Stroke is the leading cause of death and disability among adults in China， and its common complications include digestive system abnormalities， cognitive impairment， depression， stroke-associated pneumonia， and hemiplegia. The combination of traditional Chinese and Western medicine has great potential in treating post-stroke complications. Xinglou Chengqitang （XLCQT） is a representative prescription of alleviating the disease in the upper part by treating the lower part. It has definite therapeutic effect and high safety. Clinically， XLCQT is often used to treat stroke and its complications. However， the quantity and quality of clinical trials of XLCQT in treating post-stroke complications need to be improved. Additionally， since the basic research is weak， the material basis and multi-target mechanism for the efficacy of this prescription are unknown. This article reviews XLCQT in terms of the pharmacodynamic basis， medicinal properties， safety evaluation， and progress in clinical research and mechanisms in treating post-stroke complications. This article summarizes 22 key active ingredients of XLCQT in treating acute stroke complicated with syndrome of phlegm heat and fu-organ excess. Among these key active ingredients， resveratrol， kaempferol， luteolin， chrysoeriol， apigenin， （+）-catechin， and adenosine have good pharmacokinetic properties and high bioavailability. The mechanisms of XLCQT in treating post-stroke complications are complex， including inflammatory response， brain-gut axis， hypothalamic-pituitary-adrenal （HPA） axis， intestinal flora， neurotrophic factors， autophagy， oxidative stress， and free radical damage. This review helps to deeply understand the pharmacodynamic basis and mechanisms of XLCQT in treating post-stroke complications and provides a theoretical basis for the clinical application of XLCQT against post-stroke complications and the development of drugs.

ObjectiveTo investigate the therapeutic effects and mechanisms of Qinlian Hongqutang （QLHQT） on nonalcoholic steatohepatitis （NASH）. MethodsC57BL/6J mice were randomly divided into normal and modeling groups. The NASH model was established by feeding a high-fat diet for 12 weeks. After successful modeling， mice were randomly assigned to the model group， low-， medium-， and high-dose QLHQT groups （0.51， 1.02， and 2.04 g·kg^-1）， and a positive control metformin group， with six mice in each group. The mice were treated for 8 weeks. Body weight was recorded before and after treatment. Serum levels of total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C）， as well as hepatic TC， TG， and LDL-C contents， were determined by biochemical assays. Hematoxylin-eosin （HE） staining and oil red O staining were used to evaluate liver histopathology and lipid deposition， respectively. Flow cytometry， enzyme-linked immunosorbent assay （ELISA）， and Real-time polymerase chain reaction （Real-time PCR） were used to assess hepatic macrophage expression and related markers. Western blot and immunofluorescence were used to investigate the potential mechanisms of QLHQT in regulating macrophage polarization. ResultsCompared with the normal group， body weight and serum and hepatic levels of TC， TG， and LDL-C were significantly increased in the model group （P<0.01）. Liver histopathology showed unevenly distributed round lipid droplets in the hepatocyte cytoplasm， accompanied by inflammatory cell aggregation. Flow cytometry showed that the proportion of CD86-positive cells was significantly increased， whereas the proportion of CD206-positive cells was markedly decreased （P<0.05）. Hepatic inducible nitric oxide synthase （iNOS） levels and tumor necrosis factor-α （TNF-α） mRNA expression were significantly increased， while hepatic IL-10 levels and IL-4 mRNA expression were significantly decreased （P<0.01）. The protein expression levels of Toll-like receptor 4 （TLR4）， tumor necrosis factor receptor-associated factor 6 （TRAF6）， and myeloid differentiation factor 88 （MyD88） in the liver were significantly increased （P<0.01）. Compared with the model group， body weight was reduced in the high-， medium-， and low-dose QLHQT groups and in the metformin group. Serum and hepatic TC， TG， and LDL-C levels were significantly decreased （P<0.01）. Liver histopathology showed alleviated hepatic lipid deposition， with markedly reduced lipid droplets and inflammation. Immunofluorescence and flow cytometry showed that the proportions of CD86-positive cells were significantly decreased， whereas the proportions of CD206-positive cells were significantly increased in the high-， medium-， and low-dose QLHQT groups （P<0.05）. Hepatic iNOS levels and TNF-α mRNA expression were significantly decreased （P<0.01）， whereas hepatic IL-10 levels and IL-4 mRNA expression were significantly increased （P<0.01）. The hepatic protein expression levels of TLR4， TRAF6， and MyD88 were significantly decreased， while signal transducer and activator of transcription 6 （STAT6） phosphorylation was significantly increased （P<0.05， P<0.01）. There was no statistically significant difference in total STAT6 protein expression. ConclusionQLHQT effectively ameliorates hepatic inflammation in NASH mice， and the mechanism may involve STAT6- and TLR4-mediated signaling pathways driving polarization of M1 macrophages toward the M2 phenotype.

