Thirteen undescribed 2-O-(β-d-glucopyranosyl)benzyl quinates (1-13) and two reported derivatives (14, 15) were obtained from the twigs and leaves of Casearia tardieuae. The structures of the new compounds were elucidated by comprehensive spectroscopic analysis (1D/2D NMR, HRESIMS, IR, UV), coupled with acid hydrolysis and derivatization studies of the sugar moieties. Biological evaluation showed that compound 1 exhibited antihypertrophic potency comparable to the positive control prazosin, and its cytotoxicity was significantly lower than that of prazosin. Preliminary mechanism investigations revealed that compound 1 suppressed hypertrophy markers ANP/MYH7 at the protein level and downregulated Nppa/Myh7 genes at the transcriptional level, while inhibiting the cellular hypertrophy phenotype. This study first reports undescribed 2-O-(β-d-glucopyranosyl)benzyl quinates from C. tardieuae with significant anticardiac hypertrophy activity, providing important experimental basis for the development of antimyocardial hypertrophy candidate drugs and the study of active components of Casearia species.

Background: Comprehensive, standardized data on psychological and behavioral health among Chinese residents remain limited, constraining population-level research and the development of evidence-based health promotion strategies. Objective: The 2024 Psychology and Behavior Investigation of Chinese Residents aimed to establish a large-scale, multi-center, nationally representative database to support research on physical and mental health among Chinese residents and inform health policy development. Methods: This national cross-sectional survey was conducted from June to September 2024 using a three-stage stratified sampling strategy across 150 cities and 800 communities/villages in China. Of 38,793 distributed questionnaires, 35,861 valid responses were retained after excluding non-consenting, underage, non-Chinese, and insufficiently completed questionnaires, followed by logical quality checks (response rate: 99.05%; qualification rate: 98.95%). Trained investigators administered standardized questionnaires through face-to-face interviews, covering sociodemographic characteristics, personal health status, family information, social environment, psychological scales, behavioral scales, and attitudes toward topical social issues. Multi-level quality control procedures were implemented throughout data collection. Results: Data collection has been completed, yielding a nationally representative dataset with multidimensional information on psychological and behavioral characteristics across 150 cities. Detailed descriptions of sampling outcomes, response rates, and data quality metrics are presented in the full protocol. Conclusion: The 2024 Psychology and Behavior Investigation of Chinese Residents provides a comprehensive, high-quality evidence base to inform post-pandemic health promotion strategies and policy development aimed at improving physical and mental health in China and globally.

ABSTRACT Background The combined prognostic value of continuous glucose monitoring (CGM) metrics and circulating glucose biomarkers for predicting mortality in type 2 diabetes has not been fully established, particularly regarding residual risk in patients achieving glycemic targets. Methods This cohort study included 3677 patients with type 2 diabetes for a median of 7.4 years follow‐up. Cox proportional hazards models evaluated the associations of baseline CGM‐derived time in range (TIR) (target 70%) and serum 1,5‐anhydroglucitol (1,5‐AG) (threshold 6.0 μg/mL) with all‐cause and cardiovascular mortality in the overall population. We further examined the relationship between 1,5‐AG and mortality within TIR subgroups and compared its performance with metrics of glycemic variability derived from CGM. Results During follow‐up, 522 all‐cause deaths and 181 cardiovascular deaths occurred. TIR and 1,5‐AG were moderately correlated and independently predicted mortality, with concurrent low TIR (≤ 70%) and low 1,5‐AG (< 6.0 μg/mL) yielding the highest risk (hazard ratio [HR] 1.82, 95% CI 1.40–2.37). In stratified analyses, reduced 1,5‐AG was significantly associated with increased mortality risk in patients with TIR > 70% (HR 1.69, 95% CI 1.25–2.28), whereas no significant association was observed in those with TIR ≤ 70%. Adding 1,5‐AG improved traditional risk prediction in the former subgroup. Compared with 1,5‐AG, CGM‐derived glycemic variability indices such as mean amplitude of glycemic excursions, coefficient of variation, and standard deviation of glucose showed no significant association with mortality. Conclusions TIR and serum 1,5‐AG offer independent and complementary value, with low 1,5‐AG identifying residual mortality risk despite achieving TIR targets.

