Ningxia Center for Diseases Prevention and Control

This study aimed to investigate the spatiotemporal heterogeneity of human brucellosis and quantify the exposure-lag-response relationships of key socioeconomic and livestock production drivers in Ningxia, China, from 2007 to 2022. The goal was to generate evidence for developing targeted, integrated interventions in this high-burden pastoral region. We conducted a retrospective ecological study integrating human brucellosis surveillance data with county-level socioeconomic and livestock production statistics. A multi-analytic framework was employed: Joinpoint regression analyzed long-term trends; spatiotemporal scan statistics identified high-risk clusters; GeoDetector quantified the explanatory power of potential drivers on spatial heterogeneity; and Distributed Lag Nonlinear Models (DLNMs) were constructed to assess the nonlinear and lagged effects of significant drivers on monthly incidence. The human brucellosis incidence rate in Ningxia increased 167-fold, from 0.52 to 86.83 per 100,000 population between 2007 and 2022. Spatiotemporal analysis revealed a persistent high-risk cluster (Relative Risk, RR = 4.22, P < 0.001) in 11 eastern counties. GeoDetector identified livestock-related factors as primary spatial drivers, with sheep inventory (q = 0.96) and cattle inventory (q = 0.92) showing the highest explanatory power. DLNM results indicated a significant 3-year lagged risk associated with low cattle stocking levels (RR = 2.75), while sheep stocking exhibited a complex, non-linear U-shaped lag effect. In contrast, higher regional Gross Domestic Product (GDP) was associated with an immediate lower risk (RR = 0.81). The brucellosis epidemic in Ningxia is characterized by intense spatial clustering and is associated with distinct, lagged effects of livestock production structures coupled with immediate economic influences. The findings underscore that livestock production metrics can serve as effective proxies for risk mapping even in the absence of direct animal infection data. Our study highlights the necessity for a dual-strategy intervention: implementing risk-based veterinary public health measures in high-incidence clusters while leveraging economic development to strengthen long-term prevention and control capacities.

The health burden of end-stage liver disease continues to grow, and orthotopic liver transplantation remains the only curative treatment. Three-dimensional (3D) culture systems support the in vitro culture of primary liver cells, allowing them to recapitulate native tissue architecture. This technology holds considerable potential for regenerative medicine and disease modeling. However, the practical application of liver organoid (LO) technology is hindered by the inherent limitations of LOs derived from single-tissue sources. In this study, we integrated human umbilical cord mesenchymal stromal cells (hUC-MSCs) into single-source LOs and assessed their effects on organoid formation and function. During the expansion phase, co-culture with hUC-MSCs yielded a 2-fold increase in organoid number compared to LOs cultured alone, although no significant changes were observed in the expression of genes related to organoid lifespan. Liver-specific functions of LOs after 7 day incubated with differentiation medium were further investigated. Despite constructing organoids from mature hepatocytes, co-culture with MSCs promoted non-hepatocyte differentiation, as evidenced by the expression of the cholangiocyte organoid marker cytokeratin 19. Furthermore, LOs co-culture with hUC-MSCs demonstrated increased albumin and urea secretion. In contrast, glucose consumption and ammonia clearance rates showed no significant differences. Following in vivo transplantation, serum biochemical markers normalized in both transplanted and control groups. However, histological analysis revealed superior liver tissue repair in the transplanted group. Our findings indicate that MSCs positively enhance the proliferative capacity of LOs and confer limited functional benefits, and incorporation of MSCs may promote non-hepatic cell differentiation. This effect was particularly evident within the extracellular matrix components of the hydrogel culture system.

