Malignant tumor metastasis is the key factor leading to poor prognosis of patients， and it is a difficult problem to be overcome in the field of tumor therapy. Metabolic reprogramming， as a key link in the regulation of tumor metastasis activity， affects the growth， invasion， and metastasis of tumor cells by changing the metabolic pathways of intracellular substances （such as glucose， amino acids， lipids， and nucleotides）. In particular， metabolic reprogramming plays a key role in the multistage linked steps related to tumor metastasis and can play a crucial role in several key stages of tumor tissue dissociation in situ， hematogenous metastasis， and remote colonization. Malignant tumor cells can selectively adjust their own metabolic state to adapt to the growth conditions of different metastatic microenvironments and colonization sites and then choose the most favorable growth and metabolism strategy. According to the holistic concept of traditional Chinese medicine （TCM）， the metastasis of malignant tumors is generally closely related to the metabolic state of the whole body. One of the advantages of TCM in the treatment of malignant tumors is systemic regulation. With its multi-pathway， multi-target， and multi-component therapeutic characteristics， TCM can effectively control the metastasis of malignant tumors by regulating the degradation of tumor epithelial mesenchymal transformation （EMT） and extracellular matrix （ECM）， anchoring the independent growth of tumor cells and the tumor microenvironment. In this paper， the potential regulatory effects of metabolic reprogramming on the metastasis of malignant tumors were discussed， and the latest research progress of the regulation of metabolic reprogramming by TCM on tumor metastasis was reviewed. At the same time， the key targets of TCM and its bioactive components in the process of tumor metastasis intervention were reviewed. This study aims to provide a more valuable basis and clearer idea for the treatment of malignant tumor metastasis by regulating metabolic reprogramming with TCM.

Objective To investigate the therapeutic effect of combination treatment of transcatheter arterial chemoembolization(TACE),micro wave ablation(MW A)and targeted immunotherapy for hepatocellular carcinoma(HCC).Methods The clinical data of HCC patients,who were admitted to the Affiliated Central Hospital of Jiangnan University of China to receive TACE from August 2016 to August 2023,were retrospectively analyzed.Based on the inclusion criteria,a total of 252 patients were included in this study.According to the therapeutic scheme,the patients were divided into combination group(receiving TACE,MWA,targeted therapy and immunotherapy,n=41),and control group(receiving TACE alone,n=211).The overall survival(OS)and progression-free survival(PFS)of the two groups were statistically analyzed.After propensity score matching at 1∶1 ratio,the clinical effects of the two groups were analyzed.According to different data,t-test,test,Kaplan-Meier curve,logarithmic rank test,Cox regression analysis,or Cox proportional risk model analysis was used to make statistical analysis.Results Multivariate regression analysis showed that tumor number,maximum diameter,invasion of large vessels,tumor capsule,AFP level,glutamic oxalacetic transaminase,BCLC stage and Child-Pugh stage were the independent risk factors for patient survival.Imaging response and combination treatment were the protective factors for survival.After propensity score matching,a total of 37 pairs of patients were obtained,and the baseline data were comparable between the groups.The differences in OS and PFS between the two groups were statistically significant.Combination treatment of TACE,MWA,targeted therapy and immunotherapy could significantly prolong OS and PFS in HCC patients.Conclusion Compared with TACE alone,combination use of TACE,MWA,targeted therapy and immunotherapy is a more effective therapeutic scheme for HCC,it can remarkably and effectively improve OS and PFS in HCC patients.

This paper provides a survey of the research progress in and applications of radio frequency identification(RFID)technology in the entire process management of blood supply.This paper makes an in-depth analysis of the scenarios and effectiveness of the technology,focusing on such key operational stagesas donor management,health screening,blood collection and testing,component preparation,storage and distribution,and patient transfusion.Based on a comprehensive evaluation of current achievements and bottlenecks,this study offers strategies for optimization of RFID technology in the management of blood supply and gives recommendations.The findings are intended to provide data for the establishment of an intelligent and traceable modern blood management system.

