ObjectiveTo evaluate the impact of yang-reinforcing and blood-activating therapy on the long-term prognosis for patients with dilated cardiomyopathy （DCM） of yang deficiency and blood stasis syndrome. MethodsA retrospective cohort study was conducted involving 371 DCM patients with yang deficiency and blood stasis syndrome. The yang-reinforcing and blood-activating therapy was defined as the exposure factor. Patients were categorized into exposure group （186 cases） and non-exposure group （185 cases） according to whether they received yang-reinforcing and blood-activating therapy combined with conventional western medicine for 6 months or longer. The follow-up period was set at 48 months， and the Kaplan-Meier survival analysis was used to assess the cumulative incidence of major adverse cardiovascular events （MACE） in both groups. Cox regression analysis was used to explore the impact of yang-reinforcing and blood-activating therapy on the risk of MACE， and subgroup analysis was performed. Changes in traditional Chinese medicine （TCM） syndrome score， left ventricular ejection fraction （LVEF）， left ventricular fractional shortening （LVFS）， left ventricular end-diastolic diameter （LVEDD）， and Minnesota Living with Heart Failure Questionnaire （MLHFQ） score were compared between groups at the time of first combined use of yang-reinforcing and blood-activating therapy （before treatment） and 1 year after receiving the therapy （after treatment）. ResultsMACE occurred in 31 cases （16.67%） in the exposure group and 47 cases （25.41%） in the non-exposure group. The cumulative incidence of MACE in the exposure group was significantly lower than that in the non-exposure group ［HR=0.559， 95%CI（0.361，0.895）， P=0.014］. Cox regression analysis showed that yang-reinforcing and blood-activating therapy was an independent factor for reducing the risk of MACE in DCM patients ［HR=0.623， 95%CI（0.396，0.980）， P=0.041］， and consistent results were observed in different subgroups. Compared with pre-treatment， the exposure group showed decreased TCM syndrome score and MLHFQ score， reduced LVEDD， and increased LVEF and LVFS after treatment （P＜0.05）； in the non-exposure group， TCM syndrome score decreased， LVEF and LVFS increased， and LVEDD reduced after treatment （P＜0.05）. After treatment， the exposure group had higher LVEF and LVFS， smaller LVEDD， and lower TCM syndrome score and MLHFQ score compared with the non-exposure group （P＜0.05）. ConclusionCombining yang-reinforcing and blood-activating therapy with conventional western medicine can reduce the risk of MACE in DCM patients with yang deficiency and blood stasis syndrome， meanwhile improving their clinical symptoms， cardiac function， and quality of life.