Background: Artificial intelligence (AI) is increasingly embedded in routine primary care, yet how the levels of integration might affect its acceptability is unknown, especially in relationship-based service models where patients expect visible human stewardship. Prior experimental studies often treat AI adoption as a binary condition, leaving the "intensity gradient" of automation and the role of model specialization under-explored. We examine whether increasing AI integration in the clinical encounter erodes patients' intention to seek care from family doctors in China, and whether labeling the AI as a medical-specific model buffers such erosion. Methods: We conducted a nationwide online survey experiment in China (N = 2790). Participants were randomly assigned to vignettes that varied by (i) the level of AI integration (low, medium, high) and (ii) the AI type (general-purpose vs. medical-specific large language model), with a human-only care scenario as a reference. Care-seeking intention from family doctors was assessed immediately after exposure. We estimated treatment effects using OLS regression with heteroskedasticity-robust standard errors, and examined the buffering hypothesis through an interaction term between AI integration intensity and AI type. Results: Care-seeking intention declined steadily as AI integration increased (p < 0.001), with the sharpest drop under high-intensity AI integration where clinical decisions were delegated to the AI system. Across all intensity levels, framing the system as a medical-specific AI consistently resulted in higher care-seeking intention than a general-purpose model. However, the interaction between AI intensity and the AI type was not statistically significant (p = 0.508). Conclusions: Patient acceptance of AI in primary care depends not only on whether AI is involved, but on how deeply AI is positioned in the encounter. Medical-specific AI labeling may enhance acceptance across all AI integration levels. The findings underscore the need to preserve human clinical agency in AI-embedded primary care. The results contribute to research on healthcare systems, digital health, and AI-patient interaction.

This paper examines the economic consequences of mass shootings for local communities. Using a stacked difference-in-differences design, we find that mass shootings lead to a deterioration in local economic activity. Affected counties experience declines in entrepreneurship and in the number of local establishments, especially medium- and large-sized establishments. We also find that local bank deposits decline, small-business lending falls, and borrowing costs rise. We identify household out-migration as an important channel. Following a mass shooting, households are more likely to leave affected counties, especially for out-of-state destinations. The migration is stronger when shootings are more severe, receive greater public attention, and occur in politically liberal counties. Overall, the findings suggest that mass shootings impose persistent economic costs by inducing households to move away and weakening the local business and credit environment.

Fibrosis,resulting from excess extracellular matrix(ECM)deposition,is a feature of adipose tissue(AT)dysfunction and obesity-related insulin resistance.Emerging evidence indicates that adipogenic stem and precursor cells(ASPCs)are a crucial origin of ECM proteins and possess the potential to induce AT fibrosis.Here,we employed single-cell RNA-seq and identified a unique subset of ASPCs that were closely associated with ECM function.Within this subset,we discerned a notable upregulation in the expression of fibulin-7(FBLN7),a secreted glycoprotein,in obese mice.Similarly,in humans,FBLN7 levels exhibited an increase in visceral fat among obese individuals and demonstrated a correlation with clinical metabolic traits.Functional studies further revealed that,in response to caloric excess,ASPC-specific FBLN7 knockout mice displayed a diminished state of AT fibrosis inflammation,along with improved systemic metabolic health.Notably,the depletion of FBLN7 in ASPCs suppressed TGF-β-induced fibrogenic responses,whereas its overexpression amplified such responses.Mechanistically,FBLN7 interacted with thrombospondin-1(TSP1)via its EGF-like calcium-binding domain,thereby enhancing the stability of the TSP1 protein.This,in turn,facilitated the conversion of latent TGF-β to its bioactive form,subsequently promoting TGFBR1/Smad signaling pathways.Furthermore,we developed an anti-FBLN7 neutralizing antibody,which could dramatically alleviate diet-in-duced AT fibrosis.These results suggest that FBLN7,produced by ASPCs,exerts a major influence in the development of AT fibrosis and may represent a potential target for therapeutic intervention.

