From the perspective of transfusion medicine and based on the vision and framework of patient blood management, this article combines the advances in basic science, blood transfusion, laboratory, and clinical medicine. It aims to systematically review the key elements and characteristics of patient fibrinogen management by maintaining and optimizing patients' hemostatic function while reducing blood transfusions. This review enriches the connotation of transfusion medicine, especially patient blood management, and provides valuable insights for clinical practice.

Hepatocellular carcinoma （HCC） is a malignant tumor with relatively high incidence and mortality rates worldwide， and its therapeutic resistance and recurrence mechanism are closely associated with liver cancer stem cells （LCSC）. This article systematically introduces the biological characteristics of LCSC and their key role in the progression of HCC， reviews the functional characteristics of the specific surface markers （such as EpCAM and CD133） and related signaling pathways （such as Wnt/β-catenin， TGF-β， and STAT3）， elaborates on the interaction between LCSC and tumor microenvironment， and summarizes the latest clinical treatment strategies targeting LCSC and the countermeasure for existing resistance mechanisms. The article points out that LCSC promote tumor development and progression through metabolic reprogramming and immune microenvironment remodeling， and it is proposed to establish a standardized detection system for LCSC specific markers and promote a triple synergistic therapeutic paradigm combining targeted therapy， immune regulation， and traditional chemotherapy， in order to provide new ideas for the clinical intervention of HCC.

Liver cirrhosis is the final stage of the progression of various chronic liver diseases， often accompanied by serious complications and high mortality rates. Recent studies have shown that the interaction between gut microbiota and bile acid metabolism （the gut microbiota-bile acid axis） is closely associated with liver cirrhosis. This article systematically reviews the mechanism of action of the gut microbiota-bile acid axis in the progression of liver cirrhosis， elaborates on the pathological features of liver cirrhosis and its harm to the body， and summarizes the association of the gut microbiota-bile acid axis with the development and progression of liver cirrhosis. It also analyzes the key regulatory role of this axis in the progression of liver cirrhosis and explores its potential application value as a therapeutic target for liver cirrhosis， in order to provide a theoretical basis for exploring more effective clinical intervention methods.

ObjectiveType I interferon (IFN-I) signaling is essential for antiviral innate immunity, yet its sustained or excessive activation contributes to the pathogenesis of several autoimmune diseases and interferonopathies, such as systemic lupus erythematosus and Aicardi-Goutières syndrome. Current strategies targeting this pathway, exemplified by JAK inhibitors, act mainly on downstream signal transduction and provide limited direct control over upstream IFN-I production, while also carrying the risk of broad immunosuppression. Phyllanthus emblica L. has long been used in traditional medicine for inflammatory disorders, but the bioactive constituent responsible for its regulation of IFN-I signaling and the underlying molecular mechanism have not been clearly defined. This study aimed to identify the active anti-inflammatory component of P. emblica and to characterize its mechanism of action on the IFN-I pathway in macrophages. MethodsActive components ofP. emblica and their candidate targets were screened by network pharmacology using the TCMSP and DrugBank databases (oral bioavailability≥30%, drug-likeness≥0.18) and intersected with inflammation-related genes retrieved from public databases. The predicted interaction between EGCG and IFN-I pathway proteins (TBK1, IRF3, STAT1) was evaluated by molecular docking, with BX795 and GSK8612 used as reference TBK1 inhibitors. Mechanistic experiments were performed in THP-1-derived macrophages and primary bone marrow-derived macrophages (BMDM). Upstream signaling was activated by transfection of the nucleic acid analogs poly(I∶C) and poly(dA∶dT) or by lipopolysaccharide (LPS) stimulation, whereas downstream signaling was activated by exogenous IFN-β. An siRNA-mediated TREX1 knockdown model was used to mimic endogenous nucleic acid-driven interferonopathy. Expression of IFN-β1 and interferon-stimulated genes (ISGs) was measured by RT-qPCR, protein phosphorylation by Western blot, and IFN-β secretion by ELISA. Cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) were used to probe the interactionbetween EGCG and IRF3. ResultsNetwork pharmacology identified (-)-epigallocatechin-3-gallate (EGCG) as a candidate IFN-I-suppressive constituent of P. emblica, with predicted binding to TBK1, IRF3, and STAT1. Molecular docking yielded binding energies of -9.2, -7.2, and -8.2 kcal/mol for TBK1, IRF3, and STAT1, respectively, indicating an affinity for TBK1 comparable to that of the reference inhibitors BX795 (-5.7 kcal/mol) and GSK8612 (-6.4 kcal/mol). EGCG suppressed IFN-β1 and ISG mRNA expression under poly (I∶C), poly (dA∶dT), and LPS stimulation in both THP-1 macrophages and BMDM. At the protein level, EGCG reduced the phosphorylation of TBK1 and IRF3 without affecting the levels of the upstream sensors cGAS and RIG-I, and lowered IFN-β secretion in a concentration-dependent manner. CETSA and DARTS showed that EGCG did not enhance the thermal stability or protease resistance of IRF3, indicating that its effect on IRF3 is indirect. Following IFN-β stimulation, prolonged EGCG treatment reduced STAT1 phosphorylation in a time-dependent manner without an apparent change in IRF9, and partially attenuated ISG transcription; this effect was not monotonicly concentration-dependent, and CXCL10 showed the most consistent suppression. In TREX1-knockdown cells, the elevated mRNA levels of ISG15, ISG56, and CXCL10 were reduced by EGCG. ConclusionEGCG suppresses IFN-I responses by concurrently inhibiting TBK1-IRF3-dependent IFN‑β production and JAK-STAT1-mediated downstream transcription. These in vitro findings provide a mechanistic basis for the anti-inflammatory use of P. emblica in traditional medicine and identify EGCG as a candidate for further evaluation in interferon-driven autoimmune disease models.