ObjectiveTo integrate network pharmacology prediction with multi-level experimental verification methods， and to explore in depth the therapeutic efficacy and potential mechanism of luteolin in treating gout. MethodsDatabases were used to obtain potential pharmacodynamic targets of luteolin. Protein-protein interaction （PPI） network construction and network pharmacology analysis techniques were used to screen key core targets of luteolin in gout treatment. Further biological function enrichment analysis and signaling pathway analysis were performed on these targets. Molecular docking simulation was used to calculate the binding energy between luteolin and potential core targets， clarifying the strength of their interactions. In the in vivo experiment for hyperuricemia， 48 mice were randomly divided into a blank group， a model group， an allopurinol group （5 mg·kg^-1）， and low-dose （10 mg·kg^-1）， medium-dose （30 mg·kg^-1）， and high-dose （90 mg·kg^-1） luteolin groups. For the first three days， the blank and model groups were gavaged with an equal volume of normal saline， while the allopurinol group and luteolin groups were gavaged with corresponding drugs. From day 4 onwards， modeling was performed by intraperitoneal injection at 12：00 daily （normal saline for the blank group， and oxonic acid potassium-hypoxanthine mixture for other groups， with 300 mg·kg^-1 for each group）. Gavage intervention was administered at 18：00 daily （normal saline for the blank/model groups， and corresponding drugs for the treatment groups） until day 7. After sampling， levels of serum uric acid （UA）， alanine aminotransferase （ALT）， and aspartate aminotransferase （AST） were measured. Levels of xanthine oxidase （XO） in the liver and kidney， ATP-binding cassette transporter G2 （ABCG2） and malondialdehyde （MDA） in the kidney， and superoxide dismutase （SOD） in the liver were determined. Renal HE staining was also performed. In the pharmacodynamic study of gouty arthritis， 36 rats were randomly divided into a blank group， a model group， a colchicine group （0.315 mg·kg^-1）， and low-dose （7 mg·kg^-1）， medium-dose （21 mg·kg^-1）， and high-dose （63 mg·kg^-1） luteolin groups. The model was established by vertically injecting 100 µL of 25 g·L^-1 monosodium urate suspension into the posterior lateral aspect of the right ankle joint （the blank group was injected with an equal volume of normal saline）， with repeated injections every two days for reinforcement. From day 2 after modeling， daily gavage administration was performed （normal saline for the blank/model groups， and corresponding drugs for the treatment groups） for a total of 16 days. During the experiment， ankle swelling and pain threshold were measured regularly. After sampling， levels of serum tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β） were determined. Ankle joints were subjected to HE， Masson， and safranin O-fast green staining， and HE staining was also performed on ankle synovial tissue and various organs. Western blot was used to determine the expression levels of key proteins in gout-related signaling pathways. ResultsNetwork pharmacology analysis predicted that luteolin may regulate over 20 core targets， such as XO， ABCG2， nuclear factor erythroid 2-related factor 2 （Nrf2）， and SOD， through acting on signaling pathways including NF-κB， phosphoinositide 3-kinase/protein kinase B （PI3K/Akt）， and ABC transporters， thereby affecting uric acid metabolism and inflammatory responses. In the hyperuricemia model， compared with the blank group， the model group showed significantly increased serum UA level， liver and kidney XO activity， renal ABCG2 expression， and liver SOD activity （P<0.01）. Compared with the model group， the high-dose luteolin group significantly reduced serum UA level （P<0.01）， inhibited liver and kidney XO activity （P<0.01）， and significantly increased renal ABCG2 expression and liver SOD activity （P<0.01）， effectively alleviating renal oxidative stress damage and improving renal histopathological status. In the gouty arthritis model， compared with the blank group， the model group showed significant ankle swelling， decreased pain threshold， and significantly increased levels of IL-6， IL-1β， and TNF-α in serum and synovial tissue （P<0.01）. The high-dose luteolin group significantly reduced ankle swelling， prolonged hot plate pain threshold， effectively decreased the levels of the above inflammatory factors in serum and synovial tissue （P<0.01）， and significantly improved ankle pathological damage， showing good analgesic and anti-inflammatory effects. Western blot results further confirmed that luteolin significantly upregulated Nrf2 protein expression and downregulated XO and nucleotide-binding oligomerization domain （NOD）-like receptor protein 3 （NLRP3） expression in animals. ConclusionLuteolin can improve symptoms of hyperuricemia and gouty arthritis， and its potential mechanism may be related to inhibiting XO activity， increasing ABCG2 and SOD levels， and regulating Nrf2-mediated oxidative stress-related pathways.

The traditional Chinese medicine （TCM） myocardial infarction （MI） unit is a standardized， regulated， and continuous integrated care unit guided by TCM theory and built upon existing chest pain centers or emergency care units. This unit emphasizes multidisciplinary collaboration and forms a restructured clinical entity without altering current departmental settings， offering comprehensive diagnostic and therapeutic services with full participation of TCM in the treatment of MI. Its core medical model is patient-centered and disease-focused， providing horizontally integrated TCM-based care across multiple specialties and vertically constructing a full-cycle treatment unit for MI， delivering prevention， treatment， and rehabilitation during the acute， stable， and recovery phases. Additionally， the unit establishes a TCM-featured education and prevention mechanism for MI to guide patients in proactive health management， reduce the incidence of myocardial infarction， and improve quality of life.