Regulatory T (Treg) cells are considered as key regulators of adipose homeostasis and metabolic health. However, the underlying regulatory mechanisms remain unclear. Here we show that expression of G-protein-signaling modulator 1 (GPSM1) in CD4+ T cells in peripheral blood and visceral fat is significantly upregulated in humans upon obesity and glucose dysregulation. Genomic deletion of GPSM1 in CD4+ T cells or Treg cells in mice results in increased numbers of Treg cells in adipose tissues, restrained inflammation and improved insulin and glucose tolerance upon feeding with high fat diet. These metabolic changes are mediated by the maintenance of a specific CD73+CD103+ Treg cell subpopulation. By contrast, mice with CD4+ T-cell-specific overexpression of GPSM1 are characterized by decreased numbers of Treg cells and are more prone to adipose tissue dysfunction and metabolic deterioration. Mechanistically, a RHOA-cell stiffness-TAZ axis mediates the effects of GPSM1 on the abundance of Treg cells. Furthermore, adoptive transfer of GPSM1-deficent Treg cells promotes energy expenditure and improve glucose and lipid metabolism in Rag1 -/- mice. In summary, GSPM1 expression in Treg cells and especially in a subset specialized for metabolic regulation is an important regulator of the overall energy homeostasis.

Data sharing within psychiatric and behavioral research represents a novel application of ethical principles in practice; however, it suffers from a dearth of practical experience and established ethical norms. In this study, we comprehensively examined the ethical considerations surrounding the acquisition, management, sharing, and utilization of such data. We graded sensitive data and suggest ethical standards for privacy protection based on varying levels of data sensitivity. The objective of this study is to foster orderly and standardized open sharing of psychiatric and behavioral research data, thereby advancing the development and progress of related academic disciplines in China. This Chinese expert consensus has been registered on the International Guide Registration platform (Registration Number: PREPARE-2024CN412).

With the rapid pace of economic development, China has witnessed unprecedented population migration, which exerts a profound influence on migrants' health outcomes. This study used data from the 2023 Yangtze River Delta Health and Life Satisfaction Survey to explore the effects and underlying mechanisms of internal migration on health outcomes. The findings revealed that migration significantly worsened the migrants' health, and that the negative effects were more pronounced for interprovincial migration than for intraprovincial migration. Moreover, the study also found that greater social support could effectively buffer the negative health effects of migration, while the overall evaluation of the local healthcare services mediated this impact. These findings underscored the need for policymakers to reduce regional barriers, strengthen community cohesion, extend public services and social security to migrants, and promote their integration into residential communities through institutional reforms.

Purpose:To evaluate the predictive utility of genetic risk for predicting the presence and longitudinal progression of myopic maculopathy among Chinese pediatric and adult high myopia cohorts. Methods:Highly myopic participants (n = 623, spherical equivalence [SE] <-6.00 diopters [D]) were recruited from 2011 to 2012 and followed up with 2-year intervals. Multivariate logistic regression models and time-to-event analyses using Cox proportional hazards models were adopted to estimate the presence and progression of myopic maculopathy in cross-sectional analyses and follow-up visits. Conventional factors included age, gender, education level, SE, or axial length. Genetic risk factors included polygenic risk scores (PRSs) derived from genome-wide significant single-nucleotide polymorphisms associated with myopia. Results:The participants had a mean age of 21.02 ± 11.85 years and an average SE of -9.76 ± 3.25 D. For the prediction of the presence of myopia maculopathy, the PRS had an odds ratio of 2.62 (95% confidence interval [CI], 1.43-4.85; P = 0.002) and resulted in an area under the receiver operating characteristic curve (AUC) of 0.589. However, adding PRS to the conventional models did not significantly improve prediction (P = 0.155). Likewise, over a follow-up of 4.94 ± 2.75 years, participants in the uppermost PRS quartile demonstrated a 2.33-fold (95% CI, 1.17-4.84; P = 0.018) elevated risk of myopic maculopathy progression compared to the lowest-risk group. The PRS yielded an AUC of 0.578 for forecasting the progression of myopic maculopathy. Integrating the PRS with conventional models did not enhance the prediction accuracy significantly (P = 0.575). Conclusions:The PRS alone fails to predict myopic maculopathy among Chinese highly myopic pediatric and adult populations, and the enhancement in prediction performance is quite limited when it is added to conventional predictors.