ObjectiveTo investigate the therapeutic effects and mechanisms of Qinlian Hongqutang （QLHQT） on nonalcoholic steatohepatitis （NASH）. MethodsC57BL/6J mice were randomly divided into normal and modeling groups. The NASH model was established by feeding a high-fat diet for 12 weeks. After successful modeling， mice were randomly assigned to the model group， low-， medium-， and high-dose QLHQT groups （0.51， 1.02， and 2.04 g·kg^-1）， and a positive control metformin group， with six mice in each group. The mice were treated for 8 weeks. Body weight was recorded before and after treatment. Serum levels of total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C）， as well as hepatic TC， TG， and LDL-C contents， were determined by biochemical assays. Hematoxylin-eosin （HE） staining and oil red O staining were used to evaluate liver histopathology and lipid deposition， respectively. Flow cytometry， enzyme-linked immunosorbent assay （ELISA）， and Real-time polymerase chain reaction （Real-time PCR） were used to assess hepatic macrophage expression and related markers. Western blot and immunofluorescence were used to investigate the potential mechanisms of QLHQT in regulating macrophage polarization. ResultsCompared with the normal group， body weight and serum and hepatic levels of TC， TG， and LDL-C were significantly increased in the model group （P<0.01）. Liver histopathology showed unevenly distributed round lipid droplets in the hepatocyte cytoplasm， accompanied by inflammatory cell aggregation. Flow cytometry showed that the proportion of CD86-positive cells was significantly increased， whereas the proportion of CD206-positive cells was markedly decreased （P<0.05）. Hepatic inducible nitric oxide synthase （iNOS） levels and tumor necrosis factor-α （TNF-α） mRNA expression were significantly increased， while hepatic IL-10 levels and IL-4 mRNA expression were significantly decreased （P<0.01）. The protein expression levels of Toll-like receptor 4 （TLR4）， tumor necrosis factor receptor-associated factor 6 （TRAF6）， and myeloid differentiation factor 88 （MyD88） in the liver were significantly increased （P<0.01）. Compared with the model group， body weight was reduced in the high-， medium-， and low-dose QLHQT groups and in the metformin group. Serum and hepatic TC， TG， and LDL-C levels were significantly decreased （P<0.01）. Liver histopathology showed alleviated hepatic lipid deposition， with markedly reduced lipid droplets and inflammation. Immunofluorescence and flow cytometry showed that the proportions of CD86-positive cells were significantly decreased， whereas the proportions of CD206-positive cells were significantly increased in the high-， medium-， and low-dose QLHQT groups （P<0.05）. Hepatic iNOS levels and TNF-α mRNA expression were significantly decreased （P<0.01）， whereas hepatic IL-10 levels and IL-4 mRNA expression were significantly increased （P<0.01）. The hepatic protein expression levels of TLR4， TRAF6， and MyD88 were significantly decreased， while signal transducer and activator of transcription 6 （STAT6） phosphorylation was significantly increased （P<0.05， P<0.01）. There was no statistically significant difference in total STAT6 protein expression. ConclusionQLHQT effectively ameliorates hepatic inflammation in NASH mice， and the mechanism may involve STAT6- and TLR4-mediated signaling pathways driving polarization of M1 macrophages toward the M2 phenotype.

