ObjectiveTo investigate the value of serum long non-coding RNA H19(lncRNA H19) and activin A in the diagnosis and prognosis of neonatal hypoxic-ischemic encephalopathy(HIE).MethodsFrom January 2019 to January 2023, 207 children with HIE admitted to the Neonatal Department of Xianyang Central Hospital were selected as the HIE subgroup. According to the severity of the disease, they were divided into 99 cases of mild HIE subgroup, 61 cases of moderate HIE subgroup and 47 cases of severe HIE subgroup. According to the prognosis at discharge, they were divided into 62 cases of poor prognosis subgroup and 145 cases of good prognosis subgroup. In addition, 105 healthy newborns in the same period were selected as the healthy control group. Serum lncRNA H19 level was detected by real-time fluorescence quantitative PCR, and serum Activin A level was detected by enzyme-linked immunosorbent assay. Taking the prognosis of HIE children as the dependent variable, a multivariate unconditional Logistic regression model was established to determine the influencing factors. ROC curve was drawn to evaluate the value of serum lncRNA H19 and Activin A levels in judging the poor prognosis of HIE children.ResultsCompared with the healthy control group, the serum level of lncRNA H19 in the HIE subgroup was decreased, and the level of Activin A was increased(t/P=34.498/<0.001,47.114/<0.001). The levels of serum lncRNA H19 in mild, moderate and severe HIE subgroups decreased in turn, and the levels of Activin A increased in turn(F/P=267.954/<0.001,349.146/<0.001). Among the 207 children with HIE, 62 cases(29.95%) had poor prognosis. The independent risk factors of poor prognosis in children with HIE were severe HIE and elevated Activin A, the independent protective factors were increased neonatal behavioral neurological assessment score and increased lncRNA H19[OR(95%CI)=6.518(1.824-23.292),1.537(1.301-1.814),0.812(0.734-0.898),0.502(0.387-0.651)]; The area under the curve of serum lncRNA H19 combined with Activin A level in judging the poor prognosis of HIE children was 0.904, which was greater than 0.783 and 0.790 judged by serum lncRNA H19 and Activin A levels alone(Z/P=4.030/<0.001,4.048/<0.001).ConclusionThe increase of serum lncRNA H19 level and the decrease of Activin A level are related to the aggravation and poor prognosis of HIE children. The value of serum lncRNA H19 combined with Activin A level in judging the prognosis of HIE children is higher.

ObjectiveTo study whether long non-coding RNA(lncRNA) SOX21 antisense RNA1(SOX21-AS1) regulates H2O2-induced cardiomyocyte damage by targeting miR-7-5p.MethodsFrom July 2022 to February 2023, the experiment was carried out in Qinghai Provincial People' s Hospital. The H9C2 cells were treated with H2O2to mimic an oxidative stress injury model. H9C2 cells was divided into Con group, H2O2group, H2O2+si-NC group, H2O2+si-SOX21-AS1 group, H2O2+ miR-NC group, H2O2+miR-7-5p group, H2O2+si-SOX21-AS1+anti-miR-NC group, H2O2+si-SOX21-AS1+anti-miR-7-5p group. Expression of SOX21-AS1 and miR-7-5p was detected using RT-qPCR. The viability and apoptosis of H9C2 were calculated using CCK-8 method and flow cytometry. A commercial kit was used to measure the activity of SOD and the content of malondialdehyde(MDA). Dual luciferase reporter experiment was used verify the targeting relationship between SOX21-AS1 and miR-7-5p.ResultsAfter H2O2treatment, cell viability, miR-7-5p expression and SOD activity of H9C2 were significantly reduced(P<0.05), while apoptosis rate, SOX21-AS1 expression and MDA content were significantly increased(P<0.05). Interference with SOX21-AS1 or miR-7-5p overexpression can promote H9C2 cell survival(P<0.05), increase SOD activity(P<0.05), reduce MDA content(P<0.05), as well as inhibit cell apoptosis(P<0.05). miR-7-5p is the target gene of SOX21-AS1. miR-7-5p inhibition can reverse the protective effect of interference SOX21-AS1 on H2O2-induced H9C2 cells(P<0.05).ConclusionInterfering with SOX21-AS1 can reduce H2O2-induced cardiomyocyte injury by up-regulating miR-7-5p expression.

