Hepatocellular carcinoma (HCC) develops within a profoundly immunosuppressive tumor immune microenvironment (TIME), which limits the efficacy of immunotherapy. Polarization of tumor-associated macrophages (TAMs) toward a pro-tumorigenic M2 phenotype is a major driver of immune escape. Ferroptosis, an iron-dependent regulated cell death program, intersects with hepatic iron metabolism and immune regulation and thus offers promising points of therapeutic intervention. This review systematically elucidates the mechanistic role of TAM ferroptosis in HCC immune evasion and highlights a “bidirectional regulation” intervention strategy grounded in the Traditional Chinese medicine (TCM) principle of “fortifying healthy qi and eliminating pathogens” (Fuzheng Quxie). This strategy employs “eliminating pathogens” (Quxie) approaches to exploit the metabolic vulnerability of M2-like TAMs and precisely induce their ferroptosis. Moreover, it utilizes “fortifying healthy qi” (Fuzheng) approaches to protect M1-like TAMs and CD8⁺ T cells from oxidative damage. This parallel “induction-protection” paradigm demonstrates the unique advantages of TCM in systemically remodeling TIME through multitarget synergistic actions. Accordingly, precision regulation of TAM ferroptosis based on the Fuzheng Quxie theory represents a promising integrative Chinese-Western medicine strategy for overcoming current bottlenecks in HCC immunotherapy, although its clinical translational potential warrants further validation.

Objective To explore the effect of plasma-activated gas(PAG)in promoting wound healing.Methods The pro-healing effect of PAG was explored by testing the effectiveness of PAG in promoting cell proliferation and healing of infected wounds.Cell proliferation assay:five different cells(i.e.,HSF,IHSMC,WPMY-1,HaCaT,and HFF)in logarithmic growth phase were inoculated into culture plates.After the cells grew adherently to the wall,the different cells were each grouped experimentally using a suitable time gradient.After the cells were treated with PAG for different time,their activity was detected by CCK-8 method.Animal infected wound healing assay:a wound of about 1.5 cm × 1.5 cm in size was created on the back of SD rats with sterile tweezers and scissors,and then the wound was infected with P.Aeruginosa with A600nm=6.5.After the infection was completed,the wounds were treated with PAG at regular intervals,and the experiment groups were subdivided according to the different treatment durations.Wound healing photographs and changes in relative wound area were used as indicators of healing performance.Results Cell proliferation assay:PAG treatment was effective in promoting cell proliferation for a reasonable period of time,while overdose led to cell death.Therefore,the dose of cells treated with plasma activation gas was defined as=W/N(J/cell),where W is the work consumed by the activation gas device during the treatment process and N is the number of cells.The three indexes(starting dose,optimal dose and safe dose range)were used to characterize the proliferative effect of PAG.Animal infected wound healing assay:the experimental groups all showed accelerated wound healing,so the optimal treatment time was used to characterize the pro-healing effect of PAG.The sterilization mode played a primary role,with an optimal treatment time of 2 min,and the pro-healing mode played a secondary role.The treatment conditions with the best overall healing effect were 2 min for the sterilization mode and 1 min for the pro-healing mode.Conclusion PAG has the effect of promoting cell proliferation and infected wound healing,and indicators can be summarized to quantitatively describe its effect,which is conducive to further standardization of PAG research and clinical utility.

Several imaging examination means for the military training-related injuries at the knee joint were introduced in terms of the research progress,advantages and limitations,including X-ray examination,multi-slice spiral CT,ultrasound examination and MRI.It's pointed out the progress of imaging devices and image post-processing techniques and the involvement of AI diagnosis contributed to the development of the imaging diagnoses of the military training-related injuries at the knee joint.[Chinese Medical Equipment Journal,2025,46(1):101-107]

