ObjectiveThis paper aims to investigate the protective effects of the Tanyu Tongzhi Youhua prescription（TYTZP） against myocardial ischemia/reperfusion injury in rats via regulation of the cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathway. MethodsFifty-six 8-week-old male Sprague-Dawley （SD） rats were randomly divided into sham group， model group， ticagrelor group （32.4 mg·kg^-1）， RU320521 （RU.521cGAS inhibitors） group （5 mL·kg^-1）， groups of TYTZP with low dose （3.6 g·kg^-1）， medium dose （7.2 g·kg^-1）， and high dose （14.4 g·kg^-1）， with eight rats per group. The ticagrelor group and groups of TYTZP with different doses received pre-treatment for seven days according to their respective protocols. The RU.521 group received an intraperitoneal injection one hour before modeling. A rat model of the no-reflow phenomenon in myocardial ischemia/reperfusion injury was established by ligating the left anterior descending coronary artery in situ. Myocardial no-reflow area was determined by thioflavin staining. Histopathological morphology of myocardial tissue was observed via hematoxylin and eosin （HE） staining. Cardiac function was detected by echocardiography. Myocardial microcirculation function change was observed by using real-time myocardial contrast echocardiography. The myocardial enzyme levels in the serum were measured by serum biochemical analysis. The double-stranded DNA （dsDNA） levels were detected by using PicoGreen. The protein expression of cGAS， STING， and nuclear factor-κB （NF-κB） p65 in myocardial tissue was detected by Western blot. The levels of cardiac troponin Ⅰ （cTNⅠ）， cardiac troponin T （cTNT）， interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the peripheral blood were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the sham group， the model group showed a significantly increased myocardial no-reflow area （P<0.01）. Myocardial fiber rupture and disarray and inflammatory cell infiltration were observed by HE staining. The ultrasound results indicated that left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01） were significantly decreased. Real-time myocardial contrast echocardiography showed that the peak time of myocardial blood perfusion was significantly prolonged （P<0.01）， and the levels of creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， cTNⅠ， cTNT， and dsDNA were significantly elevated （P<0.01）. Western blot results showed that the myocardial protein expressions of cGAS， STING， and NF-κB p65 were upregulated （P<0.01）. ELISA results showed that the inflammatory factors in the serum such as IL-6， IL-1β， and TNF-α were increased （P<0.01）. Compared with the model group， the group of the TYTZP significantly reduced the levels of myocardial enzyme， troponins， and dsDNA （P<0.01， P<0.05）， improved cardiac function and myocardial microcirculation， alleviated histopathological morphology and inflammatory infiltration， inhibited activation of the cGAS/STING pathway， reduced the expression of NF-κB p65 （P<0.01， P<0.05）， and inhibited inflammatory response. ConclusionThe TYTZP mitigates the no-reflow phenomenon in myocardial ischemia/reperfusion injury， and its mechanism is associated with inhibiting the activation of the cGAS/STING pathway and attenuating inflammatory responses.

