Dynamic Polarization Behaviors of Equimolar CoCrFeNi High-Entropy Alloy Compared with 304 Stainless Steel in 0.5 M HSO Aerated Aqueous Solution.

Three corrosion potentials and three corrosion current densities are clearly identified before the passivation for both dynamic polarization curves of equimolar CoCrFeNi high-entropy alloy (HEA) and 304 stainless steel (304SS) in 0.5 M HSO aerated aqueous solution, by decomposing anodic and cathodic polarization curves. The passivated current density of the former is greater than the latter, compliant with not only the constant of solubility product (k) and redox equilibrium potential () of each metal hydroxide but also the sequence of bond energy () for monolayer hydroxide on their facets derived from the first principle founded on density function theory.

Cardioprotection of an I channel agonist on L-thyroxine induced rat ventricular remodeling.

Downregulation of inward rectifier potassium (I) channel is a hallmark in cardiac hypertrophy and failure. The cardioprotection of zacopride (a selective I agonist) and underlying mechanisms were investigated in L-thyroxine (T4) or Triiodothyronine (T3)-induced cardiac remodeling. In the study, adult male Sprague-Dawley (SD) rats were randomly divided into control, L-thyroxine, L-thy+zacopride, and L-thy+zacopride+chloroquine (an I antagonist) groups.

Nonvolatile molecular memory with the multilevel states based on MoS nanochannel field effect transistor through tuning gate voltage to control molecular configurations.

A new flexible memory element is crucial for mobile and wearable electronics. A new concept for memory operation and innovative device structure with new materials is certainly required to address the bottleneck of memory applications now and in the future. We report a new nonvolatile molecular memory with a new operating mechanism based on two-dimensional (2D) material nanochannel field-effect transistors (FETs).

I Channel Agonist Zacopride Alleviates Cardiac Hypertrophy and Failure Alterations in Calcium Dyshomeostasis and Electrical Remodeling in Rats.

Intracellular Ca overload, prolongation of the action potential duration (APD), and downregulation of inward rectifier potassium (I) channel are hallmarks of electrical remodeling in cardiac hypertrophy and heart failure (HF). We hypothesized that enhancement of I currents is a compensation for I deficit and a novel modulation for cardiac Ca homeostasis and pathological remodeling. In adult Sprague-Dawley (SD) rats , cardiac hypertrophy was induced by isoproterenol (Iso) injection (i.

Toward Antibiofouling PVDF Membranes.

Membranes for biologically and biomedically related applications must be bioinert, that is, resist biofouling by proteins, human cells, bacteria, algae, etc. Hydrophobic materials such as polysulfone, polypropylene, or poly(vinylidene fluoride) (PVDF) are often chosen as matrix materials but their hydrophobicity make them prone to biofouling, which in turn limits their application in biological/biomedical fields. Here, we designed PVDF-based membranes by precipitation from the vapor phase and zwitterionized them in situ to reduce their propensity to biofouling.

Electrochromic Devices Based on Poly(2,6-di(9H-carbazol-9-yl)pyridine)-Type Polymer Films and PEDOT-PSS.

2,6-Di(9H-carbazol-9-yl)pyridine (DiCP) was synthesized and its corresponding homopolymer (PDiCP) and copolymers (P(DiCP--CPDT), P(DiCP--CPDT2), P(DiCP--CPDTK), and P(DiCP--CPDTK2)) were synthesized electrochemically. The anodic copolymer with DiCP:cyclopentadithiophene ketone (CPDTK) = 1:1 feed molar ratio showed high transmittance change (Δ%) and colouration efficiency (), which were measured as 39.5% and 184.

Selection Role of Metal Oxides into Transition Metal Dichalcogenide Monolayers by a Direct Selenization Process.

Direct reduction of metal oxides into a few transition metal dichalcogenide (TMDCs) monolayers has been recently explored as an alternative method for large area and uniform deposition. However, not many studies have addressed the characteristics and requirement of the metal oxides into TMDCs by the selenization/sulfurization processes, yielding a wide range of outstanding properties to poor electrical characteristics with nonuniform films. The large difference implies that the process is yet not fully understood.

The IK1/Kir2.1 channel agonist zacopride prevents and cures acute ischemic arrhythmias in the rat.

Arrhythmogenesis in acute myocardial infarction (MI) is associated with depolarization of resting membraine potential (RMP) and decrease of inward rectifier potassium current (IK1) in cardiomyocytes. However, clinical anti-arrhythmic agents that primarily act on RMP by enhancing the IK1 channel are not currently available. We hypothesized that zacopride, a selective and moderate agonist of the IK1/Kir2.

AlN Surface Passivation of GaN-Based High Electron Mobility Transistors by Plasma-Enhanced Atomic Layer Deposition.

We report a low current collapse GaN-based high electron mobility transistor (HEMT) with an excellent thermal stability at 150 °C. The AlN was grown by N-based plasma enhanced atomic layer deposition (PEALD) and shown a refractive index of 1.94 at 633 nm of wavelength.

Activation of IK1 channel by zacopride attenuates left ventricular remodeling in rats with myocardial infarction.