Objective:To investigate the feasibility and safety of high-speed railway (HSR) transport for critically ill pediatric patients.Methods:A single-center retrospective analysis was conducted.A total of 39 children transported via HSR (HSR group) and 420 children transported via ambulance (ambulance group) from May 2019 to December 2024 at the Seventh Medical Center of the PLA General Hospital were included.Demographic data,disease types,transport distances,and outcomes were compared between the two groups,and the vital signs,blood gas analysis,mechanical ventilation parameters,and vasoactive drug usage before and after HSR transport were also compared.Results:Over the five-year period,39 HSR transports and 420 ambulance transports were completed.No significant differences were observed in gender,age,or weight between HSR group and ambulance group( P>0.05).The proportion of circulatory system diseases was significantly higher in the HSR group (74.4% vs.55.1%, P = 0.020).HSR transports covered longer distances [855(855,1 075)km vs.84(23,273) km, P<0.001] and achieved faster speeds [150(150,216) vs.80(79,80)km/h, P<0.001].No significant differences were found in heart rate,body temperature,or diastolic pressure before and after HSR transport ( P>0.05).However,systolic blood pressure and partial pressure of oxygen increased slightly post-HSR transport [(82.97±15.44) vs.(85.15 ± 14.82)mmHg, P=0.003；(84.22±25.45)mmHg vs.(88.95±28.70)mmHg, P=0.029].Mechanical ventilation parameters remained stable during HSR transport ( P>0.05). Conclusion:HSR transport is feasible and safe for critically ill children and represents a promising option for long-distance interhospital transfers of pediatric patients.

Objective To analyze the epidemiological distribution characteristics and influencing factors of treat-ment outcome of pulmonary tuberculosis(PTB)patients complicated with diabetes mellitus(DM)in Bijie City from 2017 to 2022,and provide reference for formulating prevention and control measures of PTB-DM.Methods The registered management cases of PTB patients combined with DM from the tuberculosis surveillance report informa-tion management system in Bijie City in 2017-2022 were collected.Changing trends in annual registration rates and successful treatment rates were analyzed with Joint-point regression models.Different characteristics between pa-tients with PTB-DM and PTB alone were conducted comparative analysis;the influencing factors of treatment out-come were analyzed by x2 test and binary logistic regression analysis.Results A total of 679 PTB-DM patients were registered in Bijie City from 2017 to 2022,accounting for 1.53％of total PTB patients,the annual registration rate increased from 1.11/100 000 in 2017 to 3.08/100 000 in 2022,with an increasing trend in the annual percentage change(APC=26.67％,95％CI:5.36％-52.29％,t=3.564,P=0.024).In the analysis on characteristics,the proportion of PTB-DM male patients,age ≥45 years and farmers,the ratio of direct consultation to transfer treat-ment,the pathogenicity positive rate,the proportion re-treatment,and rate of delay in consultation were all higher than those of PTB alone;successful treatment rate and proportion of floating population were all lower than PTB alone,difference were all statistically significant(all P＜0.05).The successful treatment rate of PTB-DM patients in Bijie City from 2017 to 2022 was 87.80％.Age,occupation,pathogenicity diagnosis results were influencing fac-tors for treatment outcome in patients with PTB-DM,with farmers(OR=3.68,95％CI:1.22-11.09),with pathogenicity positivity(OR=2.84,95％CI:1.24-6.50),and without pathogenic detection result+tuberculous pleurisy(OR=11.35,95％CI:2.16-59.74)being risk factors for successful treatment.Conclusion Although the proportion of PTB-DM in the total PTB patients in Bijie City from 2017 to 2022 was not high,it showed an up-ward trend;it is necessary to attach great importance to male,re-treated,farmer,and pathogenicity positivity co-morbid patients in Bijie City,and strengthen the two-way screening of PTB-DM in high-risk populations.