The elimination of biofilms is a crucial step in controlling hospital-acquired infections.Once biofilms colonize luminal instruments,it is difficult to remove them using traditional disinfection methods.Conventional disinfection approaches now face a series of challenges,including microbial resistance,corrosiveness,cytotoxicity,residual disinfection byproducts,and environmental pollution.Therefore,developing novel disinfection technologies specifically targeting biofilm removal is vitally important.New disinfection technologies,such as slightly acidic electrolyzed water,plasma technology,surface modification techniques,nanomaterial-based disinfection,bacteriophage disinfection,and enzymatic disinfection,are constantly emerging.These technologies exhibit excellent performance against biofilms by leveraging the synergistic effects of multiple mechanisms,including the reactive oxygen species(ROS)burst,photocatalytic oxidation,physical disruption,and biological targeting.This review summarizes the characteristics,underlying mechanisms,and potential application scenarios of these novel disinfection technologies,with a particular focus on their effects against biofilms formed by common pathogenic bacteria on surfaces in hospital settings.It aims to provide a reference basis for the practical application and translation of these disinfection technologies and the development of new disinfection strategies.

ObjectiveTo explore the association between triglyceride-glucose （TyG） index and major adverse cardiovascular events （MACEs） risk in coronary heart disease （CHD） patients with blood stasis syndrome after percutaneous coronary intervention （PCI）. MethodsA total of 857 CHD patients with blood stasis syndrome after PCI were enrolled and divided into four groups according to the baseline TyG index quartiles， Q1 （TyG ＜ 8.51）， Q2 （8.51 ≤ TyG ＜ 8.88）， Q3 （8.88 ≤ TyG ＜ 9.22）， and Q4 （TyG ≥ 9.22）. The clinical outcome was defined as a compound endpoint of cardiovascular events including cardiac death， non-fatal myocardial infarction， unplanned revascularization， in-stent restenosis and stroke. The machine learning Boruta algorithm was used for feature selection related to MACEs risk. Kaplan-Meier survival analysis and Cox proportional hazards regression model were used to compare the differences in MACEs risk among the four groups. Restricted cubic spline （RCS） and subgroup analysis were performed to determine the relationship between the TyG index and MACEs risk. The area under the receiver operating characteristic （ROC） curve （AUC）， calibration curve and Hosmer-Lemeshow test， and decision curve analysis （DCA） were plotted to evaluate the predictive value of the TyG index for MACEs risk. ResultsThe median follow-up time of the included patients was 2.45 years. During the follow-up period， 313 cases （36.52%） of new MACEs occurred. The incidence of MACEs in Q1， Q2， Q3， Q4 group was 28.17% （60/213）， 29.05% （61/210）， 39.45% （86/218） and 49.07% （106/216）， respectively. Kaplan-Meier survival analysis suggested statistically significant differences in MACEs risk among the four groups （P＜0.001）. Cox proportional hazards regression model analysis found that the risk of MACEs in patients with high TyG index increased by 60.1% （P＜0.01）. Using Q1 as the reference， the MACEs risk in Q2， Q3 and Q4 groups gradually increased， and the trend was statistically significant （P＜0.05）. RCS model suggested that the TyG index was nonlinearly associated with the MACEs risk （P＜0.001）. The TyG index had a good predictive performance for MACEs risk according to ROC analysis （AUC=0.758， 0.724-0.792） and Hosmer-Lemeshow test （χ² = 4.319， P = 0.827）. Additionally， DCA analysis also suggested a good clinical efficacy of the TyG index for predicting MACEs. Subgroup analysis showed that different baseline TyG index was positively correlated with the MACEs risk in the stratification of age， male， BMI， history of diabetes and hypertension， and low-density lipoprotein cholesterol （LDL-C）≥1.8 mmol·L^-1（P＜0.05）. ConclusionThe elevated TyG index is closely corrected with an increased risk of MACEs in CHD patients with blood stasis syndrome after PCI， indicating a guiding significance for early risk stratification and clinical decisions.

