Objective: To translate the common metrics for donation attitude, subjective norm, perceived behavioral control, and intention for the blood donation context (BD-ASPI) into Chinese, and to test its reliability and validity among college students. Methods: A research team was established. Following Beaton's cross-cultural adaptation guidelines, the BD-ASPI was translated, culturally adapted, and pre-tested to develop the Chinese version. Using convenience sampling, 620 students from four universities in Wuhan were surveyed form August to November 2024 to test the scale's reliability and validity. Results: The Chinese version of the scale consisted of 21 items across four dimensions: attitude towards blood donation, subjective norm, perceived behavioral control, and intention. The item-level content validity index ranged from 0.89 to 1.00, and the average scale-level content validity index was 0.984. Confirmatory factor analysis indicated a good fit for the second-order factor model. The Criterion validity was 0.509 (P<0.001). The overall Cronbach's α coefficient was 0.965, with the coefficients for each dimension ranging from 0.891 to 0.974. The test-retest reliability was 0.894. Conclusion: The Chinese version of the BD-ASPI demonstrates good reliability and validity, and can serve as an effective tool for assessing the behavioral intention of voluntary blood donation among college students in China.

ObjectiveTo investigate the molecular mechanisms by which salvianolic acid B （SalB） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） by downregulating phosphoribosylaminoimidazole carboxylase and phosphoribosylaminoimidazole succinocarboxamide synthetase （PAICS） expression. MethodsNSCLC A549 cells and normal bronchial epithelial cells （bronchial epithelium transformed with Ad12-SV40 2B， BEAS-2B） were used as models. Cell viability was assessed using the cell counting kit-8 （CCK-8） assay after treatment with SalB （0， 50， 100， 200， 300， 400， 500 μmol·L^-1 for 24 or 48 h to determine effective and safe intervention concentrations. Cell proliferation， cell cycle distribution， and apoptosis were evaluated by 5-ethynyl-2′-deoxyuridine （EdU） staining and flow cytometry， respectively. Wound healing and Transwell invasion assays were performed to assess cell migration and invasion. RNA sequencing combined with bioinformatic analysis was conducted to identify differentially expressed genes and functional enrichment. Molecular docking was used to predict the binding ability between SalB and PAICS， and the cellular thermal shift assay （CETSA） was performed to evaluate the effect of SalB on the thermal stability of the PAICS protein. Western blot （WB） was used to detect the effects of SalB on PAICS and EMT-related proteins （E-cadherin， N-cadherin， Vimentin， Snail， and Slug）. A functional rescue assay was conducted by PAICS overexpression via plasmid transfection. ResultsCompared with the control group， SalB inhibited A549 cell viability in a dose-dependent manner （P<0.05）， and the effective concentrations （≤300 μmol·L^-1） showed no significant cytotoxicity in BEAS-2B cells. Within this concentration range， SalB significantly inhibited A549 cell proliferation， migration， and invasion， and induced G₀/G₁ phase arrest and apoptosis （P<0.05）. Transcriptomic analysis showed that SalB significantly downregulated PAICS expression， and its functions were enriched in cell proliferation and EMT. Bioinformatic analysis indicated that PAICS is highly expressed in lung adenocarcinoma and is associated with poor prognosis （P<0.01）. Molecular docking showed that SalB has strong binding ability to PAICS （binding energy -9.1 kcal·mol^-1. CETSA results showed that SalB significantly increased the thermal stability of the PAICS protein （P<0.05）. WB results showed that， compared with the control group， SalB dose-dependently downregulated PAICS expression， upregulated E-cadherin， and downregulated N-cadherin， Vimentin， Snail， and Slug （P<0.05）. Functional rescue experiments showed that， compared with the empty vector group， PAICS overexpression significantly enhanced A549 cell proliferation， migration， and invasion， promoted cell cycle progression， and inhibited apoptosis （P<0.05）. Meanwhile， compared with the empty vector + SalB-H group， PAICS overexpression partially reversed the inhibitory effects of SalB on malignant phenotypes and EMT-related proteins （N-cadherin， Vimentin， Snail， and Slug）， and downregulated E-cadherin expression （P<0.05，P<0.01）， indicating that PAICS is a key functional target mediating the antitumor effects of SalB. ConclusionSalB effectively inhibits EMT progression and cell cycle progression in A549 cells by downregulating PAICS expression， thereby exerting anti-NSCLC effects. This study not only reveals that PAICS is a key functional target through which SalB regulates EMT， but also provides experimental evidence supporting SalB as a potential candidate drug for inhibiting NSCLC metastasis.

