Objective To investigate the mechanism of esketamine(ESK)in modulating the glutaminolysis in endometrial cancer(EC)via the lactate dehydrogenase A(LDHA)-hypoxia-inducible factor 1A(HIF1A)axis.Methods Human EC cell line KLE was treated with 0-10 μmol/L ESK.5 μmol/L was selected as the working concentration.The LDHA overexpression/knockdown and HIF1A overexpression models were constructed,and cell proliferation,invasion,apoptosis,glutamine uptake,adenosine triphosphate level and glutaminase(GLS)expression were measured.A C57BL/6 xenograft model was established to assess tumor growth inhibition by ESK,levels of LDHA,HIF1A and GLS in tumors were measured.Results ESK significantly inhibited KLE cell proliferation and invasion and promoted the apoptosis(P<0.05).Overexpression of LDHA reversed these effects and enhanced glutaminolysis,whereas ESK abrogated the effect of LDHA overexpression.LDHA knockdown reduced metabolic activity and malignant phenotypes,and HIF1A overexpression partially rescued these results.Xenograft experienment showed that ESK suppressed tumor growth and levels of LDHA,HIF1A and GLS in tumor tissues(P<0.05).Conclusion ESK blocks the LDHA-HIF1A pathway,inhibits glutaminolysis,proliferation and invasion,and promotes apoptosis in EC.

Objective To explore the effect of long non coding RNA small nucleolar RNA host gene 14(lncRNA SNHG14)on interleukin(IL)-1β-induced chondrocyte injury by targeting the microRNA-181a-5p(miR-181a-5p)/peroxiredoxin3 (PRDX3) axis.Methods The targeting relationships among lncRNA SNHG14,miR-181a-5p,and PRDX3 were detected using dual-luciferase reporter assay.Human chondrocytes C28/I2 were used to set up the following 10 groups:NC group,IL-1β group,sh-NC group,sh-SNHG14 group,sh-SNHG14+anti-NC group,sh-SNHG14+anti-miR-181a-5p group,miR-NC group,miR-181a-5p mimic group,miR-181a-5p mimic+pcDNA-NC group,miR-181a-5p mimic+pcDNA-PRDX3 group.Cell proliferation and apoptosis were assessed using colony formation assay and flow cytometry,respectively.The levels of IL-6,tumor necrosis factor-alpha(TNF-α),and monocyte chemoattractant protein 1(MCP-1)were measured by enzyme-linked immunosorbent assay.Nitric oxide(NO)level was detected using Griess reagent.Western blotting was performed to determine the expression levels of PRDX3,proliferating cell nuclear antigen(PCNA),Cyclin D1,B-cell lymphoma 2(Bcl-2),and Bcl-2-associated X protein(Bax).Results Dual luciferase assay indicated the targeting relationships between miR-181a-5p and both lncRNA SNHG14 and PRDX3(P<0.05).Compared with the NC group,the IL-1β group showed significantly increased apoptosis rate,IL-6,TNF-α,MCP-1,and NO levels,as well as elevated expression levels of lncRNA SNHG14,PRDX3,and Bax protein,and decreased miR-181a-5p expression,colony formation number,and protein levels of PCNA,Cyclin D1,and Bcl-2(P<0.05).Compared with the sh-NC group or miR-NC group,the sh-SNHG14 group or miR-181a-5p mimic group exhibited significantly higher miR-181a-5p expression level,colony formation number,and protein expression level of PCNA,Cyclin D1,and Bcl-2,along with notably reduced apoptosis rate,IL-6,TNF-α,MCP-1,and NO levels,as well as decreased expression levels of lncRNA SNHG14,PRDX3,and Bax protein(P<0.05).In contrast to the sh-SNHG14+anti-NC group,the sh-SNHG14+anti-miR-181a-5p group demonstrated opposite trends in all above detected indicators(P<0.05).Similarly,all trends of the above index in the miR-181a-5p mimic+pcDNA-PRDX3 group were reversed compared with those in the miR-181a-5p mimic+pcDNA-NC group(P<0.05).Conclusion LncRNA SNHG14 alleviates IL-1β-induced chondrocyte injury by targeting the miR-181a-5p/PRDX3 axis.