Objective To observe the effect of a Jianpi Huayu Jiedu formula on the NLRP3-mediated pyroptosis pathway in gastric precancerous lesion(GPL)associated with Helicobacter pylori(Hp)infection.Methods A GPL mouse model was prepared using Hp suspension gavage combined with Atp4a gene-deficient mice.The Jianpi Huayu Jiedu formula was administered as an intervention.Gastric mucosal tissue pathological damage was observed using hematoxylin and eosin(HE)staining.The presence of intestinal metaplasia(IM)was assessed using Alcian Blue-Periodic Acid Schiff(AB-PAS)staining.Ultrastructural changes in cell organelles were observed using transmission electron microscopy.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of gastrin-17(G-17),pepsinogen I(PGI),and proinflammatory cytokines IL-1β and IL-18.The expression of molecules related to the pyroptosis pathway was detected using Western blot and real-time quantitative PCR(RT-qPCR).Results Compared to the control group,Hp-related GPL mice exhibited gastric mucosal atrophy accompanied by IM and dysplasia.Damage to mitochondria and endoplasmic reticulum in parietal cells was observed.Levels of G-17,PGI,and proinflammatory cytokines IL-1β and IL-18 were elevated.The expression of molecules related to the pyroptosis pathway was increased.The Jianpi Huayu Jiedu formula significantly reduced gastric mucosal tissue pathological damage in GPL mice,decreased G-17 and PGI levels,mitigated inflammatory responses,and downregulated the expression of molecules related to the pyroptosis pathway.Conclusion The Jianpi Huayu Jiedu formula may exert its effects by inhibiting the NLRP3-mediated pyroptosis signaling pathway,thereby alleviating or even reversing the pathological damage of gastric mucosa in Hp-related GPL.

Objective To observe the effect of a Jianpi Huayu Jiedu formula on the NLRP3-mediated pyroptosis pathway in gastric precancerous lesion(GPL)associated with Helicobacter pylori(Hp)infection.Methods A GPL mouse model was prepared using Hp suspension gavage combined with Atp4a gene-deficient mice.The Jianpi Huayu Jiedu formula was administered as an intervention.Gastric mucosal tissue pathological damage was observed using hematoxylin and eosin(HE)staining.The presence of intestinal metaplasia(IM)was assessed using Alcian Blue-Periodic Acid Schiff(AB-PAS)staining.Ultrastructural changes in cell organelles were observed using transmission electron microscopy.Enzyme-linked immunosorbent assay(ELISA)was used to measure levels of gastrin-17(G-17),pepsinogen I(PGI),and proinflammatory cytokines IL-1β and IL-18.The expression of molecules related to the pyroptosis pathway was detected using Western blot and real-time quantitative PCR(RT-qPCR).Results Compared to the control group,Hp-related GPL mice exhibited gastric mucosal atrophy accompanied by IM and dysplasia.Damage to mitochondria and endoplasmic reticulum in parietal cells was observed.Levels of G-17,PGI,and proinflammatory cytokines IL-1β and IL-18 were elevated.The expression of molecules related to the pyroptosis pathway was increased.The Jianpi Huayu Jiedu formula significantly reduced gastric mucosal tissue pathological damage in GPL mice,decreased G-17 and PGI levels,mitigated inflammatory responses,and downregulated the expression of molecules related to the pyroptosis pathway.Conclusion The Jianpi Huayu Jiedu formula may exert its effects by inhibiting the NLRP3-mediated pyroptosis signaling pathway,thereby alleviating or even reversing the pathological damage of gastric mucosa in Hp-related GPL.

Nanobodies(Nb)have become novel probes for PET imaging instead of traditional antibodies,which have broad application prospects due to advantages of small molecular weight,strong stability and permeability,passing through the blood-brain barrier and low immunogenicity.The research progresses of structural characteristics of Nb,labeling methods of positron isotopes and application of labeled products in PET imaging were reviewed in this article.

Nanobodies(Nb)have become novel probes for PET imaging instead of traditional antibodies,which have broad application prospects due to advantages of small molecular weight,strong stability and permeability,passing through the blood-brain barrier and low immunogenicity.The research progresses of structural characteristics of Nb,labeling methods of positron isotopes and application of labeled products in PET imaging were reviewed in this article.

