AIM:This study aims to investigate the synergistic cytotoxic effects of chrysin and venetoclax on acute myeloid leukemia(AML)cells and to elucidate the underlying mechanisms.METHODS:Human AML cell lines MV411 and MOLM13 were cultured in vitro and treated with chrysin in combination with venetoclax.Cell viability was as-sessed using the CCK8 assay,while flow cytometry was employed to measure cell cycle distribution and apoptosis rates.Western blot was used to detect the expression of apoptosis-related proteins and protein kinase B(PKB/Akt)/nuclear factor-κB(NF-κB)signaling pathway-related proteins.RESULTS:The results from the CCK8 assay and flow cytometry demon-strated that treatment with 16 and 32 μmol/L chrysin significantly inhibited the viability of AML cells and increased the proportion of cells in G1 phase,as well as the apoptosis rate.Notably,the cells in combination treatment group exhibited a marked reduction in proliferation and an elevated apoptosis rate compared with either chrysin or venetoclax group alone.Western blot analysis indicated that increasing concentrations of chrysin led to an elevation in cleaved poly(ADP-ribose)polymerase(PARP)level,alongside a down-regulation of proteins associated with the Akt/NF-κB signaling pathway.Fur-thermore,the combination treatment significantly up-regulated cleaved PARP level and down-regulated Akt/NF-κB path-way-related proteins compared with the treatment with chrysin or venetoclax alone.CONCLUSION:Chrysin and veneto-clax synergistically inhibit the proliferation of AML cells and promote apoptosis by modulating the Akt/NF-κB signaling pathway.

Objective:To investigate the effects of the transforming growth factor-β/Wingless 5a/c-Jun N-terminal kinase (TGF-β/WNT5a/JNK) signaling pathway on fibrosis of lens epithelial cells (LECs).Methods:The human LECs line SRA01/04 was divided into three groups, control group cultured with conventional medium, TGF-β group treated with TGF-β1 for 24 hours and WNT5a group treated with WNT5a for 24 hours.Western blot was performed to detect the relative protein expression levels of WNT5a, JNK, and phosphorylated JNK (p-JNK) in cells of the three groups.The SRA01/04 cell line was further divided into four groups, control group cultured with conventional medium, TGF-β group treated with TGF-β 1 for 24 hours, TGF-β+ SP600125 group treated with TGF-β1 for 24 hours+ JNK inhibitor SP600125 for 2 hours, and WNT5a+ SP600125 group treated with WNT5a for 24 hours+ SP600125 for 2 hours.The relative expression of WNT5a, JNK, p-JNK, type Ⅰ collagen (Col-Ⅰ), fibronectin (FN), and α-smooth muscle actin (α-SMA) in cells of the four groups was detected by Western blot.The distribution of α-SMA in cells was determined by immunofluorescence staining.Cell migration was evaluated via Transwell assay, and Col-Ⅰ gel area ratio was measured at 8, 16, 24, and 48 hours of culture by gel contraction experiment. Results:Western blot revealed that the relative protein expression levels of WNT5a, JNK, and p-JNK were significantly higher in the TGF-β and WNT5a groups than in the control group (all P<0.05).The expression levels of Col-Ⅰ, FN, and α-SMA were significantly higher in the TGF-β, TGF-β+ SP600125, and WNT5a+ SP600125 groups than in the control group and significantly lower in the TGF-β+ SP600125 and WNT5a+ SP600125 groups than in the TGF-β group (all P<0.05).Immunofluorescence staining showed that TGF-β-treated SRA01/04 cells transformed from columnar epithelial cells to spindle-shaped myofibroblasts in TGF-β group, whereas most cells in the TGF-β+ SP600125 and WNT5a+ SP600125 groups were still columnar epithelial cells.The relative fluorescence intensity of α-SMA was significantly higher in the TGF-β, TGF-β+ SP600125 and WNT5a+ SP600125 groups than in the control group, and the relative fluorescence intensity of α-SMA was significantly lower in the TGF-β+ SP600125 and WNT5a+ SP600125 groups than in the TGF-β group (all P<0.05).Transwell assay showed that there were more migrating cells in TGF-β group than in the control group, and the migrating cell count was lower in TGF-β+ SP600125 group and WNT5a+ SP600125 group than in the control group, with statistically significant differences (all P<0.05).Col-Ⅰ gel contraction experiment results showed that with the extension of culture time, the Col-Ⅰ gel area in each group decreased significantly, with significant overall comparison differences in the Col-Ⅰ gel area shrinkage ratios in each group at different time points ( Ftime=71.599, P<0.001) and among different groups ( Fgroup=71.604, P<0.001).After 48 hours of culture, the Col-Ⅰ gel shrinkage ratios in TGF-β group, TGF-β+ SP600125 and WNT5a+ SP600125 groups were (26.24±0.28)%, (64.02±1.05)%, and (76.81±0.28)%, respectively, which were significantly lower than (90.20±0.31)% of the control group (all P<0.05). Conclusions:The WNT5a/JNK signaling pathway, acting as a downstream target of the TGF-β signaling pathway, promotes epithelial-mesenchymal transition and extracellular matrix deposition in LECs, and enhances cell contractility.

