesion-background differentiation and outline the lesions distinctly. We evaluated our approach on the MS public and local datasets of MS and NMOSD. Compared to U-Net, ResUNet, FC-DenseNet, AttentionUNet, lesion prediction algorithm (LPA) and Sequence Adaptive Multimodal SEGmentation (SAMSEG), the 2.5D FrC-ResUnet achieved the highest Dice similarity coefficient (DSC) on three different datasets, with values of 0.710, 0.667, and 0.822, respectively. The 2.5D FrC-ResUnet demonstrates accurate and robust segmentation of NMOSD brain WMH. Meanwhile, the model excels in segmenting MS brain WMH, particularly when confronted with irregularly shaped and dispersed lesions. Show less

Although light-intensity physical activity (LPA) has been suggested to be associated with a lower risk of mortality, the minimal and optimal volumes of LPA remain unclear. We aimed to examine the minimal and optimal volumes of LPA associated with the risks of mortality and disease incidence (i.e., cardiovascular diseases and cancer). Data were derived from the population-based UK Biobank cohort study, including 69,492 adults aged 43-78 years. Accelerometer-measured LPA was defined using a validated, published machine learning-based Random Forest activity method, which was categorized into 4 quartile groups. All-cause and cause-specific mortality (cardiovascular disease- and cancer-specific) were determined according to the International Classification of Diseases, 10th version codes. Disease incidence was defined based on primary care, hospitalization, or death records. During a median follow-up period of 8.04 years, 2024 adults died from all causes, 539 from cardiovascular disease, and 1175 from cancer. For all-cause mortality, compared with participants in the lowest quartile of LPA (<3.9 h/day), the hazard ratios (HRs) and 95% confidence intervals (95%CIs) were 0.82 (95%CI: 0.73‒0.93) for those with 3.9 to <5.0 h/day, 0.75 (95%CI: 0.66‒0.85) for those with 5.0 to <6.1 h/day, and 0.77 (95%CI: 0.68‒0.88) for those with ≥6.1 h/day, respectively. There was an inverse non-linear dose-response association between LPA and all-cause mortality, with an optimal dose of 5.72 h/day (95%CI: 5.45‒6.41; HR = 0.63, 95%CI: 0.56‒0.71) and a minimal dose of 3.59 h/day (95%CI: 3.53-8.56; HR = 0.81, 95%CI: 0.78‒0.86), with the 5th percentile as the reference. Similar patterns were observed for cause-specific mortality and disease incidence (cardiovascular disease and cancer). Engaging in LPA for ∼3.5 h/day was conservatively associated with lower risk of mortality and disease incidence, with further risk reductions observed up to an optimal dose of ∼6.0 h/day. These findings suggest that sufficient LPA offers important health benefits, which can inform the development of future PA guidelines. Show less

This study systematically examines the relationship between mindfulness and metacognition among Chinese college students through a person-centered analytical approach. Using latent profile analysis (LPA) of Five Facet Mindfulness Questionnaire (FFMQ) responses, we identified four distinct mindfulness profiles: (1) High Observation/Low Non-reactivity, (2) High Awareness/Judging, (3) Moderately Mindful, and (4) Highly Mindful. Gender differences were observed across profiles, with female students more represented in the Highly Mindful group. Hierarchical regression analyses revealed that mindfulness profiles significantly predicted metacognitive ability, with the Highly Mindful group demonstrating superior metacognitive self-regulation and learning strategy application. These findings contribute to the literature by identifying distinct mindfulness subtypes and their differential relationships with metacognition. The results suggest that educational interventions emphasizing non-judgmental present-moment awareness may be particularly effective for fostering students' metacognitive development, while highlighting the importance of considering individual differences in mindfulness training approaches. Show less

