Over the past three decades， China has made significant progress in the prevention and control of viral hepatitis， and the incidence rates of new-onset pediatric hepatitis B virus infections and acute viral hepatitis in the population have reduced to a relatively low level； however， there is still a heavy disease burden of chronic viral hepatitis in China， which severely affects the health status of the population. This study systematically summarizes the achievements of viral hepatitis prevention and control in China， analyzes existing problems and challenges， and proposes comprehensive prevention and control strategies and measures to eliminate viral hepatitis as a public health threat based on the national conditions of China， in order to provide a reference for related departments in China on how to achieve the action targets for eliminating viral hepatitis as a public health threat by 2030.

OBJECTIVE To establish population pharmacokinetic model of levetiracetam （Lev） for Chinese patients with post- stroke epilepsy （PSE）， and provide reference for formulating individualized dosing regimens for Lev therapy in this specific population. METHODS Blood concentration data and clinical diagnosis and treatment information of PSE patients meeting the inclusion criteria were retrospectively collected and divided into model group and validation group at an 8∶2 ratio using a random number method. Based on the model group data， a population pharmacokinetic model was developed using nonlinear mixed-effects modeling. Internal evaluation was performed through goodness-of-fit tests and bootstrap analysis， while external validation was conducted using the validation group data. RESULTS A total of 75 blood concentration measurements from 70 PSE patients were collected， with 60 measurements from 55 patients used for model development and 15 measurements from 15 patients reserved for external validation. The final model estimated a population typical value of clearance at 2.98 L/h. Estimated glomerular filtration rate， daily dose， and homocysteine level significantly influenced clearance of Lev （P＜0.01）. The model demonstrated satisfactory predictive performance， as evidenced by goodness-of-fit tests， bootstrap analysis， and external validation results. CONCLUSIONS Daily dose， estimated glomerular filtration rate， and homocysteine level are identified as significant covariates influencing Lev clearance in Chinese PSE patients. When making clinical decisions， comprehensive consideration should be given to the patient’s treatment response， physiological and pathological conditions， and the occurrence of adverse reactions， etc. The dosage of Lev should be adjusted based on the results of population pharmacokinetic model.

With the rapid development of generative artificial intelligence(GAI)technologies,their widespread application in academic research and writing is continuously expanding the boundaries of sci-entific inquiry.However,this trend has also raised a series of ethical and regulatory challenges,inclu-ding issues related to authorship,content authenticity,citation accuracy,and accountability.In light of the growing involvement of AI in generating academic content,establishing an open,controllable,and trustworthy ethical governance framework has become a key task for safeguarding research integrity and maintaining trust within the academic community.This expert consensus outlines ethical requirements across key stages of AI-assisted academic writing-including topic selection,data management,citation practices,and authorship attribution.It aims to clarify the boundaries and ethical obligations surrounding AI use in academic writing,ensuring that technological tools enhance efficiency without compromising in-tegrity.The goal is to provide guidance and institutional support for building a responsible and sustainable research ecosystem.

Objective The pathophysiological process of acute high-altitude hypoxia-induced lung injury affects protein expression levels,which are mainly evaluated by Western blot.No systematic study has investigated changes in internal control proteins as calibration loading amounts.Methods Lung injury at an altitude of 6000 m was induced in a low-pressure,low-oxygen chamber for 8,24,and 72 h using C57BL/6J mice.Establishment of the model was confirmed by hematoxylin and eosin staining.Expression levels of various internal control proteins,including vinculin,α-tubulin,eukaryotic translation initiation factor 5(EIF5),β-actin,and glyceraldehyde 3-phosphate dehydrogenase(GAPDH)were detected by Western blot,and total protein expression was detected by Coomassie blue staining.Furthermore,the lung injury model in vitro was establised by using,Bronchial epithelial cell(BZAS-2B)andhunman umbilical vein endothelial cells(HUVECS)confirmed by TUNEL staining.Expression levels of internal control proteins were detected by Western blot,and total protein expression was detected by Coomassie Blue staining.Results Acute 8,24,and 72 h hypoxic models were successfully established in lung tissue,demonstrating consistent total protein expression and stable levels of the internal reference proteins vinculin,α-tubulin,EIF5,andβ-actin.GAPDH expression was elevated in the HH8 h,HH24 h,and HH72 h groups compared with the normoxia(Nor)group,but only the increase at HH72 h groups was significant.Similarly,8,24,and 48 h hypoxic models were successfully established in BEAS-2B cells and HUVECs,with consistent total protein expression.In BEAS-2B cells,expression levels of the internal reference proteins β-actin and GAPDH were consistent with the normoxic control(NC)group,while vinculin,α-tubulin,and EIF5 expression levels were significantly reduced under hypoxic conditions for up to 24 h.In HUVECs,vinculin and α-tubulin expression levels were also consistent with the NC group,while EIF5,β-actin,and GAPDH expression levels were significantly reduced at 8 h and increased at 48 h.Conclusions Acute hypoxia induces lung tissue injury,and protein expression levels of the internal reference proteins vinculin,α-tubulin,EIF5,and β-actin are stable,making them suitable internal references for Western blot.Additionally,Western blot detected differential expression levels of the internal reference proteins vinculin,α-tubulin,EIF5,β-actin,and GAPDH in BEAS-2B cells and HUVECs,as the most important in vitro lung tissue models of hypoxia-induced injury.