ObjectiveTo explore the role of cinobufacini in colon cancer invasion and metastasis and its mechanism.MethodsThe experiment was conducted in the laboratory of the Second Affiliated Hospital of the Air Force Military Medical University from September 2022 to March 2023. Human colon cancer cell line HCT 116 and human normal colon epithelial cell line NCM 460 were treated with different concentrations of cinobufacini(0, 2.5, 5, 10, 20, 40, 80, 160 mg/L) for treatment, and the effects of cinobufacini on the proliferation of colon cancer cells and normal cells were detected by CCK-8 method. HCT 116 cells were randomly divided into the control group and the cinobufacini(80 mg/L) group, and the morphological changes of the cells were observed under the light microscope; apoptosis was detected by Annexin V-FITC/PI double staining; cell migration and invasion were detected by Transwell assay; and metastasis of the cancer cells, EMT, and Wnt/β-catenin related protein expression.ResultsCCK-8 results showed that the proliferation inhibition rate of HCT 116 cells was gradually increased in a dose and time dependent manner(P<0.001) after treatment with different concentrations of cinobufacini, and the 24 h semi-inhibitory concentration(IC50) was about 80 mg/L, whereas it did not affect the proliferative ability of normal colonic epithelial cells NCM460. The HCT 116 cells in the control group were in good condition, while the cells in the cinobufacini group showed decreased wall adhesion ability, increased secretion, and wrinkled morphology with a round epithelial cell like phenotype, accompanied by cell membrane rupture of varying degrees; the results of flow cytometry showed that the apoptosis rate of the HCT 116 cells was significantly increased compared with that of the treatment at 0 h after cinobufacini treatment for 24, 48, and 72 h, respectively(t=17.222,17.041,23.651,P<0.001); and the results of the Transwell experiments showed that the apoptotic rate of HCT 116 cells increased significantly compared with that of the control group. Transwell assay showed that the number of migrating and invading cells of HCT 116 cells in the cinobufacini group was significantly lower compared with the control group(t/P=52.754/<0.001,7.584/0.002); Western blot results showed that the expression of MMP-2 and MMP-9 in the cells of the cinobufacini group was reduced compared with the control group, the expression of epithelial markers E cadherin was increased, whereas the expression of mesenchymal markers N cadherin and Snail was reduced, and the expression of β-catenin, Wnt3a, c-myc, cyclin D1 and MMP-7 proteins were down regulated, while APC protein expression was up-regulated(t/P=8.908/0.001,29.394/0.001,36.406/0.001,12.860/0.001,14.203/0.001,27.862/0.001,20.176/0.001,24.012/0.001,37.245/0.001,33.627/0.001,6.971/0.002).ConclusionCinobufacini can inhibit colon cancer cell invasion and metastasis, and its mechanism may be related to the inhibition of EMT and blocking of Wnt/β-catenin signaling pathway.

Anemia is a common complication of chronic kidney disease(CKD), especially in CKD patients with maintenance hemodialysis. In the past, anemia was mainly thought to be related to insufficient erythropoiesis and excessive loss in patients, therefore erythropoiesis stimulators were often used for treatment. In recent years, with the deepening of research, new pathogenesis such as abnormal bone mineral metabolism and abnormal thyroid function have been gradually discovered, and with the development and application of new drugs such as roxadustat and enarodustat, the diagnosis and treatment situation of CKD maintenance hemodialysis-related anemia has been improved. The study reviews the characteristics and treatment methods of CKD maintenance hemodialysis-related anemia in order to provide new ideas for the treatment of the disease.

Surgical treatment for malignant obstructive jaundice(MOJ) depends on the cause, location, and severity of the obstruction. In recent years, perioperative management of MOJ has garnered significant attention. Based on the patient's condition, preoperative biliary drainage, endoscopic interventions, and stent placement are used to relieve the obstruction during the perioperative period. Postoperatively, appropriate enteral nutritional support can be provided to reduce complications and improve the quality of life. At present, treatment strategies for malignant obstructive jaundice have become more diverse and comprehensive. Different treatment plans are selected based on the patient's disease course, obstruction location, and tumor staging. This article reviews the recent advances in the comprehensive treatment of malignant obstructive jaundice and proposes future research directions to provide references for clinical application.