Physical fitness in preschoolers, encompassing muscular strength, speed-agility, balance, and cardiorespiratory fitness, serves as a key health indicator. While preschools are ideal settings for promoting physical fitness, the association between preschool-based movement behaviors and physical fitness remains unclear. This cross-sectional study included 1144 Chinese preschoolers aged 3-6 years. Preschool-based movement behaviors including moderate-to-vigorous physical activity (MVPA), light physical activity (LPA), and sedentary behavior (SB), were measured using ActiGraph GT9X accelerometers. Physical fitness was assessed via the PREFIT battery, which includes handgrip strength, standing long jump, 4 × 10 m shuttle run, one-leg stance, and 20 m shuttle run. Compositional linear regression and isotemporal substitution modeling were employed to examine associations and time-reallocation effects, respectively. Greater amounts of MVPA during preschool hours were positively associated with better performance in muscular strength, speed-agility, and cardiorespiratory fitness. Reallocating time from SB or LPA to MVPA enhanced physical fitness, whereas substituting MVPA with SB or LPA reduced fitness levels, demonstrating an asymmetric effect. Moderate-to-vigorous physical activity during preschool hours significantly enhances physical fitness. Prioritizing the implementation of physical activity programs to increase MVPA in preschool settings is crucial for improving physical fitness and addressing insufficient MVPA in this age group. First large-scale study (N = 1144) demonstrating preschool-based moderate-to-vigorous physical activity (MVPA) is essential for developing preschoolers' muscular strength, speed-agility, and cardiorespiratory fitness, complementing existing 24-h movement behavior research. Reveals critical asymmetry: Reducing MVPA time significantly harms fitness, with losses exceeding the benefits from equivalent MVPA increases. Provides objective evidence to guide policymakers in optimizing preschool schedules to prioritize MVPA for enhancing children's physical fitness. Show less

The mediation effect of 24-hour physical activities on the association between type 2 diabetes and mortality is unclear. Additionally, Little evidence was found on the isotemporal substitution effect of 24-hour physical activities components on changing Life expectancy among patients with type 2 diabetes diagnosed. To address the abovementioned research gap, the study has a two-fold aims: first, to examine the mediation effect of 24-hour physical activities in type 2 diabetes and mortality; and second, to address how reallocating time on different daily activities would affect life expectancy. Analysis was conducted on the accelerometer data of 103,359 participants in the UK Biobank, with a median age of 57 years (range 39 to 70). Compositional mediation cox model was conducted to analyze the mediating effects of 24-hour physical activities. Additionally, the cohort Life table method was utilized to estimate the changes of Life-years over the next 10 years resulting from the substitution effect of different physical activities. During a mean follow-up of 13.95 (range 2.95-16.28) years, 2,649 deaths were recorded. Diabetes was significantly associated with increased time spent engaging in sedentary behavior (SB), and reduced time spent on moderate-to-vigorous physical activity (MVPA) and light-intensive physical activity (LPA), thereby demonstrating an association with higher mortality risk. The indirect effect of physical activity (HR = 1.27, 95% CI 1.23-1.30) accounted for 41.9% of the total effect of diabetes on mortality. Furthermore, the Life expectancy gains with a maximum of 1.32 years over the next 10 years was found when reallocating SB time to MVPA. The results revealed that 24-hour physical activities might mediate the association between diabetes and mortality. Therefore, promoting participation in MVPA and reducing sedentary activities among diabetes patients was expected to have a positive effect on Life expectancy over the next 10 years. Show less

This study examines how distinct Information and Communication Technology (ICT) engagement profiles impact life satisfaction among older adults, aiming to inform digital inclusion policies for aging populations. Cross-sectional data from 717 older adults in Central China were analyzed using latent profile analysis (LPA) to identify distinct ICT engagement profiles, followed by multinomial logistic regression to examine predictors of profile membership. LPA identified 3 profiles: Quiescent (39.75%), Compliant (42.96%), and Active (17.29%) Users. Active Users reported significantly higher life satisfaction ( Show less

