The pathogenesis of metabolic dysfunction-associated steatotic liver disease （MASLD） is fundamentally rooted in spleen deficiency and is closely associated with phlegm turbidity， damp-heat and blood stasis. Clinically， liver constraint with spleen deficiency and internal retention of damp turbidity represent the predominant traditional Chinese medicine （TCM） syndrome patterns. Researches have indicated intrinsic connections between the syndrome patterns and biological indicators such as gut microbiota and metabolic profiles. Regarding treatment， classical famous formulas， modern empirical formulas， and newly developed TCM drugs show positive effects in regulating glucose and lipid metabolism， improving insulin resistance， and alleviating metabolic inflammation， exhibiting multi-target mechanisms of action； acupuncture and other external therapies also provide adjunctive value. Nevertheless， current researches still have limitations such as the lack of high-quality clinical evidence and insufficient systematic elucidation of the uncerlying mechanisms. Future efforts should focus on conducting high-quality TCM clinical trials with hard endpoint outcomes such as hepatic histology outcomes， and utilizing modern technologies like multi-omics to elucidate TCM's mechanisms of action， thereby advancing the position of TCM as a first-line therapeutic strategy for MASLD.

As a coagulase-negative staphylococcus， Staphylococcus lugdunensis has stronger virulence and pathogenicity than other Staphylococcus bacteria and is comparable to Staphylococcus aureus. In recent years， there has been a gradual increase in the number of related case reports， A patient with hepatitis B cirrhosis and Staphylococcus lugdunensis bloodstream infection was admitted to our department and was followed up for more than 2 years， and the patient was analyzed in terms of clinical features， pathogenicity， invasion， and the application of related antibiotics.

Autoimmune hepatitis （AIH） is an immune-mediated chronic liver inflammatory disease with unknown pathogenesis， and intestinal barrier dysfunction is considered an important factor. Meanwhile， there are sex and age differences in the incidence rate of AIH， suggesting that hormone may be involved in regulation. On this basis， this article focuses on the association between estrogen， intestinal barrier， and immune homeostasis， systematically reviews the evidence that estrogen deficiency disrupts intestinal barrier homeostasis， and further summarizes the potential mechanism of estrogen in regulating the development and progression of AIH via intestinal barrier.

Objective: To understand the epidemiological characteristics and disease burden of influenza like illness (ILI) among student populations, so as to provide data support for policy formulation and optimal allocation of health resources. Methods: From January 2024 to February 2025, a questionnaire survey was conducted among parents of kindergarten, primary school, junior and senior high school students in 9 districts of Shenzhen, including Longhua, Futian, Bao an, Longgang, Luohu, Nanshan, Guangming, Pingshan and Yantian. Parents were asked to complete the questionnaire based on whether their children had fever, cough, vomiting, diarrhea, rash and other common symptoms in 2024. A total of 3 537 parents were investigated, and 444 ILI cases were included as study subjects. The epidemiological burden, including incidence rate of influenza, visitation rate, years lived with disability (YLDs) and economic burden (including direct economic burden, indirect economic burden and intangible burden) were analyzed. Results: The incidence rate of influenza among students in Shenzhen in 2024 was 12.55%. The ILI incidence rates in kindergarten, primary school, junior and senior high school were 14.01%, 11.69% and 5.23%, respectively, with a statistically significant difference ( χ 2= 45.20, P <0.01). The ILI consultation rate among students was 85.36%, and the consultation rates in kindergarten (87.36%) and primary school students (84.62%) were higher than those in junior and senior high school students ( 56.52 %) ( χ 2=16.47, P <0.01). A total of 78.88% of cases did not receive etiological detection.The median total economic burden per ILI case was 2 354.62 yuan, including direct medical costs of 300.00 yuan, direct non medical costs of 212.50 yuan, indirect costs of 1 000.00 yuan, and intangible burden of 500.00 yuan. Conclusions Schools are high risk environment for influenza, and younger students are a high risk group for ILI. The disease burden caused by student ILI remains substantial.