BackgroundAllergic asthma is a major health burden. The “hygiene hypothesis” links parasitic infections to the prevention and treatment of allergic asthma. Recombinant Echinococcus granulosus P29 protein (rEg.P29) has been shown to induce the conversion of CD4+ T cells to Th1 in mice, and is widely sourced for translational applications given its composition and biological safety compared with using fine-grained Echinococcus granulosus or antigenic extracts of cystic fluid. However, its effects on allergic asthma remain unclear. Therefore, in this study, we used experiments to investigate how rEg.P29 relieves airway inflammation in mice with allergic asthma and understand the underlying immune mechanisms.MethodsLung histiocytes from mice were examined using single-cell transcriptome sequencing in combination with experimental methods, such as flow cytometry. Serum levels of total immunoglobulin E (IgE), ovalbumin (OVA)-IgE, and inflammatory factors were measured using enzyme-linked immunosorbent assays and cytometric bead array. Finally, cellular communication analysis of target immune cells was performed using bioinformatics approaches.ResultsrEg.P29 significantly alleviated OVA-induced histopathological changes in the lungs of mice with allergic asthma; downregulated serum IgE levels; reduced lung tissue eosinophils, Th2, and Th17 cells; and increased Th1 and Treg cells in mouse lung tissues. The possibility of an interconversion between proliferative pathogenic Th2 cells and stem cell-like Th2 cells was noted. In Treg cells, Nr4a1 targets were detected, and a Lag3+Tnfrsf9+ Treg cell population was identified, which may play an important immunosuppressive role. Finally, CellChat analysis showed significant interactions between stem cell-like Th2 and Th1 cells, proliferative pathogenic Th2 and stem cell-like Th2 cells, and Treg and Th1 cells.ConclusionsrEg.P29 can effectively alleviate OVA-induced airway inflammation in mice with allergic asthma, and multiple T cell subpopulations in lung tissues are collectively involved in the immunological effects of rEg.P29.Graphical abstractSupplementary InformationThe online version contains supplementary material available at 10.1186/s13071-026-07256-w.

BackgroundAlthough skipping breakfast has been associated with an increased risk of metabolic syndrome (MetS), evidence remains limited. Herein, we examined the association between breakfast skipping and MetS, as well as its individual components, among adults aged 35–74 years in Northwest China.MethodsBaseline data were obtained from the Northwest China Cohort–Ningxia Project (CNC-NX), which initially recruited 20,837 participants; 15,959 were included in the final analysis. Demographic characteristics, lifestyle factors, and laboratory results were collected. Logistic regression analyses were performed to evaluate the association between breakfast skipping frequency and MetS. Associations were reported as odds ratios (ORs) with 95% confidence intervals (CIs).ResultsThe prevalence of MetS was 76.7%, with males accounting for 40.2% and females for 59.8%. Compared with participants who never skipped breakfast, those who skipped breakfast ≥4 times per week had a significantly higher likelihood of developing MetS (OR: 1.250, 95% CI: 1.098–1.419). Subgroup analyses revealed that this association was particularly pronounced among males (OR: 1.333, 95% CI: 1.074–1.645) and individuals with a BMI of 24.0–27.9 kg/m2 (OR: 1.328, 95% CI: 1.071–1.637). Frequent breakfast skipping (≥4 times/week) was also significantly associated with an increased risk of several individual MetS components, including elevated fasting blood glucose (OR: 1.328, 95% CI: 1.176–1.502), hypertension (OR: 1.249, 95% CI: 1.075–1.467), and reduced HDL-C levels (OR: 1.377, 95% CI: 1.165–1.638), even after adjusting for confounders.ConclusionBreakfast skipping was significantly associated with MetS among adults aged 35–74 years in Northwest China. Promoting regular breakfast consumption may represent a feasible public health strategy for MetS prevention in this high-risk population.

