Metal diffusion from magnesium–silver cathodes and indium–tin–oxide anodes in organic light-emitting diodes has been investigated. Magnesium showed no substantial diffusion under device operation and had no significant effects on luminance decay with operation time. Indium was immobile in storage at room temperature, while indium penetration into organic layers was observed after device operation. The presence of indium in organic films showed a correlation with performance degradation.

In the fabrication of polymeric electroluminescent devices with indium-tin oxide (ITO) as anode, indium contamination of the polymers can greatly degrade the device performance. In the present study, we have used x-ray photoelectron spectroscopy to measure indium incorporation in poly(3,4-ethylene dioxythiophene):poly(styrene sulphonate), referred to as PEDOT:PSS, which were spincast on bare ITO and encapsulated ITO. We found that the deposition of a self-assembled monolayer of alkylsiloxanes on ITO prior to spincasting PEDOT:PSS was effective and practical in blocking the reactions between ITO and PEDOT:PSS.

Background: MicroRNA-21 is important in hepatic fibrosis development, but the mechanism is unclear. Results: MicroRNA-21 is predominantly up-regulated in activated hepatic stellate cells and could form a double negative feedback loop that links fibrogenic machinery. Conclusion:The microRNA-21-mediated loop is a main driving force for hepatic fibrosis progression. Significance: It suggests a mechanism for how microRNA-21 contributes to hepatic fibrosis.Sustained activation of hepatic stellate cells (HSCs) leads to hepatic fibrosis, which is characterized by excessive collagen production, and for which there is no available drug clinically. Despite tremendous progress, the cellular activities underlying HSC activation, especially the driving force in the perpetuation stage, are only partially understood. Recently, microRNA-21 (miR-21) has been found to be prevalently up-regulated during fibrogenesis in different tissues, although its detailed role needs to be further elucidated. In the present study, miR-21 expression was examined in human cirrhotic liver samples and in murine fibrotic livers induced by thioacetamide or carbon tetrachloride. A dramatic miR-21 increase was noted in activated HSCs. We further found that miR-21 maintained itself at constant high levels by using a microRNA-21/programmed cell death protein 4/activation protein-1 (miR-21/PDCD4/AP-1) feedback loop. Disrupting this loop with miR-21 antagomir or AP-1 inhibitors significantly suppressed fibrogenic activities in HSCs and ameliorated liver fibrosis. In contrast, reinforcing this loop with small interfering RNA (siRNA) against PDCD4 promoted fibrogenesis in HSCs. Further analysis indicated that the up-regulated miR-21 promoted the central transforming growth factor-␤ (TGF-␤) signaling pathway underlying HSC activation. In summary, we suggest that the miR-21/PDCD4/AP-1 autoregulatory loop is one of the main driving forces for hepatic fibrosis progression. Targeting this aberrantly activated feedback loop may provide a new therapeutic strategy and facilitate drug discovery against hepatic fibrosis.Hepatic fibrosis is a wound healing process in response to chronic liver injuries that leads to unbalanced extracellular matrix (ECM) 3 deposition and resolution. The persistent activation of wound healing responses causes quantitative and qualitative changes in the ECM components and could finally distort liver parenchyma and vascular architecture, which could impair liver function and potentially lead to liver failure and hepatocellular carcinoma. Following liver injury, quiescent hepatic stellate cells (HSCs) transdifferentiate into myofibroblast-like cells that are characterized by the expression of smooth muscle ␣-actin (␣-SMA) and enhanced production of ECM (1). Despite the tremendous progress in understanding the mechanisms during fibrogenesis, the driving force underlying the persistent fibrogenic activities is still only partially understood.Extensive studies have suggested the central role of feedback networks in dictating disease progressi...

