Composites of Vanadium (III) Oxide (VO) Incorporating with Amorphous C as Pt-Free Counter Electrodes for Low-Cost and High-Performance Dye-Sensitized Solar Cells.

To replace precious Pt-based counter electrodes (CEs) with a low-cost Pt-free catalyst of CEs is still a motivating hotspot to decrease the fabrication cost of dye-sensitized solar cells (DSSCs). Herein, four different VO@C composite catalysts were synthesized by pyrolysis of a precursor under N flow at 1100 °C and further served as catalytic materials of CEs for the encapsulation of DSSCs. The precursors of VO@C composites have been prepared via a sol-gel method using different proportions of VO with soluble starch in a HO solution.

Highly efficient Mo2C nanotubes as a counter electrode catalyst for organic redox shuttles in dye-sensitized solar cells.

Molybdenum carbide nanotubes (Mo2C-NTs) were synthesized and showed remarkable catalytic activity for regeneration of an organic sulfide redox shuttle. The dye-sensitized solar cells (DSCs) using Mo2C-NTs as the counter electrode (CE) showed a high power conversion efficiency of 6.22%, which is much higher than the DSCs using a conventional Pt CE (3.

Differential effects of the β-adrenoceptor blockers carvedilol and metoprolol on SQT1- and SQT2-mutant channels.

Background: N588K-KCNH2 and V307L-KCNQ1 mutations lead to a gain-of-function of IKr and IKs thus causing short-QT syndromes (SQT1, SQT2). Combined pharmacotherapies using K(+) -channel-blockers and β-blockers are effective in SQTS. Since β-blockers can block IKr and IKs , we aimed at determining carvedilol's and metoprolol's electrophysiological effects on N588K-KCNH2 and V307L-KCNQ1 channels.

Standard molar enthalpy of combustion and formation of quaternary ammonium tetrachlorozincate [n-CnH2n+1 N(CH3)3]2 ZnCl4.

The standard molar enthalpy of combustion (Δc H (o) m) and formation (Δf H (o) m) of quaternary ammonium tetrachlorozincate [n-CnH2n+1N(CH3)3]2ZnCl4 have been determined for the hydrocarbon chain length from even number 8 to 18 of carbon atoms (n) by an oxygen-bomb combustion calorimeter. The results indicated that the values of Δc H (o) m increased and Δf H (o) m decreased with increasing chain length and showed a linear dependence on the number of carbon atoms, which were caused by that the order and rigidity of the hydrocarbon chain decreased with increasing the carbon atoms. The linear regression equations are -Δc H (o) m =1440.

Great improvement of catalytic activity of oxide counter electrodes fabricated in N2 atmosphere for dye-sensitized solar cells.

The dye-sensitized solar cells (DSCs) using SnO(2) and Nb(2)O(5) counter electrodes (CEs) prepared in N(2) atmosphere yielded power conversion efficiencies (PCE) of 6.09% and 4.65%, much higher than the PCE values (1.

Pharmacological activation of Kv11.1 in transgenic long QT-1 rabbits.

Transgenic rabbits expressing pore mutants of K(V)7.1 display a long QT syndrome 1 (LQT1) phenotype. Recently, NS1643 has been described to increase I(Kr).

Nicorandil normalizes prolonged repolarisation in the first transgenic rabbit model with Long-QT syndrome 1 both in vitro and in vivo.

Transgenic rabbits expressing loss-of-function pore mutants of the human gene KCNQ1 (K(v)LQT1-Y315S) have a Long QT-Syndrome 1 (LQT1) phenotype. We evaluated for the first time the effect of nicorandil, an opener of ATP-sensitive potassium channels, and of isoproterenol on cardiac action potential duration and heart rate dependent dispersion of repolarisation in transgenic LQT1 rabbits. In vivo LQT1 and littermate control were subjected to transvenous electrophysiological studies; in vitro monophasic action potentials were recorded from explanted Langendorff-perfused hearts.

Prosthetic valve endocarditis due to Actinomyces neuii successfully treated with antibiotic therapy.

Endocarditis due to Actinomyces neuii is a rare disease, with only 14 reported cases. Recently, A. neuii was added to the list of species implicated in endocarditis of native valves.

Direct block of hERG potassium channels by the protein kinase C inhibitor bisindolylmaleimide I (GF109203X).