Objective To explore the reasons for the activation of the RNA-binding protein ZC3H15 in non-small cell lung canc-er and its biological functions in the tumorigenesis of non-small cell lung cancer.Methods Based on the whole genome sequencing data of The Cancer Genome Atlas(TCGA)database,the relationship between ZC3H15 copy number variation and its expression was analyzed,and the differential expression of ZC3H15 between normal and non-small cell lung cancer groups,its variation across different TNM sta-ges,and its prognostic analysis were investigated.A549 cells and PC9 cells were divided into si-NC group and si-c-Myc group,re-spectively.Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and chromatin immunoprecipitation were used to explore the regulatory relationship between the transcription factor c-Myc and ZC3H15.A549 cells and PC9 cells were divided into si-NC group,si-ZC3H15 1# group,si-ZC3H15 2# group,Vector group,pcDNA-ZC3H15group.RT-qPCR was used to detect the ex-pression of ZC3H15,MTT assay was used to detect cell viability,colony formation assay was used to examine cell proliferation capacity,and Transwell assay was used to measure cell migration ability.The A549 cells were stably transfected with sh-Ctrl and sh-ZC3H15,and the nude mouse xenograft model was used to detect the impact of ZC3H15 on the proliferation ability of non-small cell lung cancer cells in vivo.Results TCGA non-small cell lung cancer data analysis showed that the expression level of ZC3H15 in the copy-number-amplified group was higher than that in the copy-number-deleted group(P＜0.05).ZC3H15 copy number was positively correlated with expression level(P＜0.05).In both paired and unpaired non-small cell lung cancer groups,the expression level of ZC3H15 was up-regulated compared to the normal group(P＜0.05).The expression level of ZC3H15 was higher in stage Ⅲ/Ⅳ group than that in stage Ⅰ/Ⅱ group(P＜0.05).The low-expression ZC3H15group had a higher survival rate than the high-expression group(P＜0.05).Compared to the si-NC group,the expression level of ZC3H15 and Input reference percentage after c-Myc antibody treatment in the si-c-Myc group were both decreased(P＜0.05).The results of RT-qPCR showed that in A549 cells and PC9 cells,the expression level of ZC3H15 in the si-ZC3H15 1# and si-ZC3H15 2# groups were lower than those in the si-NC group(P＜0.05),while the expression level of ZC3H15 in the pcDNA-ZC3H15group was higher than that in the Vector group(P＜0.05).Further cell func-tion studies found that the proliferation and migration capacity of non-small cell lung cancer cells with ZC3H15 knockdown were decreased(P＜0.05),and the overexpression of ZC3H15 could enhance the proliferation and migration capacity of non-small cell lung cancer cells(P＜0.05).At the in vivo level,subcutaneous tumor-bearing experiments in nude mice showed that ZC3H15 knockdown could significant-ly reduced the tumor growth rate(P＜0.05).Conclusion Copy number amplification and c-Myc transcriptional activation were important reasons for ZC3H15 activation in non-small cell lung cancer.ZC3H15 is a key functional molecule to promote the tumorigenesis of non-small cell lung cancer,and can provide some theoretical basis for clinical diagnosis and treatment of non-small cell lung cancer.

