ObjectiveTo establish a reliable chronic obstructive pulmonary disease (COPD) mouse model based on a self-developed multichannel automatic control system for long-term continuous cigarette smoke exposure in small animals using a novel continuous cigarette smoke exposure method, and to conduct phenotypic evaluation and analysis, thereby providing an animal experimental basis for investigating COPD pathogenesis and prevention strategies. MethodsTwenty male C57BL/6J mice aged 6 weeks were randomly and equally divided into a control group and a model group. The model group (n=10) underwent 6 h of continuous cigarette smoke exposure daily (6 cigarettes per day for 12 consecutive weeks), while the control group (n=10) received no intervention. Body weight was monitored biweekly. Post-exposure, in vivo micro-CT imaging was performed. After euthanasia, serum and bronchoalveolar lavage fluid (BALF) levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were quantified by ELISA. Lung tissues underwent H&E and Masson's trichrome staining to observe changes in lung morphology and inflammatory cell infiltration, and the mean linear intercept (MLI) was calculated, thereby comprehensively evaluating the clinical features of COPD in the mouse model. ResultsCompared with the control group, the model group showed significantly reduced body weight (P<0.01) from the fourth week. Compared with the control group, IL-6 level in the serum and BALF of the model group increased by 27.2% and 140.0%, respectively (P<0.01). TNF-α level in the serum and bronchoalveolar lavage fluid of the model group increased by 16.7% (P<0.01) and 19.3% (P<0.05), respectively. Histopathological examination revealed alveolar wall thinning, septal rupture, emphysematous bullae formation, reduced alveolar count, bronchial wall thickening with lumen narrowing, and inflammatory cell infiltration. MLI was significantly elevated (P<0.01). Masson's staining confirmed collagen deposition and bronchial remodeling. Micro-CT demonstrated localized high-density shadows exhibiting typical features of chronic bronchitis. Conclusion The self-developed device enables long-term continuous smoke exposure, and the successfully established COPD mouse model exhibits pathological features highly consistent with clinical manifestations, offering an efficient and reliable tool for COPD research.

ObjectiveTo evaluate the clinical efficacy of Fuzheng Huaji Formula （扶正化积方） for chronic hepatitis B to reduce the incidence of liver cirrhosis and hepatocellular carcinoma. MethodsA retrospective cohort study was conducted， collecting medical records of 118 patients with chronic hepatitis B and 234 patients with hepatitis B-related cirrhosis who visited the hospital between January 1， 2014， and December 31， 2018. The use of Fuzheng Huaji Formula was designated as the exposure factor. Patients receiving antiviral treatment for hepatitis B without concurrent Fuzheng Huaji Formula therapy were included in the western medicine group， while those receiving antiviral treatment combined with Fuzheng Huaji Formula for a cumulative treatment lasting longer than 3 months were included in the combined treatment group. The follow-up observation period was five years. Kaplan-Meier survival analysis was used to assess the cumulative incidence of cirrhosis in patients with chronic hepatitis B and the cumulative incidence of hepatocellular carcinoma in patients with hepatitis B-related cirrhosis. Univariate and multivariate Cox regression analyses were employed to examine the factors influencing the occurrence of cirrhosis and hepatocellular carcinoma. ResultsAmong patients with chronic hepatitis B， there were 55 cases in the combined treatment group and 63 cases in the western medicine group； among patients with hepatitis B-related cirrhosis， there were 110 cases in the combined treatment group and 124 cases in the western medicine group. Five-year follow-up outcomes for chronic hepatitis B patients showed that the cumulative incidence of cirrhosis was 5.45% （3/55） in the combined treatment group and 17.46% （11/63） in the western medicine group， with a statistically significant difference between groups （Z = 2.003， P = 0.045）. Five-year follow-up outcomes for hepatitis B-related cirrhosis patients showed that the cumulative incidence of hepatocellular carcinoma was 8.18% （9/110） in the combined treatment group and 22.58% （28/124） in the western medicine group， also showing a statistically significant difference （Z = 3.007， P = 0.003）. Univariate and multivariate Cox regression analyses indicated that treatment with Fuzheng Huaji Formula is an independent protective factor in preventing the progression of chronic hepatitis B to cirrhosis and the progression of hepatitis B-related cirrhosis to hepatocellular carcinoma （P＜0.05）. ConclusionCombining Fuzheng Huaji Formula with antiviral therapy for hepatitis B can effectively intervene in the disease progression of chronic hepatitis B， reducing the incidence of cirrhosis and hepatocellular carcinoma.