Methanol (MeOH) is a volatile and flammable liquid commonly used in the construction, automotive, and pharmaceutical industries. It has systemic and ocular toxicity, and most patients with methanol poisoning have severe metabolic acidosis. Occupational inhalation can cause toxic optic neuropathy and bilateral optic atrophy. In this study, we investigated whether the 5'-AMP-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1-alpha/sirtuin-3 (AMPK/PGC-1α/SIRT3) pathway is involved in the methanol-induced mitochondrial dysfunction. A series of behavioral, histological, and pathological assessments was performed. Methanol exposure slowed down the weight growth rate of rats and prolonged escape latencies. In addition, methanol exposure decreased the number of upright times and horizontal movements, damaged cortical neurons, and caused oxidative stress injury. These alterations coincided with neurobehavioral impairments, indicating that methanol exposure may cause oxidative damage and mitochondrial dysfunction by down-regulating the expression levels of the AMPK/PGC-1α/SIRT3 pathway proteins. Treatment with ZLN005, a PGC-1α activator, partially alleviated methanol-induced neurobehavioral deficits and mitochondrial dysfunction, likely via the modulation of the AMPK/PGC-1α/SIRT3 pathway, which may be a novel target for therapeutics aimed to alleviate the effects of environmental neurotoxicants.

BackgroundThe association between multimorbidity and health-related quality of life has been extensively studied. This study aimed to investigate the longitudinal association between multimorbidity and health-related quality of life in a rural Chinese population. Specifically, we sought to: (1) examine how the trajectory of multimorbidity burden influences subsequent health-related quality of life, and (2) explore how the trajectory of health-related quality of life, in turn, influences the incidence of multimorbidity.MethodsBased on a longitudinal survey of the health status of rural community residents aged 18 years and above in 2012, 2015, 2019, and 2022, a group-based trajectory model was used to fit the trajectory of multimorbidity and health-related quality of life utility index over time. Multinomial logistic regression was employed to analyze the association trajectory with outcomes between the health-related quality of life utility index and multimorbidity. A series of sensitivity analyses was used to ensure the robustness of results.ResultsA total of 1,398 residents who completed the four follow-up surveys were included in the analysis. Two trajectories of the health-related quality of life utility index were identified, and the risk of two and three or more multimorbidities in the decline trajectory was 1.95 and 3.78 times greater than that in the stable trajectory, respectively. Two trajectories of multimorbidity were identified: the health-related quality of life utility index decreased by 0.09 in the rapid increase trajectory compared with the slow increase trajectory. The results of the sensitivity analysis remained robust.ConclusionThe trajectory of the health-related quality of life utility index can be used to predict the risk of multimorbidity. Heterogeneous trajectories of chronic disease multimorbidity development lead to differential impacts on the health-related quality of life utility index.

BackgroundAlveolar echinococcosis (AE) is a zoonotic parasitic disease that poses a grave threat to human health. Recent studies have indicated that the gut microbiota plays a significant role in the pathogenesis of alveolar echinococcosis. Consequently, the quest for innovative microbial targeted modulators is anticipated to address the treatment of alveolar echinococcosis. Oxymatrine, an alkaloid extracted from the legume plant Sophora flavescens, has been demonstrated in research studies to regulate gut microbiota, thus treating various diseases, including rheumatoid arthritis and autoimmune encephalomyelitis. Nevertheless, the role of the aforementioned organism in alveolar echinococcosis remains to be elucidated.MethodsThis study evaluated the effects of oxymatrine (OMT) at concentrations of 0.25 mM, 0.35 mM, 0.75 mM, 1 mM, and 1.25 mM on Echinococcus multilocularis protoscoleces in vitro over 48 hours, with cell viability assessed using the CCK-8 assay. Subsequently, an E. multilocularis infection model was established by intraperitoneal injection in mice. After three months of infection, the mice were treated daily with intraperitoneal injections of OMT at doses of 25 mg/kg, 50 mg/kg, or 100 mg/kg, alongside albendazole as a reference treatment, for two months. Fecal samples from each group were collected for 16S rRNA sequencing. Following treatment, tissue samples were analyzed. The liver and spleen indices were calculated by measuring mouse body weight, cyst weight, liver weight, and spleen weight. Hepatic pathological changes were examined using hematoxylin-eosin (H&E) and Masson’s trichrome staining. Additionally, flow cytometry was performed to quantify changes in hepatic CD4+ T cells, CD8+ T cells, and B cells.ResultsIn vitro experimental results demonstrated that treatment with oxymatrine at concentrations of 0.35 mM, 0.5 mM, 0.75 mM, 1.0 mM, and 1.25 mM significantly reduced the viability of Echinococcus multilocularis protoscoleces compared to the control group. The in vivo experimental results demonstrated that, compared with the control group, the 25 mg/kg, 50 mg/kg, and 100 mg/kg OMT-treated groups exhibited significantly reduced cyst weights, marked alleviation of liver inflammatory cell infiltration and fibrosis, and a significant increase in the number of hepatic CD8+ T cells. Furthermore, the 16S rRNA sequencing analysis revealed that OMT intervention enhanced the diversity of gut microbiota.ConclusionOur data indicate that matrine can directly inhibit the growth of Echinococcus multilocularis in vitro, suggesting that matrine may play a therapeutic role in the early stage of alveolar echinococcosis. In vivo studies have shown that three months after infection, matrine can exert an anti-infection effect in the middle and late stages of alveolar echinococcosis by increasing the diversity of intestinal microbiota and the number of CD8+ T cells.