ObjectiveThis paper aims to investigate the protective effects of the Tanyu Tongzhi Youhua prescription（TYTZP） against myocardial ischemia/reperfusion injury in rats via regulation of the cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathway. MethodsFifty-six 8-week-old male Sprague-Dawley （SD） rats were randomly divided into sham group， model group， ticagrelor group （32.4 mg·kg^-1）， RU320521 （RU.521cGAS inhibitors） group （5 mL·kg^-1）， groups of TYTZP with low dose （3.6 g·kg^-1）， medium dose （7.2 g·kg^-1）， and high dose （14.4 g·kg^-1）， with eight rats per group. The ticagrelor group and groups of TYTZP with different doses received pre-treatment for seven days according to their respective protocols. The RU.521 group received an intraperitoneal injection one hour before modeling. A rat model of the no-reflow phenomenon in myocardial ischemia/reperfusion injury was established by ligating the left anterior descending coronary artery in situ. Myocardial no-reflow area was determined by thioflavin staining. Histopathological morphology of myocardial tissue was observed via hematoxylin and eosin （HE） staining. Cardiac function was detected by echocardiography. Myocardial microcirculation function change was observed by using real-time myocardial contrast echocardiography. The myocardial enzyme levels in the serum were measured by serum biochemical analysis. The double-stranded DNA （dsDNA） levels were detected by using PicoGreen. The protein expression of cGAS， STING， and nuclear factor-κB （NF-κB） p65 in myocardial tissue was detected by Western blot. The levels of cardiac troponin Ⅰ （cTNⅠ）， cardiac troponin T （cTNT）， interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the peripheral blood were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the sham group， the model group showed a significantly increased myocardial no-reflow area （P<0.01）. Myocardial fiber rupture and disarray and inflammatory cell infiltration were observed by HE staining. The ultrasound results indicated that left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01） were significantly decreased. Real-time myocardial contrast echocardiography showed that the peak time of myocardial blood perfusion was significantly prolonged （P<0.01）， and the levels of creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， cTNⅠ， cTNT， and dsDNA were significantly elevated （P<0.01）. Western blot results showed that the myocardial protein expressions of cGAS， STING， and NF-κB p65 were upregulated （P<0.01）. ELISA results showed that the inflammatory factors in the serum such as IL-6， IL-1β， and TNF-α were increased （P<0.01）. Compared with the model group， the group of the TYTZP significantly reduced the levels of myocardial enzyme， troponins， and dsDNA （P<0.01， P<0.05）， improved cardiac function and myocardial microcirculation， alleviated histopathological morphology and inflammatory infiltration， inhibited activation of the cGAS/STING pathway， reduced the expression of NF-κB p65 （P<0.01， P<0.05）， and inhibited inflammatory response. ConclusionThe TYTZP mitigates the no-reflow phenomenon in myocardial ischemia/reperfusion injury， and its mechanism is associated with inhibiting the activation of the cGAS/STING pathway and attenuating inflammatory responses.

Atherosclerosis （AS） is a chronic and inflammatory vascular disease. Macrophages are common immune cells and play an important role in the development of AS. In recent years， research has found that the formation of AS plaques is closely related to pathological and physiological processes such as macrophage polarization， energy metabolism， and lipid phagocytosis. This review aims to summarize the mechanism of macrophages in the development of AS， and to explore potential therapeutic methods for delaying AS by regulating macrophages， providing new ideas for the treatment and research of AS.

Objective:To analyze the clinical characteristics of adverse reactions caused by dinutuximab β for the treatment of neuro-blastoma(NB)in China and to provide safety evidence for the rational use of dinutuximab β in clinical practice.Methods:Clinical data were retrospectively collected from 16 pediatric patients with NB who had been treated with dinutuximab β at Shanghai Children's Medical Center Affiliated to Shanghai Jiao Tong University School of Medicine from January 2022 to November 2023,and the adverse reactions caused by dinutuximab β were summarized and analyzed.Results:The male-to-female ratio was 5:3 among the 16 children with NB.The retroperitoneum was the main initial site of involvement,accounting for 75%.Thirteen(81.25%)patients had high-risk NB.The adverse reactions caused by dinutuximab β mainly included decreased hemoglobin,fever,vomiting,and diarrhea.The inci-dence of adverse reactions was highest in the first course of treatment,and the median time of adverse reactions was 2-5 days.Conclu-sion:Targeted monitoring should be carried out at an early stage during dinutuximab β administration.Adverse reactions should be de-tected and managed early to ensure the safety of medication for children.

Objective To explore the interaction mechanisms among different dimensions of online learning competence in undergraduates,providing scientific evidence for optimizing software design and online education strategies.Methods A cross-sectional study was conducted with 347 undergraduates from Kunming Medical University via an online questionnaire in October 2024.Reliability testing and exploratory factor analysis were performed using SPSS 26.0,while structural equation modeling was constructed with Amos 24.0.Results Driving force directly and positively influenced regulatory force(β=0.778,P<0.001)and reciprocal force(β=0.302,P=0.003),but had no significant direct effect on adaptive force(β=0.131,P=0.182).Regulatory force and reciprocal force both exerted direct positive effects on adaptive force(β=0.262,P=0.022;β=0.410,P<0.001).The indirect effect of driving force on adaptive force accounted for 78.1%of the total effect(P=0.007),with regulatory force showing a significant mediating role(β=0.178,P=0.023),while reciprocal force alone did not(β=0.108,P=0.060).A chain mediating effect(driving force→regulatory force→reciprocal force→adaptive force)was confirmed(β=0.124,P=0.004).Conclusion Driving force serves as the core of online learning competence,and adaptive capacity is enhanced through regulatory and reciprocal forces.To promote knowledge internalization and adaptability,it is required to optimize feedback mechanisms and deepen interactive designs in online learning platforms.