Objective To explore the effect of sodium aescinate on intestinal mucosal barrier in rats with ulcerative colitis(UC).Methods A total of 65 SD rats were divided into 6 groups:sham operation group,model group,low-dose,medium-dose and high-dose sodium aescinate groups(2.5,5,10 mg/kg),and positive control group(mesalazine,360 mg/kg),10 rats in each group.UC rat models were induced by DSS.Disease activity index(DAI)scores were recorded after drug intervention.The levels of serum D-lactic acid(D-LA),diamine oxidase(DAO),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and IL-6 were detected.The ulcer area,length and weight of colon,expression levels of myeloperoxidase(MPO),Occludin,zonula occludens-1(ZO-1),nuclear factor-erythroid 2-related factor 2(Nrf-2),antioxidant response element(ARE)and heme oxygenase-1(HO-1)proteins in colon tissues were compared among different groups.HE staining was performed and pathological scores were recorded.Results Medium-dose and high-dose sodium aescinate significantly reduced DAI score and pathological score,alleviated colonic ulcers,reduced colon weight and increased colon length(P<0.05).The levels of serum D-LA,DAO,TNF-α,IL-1β,IL-6,and colonic MPO were significantly reduced,and the expression of Occludin,ZO-1,p-Nrf2/Nrf2,ARE and HO-1 proteins in colonic tissues was upregulated in the medium- and high-dose sodium aescinate groups(P<0.05).Conclusion Sodium aescinate can ameliorate intestinal mucosal barrier dysfunction in DSS-induced UC rats,and the mechanisms may be related to the inflammation and Nrf-2/ARE/HO-1 signaling pathway.

Objective To investigate the effect of stachydrine hydrochloride(Sta)on myocardial hypertrophy and the underlying mechanism.Methods C57BL/6 J mice were subjected to subcutaneous implantation of an osmotic pump for continuous administration of phenylephrine(PE)over 14 days and were orally treated with Sta.The small animal ultrasound imaging system was used to detect the cardiac function and structural parameters.HE staining and WGA staining were used to observe the morphological changes of heart and myocardial cells.The mRNA expression of cardiac hypertrophy biomarkers(ANP and BNP)was detected by RT-PCR.Cardiomyocytes were stimulated by PE to mimic hypertrophy,and the cells in the Sta group were treated with 5×10^-5 mol/L Sta for 48 h.Cytoskeleton was labeled with fluorescent dyes to measure cell surface,and the expression of fetal genes was detected by RT-PCR.Moreover,the activity of CaN was tested by ELISA.Calcium transient was detected by ion imaging system.The nuclear translocation of NFATc3 was detected by immunofluorescence.Dual-luciferase reporter assay was conducted to detect the GATA4 transcriptional activity.Results Compared with the sham group,the PE group exhibited an increase in ventricular wall thickness(values of IVSd,LVPWd,and LVPWs were elevated),a significant rise in the cardiac index,and a marked enlargement in the cross-sectional area of cardiomyocytes,accompanied by an upsurge in the mRNA expression levels of hypertrophy-related genes.Sta intervention notably attenuated the increase in these parameters induced by PE stimulation.Cellular experienments showed that cardiomyocytes stimulated with PE demonstrated increases in the cell surface and the expression levels of hypertrophy-related genes,and the increase of calcium transients caused the calcium dysregulation,resulting in an excessive activation of CaN enzyme activity,which in turn promoted the translocation of NFATc3 from the cytoplasm to the nucleus.PE stimulation also significantly enhanced the transcriptional activity of GATA4 in H9c2 cells.Sta intervention significantly inhibited the alterations induced by PE in cardiomyocytes.Conclusion Sta can effectively ameliorate PE-induced myocardial hypertrophy through modulation of the Ca²⁺/CaN/NFATc3/GATA4 signaling pathway.