Objective To monitor the susceptibility of clinical isolates to antimicrobial agents in healthcare facilities in major regions of China in 2023.Methods Clinical isolates collected from 73 hospitals across China were tested for antimicrobial susceptibility using a unified protocol based on disc diffusion method or automated testing systems.Results were interpreted using the 2023 Clinical & Laboratory Standards Institute (CLSI) breakpoints.Results A total of 445199 clinical isolates were collected in 2023,of which 29.0％ were gram-positive and 71.0％ were gram-negative.The prevalence of methicillin-resistant strains in Staphylococcus aureus,Staphylococcus epidermidis and other coagulase-negative Staphylococcus species (excluding Staphylococcus pseudintermedius and Staphylococcus schleiferi) (MRSA,MRSE and MRCNS) was 29.6％,81.9％ and 78.5％,respectively.Methicillin-resistant strains showed significantly higher resistance rates to most antimicrobial agents than methicillin-susceptible strains (MSSA,MSSE and MSCNS).Overall,92.9％ of MRSA strains were susceptible to trimethoprim-sulfamethoxazole and 91.4％ of MRSE strains were susceptible to rifampicin.No vancomycin-resistant strains were found.Enterococcus faecalis had significantly lower resistance rates to most antimicrobial agents tested than Enterococcus faecium.A few vancomycin-resistant strains were identified in both E.faecalis and E.faecium.The prevalence of penicillin-susceptible Streptococcus pneumoniae was 93.1％ in the isolates from children and and 95.9％ in the isolates from adults.The resistance rate to carbapenems was lower than 15.0％ for most Enterobacterales species except for Klebsiella,22.5％ and 23.6％ of which were resistant to imipenem and meropenem,respectively .Most Enterobacterales isolates were highly susceptible to tigecycline,colistin and polymyxin B,with resistance rates ranging from 0.6％ to 10.0％.The resistance rate to imipenem and meropenem was 21.9％ and 17.4％ for Pseudomonas aeruginosa,respectively,and 67.5％ and 68.1％ for Acinetobacter baumannii,respectively.Conclusions Increasing resistance to the commonly used antimicrobial agents is still observed in clinical bacterial isolates.However,the prevalence of important crabapenem-resistant organisms such as crabapenem-resistant K.pneumoniae,P.aeruginosa,and A.baumannii showed a slightly decreasing trend.This finding suggests that strengthening bacterial resistance surveillance and multidisciplinary linkage are important for preventing the occurrence and development of bacterial resistance.

Background: Insulin resistance (IR) is the key pathological basis of many metabolic disorders. Lack of asialoglycoprotein receptor 1 (ASGR1) decreased the serum lipid levels and reduced the risk of coronary artery disease. However, whether ASGR1 also participates in the regulatory network of insulin sensitivity and glucose metabolism remains unknown. Methods: The constructed ASGR1 knockout mice and ASGR1-/- HepG2 cell lines were used to establish the animal model of metabolic syndrome and the IR cell model by high-fat diet (HFD) or drug induction, respectively. Then we evaluated the glucose metabolism and insulin signaling in vivo and in vitro. Results: ASGR1 deficiency ameliorated systemic IR in mice fed with HFD, evidenced by improved insulin intolerance, serum insulin, and homeostasis model assessment of IR index, mainly contributed from increased insulin signaling in the liver, but not in muscle or adipose tissues. Meanwhile, the insulin signal transduction was significantly enhanced in ASGR1-/- HepG2 cells. By transcriptome analyses and comparison, those differentially expressed genes between ASGR1 null and wild type were enriched in the insulin signal pathway, particularly in phosphoinositide 3-kinase-AKT signaling. Notably, ASGR1 deficiency significantly reduced hepatic gluconeogenesis and glycogenolysis. Conclusion The ASGR1 deficiency was consequentially linked with improved hepatic insulin sensitivity under metabolic stress, hepatic IR was the core factor of systemic IR, and overcoming hepatic IR significantly relieved the systemic IR. It suggests that ASGR1 is a potential intervention target for improving systemic IR in metabolic disorders.

Objectives: This study aimed to explore the influence of depression severity, disease course, treatment status, and other factors on cognitive function in adolescents with depressive disorders. Methods: Participants who met the inclusion criteria were enrolled in the study. Sociodemographic data of each participant were recorded, including age, sex, and family history of mental disorders. Zung’s Self-Rating Depression Scale was used to assess depression status in adolescents. Moreover, P300 and mismatch negativity (MMN) were used to objectively evaluate the participants’ cognitive function. Results: Only 26.8% of the adolescents with depression received standard antidepressant treatment. The latencies of N2 (267.80±23.34 ms), P3 (357.71±32.09 ms), and MMN (212.10±15.61 ms) in the adolescent depression group were longer than those in the healthy control group (p<0.01). Further analysis revealed that the latency of MMN was extended with increased levels of depression in adolescents.The MMN latency was short in participants with depression receiving standardized treatment. Furthermore, the latency of MMN was positively correlated with the severity and duration of depression (correlation coefficients were 0.465 and 0.479, respectively) (p<0.01). Conclusion Receiving standardized treatment and shortening the course of depression can reduce cognitive impairment in adolescents with depression.