Objective To explore the reasons for the activation of the RNA-binding protein ZC3H15 in non-small cell lung canc-er and its biological functions in the tumorigenesis of non-small cell lung cancer.Methods Based on the whole genome sequencing data of The Cancer Genome Atlas(TCGA)database,the relationship between ZC3H15 copy number variation and its expression was analyzed,and the differential expression of ZC3H15 between normal and non-small cell lung cancer groups,its variation across different TNM sta-ges,and its prognostic analysis were investigated.A549 cells and PC9 cells were divided into si-NC group and si-c-Myc group,re-spectively.Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and chromatin immunoprecipitation were used to explore the regulatory relationship between the transcription factor c-Myc and ZC3H15.A549 cells and PC9 cells were divided into si-NC group,si-ZC3H15 1# group,si-ZC3H15 2# group,Vector group,pcDNA-ZC3H15group.RT-qPCR was used to detect the ex-pression of ZC3H15,MTT assay was used to detect cell viability,colony formation assay was used to examine cell proliferation capacity,and Transwell assay was used to measure cell migration ability.The A549 cells were stably transfected with sh-Ctrl and sh-ZC3H15,and the nude mouse xenograft model was used to detect the impact of ZC3H15 on the proliferation ability of non-small cell lung cancer cells in vivo.Results TCGA non-small cell lung cancer data analysis showed that the expression level of ZC3H15 in the copy-number-amplified group was higher than that in the copy-number-deleted group(P＜0.05).ZC3H15 copy number was positively correlated with expression level(P＜0.05).In both paired and unpaired non-small cell lung cancer groups,the expression level of ZC3H15 was up-regulated compared to the normal group(P＜0.05).The expression level of ZC3H15 was higher in stage Ⅲ/Ⅳ group than that in stage Ⅰ/Ⅱ group(P＜0.05).The low-expression ZC3H15group had a higher survival rate than the high-expression group(P＜0.05).Compared to the si-NC group,the expression level of ZC3H15 and Input reference percentage after c-Myc antibody treatment in the si-c-Myc group were both decreased(P＜0.05).The results of RT-qPCR showed that in A549 cells and PC9 cells,the expression level of ZC3H15 in the si-ZC3H15 1# and si-ZC3H15 2# groups were lower than those in the si-NC group(P＜0.05),while the expression level of ZC3H15 in the pcDNA-ZC3H15group was higher than that in the Vector group(P＜0.05).Further cell func-tion studies found that the proliferation and migration capacity of non-small cell lung cancer cells with ZC3H15 knockdown were decreased(P＜0.05),and the overexpression of ZC3H15 could enhance the proliferation and migration capacity of non-small cell lung cancer cells(P＜0.05).At the in vivo level,subcutaneous tumor-bearing experiments in nude mice showed that ZC3H15 knockdown could significant-ly reduced the tumor growth rate(P＜0.05).Conclusion Copy number amplification and c-Myc transcriptional activation were important reasons for ZC3H15 activation in non-small cell lung cancer.ZC3H15 is a key functional molecule to promote the tumorigenesis of non-small cell lung cancer,and can provide some theoretical basis for clinical diagnosis and treatment of non-small cell lung cancer.

Objective:To investigate the selection preference and heterogeneity of intervention measures for high-risk population of Cardiovascular Disease in rural areas,and to provide new empirical evidence and path reference for evidence-based CVD intervention strategies.Methods:Using cluster sampling method,a discrete choice experiment was designed to conduct an offline survey on 345 CVD high-risk subjects in one of the CVD high-risk screening sites in Hubei Province.Mixed logit model was used for data analysis.Results:The attributes of"Primary medical staff+County-level medical staff+Experts above county-level","Monthly or longer","Non-drug intervention","Drug intervention+non-drug intervention","One hour",all significantly increased the probability of high-risk population to choose the project,and"Online"mode and"Personalized service package"will significantly reduce the probability of respondents to choose a solution,there were significant differences in the selection preferences of high-risk population with different gender,age,education level,income level and health status.Conclusion:The rural CVD high-risk population obviously prefer the intervention model with high level of service subject,off-line implementation,low frequency,medium intensity,non-drug intervention or combined with drug intervention,and free basic service content.It is necessary to explore a more efficient and suitable intervention scheme for CVD in rural high-risk population according to the demand-side preference and its heterogeneity.

Objective:In the context of China's cardiovascular disease(CVD)high-risk population screening and intervention project,this study systematically evaluates the applicability of the EQ-5D-5L and SF-6Dv2 instruments among individuals at high risk of CVD.Methods:Convergent validity was assessed using Spearman's correlation coefficient.Measurement agreement was evaluated through intraclass correlation coefficients(ICC)and Bland-Altman plots.Factors influencing utility differences were explored using multiple linear regression analysis.Kruskal-Wallis test and t-test were used to examine discriminant validity.Sensitivity was compared by effect size(ES),relative efficiency(RE),and the area under the receiver operating characteristic curve(ROC-AUC).Floor and ceiling effects were also compared.Results:Among 5,415 individuals at high risk of CVD,the two instruments showed moderate overall correlation and acceptable convergent validity,but dimension-specific correlations were weak,and measurement consistency was low(ICC=0.367).Both instruments effectively distinguished different health states,yet the SF-6Dv2 demonstrated superior sensitivity and a milder ceiling effect.Conclusion:When measuring the health utility value of CVD patients,scale selection should be cautious,especially for high-risk groups,and SF-6Dv2 is more appropriate.