ObjectiveTo investigate the mechanisms by which eupatilin （Eup） inhibits proliferation， invasion， and metastasis of non-small cell lung cancer （NSCLC） through the enhancer of zeste homolog 2/histone H3 lysine 27 trimethylation （EZH2/H3K27me3） signaling pathway. MethodsIn vivo， a subcutaneous xenograft tumor model was established in nude mice using H1299 cells to evaluate the anti-NSCLC effects of Eup. Immunohistochemistry （IHC-P） was used to detect the expression of proliferation- and invasion/metastasis-related proteins， including proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA）. In vitro， cell counting kit-8 （CCK-8） assays were performed to determine the viability of H1299 cells treated with different concentrations of Eup （0-200 μmol·L^-1） and to select appropriate concentrations. Colony formation and 5-ethynyl-2′-deoxyuridine （EdU） assays were used to evaluate cell proliferation. Wound healing and invasion assays were conducted to assess cell migration and invasion. Human umbilical vein endothelial cell （HUVEC） angiogenesis assays were used to evaluate the effects of Eup on angiogenesis. Transcriptomic analysis was performed to identify the targets of Eup in H1299 cells and to explore its major functions. Molecular docking and molecular dynamics simulations were conducted to predict the binding affinity and interaction stability between Eup and its target proteins. Western blot was used to detect the effects of Eup on the expression levels of EZH2/H3K27me3 pathway-related proteins and proliferation- and invasion/metastasis-related proteins， including PCNA， MMP-2， MMP-9， and VEGFA. ResultsIn the subcutaneous xenograft model， compared with the model group， Eup treatment dose-dependently inhibited the growth of H1299 xenograft tumors， and the tumor inhibition rate was significantly increased （P<0.05）. IHC-P results showed that， compared with the model group， high-dose Eup significantly reduced the expression levels of PCNA， MMP-2， MMP-9， and VEGFA in vivo （P<0.05）. In vitro， compared with the control group， Eup inhibited the proliferation， invasion， and metastasis of NSCLC cells in a concentration-dependent manner. Transcriptomic analysis further showed that， compared with the control group， Eup significantly downregulated EZH2 expression， and its functional effects were associated with inhibition of tumor metastasis. Molecular docking and molecular dynamics simulations indicated that Eup exhibited strong binding affinity with EZH2 and stable interactions. Western blot results demonstrated that， compared with the model group， Eup significantly inhibited， in a dose-dependent manner， the expression levels of EZH2， H3K27me3， and proliferation- and invasion/metastasis-related proteins （PCNA， MMP-2， MMP-9， and VEGFA） in both in vivo and in vitro experiments （P<0.05）. In vitro， compared with the control group， overexpression of EZH2 via plasmid transfection partially reversed the inhibitory effects of Eup on the expression of key proteins involved in proliferation and invasion/metastasis in H1299 cells. ConclusionEup effectively inhibits the proliferation， migration， and invasion of H1299 cells both in vivo and in vitro. The underlying mechanism may be related to inhibition of the EZH2/H3K27me3 signaling pathway and downregulation of proliferation- and invasion/metastasis-related proteins， including PCNA， MMP-2， MMP-9， and VEGFA. Eup may serve as a potential therapeutic agent for suppressing proliferation and invasion/metastasis in NSCLC.