Cardiac fibroblasts (CFs) are activated into cardiac myofibroblasts (CMFs) in myocardial infarction (MI) and promote fibrosis, playing a crucial role in deteriorating cardiac function and inducing fatal arrhythmias. Transplantation of bone marrow mesenchymal stem cells (BMSCs) has emerged as a promising therapeutic approach for ischemic heart diseases, including MI. Recent studies have indicated that BMSCs can modulate the survival, differentiation, and antifibrotic activity of CFs. Kruppel-like factor 5 (KLF5) is a significant transcription factor involved in maintaining stem cell properties. In this study, we aimed to investigate whether overexpression of KLF5 could enhance the cardioprotective characteristics of BMSCs, particularly in terms of mitigating structural and electrical remodeling. Our in vivo experiments revealed that transplantation of KLF5-overexpressing BMSCs in mice with MI led to a substantial reduction in ventricular fibrosis and the occurrence of ventricular arrhythmias (VAs). In vitro coculture experiments demonstrated that BMSCs could inhibit CFs activation and cytoskeleton protein bundling induced by hypoxia through paracrine effects, resulting in reduced expression of α-SMA and Collagen I. Furthermore, coculturing BMSCs significantly reduced the expression of connexin 43, alleviated hypoxia, increased the expression of inward-rectifier K+ current (Kir), and decreased voltage-dependent K+ (Kv) currents. Mechanistically, KLF5 enhanced the effects of BMSCs by facilitating the transfer of miR-152-3 p from BMSCs-derived exosomes to CFs. Overall, our findings show that BMSCs transplantation promotes the recovery of cardiac function and reduces the incidence of arrhythmias by inhibiting CFs activation and modulating CFs Kir current remodeling. Additionally, overexpression of KLF5 enhances the cardioprotective effects of BMSCs.

Background:The peritoneal cavity (PerC) constitutes a distinct anatomical compartment that harbors various subpopulations of peritoneal macrophages. However, there remains a significant gap in our understanding of the functions of these macrophage subpopulations in the context of peritoneal metastasis of colorectal cancer (PM-CRC) and their roles in the tumor progression process. This investigation seeks to analyze the characteristics of large peritoneal macrophages (LPMs) and small peritoneal macrophages (SPMs), in the context of PM-CRC. Methods:A murine model of PM-CRC was developed through the intraperitoneal administration of the MC38 colorectal cancer cell line into C57BL/6 mice. Peritoneal effusions were subsequently collected at various time points post-injection and subjected to analysis via flow cytometry, cell co-culture assays, among other techniques. Additionally, clodronate liposomes were employed to deplete peritoneal macrophages in order to investigate the impact of SPMs on tumor progression and survival in the PM-CRC mouse model. Results:The findings of this study demonstrated a significant increase in the number of SPMs during the progression of PM-CRC, concomitant with a decrease in the proportion of LPMs. Notably, SPMs exhibited a macrophage phenotype conducive to tumor growth. In the PM-CRC mouse model, the dynamic escalation of SPMs following lipopolysaccharide stimulation was associated with a reduced survival rate. However, the depletion of SPMs using clodronate liposomes in the later stages of the model effectively extended the survival period in cases of PM-CRC. Conclusions:The findings of this study suggest that SPMs acts as a catalyst in the progression of peritoneal metastasis in colorectal cancer, thereby identifying it as a potential therapeutic target for managing this condition.

