Objective To investigate the effect of drug-eluting bead DACE(DEB-TACE)combined with systemic treatment for hepatocellular carcinoma(HCC)in different locations.Methods A total of 204 HCC patients who underwent DEB-TACE combined with systemic therapy(targeted and immunotherapy)were retrospectively collected.According to the anatomical location of HCC,86 cases with lesions located at the main trunk of portal vein(PV)or within 1 cm of the first PV branch were classified into central type group,while 118 cases with lesions located at the other areas were classified as peripheral type group.Follow-up was regularly performed after DEB-TACE until August,2024.The objective response rate(ORR)and disease control rate(DCR)at 1,3,6 and 12 months after DEB-TACE,also patients'progression-free survival(PFS)and overall survival(OS)were compared between groups.Results All patients were followed up for a median of 32.6 months,during which 164 cases died.Significant differences of ORR at 1 and 3 months after DEB-TACE(77.91％[67/86]vs.89.83％[106/118],34.88％[30/86]vs.54.24％[64/118])and DCR at 3 and 6 months after DEB-TACE(51.16％[44/86]vs.66.95％[79/118],34.88％[30/86]vs.50.00％[59/118])were found between groups(all P＜0.05).Patients'PFS(30.18[9.12,48.54]months)and OS(37.36[17.79,56.68])in peripheral type group were better than those in central type group(20.11[11.35,28.87]months and 23.24[3.11,43.47]months,x2=3.971,4.162,P=0.048,0.041).Conclusion The effect of DEB-TACE combined with systemic treatment for peripheral type HCC was better than for central type HCC.

AIM:To investigate the role and mechanism of the glucagon-like peptide-1 receptor agonist lira-glutide(Lira)in regulating ferroptosis of mouse insulinoma MIN6 cells induced by high glucose and high fat.METHODS:The mouse insulinoma MIN6 cells were exposed to 30 mmol/L glucose and 500 μmol/L palmitic acid to establish an islet β cell injury model.On this basis,a ferroptosis inducer erastin,a ferroptosis inhibitor ferrostatin-1(Fer-1),and low and high concentrations of Lira were administered.Cell viability of different treatment groups were detected by CCK-8 assay.The malondialdehyde(MDA)kit was used to determine the changes in intracellular MDA content.The reactive oxygen species(ROS)kit was used to detect the changes in the ROS level of cells.The Fe2+fluorescence probe FerroOrange and mitochondrial membrane potential(JC-1)were used to detect the intracellular Fe2+levels and mitochondrial functions in different treatment groups.The mouse insulin ELISA kit was used to detect the insulin secretion of cells.RT-qPCR was used to detect the changes in the expression levels of key ferroptosis genes and insulin secretion genes in different treat-ment groups.Western blot was used to detect the expression levels of key ferroptosis proteins,glutathione peroxidase 4(GPX4)and solute carrier family 7 member 11(SLC7A11)in different treatment groups.RESULTS:Compared with the cells treated with high glucose and high fat,after treatment with Fer-1 and high-dose Lira,the cell viability,insulin secre-tion of the cells,and mitochondrial membrane potential all increased significantly,the levels of ROS,MDA and Fe2+were decreased(P<0.05).The results of RT-qPCR showed that Fer-1 and high-dose Lira significantly upregulated the expres-sion of genes promoting insulin secretion(P<0.05).The results of Western blot showed that Fer-1 and high-dose Lira sig-nificantly upregulated the expression of ferroptosis-inhibiting proteins GPX4 and SLC7A11(P<0.05).CONCLUSION:Liraglutide inhibits ferroptosis of mouse insulinoma MIN6 cells by regulating the SLC7A11/GPX4 signaling pathway,there-by improving the damage and dysfunction of MIN6 cells induced by high glucose and high fat.