ObjectiveTo investigate the molecular mechanisms by which salvianolic acid B （SalB） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） by downregulating phosphoribosylaminoimidazole carboxylase and phosphoribosylaminoimidazole succinocarboxamide synthetase （PAICS） expression. MethodsNSCLC A549 cells and normal bronchial epithelial cells （bronchial epithelium transformed with Ad12-SV40 2B， BEAS-2B） were used as models. Cell viability was assessed using the cell counting kit-8 （CCK-8） assay after treatment with SalB （0， 50， 100， 200， 300， 400， 500 μmol·L^-1 for 24 or 48 h to determine effective and safe intervention concentrations. Cell proliferation， cell cycle distribution， and apoptosis were evaluated by 5-ethynyl-2′-deoxyuridine （EdU） staining and flow cytometry， respectively. Wound healing and Transwell invasion assays were performed to assess cell migration and invasion. RNA sequencing combined with bioinformatic analysis was conducted to identify differentially expressed genes and functional enrichment. Molecular docking was used to predict the binding ability between SalB and PAICS， and the cellular thermal shift assay （CETSA） was performed to evaluate the effect of SalB on the thermal stability of the PAICS protein. Western blot （WB） was used to detect the effects of SalB on PAICS and EMT-related proteins （E-cadherin， N-cadherin， Vimentin， Snail， and Slug）. A functional rescue assay was conducted by PAICS overexpression via plasmid transfection. ResultsCompared with the control group， SalB inhibited A549 cell viability in a dose-dependent manner （P<0.05）， and the effective concentrations （≤300 μmol·L^-1） showed no significant cytotoxicity in BEAS-2B cells. Within this concentration range， SalB significantly inhibited A549 cell proliferation， migration， and invasion， and induced G₀/G₁ phase arrest and apoptosis （P<0.05）. Transcriptomic analysis showed that SalB significantly downregulated PAICS expression， and its functions were enriched in cell proliferation and EMT. Bioinformatic analysis indicated that PAICS is highly expressed in lung adenocarcinoma and is associated with poor prognosis （P<0.01）. Molecular docking showed that SalB has strong binding ability to PAICS （binding energy -9.1 kcal·mol^-1. CETSA results showed that SalB significantly increased the thermal stability of the PAICS protein （P<0.05）. WB results showed that， compared with the control group， SalB dose-dependently downregulated PAICS expression， upregulated E-cadherin， and downregulated N-cadherin， Vimentin， Snail， and Slug （P<0.05）. Functional rescue experiments showed that， compared with the empty vector group， PAICS overexpression significantly enhanced A549 cell proliferation， migration， and invasion， promoted cell cycle progression， and inhibited apoptosis （P<0.05）. Meanwhile， compared with the empty vector + SalB-H group， PAICS overexpression partially reversed the inhibitory effects of SalB on malignant phenotypes and EMT-related proteins （N-cadherin， Vimentin， Snail， and Slug）， and downregulated E-cadherin expression （P<0.05，P<0.01）， indicating that PAICS is a key functional target mediating the antitumor effects of SalB. ConclusionSalB effectively inhibits EMT progression and cell cycle progression in A549 cells by downregulating PAICS expression， thereby exerting anti-NSCLC effects. This study not only reveals that PAICS is a key functional target through which SalB regulates EMT， but also provides experimental evidence supporting SalB as a potential candidate drug for inhibiting NSCLC metastasis.