Portal vein thrombosis (PVT) is one of the most common complications of liver cirrhosis. The formation of PVT can increase the mortality rate of cirrhotic patients and adversely affect the successful implementation and prognosis of liver transplantation. A hypercoagulable state is a unique mechanism underlying PVT formation in cirrhotic patients. In recent years, the pathogenesis of PVT has gradually been elucidated, with specific mechanisms including the following aspects: systemic and local inflammatory responses lead to vascular endothelial cell dysfunction, thereby promoting the activation of the coagulation system; abnormal activation of the monocyte-macrophage system exacerbates local inflammation, enhancing platelet adhesion and aggregation, and facilitating thrombus formation; an imbalance between the coagulation and fibrinolytic systems results in a sustained hypercoagulable state; and intestinal microbiota dysbiosis induces inflammation and metabolic disturbances, thereby increasing the risk of PVT. This article summarizes the latest research progress on these key mechanisms and their interactions, providing new insights into the molecular and cellular mechanisms of PVT. It also offers directions for the early diagnosis of PVT and the exploration of novel intervention strategies in the future.

Primary liver cancer is one of the most common malignant tumors of the digestive system， and the “inflammation-to-cancer transformation” （ICT） of chronic hepatitis is the core pathological process of the progression of chronic hepatitis to liver cancer. Persistent and uncontrolled liver inflammation in patients with chronic hepatitis often leads to repeated liver tissue damage and repair， which gradually develops into liver fibrosis and cirrhosis， eventually leading to malignant transformation through the mechanisms such as gene mutation and microenvironment imbalance. ICT in chronic hepatitis is the key link between chronic hepatitis and liver cancer， and its dynamic evolution involves various pathogenic factors such as dampness， heat， deficiency， toxin， and stasis； among which damp-heat and vital energy deficiency are the initiating factors for ICT of chronic hepatitis， while intermingled stasis and toxin are the key pathological products that promote malignant transformation. Based on the concept of preventive treatment， traditional Chinese medicine can effectively delay and even block the ICT of chronic hepatitis by regulating inflammation， metabolism， and abnormal cell proliferation through multiple targets， which provides important strategies and research directions for the prevention and treatment of liver cancer.

Objective To establish a prediction model for the occurrence of non-occupational carbon monoxide poisoning events in Beijing, and to provide scientific basis and theoretical support for the prevention and warning of poisoning events. Methods Based on the monitoring data of non-occupational carbon monoxide poisoning events in Beijing from 2016 to 2024, the seasonal ARIMA model and seasonal index model were established to analyze the data and predict the occurrence of events. Results Between 2016 and 2024, a total of 436 cases of non-occupational carbon monoxide poisoning were reported in Beijing, showing a downward trend. The established SARIMA model and seasonal index model were SARIMA (1,0,0) (1,1,0) 12, Yt = (-0.0339t+5.8863) × St, and the average relative errors were 65.42% and 29.19%, respectively. In terms of months, the SARIMA model had better predictive performance during April and summer (June to August), while the seasonal index model was superior in other months. By combining the two models, the predicted number of events in 2025 was as follows: 3, 2, 2, 3, 1, 5, 2, 7, 1, 1, 1, and 2. Conclusion The seasonal index model has the best prediction effect on the non-occupational carbon monoxide poisoning events in Beijing throughout the year, and the number of summer events predicted by SARIMA model is closer to the actual values. The two models can be combined to predict the trend of non-occupational carbon monoxide poisoning, which provides a scientific basis for the prevention and control of carbon monoxide poisoning in the future.