Objective To observe the effect of specialist team-led walking-cognition dual-task train-ing combined with active self-disclosure on control and balance abilities in elderly patients with acute ischemic stroke(AIS).Methods A total of 90 elderly AIS patients treated in our hospital from January 2022 to January 2024 were enrolled and randomly assigned into the control group and the observation group,with 45 cases in each group.The control group received routine walk-ing training,while the observation group received specialist team-led walking-cognition dual-task training combined with active self-disclosure intervention.Control ability,balance ability,walking ability,cognitive function and psychological status were compared between the two groups.Results After intervention,the scores of Sheikh Trunk Control Scale and Fugl-Meyer Assessment(FMA),and the static balance score,dynamic balance score and total score of Berg Balance Scale(BBS)were significantly increased in both the observation and the control groups(P＜0.05),and all above scores were obviously higher in the former group than the latter one(P＜0.01).The two groups also obtained notably shorter single-and dual-task walking time after intervention,but there were no statistical difference in the single-task walking time in both groups before and after intervention(P＞0.05).After intervention,the observation group had significantly shorter dual-task walking time(22.87±7.36 s vs 27.52±8.71 s,P=0.008)and lower walking time cost of dual task[(11.16±4.07)％vs(25.61±7.82)％,P=0.000]when compared with the control group.After intervention,the scores of Mini-Mental Status Examination were increased,and the scores of Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale were decreased in the two groups(P＜0.05).Conclusion Specialist team-led walking-cognition dual-task training com-bined with active self-disclosure intervention can effectively improve trunk control ability,balance ability,walking ability,cognitive function and psychological state in elderly AIS patients,has cer-tian clinical application value.

Objective:To investigate the potential of praeruptorin A (PA) in alleviating inflammatory damage in sepsis through the inhibition of ferritin expression.Methods:C57BL/6 mice were intraperitoneally injected with lipopolysaccharide (LPS) to establish the model of sepsis. After 6 and 12 h of PA intervention, serum levels of inflammatory cytokines IL-6 and TNF-α were measured by ELISA. Kidney tissues were collected at 72 h for HE staining to assess inflammatory cell infiltration and tissue damage. Human neutrophils were divided into four groups: control, LPS, ferritin, and LPS+ ferritin groups. After 12 h of intervention, qRT-PCR was used to detect the expression of IL-6 and TNF-α mRNA. In order to observe the effect of PA on the expression of inflammatory cytokines and ferritin, human neutrophils were grouped into control, LPS, and LPS+ PA (2/3/4 μmol/L) groups. After 12 h of intervention, qRT-PCR was performed to measure the expression of IL-1β, IL-6, TNF-α, and ferritin mRNA; ELISA was used to quantify the levels of IL-1β, IL-6, and TNF-α in culture supernatants; Western blot was used to analyze the expression of ferritin. Molecular docking was conducted to verify interactions between PA and ferritin.Results:Significant inflammatory cell recruitment, tissue damage, and elevated serum levels of IL-6 and TNF-α ( P<0.01) were observed in mice with LPS-induced sepsis. PA significantly inhibited cytokine secretion ( P<0.01) and alleviated tissue injury in sepsis mice. In human neutrophil models, ferritin upregulated the expression of IL-6 and TNF-α mRNA ( P<0.01); LPS stimulation alone increased the expression of IL-1β, IL-6, TNF-α, and ferritin at both mRNA and protein levels ( P<0.01), while co-stimulation with PA (3/4 μmol/L) significantly reversed the aforementioned results ( P<0.01). Molecular docking confirmed there were interaction sites between PA and ferritin. Conclusion:PA inhibits the release of inflammatory cytokines and alleviates tissue damage in sepsis, and the potential mechanism may involve modulating ferritin expression to suppress inflammatory responses.