Mitochondrial membrane potential （MMP） is one of the most sensitive indicators of cell damage and one of the potential targets of traditional Chinese medicine （TCM） intervention in the cardiac function. Cardiovascular diseases， with complex mechanisms of the occurrence and development， often involve the myocardium and other organs and present slow development and high mortality， seriously affecting the quality of life of patients. The TCM treatment of cardiovascular diseases is praised for small side effects， low drug resistance， and holistic treatment and can effectively relieve symptoms and improve prognosis. In recent years， the research on the occurrence mechanism of cardiovascular diseases from mitochondrial function has gained increasing attention. MMP is closely related to the functioning mechanism of mitochondria. Studies have shown that TCM regulates MMP to treat cardiovascular diseases by modulating energy metabolism， improving mitochondrial structure and function， and inhibiting oxidative stress and apoptosis， thus protecting the heart function， improving the cure rate， and reducing the mortality of patients. This paper systematically reviews the studies about the mechanisms of TCM regulation of MMP in cardiovascular diseases including atherosclerosis， heart failure， myocardial ischemia-reperfusion injury， diabetic cardiomyopathy disease， and pulmonary artery hypertension. Most of Chinese medicine compound prescriptions， Chinese medicinal herbs， effective fraction， and active components can protect mitochondrial function by regulating MMP. However， relevant clinical trials and TCM theoretical studies of MMP remain to be carried out to provide more ideas for TCM treatment of cardiovascular diseases.

Japanese encephalitis is an acute central nervous system infectious disease caused by Japanese encephalitis virus (JEV) with brain parenchyma inflammation, characterized by high fever, headache, positive meningeal irritation, impaired consciousness, convulsion, and respiratory failure, with mortality rate as high as 20%-30%, and with neurological sequelae in 30%-50% of survivors. The mechanism of brain damage caused by JEV infection is still unclear, and some studies imply its close relation with immune-inflammatory response. This article reviews the research progress on immune-inflammatory response mechanism of Japanese encephalitis to help to understand its pathogenesis.

ObjectiveTo investigate the protective effect of Geju Hugan tablets on the liver of mice with alcohol-induced liver injury， and explore the underlying mechanism based on nuclear factor-κB p65 （NF-κB p65） and B-cell lymphoma-2 （Bcl-2）/Bcl-2-associated X protein （Bax） signaling pathways. MethodAccording to the body weight， 60 SPF-grade male ICR mice were randomized into normal， model， Compound Yiganling tablets （0.16 g·kg^-1）， and low-， medium-， and high-dose （0.2， 0.4， 0.8 g·kg^-1， respectively） Geju Hugan tablets groups. The drugs were administrated at the corresponding doses by gavage， and the normal and model groups with equal volume of pure water once a day for 28 consecutive days. On day 29， the mice in other groups except the normal group were administrated with liquor （53% Vol） by gavage twice a day at the doses of 20， 10 mL·kg^-1 and with the interval of 6 h. Samples were harvested on day 30. The histopathological changes in the liver were observed by hematoxylin-eosin （HE） staining， and the ultrastructural changes in hepatocytes were observed by transmission electron microscopy. The enzyme-linked immunosorbent assay was employed to measure the levels of malonaldehyde （MDA）， reduced glutathione （GSH）， and triglycerides （TG） in the liver tissue and the levels of alanine aminotransferase （ALT） and aspartate aminotransferase （AST） in the serum. Western blotting was employed to determine the protein levels of NF-κB p65， phosphorylated p-inhibitor kappa B alpha （p-IκBα）， Bcl-2， and Bax in the liver tissue. ResultCompared with the normal group， the model group showed increases in the ALT， AST， MDA， and TG levels， a decrease in the GSH level， and increases in the liver injury scores evaluated based on the HE， oil red O， and transmission electron microscopy （P<0.01）. Moreover， the model group showed up-regulated expression of NF-κB， p-IκBα， and Bax （P<0.05， P<0.01） and down-regulated expression of Bcl-2 （P<0.05） in the liver tissue. Compared with the model group， Geju Hugan tablets of all the doses lowered the ALT， AST， MDA， and TG levels and elevated the GSH level （P<0.01）. The liver injury scores assessed based on HE staining and transmission electron microscopy in the medium- and high-dose Geju Hugan tablets groups were lower than those in the model group （P<0.01）. Compared with the model group， medium- and high-dose Geju Hugan tablets down-regulated the protein levels of NF-κB， p-IκBα， and Bax （P<0.01） and all doses of Geju Hugan tablets up-regulated the protein level of Bcl-2 （P<0.01）. ConclusionGeju Hugan tablets protect mice from alcohol-induced liver injury by down-regulating NF-κB signaling pathway to alleviate inflammation in the liver tissue and down-regulating the expression of Bax and up-regulating the expression of Bcl-2 to inhibit hepatocyte apoptosis.