Pancreatic cancer has emerged as one of the most challenging malignancies worldwide,with its high resistance to chemotherapy being the primary cause of treatment failure.Therefore,enhancing the chemosensitivity of pancreatic cancer has become a major focus of current research.In this study,we in-vestigated how Bufotaline,a bufadienolide extracted from the traditional Chinese medicine toad venom,exhibits its antitumor activity.Specifically,we explored the potential of Bufotaline to enhance the chemo-sensitivity of pancreatic cancer cells to Adriamycin and elucidated its underlying molecular mechanisms.Using CCK-8 and colony formation assays,we demonstrated that Bufotaline enhances the inhibitory effect of Adriamycin on the survival of pancreatic cancer cell lines Patu-8988T,Aspc-1,and Patu-8988S.No-tably,Bufotaline treatment reduced the IC50 of Adriamycin in drug-resistant pancreatic cancer cells to lev-els comparable to those in non-resistant cells.Results from Western blot,immunofluorescence,comet as-say,and TUNEL assays revealed that Bufotaline promotes Adriamycin-induced DNA damage in pancreatic cancer cells.RNA-seq analysis of Patu-8988T cells treated with Adriamycin alone or in combination with Bufotaline showed significant changes in gene expression,and qRT-PCR analysis further confirmed that Bu-fotaline downregulates the expression of DNA damage repair proteins NBS1 and RAD50.Moreover,Western blot analysis revealed that Bufotaline reduces the levels of DNA damage response repair proteins,and Im-munofluorescence experiments indicated that Bufotaline inhibits the activation of the ATM/CHK2 signaling pathway.Finally,in a subcutaneous xenograft mouse model,the combination of Adriamycin and Bufotaline treatment significantly suppressed pancreatic cancer cell growth.In conclusion,Bufotaline enhances Adria-mycin-induced chemosensitivity in pancreatic cancer cells;the combination of Adriamycin and Bufotaline downregulates the expression of DNA damage response repair proteins NBS1 and RAD50,and inhibits the ATM/CHK2-mediated DDR signaling pathway,thereby delaying DNA damage repair.