ObjectiveTo investigate the safety and efficacy of transparent cap-assisted peroral cholangiopancreatoscopy-guided electrohydraulic lithotripsy （EHL）. MethodsA retrospective analysis was performed for the clinical data of 60 patients with large common bile duct stones who were admitted to Department of Gastroenterology， Jilin People’s Hospital， from May 1， 2023 to January 31， 2026， and according to the treatment method， the patients were divided into transparent cap-assisted peroral cholangiopancreatoscopy-guided electrohydraulic lithotripsy group and peroral cholangiopancreatoscopy-guided electrohydraulic lithotripsy group， with 30 patients in each group. The two groups were compared in terms of the rate of successful single-session stone fragmentation and removal， procedural time， duration of electrohydraulic lithotripsy， clinical success rate， and complications. The independent-samples t test or the Mann-Whitney U test was used for comparison of continuous data between two groups， and the chi-square test or the Fisher’s exact test was used for comparison of categorical data between two groups. ResultsCompared with the peroral cholangiopancreatoscopy-guided electrohydraulic lithotripsy group， the transparent cap-assisted peroral cholangiopancreatoscopy-guided electrohydraulic lithotripsy group had a significantly higher technical success rate （83.33% vs 60.00%， χ²=4.022， P=0.045） and significantly shorter procedural time ［46.00 （42.25 — 49.00） min vs 54.50 （42.00 — 65.00） min， Z=2.012， P=0.044］ and duration of electrohydraulic lithotripsy ［8.00 （6.25 — 11.75） min vs 13.50 （9.25 — 17.75） min， Z=2.749， P=0.006］. Both groups achieved a clinical success rate of 100%， with no significant difference in the incidence rate of complications （P>0.05）. ConclusionTransparent cap-assisted peroral cholangiopancreatoscopy-guided electrohydraulic lithotripsy has a high rate of successful single-session stone fragmentation and removal and a short procedural time， with good safety and efficacy， and therefore， it holds promise for clinical application.

Objective Mendelian randomization(MR)analysis was used to explore the genetic link between immunophenotype and breast cancer(BC)risk and how cerebrospinal fluid(CSF)metabolites play a part in mediating this.Methods We used MR to assess the genetic associations between immune cells and BC risk and their possible mediators.Genetic statistics for immune cells and CSF metabolites were obtained from the Genome-Wide Association Study(GWAS)catalog,whereas those for BC were obtained from the Japan Biobank,the UK Biobank,and FinnGen's cross-ethnic meta-analysis.We performed a two-sample MR analysis using inverse variance weighting(IVW)to investigate the genetic association between immunoepidemiology and BC.We also analyzed CSF metabolites as mediators between them.Heterogeneity was tested using the Cochran's Q statistic,horizontal pleiotropy was tested using the MR Egger intercept,and sensitivity analysis was performed using the"leave-one-out"method.Results MR analysis by the IVW method showed that HLA DR+CD4+T cells were associated with a reduced risk of BC(OR=0.972,95％ CI:0.955-0.990,P=0.003),and there was a negative genetic association between HLA DR+CD4+T cells and methylsuccinimidyl carnitine level(OR=0.922,95％ CI:0.861-0.986,P=0.018),but there was a positive genetic association between the latter and BC risk(OR=1.029,95％ CI:1.012-1.047,P＜0.001).Mediation analysis showed that the direct effect remained significant after correction for CSF methylsuccinylcarnitine level(β=-0.026,SE=0.008,P=0.002).And the indirect effect(β=-0.002,Delta Method SE=0.001)suggested that this CSF metabolite might mediate 8.36％of the association in the protective effect of immune cells against BC risk(95％ CI:-12.4％-29.1％).Conclusion Genetically predicted HLA DR+CD4+T cells may reduce the risk of BC development by modulating the level of methylsuccinylcarnitine,the CSF metabolite.

Objective To investigate the causal relationship between circulating white blood cells(WBC)and juvenile idiopathic arthritis(JIA)using a two-sample Mendelian randomization(MR)analysis,and to provide a reference for the treatment strategy of JIA.Methods Relevant data of WBC and JIA were extracted from the public data of genome-wide association studies.Then,bidirectional MR analysis was conducted using the inverse variance weighted method(IVW),MR-Egger regression method,mixed contamination method,and Bayesian weighted Mendelian randomization.A series of sensitivity analyses were used to verify the robustness of the results.Results After MR analysis,false discovery rate(FDR)correction and sensitivity verification,calculations using IVW as the main method showed that neutrophils could reduce the risk of JIA(OR=0.752,95%CI:0.622,0.908,P=0.003,PFDR=0.003),and that JIA could lead to increased monocyte counts(bete=0.015,95%CI:0.007,0.022,P=1.90E-04,PFDR=1.14E-03).Conclusion A bidirectional causal association is identified between WBC and the risk of JIA occurrence.

