Barbaloin inhibits ventricular arrhythmias in rabbits by modulating voltage-gated ion channels.

Barbaloin (10-ß-D-glucopyranosyl-1,8-dihydroxy-3-(hydroxymethyl)-9(10H)-anthracenone) is extracted from the aloe plant and has been reported to have anti-inflammatory, antitumor, antibacterial, and other biological activities. Here, we investigated the effects of barbaloin on cardiac electrophysiology, which has not been reported thus far. Cardiac action potentials (APs) and ionic currents were recorded in isolated rabbit ventricular myocytes using whole-cell patch-clamp technique. Additionally, the antiarrhythmic effect of barbaloin was examined in Langendorff-perfused rabbit hearts. In current-clamp recording, application of barbaloin (100 and 200 µmol/L) dose-dependently reduced the action potential duration (APD) and the maximum depolarization velocity (Vmax), and attenuated APD reverse-rate dependence (RRD) in ventricular myocytes. Furthermore, barbaloin (100 and 200 µmol/L) effectively eliminated ATX II-induced early afterdepolarizations (EADs) and Ca2+-induced delayed afterdepolarizations (DADs) in ventricular myocytes. In voltage-clamp recording, barbaloin (10-200 µmol/L) dose-dependently inhibited L-type calcium current (ICa.L) and peak sodium current (INa.P) with IC50 values of 137.06 and 559.80 µmol/L, respectively. Application of barbaloin (100, 200 µmol/L) decreased ATX II-enhanced late sodium current (INa.L) by 36.6%±3.3% and 71.8%±6.5%, respectively. However, barbaloin up to 800 µmol/L did not affect the inward rectifier potassium current (IK1) or the rapidly activated delayed rectifier potassium current (IKr) in ventricular myocytes. In Langendorff-perfused rabbit hearts, barbaloin (200 µmol/L) significantly inhibited aconitine-induced ventricular arrhythmias. These results demonstrate that barbaloin has potential as an antiarrhythmic drug.

Performance of field-effect transistors based on Nb(x)W(1-x)S2 monolayers.

The Schottky barrier has been detected in many field-effect transistors (FETs) based on transition metal dichalcogenide (TMD) semiconductors and has seriously affected the electronic properties of the devices. In order to decrease the Schottky barrier in WS2 FETs, novel Nb doping in WS2 monolayers has been performed and p-FETs based on Nb-doped WS2 (Nb(x)W(1-x)S2) monolayers as the active channel have been fabricated for the first time. The monolayer Nb0.15W0.85S2 p-FET has a drain current of 330 µA µm(-1), an impressive I(ON)/I(OFF) of 10(7), and a high effective hole mobility of ∼146 cm(2) V(-1) s(-1). The novel Nb doping in monolayer WS2 has eliminated the ambipolar behavior and reduced the Schottky barrier in WS2 FETs. The reduction of the Schottky barrier is ascribed to the hybridization between W 5d, Nb 4d and S 3p states near the EF and to the enhancement of the metallization of the contact between the Pd metal and monolayer Nb(x)W(1-x)S2 after Nb doping.

Decreased expression of spine-associated Rap guanosine triphosphatase-activating protein (SPAR) in glutamate-treated primary hippocampal neurons.

Spine-associated Rap guanosine triphosphatase-activating protein (SPAR) is an important regulator of activity-dependent remodeling of synapses. It is also critically involved in both mature dendritic spine formation and the maintenance of spine maturity. Glutamate is a major neurotransmitter of the brain, and is involved in all aspects of cognitive function, as it is the primary transmitter utilized by the cortical and hippocampal pyramidal neurons. Glutamate has also been associated with neuronal dendritic spine damage. The precise molecular mechanisms underlying dendritic spine damage following glutamate-induced neurotoxicity remain unknown. In the current study, we measured mRNA and protein expression levels of SPAR and serum-inducible kinase (SNK) in primary hippocampal neurons following glutamate treatment. Expression of SPAR and SNK was altered by glutamate treatment, indicating that the SPAR and SNK signaling pathways may be involved in the damage to dendritic spines in hippocampal neurons following excitotoxicity induced by glutamate.