Strategies to modify nanoparticles with biological ligands for targeted drug delivery in vivo have been widely studied but met with limited clinical success. A possible reason is that, in the blood circulation, serum proteins could rapidly form a layer of protein "corona" on the vehicle surface, which might block the modified ligands and hamper their targeting functions. We speculate that strategies for drug delivery can be designed based upon elegant control of the corona formation on the vehicle surfaces. In this study, we demonstrate a retinol-conjugated polyetherimine (RcP) nanoparticle system that selectively recruited the retinol binding protein 4 (RBP) in its corona components. RBP was found to bind retinol, and direct the antisense oligonucleotide (ASO)-laden RcP carrier to hepatic stellate cells (HSC), which play essential roles in the progression of hepatic fibrosis. In both mouse fibrosis models, induced by carbon tetrachloride (CCl4) and bile duct ligation (BDL), respectively, the ASO-laden RcP particles effectively suppressed the expression of type I collagen (collagen I), and consequently ameliorated hepatic fibrosis. Such findings suggest that this delivery system, designed to exploit the power of corona proteins, can serve as a promising tool for targeted delivery of therapeutic agents for the treatment of hepatic fibrosis.

A bright-blue electroluminescent device has been fabricated by using an emissive dopant and an electron-transporting host. The dopant was a highly photoluminescent silyl-substituted ter-(phenylene–vinylene) derivative [1,4-bis[4-(2-trimethylsilylvinly) styryl]-2,5-dibutoxybenzene (BTSB)]. BTSB was doped into a trimer of N-arylbenzimidazoles (TPBI) which functioned as the host and electron transporter. N,N′-bis-(1-naphthyl)-N,N′-diphenyl-1,1′-biphenyl-4-4′-diamine (NPB) was used as the hole transporter. The device, with a structure of indium tin oxide\NPB\TPBI:10%BTSB\TPBI\Mg:Ag, shows a bright blue emission of 11000 cd/m2 at a current density of 360 mA/cm2. The current efficiency of this device is about 3.2 cd/A at 20 mA/cm2.

General Information: All reactions were performed under nitrogen. Solvents were carefully dried and distilled from appropriate drying agents prior to use. Commercially available reagents were used without further purification unless otherwise stated. All reactions were monitored by thin-layer chromatography (TLC) with Merck pre-coated glass plates. Flash column chromatography and preparative TLC were carried out using silica gel from Merck (230-400 mesh). Fast atom bombardment (FAB) mass spectra were recorded on a Finnigan MAT SSQ710 system. Proton NMR spectra were Ferrocene was added as a calibrant after each set of measurements, and all potentials reported were quoted with reference to the ferrocene-ferrocenium (Fc/Fc + ) couple at a scan rate of 100 mV s −1 .Thermal analyses were performed with the Perkin-Elmer TGA6 thermal analyzer.

An anthracene carboxamide derivative of the excited-state intramolecular proton-transfer compound of 2-(2'-hydroxyphenyl)benzothiazole has been newly developed to produce the prominent characteristics of aggregation-induced enhanced emission (AIEE) with a high solid-state fluorescence quantum efficiency of 78.1%. Compared with our previously reported phenyl carboxamide derivatives, a small tailoring of the molecular structure was found to result in a big difference in the dominant factor of the AIEE mechanism. In the phenyl carboxamide derivatives, the dominant factor of the AIEE mechanism is the restriction of the twisted intramolecular charge transfer (TICT) of the enol excited state, regardless of their different aggregation modes. In the anthracene carboxamide derivative, N-(3-(benzo[d]thiazol-2-yl)-4-hydroxyphenyl) anthracene-9-carboxamide, the AIEE characteristics are not dependent on the restriction of TICT, but mainly attributed to the cooperative effects of J-aggregation and the restriction of the cis-trans tautomerization in the keto excited state. A specific N···π interaction was found to be the main driving force for this J-aggregation, as revealed by the single crystal analysis. The AIEE mechanism of this anthracene carboxamide derivative was studied in detail through photophysical investigations and theoretical calculations. On the basis of its AIEE characteristics, a stable non-doped organic light-emitting diode was achieved, with high color purity and a remarkably low efficiency roll-off.

Electron mobility in tris(8-hydroxyquinoline)aluminum ( Al q 3 ) films by transient electroluminescence from single layer organic light emitting diodes A dinuclear aluminum 8-hydroxyquinoline complex with high electron mobility for organic light-emitting diodes Electron mobility in tris(8-hydroxy-quinoline)aluminum thin films determined via transient electroluminescence from single-and multilayer organic light-emitting diodes