Paraneoplastic syndromes arise when tumor-derived cytokines reprogram distant organs. Although mediators such as Interleukin-6 have been implicated, how these signals impair host organ function remains incompletely defined. Here, we identify a cytokine-lipid axis that drives hepatic autophagy dysfunction. Specifically, in Show less

Lymphoplasmacytic Lymphoma (LPL) with immunoglobulin (Ig)A paraprotein is rare. When plasma cells dominate, the diagnosis becomes more challenging. We reported a case of a 71-year-old male with elevated creatinine, splenomegaly, monoclonal IgA, and MYD88 mutation. Only monoclonal plasma cells were detected first, leading to a misdiagnosis of multiple myeloma. When progressive spleen enlargement was observed, re-evaluation revealed the emergence of monoclonal lymphocytes and the diagnosis was revised to LPL. The addition of rituximab to DVD regimen led to a partial response. For cases where an initial definitive diagnosis cannot be established, close follow-up is required for timely diagnosis revision and therapeutic adjustment. Show less

Metabolic dysfunction-associated fatty liver disease (MAFLD), driven by dyslipidemia and hepatic lipid deposition, has become a major public health concern. Angiopoietin-like protein 3 (ANGPTL3), a lipoprotein lipase (LPL) activity inhibitor, can inhibit triglycerides (TGs) decomposition, and fibroblast growth factor 21 (FGF21) enhances fatty acids' β-oxidation in liver. We constructed a novel fusion protein combining the anti-ANGPTL3 nanobody FD03 and FGF21 (FD03-FGF21), which exerted appropriate binding affinities to ANGPTL3 and β-Klotho respectively. Our results showed FD03-FGF21 restored bioactivity of LPL which inhibited by ANGPTL3 and activated downstream pathway of FGF21 in iLite FGF21 assay-ready cells. Next, FD03-FGF21 showed a significant therapeutic effect in MAFLD mice, including attenuation of metabolic dyslipidemia, hepatic lipid accumulation, and impaired glucose tolerance. Compared to other treatments, FD03-FGF21 achieved the most significant therapeutic effect with a 79.78 % attenuation of low-density lipoprotein cholesterol (LDL-C) and a 95.8 % reduction of hepatic lipid accumulation. Mechanistically, transcriptomic analysis revealed that differential expression genes (DEGs) were principally clustered into lipid metabolism and oxidative stress pathways after the fusion protein treatment, especially the key lipid metabolism genes of LDLR and CD36 were significantly upregulated and downregulated respectively, as confirmed by WB. Furthermore, lipidomic and metabolomic analysis indicated the fusion protein ameliorated disorders in lipid and protein metabolism mainly through the downregulation of DG and upregulation of PC. Hepatic oxidative stress and inflammation were significantly reduced after administration of the fusion protein in MAFLD mice. Collectively, FD03-FGF21 represents an effective therapeutic strategy for MAFLD therapy through ameliorating lipid metabolism and oxidative stress. Show less

2,2',4,4'-tetrabromodiphenyl ether (BDE-47) is a common environmental contaminant and widely detected in aquatic surroundings, while only a few reports exist on the hazard mechanism in economic aquatic animals. It has been shown that 40 and 4000 ng/g of BDE-47 dietary exposure over 42 days significantly increased the levels of blood triglycerides, glucose, and liver glycogen in carp ( Show less