Objective:To investigate the effects of the transforming growth factor-β/Wingless 5a/c-Jun N-terminal kinase (TGF-β/WNT5a/JNK) signaling pathway on fibrosis of lens epithelial cells (LECs).Methods:The human LECs line SRA01/04 was divided into three groups, control group cultured with conventional medium, TGF-β group treated with TGF-β1 for 24 hours and WNT5a group treated with WNT5a for 24 hours.Western blot was performed to detect the relative protein expression levels of WNT5a, JNK, and phosphorylated JNK (p-JNK) in cells of the three groups.The SRA01/04 cell line was further divided into four groups, control group cultured with conventional medium, TGF-β group treated with TGF-β 1 for 24 hours, TGF-β+ SP600125 group treated with TGF-β1 for 24 hours+ JNK inhibitor SP600125 for 2 hours, and WNT5a+ SP600125 group treated with WNT5a for 24 hours+ SP600125 for 2 hours.The relative expression of WNT5a, JNK, p-JNK, type Ⅰ collagen (Col-Ⅰ), fibronectin (FN), and α-smooth muscle actin (α-SMA) in cells of the four groups was detected by Western blot.The distribution of α-SMA in cells was determined by immunofluorescence staining.Cell migration was evaluated via Transwell assay, and Col-Ⅰ gel area ratio was measured at 8, 16, 24, and 48 hours of culture by gel contraction experiment. Results:Western blot revealed that the relative protein expression levels of WNT5a, JNK, and p-JNK were significantly higher in the TGF-β and WNT5a groups than in the control group (all P<0.05).The expression levels of Col-Ⅰ, FN, and α-SMA were significantly higher in the TGF-β, TGF-β+ SP600125, and WNT5a+ SP600125 groups than in the control group and significantly lower in the TGF-β+ SP600125 and WNT5a+ SP600125 groups than in the TGF-β group (all P<0.05).Immunofluorescence staining showed that TGF-β-treated SRA01/04 cells transformed from columnar epithelial cells to spindle-shaped myofibroblasts in TGF-β group, whereas most cells in the TGF-β+ SP600125 and WNT5a+ SP600125 groups were still columnar epithelial cells.The relative fluorescence intensity of α-SMA was significantly higher in the TGF-β, TGF-β+ SP600125 and WNT5a+ SP600125 groups than in the control group, and the relative fluorescence intensity of α-SMA was significantly lower in the TGF-β+ SP600125 and WNT5a+ SP600125 groups than in the TGF-β group (all P<0.05).Transwell assay showed that there were more migrating cells in TGF-β group than in the control group, and the migrating cell count was lower in TGF-β+ SP600125 group and WNT5a+ SP600125 group than in the control group, with statistically significant differences (all P<0.05).Col-Ⅰ gel contraction experiment results showed that with the extension of culture time, the Col-Ⅰ gel area in each group decreased significantly, with significant overall comparison differences in the Col-Ⅰ gel area shrinkage ratios in each group at different time points ( Ftime=71.599, P<0.001) and among different groups ( Fgroup=71.604, P<0.001).After 48 hours of culture, the Col-Ⅰ gel shrinkage ratios in TGF-β group, TGF-β+ SP600125 and WNT5a+ SP600125 groups were (26.24±0.28)%, (64.02±1.05)%, and (76.81±0.28)%, respectively, which were significantly lower than (90.20±0.31)% of the control group (all P<0.05). Conclusions:The WNT5a/JNK signaling pathway, acting as a downstream target of the TGF-β signaling pathway, promotes epithelial-mesenchymal transition and extracellular matrix deposition in LECs, and enhances cell contractility.

