OBJECTIVE Peripherally inserted central catheter (PICC) is being increasingly used in critical care settings. However, PICC is associated with various complications, particularly venous thrombosis. Our aim was to observe the effects of preventive application of low molecular weight heparin on venous thrombosis in a PICC model. METHODS All rabbits were randomly divided into four groups a control group, and low/medium/high concentration of low molecular weight heparin groups. All rabbits were injected prophylactically with normal saline or low molecular weight heparin once a day for 7 days. A PICC model was constructed. The pathologic changes of ear vein, anterior vena cava, and venous thrombosis were investigated using hematoxylin and eosin (H&E). Biochemical testing was performed including prothrombin time (PT), activated partial thromboplastin time (APTT), and thrombin time (TT). Serum D-dimer (D2D) and fibrinogen (FG) levels were detected using Enzyme-linked immunosorbent assay (ELISA). RESULTS X-ray results showed that the PICC model was successfully constructed. H&E results showed that preventive application of low molecular weight heparin significantly ameliorated the pathologic damage to ear vein and anterior vena cava in the PICC model. Furthermore, we found that preventive application of low molecular weight heparin inhibited venous thrombosis in the model by H&E stain. Moreover, it significantly reduced serum FG and D2D levels in PICC model. Biochemical testing results showed that PT, APTT, and TT were significantly elevated in the PICC model. CONCLUSION Our findings revealed that preventive application of low molecular weight heparin significantly ameliorates venous thrombosis in a PICC model. IJCEP Copyright © 2020.BACKGROUND Breast cancer (BC) is a common cancer with high incidence in women worldwide. Although there are some studies focusing on the pathogenesis of BC, the regulatory mechanism needs to be further investigated. The function of lncRNA and miRNA has been demonstrated to participate in cell progression of BC. However, the function of SNHG12 has not been clearly elucidated. METHODS We detected the expression of SNHG12 and miR-451a using quantitative real-time PCR (qRT-PCR). The protein expression of AKT, p-AKT, mTOR and p-mTOR were measured using western blot. The relationship between SNHG12 and miR-451a was confirmed by luciferase reporter assay. Cell proliferation was measured using MTT assay. Transwell assay was used to detect cell migration and invasion. Xenograft transplantation was used to detect the function of SNHG12 in vivo. RESULTS In this study, we found that SNHG12 was significantly increased in BC tissues and cells. Knockdown of SNHG12 inhibited BC cell proliferation, invasion, and migration in vitro as well as suppressed tumor growth in vivo. In addition, miR-451a expression was obviously down-regulated in BC tissues and had negative correlation with SNHG12.  https://www.selleckchem.com/products/pf-06821497.html  Luciferase reporter assay determined that miR-451a was a target miRNA of SNHG12. Notably, SNHG12 knockdown decreased cell proliferation, migration, invasion, and AKT/mTOR pathway activation which could be reversed by down-regulation of miR-451a. CONCLUSION Knockdown of SNHG12 inhibited cell proliferation, invasion, and migration by regulating miR-451a through suppression of AKT/mTOR pathway in BC. IJCEP Copyright © 2020.We aimed to investigate the effect of Keap1/Nrf2 pathway on the biologic function of trophoblast cells in the oxidative stress model at the cellular level, and analyze the expression levels and clinical significance of Keap1/Nrf2 related antioxidant factors in placental tissues of preeclampsia (PE) patients at clinical level. In this study, we found that under hypoxia/reoxygenation conditions, the activities of oxidative stress-related enzymes (CAT, GSH-Px, SOD) in HTR8/SVneo cells were significantly lower than those before treatment (P less then 0.01). The activities of CAT, GSH-Px and SOD in HTR8/SVneo cells in siRNA+H/R group decreased significantly (P less then 0.01), which indicated the important defensive effect of Keap1/Nrf2 pathway in oxidative stress. Compared with Nrf2 siRNA+H/R group, Si-NC+H/R group had CAT, GSH-Px and SOD activities decreasing, which were similar to those in the H/R group. Moreover, the activities of oxidative stress-related active enzymes in patients with preeclampsia were further confirmed by detecting and comparing the activities of CAT, GSH-Px and SOD in placental tissues. The results showed that the activities of SOD (P less then 0.001), GSH-Px (P less then 0.01) and CAT (P less then 0.01) in placental tissues of patients with PE were significant different from those of normal placental tissues. The expression level of Keap1 in placenta of patients with PE was slightly lower than that of normal placenta, while the expression of Nrf2 and HO-1 in placenta of patients with PE were significantly higher than those of normal placenta, which implicated the importance of Keap-1/Nrf2 pathway in PE. IJCEP Copyright © 2020.The purpose of the present study was to enhance understanding of the molecular mechanisms underpinning head and neck squamous cell carcinoma (HNSCC). Microarray datasets were obtained from the gene expression omnibus database. By a bioinformatics method, 109 differentially expressed genes were identified between the two mRNA datasets, and these genes were classified primarily into biological process, molecular function, or cellular component. In the protein-protein interaction network analysis, top 20 hub genes were identified, and five (SERPINE1, SERPINH1, SPP1, PLAU and MMP1) of them were associated with the prognosis of HNSCC patients. Immunohistochemistry result also showed that the expression of the proteins encoded by these five genes were significantly upregulated in HNSCC, matching the bioinformatics analysis. Moreover, 28 differentially expressed miRNAs were also identified, with miR-196a and miR-1 being most upregulated and downregulated respectively. Our results provide potential biomarkers for HNSCC and may improve understanding of the molecular mechanisms underlying HNSCC. IJCEP Copyright © 2020.