Lung adenocarcinoma (LUAD) has become the most common pathological pattern of lung cancer in recent decades. Prediction of biological behavior of LUAD is crucial for disease management and treatment options. The objective of this study was to identify significant genes related with prognosis of LUAD, and to investigate the role and biological mechanism of caveolin-1 (CAV1) in LUAD. Bioinformatical analysis was used to identify significant genes related to the prognosis of LUAD based on GEO datasets. Then the mechanisms underlying these critical genes were explored. Enrichment analysis was implemented based on CAV1 related differentially expressed genes subsequently. The expressions of CAV1 and EGFR in LUAD tissues and adjacent tissues were detected by Western blotting, immunohistochemistry and microarray technology. Kaplan-Meier survival analysis and cox regression analysis were performed to verify the correlation between CAV1 expression level and the prognosis of LUAD. The expression of CAV1 in PC-9, H1299 and H1975 cells was inhibited by siRNA transfection. CAV1 overexpression plasmid was constructed and transfected into A549 cells. Cell proliferation was detected by cell Titer-Glo, CCK-8 and colony formation assay. Scratch test was used to compare cell migration ability. Transwell assay was used to compare cell invasion ability. Cell apoptosis and cell cycle were detected by flow cytometry. The effect of CAV1 on EGFR degradation was verified by cycloheximide inhibition assay. Western blotting was used to detect the phosphorylation of AKT and STAT3, the expression of epithelial-mesenchymal transition (EMT) -related molecular markers and apoptosis-related Bax/Caspase-3/Bcl-2 pathway. The GFP plasmid loaded with shRNA was transfected into PC-9 cell line by lentivirus infection. Three groups of stable PC-9 cell lines, including shNC, shCAV1-1 and shCAV1-2 were obtained. The phenotypic experiments of proliferation, invasion, migration and apoptosis were completed. Western blotting was used to detect the phosphorylation of AKT and STAT3, as well as apoptosis-related Bax/Caspase-3/Bcl-2 pathway markers. In vivo experiments, including subcutaneous tumor formation experiment and immunohistochemical detection of CAV1, EGFR and Ki-67 were performed. Comprehensive analysis of GSE130779, GSE32863 and GSE85841 datasets identified 3 up-regulated DEGs and 86 down-regulated DEGs, which were significantly enriched in malaria pathway and proteoglycans in cancer pathway. CAV1 and CAV2 may inhibit tumor growth by degrading EGFR. Thirteen core genes including ADH1B, ALDH1A1, CAV1, CAV2, CLDN18, CXCL2 (GRO2), EDNRB, GNG11, LPL, PDK4, SCGB1A1, SDPR and SFTPC were down-regulated in LUAD tissues, which were associated with better prognosis of lung cancer significantly. Enrichment analysis of CAV1-related DEGs identified the endocytosis pathway, suggesting that CAV1 was involved in the development of LUAD by degrading EGFR through endocytosis. CAV1 was highly expressed in paracancerous tissues, and there was a negative correlation between the tissue locations of CAV1 and EGFR. Kaplan-Meier survival analysis of the cohort study showed that higher Cav-1 levels were associated with longer overall survival, and the difference was significant. Both in vitro and in vivo, CAV1 knockdown increased EGFR level, while CAV1 overexpression decreased EGFR level. This effect was mediated by Cav-1 promoting EGFR degradation. Cav-1 further inhibited the phosphorylation of downstream AKT/STAT3 pathway of EGFR. Caveolin-1 positively regulated the Bax/Caspase-3/Bcl-2 pathway, thereby participating in mediating apoptosis. Cav-1 can suppress the proliferation, migration and invasion of LUAD, while promote cell apoptosis. Our findings demonstrate that CAV1 exerts its anti-tumor effects, at least in part, by inhibiting EGFR degradation and modulating the AKT/STAT3 pathway, as well as enhancing the Bax/Caspase-3/Bcl-2 signaling pathway in LUAD cells. These results suggest that targeting CAV1 may represent a promising therapeutic strategy for the treatment of LUAD patients. Show less