Objective:To investigate the role of dendritic cells (DC) in Chlamydia muridarum ( Cm) respiratory infection and their effect on adaptive immune response. Methods:C57BL/6 mice were exposed to 1×10 3 inclusion-forming units (IFU) of Cm through inhalation to establish the mouse model of Cm respiratory infection. The proportion of CD11c + MHCⅡ + DC and the expression of costimulatory molecules (CD40, CD80 and CD86) in spleen tissues were detected by flow cytometry on 0, 3 and 7 d after infection. The expression of IL-12p40, IL-10 and IL-6 at mRNA level in spleen tissues was detected by qPCR. Mouse splenic DC isolated on 7 d after Cm infection were sorted by magnetic beads and then transferred to recipient mice. Th1 response in the recipient mice was measured using intracellular cytokine staining 14 d after infection. Results:Cm respiratory infection induced massive infiltration of DC and promoted the expression of costimulatory molecules on splenic DC. The expression of IL-12 and IL-10 at mRNA level in splenic DC reached the peak on 3 d after infection. Transferring the splenic DC of Cm-infected mice into the recipient mice could alleviate the disease condition in the recipient mice after Cm infection with reduced Cm inclusion-forming units in lung tissues and significantly increased proportion of Th1 cells in lung and spleen tissues. Conclusions:Cm respiratory infection could induce the maturation and activation of DC, which promoted Th1 immune response. DC played an important role in Cm infection.

Objective:To investigate the role of IL-21/IL-21R-mediated CD4 + T cells in Chlamydia muridarum ( Cm) respiratory infection. Methods:C57BL/6 mice (WT mice) and IL-21R -/- mice were used to establish the models of Cm respiratory infection through intranasal inhalation of Cm. Flow cytometry was used to detect the proportion, number, activity and function of CD4 + T cells in lung and spleen tissues at 0, 3, 7 and 14 d after Cm respiratory tract infection. IFN-γ and IL-4 levels in spleen cell culture supernatants were detected by ELISA. Na?ve WT mice were transferred with CD4 + T cells in the spleen tissues of IL-21R -/- mice or WT mice on 7 d after infection and given Cm intranasally 2 h later. Then the mice were weighed daily and sacrificed on 14 d after infection. The bacterial load and pathological changes in lung were analyzed. Flow cytometry was performed to detect the proportions and numbers of neutrophils (CD45 + CD11b + Gr-1 high) and alveolar macrophages (CD45 + F4/80 + CD11c high)as well as the proportions of Th1 (IFN-γ + CD4 + ) and Th2 (IL-4 + CD4 + ) cells. ELISA was also performed to measure IFN-γ and IL-4 levels in spleen cell culture supernatants. Results:Compared with WT mice, IL-21R -/- mice showed elevated numbers and enhanced activation of CD4 + T cells, increased proportion of Th1 cells and decreased proportion of Th2 cells in spleen and lung tissues after Cm respiratory infection. Besides, IFN-γ levels increased, while IL-4 levels decreased in spleen cell culture supernatants of IL-21R -/- mice. After Cm infection, the na?ve WT transferred with CD4 + T cells from IL-21R -/- mice showed less body weight loss, reduced bacterial load and alleviated pathological changes in lung tissues, increased proportion of Th1 cells in lung tissue and higher IFN-γ level in spleen cell culture supernatants. Conclusions:IL-21/IL-21R-mediated CD4 + T cells could aggravate Cm respiratory infection by suppressing Th1 cell immune responses.