Objective: To investigate the role of STAT3 phosphorylation in ferroptosis regulation and its impact on cisplatin resistance mechanisms in human osteosarcoma cells． Methods: Human osteosarcoma HOS cells and cispl- atin-resistant HOS / DDP cells were treated with cisplatin ( 0. 5，1，2，4，8，16，32 mg / L) ，the ferroptosis inducer Erastin ( Era) ( 2 μmol / L) ，and / or the ferroptosis inhibitor Ferrostatin-1 ( Fer1) ( 10 μmol / L) ．Cell viability and proliferation were assessed using the Cell Counting Kit-8 ( CCK-8) and colony formation assays，and cell migration was evaluated via a scratch assay．Reactive oxygen species ( ROS) ，intracellular ferrous iron levels，mitochondrial membrane potential，mitochondrial function，malondialdehyde ( MDA) levels，and the reduced glutathione / oxi- dized glutathione ( GSH / GSSG) ratio were measured using commercial kits．The mRNA expression of ferroptosis- related genes was analyzed by quantitative reverse transcription polymerase chain reaction ( RT-qPCR) ．The protein levels of glutathione peroxidase 4 ( GPX4) ，solute carrier family 7 member 11 ( SLC7A11) ，phosphorylated STAT3 ( p-STAT3) ，and total STAT3 were determined by Western blot． Results: With cisplatin treatment，HOS cells ex- hibited decreased cell viability，mitochondrial membrane potential，and GSH / GSSG ratio ( P＜0. 01) ，along with elevated levels of ROS，ferrous ion，and MDA content ( P ＜0. 01) ． The protein levels of GPX4 ( P ＜0. 01) ， SLC7A11，and p-STAT3 also decreased ( P ＜0. 05) ．Coadministration with the ferroptosis inhibitor Ferrostatin-1 ( Fer-1) reversed these aforementioned effects ( P ＜0. 05) ．In HOS / DDP cells，the mRNA levels of ferroptosis- suppressive genes ( GPX4，FTH1，SLC7A11，and AIFM2) were significantly higher than those in HOS cells ( P < 0. 05) ，whereas the expression of ferroptosis-promoting genes ( ACSL4 and PTGS2) was significantly lower ( P < 0. 05) ．The cisplatin-induced reductions in cell viability and mitochondrial membrane potential，as well as the in- creases in ROS，ferrous ion，and MDA levels，were less pronounced in HOS / DDP cells than in HOS cells．The SLC7A11 protein level showed no significant change． However，combined treatment with the ferroptosis inducer Erastin ( Era) resulted in significant decreases in viability，mitochondrial membrane potential，and the GSH / GSSG ratio in HOS / DDP cells ( P＜0. 05) ．Furthermore，the protein levels of p-STAT3，GPX4，and SLC7A11 were also markedly reduced ( P＜0. 05) ． Conclusion The activation of ferroptosis mediated by p-STAT3 enhances cisplatin sensitivity in HOS / DDP cells．

AIM:To investigate the role and mechanism of the glucagon-like peptide-1 receptor agonist lira-glutide(Lira)in regulating ferroptosis of mouse insulinoma MIN6 cells induced by high glucose and high fat.METHODS:The mouse insulinoma MIN6 cells were exposed to 30 mmol/L glucose and 500 μmol/L palmitic acid to establish an islet β cell injury model.On this basis,a ferroptosis inducer erastin,a ferroptosis inhibitor ferrostatin-1(Fer-1),and low and high concentrations of Lira were administered.Cell viability of different treatment groups were detected by CCK-8 assay.The malondialdehyde(MDA)kit was used to determine the changes in intracellular MDA content.The reactive oxygen species(ROS)kit was used to detect the changes in the ROS level of cells.The Fe2+fluorescence probe FerroOrange and mitochondrial membrane potential(JC-1)were used to detect the intracellular Fe2+levels and mitochondrial functions in different treatment groups.The mouse insulin ELISA kit was used to detect the insulin secretion of cells.RT-qPCR was used to detect the changes in the expression levels of key ferroptosis genes and insulin secretion genes in different treat-ment groups.Western blot was used to detect the expression levels of key ferroptosis proteins,glutathione peroxidase 4(GPX4)and solute carrier family 7 member 11(SLC7A11)in different treatment groups.RESULTS:Compared with the cells treated with high glucose and high fat,after treatment with Fer-1 and high-dose Lira,the cell viability,insulin secre-tion of the cells,and mitochondrial membrane potential all increased significantly,the levels of ROS,MDA and Fe2+were decreased(P<0.05).The results of RT-qPCR showed that Fer-1 and high-dose Lira significantly upregulated the expres-sion of genes promoting insulin secretion(P<0.05).The results of Western blot showed that Fer-1 and high-dose Lira sig-nificantly upregulated the expression of ferroptosis-inhibiting proteins GPX4 and SLC7A11(P<0.05).CONCLUSION:Liraglutide inhibits ferroptosis of mouse insulinoma MIN6 cells by regulating the SLC7A11/GPX4 signaling pathway,there-by improving the damage and dysfunction of MIN6 cells induced by high glucose and high fat.