There is a dearth of information on wellness program preferences and influencing factors among Chinese health care professionals (HCPs). This study begins to establish a foundation for wellness programming for HCPs in China, especially during public health crises. It sought to (a) examine differences in wellness program preferences across the COVID-19 pandemic phases; (b) identify wellness program patterns and preferences; and (c) explore the influence of sociodemographic and psychological factors on these preferences. One hundred eighty participants (mean age of 33.1 ± 7.8 years) were HCPs from two hospitals in China who completed a battery of measures regarding preference for wellness programs (Wellness Programming Preferences Questionnaire), psychological symptoms (Patient Health Questionnaire-9; Depression, Anxiety, and Stress Scale-21), attitudes about professional help-seeking (Attitude Toward Seeking Professional Psychological Help-Short Form), and coping styles (Simplified Coping Style Questionnaire). Findings revealed that interactive and interpersonal wellness programs were preferred consistently throughout the pandemic. Peer support outreach (53.1%) and various onsite interactive programs, including wellness programming activities (50.6%), relaxation groups (46.7%), and in-person counseling (41.1%), were among the most preferred options. Further, HCPs with higher levels of help-seeking attitudes, t(145) = 3.28, p = .001, and positive coping styles, t(154) = 2.70, p = .008, endorsed higher preferences for an array of wellness programs. Our findings underscore the importance of developing and implementing interactive and interpersonally focused wellness programs to enhance the psychological well-being of Chinese HCPs. Future research should evaluate the effectiveness of culturally sensitive wellness programs for HCPs and compare wellness programming preferences worldwide. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

BackgroundThe COVID-19 pandemic significantly increased the levels of burnout and symptoms of depression, anxiety, and stress among healthcare professionals. However, research on the interrelations between burnout and psychological symptoms is scarce, particularly among psychiatrists. This study addresses this gap in a national sample.MethodData was collected via an online survey conducted in Mainland China from January to March 2021 with a sample size of 3,783 participants. Psychological symptoms were assessed using the Depression, Anxiety, and Stress Scale-21 (DASS-21), and physician burnout was assessed using the Maslach Burnout Inventory-Human Service Survey (MBIHSS). Network analysis was used to examine the interconnection between physician burnout and psychological symptoms, with further analysis conducted on multiple levels, including individual symptoms in central positions or acting as bridges between clusters, and identifying core symptom combinations with significant correlations.ResultsStress emerged as the highest Expected Influence (EI) index, with emotional exhaustion in the burnout cluster being the singular bridge symptom. Furthermore, depressive symptoms such as hopelessness and anhedonia showed a strong and the most straightforward association with emotional exhaustion, while stress-related overreaction was closely associated with depersonalization.ConclusionNetwork analysis between burnout and psychological symptoms identified critical symptoms like stress and emotional exhaustion in Chinese psychiatrists. Close monitoring of these symptoms may be crucial for mitigating the risk of common psychological disturbances and preventing their exacerbation in this population.

Bone cancer pain (BCP) is a complex condition that severely affects patients' quality of life, and its treatment remains challenging. Astaxanthin, a potent antioxidant with anti-inflammatory and neuroprotective effects, and celecoxib, a selective COX-2 inhibitor, have shown synergistic effects in various disease models, but their potential in BCP is unclear. In this study, a mouse BCP model was used to evaluate the analgesic effects of astaxanthin alone and combined with celecoxib on pain-related behaviors, including mechanical allodynia, thermal hyperalgesia, and spontaneous leg-lifting. The combination showed significant synergistic analgesic effects. Transcriptomic data from the Gene Expression Omnibus (GEO) database were analyzed to identify differentially expressed genes (DEGs), and nine core genes were screened by integrating DEGs with BCP-related targets. Machine learning methods (LASSO, random forest, SVM) and cross-validation identified CASP1 and TLR7 as key genes. Immune infiltration analysis, gene immune cell correlation, and molecular docking further supported the therapeutic potential of the drug combination and the importance of CASP1 and TLR7. This study provides new molecular targets and candidate drugs for BCP treatment, laying a foundation for future research.