The relationship between high-density lipoprotein (HDL) and atherosclerotic risk remains incompletely elucidated, potentially due to the inherent heterogeneity of HDL particles. Hypertriglyceridemia is associated with alterations in HDL composition. This study investigated the impact of elevated triglycerides (TG) on HDL and its association with coronary artery disease (CAD) risk using a large prospective cohort study and Mendelian randomization (MR). We found that elevated TG was associated with reduced HDL particle size, decreased concentrations of HDL components, and increased triglycerides in HDL (HDL-TG) (all P for trend < 0.001). The protective effects of HDL particle concentration and HDL cholesterol on CAD are attenuated with increasing serum TG levels. An independent and positive association between HDL-TG levels and incident CAD events (hazard ratio [HR] per 1 standard deviation increase: 1.066, 95% CI: 1.052-1.080, P < 0.001) was confirmed even after adjustment for established cardiovascular disease risk factors. MR analyses supported a causal role for HDL-TG in CAD development (inverse-variance weighted [IVW] method: odds ratios [ORs] of 1.120 (95% CI: 1.053-1.192, P < 0.001) and 1.141 (95% CI: 1.032-1.263, P = 0.010) for dataset groups 1 and 2, respectively). Drug-target MR analyses suggested a potential association between omega-3 fatty acids (OM3-FA) and lower HDL-TG levels, with LPL and DGAT2 as key pharmacological targets. Our findings suggest that elevated TG contributes to adverse alterations in HDL, elevating CAD risk. HDL-TG is an independent positive risk factor for CAD and a potential causal contributor to CAD development. OM3-FA supplementation may offer a therapeutic strategy for mitigating the CAD risk associated with elevated HDL-TG. Show less

Light-responsive porous liquids (LPLs) attract significant attention for their controllable gas uptake under light irradiation, while their preparation has remained a great challenge. Here we report the fabrication of type II LPLs with enhanced light-responsive efficiency by tailoring the host's functionality for the first time. The functionality of light-responsive metal-organic cage (MOC-RL, constructed from dicopper and responsive ligands) is modified by introducing the second long-chain alkyl ligand, producing MOC-RL-AL as a new host. A spatially hindered solvent based on polyethylene glycol, IL-NTf Show less

Dynamic responsive structural colored materials have drawn increased consideration in a wide range of applications, such as colorimetric sensors and high-safety tags. However, the sophisticated interactions among the individual responsive parts restrict the advanced design of multimodal responsive photonic materials. Inspired by stimuli-responsive color change in chameleon skin, a simple and effective photo-crosslinking strategy is proposed to construct hydroxypropyl cellulose (HPC) based hydrogels with multiple responsive structured colors. By controlling UV exposure time, the structural color of HPC hydrogels can be effectively controlled in a full-color spectrum. At the same time, HPC hydrogels showcase temperature and mechanical dual-responsive structural colors. In particular, the microstructure of HPC hydrogels undergoes a transition from the chiral nematic phase to the nematic phase under the action of external stretching, leading to a significant reflection of circularly polarized light (CPL) to linearly polarized light (LPL). Given the diverse responsiveness exhibited by HPC hydrogels and their unique structural transition properties under external forces, we have explored their potential applications as dynamic anti-counterfeiting labels and optical skins. This work reveals the great possibility of using structural colored cellulose hydrogels in multi-sensing and optical displays, opening up a new path for the exploration of next-generation flexible photonic devices. Show less