The concept of amplification feedback pathways represents an intersection between electronics and control theory,involving both amplification and feedback processes.It reveals the dynamic evolution mechanisms of systems under the combined influence of these two processes.In Traditional Chinese Medicine(TCM),Chest Bi syndrome is considered a"ben xu biao shi"condition,with its primary pathology located in the heart and closely related to other organs such as the liver,spleen and kidneys.This article focuses on the interrelationship between organ dysfunction and the imbalance of the Five Elements Theory.By applying amplification feedback theory and models,the study constructs and analyzes single-stage amplification feedback pathways involving the heart,liver and kidneys,as well as double-stage amplification feedback pathways involving the heart,liver,kidneys and spleen,in the context of multifactorial interactions such as heart and kidney Yang deficiency,Qi stagnation in the heart and chest,and spleen-stomach dysfunction.Particular emphasis is placed on analyzing the phenomena of deep feedback and self-excited oscillation,and specific formulas and clinical evidence are used to validate the analysis results,clarifying the role of relevant organ function changes in the pathogenesis of Chest Bi syndrome.The article aims to provide new insights into the complex pathogenesis of refractory diseases from a control theory perspective,offering new directions for modernizing TCM research with digital technology and theoretical support for future simulation-based digital systems guided by TCM theory.

The concept of amplification feedback pathways represents an intersection between electronics and control theory,involving both amplification and feedback processes.It reveals the dynamic evolution mechanisms of systems under the combined influence of these two processes.In Traditional Chinese Medicine(TCM),Chest Bi syndrome is considered a"ben xu biao shi"condition,with its primary pathology located in the heart and closely related to other organs such as the liver,spleen and kidneys.This article focuses on the interrelationship between organ dysfunction and the imbalance of the Five Elements Theory.By applying amplification feedback theory and models,the study constructs and analyzes single-stage amplification feedback pathways involving the heart,liver and kidneys,as well as double-stage amplification feedback pathways involving the heart,liver,kidneys and spleen,in the context of multifactorial interactions such as heart and kidney Yang deficiency,Qi stagnation in the heart and chest,and spleen-stomach dysfunction.Particular emphasis is placed on analyzing the phenomena of deep feedback and self-excited oscillation,and specific formulas and clinical evidence are used to validate the analysis results,clarifying the role of relevant organ function changes in the pathogenesis of Chest Bi syndrome.The article aims to provide new insights into the complex pathogenesis of refractory diseases from a control theory perspective,offering new directions for modernizing TCM research with digital technology and theoretical support for future simulation-based digital systems guided by TCM theory.

To investigate the in vitro inhibitory mechanism of Nymphaea candida total flavonoids(NCTF)against Staphylococcus aureus(S.aureus)and its safety in mice,this study first deter-mined the antibacterial effect of NCTF on the clinically isolated strain S.aureus-C1.Subsequently,the inhibitory mechanism of NCTF on S.aureus-C1 was explored by measuring its effects on bac-terial growth curves,microstructure,intracellular AKP and LDH levels,and biofilm formation.Safety evaluation included determination of LD50 and MDT in mice,as well as analysis of serum biochemical parameters,organ indices,and histopathological observations.Results showed that NCTF effectively inhibited S.aureus-C1 proliferation,with an inhibition zone diameter of(18.98±0.67)mm and a MIC of 6.25 g/L.A concentration of 2×MIC nearly completely suppressed bacte-rial growth.Scanning electron microscopy revealed structural damage to bacterial cells,including collapse and shrinkage.AKP and LDH assays indicated significantly increased AKP activity(P＜0.05)and decreased intracellular LDH activity(P＜0.05)in the supernatant of drug-treated groups,demonstrating NCTF-induced disruption of cell walls and membranes leading to leakage of AKP and LDH.Crystal violet staining of biofilms showed significant inhibition rates of(43.77±9.16)％and(61.71±9.82)％at 2 × MIC and 4 × MIC concentrations,respectively(P＜0.05).Safe-ty assessments indicated low toxicity of NCTF in mice,with transient effects that returned to nor-mal levels within a short period.These findings demonstrate that NCTF exhibits potent antibacte-rial activity against S.aureus-C1 by damaging bacterial cell structures,increasing cell wall/mem-brane permeability,reducing biofilm formation,and displaying low toxicity.This study provides scientific evidence for clinical drug screening against bovine mastitis and the development of Nym-phaea candida resources.