Objective To investigate the epidemiological characteristics and control measures of dengue fever in Zhongshan City in 2024, so as to provide insights into optimization of dengue fever control strategies in the city. Methods Data pertaining to dengue fever cases in Zhongshan City in 2024 were collected from the Infectious Disease Reporting System of China Disease Prevention and Control Information System, and the epidemiological characteristics of the cases were analyzed using a descriptive statistical method. The density of Aedes albopictus mosquito was monitored across all 23 townships (subdistricts) using Breteau index (BI) and mosquito ovitrap index (MOI) at midmonth each month from March to December 2024. In addition, the climatic characteristics, case reporting patterns, and corresponding control measures were analyzed during different phases of dengue fever epidemics in Zhongshan in 2024. Furthermore, real-time quantitative reverse transcription PCR (RT-qPCR) assay was employed to serotype the dengue virus among local dengue fever cases with unknown sources of infections. The dengue virus envelope (E) gene was sequenced using Sanger sequencing among dengue fever cases without apparent epidemiological links. A phylogenetic tree was constructed using the neighbor-joining method to infer major transmission chains during the dengue fever epi demics. Results A total of 952 dengue fever cases were reported in Zhongshan City in 2024, including 879 local cases, 57 domestically imported cases from other regions, and 16 overseas imported cases, representing the largest outbreak in nearly two decades. The first local dengue fever case was reported on July 5, and the last one was detected on December 19, with all townships and subdistricts affected. Mosquito monitoring data indicated that both MOI and BI rose rapidly from March to May, and then remained at high levels with fluctuations, and began to decline in October. The dengue fever epidemic was categorized into five distinct phases in Zhongshan, including non-epidemic, pre-epidemic, early-epidemic, peak, and receding stages. During the pre-epidemic and early-epidemic phases, key measures included enhancing sensitivity of case detection, implementing isolation and treatment of hospitalized cases, and carrying out standardized vector control measures in affected communities. In the peak phase, the strategy shifted towards targeted mosquito control in key communities and clinical rescue and treatment emphasized on “preventing severe cases and deaths”. Among 481 local cases with unknown sources of infections, RT-qPCR assay revealed that 68.8% (331/481) were infected with dengue virus type I and 31.2% (150/481) with type II among local dengue fever cases in Zhongshan City in 2024. Phylogenetic analysis revealed two major transmission chains: one originating from imported cases within Guangdong Province around Zhongshan City, and another from cases imported from Malaysia. Late detection of local dengue fever cases contributed to widespread community outbreaks. Conclusions The 2024 dengue fever epidemic in Zhongshan City was of considerable scale, which was primarily driven by imported cases from overseas and surrounding regions, leading to local community outbreaks. The epidemic began in early July, increased rapidly during August and September, peaked in October, and subsequently declined, with a trend consistent with the average pattern observed in previous high-incidence years. By implementing differentiated control measures tailored to each phase of the epidemic, the local transmission of dengue fever was successfully contained in Zhongshan City in 2024.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract, which increases the incidence of colorectal cancer (CRC). In the pathophysiology of IBD, ubiquitination/deubiquitination plays a critical regulatory function. Josephin domain containing 2 (JOSD2), a deubiquitinating enzyme, controls cell proliferation and carcinogenesis. However, its role in IBD remains unknown. Colitis mice model developed by dextran sodium sulfate (DSS) or colon tissues from individuals with ulcerative colitis and Crohn's disease showed a significant upregulation of JOSD2 expression in the macrophages. JOSD2 deficiency exacerbated the phenotypes of DSS-induced colitis by enhancing colon inflammation. DSS-challenged mice with myeloid-specific JOSD2 deletion developed severe colitis after bone marrow transplantation. Mechanistically, JOSD2 binds to the C-terminal of inosine-5'-monophosphate dehydrogenase 2 (IMPDH2) and preferentially cleaves K63-linked polyubiquitin chains at the K134 site, suppressing IMPDH2 activity and preventing activation of nuclear factor kappa B (NF-κB) and inflammation in macrophages. It was also shown that JOSD2 knockout significantly exacerbated increased azoxymethane (AOM)/DSS-induced CRC, and AAV6-mediated JOSD2 overexpression in macrophages prevented the development of colitis in mice. These outcomes reveal a novel role for JOSD2 in colitis through deubiquitinating IMPDH2, suggesting that targeting JOSD2 is a potential strategy for treating IBD.

[This corrects the article DOI: 10.1016/j.apsb.2024.09.010.].

