Objective To explore the clinical application effect of squamous cell carcinoma antigen (SCC) ,cancer embryo antigen (CEA) and carbohydrate antigen 125(CA125) chemiluminescence combined detection in early diagnosis of lung cancer .Methods The SCC ,CEA and CA125 levels in the patients with early stage lung cancer ,benign lung diseases and healthy subjects undergoing physical examination were detected by using the automatic chemiluminescence immune analyzer .Results The concentrations of three tumor markers in the lung cancer group were significantly higher than those in the benign disease group and control group (P<0 .05);t he concentrations of CEA and CA125 in the adenocarcinoma patients with were significantly higher than those in the patients with squamous cell carcinoma and small cell carcinoma (P<0 .05) .The concentration of SCC in the patients with squamous cell carcinoma was significantly higher than that in the patients with adenocarcinoma and small cell lung cancer (P<0 .05) .The sen-sitivity ,specificity ,positive predictive value and negative predictive value of combined detection of three tumor markers were signifi-cantly better than that of single tumor marker ,and the difference was statistically significant (P<0 .05) .Conclusion The combined detection of SCC ,CEA and CA125 can be used in the early diagnosis of lung cancer and has the promotion value .

Pulmonary hypertension (PH) is an extremely malignant pulmonary vascular disease of unknown etiology. ADAR1 is an RNA editing enzyme that converts adenosine in RNA to inosine, thereby affecting RNA expression. However, the role of ADAR1 in PH development remains unclear. In the present study, we investigated the biological role and molecular mechanism of ADAR1 in PH pulmonary vascular remodeling. Overexpression of ADAR1 aggravated PH progression and promoted the proliferation of pulmonary artery smooth muscle cells (PASMCs). Conversely, inhibition of ADAR1 produced opposite effects. High-throughput whole transcriptome sequencing showed that ADAR1 was an important regulator of circRNAs in PH. CircCDK17 level was significantly lowered in the serum of PH patients. The effects of ADAR1 on cell cycle progression and proliferation were mediated by circCDK17. ADAR1 affects the stability of circCDK17 by mediating A-to-I modification at the A5 and A293 sites of circCDK17 to prevent it from m1A modification. We demonstrate for the first time that ADAR1 contributes to the PH development, at least partially, through m1A modification of circCDK17 and the subsequent PASMCs proliferation. Our study provides a novel therapeutic strategy for treatment of PH and the evidence for circCDK17 as a potential novel marker for the diagnosis of this disease.