Objective: To investigate the effects and mechanisms of Astragalus Polysacharin(APS) on the proliferation and metastasis of breast cancer cells by regulating miR-107 and miR-346-mediated macrophage polarization in breast cancer-derived exosomes. Methods: Forty 8-week-old female BALB/c mice were selected and breast cancer xenograft models and 4T1 transplanted tumor models were established. The mice were divided into the control group and the APS group. The APS group mice received daily intragastric administration of APS for 25 days, while the control group mice were given the same amount of normal saline. After all treatments were completed, the mice were euthanized, and tumor tissues were isolated. Western blot and flow cytometry were used to detect the expressions of proliferating cell nuclear antigen(PCNA), Ki-67, CD206, CD163, inducible nitric-oxide synthase(iNOS), and CD86. The apoptosis of single-cell suspensions in tumor tissues was analyzed. Human breast cancer cell line MDA-MB-231 was cultured and stimulated with APS, and exosomes from the cell culture medium were collected. The proliferation, migration, and invasion of cells were detected by CCK-8 assay, scratch assay, permeability chamber cell invasion assay, and qRT-PCR. Differentially expressed genes were screened by bioinformatics. Results : By measuring the expressions of molecules related to breast cancer cell proliferation and metastasis, it was shown that APS treatment reduced the expressions of proliferation-related proteins(PCNA and Ki-67) and metastasis-related proteins(Vimentin) in MDA-MB-231 xenograft tumor tissues; and the polarization of tumor-associated macrophages was observed. APS treatment of 4T1 transplanted tumor tissues could reduce the number of M2 macrophages and increase the number of M1 macrophages, resulting in a decrease in the ratio of M2/M1 macrophages and an increase in cell apoptosis in 4T1 transplanted tumor tissues. The expressions of related proteins iNOS and CD86 increased, and CD206 and CD163 decreased. After APS treatment, the exosomes produced by MDA-MB-231 reduced the polarization of M2 macrophages and affected the expressions of miR-107 and miR-346. Conclusion APS inhibits the polarization of M2 macrophages by regulating the expression of miR-107 or miR-346 in breast cancer cell-derived exosomes, ultimately inhibiting the proliferation and metastasis of breast cancer cells.

Objective To analyze the risk factors of critically ill patients infected with Acinetobacter bau-mannii(AB)and carbapenem resistant Acinetobacter baumannii(CRAB).Methods From January 2022 to June 2023,the data of Intensive Care Unit(ICU)patients admitted to Second Hospital of Shanxi Medical Uni-versity in Shanxi Province were collected.According to whether they were infected with AB,the patients were divided into an observation group and a control group(98 cases each).The observation group was further di-vided into a carbapenem sensitive Acinetobacter baumannii(CSAB)group(72 cases)and a CRAB group(26 cases).Mann-Whitney U test,chi-square test and other univariate and multivariate binary Logistic regression were used to analyze the risk factors of AB and CRAB infection for critically ill patients.The prognosis was analyzed by Kaplan Meier survival analysis.Results Long stay in ICU,previous use of carbapenem drugs and high Acute Physiology and Health Evaluation(APACHE Ⅱ)score were independent risk factors for AB sus-ceptibility(P＜0.05),while the independent risk factors for CRAB susceptibility were invasive ventilation and delayed surgery(P＜0.01).In addition,CRAB infection,COVID-19 and shock was risk factors for death in critically ill patients,and invasive ventilation,indwelling drainage tube and operation could reduce the risk of death in critically ill patients(P＜0.05).Conclusion ICU stay time,APACHE Ⅱ score,previous use of car-bapenem drugs and invasive ventilation increase the risk of AB and CRAB infection in critically ill patients.In-vasive ventilation,indwelling drainage and early surgery could reduce the risk of death from AB and CRAB in-fection in critically ill patients.