Objective: The human ether-a-go-go-related gene (hERG) encodes the rapid component of the cardiac repolarizing delayed rectifier potassium current, I(Kr). The direct interaction of the commonly used protein kinase C (PKC) inhibitor bisindolylmaleimide I (BIM I) with hERG, KvLQT1/minK, and I(Kr) currents was investigated in this study.

Methods: hERG and KvLQT1/minK channels were heterologously expressed in Xenopus laevis oocytes, and currents were measured using the two-microelectrode voltage clamp technique.

Activation of cardiac human ether-a-go-go related gene potassium currents is regulated by alpha(1A)-adrenoceptors.

Patients with cardiac disease typically develop life-threatening ventricular arrhythmias during physical or emotional stress, suggesting a link between adrenergic stimulation and regulation of the cardiac action potential. Human ether-a-go-go related gene (hERG) potassium channels conduct the rapid component of the repolarizing delayed rectifier potassium current, I(Kr). Previous studies have revealed that hERG channel activation is modulated by activation of the beta-adrenergic system.

Inhibition of cardiac HERG currents by the DNA topoisomerase II inhibitor amsacrine: mode of action.

1 The topoisomerase II inhibitor amsacrine is used in the treatment of acute myelogenous leukemia. Although most anticancer drugs are believed not to cause acquired long QT syndrome (LQTS), concerns have been raised by reports of QT interval prolongation, ventricular fibrillation and death associated with amsacrine treatment. Since blockade of cardiac human ether-a-go-go-related gene (HERG) potassium currents is an important cause of acquired LQTS, we investigated the acute effects of amsacrine on cloned HERG channels to determine the electrophysiological basis for its proarrhythmic potential.

Inhibition of human ether-a-go-go-related gene potassium channels by alpha 1-adrenoceptor antagonists prazosin, doxazosin, and terazosin.

Human ether-a-go-go-related gene (HERG) potassium channels are expressed in multiple tissues including the heart and adenocarcinomas. In cardiomyocytes, HERG encodes the alpha-subunit underlying the rapid component of the delayed rectifier potassium current, I(Kr), and pharmacological reduction of HERG currents may cause acquired long QT syndrome. In addition, HERG currents have been shown to be involved in the regulation of cell proliferation and apoptosis.

Acute effects of dronedarone on both components of the cardiac delayed rectifier K+ current, HERG and KvLQT1/minK potassium channels.

Dronedarone is a noniodinated benzofuran derivative that has been synthesized to overcome the limiting iodine-associated adverse effects of the potent antiarrhythmic drug amiodarone. In this study, the acute electrophysiological effects of dronedarone on repolarizing potassium channels were investigated to determine the class III antiarrhythmic action of this compound. HERG and KvLQT1/minK potassium channels conduct the delayed rectifier potassium current IK in human heart, being a primary target for class III antiarrhythmic therapy.

Regulation of HERG potassium channel activation by protein kinase C independent of direct phosphorylation of the channel protein.

Objective: Patients with HERG-associated long QT syndrome typically develop tachyarrhythmias during physical or emotional stress. Previous studies have revealed that activation of the beta-adrenergic system and consecutive elevation of the intracellular cAMP concentration regulate HERG channels via protein kinase A-mediated phosphorylation of the channel protein and via direct interaction with the cAMP binding site of HERG. In contrast, the influence of the alpha-adrenergic signal transduction cascade on HERG currents as suggested by recent reports is less well understood.

Inhibition of cloned HERG potassium channels by the antiestrogen tamoxifen.

Tamoxifen is a nonsteroidal antiestrogen that is commonly used in the treatment of breast cancer. Although antiestrogenic drugs are generally believed not to cause acquired long QT syndrome (LQTS), concerns have been raised by recent reports of QT interval prolongation associated with tamoxifen treatment. Since blockade of human ether-a-go-go-related gene (HERG) potassium channels is critical in the development of acquired LQTS, we investigated the effects of tamoxifen on cloned HERG potassium channels to determine the electrophysiological basis for the arrhythmogenic potential of this drug.

The antipsychotic drug chlorpromazine inhibits HERG potassium channels.

(1) Acquired long QT syndrome (aLQTS) is caused by prolongation of the cardiac action potential because of blockade of cardiac ion channels and delayed repolarization of the heart. Patients with aLQTS carry an increased risk for torsade de pointes arrhythmias and sudden cardiac death. Several antipsychotic drugs may cause aLQTS.