Objective To explore and compare the diagnostic value of blood pressure, brain natriuretic peptide (BNP), pulmonary artery systolic pressure (PASP) in evaluating right ventricular dysfunction (RVD) in patients with acute pulmonary embolism (APE). Methods A retrospective study was conducted on 84 APE patients who were diagnosed by computed tomographic pulmonary angiography. The patients were divided into a RVD group and a non-RVD group by echocardiography. Eighteen clinical and auxiliary examination variables were used as the research factors and RVD as the related factor. The relationship between these research factors and RVD were evaluated by logistic regression model, the diagnostic value of BNP and PASP to predict RVD was analyzed by receiver-operating characteristic (ROC) curve analysis. Results The patients with RVD had more rapid heart rate, higher diastolic blood pressure, higher mean arterial pressure, higher incidence of BNP>100 pg/ml and higher incidence of PASP>40 mm Hg (allP<0 05="" upon="" logistic="" regression="" model="" bnp="">100 pg/ml (OR=4.904, 95%CI 1.431–16.806, P=0.011) and PASP>40 mm Hg (OR=6.415, 95%CI 1.509–27.261, P=0.012) were independent predictors of RVD. The areas under the ROC curve to predict RVD were 0.823 (95%CI 0.729–0.917) for BNP, and 0.798 (95%CI 0.700–0.896) for PASP. Conclusions Blood pressure related parameters can not serve as a predictor of RVD. Combined monitoring of BNP level and PASP is helpful for accurate prediction of RVD in patients with APE.
ObjectiveTo study the early functional change of sinusoid endothelial cell after liver transplantation in rat, and to investigate the endothelia protective effect of prostaglandin E1(PGE1). MethodsRat orthotopic liver transplantation model was performed in “twocuff method”, grouped as follows: group A served as normal rat blank control, group B as operative control with normal donor, group C as experimental control with shock donor, and group D as experimental group with shock donor and PGE1 administration (n=8 in each group). Transplanted groups (referring to recipients without specific definition) were sacrificed 6 h after operation for blood taken to detect serum liver enzymes (ALT, LDH), malondialdehyde (MDA), nitric oxide (NO) and plasm endothelin (ET). Liver tissue was resected at the same time for standard pathologic examination. Comparison of the difference the results was made between groups. ResultsCold preservation time and anhepatic phase were similar in each group, (2±0.5) h and (15±3) min respectively. All survived 6 h after transplantation (8/8) in group B and D with a survival rate of 100%, only 5 survived 6 h after transplantation in group C (5/8) with a survival rate of 62.5%. Comparing with group C, blood ALT, LDH, MDA, ET decreased and NO increased significantly in group D (Plt;0.05). Marked histologic structural damage was observed in group C, while normal light microscope appearance was better preserved in group C and D. ConclusionMarked sinusoid endothelia injury occurs during liver transplantation. Concentration of serum NO and plasm ET well presents its function. PGE1 relieves endothelia injury by improving hemodynamics and stabilizing sinusoid endothelial cell plasma membrane.
ObjectiveTo explore the mechanism by which the tumor suppressor gene Testin affects the proliferation, migration, and invasive biological activity of lung adenocarcinoma cell lines by regulating the RhoA pathway. MethodThe cbioportal tumor gene expression was used to screen for genes with high correlation with TES gene expression in lung adenocarcinoma, and the 200 genes with the highest correlation were selected for pathway enrichment analysis. Upload these 200 genes to the David gene annotation tool for GO_Biological Process pathway analysis, GO Molecular Function pathway analysis, KEGG pathway analysis, and Reactome pathway analysis. The lung adenocarcinoma cell line H1299 was cultured, and an overexpression Testin plasmid was constructed and transfected into H1299 cells. The mRNA and protein expression of RhoA, Rac1, and Cdc42 were detected using qRT PCR and western blot. On the basis of downregulating RhoA expression through overexpression of Testin, the overexpression plasmid of RhoA (TES+RhoA) was transfected simultaneously to induce a downregulation of RhoA expression, and the changes in malignant phenotype of lung adenocarcinoma cells were detected. The biological activity changes of adenocarcinoma cell lines after the above intervention were verified through CCK-8 experiment, Transwell experiment, and Matrigel experiment. Results The results of pathway analysis prediction showed that Testin may be involved in regulating the Rho GTPase signaling pathway. Overexpression of Testin did not affect the mRNA levels of RhoA, Rac1, and Cdc42 (all P>0.05), nor did it affect the protein expression levels of Rac1 and Cdc42 (all P>0.05), but it significantly reduced the protein level of RhoA (P<0.05). Knocking down RhoA in lung adenocarcinoma cell H1299 can significantly inhibit cell proliferation, migration, and invasion ability (all P<0.05). Simultaneously transfecting RhoA overexpression plasmid on the basis of overexpression of Testin can downregulate RhoA expression, but does not affect Testin expression. ConclusionsRhoA plays a pro-cancer role in lung adenocarcinoma, and Testin can inhibit RhoA expression. Overexpression of RhoA can rescue Testin's effect on lung adenocarcinoma cell proliferation, migration, and invasion. Testin exerts its anti-cancer biological activity by regulating RhoA.