Objective To investigate the effect of Qihong capsules on mitochondrial oxidative stress in mice with coronary microvascular disease(CMVD)via the TLR4/NF-κB/GPX4 pathway.Methods Twenty CMVD model mice were randomly assigned to 2 groups:model group and Qihong capsules treatment group[0.648 g/(kg·d),intragastric administration for 4 weeks],and additional 10 mice were served as the control group.Hematoxylin-eosin(HE)staining,oil red O staining,and immunohistochemistry were employed to assess coronary pathology and macrophage infiltration.Western blotting and enzyme-linked immunosorbent assay(ELISA)were utilized to detect the expression of relevant proteins and levels of reactive oxygen species(ROS).Results Compared with the control group,the model group exhibited severe coronary artery injury,elevated expression of inflammatory cytokines(TNF-α,IL-1β,IL-6),enhanced activation of the TLR4/NF-κB pathway,downregulated expression of GPX4,Sirt1,and HO-1,and increased ROS levels(all P<0.001).Following intervention with Qihong capsules,the aforementioned pathological changes were significantly ameliorated,inflammation and oxidative stress were suppressed,and the expression of protective proteins was upregulated(all P<0.001).Conclusion Qihong capsules can alleviate oxidative stress by inhibiting the TLR4/NF-κB inflammatory pathway and upregulating the expression of GPX4/Sirt1/HO-1,thereby improving microvascular dysfunction in CMVD mice.Its mechanism may be associated with the inhibition of ferroptosis,reflecting its potential for multi-target intervention.

Objective To evaluate the effect of Qidi Xiaoke capsule combined with dapagliflozin on renal function and pyroptosis factors levels in patients with diabetic nephropathy(DN). Methods A total of 121 DN patients were divided into study group(n=60)and control group(n=61). The control group was given dapagliflozin, and study group received Qidi Xiaoke capsule combined with dapagliflozin. The traditional Chinese medicine(TCM)syndrome score, fasting blood glucose(FPG), 2-h postprandial blood glucose(2hPG), glycated hemoglobin(HbA1c), urea nitrogen(BUN), blood creatinine(Scr), 24-h urinary protein(24 h UP), NOD-like receptor thermal protein domain associated protein 3(NLRP3), cysteine aspartate-specific proteinase-1(Caspase-1), interleukin-18(IL-18), interleukin-1β(IL-1β), clinical efficacy and adverse reactions were compared between the two groups. Results After treatment, the TCM syndrome score of study group was lower than that of control group(P<0. 05). The HbA1c, 2hPG and FBG of study group were lower than those of control group(P<0. 05). The eGFR of study group was higher than that of control group, BUN, Scr and 24 h UP were lower than in the control group(P<0. 05). The NLRP3, Caspase-1, IL-18 and IL-1β of study group were lower than control group(P<0. 05). The clinical efficacy of study group was better than that of control group(P<0. 05). There was no significance in adverse reactions between the two groups(P＞0. 05). Conclusion Qidi Xiaoke capsule combined with Dapagliflozin in the treatment of DN is safe and effective, and can improve clinical symptoms, blood glucose level and renal function, the mechanism may be related to regulation of pyroptosis factors.

Objective To explore the effect of Platycodon grandiflorum polysaccharides on oxidative stress,and expression of Toll-like receptor(TLR)/nuclear transcription factor kappa B(NF-κB)and Janus kinase 2(JAK2)/signal transduction and activator of transcription 3(STAT3)signaling pathways-related factors in rats with ulcerative colitis(UC).Methods The UC rat model was constructed by dextran sulfate sodium(DSS),then UC rats were treated with different doses of Platycodon grandiflorum polysaccharides for 2 weeks.The disease activity index,pathological changes of colon,apoptosis,levels of inflammatory and oxidative stress factors,and expression levels of TLR4/NF-κB and JAK2/STAT3 related mRNA and proteins were observed.Results After treatment with Platycodon grandiflorum polysaccharides,the disease activity index,apoptosis rate of colon tissues,levels of IL-6,TNF-α,IL-17 and MDA were decreased,levels of IL-10,SOD and GSH-px were increased,expression levels of TLR4,NF-κB,JAK2,STAT3,and p-JAK2 and p-STAT3 in colon tissues were decreased,with a dose dependent manner(P<0.05).Conclusion Platycodon grandiflorum polysaccharides can alleviate colon injury and oxidative stress in colon tissues in UC rats,and inhibit the activation of TLR/NF-κB and JAK2/STAT3 pathways.