BackgroundSleep disorders are common among pregnant women and can adversely affect maternal and infant health. Traditional statistical methods have limitations in predicting these disorders, highlighting the need for advanced machine learning (ML) approaches. This study aimed to develop a reliable ML model for early prediction of pregnancy-related sleep disorders.MethodsData from 1,681 pregnant women in western China were analyzed. Logistic regression and LASSO regression identified key predictors, with 10 variables selected for Model training. Eight ML algorithms were evaluated using 5-fold cross-validation. SHAP analysis interpreted the model’s decisions.ResultsTen predictors were identified: age, standardized gestational weight gain, gestational weeks, severity of morning sickness, pregnancy intention, pre-pregnancy health, underlying diseases, anxiety, depression, and the combined effect of anxiety and depression. LightGBM achieved the highest AUC (0.718) in the test set, with accuracy of 0.670 and specificity of 0.764. SHAP analysis revealed depression as the strongest predictor (mean |SHAP|=0.26), followed by gestational weeks and Std. GWG.ConclusionThe interpretable and accurate LightGBM model, using clinically feasible variables, is a practical tool for early identification of pregnant women at high risk of sleep disorders. It enables targeted interventions to mitigate sleep - related adverse outcomes, thus improving maternal and infant health.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12884-025-08026-9.

Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus primarily associated with central nervous system disorders. Recent studies have indicated that JEV infection can lead to Guillain-Barré syndrome (GBS), a peripheral nervous system (PNS) disorder; however, the underlying mechanisms remain unclear. In this study, we investigated the tropism of different genotypes of JEV strains for peripheral nerves and their potential impact on peripheral nerves. Four JEV strains-GI NX1889, GI GZ56, GIII P3, and GV XZ0934-representing three prevalent genotypes in China were selected for analysis. Compared with other JEV strains, NX1889 exhibited greater peripheral nerve tropism, leading to peripheral nerve dysfunction, severe pathological changes, and inflammatory responses. Further investigation revealed that Schwann cells (SCs) supported productive replication of GI JEV, but not GIII or GV strains. Although both GI strains infected SCs and caused proliferation inhibition and G1 phase arrest, only NX1889 induced apoptosis. At the symptomatic peak, NX1889-infected mice demonstrated significantly higher viral loads in sciatic nerves and dorsal root ganglia compared to peripheral non-neural tissues and organs. Sciatic nerves exhibited extensive infiltration of CD45 + inflammatory cells and upregulated pro-inflammatory mediators, and the viral load and CCL2 expression in sciatic nerves were positively correlated with limb motor deficits. These findings demonstrate that JEV strains exhibit distinct abilities to induce peripheral nerve injury (PNI), with the variation being a strain-specific characteristic of NX1889 rather than a genotype-specific feature of GI. The peripheral nerve is a vital site for JEV NX1889 replication, and the direct viral invasion of SCs leads to demyelinating neuropathy, with subsequent immune-inflammatory responses exacerbating this injury. This study broadens the spectrum of pathogens known to directly invade and damage peripheral nerves and provides new insights into the pathogenesis of JEV-associated PNI.