Objective To explore the relationship between serum S100 calcium-binding protein(S100)A4,S100A12 and the infection type and prognosis of neonatal infectious pneumonia(NIP).Methods A total of 300 children with NIP admitted to the Neijiang Second People's Hospital from January 2021 to March 2024 were selected and divided into the bacterial infection group(214 cases)and the non-bacterial infection group(86 cases)according to the types of pathogenic bacteria.Another 150 healthy newborns in the same hospital during the same period were selected as the control group.The levels of serum S100A4 and S100A12 were de-tected by enzyme-linked immunosorbent assay.Pearson correlation analysis was conducted to examine the cor-relations between serum S100A4,S100A12 and procalcitonin(PCT),white blood cell count(WBC),albumin(Alb),and platelet count(PLT).The receiver operating characteristic(ROC)curve was used to evaluate the differential value of serum S100A4,S100A12,PCT,WBC,Alb,and PLT alone and in combination for NIP bac-terial infection.According to the prognosis,children with NIP were divided into the poor prognosis group(63 cases)and the good prognosis group(237 cases).Multivariate Logistic regression model was used to analyze the influencing factors of poor prognosis in children with NIP,and ROC curve was used to analyze the value of each factor in predicting poor prognosis in children with NIP.Results The levels of serum S100A4,S100A12,PCT,WBC,and PLT in the bacterial infection group were higher than those in the non-bacterial infection group and the control group,while Alb was lower than that in the non-bacterial infection group and the control group,the differences were statistically significant(P<0.05).Pearson correlation analysis showed that serum S100A4 and S100A12 in children with NIP were positively correlated with PCT,WBC and PLT(P<0.05),and negatively correlated with Alb(P<0.05).The results of ROC curve analysis showed that the area under the curve(AUC)of serum S100A4 and S100A12 in differentiating NIP infection types was slightly lower than that of PCT,WBC,Alb,and PLT in differentiating NIP infection types.The results of multivariate Logistic re-gression analysis showed that elevated S100A4,elevated S100A12,elevated PCT,bacterial infection,and lung consolidation were independent risk factors for poor prognosis in children with NIP(P<0.05).The AUC of bacterial infection,lung consolidation,PCT,S100A4,and S100A12 for predicting the poor prognosis of chil-dren with NIP was 0.903.It was greater than the AUC predicted separately by bacterial infection,lung consol-idation,PCT,S100A4,and S100A12 levels(Z=9.989,9.460,5.514,4.084,4.376,P<0.001).Conclusion The combination of serum S100A4 and S100A12 with traditional markers has certain discrimina-tory value for the infection types of NIP,and the levels of serum S100A4 and S100A12 are related to the prog-nosis of NIP.

ObjectiveTo investigate the induction of ferroptosis by polyphyllin Ⅱ （PPⅡ） in hepatocellular carcinoma HepG2 cells and its underlying mechanism. MethodThe effect of PPⅡ （0， 1.5， 3.0， 4.5， 6.0， 9.0， 18.0 mg·L^-1） on the in vitro proliferation of HepG2 cells was assessed using the methyl thiazolyl tetrazolium （MTT） assay. Colony formation ability of HepG2 cells was evaluated through a colony formation assay. Cell migration ability was assessed via a scratch assay. Lactate dehydrogenase （LDH） content in HepG2 cells was measured using a kit. Reactive oxygen species （ROS） levels in HepG2 cells were observed using a fluorescence inverted microscope. Malondialdehyde （MDA）， glutathione （GSH）， and free Fe²⁺ content in HepG2 cells were detected using respective kits. The mitochondrial ultrastructure in HepG2 cells was observed by transmission electron microscopy. The expression of ferroptosis-related proteins p53， solute carrier family 7 member 11 （SLC7A11）， glutathione peroxidase 4 （GPX4）， long-chain acyl-CoA synthetase 4 （ACSL4）， and transferrin receptor 1 （TFR1） in HepG2 cells was detected using Western blot. ResultCompared with the control group， the PPⅡ treatment groups showed significantly decreased survival rate of HepG2 cells in a dose-dependent manner （P<0.01）， significantly reduced number of cell colonies （P<0.01）， significantly shortened scratch healing distance， inverse correlation of the migration distance with drug concentration （P<0.01）， significantly increased LDH leakage in cells （P<0.01）， significantly enhanced relative fluorescence intensity of intracellular ROS， and significantly increased accumulation of lipid peroxide MDA （P<0.01）， decreased intracellular GSH content with increasing drug concentration （P<0.01）， and significantly enhanced fluorescence intensity of FeRhoNox-1 in cells （P<0.01）. Moreover， cells exhibited vacuolation， and mitochondria showed significant shrinkage with reduced or even disappeared cristae. Compared with the results in the control group， the expression of p53， ACSL4， and TFR1 proteins significantly increased， while the expression of SLC7A11 and GPX4 proteins significantly decreased in the PPⅡ treatment groups （P<0.05）. ConclusionIn summary， PPⅡ induces ferroptosis in HepG2 cells by regulating the p53/SLC7A11/GPX4 signaling axis， promoting ACSL4 expression and Fe³⁺ uptake， leading to an imbalance in the antioxidant system.