Objective To investigate the effect of matrix metalloproteinase 2(MMP2)on the sensitivity of poly-ADP ribose polymerase inhibitor(PARPi)in high-grade serous ovarian cancer(HGSOC)cells and the underlying mechanism.Methods The HGSOC cell line HeyA8 cells were divided into 3 groups:control group,sh-NC group,sh-MMP2 group.RT-qPCR and Western blotting were used to detect the expression of MMP2.CCK-8 method was used to detect the cell survival rate under different concentrations of Olaparib.Then HeyA8 cells were divided into 4 groups:sh-NC group,sh-MMP2 group,sh-NC+PARPi group,sh-MMP2+PARPi group.Wound-healing assay,Annexin V-FITC/PI method and Hochest 33258 staining were used to detect cell migration and apoptosis,respectively.Western blotting was used to determine the expression levels of proteins related to the vascular endothelial growth factor(VEGF)/phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt).Results Compared with those in the control group and the sh-NC group,the relative expression levels of MMP2 mRNA and protein of HeyA8 cells in the sh-MMP2 group were downregulated,and the cell survival rate after Olaparib treatment was reduced(P<0.05).Compared with those in the sh-NC group,the wound-healing rate of HeyA8 cells in the sh-MMP2 group was decreased,the apoptosis rate was increased,nuclear condensation and fragmentation of apoptotic cells were observed,the relative protein expression levels of vascular endothelial growth factor A(VEGFA),vascular endothelial growth factor receptor 2(VEGFR-2),phosphorylated PI3K(Tyr458)[p-PI3K(Tyr458)]and phosphorylated Akt(Ser473)[p-Akt(Ser473)]were all downregulated(P<0.05).Compared with those in the sh-NC+PARPi group,the wound-healing rate of HeyA8 cells in the sh-MMP2+PARPi group was decreased,the apoptosis rate was increased,more apoptotic cells with nuclear condensation and fragmentation were observed,the relative protein expression levels of VEGFA,VEGFR2,p-PI3K(Tyr458)and p-Akt(Ser473)were downregulated(P<0.05).Conclusion Silencing MMP2 expression can promote PARPi-induced apoptosis in HGSOC cells,and increase PARPi sensitivity.

Objective To investigate the effect of high-dose red meat diet(H-red)on ulcerative colitis(UC)in mice and the potential mechanism of M1 macrophage polarization promoted by sirtuin 1(Sirt1)/nuclear factor-κB(NF-κB)pathway.Methods Mouse UC model was established with dextran sulfate sodium(DSS)and fed on H-red.Mice were divided into 5 groups:Normal group,UC group,H-red+UC group,resveratrol(RES)treatment group(RES+H-red+UC group),and RES combined with NF-κB inhibitor(quininib,QNZ)treatment group(QNZ+RES+H-red+UC group),10 mice in each group.Body weight,colon length,disease activity index(DAI),myeloperoxidase(MPO)activity were detected.The expression levels of Sirt1/NF-κB signaling pathway proteins and the acetylated NF-κB-p65 in colon tissues were detected by Western blotting.The number of M1 macrophages(F4/80⁺iNOS⁺)was detected by immunofluorescence chemistry,and the mRNA expression levels of inflammatory factors such as IL-6 and TNF-α were detected by qPCR.Results Compared with the UC group,the H-red+UC group had more weight loss,shorter colon length,and further aggravated abnormalities in DAI,pathological changes and MPO activity(all P<0.05),In addition,the Sirt1 expression was inhibited,while acetylated NF-κB-p65 expression,M1 macrophage count and mRNA expression of IL-6,TNF-α,IL-1β,MCP-1,CXCL10 and COX-2 were increased in the H-red+UC group(all P<0.05).Compared with the H-red+UC group,the RES+H-red+UC group showed significant improvement in inflammatory injury,upregulated Sirt1 expression,and significant improvement in the above abnormal indicators(all P<0.05),the QNZ+RES+H-red+UC group had an even better therapeutic effect than the RES+H-red+UC group.Conclusion High red meat diet promotes M1 macrophage polarization and aggravates UC in mice through the Sirt1/NF-κB signaling pathway.