Aim To predict the mechanism of action of ginsenoside Rg1(G-Rg1)paired with hirudin in the treatment of myocardial fibrosis in acute myocardial in-farction(AMI)based on the network pharmacology ap-proach,and to validate it by in vivo and in vitro experi-ments.Methods The corresponding targets of G-Rg1 and Hirudin were collected using SwissTargetPredic-tion,TargetNet,ETCM and ChEMBL databases,and the targets related to AMI and myocardial fibrosis were collected using GeneCards,OMIM and DisGeNET da-tabases.The drug-disease intersection targets were subjected to protein-protein interaction network(PPI)network analysis,gene ontology(GO)functional en-richment analysis and kyoto encyclopedia of genomes(KEGG)pathway enrichment analysis.Key targets and pathways were validated using an AMI mouse mod-el induced by ligation of the anterior descending branch of the left coronary artery in mice versus a hypoxia-in-duced injury model of human cardiac microvascular en-dothelial cells(HCMECs).Results G-Rg1 paired with hirudin had 229 drug targets,816 AMI and myo-cardial fibrosis disease targets,and 65 intersecting tar-gets.PPI analysis showed that tumor necrosis factor(TNF),interleukin-1[3(IL-1 β),transforming growth factor beta-1(TGF-β1),nuclear factor kappa-B(NF-κB),and interleukin-6(IL-6)might be the core tar-gets of G-Rg1 paired with Hirudin in the treatment of post-MI myocardial fibrosis;KEGG was enriched for a total of 141 pathways involving endocrine and metabo-lism,inflammation,and immunity,mainly TNF signa-ling pathway,PI3K/Akt signaling pathway and TGF-βsignaling pathway.In vivo experiments confirmed that G-Rg1 paired with hirudin attenuated myocardial fibro-sis after AMI in mice,and down-regulated the expres-sion of TNF-α,IL-1β,NF-κB,TGF-β1,and Smad2/3 proteins in myocardial tissues.In vitro experiments confirmed that G-Rg1 paired with Hirudin inhibited cellular NF-κB/TGF-β1 pathway,reduced hypoxia-in-duced cellular TNF-α and IL-1β expression,and su-perimposed NF-κB inhibitor significantly reduced IL-1 β expression and attenuated cellular inflammatory re-sponse.Conclusions G-Rg1 with Hirudin treats post-MI myocardial fibrosis by regulating TNF-α,IL-1 β and other targets and NF-KB/TGF-β1 pathway,reflecting its multi-pathway and multi-target action characteris-tics,and providing a pharmacological basis for the treatment of post-MI myocardial fibrosis with G-Rg1 with Hirudin.