Objective To investigate the effect of drug-eluting bead DACE(DEB-TACE)combined with systemic treatment for hepatocellular carcinoma(HCC)in different locations.Methods A total of 204 HCC patients who underwent DEB-TACE combined with systemic therapy(targeted and immunotherapy)were retrospectively collected.According to the anatomical location of HCC,86 cases with lesions located at the main trunk of portal vein(PV)or within 1 cm of the first PV branch were classified into central type group,while 118 cases with lesions located at the other areas were classified as peripheral type group.Follow-up was regularly performed after DEB-TACE until August,2024.The objective response rate(ORR)and disease control rate(DCR)at 1,3,6 and 12 months after DEB-TACE,also patients'progression-free survival(PFS)and overall survival(OS)were compared between groups.Results All patients were followed up for a median of 32.6 months,during which 164 cases died.Significant differences of ORR at 1 and 3 months after DEB-TACE(77.91％[67/86]vs.89.83％[106/118],34.88％[30/86]vs.54.24％[64/118])and DCR at 3 and 6 months after DEB-TACE(51.16％[44/86]vs.66.95％[79/118],34.88％[30/86]vs.50.00％[59/118])were found between groups(all P＜0.05).Patients'PFS(30.18[9.12,48.54]months)and OS(37.36[17.79,56.68])in peripheral type group were better than those in central type group(20.11[11.35,28.87]months and 23.24[3.11,43.47]months,x2=3.971,4.162,P=0.048,0.041).Conclusion The effect of DEB-TACE combined with systemic treatment for peripheral type HCC was better than for central type HCC.

Objective To observe the effect of specialist team-led walking-cognition dual-task train-ing combined with active self-disclosure on control and balance abilities in elderly patients with acute ischemic stroke(AIS).Methods A total of 90 elderly AIS patients treated in our hospital from January 2022 to January 2024 were enrolled and randomly assigned into the control group and the observation group,with 45 cases in each group.The control group received routine walk-ing training,while the observation group received specialist team-led walking-cognition dual-task training combined with active self-disclosure intervention.Control ability,balance ability,walking ability,cognitive function and psychological status were compared between the two groups.Results After intervention,the scores of Sheikh Trunk Control Scale and Fugl-Meyer Assessment(FMA),and the static balance score,dynamic balance score and total score of Berg Balance Scale(BBS)were significantly increased in both the observation and the control groups(P＜0.05),and all above scores were obviously higher in the former group than the latter one(P＜0.01).The two groups also obtained notably shorter single-and dual-task walking time after intervention,but there were no statistical difference in the single-task walking time in both groups before and after intervention(P＞0.05).After intervention,the observation group had significantly shorter dual-task walking time(22.87±7.36 s vs 27.52±8.71 s,P=0.008)and lower walking time cost of dual task[(11.16±4.07)％vs(25.61±7.82)％,P=0.000]when compared with the control group.After intervention,the scores of Mini-Mental Status Examination were increased,and the scores of Hamilton Depression Rating Scale and Hamilton Anxiety Rating Scale were decreased in the two groups(P＜0.05).Conclusion Specialist team-led walking-cognition dual-task training com-bined with active self-disclosure intervention can effectively improve trunk control ability,balance ability,walking ability,cognitive function and psychological state in elderly AIS patients,has cer-tian clinical application value.