Objective To investigate the effect of microRNA(miRNA)-181 a-3 p on the malignant progression of acute lymphoblastic leukemia(ALL)cells by targeting suppressor of cytokine signaling 5(SOCS5).Methods The expression levels of miR-181a-3p and SOCS5 in ALL cells were detected by RT-qPCR and Western blotting.MoIt4 cells were divided into 6 groups:anti-miR-NC group,anti-miR-181a-3p group,pcDNA group,PCDNA-SOCS5 group,anti-miR-181a-3p+si-NC group and anti-miR-181a-3p+si-SOCS5 group.RT-qPCR was used to detect the expression levels of miR-181a-3p and SOCS5.CCK8 and Transwell assay were used to detect cell proliferation,migration and invasion.Western blotting was used to detect the expression of SOCS5,CDK2,N-cadherin,E-cadherin and Vimentin.Dual luciferase gene reporter assay was used to detect the targeting relationship between miR-181a-3p and SOCS5.Results Compared with that in the PBMCS cells,the expression level of miR-181a-3p in the MoIt4 and Jurkat cells was increased(P<0.05),while the expression levels of SOCS5 mRNA and protein were decreased(P<0.05).Inhibition of miR-181a-3p or overexpression of SOCS5 decreased the proliferative activity,migration and invasion of MoIt4 cells,and the expression levels of N-cadherin,CDK2 and Vimentin,and increased the expression level of E-cadherin(P<0.05).miR-181a-3p negatively targeted SOCS5,inhibition of SOCS5 reversed the effect of miR-181a-3p on the proliferation,migration,invasion and epithelial-to-mesenchymal transition(EMT)in MoIt4 cells.Conclusion miR-181a-3p targets SOCS5 and negatively regulates the proliferation,migration,invasion and EMT of ALL cells.

Objective To explore the effect of miR-330-3p on proliferation,migration,and invasion of endometrial cancer by targeting LIM homeobox 6(LHX6).Methods The clinical significance of miR-330-3p and LHX6 in endometrial cancer was analyzed by TCGA database.The binding site between miR-330-3p and LHX6 was predicted by Starbase and was then validated.HEC108 and Ishikawa cell lines with miR-330-3p overexpression or miR-330-3p/LHX6 overexpression were constructed to observe cells proliferation,migration and invasion.The xenograft nude mice model with miR-330-3p overexpressed HEC108 cells were constructed to observe the growth of transplanted tumors.Results The expression level of miR-330-3p was increased,while the expression level of LHX6 was decreased in endometrial cancer tissues,and miR-330-3p could inhibit the expression of LHX6.Overexpression of miR-330-3p could promote the proliferation,migration and invasion of HEC108 and Ishikawa cells and the growth of transplanted tumors.Overexpression of LHX6 could partially reverse the effect of miR-330-3p overexpression in cells.Conclusion miR-330-3p can promote proliferation,migration and invasion of endometrial cancer by inhibiting the expression of LHX6.

Objective To construct a prognostic model for iron death related genes in lung adenocarcinoma(LUAD)and lung squamous cell carcinoma(LUSC),compare the differences in molecular pathways,immunity and epigenetic characteristics between the two,and explore the mechanisms of immune checkpoints and m6A factors regulating iron death.Methods Based on the TCGA data and the FerrDb gene set,the models were constructed after differential expression analysis,COX regression,and LASSO regression.The model performance was evaluated using the Kaplan-Meier method and ROC curves.The differentially expressed genes(P<0.001)were analyzed by GSEA and literature screening,and the hypotheses were proposed.Results The LUAD prognostic model(CYBB,GLS2,CAV1,DDIT4,SLC7A5,TRIB3,IL33,RRM2)had the AUC of 0.720,0.690,and 0.640 for 1,3,and 5 years respectively(P<0.001),while the LUSC prognostic model(ALOX5,MIOX,JUN,SLC7A5,ARRDC3)had the AUC of 0.608,0.637,and 0.652 respectively(P=0.003),which was superior to existing models.The risk score was an independent prognostic factor(P<0.05).LUAD enriched in the pathways of proteasome and TCA cycle,while LUSC enriched in pathways of leukocyte migration and focal adhesion(P<0.05).In addition,LUAD showed low expression of TNFSF18 and METTL3,while LUSC showed high expression of NRP1 and FTO(P<0.001).Therefore,the mechanism hypothesis was proposed:In LUSC,CD28 affected iron death sensitivity,and FTO/YTHDF2 drived resistance;in LUAD,TNFSF18 weakened the inhibition of GPX4,and there was a bidirectional regulatory network.Conclusion By construction of the highly efficient prognostic models and analysis of the essential differences between the two subtypes from multiple dimensions,the key targets and theoretical frameworks for the study of the synergistic mechanism of iron death is therefore provided for the subsequent experimental verification.