Objective The pathophysiological process of acute high-altitude hypoxia-induced lung injury affects protein expression levels,which are mainly evaluated by Western blot.No systematic study has investigated changes in internal control proteins as calibration loading amounts.Methods Lung injury at an altitude of 6000 m was induced in a low-pressure,low-oxygen chamber for 8,24,and 72 h using C57BL/6J mice.Establishment of the model was confirmed by hematoxylin and eosin staining.Expression levels of various internal control proteins,including vinculin,α-tubulin,eukaryotic translation initiation factor 5(EIF5),β-actin,and glyceraldehyde 3-phosphate dehydrogenase(GAPDH)were detected by Western blot,and total protein expression was detected by Coomassie blue staining.Furthermore,the lung injury model in vitro was establised by using,Bronchial epithelial cell(BZAS-2B)andhunman umbilical vein endothelial cells(HUVECS)confirmed by TUNEL staining.Expression levels of internal control proteins were detected by Western blot,and total protein expression was detected by Coomassie Blue staining.Results Acute 8,24,and 72 h hypoxic models were successfully established in lung tissue,demonstrating consistent total protein expression and stable levels of the internal reference proteins vinculin,α-tubulin,EIF5,andβ-actin.GAPDH expression was elevated in the HH8 h,HH24 h,and HH72 h groups compared with the normoxia(Nor)group,but only the increase at HH72 h groups was significant.Similarly,8,24,and 48 h hypoxic models were successfully established in BEAS-2B cells and HUVECs,with consistent total protein expression.In BEAS-2B cells,expression levels of the internal reference proteins β-actin and GAPDH were consistent with the normoxic control(NC)group,while vinculin,α-tubulin,and EIF5 expression levels were significantly reduced under hypoxic conditions for up to 24 h.In HUVECs,vinculin and α-tubulin expression levels were also consistent with the NC group,while EIF5,β-actin,and GAPDH expression levels were significantly reduced at 8 h and increased at 48 h.Conclusions Acute hypoxia induces lung tissue injury,and protein expression levels of the internal reference proteins vinculin,α-tubulin,EIF5,and β-actin are stable,making them suitable internal references for Western blot.Additionally,Western blot detected differential expression levels of the internal reference proteins vinculin,α-tubulin,EIF5,β-actin,and GAPDH in BEAS-2B cells and HUVECs,as the most important in vitro lung tissue models of hypoxia-induced injury.

Aim To predict the mechanism of action of ginsenoside Rg1(G-Rg1)paired with hirudin in the treatment of myocardial fibrosis in acute myocardial in-farction(AMI)based on the network pharmacology ap-proach,and to validate it by in vivo and in vitro experi-ments.Methods The corresponding targets of G-Rg1 and Hirudin were collected using SwissTargetPredic-tion,TargetNet,ETCM and ChEMBL databases,and the targets related to AMI and myocardial fibrosis were collected using GeneCards,OMIM and DisGeNET da-tabases.The drug-disease intersection targets were subjected to protein-protein interaction network(PPI)network analysis,gene ontology(GO)functional en-richment analysis and kyoto encyclopedia of genomes(KEGG)pathway enrichment analysis.Key targets and pathways were validated using an AMI mouse mod-el induced by ligation of the anterior descending branch of the left coronary artery in mice versus a hypoxia-in-duced injury model of human cardiac microvascular en-dothelial cells(HCMECs).Results G-Rg1 paired with hirudin had 229 drug targets,816 AMI and myo-cardial fibrosis disease targets,and 65 intersecting tar-gets.PPI analysis showed that tumor necrosis factor(TNF),interleukin-1[3(IL-1 β),transforming growth factor beta-1(TGF-β1),nuclear factor kappa-B(NF-κB),and interleukin-6(IL-6)might be the core tar-gets of G-Rg1 paired with Hirudin in the treatment of post-MI myocardial fibrosis;KEGG was enriched for a total of 141 pathways involving endocrine and metabo-lism,inflammation,and immunity,mainly TNF signa-ling pathway,PI3K/Akt signaling pathway and TGF-βsignaling pathway.In vivo experiments confirmed that G-Rg1 paired with hirudin attenuated myocardial fibro-sis after AMI in mice,and down-regulated the expres-sion of TNF-α,IL-1β,NF-κB,TGF-β1,and Smad2/3 proteins in myocardial tissues.In vitro experiments confirmed that G-Rg1 paired with Hirudin inhibited cellular NF-κB/TGF-β1 pathway,reduced hypoxia-in-duced cellular TNF-α and IL-1β expression,and su-perimposed NF-κB inhibitor significantly reduced IL-1 β expression and attenuated cellular inflammatory re-sponse.Conclusions G-Rg1 with Hirudin treats post-MI myocardial fibrosis by regulating TNF-α,IL-1 β and other targets and NF-KB/TGF-β1 pathway,reflecting its multi-pathway and multi-target action characteris-tics,and providing a pharmacological basis for the treatment of post-MI myocardial fibrosis with G-Rg1 with Hirudin.