Objective:To investigate the potential of praeruptorin A (PA) in alleviating inflammatory damage in sepsis through the inhibition of ferritin expression.Methods:C57BL/6 mice were intraperitoneally injected with lipopolysaccharide (LPS) to establish the model of sepsis. After 6 and 12 h of PA intervention, serum levels of inflammatory cytokines IL-6 and TNF-α were measured by ELISA. Kidney tissues were collected at 72 h for HE staining to assess inflammatory cell infiltration and tissue damage. Human neutrophils were divided into four groups: control, LPS, ferritin, and LPS+ ferritin groups. After 12 h of intervention, qRT-PCR was used to detect the expression of IL-6 and TNF-α mRNA. In order to observe the effect of PA on the expression of inflammatory cytokines and ferritin, human neutrophils were grouped into control, LPS, and LPS+ PA (2/3/4 μmol/L) groups. After 12 h of intervention, qRT-PCR was performed to measure the expression of IL-1β, IL-6, TNF-α, and ferritin mRNA; ELISA was used to quantify the levels of IL-1β, IL-6, and TNF-α in culture supernatants; Western blot was used to analyze the expression of ferritin. Molecular docking was conducted to verify interactions between PA and ferritin.Results:Significant inflammatory cell recruitment, tissue damage, and elevated serum levels of IL-6 and TNF-α ( P<0.01) were observed in mice with LPS-induced sepsis. PA significantly inhibited cytokine secretion ( P<0.01) and alleviated tissue injury in sepsis mice. In human neutrophil models, ferritin upregulated the expression of IL-6 and TNF-α mRNA ( P<0.01); LPS stimulation alone increased the expression of IL-1β, IL-6, TNF-α, and ferritin at both mRNA and protein levels ( P<0.01), while co-stimulation with PA (3/4 μmol/L) significantly reversed the aforementioned results ( P<0.01). Molecular docking confirmed there were interaction sites between PA and ferritin. Conclusion:PA inhibits the release of inflammatory cytokines and alleviates tissue damage in sepsis, and the potential mechanism may involve modulating ferritin expression to suppress inflammatory responses.

Objective:To investigate the value of CT quantitative parameters of tumor and spleen in predicting the clinical stage of gastric cancer (Ⅰ/Ⅱ stage and Ⅲ/Ⅳ stage).Methods:This study was a case-control study. The data of 145 patients with gastric cancer confirmed by pathology in the First Affiliated Hospital of Zhengzhou University from February 2019 to June 2021 were retrospectively collected, including 70 cases of Ⅰ/Ⅱ stage and 75 cases of Ⅲ/Ⅳ stage. On the baseline CT images, the tumor related parameters, including tumor thickness, length of tumor, CT attenuation of tumor unenhanced phase, CT attenuation of tumor arterial phase, CT attenuation of tumor venous phase were measured. The spleen related parameters, including splenic thickness, CT attenuation of splenic unenhanced phase, CT attenuation of splenic arterial phase, CT attenuation of splenic venous phase, and standard deviation of CT attenuation (CTsd) in splenic unenhanced phase were also measured. The independent sample t test or Mann-Whitney U test was used to compare the parameters between the Ⅰ/Ⅱ stage and Ⅲ/Ⅳ stage patients. The multi-factor logistic regression analysis was used to find the independent predictors of gastric cancer clinical stage, and establish the combined parameters. The efficiency to the diagnosis of gastric cancer stage of single and combined parameters was evaluated using the operating characteristic curve, and the DeLong test was used to compare the differences of area under the curve (AUC). Results:There were significant differences in tumor thickness, length of tumor, CT attenuation of tumor venous phase, CT attenuation of splenic unenhanced phase, CT attenuation of splenic venous phase, CTsd in splenic unenhanced phase between the Ⅰ/Ⅱ stage and Ⅲ/Ⅳ stage of gastric cancer ( P<0.05). Multivariate analysis showed that tumor thickness ( OR=1.073, 95% CI 1.026-1.123, P=0.002), CT attenuation of splenic venous phase ( OR=1.040, 95% CI 1.011-1.070, P=0.006) and CTsd in splenic unenhanced phase ( OR=1.625, 95% CI 1.330-1.987, P<0.001) were independent risk factors for the clinical stage of gastric cancer and the combined parameters were established. The AUC values of tumor thickness, CT attenuation of splenic venous phase, CTsd in splenic unenhanced phase and combined parameters were 0.655, 0.614, 0.749 and 0.806, respectively. The AUC of combined parameters was higher than those of tumor thickness and CT attenuation of splenic venous phase, and the differences were statistically significant ( Z=3.37, 3.82, both P<0.001). Conclusion:Tumor thickness, CT attenuation of splenic venous phase and CTsd in splenic unenhanced phase are independent risk factors for the clinical stage of gastric cancer, and combined parameters can improve the diagnostic efficiency.