Objective To explore the molecular mechanism of Jianfu mixture in the treatment of erectile dysfunction （ED） by network pharmacology and molecular docking techniques, and validate its core targets and mechanisms through in vitro experiments. Methods The active components and corresponding molecular targets of Jianfu mixture were searched by searching TCMSP and Batman-TCM databases, and the disease targets of ED were searched by using GeneCards database. Find the intersection of drug ingredient target and disease target. The interaction between intersected targets was described and analyzed by String database, and the analysis results were visualized by Cytoscape software to determine the core target and the corresponding active components. GO functional enrichment analysis and KEGG pathway enrichment analysis were performed for intersection targets; the core target within the intersection were found through MCODE plug-in on Cytoscape software and molecular docking was performed with the corresponding active ingredients. An endothelial dysfunction model was established by transfecting HUVECs with si-eNOS. Intervene with different concentrations of the Jianfu mixture for the model cells for 24 h. QPCR was used to detect mRNA expression of core targets （MAPK1, MAPK3, JUN, ESR1, MAPK8）; Western blot was used to analyze protein expression （eNOS, JUN, p-JUN, MAPK, p-MAPK） and phosphorylation levels. Results 144 effective active components and 168 active components target-disease targe intersection of Jianfu mixture were obtained. GO analysis revealed 200 5 biological processes, 151 molecular functions, and 63 cellular components. KEGG analysis yielded 181 pathways. 5 core targets including MAPK1, MAPK3, JUN, ESR1 and MAPK8 were screened out. The active components such as β-sitosterol, kaempferol, astapterocarpan had good binding affinity with the core target. In vitro experiments confirmed successful construction of the endothelial dysfunction model （eNOS expression significantly decreased after si-eNOS transfection）. Jianfu mixture dose-dependently inhibited mRNA expression of MAPK1, MAPK3, JUN, ESR1, and MAPK8. Additionally, it reduced phosphorylation levels of JUN and MAPK, indicating inhibition of the JNK/c-Jun and ERK/MAPK signaling pathways to improve endothelial function. Conclusion Jianfu mixture treats ED by suppressing abnormal activation of multi-target signaling pathways （MAPK/JUN/ESR1）, reducing endothelial apoptosis, and promoting NO synthesis. This mechanism aligns with the traditional Chinese medicine principle of “activating blood circulation, resolving stasis, tonifying Qi, and strengthening cardiovascular function.” The study provided molecular-level evidence for the therapeutic efficacy of Jianfu mixture in ED management.

Objective To explore the molecular mechanism of Jianfu mixture in the treatment of erectile dysfunction （ED） by network pharmacology and molecular docking techniques, and validate its core targets and mechanisms through in vitro experiments. Methods The active components and corresponding molecular targets of Jianfu mixture were searched by searching TCMSP and Batman-TCM databases, and the disease targets of ED were searched by using GeneCards database. Find the intersection of drug ingredient target and disease target. The interaction between intersected targets was described and analyzed by String database, and the analysis results were visualized by Cytoscape software to determine the core target and the corresponding active components. GO functional enrichment analysis and KEGG pathway enrichment analysis were performed for intersection targets; the core target within the intersection were found through MCODE plug-in on Cytoscape software and molecular docking was performed with the corresponding active ingredients. An endothelial dysfunction model was established by transfecting HUVECs with si-eNOS. Intervene with different concentrations of the Jianfu mixture for the model cells for 24 h. QPCR was used to detect mRNA expression of core targets （MAPK1, MAPK3, JUN, ESR1, MAPK8）; Western blot was used to analyze protein expression （eNOS, JUN, p-JUN, MAPK, p-MAPK） and phosphorylation levels. Results 144 effective active components and 168 active components target-disease targe intersection of Jianfu mixture were obtained. GO analysis revealed 200 5 biological processes, 151 molecular functions, and 63 cellular components. KEGG analysis yielded 181 pathways. 5 core targets including MAPK1, MAPK3, JUN, ESR1 and MAPK8 were screened out. The active components such as β-sitosterol, kaempferol, astapterocarpan had good binding affinity with the core target. In vitro experiments confirmed successful construction of the endothelial dysfunction model （eNOS expression significantly decreased after si-eNOS transfection）. Jianfu mixture dose-dependently inhibited mRNA expression of MAPK1, MAPK3, JUN, ESR1, and MAPK8. Additionally, it reduced phosphorylation levels of JUN and MAPK, indicating inhibition of the JNK/c-Jun and ERK/MAPK signaling pathways to improve endothelial function. Conclusion Jianfu mixture treats ED by suppressing abnormal activation of multi-target signaling pathways （MAPK/JUN/ESR1）, reducing endothelial apoptosis, and promoting NO synthesis. This mechanism aligns with the traditional Chinese medicine principle of “activating blood circulation, resolving stasis, tonifying Qi, and strengthening cardiovascular function.” The study provided molecular-level evidence for the therapeutic efficacy of Jianfu mixture in ED management.