The activation of blood monocytes and the infiltration of monocyte-derived macrophages into the vessel walls are the central part of atherosclerosis. However, the mechanisms underlying the processes remain unclear. Here, we report that G-protein signaling modulator 1 (GPSM1) plays a critical role in atherogenesis. We found that GPSM1 expression in lesional macrophages was increased during atherosclerosis development both in mice and humans. Myeloid-specific GPSM1 ablation protects mice against atherosclerosis and reduces aortic inflammation in both Apoe −/− mice and an AAV-PCSK9 injection model. Conversely, myeloid-restricted overexpression of GPSM1 accelerates aortic inflammation and promotes atherosclerosis development in mice. Mechanistically, GPSM1 deficiency suppressed monocyte activation including chemotaxis and adhesion through inhibition of the p38/ERK MAPK pathway regulated by the cAMP/PKA/KLF4/PMP22 axis, thereby alleviating proinflammatory responses within atherosclerotic plaques. Blockade of PMP22 using siRNA-loaded liposomes protected GPSM1 overexpression mice from atherosclerosis. Furthermore, a small-molecule compound inhibiting GPSM1 function could suppress atherosclerosis in vivo. In conclusion, our findings establish that GPSM1 is a regulator of atherosclerosis development and targeting GPSM1 might be a promising therapy against atherosclerosis.

Colorectal cancer (CRC) is a major global health issue. Despite advancements in treatment, CRC patients still face challenges of metastasis and variable prognosis. Circulating tumor cells (CTCs) shed from the primary tumor into the peripheral blood circulation provide new insights into the potential molecular mechanisms driving tumor progression and metastasis.In this study, we comprehensively analyzed CTC data, primary tumor tissue data, and metastatic tumor tissue data from CRC patients to identify pathways associated with CRC metastasis, with a specific focus on the transport processes of vitamins, nucleosides, and related molecules. Using machine learning techniques, we identified Solute Carrier Family 27 Member 1 (SLC27A1) as the biomarker most closely associated with CRC metastasis. SLC27A1 is responsible for transporting extracellular long-chain fatty acids (LCFAs) into cells, and the model constructed based on the expression level of this gene achieved an accuracy of over 95% in assisting the assessment of patients' metastatic risk across different datasets.Further studies revealed that the process of intracellular LCFAs being catalyzed to synthesize diacylglycerol-3-phosphate (DAG-3P) is closely related to CRC metastasis. Laboratory experiments confirmed that downregulation of SLC27A1 expression in colorectal cancer cell lines (Caco-2 and T84) significantly inhibited cell migration and invasion abilities, directly validating the functional role of this gene in promoting tumor metastasis. Additionally, statistical analysis using data from the National Health and Nutrition Examination Survey database (2017-2020) showed a slightly higher incidence of cancer in populations with high-fat intake.These findings, integrating computational predictions and experimental validation, deepen our understanding of the biological mechanisms of colorectal cancer and provide potential targets for therapeutic interventions and personalized treatment strategies.

Lung cancer is one of the most prevalent and lethal malignant tumors worldwide. Currently, clinical diagnosis primarily relies on chest X-ray examinations, histopathological analysis, and the detection of tumor markers in blood. However, each of these methods has inherent limitations. The current study aims to explore novel diagnostic approaches for lung cancer by employing attenuated total reflection-Fourier transform infrared (ATR-FTIR) spectroscopy in conjunction with multiple machine learning models. Fourier transform infrared spectroscopy can detect subtle differences in the material structures that reflect the carcinogenic process between lung cancer tissues and normal tissues. By applying principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA) to analyze infrared spectral data, these subtle differences can be amplified. The study revealed that the combination of spectral bands within the 3500-3000 cm-1 and 1600-1500 cm-1 ranges is particularly significant for differentiating between the two groups. Three classification models—Support Vector Machine (SVM), k-Nearest Neighbor (kNN), and Linear Discriminant Analysis (LDA)—were constructed for spectral analysis of various band combinations. The results indicated that in detecting lung cancer samples, the combination of the 3500-3000 cm-1 and 1600-1500 cm-1 bands offers significant advantages. The analysis of the receiver operating characteristic (ROC) curve demonstrated that the area under the curve (AUC) exceeded 0.95 for all models, with the LDA model achieving an accuracy rate of 99.4% in identifying lung cancer patients compared to healthy individuals. The findings suggest that the integration of ATR-FTIR spectroscopy with multiple machine learning models represents a promising auxiliary diagnostic method for clinical lung cancer diagnosis, enabling detection at the molecular level.