OBJECTIVE: To observe the clinical effect of cinobufacini injection in treating moderate and advanced primary liver cancer (PLC). METHODS: One hundred patients with moderate and advanced PLC were randomly divided into cino-treated group (50 patients) and control group (50 patients). The quality of life, tumor size, some changes of laboratory tests, and survival time were observed. RESULTS: The progressive rate of cino-treated group (18%) was lower than that of the control group (32%). The quality of life of the cino-treated group (80%) was better than that of the control group (72%), but without statistical significance. The survival rate of >12 months of the cino-treated group (30%) was higher than that of the control group (18%). The patients' liver function such as serum total bilirubin and ALT decreased obviously in the cino-treated group while increased a lot in the control group. The level of AFP increased after treatment with statistical significance in the control group while there was no statistical significance in the cino-treated group. CONCLUSION: Cinobufacini injection can not only inhibit the proliferation of cancer, but also protect liver function, improve quality of life and prolong survival time.

Objective:To study the clinical characteristics of ureaplasma urealyticum (UU) infection in preterm infants with gestational age <34 weeks.Methods:From January 2017 to December 2021, premature infants with gestational age <34 weeks admitted to neonatal department of our hospital were enrolled in this prospective cohort study. UU-DNA from respiratory tract samples were examined using quantitative fluorescence polymerase chain reaction method. The infants were assigned into UU (+) group and UU (-) group. Perinatal factors and clinical characteristics were compared between the two groups.Results:A total of 182 preterm infants were enrolled, including 59 cases (32.4%) in UU (+) group and 123 (67.6%) in UU (-) group. UU (+) group had significantly lower gestational age and birth weight and significantly higher incidences of vaginal delivery, premature rupture of membranes (PROM) >18 h and maternal chorioamnionitis than UU (-) group ( P<0.05). Compared with UU (-) group, UU (+) group had significantly higher leucocyte count, neutrophil count and interleukin-6 at 1, 24 and 72 h after birth ( P<0.05). No significant differences existed in C-reactive protein and procalcitonin between the two groups at each time point ( P>0.05). In UU (+) group, the incidences of intrauterine pulmonary infection and bronchopulmonary dysplasia (BPD) were higher and the incidence of respiratory distress syndrome was lower than UU (-) group ( P<0.05). No significant differences existed in the incidences of intraventricular hemorrhage, periventricular leukomalacia, feeding intolerance, necrotizing enterocolitis, retinopathy of prematurity between the two groups ( P>0.0 5). UU (+) group had significantly longer duration of oxygen therapy than UU (-) group ( P<0.05). No significant differences existed in the duration of invasive mechanical ventilation and hospital stay between the two groups ( P>0.05). Conclusions:Preterm infants <34 weeks with positive UU in respiratory tract secretions have higher incidences of vaginal delivery, PROM>18 h and maternal chorioamnionitis. Leukocyte and neutrophil count and interleukin -6 are higher in these infants. They need prolonged oxygen therapy and have increased risks of intrauterine pulmonary infection and BPD.

Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes. Methods: The degree of tissue injury was observed by pathological staining. Inflammatory cell infiltration was analyzed by immunohistochemical staining. Serum EPO levels were detected by enzyme-linked immunosorbent assay, and EPO production and renal interstitial fibrosis were analyzed by immunofluorescence. Quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of key inflammatory factors and the activation of signaling pathways. In vitro, the interaction between peripheral blood mononuclear cells (PBMCs) and C3H10T1/2 cells was investigated via cell coculture experiments. Results: RasGRP4 decreased the expression of hypoxia-inducible factor 2-alpha (HIF2A) via the ubiquitination–proteasome degradation pathway and promoted myofibroblastic transformation by activating critical inflammatory pathways, consequently reducing the production of EPO in T2DM mice. Conclusion RasGRP4 participates in the production of renal EPO in diabetic mice by affecting the secretion of proinflammatory cytokines in PBMCs, degrading HIF2A, and promoting the myofibroblastic transformation of C3H10T1/2 cells.

Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes. Methods: The degree of tissue injury was observed by pathological staining. Inflammatory cell infiltration was analyzed by immunohistochemical staining. Serum EPO levels were detected by enzyme-linked immunosorbent assay, and EPO production and renal interstitial fibrosis were analyzed by immunofluorescence. Quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of key inflammatory factors and the activation of signaling pathways. In vitro, the interaction between peripheral blood mononuclear cells (PBMCs) and C3H10T1/2 cells was investigated via cell coculture experiments. Results: RasGRP4 decreased the expression of hypoxia-inducible factor 2-alpha (HIF2A) via the ubiquitination–proteasome degradation pathway and promoted myofibroblastic transformation by activating critical inflammatory pathways, consequently reducing the production of EPO in T2DM mice. Conclusion RasGRP4 participates in the production of renal EPO in diabetic mice by affecting the secretion of proinflammatory cytokines in PBMCs, degrading HIF2A, and promoting the myofibroblastic transformation of C3H10T1/2 cells.

Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes. Methods: The degree of tissue injury was observed by pathological staining. Inflammatory cell infiltration was analyzed by immunohistochemical staining. Serum EPO levels were detected by enzyme-linked immunosorbent assay, and EPO production and renal interstitial fibrosis were analyzed by immunofluorescence. Quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of key inflammatory factors and the activation of signaling pathways. In vitro, the interaction between peripheral blood mononuclear cells (PBMCs) and C3H10T1/2 cells was investigated via cell coculture experiments. Results: RasGRP4 decreased the expression of hypoxia-inducible factor 2-alpha (HIF2A) via the ubiquitination–proteasome degradation pathway and promoted myofibroblastic transformation by activating critical inflammatory pathways, consequently reducing the production of EPO in T2DM mice. Conclusion RasGRP4 participates in the production of renal EPO in diabetic mice by affecting the secretion of proinflammatory cytokines in PBMCs, degrading HIF2A, and promoting the myofibroblastic transformation of C3H10T1/2 cells.

Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes. Methods: The degree of tissue injury was observed by pathological staining. Inflammatory cell infiltration was analyzed by immunohistochemical staining. Serum EPO levels were detected by enzyme-linked immunosorbent assay, and EPO production and renal interstitial fibrosis were analyzed by immunofluorescence. Quantitative real-time polymerase chain reaction and Western blotting were used to detect the expression of key inflammatory factors and the activation of signaling pathways. In vitro, the interaction between peripheral blood mononuclear cells (PBMCs) and C3H10T1/2 cells was investigated via cell coculture experiments. Results: RasGRP4 decreased the expression of hypoxia-inducible factor 2-alpha (HIF2A) via the ubiquitination–proteasome degradation pathway and promoted myofibroblastic transformation by activating critical inflammatory pathways, consequently reducing the production of EPO in T2DM mice. Conclusion RasGRP4 participates in the production of renal EPO in diabetic mice by affecting the secretion of proinflammatory cytokines in PBMCs, degrading HIF2A, and promoting the myofibroblastic transformation of C3H10T1/2 cells.