Inflammation is a complex factor in the pathogenesis of intracranial aneurysms (IA), but its specific cellular inflammatory factors remain uncertain. We collected two cohorts and measured the representation of vascular inflammation-related proteins using the Olink CVD II Vascular Inflammation Panel. We subsequently validated our findings using ELISA and RT-qPCR. Our proteomic analysis identified 11 vascular inflammation-related markers that were significantly differentially represented between the IA and control groups. These markers were implicated in leukocyte migration, immune response, triglyceride and lipoprotein metabolism, acute phase response, T cell regulation, and several key biological pathways, including PPAR, HIF-1, cytokine-cytokine interactions, and PI3K-AKT signaling. Further validation with ELISA and RT-qPCR confirmed the differential representation of IL6, PTX3, LPL, and OLR1 between the two groups. Notably, a combination marker incorporating these four factors demonstrated high diagnostic potential for the early detection of IA. Our study has identified a set of informative biomarkers (IL6, PTX3, LPL, and OLR1) that could be valuable for the early diagnosis of IA. Importantly, this is the first report of significantly elevated OLR1 representation in the plasma of IA patients. Further investigation into the role of OLR1 in the pathogenesis of IA is warranted. SIGNIFICANCE: This study significantly advances our understanding of the molecular mechanisms underlying intracranial aneurysm (IA) pathogenesis. By identifying a panel of novel biomarkers, including the previously unreported elevated expression of OLR1 in IA patients, we provide crucial insights into the inflammatory processes involved in aneurysm formation and development. These findings have important clinical implications, as the identified biomarkers could serve as valuable tools for early diagnosis and potentially targeted therapeutic interventions. Furthermore, the study highlights the complex interplay of inflammatory pathways in IA, suggesting that a multi-faceted approach may be necessary for effective management. Show less

Studies showed that contaminants adhered to the surface of nano-polystyrene microplastics (NPs) have a toxicological effect. Juveniles tilapia were dispersed into four groups: the control group A, 75 nm NPs exposed group B, 5 ng·L Show less

The aim of this study was to investigate the ameliorative effects of pterostilbene (PTE), a polyphenolic compound, on stress-induced lipid metabolic disorders in the liver of broiler chickens. Six hundred healthy, 1-day-old Arbor Acres with similar weight were randomly assigned to five groups, each consisting of eight replicates with 15 broilers per replicate. The groups included: a control group (fed a basal diet), and four groups treated with corticosterone (CORT) at varying dietary levels of PTE supplementation: CORT (0 mg/kg PTE), CORT-PT200 (200 mg/kg PTE), CORT-PT400 (400 mg/kg PTE), and CORT-PT600 (600 mg/kg PTE). The results indicated that PTE administration to corticosterone (CORT)-injected broilers significantly improved weight gain, reduced liver index, and lowered the elevation of serum aspartate aminotransferase, gamma-glutamyl transferase, glucose, total cholesterol, triglycerides, and lipoprotein cholesterol concentrations induced by CORT injection (P<.05), but had no significant effect on serum CORT concentration (P>.05). PTE also significantly reduced the increased rate of abdominal fat deposition induced by CORT, decreased the average size of adipocytes, and downregulated the expression of the FAS gene (P<.05). It reversed the increase in liver total cholesterol, triglycerides, lipoprotein cholesterol, and non-esterified fatty acids content induced by CORT (P<.05). PTE had no significant effect on the expression of the glucocorticoid receptor (P>.05), but significantly upregulated the protein expression of Sirt1 and p-AMPK (P<.05), promoted the expression of lipid autophagy genes MAP1LC3B and lipolytic genes LPL, but inhibited the expression of fatty acid synthesis genes SREBP-1c, ACC, and SCD (P<.05). The addition of PTE to the diet alleviated CORT-induced oxidative stress and inflammation by enhancing T-SOD and GSH-Px activities, reducing MDA content, inhibiting p-NF-κB p65 and NLRP3 expression and the release of TNF-α and IL-1β in the serum, and increasing IL-4 content (P<.05). Overall, dietary PTE effectively regulates lipid metabolism and antioxidant status, offering a potential strategy to mitigate stress-induced metabolic disruptions in broilers. Show less

Emodin has been proven to have weight-reducing and lipid-lowering effects. In order to make emodin play a better anti-obesity role, we designed and developed an emodin loaded dissolving microneedle patch, in which emodin existed in the form of emodin-polyvinylpyrrolidone co-precipitate (Emodin-PVP). Meanwhile, polydopamine (PDA) was added to the microneedle patch (PDA-Emodin-PVP-MN) for photothermal-enhanced chemotherapy of obesity. The average weight of the patch was 0.1 ± 0.05 g and the drug loading was 0.37 ± 0.031 mg. After 5 min of NIR irradiation (808 nm, 0.6 W/cm Show less

