The relative expressions of CyclinA and CDK2 proteins and mRNA in the cervical cancer group were significantly higher than those in the control group (P less then 0.05). Pearson correlation analysis showed a positive correlation between CyclinA and CDK2 proteins and mRNA expressions. After treatment, the expressions of CyclinA, CDK2 mRNA and SCCA, CEA and VEGF were significantly lower than those before treatment (P less then 0.05). The 3-year survival rate of CyclinA and CDK2 in the high expression group was significantly lower than that of the low expression group. CyclinA and CDK2 are highly expressed in advanced cervical cancer. The expression is decreased after chemotherapy. The prognosis of both low expressions is higher and the expression is good. It can be used to predict the efficacy and prognosis of cervical cancer in the clinic.This study aimed to explore the effects of miR-27a-3p-mediated Smurf2 on bleomycin A5-induced pulmonary fibrosis in rats. Sixty clean-grade SD rats were made into models of pulmonary fibrosis induced by bleomycin A5. They were randomly divided into the control group (fed as usual), the bleomycin A5 group, and the miR-27a-3p group according to the modeling. Pathological sections and morphological observations were performed on the lung tissues of all rats, and the expression of miR-27a-3p, Smurf2 mRNA, Smurf2 protein, collagen type I (Col I), collagen type III (Col III), and related inflammatory factors in lung tissues were measured. Dual fluorescein detection was performed for miR-27a-3p and Smurf2 in lung tissues. The lung tissue of rats in the bleomycin A5 group showed obvious pathological changes. The degree of pulmonary fibrosis in the miR-27a-3p group was significantly lower than that in the bleomycin A5 group. The expression levels of Smurf2 mRNA, Smurf2 protein, Col I, Col III, and related inflammatory factors in the lung tissue of rats in the control group were notably lower than rats in the bleomycin A5 group and the miR-27a-3p group (levels of those factors in the miR-27a-3p group were lower than the bleomycin A5 group). The expression level of miR-27a-3p in the lung tissue of rats in the control group was significantly higher than that in the bleomycin A5 group and the miR-27a-3p group (miR-27a-3p level in the miR-27a-3p group was significantly higher than in the bleomycin A5 group). Results of dual fluorescein detection demonstrated that Smurf2 was a direct target gene of miR-27a-3p, and the expression of miR-27a-3p negatively associated with Smurf2. Up-regulation of miR-27a-3p expression can effectively improve the disease degree and inflammatory response in rats with pulmonary fibrosis. Its mechanism may be achieved by regulating Smurf2.This study aimed to explore the expression of lncRNA-metastasis associated lung adenocarcinoma transcript 1 (lncRNA-MALAT1) in breast cancer (BC) patients and its influences on the prognosis of the patients. A total of 120 BC patients admitted to our hospital were enrolled as a BC group, of which 58 patients at I/II stage were treated with breast-conserving surgery as an operation group, and the other 62 patients at III/IV stage were treated with neoadjuvant chemotherapy combined with breast-conserving surgery as a combination group. Meantime, 100 healthy people in physical examination during the same period were enrolled as a normal group. The expression of serum lncRNA-MALAT1 in the subjects was determined, and the expression in BC patients and its influences on the patients were analyzed. LncRNA-MALAT1 was over-expressed in patients from the BC group, and the area-under-the-curve (AUC) of it for diagnosing BC was 0.911. After treatment, the expression of lncRNA-MALAT1 in the operation group and the combination group significantly decreased, and the expression of it in patients with good prognosis was greatly lower than that in patients with poor prognosis. The AUC of lncRNA-MALAT1 for predicting poor prognosis was 0.838, and TNM staging, pathological differentiation, tumor diameter, and lncRNA-MALAT1 were independent prognostic factors for poor prognosis of the patients. Furthermore, low expression of lncRNA-MALAT1 was associated with a relatively high 5-year overall survival (OS) of BC patients. The expression of lncRNA-MALAT1 was up-regulated in BC patients, while it was down-regulated in BC patients treated with breast-conserving surgery combined with neo-adjuvant chemotherapy, so lncRNA-MALAT1 can be used as a potential indicator for early diagnosis and prognosis prediction of BC patients.Intervertebral Disc (IVD) is a moderately moving joint that provides load transfer and flexibility to the entire spine. Although healthy IVD can balance the turnover of slow-synthesis matrices, this balance is often disrupted that leading to the development of degenerative diseases. The pathogenesis and treatment mechanism of Intervertebral Disc Degeneration (IDD) has always been the focus of scientific research, but its pathogenesis is still unknown. Therefore, this study is based on a modular approach to in-depth analysis and explore the genes of IDD, intended to identify the molecular process of disc degeneration. Firstly, the data related to Intervertebral Disc Degeneration and normal intervertebral disc were downloaded from the GEO database. The differential analysis of two kinds of data was performed to obtain differential gene expression profiles.  https://www.selleckchem.com/products/rk-701.html  Secondly, mapping those differential genes to Cytoscape to construct protein-protein interaction networks (PPIs). Then, the module gene was subjected to enrichment analysis of GO function and KEGG pathway. Finally, non-coding RNAs (ncRNAs) and transcription factors that regulate the module are predicted based on hypergeometric testing. In summary, we identified 22 co-expression modules, and the enrichment analysis results revealed that the module genes were significantly involved in the regulation of definite biotic procedures. In conclusion, we recognized the ncRNA pivot (including miR-193b-3p, CRNDE, etc.) and TF pivot (including E2F1, E2F4, etc.) that significantly regulate dysfunction modules.Cardiovascular disease (CVDs) is the leading cause of morbidity and death worldwide. Most genetic variants could be identified by several genome-wide-association-studies (GWAS), including within genes encoding proteins involved in the AKT/PI3K pathways that are related with an increased risk of metabolic syndrome and CVDs. Therefore, due to the importance of genetic variants in the prognosis of diseases, we examined the genetic polymorphism of AKT-rs1130233 located on chromosome 14 with cardiovascular risk factors. In this cross-sectional study, 721 subjects recruited from the Mashhad-Stroke and Heart-Atherosclerotic-Disorders (MASHAD) cohort study. The participants including 257 subjects with metabolic syndrome, 144 subjects with cardiovascular disease and 320 subjects as a control group. Anthropometric, biochemical and demographic information measures were prepared. Dietary assessment was managed by 24h dietary recall. DNA extraction and genotyping were carried out by using the TaqMan real-time-PCR based method.