Objective To address the bottlenecks in the application of wastewater biological treatment technology under space conditions,an experimental system for the biological treatment of space wastewater was constructed and its biochemical performance examined.The findings of this study will provide technical support for the biological treatment of space wastewater.Methods Based on the Membrane Aerated Biofilm Reactor(MABR)process,a biological treatment experimental system for space wastewater was constructed and conducted the continuous flow test for 77 days to investigate the performance of PVDF and PP membrane modules in the treatment of simulated air condensate.Results The results demonstrated that both membrane modules exhibited an average TOC removal rate of 90%,indicative of their effective organic matter removal capacity.In the air supply mode,the ammonia oxidation capacity was observed to be comparatively lower,whereas in the oxygen source without bubbling mode,the nitrogen oxidation rate and total nitrogen removal rate could be attained above 90%,indicating a notable degree of simultaneous nitrification and denitrification.The results demonstrated that the mode of gas supply had a significant impact on the nitrogen conversion performance.The abundance of nitrogen-converting bacteria in PP membrane module is higher than that in PVDF membrane module,indicating a better nitrogen-converting performance in PP membrane module.Conclusion The constructed wastewater biological treatment system is optimally suited for the treatment of air condensate,thereby offering a novel technical approach for space wastewater treatment.

The control and utilization of microorganisms in space-based animal culture constitute a pivotal challenge underpinning research domains such as space life sciences and extraterrestrial life-support system.This paper systematically examines the origins,transmission routes,and latent risks of microbial contamination in space-based animal culture facilities.A comprehensive analysis is conducted on the advancements in on-orbit implementation of microbial containment strategies,including physical filtration systems,antimicrobial surface coatings,and environmental parameter optimization.Additionally,the study evaluates the prospective applications of probiotic consortia and functionally engineered microorganisms in enhancing animal welfare,stabilizing biosphere conditions,and enabling closed-loop waste recycling.Notably,this work highlights the paradigm shift from reactive microbial suppression to proactive microbiome engineering in space-based animal husbandry,thereby establishing a theoretical framework for sustainable development of space-based animal culture.

Objective To investigate the therapeutic mechanism of Thesium chinense Turcz.(TCT)for antibiotic-associated diarrhea(AAD).Methods Network pharmacology,KEGG pathway enrichment analysis and molecular docking were used to identify the shared targets and genes of TCT and AAD,the key signaling pathways and the binding between the active components in TCT and the core protein targets.In a Kunming mouse model of AAD established by intragastric administration of lincomycin hydrochloride,the effects of daily gavage of 1%carboxymethyl cellulose sodium or TCT gel solutions at 1.5 g/kg and 3 g/kg(n=10)on body weight and diarrhea were observed.HE staining,ELISA,16S rRNA sequencing,and Western blotting were used to examine pathologies,expression levels of IL-6 and TNF-α,changes in gut microbiota,and protein expressions of EGFR,p-EGFR,PI3K,p-PI3K,Akt,and p-Akt in the colon tissues of the mice.Results We identified a total of 66 active components of TCT and 68 core targets including EGFR,STAT3 and PIK3CA.KEGG pathway enrichment analysis suggested that the therapeutic effects of TCT was mediated primarily through the PI3K/Akt signaling pathway.Molecular docking showed that EGFR had the highest binding affinity with coniferin,and the EGFR-coniferin complex maintained a stable conformation at 10 ns,whose stability was also confirmed by Gibbs free energy analysis.In the mouse models of AAD,treatment with TCT significantly improved colonic tissue morphology,decreased colonic levels of TNF-α and IL-6,increased gut microbiota diversity,and modulated the relative abundances of the key genera including Lactobacillus and Bacteroides.TCT treatment also markedly reduced protein expressions of p-EGFR,p-PI3K and p-Akt in the colon tissues of the mice.Conclusion TCT can alleviate AAD in mice by modulating gut microbiota composition,regulating the EGFR/PI3K/Akt signaling pathway,and reducing TNF-α and IL-6 expressions.