OBJECTIVE To explore the improvement effect and potential mechanism of ginsenoside F1 （GF1） on allergic rhinitis （AR） rats based on the mitogen-activated protein kinase （MAPK）/signal transducer and activator of transcription 3 （STAT3） pathway. METHODS Male SD rats were divided into a control group （ n ＝15） and a modeling group （ n ＝55）. The AR rat model was established by basic sensitization with ovalbumin followed by local challenge. The successfully modeled rats were randomly assigned to the AR group， low-dose GF1 group [2.5 mg/（kg·d） ] ， high-dose GF1 group [5 mg/（kg·d） ] ， loratadine group （positive control， 1.5 mg/（kg·d） ] ， and high-dose GF1+MAPK activator group [5 mg/（kg·d） GF1+0.2 nmol C16-PAF ] ， with 10 rats in each group. Another 10 rats from the control group were randomly selected as the blank control group. Rats in each group received corresponding drug solutions or normal saline via intranasal instillation and/or oral gavage once daily for 28 consecutive days. After the final administration， AR symptoms were observed and rhinitis symptom scores were assessed. Histopathological changes of the nasal mucosa were examined. The number of inflammatory cells in nasal lavage fluid， serum levels of inflammatory cytokines [interleukin-4 （IL-4）， IL-17， interferon-γ （IFN-γ） ] and immunoglobulin E （IgE）， as well as the density of goblet cells， the number of mast cells， and the expression of MAPK/STAT3 pathway-related proteins in nasal mucosal tissues were measured. RESULTS Compared with the blank control group， the AR group exhibited marked pathological damage to the nasal mucosal epithelium， characterized by interstitial edema and inflammatory cell infiltration. The rhinitis symptom score， the number of macrophages， lymphocytes， eosinophils， neutrophils and mast cells， the density of goblet cells， the levels of IL-4， IL-17 and IgE， as well as the protein phosphorylation levels of p38 MAPK and STAT3 were significantly increased or elevated， while the level of IFN-γ was significantly decreased in the AR group （ P ＜0.05）. Compared with the AR group， all administration groups showed recovery of nasal mucosal epithelial pathological damage and significant improvements in all quantitative indicators， with the high-dose GF1 group and loratadine group showing more pronounced improvements than the low-dose GF1 group （ P ＜0.05）. C16-PAF significantly reversed the ameliorative effects of GF1 on all quantitative indicators （ P ＜0.05）. CONCLUSIONS GF1 can alleviate rhinitis symptoms in AR rats and inhibit inflammatory responses， which may be related to the inhibition of the MAPK/STAT3 pathway activation.

ObjectiveTo investigate the molecular mechanism by which Feiyanning formula（FYN） regulated exosomal miR-328 to suppress the invasion and metastasis of lung cancer. MethodsIn vitro models using low-metastatic 95C and high-metastatic 95D lung cancer cell lines， along with isolated exosomes， were established. Initially， 95C and 95D cells were cultured， and exosomes were isolated from their supernatants. The exosomes were identified using transmission electron microscopy （TEM）， nanoparticle tracking analysis （NTA）， and Western blot. Exosome uptake assays confirmed that both 95C and 95D cells could internalize exosomes derived from lung cancer patients' plasma. Cell counting kit-8 （CCK-8） assays were performed to assess the inhibitory effects of FYN （0， 0.1， 0.2， 0.4， 0.8， 1.6， 3.2， 6.4 g·L^-1） on 95C and 95D cell proliferation. Subsequent experiments were divided into three groups of control， low-dose FYN （1 g·L^-1）， and high-dose FYN （2 g·L^-1） groups. Wound-healing and Transwell assays were used to evaluate the inhibitory effects of FYN on the migration and invasion of 95C and 95D cells. Western blot was employed to detect the protein expression levels of Janus kinase 2 （JAK2）， signal transducer and activator of transcription 3 （STAT3）， cellular oncogene Fos （c-Fos）， and nuclear factor of activated T cells 1 （NFATc1）. The mRNA expression of miR-328 was measured by Real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsLung cancer plasma-derived exosomes （EXO） enhanced the migration， invasion， and miR-328 expression levels in 95C and 95D cells （P<0.05， P<0.01）. FYN inhibited the proliferation， invasion， and metastasis of 95C and 95D cells in a dose-dependent manner （P<0.01）， with more pronounced effects on 95C cells. Additionally， FYN downregulated exosomal miR-328 expression and suppressed the protein levels of JAK2， STAT3， and its downstream target genes c-Fos and NFATc1 （P<0.01）. ConclusionFYN may inhibit lung cancer metastasis by downregulating exosomal miR-328 expression， potentially through the STAT3/c-Fos/NFATc1 signaling pathway. Further studies are warranted to elucidate its detailed mechanisms and facilitate clinical application， providing insights into traditional Chinese medicine-based strategies for lung cancer treatment.