To investigate the regulatory role of MACF1 and its upstream transcriptional control in focal adhesion remodeling and tumor progression in lung adenocarcinoma (LUAD). We employed in vitro loss- and gain-of-function assays using shRNA-mediated knockdown and ectopic overexpression of MACF1 and NR2F1 in LUAD cell lines (H1299 and Calu-3). Cell proliferation, adhesion, and migration were assessed by CCK-8, EdU, crystal violet, and Transwell assays. In vivo tumor growth and metastasis were evaluated using subcutaneous and tail vein xenograft models in nude mice. RNA-seq and GSEA were performed to identify MACF1-regulated pathways, followed by nuclear-cytoplasmic fractionation, dual-luciferase reporter assays, and immunofluorescence to assess WNT/β-catenin activity. ChIP-qPCR and ChIP-seq data from ENCODE were used to validate NR2F1 binding to the MACF1 promoter. MACF1 knockdown significantly suppressed LUAD cell proliferation, DNA replication, adhesion, and migration, and reduced tumor burden and lung metastases in vivo. Mechanistically, MACF1 activated WNT/β-catenin signaling by promoting CTNNB1 nuclear translocation, which upregulated focal adhesion genes (Paxillin, FAK, ITGB1). CTNNB1 agonist TWS119 restored focal adhesion in MACF1-deficient cells. Bioinformatic prediction and ChIP validation identified NR2F1 as a transcription factor directly targeting the MACF1 promoter. NR2F1 deficiency reduced MACF1 expression and phenocopied its functional loss, while MACF1 overexpression rescued the impaired phenotype. Our study uncovers a previously unrecognized NR2F1-MACF1-WNT axis that drives focal adhesion formation and LUAD progression. Targeting this regulatory circuit may offer new avenues for anti-metastatic therapy in lung adenocarcinoma. 1. NR2F1 is identified as a direct upstream transcription factor that activates MACF1 expression in LUAD. 2. MACF1 promotes LUAD cell proliferation, adhesion, and migration by enhancing focal adhesion assembly. 3. MACF1 activates the WNT/CTNNB1 signaling cascade, facilitating CTNNB1 nuclear translocation and downstream target expression. 4. Loss of MACF1 impairs focal adhesion formation and metastatic potential both in vitro and in xenograft and tail vein models. 5. The NR2F1-MACF1-WNT axis represents a novel regulatory circuit driving LUAD metastasis and offers potential therapeutic targets. Show less

The microtubule actin crosslinking factor 1 ( Trios-based whole-exome sequencing was performed on a cohort with generalised epilepsy from the China Epilepsy Gene 1.0 project. The spatial-temporal expression, single-cell sequencing and genotype-phenotype correlation were analysed to explore the role of Two de novo heterozygous and eight biallelic Show less

Citrin deficiency (CD) is caused by the inactivation of SLC25A13, a mitochondrial membrane protein required to move electrons from cytosolic NADH to the mitochondrial matrix in hepatocytes. People with CD do not like sweets. Here we show that SLC25A13 loss causes the accumulation of glycerol-3-phosphate (G3P), which activates the carbohydrate response element-binding protein (ChREBP) to transcribe FGF21, which acts in the brain to restrain intake of sweets and alcohol and to transcribe key genes driving lipogenesis. Mouse and human data suggest that G3P-ChREBP is a mechanistic component of the Randle Cycle that contributes to metabolic-dysfunction-associated steatotic liver disease and forms part of a system that communicates metabolic states from the liver to the brain in a manner that alters food and alcohol choices. The data provide a framework for understanding FGF21 induction in varied conditions, suggest ways to develop FGF21-inducing drugs and suggest potential drug candidates for lean metabolic-dysfunction-associated steatotic liver disease and support of urea cycle function in CD. Show less