Objective To analyze the relationship between levels of glycogen synthase kinase-3(GSK-3),intercellular adhesion molecule-1(ICAM-1),and the progression of acute ST segment elevation myocardial infarction(STEMI),as well as their predictive value for major adverse cardiovascular events(MACE)after emergency percutaneous coronary intervention(PCI).Methods A total of 102 STEMI patients who underwent emergency PCI at Liangjiang New District People’s Hospital in Chongqing from April 2022 to March 2023 were selected as the study subjects,with 40 patients in the severe group and 62 patients in the moderate to mild group.After 2-year follow-up,the patients were divided into two groups according to the occurrence of MACE:MACE group(n=32)and non-MACE group(n=70).The biochemical indicators,cardiac function,and the incidence of MACE in STEMI patients with different conditions were compared and the correlation between patient’s condition,cardiac function,biochemical indicators and levels of GSK-3β,ICAM-1 were analyzed.The clinical data between the MACE and non-MACE groups were compared and the factors influencing the occurrence of MACE were analyzed by logistic regression analysis.The receiver operating characteristic(ROC)curves were drown to analyze the efficacy of GSK-3β and ICAM-1 in predicting MACE occurrence.Results The levels of GSK-3β,ICAM-1,TNF-α,NT proBNP,HMGB1,the values of LVESD,LVEDD,and the incidence of MACE were higher in the severe group than in the moderate to mild group,while LVEF value was lower in the moderate to mild group(P<0.05).The levels of GSK-3β and ICAM-1 in STEMI patients were positively correlated with Killip grading and values of LVESD and LVEDD,respectively,and negatively correlated with LVEF value(P<0.05).Logistic regression analysis showed that GSK-3β(OR=1.962),ICAM-1(OR=1.702),LVESD(OR=1.621),LVEDD(OR=1.606),TNF-α(OR=1.388),NT-proBNP(OR=1.443)and HMGB1(OR=1.425)were independent risk factors for MACE after emergency PCI in STEMI patients(P<0.05),while LVEF(OR=0.581)was a protective factor(P<0.05).The ROC curve showed that the sensitivity and specificity of combining GSK-3β and ICAM-1 in predicting MACE after emergency PCI in STEMI patients were 83.45% and 81.27 %,respectively.The area under the curve of combining GSK-3β and ICAM-1 was 0.832,which was higher than that of the single indicators of GSK-3β(Z=2.643)and ICAM-1(Z=2.872)(P<0.05).Conclusion GSK-3β and ICAM-1 are highly expressed in the serum of STEMI patients,and their expression levels are closely related to the patient’s cardiac function.Both can be used to evaluate the occurrence of MACE after emergency PCI in STEMI patients,and their combined predictive power is greater.

Objective To investigate the expression levels of catenin beta 1(CTNNB1)and growth factor receptor-bound protein 2(Grb2)in ovarian cancer tissues and their prognostic significance.Methods A total of 126 patients with ovarian cancer who were treated in Cangzhou Central Hospital from January 2019 to January 2022 were selected.Samples of the cancer tissue were included in the ovarian cancer group(n= 126),and samples of adjacent tissues at least 1 cm away from the lesion margin were included in the adjacent tissue group(n= 126).The expression of CTNNB1 and Grb2 in the tissues was detected by immunohistochemistry.The relationship between the CTNNB1,Grb2 and the clinicopathological characteristics of ovarian cancer patients were analyzed by χ² test.The influencing factors of prognosis in ovarian cancer patients were analyzed by multivariate Cox regression.Results The positive rate of CTNNB1 and Grb2 in the ovarian cancer group was higher than that in the adjacent tissue group(61.90 % vs 30.95 %,65.08 % vs 33.33 %;P<0.05).The positive expression rate of CTNNB1 and Grb2 in patients with low differentiation,FIGO stage Ⅲ-Ⅳ,lymph node metastasis,and ascites was higher than that in those with moderate/high differentiation,FIGO stage Ⅰ-Ⅱ,no lymph node metastasis,and no ascites(P<0.05).The 3-year overall survival rate of patients with positive CTNNB1 and Grb2 was lower than that of those with negative CTNNB1 and Grb2(53.85 %vs 81.25 %,54.88 %vs 81.81 %,P<0.05).Multivariate analysis showed that low differentiation(HR=3.065,95 %CI:1.348-6.967),lymph node metastasis(HR=2.765,95 %CI:1.401-5.458),positive CTNNB1(HR=3.080,95 %CI:1.594-5.951),and positive Grb2(HR=3.062,95 %CI:1.536-6.104)were independent risk factors affecting the prognosis of ovarian cancer patients(P<0.05).Conclusion CTNNB1 and Grb2 are highly expressed in ovarian cancer tissues and are significantly associated with FIGO stage,differentiation degree,lymph node metastasis,and ascites.Both of them can be used as biomarkers for auxiliary assessment of patient prognosis.