ObjectiveTo investigate the mechanisms by which eupatilin （Eup） inhibits proliferation， invasion， and metastasis of non-small cell lung cancer （NSCLC） through the enhancer of zeste homolog 2/histone H3 lysine 27 trimethylation （EZH2/H3K27me3） signaling pathway. MethodsIn vivo， a subcutaneous xenograft tumor model was established in nude mice using H1299 cells to evaluate the anti-NSCLC effects of Eup. Immunohistochemistry （IHC-P） was used to detect the expression of proliferation- and invasion/metastasis-related proteins， including proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA）. In vitro， cell counting kit-8 （CCK-8） assays were performed to determine the viability of H1299 cells treated with different concentrations of Eup （0-200 μmol·L^-1） and to select appropriate concentrations. Colony formation and 5-ethynyl-2′-deoxyuridine （EdU） assays were used to evaluate cell proliferation. Wound healing and invasion assays were conducted to assess cell migration and invasion. Human umbilical vein endothelial cell （HUVEC） angiogenesis assays were used to evaluate the effects of Eup on angiogenesis. Transcriptomic analysis was performed to identify the targets of Eup in H1299 cells and to explore its major functions. Molecular docking and molecular dynamics simulations were conducted to predict the binding affinity and interaction stability between Eup and its target proteins. Western blot was used to detect the effects of Eup on the expression levels of EZH2/H3K27me3 pathway-related proteins and proliferation- and invasion/metastasis-related proteins， including PCNA， MMP-2， MMP-9， and VEGFA. ResultsIn the subcutaneous xenograft model， compared with the model group， Eup treatment dose-dependently inhibited the growth of H1299 xenograft tumors， and the tumor inhibition rate was significantly increased （P<0.05）. IHC-P results showed that， compared with the model group， high-dose Eup significantly reduced the expression levels of PCNA， MMP-2， MMP-9， and VEGFA in vivo （P<0.05）. In vitro， compared with the control group， Eup inhibited the proliferation， invasion， and metastasis of NSCLC cells in a concentration-dependent manner. Transcriptomic analysis further showed that， compared with the control group， Eup significantly downregulated EZH2 expression， and its functional effects were associated with inhibition of tumor metastasis. Molecular docking and molecular dynamics simulations indicated that Eup exhibited strong binding affinity with EZH2 and stable interactions. Western blot results demonstrated that， compared with the model group， Eup significantly inhibited， in a dose-dependent manner， the expression levels of EZH2， H3K27me3， and proliferation- and invasion/metastasis-related proteins （PCNA， MMP-2， MMP-9， and VEGFA） in both in vivo and in vitro experiments （P<0.05）. In vitro， compared with the control group， overexpression of EZH2 via plasmid transfection partially reversed the inhibitory effects of Eup on the expression of key proteins involved in proliferation and invasion/metastasis in H1299 cells. ConclusionEup effectively inhibits the proliferation， migration， and invasion of H1299 cells both in vivo and in vitro. The underlying mechanism may be related to inhibition of the EZH2/H3K27me3 signaling pathway and downregulation of proliferation- and invasion/metastasis-related proteins， including PCNA， MMP-2， MMP-9， and VEGFA. Eup may serve as a potential therapeutic agent for suppressing proliferation and invasion/metastasis in NSCLC.

Hepatolenticular degeneration is a rare disease,and the number of cases of primary liver cancer occurring on the basis of liver cirrhosis caused by hepatolenticular degeneration is very small.This paper reports a case of hepatolenticular degeneration with primary liver cancer,and then reviews and summarizes current cases of this disease both domestically and internationally.
Humans ; Hepatolenticular Degeneration/complications* ; Liver Neoplasms/complications*

In recent years,the incidence and mortality of heatstroke have been increasing annually alongside global warming,with a marked rise in cases exhibiting atypical symptoms.To address the increasingly complex challenges in heatstroke prevention and treatment,Heatstroke Prevention and Treatment Research Center of Chinese PLA,Expert Group of Heatstroke Prevention and Treatment of Chinese PLA,and Chinese PLA Professional Committee of Critical Care Medicine have jointly developed this guideline(2025 edition).Utilizing the Grading of Recommendations Assessment,Development and Evaluation(GRADE)system,Appraisal of Guidelines for Research and Evaluation(AGREE)criteria,and Reporting Items for Practice Guidelines in Healthcare(RIGHT)standards,and based on the 2015 draft"Expert Consensus on the Standardized Diagnosis and Treatment of Heatstroke"and the 2019"Chinese Expert Consensus on the Diagnosis and Treatment of Heatstroke",this guideline has been crafted.This guideline provides 25 evidence-based recommendations to guide the prevention,treatment and research of heatstroke,which thoroughly covers 8 critical domains:clinical classification,pathophysiological mechanisms,clinical manifestations,diagnostic criteria,differential diagnosis,treatment protocols,rehabilitation and return to work,and prevention.

