Objective To study the eorrelation between the plasma cardiotrophin-1(CT-1)level and cardiac function of patients with diabetic cardiopathy.Methods Using the Biotin-StreptAvidin-enzyme-linked immunosorbent assay(BSA-ELISA),the level of plasma CT-1 jn 35 normal controls,40 patients with type 2 diabetes and 60 patients with diabetic cardiopathy was measured.The relation to heart function was observed.Results The difference of plasma CT-1 level in the three groups was significant(all P＜0.05).The level of plasma CT-1 in diabetic cardiopathy group was apparently higher than that of type 2 diabetes group and normal controls(all P＜0.01);The level in type 2 diabetes group was significantly higher than that of normal controls(P＜0.01).The level of plasma CT-1 elevated with the worsening of heart failure(NYHA classification).The level of plasma CT-1 was correlated with EF(r=0.669,P＜0.01);LAD(r=0.528,P＜0.01);PVE(r=0.502,P＜0.01);CK-MB(r=0.312,P＜0.01);TG(r=0.187,P＜0.05);DBP(r=0.158,P＜0.05)o Stepwise regression analysis revealed that EF and LAD were the most significant agents affecting the plasma CT-1.Conclusion The plasma CT-1 level could reflect the state of cardiac function of diabetic cardiopathy patient,it could help to diagnose diabetic cardiopathy earlier.

BACKGROUND: The occurrence and development of lung cancer are closely linked to epigenetic modification. Abnormal DNA methylation in the CpG island region of genes has been found in many cancers. Protein kinase C delta binding protein (PRKCDBP) is a potential tumor suppressor and its epigenetic changes are found in many human malignancies. This study investigated the possibility of PRKCDBP methylation as a potential biomarker for non-small cell lung cancer (NSCLC). METHODS: We measured the methylation levels of PRKCDBP in the three groups of NSCLC tissues. Promoter activity was measured by the dual luciferase assay, with 5'-aza-deoxycytidine to examine the effect of demethylation on the expression level of PRKCDBP. RESULTS: The methylation levels of PRKCDBP in tumor tissues and 3 cm para-tumor were higher than those of distant (>10 cm) non-tumor tissues. Receiver operating characteristic (ROC) curve analysis between tumor tissues and distant non-tumor tissues showed that the area under the line (AUC) was 0.717. Dual luciferase experiment confirmed that the promoter region was able to promote gene expression. Meanwhile, in vitro methylation of the fragment (PRKCDBP_Me) could significantly reduce the promoter activity of the fragment. Demethylation of 5'-aza-deoxycytidine in lung cancer cell lines A549 and H1299 showed a significant up-regulation of PRKCDBP mRNA levels. CONCLUSIONS PRKCDBP methylation is a potential and promising candidate biomarker for non-small cell lung cancer.
Biomarkers/metabolism* ; Carcinoma, Non-Small-Cell Lung/pathology* ; Cell Line, Tumor ; DNA Methylation ; Gene Expression Regulation, Neoplastic ; Humans ; Intracellular Signaling Peptides and Proteins/genetics* ; Lung Neoplasms/pathology* ; Promoter Regions, Genetic