AIM:This study aims to investigate the synergistic cytotoxic effects of chrysin and venetoclax on acute myeloid leukemia(AML)cells and to elucidate the underlying mechanisms.METHODS:Human AML cell lines MV411 and MOLM13 were cultured in vitro and treated with chrysin in combination with venetoclax.Cell viability was as-sessed using the CCK8 assay,while flow cytometry was employed to measure cell cycle distribution and apoptosis rates.Western blot was used to detect the expression of apoptosis-related proteins and protein kinase B(PKB/Akt)/nuclear factor-κB(NF-κB)signaling pathway-related proteins.RESULTS:The results from the CCK8 assay and flow cytometry demon-strated that treatment with 16 and 32 μmol/L chrysin significantly inhibited the viability of AML cells and increased the proportion of cells in G1 phase,as well as the apoptosis rate.Notably,the cells in combination treatment group exhibited a marked reduction in proliferation and an elevated apoptosis rate compared with either chrysin or venetoclax group alone.Western blot analysis indicated that increasing concentrations of chrysin led to an elevation in cleaved poly(ADP-ribose)polymerase(PARP)level,alongside a down-regulation of proteins associated with the Akt/NF-κB signaling pathway.Fur-thermore,the combination treatment significantly up-regulated cleaved PARP level and down-regulated Akt/NF-κB path-way-related proteins compared with the treatment with chrysin or venetoclax alone.CONCLUSION:Chrysin and veneto-clax synergistically inhibit the proliferation of AML cells and promote apoptosis by modulating the Akt/NF-κB signaling pathway.

Objective　To explore the effect of Mp1p on host macrophages through transcriptomics combined with metabolomics. Methods Firstly, a THP-1 macrophage strain (THP-1-Mp1p+) stably expressing Mp1p was constructed using lentivirus. Secondly, using high-throughput RNA sequencing (RNA Seq) technology, the expression level of intracellular mRNA was detected in transcriptomics analysis to determine differentially expressed genes; In metabolomics analysis, metabolite identification was performed through database comparison, and pathway analysis was performed on differential metabolites to reveal potential mechanisms of action. Finally, the results of metabolomics and transcriptomics were combined for analysis, and differential metabolites and genes were analyzed to further elucidate the mechanism of action of Mp1p on macrophages. Results Transcriptome analysis showed that, compared with the negative control group, the THP-1-Mp1p+ group had a total of 1 180 differentially expressed genes (DEGs), with 345 upregulated genes and 835 downregulated genes. GO enrichment analysis of DEGs showed that there were 135 differentially expressed genes, including 105 in biological processes (BP), 28 in cellular components (CC), and 2 in molecular functions (MF). The KEGG analysis results showed that the effect of Mp1p on THP-1 macrophages was highly correlated with the TNF pathway. The metabolomic analysis found that both the blank control group and the THP-1-Mp1p+ macrophage group achieved good separation between QC samples in both positive and negative ion modes. The threshold for significant differential metabolites was set at: VIP≥1 and T-test P<0.05, resulting in the identification of 488 differential metabolites, with 230 in the positive ion mode and 258 in the negative ion mode. Pathway enrichment analysis of the identified metabolites pointed to significant enrichment in metabolic pathways. The combined analysis confirmed that the tumor necrosis factor signaling pathway, interleukin-17 signaling pathway, and NF-kappaB signaling pathway were important metabolic pathways involved. Conclusions The virulence factor Mp1p may affect host macrophages by modulating the tumor necrosis factor signaling pathway, interleukin-17 signaling pathway, and NF-kappaB signaling pathway. The findings contribute to a better understanding of the mechanisms of action of Mp1p and may offer potential directions for the selection of relevant diagnostic and therapeutic targets in the future.