Objective To explore the expression of heat shock protein 70(HSP70)and nuclear distribution protein C(NUDC)in ovarian cancer tissues and their relationship with disease progression.Methods A total of 150 patients with ovarian cancer(observation group)and 134 patients with non-tumor gynecological diseases(control group)were selected.The expression levels of HSP70 and NUDC in ovarian tissues were detected in the two groups.The influencing factors of ovarian cancer progression were explored by univariate and multivariate logistic regression analyses.Results The expression levels of HSP70 and NUDC in ovarian tissues in the observation group were significantly higher than those in the control group(P<0.05).Logistic regression analysis suggested that the influencing factors of ovarian cancer progression were clinical staging,other organ metastasis,high expression level of HSP70,and high expression level of NUDC(P<0.05).Conclusion The expression levels of HSP70 and NUDC in ovarian cancer tissues are significantly higher than those in non-tumor ovarian tissues,and the high expression of HSP70 and NUDC are influence factors for ovarian cancer progression.

Objective To investigate the association between serum thioredoxin interacting protein(Txnip),NADPH oxidase 4(Nox4),carbohydrate response element binding protein(ChREBP)and diabetic retinopathy(DR)in newly diagnosed type 2 diabetes mellitus(T2DM)patients.Methods A total of 324 newly diagnosed T2DM patients admitted to Xi’an Trade Union Hospital from January 2022 to May 2023 were selected and divided into DR group with DR(n=106)and control group without DR(n=218)according to the results of fundus photography.Serum Txnip,Nox4 and ChREBP levels were detected.The serum Txnip,Nox4,ChREBP levels and various clinical data were compared between the two groups.Logistic regression model was used to analyze the influencing factors of DR,and receiver operating characteristic curve was used to analyze the diagnostic value of Txnip,Nox4,ChREBP for DR.Results The levels of Txnip,Nox4,ChREBP,hypertension,the levels of triglyceride,fasting insulin and HbA1c in DR group were higher than those in the control group(P<0.05).Increased serum Txnip,Nox4 and ChREBP levels were risk factors for DR of newly diagnosed T2DM patients(P<0.05).Serum Txnip,Nox4,and ChREBP levels alone and in combination had diagnostic value for T2DM patients with DR.The area under the curve was 0.804(95 %CI:0.753-0.854),0.799(95 %CI:0.744-0.855),0.781(95 %CI:0.727-0.834),0.926(95 %CI:0.898-0.954),respectively.Conclusion The increase of serum Txnip,Nox4 and ChREBP levels is associated with the occurrence of DR in newly diagnosed T2DM patients,and the three serum indexes have good diagnostic value for DR.

Artificial intelligence(AI)technology has been applied to various aspects of scientific activities,and artificial intelligence generated content(AIGC)has permeated the process of academic research writing.Guidelines and standards for the use of AIGC in academic writing are an unavoidable issue in the promotion of research integrity.Based on existing policy documents and relevant statements from international publishing organizations and academic journals,this article summarizes the current regulatory requirements regarding authorship,citation,disclosure,and the use of AIGC in text,figures,data,and references in academic publications.The aim is to help authors enhance their awareness and ability to use AIGC appropriately,thereby further improving the standardization of journal management.