Objective:To explore the high-risk factors affecting the severity of neonatal necrotizing enterocolitis (NEC).Methods:This study involved 153 NEC patients admitted to the Neonatology Department of the Children's Hospital of Soochow University from January 1, 2017, to December 30, 2023. Based on the severity of NEC determined by Bell's criteria, these patients were divided into two groups: mild group (Bell stage Ⅱ, n=70) and severe group (Bell stage Ⅲ, n=83). Clinical data including general conditions, clinical treatment and disease status before the onset of NEC, laboratory test results, and perinatal conditions of the mothers were retrospectively collected. Univariate analysis (rank-sum test and Chi-square test) and multivariate analysis (logistic regression analysis) were used to explore the risk factors affecting the severity of NEC. Results:The proportion of infants with gestational age<37 weeks or birth weight<1 500 g, the rate of antibiotic usage, sepsis or shock were higher in the severe group than in the mild group [91.6% (76/83) vs. 75.7% (53/70); 55.4% (46/83) vs. 34.3% (24/70); 85.5% (71/83) vs. 71.4% (50/70); 55.4% (46/83) vs. 17.1% (12/70); 30.1% (25/83) vs. 8.6% (6/70); with χ 2 values of 7.22, 6.84, 4.57, 23.64, and 10.91, respectively, all P<0.05]. Furthermore, the severe group had a late initiation of breastfeeding and longer durations of peripherally inserted central catheter (PICC) placement and parenteral nutrition [2.00 d (1.00-2.00 d) vs. 1.00 d (1.00-2.00 d); 0.00 d (0.00-18.00 d) vs. 0.00 d (0.00-7.50 d); 14.00 d (5.00-21.00 d) vs. 10.50 d (0.00-18.25 d), with Z values of -2.90, -1.98, and -2.09, respectively, all P<0.05]. (2) Within 48 h before the onset, the severe group had higher proportions of infants with decreased white blood cell count, decreased platelet count, electrolyte imbalance, and metabolic acidosis than the mild group [53.0% (44/83) vs. 14.3% (10/70); 49.4% (41/83) vs. 10.0% (7/70); 38.6% (32/83) vs. 14.3% (10/70); 37.3% (31/83) vs. 14.3% (10/70), with χ2 values of 24.94, 27.38, 11.23, and 10.30, respectively, all P<0.05]. Besides, the levels of procalcitonin and C-reactive protein were higher in the severe group than in the mild group [2.31 ng/ml (0.26-11.71 ng/ml) vs. 0.22 ng/ml (0.00-2.19 ng/ml); 58.50 mg/L (14.34-125.25 mg/L) vs. 8.20 mg/L (0.23-34.56 mg/L), with Z values of -3.88 and -5.02, respectively, both P<0.05]. (3) Multivariate logistic regression analysis showed that prolonged duration of PICC placement, decreased platelet count, electrolyte imbalance, metabolic acidosis, and concurrent sepsis were independent risk factors affecting the severity of NEC [ OR (95% CI) values were 1.104 (1.020-1.196), 5.364 (1.667-17.253), 4.047 (1.171-13.986), 4.333 (1.290-14.556), and 3.290 (1.005-10.774), respectively, with all P<0.05]. Conclusions:Prolonged duration of PICC placement, concurrent sepsis, decreased platelet count, electrolyte imbalance, and metabolic acidosis in NEC patients are more likely to lead to severe cases. In clinical practice, attention should be paid to relevant indicators, and abnormal changes should be identified and intervened in a timely manner to reduce the occurrence of severe NEC.

Pancreatic cancer has emerged as one of the most challenging malignancies worldwide,with its high resistance to chemotherapy being the primary cause of treatment failure.Therefore,enhancing the chemosensitivity of pancreatic cancer has become a major focus of current research.In this study,we in-vestigated how Bufotaline,a bufadienolide extracted from the traditional Chinese medicine toad venom,exhibits its antitumor activity.Specifically,we explored the potential of Bufotaline to enhance the chemo-sensitivity of pancreatic cancer cells to Adriamycin and elucidated its underlying molecular mechanisms.Using CCK-8 and colony formation assays,we demonstrated that Bufotaline enhances the inhibitory effect of Adriamycin on the survival of pancreatic cancer cell lines Patu-8988T,Aspc-1,and Patu-8988S.No-tably,Bufotaline treatment reduced the IC50 of Adriamycin in drug-resistant pancreatic cancer cells to lev-els comparable to those in non-resistant cells.Results from Western blot,immunofluorescence,comet as-say,and TUNEL assays revealed that Bufotaline promotes Adriamycin-induced DNA damage in pancreatic cancer cells.RNA-seq analysis of Patu-8988T cells treated with Adriamycin alone or in combination with Bufotaline showed significant changes in gene expression,and qRT-PCR analysis further confirmed that Bu-fotaline downregulates the expression of DNA damage repair proteins NBS1 and RAD50.Moreover,Western blot analysis revealed that Bufotaline reduces the levels of DNA damage response repair proteins,and Im-munofluorescence experiments indicated that Bufotaline inhibits the activation of the ATM/CHK2 signaling pathway.Finally,in a subcutaneous xenograft mouse model,the combination of Adriamycin and Bufotaline treatment significantly suppressed pancreatic cancer cell growth.In conclusion,Bufotaline enhances Adria-mycin-induced chemosensitivity in pancreatic cancer cells;the combination of Adriamycin and Bufotaline downregulates the expression of DNA damage response repair proteins NBS1 and RAD50,and inhibits the ATM/CHK2-mediated DDR signaling pathway,thereby delaying DNA damage repair.