The sepsis and sepsis-induce lung inju-ry threats seriously human health.Dexmedetomi-dine(DEX),a sedative drug,plays an active role in preventing sepsis-induced lung injury during the ba-sic and clinical practice.The current article reviews the role and mechanism of DEX dexmedetomidine alleviating sepsis-induced lung injury from the as-pects of inflammation,oxidative stress,apoptosis,mitochondrial dynamics,autophagy,vascular per-meability,neuro-regulation,targeting miR-128-3p/MAPK14 and DNA methylation,etc.This review looks forward to deepen the understanding the ap-plication of DEX in the field of critical care medi-cine,expand the pharmacological effect of DEX and provide a new idea for the prevention and treat-ment of sepsis from the sedation approach.

Objective:To develop a health education intervention program for minor stroke patients based on the information-knowledge-attitude-practice (IKAP) theory and to verify its application effectiveness.Methods:A convenience sampling method was used to select 31 minor stroke patients admitted to the Emergency Department of Xuanwu Hospital, Capital Medical University, from September to October 2023 as the control group, and another 31 patients admitted from November to December 2023 as the experimental group. The control group received routine health education, while the experimental group implemented the health education program based on the IKAP theory. Knowledge, attitude, and practice of the patients were assessed using the Stroke Knowledge, Attitude, and Practice Questionnaire before the intervention, immediately after the intervention, and 3 months post-intervention.Results:Immediately after the intervention, the knowledge, attitude, and behavior scores of patients in the experimental group were higher than those of the control group, and the differences were statistically significant (all P<0.05); three months after the intervention, the knowledge and attitude scores of patients in the experimental group were higher than those of the control group, and the differences were statistically significant (all P<0.05). Conclusions:The health education intervention program based on the IKAP theory can effectively improve the knowledge, attitude, and practice levels of minor stroke patients, with lasting effects.

Objective Mendelian randomization(MR)analysis was used to explore the genetic link between immunophenotype and breast cancer(BC)risk and how cerebrospinal fluid(CSF)metabolites play a part in mediating this.Methods We used MR to assess the genetic associations between immune cells and BC risk and their possible mediators.Genetic statistics for immune cells and CSF metabolites were obtained from the Genome-Wide Association Study(GWAS)catalog,whereas those for BC were obtained from the Japan Biobank,the UK Biobank,and FinnGen's cross-ethnic meta-analysis.We performed a two-sample MR analysis using inverse variance weighting(IVW)to investigate the genetic association between immunoepidemiology and BC.We also analyzed CSF metabolites as mediators between them.Heterogeneity was tested using the Cochran's Q statistic,horizontal pleiotropy was tested using the MR Egger intercept,and sensitivity analysis was performed using the"leave-one-out"method.Results MR analysis by the IVW method showed that HLA DR+CD4+T cells were associated with a reduced risk of BC(OR=0.972,95％ CI:0.955-0.990,P=0.003),and there was a negative genetic association between HLA DR+CD4+T cells and methylsuccinimidyl carnitine level(OR=0.922,95％ CI:0.861-0.986,P=0.018),but there was a positive genetic association between the latter and BC risk(OR=1.029,95％ CI:1.012-1.047,P＜0.001).Mediation analysis showed that the direct effect remained significant after correction for CSF methylsuccinylcarnitine level(β=-0.026,SE=0.008,P=0.002).And the indirect effect(β=-0.002,Delta Method SE=0.001)suggested that this CSF metabolite might mediate 8.36％of the association in the protective effect of immune cells against BC risk(95％ CI:-12.4％-29.1％).Conclusion Genetically predicted HLA DR+CD4+T cells may reduce the risk of BC development by modulating the level of methylsuccinylcarnitine,the CSF metabolite.

Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis, which is primarily transmitted through the respiratory tract, and remains one of the diseases with the highest mortality rate of single-pathogen infections globally. The cell wall polysaccharides of M. tuberculosis are critical for maintaining bacterial structure, mediating pathogenesis, and enabling immune evasion. Lipoarabinomannan (LAM), a key polysaccharide component, has revolutionized non-invasive diagnostic technologies as a TB biomarker, while polysaccharide-based vaccines have emerged as innovative strategies for TB prevention. This review systematically examines the composition, subcellular distribution, and functional roles of M. tuberculosis cell wall polysaccharides in bacterial metabolism, drug resistance, and immune regulation. A particular emphasis is placed on recent advancements in LAM-based diagnostics and vaccine development. Future studies should utilize advanced technologies to precisely characterize the structural features of TB polysaccharides and explore their biological functions, providing a foundation for targeted diagnostic and therapeutic innovations. This article aims to provide reference for advancing both basic research and clinical applications related to M. tuberculosis.