Search

Non-small cell lung cancer (NSCLC) is the first cause of cancer related death in the world. Biomarkers to predict the relapse and drug resistance could be extremely useful for a clinical doctor to monitor high risk patients and select rational regimen. miRNAs play an important role in lung cancer and detection samples are relatively easy to be obtained, miRNAs could become a promising means of comprehending the oncogenesis and pathogenesis of lung cancer. This study aimed to investigate the function of miR-145 to work as a biomarker in NSCLC. miR-145 expression level in 48 NSCLC tumor tissues and their matched normal tissues were detected by qRT-PCR. miR-145 in 18 paraffin-embedded samples underwent chemotherapy and were assessed by in situ hybridization (ISH). Here we show that miR-145 was down-regulated in NSCLC tissues; down-regulation of miR-145 was correlated with late clinical stage and poorly differentiated carcinoma, and, low expression level of miR-145 could also predict chemotherapy resistance and shorter disease-free survival (DFS). These findings indicated that miR-145 expression may be a useful prognostic marker that could be used for predicting poor differentiation, chemo-resistance and shore DFS. [ABSTRACT FROM AUTHOR]

With the increasing penetration of information and communication technologies (ICTs) in energy systems, traditional energy systems are being digitized. Advanced analysis of the energy production and consumption data and data-driven decision support can be combined to promote the formation and development of smart energy systems. Smart grids are a specific application of smart energy systems. Different electricity consumption patterns of residential users can be discovered and extracted by clustering analysis of the electricity consumption data collected by smart meters and other data acquisition terminals in a smart grid. This research explores daily electricity consumption patterns of low-voltage residential users in China. The service architecture of smart power use and the structure of electric energy data acquisition system of the State Grid Corporation of China (SGCC) are introduced and a process model for mining daily electricity consumption data is presented. The analysis is based on the fuzzy c-means (FCM) clustering method and a fuzzy cluster validity index (PBMF). A case study of Kunshan City, Jiangsu Province, China is presented, using the daily electricity consumption data of 1312 low-voltage users within a month. [ABSTRACT FROM AUTHOR]

Background TKI-acquired resistance is a tough obstacle for effectively treating NSCLC patients with EGFR mutant characteristics. T790M mutations and MET amplifications account for 70% of the acquired resistance, but the causes for the remaining 30% need elucidation. Methods We detected TGF-β1and PTEN expression levels in 51 NSCLC patients undergoing EGFR-TKI treatment using Immunohistochemistry (IHC) assay. We examined erlotinib sensitivity, apoptosis rate, and invasion ability in PC-9 cells and PC-9/TGF-β1 cells with CCK-8, flow cytometry, and trans-well assays. We examined and analyzed the AKT and ERK pathways’ expression levels using western blot. Results High TGF-β1 and low PTEN expression levels were correlated with poor EGFR-TKI sensitivity and overall survival in 51 NSCLC samples. In vitro analysis revealed that TGF-β1 could reduce erlotinib sensitivity, increase anti-apoptosis ability and invasive characteristic in TKI-sensitive PC-9 cell lines by down-regulating PTEN and activating the Akt and ERK pathways. Conclusions The results suggest that TGF-β1 demonstrated another acquired erlotinib resistance by down-regulating PTEN expression. [ABSTRACT FROM AUTHOR]

NbMoSiN composite and gradient films were deposited by magnetron sputtering with nitrogen flow design, and their structural, electrochemical and tribological behaviors in simulated body fluids were investigated. The results revealed that the NbMoSiN composite film composed β -Nb 2 N, MoSi 2 nanocrystals, Si 3 N 4 , and amorphous phases, while the NbMoSiN gradient film was completely amorphous. The film with 30 sccm nitrogen flow demonstrated enhanced corrosion resistance, attributed to the increased MoSi 2 and Si 3 N 4. The gradient film exhibited poor passivation ability and compositional inhomogeneity, leading to accelerated corrosion. The film's wear rate at 10 sccm nitrogen flow was significantly lower due to the hard nitride phase and multiphase interface strengthening. Higher nitrogen flow increased the silicide phase and reduced the friction coefficient through hydration. • NbMoSiN composite and gradient films were deposited by DC magnetron sputtering. • Tribological and anticorrosion mechanisms in simulated body fluids were discussed. • The hydration lubrication at the wear track resulted in a lower friction coefficient. • This study provides a potential method for surface modification of 316 L implants. [ABSTRACT FROM AUTHOR]

[Display omitted] Berberine, a natural isoquinoline alkaloid, exhibits a variety of pharmacological effects, but the pharmacological targets and mechanisms remain elusive. Here, we report a novel finding that berberine inhibits acetylcholine (ACh)-induced intracellular Ca2+ oscillations, mediated through an inhibition of the muscarinic subtype 3 (M 3) receptor. Patch-clamp recordings and confocal Ca2+ imaging were applied to acute dissociated pancreatic acinar cells prepared from CD1 mice to examine the effects of berberine on ACh-induced Ca2+ oscillations. Whole-cell patch-clamp recordings showed that berberine (from 0.1 to 10 µM) reduced ACh-induced Ca2+ oscillations in a concentration-dependent manner, and this inhibition also depended on ACh concentrations. The inhibitory effect of berberine neither occurred in intracellular targets nor extracellular cholecystokinin (CCK) receptors, chloride (Cl-) channels, and store-operated Ca2+ channels. Together, the results demonstrate that berberine directly inhibits the muscarinic M 3 receptors, further confirmed by evidence of the interaction between berberine and M 3 receptors in pancreatic acinar cells. [ABSTRACT FROM AUTHOR]

The α7 nicotinic acetylcholine receptor (α7 nAChR) is highly expressed in the brain, where it maintains various neuronal functions including (but not limited to) learning and memory. In addition, the protein expression levels of α7 nAChRs are altered in various brain disorders. The classic rule governing α7 nAChR assembly in the mammalian brain was that it was assembled from five α7 subunits to form a homomeric receptor pentamer. However, emerging evidence demonstrates the presence of heteromeric α7 nAChRs in heterologously expressed systems and naturally in brain neurons, where α7 subunits are co-assembled with β2 subunits to form a novel type of α7β2 nAChR. Interestingly, the α7β2 nAChR exhibits distinctive function and pharmacology from traditional homomeric α7 nAChRs. We review recent advances in probing the distribution, function, pharmacology, pathophysiology, and stoichiometry of the heteromeric α7β2 nAChR, which have provided new insights into the understanding of a novel target of cholinergic signaling. [ABSTRACT FROM AUTHOR]