Objective The myocardial injury was induced by hypobaric hypoxia through regulating the expression of various proteins.The expression of proteins was mainly detected by western blot,but the selection of internal reference proteins and their variations have not been systematically studied.Methods Myocardial injury was induced in a low-pressure,low-oxygen chamber simulating an altitude of 6000 m,for 24 and 72 h.Establishment of the myocardial injury model was confirmed by hematoxylin eosin(HE)staining.Expression levels of internal control proteins,including vinculin,α-tubulin,eukaryotic translation initiation factor-5(EIF5),β-actin,glyceraldehyde-3-phosphate dehydrogenase(GAPDH),cyclophilin B,and cofilin,were detected by Western Blot and total protein expression was detected by Ponceau S and Coomassie Blue staining.An adult mouse cardiomyocytes(AMCMs)injury model was induced by hypoxia for 12 and 24 h and confirmed by terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL staining).Internal control proteins were detected by Western Blot,as in the in vivo model,and total protein expression was detected by Ponceau S and Coomassie Blue staining.Results A myocardial injury model was established by hypobaric hypoxia for 24 and 72 h,the total protein expression levels remained consistent.The expression of internal control proteins including vinculin,EIF5,β-actin,cyclophilin B,and cofilin was consistent between the control and model groups.Expression levels of α-tubulin were similar in the plain control and 24 h hypobaric hypoxia group,but were significantly lower in the 72 h hypobaric hypoxia group compared with the plain control group.GAPDH expression was significantly higher in the 24 and 72 h hypobaric hypoxia groups than in the plain control group.An AMCM injury model was established by hypoxia for 12 and 24 h.Total protein levels and expression levels of the internal control proteins EIF5 and β-actin were consistent,but vinculin,α-tubulin,GAPDH,cyclophilin B,and cofilin expression levels were higher in both hypoxia groups compared with the normoxic control group.Conclusions EIF5 and β-actin may be the suitable loading control proteins for studies of hypobaric hypoxia-induced myocardial injury using Western Blot.Total protein is also a good choice for hypobaric hypoxia studies.

This study was aimed at understanding the prevalence and drug resistance status of Salmonella of waterfowl ori-gin in the Guangdong region in the past decade,to guide prevention and control efforts.The drug-sensitive paper slide method was used to conduct drug susceptibility testing on 314 waterfowl-originating Salmonella strains isolated from 238 waterfowl farms in the Guangdong region from 2013 to 2023.The isolated Salmonella strains were most resistant to penicillin,amoxicil-lin,cefradine,and cefazolin in the β-lactam group;sulphadoxine dimethylpyrimidine in the sulphonamide group;and tetracy-cline in the tetracycline group.The resistance rates ranged from 73.57％to 89.49％.The highest sensitivity was observed to amikacin,gentamicin,and kanamycin in the aminoglycoside group,and norfloxacin in the quinolone group,with susceptibility rates all exceeding 50％.The 280 strains of Salmonella showed multi-drug resistance to six classes of antimicrobial drugs and high resistance(as much as 60.83％)to five drug classes.Correlation analysis revealed the highest correlations for florfenicol with gentamicin,and for amoxicillin with penicillin(r=0.650 for both),followed by gentamicin with kanamycin(r=0.620).Salmonella resistance in waterfowl in Guangdong Province was generally severe and showed a complex pattern of drug resist-ance.Detection of waterfowl pathogens should be strengthened to prevent the spread of drug-resistant bacteria and support ra-tional use of antibiotics.This work provides a reference for Salmonella prevention and control in waterfowl farms.

The stability of ammonium ion selective electrode is an important indicator to ensure accurate monitoring of ammonia nitrogen concentration in drinking water.However,in long-term monitoring process,interfering ions and water molecules in water samples may penetrate into the interior of the ammonium ion selective electrode to form a water layer,which affects the potential response and stability of the electrode.Perfluorooctanoic acid is a low surface energy material,and doping it in polyaniline can reduce surface energy of the composite and improve surface roughness.In this work,five ammonium ion selective electrodes were prepared by doping polyaniline with different concentrations of perfluorooctanoic acid as a solid contact layer,which made the solid contact layer of electrode had hydrophobic properties,thereby improving stability of the ammonium ion selective electrode.The stability of the ion-selective electrode was evaluated by potential drift experiment,and the optimal doping concentration of perfluorooctanoic acid in the sediment solution was determined to be 5 mmol/L.The experiment results showed that the solid contact layer had a water contact angle of 132o under the doping concentration,the potential drift rate was 41.66 μV/h,and potential drift rate in the aqueous layer test was 1.31 mV/h,which were all better than those of the unmodified electrode.The standard deviation of the electrode potential was 1.42 mV,which was obviously superior to that of the unmodified electrode.The characteristics of high stability of the electrode made it suitable for long-term monitoring of ammonia nitrogen content in water samples.