With the continuous improvement of the national management requirements for medical quality and safety,it is particularly important to improve the level of refinement,scientificity,and standardization of medical quality and safety manage-ment.Based on the evaluation criteria of tertiary hospitals,a hospital in Tianjin has constructed a medical quality indicator moni-toring system,which has improved the management efficiency of medical data and assisted the hospital in successfully meeting the evaluation and achieved good results.This paper discusses the system's requirements analysis,construction process,application results,and shares experiences and shortcomings to provide reference for other medical institutions to improve the effectiveness of medical quality and safety management.

Objective To investigate the expression of arginase Ⅱ(ArgⅡ)in kidney tissue of rats with diabetic nephropathy(DN)and its significance in the development of DN.Methods A total of 10 male SD rats were randomly divided into the control group and the model group,with 5 rats in each group.An rat model of DN was developed by feeding with high-sugar and high-fat diet combined with intra-peritoneal injection of low-dose streptozotocin(45 mg/kg),and they were sacrificed after 11 weeks of continued feeding.The body weight,and biochemical indexes of blood and urine of rats were determined.The right kidney was weighed and histopathological examination was performed.The pathological changes of kidney tissues and protein expression of ArgⅡ and CD68+were observed,and the immunofluores-cence double staining was used to observe the distribution and expression of ArgⅡand a marker of renal macrophage activation CD68+;the protein expression of ArgⅡ,NF-κB,TNF-α and IL-6 in kidney tissues was determined by Western blot.Results Compared with the control group,the ratio of kidney weight to body weight,24-hour urine volume,24-hour urine protein,fasting blood glucose,urea nitrogen and insulin level in the model group were significantly increased(P<0.05).The renal histopathology showed that the mesangial cells of the renal glomerular were necrotic with vascular dilatation,and the renal tubular epithelial cells were steatosis and congestion.Compared with the control group,the protein expression of ArgⅡ,CD68+,NF-κB,TNF-α and IL-6 in the kidney tissues of the model group were significantly increased(P<0.05).Immunofluorescence double staining demonstrated the co-expression of ArgⅡ and CD68+in renal tissue,and the fluorescence intensities of both ArgⅡ and CD68+in the model group were significantly stronger than those in the control group(P<0.01).Conclusion The expression of ArgⅡ is increased in DN,which may be participated in the occurrence of inflammatory lesions in DN.

Objective To propose a dynamic early warning model based on machine learning methods and validate its predi-ctive efficacy so as to achieve precise assessment and early warning of mortality risk in patients with traumatic hypothermia.Methods Firstly,a total of 480 patients who met inclusion criteria were retrospectively selected from the eICU database and randomly divided into training and test sets at an 8∶2 ratio.Secondly,physiological parameters were extracted from these patients,and five machine learning algorithms including XGBoost,AdaBoost,LightGBM,logistic regression(LR)and random forest(RF)were employed respectively to develop dynamic mortality risk warning models for traumatic hypothermia patients,utilizing a 1-hour observation window.Thirdly,receiver operating characteristic curves(ROC)were plotted using the test set data and the effects of different warning windows on the model performance were analyzed by calculating the AUC.Finally,the interpretability of the models was analyzed using the SHapley Additive exPlanations(SHAP)algorithm to elucidate the contribution of each feature to predictive performance.Results The optimal warning window for the dynamic warning model constructed using the eICU database was 12 hours,and in case of 12-hour warning window the logistic regression model achieved the highest AUC of 0.935 and showed optimal predictive performance.The results of the interpretability analysis by the SHAP algorithm showed that body temperature was the feature that had the greatest impact on the model results,and its reduction was positively correlated with the increased risk of death.Conclusion The machine learning-based dynamic warning model for mortality risk in traumatic hypothermia patients enables real-time dynamic risk assessment,providing robust support for clinicians to identify the patient's condition changes at an early stage and references for the adjustment of clinical treatment programs.[Chinese Medical Equipment Journal,2025,46(3):9-14]