LncRNA CASC11 upregulation promotes HDAC4 to alleviate oxidized low-density lipoprotein-induced injury of cardiac microvascular endothelial cells.

Long noncoding RNAs (LncRNAs) are essential to regulate the pathogenesis of coronary artery disease (CAD). This study was conducted to analyze the functionality of long noncoding RNA cancer susceptibility candidate 11 (lncRNA CASC11) in oxidized low-density lipoprotein (ox-LDL)-induced injury of cardiac microvascular endothelial cells (CMECs). CMECs were treated with ox-LDL to induce the CAD cell model. The cellular expression levels of CASC11 and histone deacetylase 4 (HDAC4) were determined by real-time quantitative polymerase chain reaction or Western blot assay. Cell absorbance, apoptosis, angiogenesis, and inflammation were evaluated by cell counting kit-8, flow cytometry, tube formation, and enzyme-linked immunosorbent assays. The subcellular localization of CASC11 was examined by the nuclear/cytoplasmic fractionation assay. The binding of human antigen R (HuR) to CASC11 and HDAC4 was analyzed by RNA immunoprecipitation. HDAC4 stability was determined after actinomycin D treatment. CASC11 was found to be decreased in the CAD cell model. CASC11 upregulation increased cell viability and angiogenesis and reduced apoptosis and inflammation. CASC11 bound to HuR and improved HDAC4 expression. HDAC4 downregulation counteracted the protective role of CASC11 overexpression in CMECs. In summary, CASC11 alleviated ox-LDL-induced injury of CMECs by binding to HuR and stabilizing HDAC4.

An ultra-sensitive and selective nitrogen dioxide sensor based on a novel P2C2 monolayer from a theoretical perspective.

The sensing properties of an α phase black phosphorus carbide (P2C2) monolayer for the adsorption of CO2, H2, H2O, N2, H2S, NH3, O2 and NO2 gases are theoretically investigated using first-principles calculations. We calculate the adsorption energy, equilibrium distance, Mulliken charge transfer, electron localization function, and work function to explore whether P2C2 is suitable for detecting NO2 gas. The results demonstrate that the P2C2 monolayer is highly sensitive and selective to NO2 gas molecules with robust adsorption energy and superior charge transfer due to the existence of strong orbital hybridization between the NO2 molecule and monolayer P2C2. In addition, the results of the work function calculations indicate that field effect transistor type NO2 gas sensors based on P2C2 monolayers are also feasible. Furthermore, the current-voltage curves reveal that the adsorption of NO2 can greatly modify the resistance of the P2C2 monolayer. Our results show that gas sensors based on P2C2 monolayers could be better than those based on black phosphorene (BP) for detecting NO2 molecules in an air mixture. In addition, the recovery time of the P2C2 sensor at T = 300 K was estimated to be short (and even shorter at higher temperatures) for NO2 which satisfies the demands for sustainable use.

Increasing FLAIR signal intensity in the postoperative cavity predicts progression in gross-total resected high-grade gliomas.

To evaluate the prognostic value of fluid-attenuated inversion recovery (FLAIR) signal intensity of postoperative cavity on progression free survival (PFS) and overall survival (OS) in patients with high-grade gliomas (HGG). This study retrospectively enrolled 45 consecutive HGG patients. These patients had chemoradiotherapy after gross-total resection of tumors. Quantitative analysis of the FLAIR signal intensity in postoperative cavity and background was made. We evaluated the threshold value, accuracy, sensitivity, specificity, and survival state with this technique. The patients who progressed and patients who did not progress were 33 and 12 cases separately. The ratio of postoperative cavity and background (C-B) on FLAIR sequence in patients who progressed was higher than that of patients who did not progress (P = 0.014). The PFS of the patients who progressed was shorter than that of patients who did not progress (P = 0.008). The area under ROC curve, threshold, sensitivity, specificity of C-B ratio for predicting tumor progression were 0.875, 62.3, 69.7, 0.84, and 0.50% respectively. The PFS of lower signal group was much longer than that of higher signal group (P = 0.004). The OS of the patients with higher signal was shorter than that of patients with lower signal (P = 0.034). The increase of gray value of FLAIR in postoperative cavity may be used as an imaging marker for predicting tumor progression.

Relaxin ameliorates high glucose-induced cardiomyocyte hypertrophy and apoptosis via the Notch1 pathway.

The present study aimed to investigate the role of relaxin (RLX) on high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis, as well as the possible molecular mechanism. H9c2 cells were exposed to 33 mmol/l HG with or without RLX (100 nmol/ml). Cell viability, apoptosis, oxidative stress, cell hypertrophy and the levels of Notch1, hairy and enhancer of split 1 (hes1), atrial natriuretic polypeptide (ANP), brain natriuretic peptide (BNP), manganese superoxide dismutase (MnSOD), cytochrome C and caspase-3 were assessed in cardiomyocytes. Compared with the HG group, the viability of H9c2 cells was increased by RLX in a time- and dose-dependent manner, and was accompanied with a significant reduction in apoptosis. Furthermore, RLX significantly suppressed the formation of reactive oxygen species and malondialdehyde, and enhanced the activity of SOD. In addition, the levels of ANP, BNP, cytochrome C and caspase-3 were increased and Notch1, hes1 and MnSOD were inhibited in the HG group compared with those in the normal group. However, the Notch inhibitor DAPT almost abolished the protective effects of RLX. These results suggested that RLX protected cardiomyocytes from HG-induced hypertrophy and apoptosis partly through a Notch1-dependent pathway, which may be associated with reducing oxidative stress.