Objective:To explore the level and influencing factors of treatment costs for patients with pneumoconiosis, and to provide a basis for reducing the economic burden of patients with pneumoconiosis and optimizing the rational allocation of medical resources.Methods:In August 2020, the multi-stage stratified sampling method was used to obtain the treatment cost information of pneumoconiosis patients from January to December 2018 in 1123 sample medical institutions. The average cost per time of 2178 outpatients and 7425 inpatients was described, and the differences in the distribution of hospitalization costs for patients with pneumoconiosis were compared by one-way analysis of variance, and a multiple linear regression model was constructed to analyze the influencing factors of hospitalization costs for patients with pneumoconiosis.Results:The average cost of outpatients with pneumoconiosis was 465.88 yuan, and the average cost of inpatients was 12280.63 yuan. There were statistically significant differences in hospitalization expenses among different age, institution level, institution type, length of hospital stay and type of insured ( F=10.49, 402.92, 416.35, 2390.48, 1298.14, P<0.001) . Age, length of hospital stay, reimbursement ratio, and institution level were influencing factors of the total hospitalization expenses of patients with pneumoconiosis ( t=5.27, 62.20, 22.35, 21.20, P<0.001) . Conclusion:Patients with pneumoconiosis have a heavy burden of treatment costs. Age, length of hospital stay, institution level and reimbursement ratio are the main influencing factors of hospitalization costs. It is recommended to strengthen the prevention and treatment of key populations, standardize the use of medical insurance, and promote the rational allocation of medical resource to reduce the cost burden of pneumoconiosis patients.

Objective:To explore the level and influencing factors of treatment costs for patients with pneumoconiosis, and to provide a basis for reducing the economic burden of patients with pneumoconiosis and optimizing the rational allocation of medical resources.Methods:In August 2020, the multi-stage stratified sampling method was used to obtain the treatment cost information of pneumoconiosis patients from January to December 2018 in 1123 sample medical institutions. The average cost per time of 2178 outpatients and 7425 inpatients was described, and the differences in the distribution of hospitalization costs for patients with pneumoconiosis were compared by one-way analysis of variance, and a multiple linear regression model was constructed to analyze the influencing factors of hospitalization costs for patients with pneumoconiosis.Results:The average cost of outpatients with pneumoconiosis was 465.88 yuan, and the average cost of inpatients was 12280.63 yuan. There were statistically significant differences in hospitalization expenses among different age, institution level, institution type, length of hospital stay and type of insured ( F=10.49, 402.92, 416.35, 2390.48, 1298.14, P<0.001) . Age, length of hospital stay, reimbursement ratio, and institution level were influencing factors of the total hospitalization expenses of patients with pneumoconiosis ( t=5.27, 62.20, 22.35, 21.20, P<0.001) . Conclusion:Patients with pneumoconiosis have a heavy burden of treatment costs. Age, length of hospital stay, institution level and reimbursement ratio are the main influencing factors of hospitalization costs. It is recommended to strengthen the prevention and treatment of key populations, standardize the use of medical insurance, and promote the rational allocation of medical resource to reduce the cost burden of pneumoconiosis patients.