ObjectiveTo assess changes in the incidence， prevalence， and disability-adjusted life-year （DALY） burden of ulcerative colitis （UC） in China and worldwide from 1990 to 2023 using data from the Global Burden of Disease Study 2023 （GBD 2023）， and to examine demographic drivers and future trends. MethodsUC data for China， the world， and 204 countries and territories were extracted from the GBD 2023 Results Tool. Age-standardized incidence rate （ASIR）， age-standardized prevalence rate （ASPR）， and age-standardized DALY rate （ASDR）， with 95% uncertainty interval （UI）， were obtained. Joinpoint regression was used to estimate average annual percent change （AAPC） and 95% confidence interval （CI）. Spearman rank correlation， inequality and frontier analyses， Das Gupta decomposition， and autoregressive integrated moving average （ARIMA） models were used to assess associations with the sociodemographic index （SDI）， cross-country burden disparities， demographic drivers， and trends from 2024 to 2035， respectively. ResultsIn 2023， the ASIR， ASPR， and ASDR in China were 0.94， 5.95， and 5.94 per 100 000 population， respectively， lower than the corresponding global estimates of 2.87， 28.48， and 13.82 per 100 000 population. From 1990 to 2023， China’s ASIR and ASPR increased， with AAPCs of 2.720% （95% CI： 2.133%-3.309%） and 2.261% （95% CI： 1.617%-2.908%）， whereas the ASDR decreased （AAPC=-3.056%， 95% CI： -3.449% to -2.662%）. Globally， ASIR increased slightly， whereas ASPR and ASDR decreased. In China， the crude incidence， prevalence， and DALY rates peaked at ages 50-54 years， 60-64 years， and ≥95 years， respectively. ASIR and ASPR were positively correlated with SDI （r_s=0.5794 and 0.6177， both P<0.001）， whereas the correlation between ASDR and SDI was not statistically significant （r_s=0.0666， P=0.343）. In China， epidemiological change contributed most to increases in incident and prevalent cases， and changes in age-specific rates contributed most to the decline in DALYs； globally， population growth and population aging contributed most to the increase in DALYs. By 2035， China’s ASIR， ASPR， and ASDR were projected to be 1.23， 6.37， and 2.55 per 100 000 population， respectively. ConclusionsFrom 1990 to 2023， the age-standardized incidence and prevalence rates of UC increased in China， whereas the age-standardized DALY rate decreased， and peaks in absolute burden generally shifted toward middle-aged and older age groups. The projected directions may persist. These findings may provide reference for long-term UC management and health-resource planning.

ObjectiveTo assess changes in the incidence， prevalence， and disability-adjusted life-year （DALY） burden of ulcerative colitis （UC） in China and worldwide from 1990 to 2023 using data from the Global Burden of Disease Study 2023 （GBD 2023）， and to examine demographic drivers and future trends. MethodsUC data for China， the world， and 204 countries and territories were extracted from the GBD 2023 Results Tool. Age-standardized incidence rate （ASIR）， age-standardized prevalence rate （ASPR）， and age-standardized DALY rate （ASDR）， with 95% uncertainty interval （UI）， were obtained. Joinpoint regression was used to estimate average annual percent change （AAPC） and 95% confidence interval （CI）. Spearman rank correlation， inequality and frontier analyses， Das Gupta decomposition， and autoregressive integrated moving average （ARIMA） models were used to assess associations with the sociodemographic index （SDI）， cross-country burden disparities， demographic drivers， and trends from 2024 to 2035， respectively. ResultsIn 2023， the ASIR， ASPR， and ASDR in China were 0.94， 5.95， and 5.94 per 100 000 population， respectively， lower than the corresponding global estimates of 2.87， 28.48， and 13.82 per 100 000 population. From 1990 to 2023， China’s ASIR and ASPR increased， with AAPCs of 2.720% （95% CI： 2.133%-3.309%） and 2.261% （95% CI： 1.617%-2.908%）， whereas the ASDR decreased （AAPC=-3.056%， 95% CI： -3.449% to -2.662%）. Globally， ASIR increased slightly， whereas ASPR and ASDR decreased. In China， the crude incidence， prevalence， and DALY rates peaked at ages 50-54 years， 60-64 years， and ≥95 years， respectively. ASIR and ASPR were positively correlated with SDI （r_s=0.5794 and 0.6177， both P<0.001）， whereas the correlation between ASDR and SDI was not statistically significant （r_s=0.0666， P=0.343）. In China， epidemiological change contributed most to increases in incident and prevalent cases， and changes in age-specific rates contributed most to the decline in DALYs； globally， population growth and population aging contributed most to the increase in DALYs. By 2035， China’s ASIR， ASPR， and ASDR were projected to be 1.23， 6.37， and 2.55 per 100 000 population， respectively. ConclusionsFrom 1990 to 2023， the age-standardized incidence and prevalence rates of UC increased in China， whereas the age-standardized DALY rate decreased， and peaks in absolute burden generally shifted toward middle-aged and older age groups. The projected directions may persist. These findings may provide reference for long-term UC management and health-resource planning.