Objective:To investigate the effects of Dickkopf-1(DKK1) on the proliferation of human lens epithelial cells (LECs) and its possible mechanism in order to search a new target for the treatment of posterior capsular opacification (PCO).Methods:Human LECs line (SRA 01/04 cells )were divided into Wnt3a overexpression group, DKK1 group and control group.Wnt3a gene expression vector was transfected into SRA 01/04 cells by liposome mediated transfection to establish a PCO model in the Wnt3a overexpression group, DKK1 of 100 μg/ml was added into the medium 48 hours after transfection of Wnt3a gene vector in the DKK1 group, and only pcDNA3-HA vector was transfected in the control group.The survival rate of SRA 01/04 cells was detected with a cell counting kit-8 (CCK-8) assay.The expression rate of proliferating cell nuclear antigen (PCNA) in the cells was detecteds by immunocytochemistry.The expression of β-catenin in the cells was detected and located by immunofluorescence.The expression of Wnt3a CyclinD1 and C-Myc were detected by Western blot assay.Results:The relative expression of Wnt3a protein in the control group was 0.49±0.07, which was significantly lower than that in the Wnt3a overexpression group (0.84±0.06) ( t=3.704, P=0.02). The survival rate in the Wnt3a overexpression group, DKK1 group and control group showed significant difference over time ( Fgroup=10.910, P<0.05; Ftime=6.041, P<0.05). The survival rate in the Wnt3a overexpression group was significantly increased in comparison with the control group and that in the DKK1 group was significantly reduced in comparison with the Wnt3a overexpression group(all at P<0.05). β-Catenin was expressed mainly in cytoplasm and cell nucleus in the Wnt3a overexpression group and only in cytoplasm in the DKK1 group. in the control group, β-catenin showed a weaked expression in the cytoplasm and nucleus in comparison with the Wnt3a overexpression group.The expression rates of PCNA protein were (9.4±1.4)%, (43.4±5.4)%, and (14.2±2.3)% in the control group, Wnt3a overexpression group and DKK1 group, respectively, with a significant difference among the groups ( F=28.250, P<0.05), and the expression rates of PCNA protein were significantly reduced in the control group and DKK1 group compared with the Wnt3a overexpression group (both at P<0.05). β-Catenin protein were expressed mainly in the cytoplasm and nucleus in the Wnt3a overexpression group and only in the cytoplasm in the control group.In the DKK1 group, the expression of β-catenin protein was weakened in the cytoplasm and nucleus in comparison with the Wnt3a overexpression group.The relative expressions of CyclinD1 were 0.64±0.07、0.84±0.03 and 0.55±0.10, C-Myc were 0.59±0.05、0.93±0.02 and 0.47±0.08 in the control group, Wnt3a overexpression group and the DKK1 group, respectively with significant differences among the groups ( F=20.580, 5.040, both at P<0.05). The relative expressions of CyclinD1 and C-Myc in the Wnt3a overexpression group were significantly higher than those in the DKK1 group and the control group (all at P<0.05). Conclusions:DKK1 inhibits activation of Wnt/β-catenin signaling pathway induced by Wnt3a overexpression in SRA01/04 cells, and down-regulation of downstream target proteins cyclin D1 and C-Mgc may be the biological mechanism of Dkk1 inhibiting human LECs proliferation.

Objective To discuss the perioperative nursing measures for patients with osteoporotic vertebral compression fractures who are receiving percutaneous vertebroplasty (PVP) treatment by using high viscosity bone cement.Methods A total of 30 patients with osteoporotic vertebral compression fractures were included in this study.All patients were treated with PVP by using high viscosity bone cement.Preoperative routine nursing,psychological intervention,dietary intervention,postoperative guidance of rehabilitation exercise of limbs,close observation of bone cement leakage were strictly implemented,and the corresponding nursing measures were promptly taken when needed.Results Through strict implement of the nursing intervention all 30 patients could actively cooperate with PVP treatment,and after PVP the pain was significantly relieved in all patients.Conclusion Adequate preoperative preparation,proper postoperative guidance,careful observation and effective nursing can help the patients resume their daily life activities as soon as possible,relieve the pain,and improve the quality of life as well.(J Intervent Radiol,2017,26:274-276)

Objective To explore pediatric nurses' perceptions about patients' safety culture and identify the factors that affect patients' safety culture so as to provide evidences for improving patients' safety. Methods A cross-sectional study with convenience sampling was performed on 886 pediatric nurses working in a children's hospital from July 2016 to September 2016. Patients' safety culture was assessed using the Chinese version of the Hospital Survey on Patient Safety Culture.Results 74.1% of nurses evaluated patients' safety grade as either 'very good' or 'good'. The advantage areas with positive responsive rates higher than 75% were described as follows "feedback and communication about error", "teamwork within units" and "organizational learning and continuous improvement". Areas need to be improved with positive responsive rates lower than 50% included "staffing" and "frequency of events reported". Multiple linear regression analysis indicated that ages and overtime work of nurses were main factors that affected nurses' knowledge of patients' safety culture. The two factors explained 10.8% of total variation.Conclusions Nurses in the children's hospital has an overall high level of knowledge to patients' safety culture. However, several aspects need to be improved. It is necessary to provide positive interventions to factors that affect knowledge of safety culture.