Activating IK1 channels is considered to be a promising antiarrhythmic strategy. Zacopride has been identified as a selective IK1 channel agonist and can suppress triggered arrhythmias. Whether this drug also exerts a beneficial effect on cardiac remodeling is unknown, and the present study sought to address this question.

On the risk concerns of zacopride, a moderate IK1 channel agonist with cardiac protective action.

Zacopride, an IK1 agonist with moderate potency, could exert significant antiarrhythmic and cardiac protective effects. To date, there is no report to show that zacopride is proarrhythmic in both experimental studies and clinical trials. However, in certain cardiac pathological conditions, especially short QT syndrome and certain reentry tachycardia, zacopride is not suggested.

Multi-walled carbon nanotubes impair Kv4.2/4.3 channel activities, delay membrane repolarization and induce bradyarrhythmias in the rat.

Purpose: The potential hazardous effects of multi-walled carbon nanotubes (MWCNTs) on cardiac electrophysiology are seldom evaluated. This study aimed to investigate the impacts of MWCNTs on the Kv4/Ito channel, action potential and heart rhythm and the underlying mechanisms.

Methods: HEK293 cells were engineered to express Kv4.

[Cardiac inwardly rectifying potassium channel and arrhythmias].

The cardiac inwardly rectifying potassium channel (I(K1)), which is mainly expressed in mammalian atrial and ventricular myocytes, has been considered as the primary conductance controlling the resting potential (RP) and permitting a significant repolarizing current during the terminal phase of action potential. Therefore, I(K1) is highly influential on the RP, and the modulation of I(K1) would likely have profound effects on cardiac excitability and arrhythmogenesis. This article may shed light on the fundamental properties of cardiac I(K1), the mechanisms of inward rectification and I(K1) subunits composition.

A novel discovery of IK1 channel agonist: zacopride selectively enhances IK1 current and suppresses triggered arrhythmias in the rat.

Modulation of the inward rectifier K current (IK1) has profound effect on cardiac excitability and underlies new antiarrhythmic strategies. However, IK1-specific pharmacological tools, especially the selective IK1 agonists, are still lacking in the market. Zacopride, a gastrointestinal prokinetic drug, was found to be a selective IK1 channel agonist.

Inhibitory effects of purified antibody against α-1 repeat (117-137) on Na(+)-Ca(2+) exchange and L-type Ca(2+) currents in rat cardiomyocytes.

Considering that α-1 repeat region may be involved in the ion binding and translocation of Na(+)-Ca(2+) exchanger (NCX), it is possible that the antibodies against NCX α-1 repeat may have a crucial action on NCX activity. The aim of the present study is to investigate the effect of antibody against α-1 repeat (117-137), designated as α-1(117-137), on NCX activity. The antibody against the synthesized α-1(117-137) was prepared and affinity-purified.

Dofetilide enhances the contractility of rat ventricular myocytes via augmentation of Na+-Ca 2+ exchange.

Purpose: Dofetilide (DOF), a novel Class III antiarrhythmic drug, prolongs the action potential duration (APD) and shows a positive inotropic effect in guinea pig papillary muscle. The present experiments were designed to study the positive inotropic effect of DOF on rat ventricle and explore its possible mechanism(s).

Methods: Hearts from male Wistar rats (260-320 g) were divided into five groups and perfused in Langendorff mode.

Stimulation of Na+-Ca2+ exchange by purified antibody against alpha-2 repeat of Na+-Ca2+ exchanger in rat cardiomyocytes.

Aim: The aim of the present study was to investigate the effect of the antibody against alpha-2 repeat on Na+-Ca2+ exchanger (NCX) current (I(Na/Ca)). To evaluate the functional specificity of this antibody, its effects on L-type Ca2+ current (I(Ca,L)), voltage-gated Na+ current (I(Na)) and delayed rectifier K+ current (I(K)) were also observed.

Methods: The whole-cell patch-clamp technique was used in this study.

[Bioinformatics analysis of mouse adiponectin receptor-1 and its antibody preparation].

To establish a method for preparation of anti-mouse adiponectin receptor-1 (AdipoR-1) polyclonal antibody, the polypeptide antigen corresponding to AdipoR-1 was designed by bioinformatics analysis. The possible physicochemical property and trans-membrane structure were predicted by ExPASy and TMHMM, respectively. The antigen epitopes of mouse AdipoR-1 and its immunogenicity were analyzed by Antigenic Prediction and AntigenProfiler, respectively.

Activation of δ-opioid receptors inhibits L-type Ca(2+) current and transient outward K(+) current in rat ventricular myocytes.

In the present study, whole-cell patch-clamp technique was used to observe the effects of SNC162, a selective agonist of δ-opioid receptors, on L-type Ca(2+) current (I(Ca-L)) and transient outward K(+) current (I(to)) in rat ventricular myocytes. The results showed that SNC162 significantly inhibited I(Ca-L) and I(to) in rat ventricular myocytes. The maximal inhibition rate of I(Ca-L) and I(to) reached (46.

Carbachol exhibited positive inotropic effect on rat ventricular myocytes via M₂ muscarinic receptors.

The present study was aimed to investigate the positive inotropic mechanism of carbachol (CCh) on rat ventricular myocytes. The effects of CCh on L-type calcium current (I(Ca,L)) and Na(+)/Ca(2+) exchange current (I(Na/Ca)) were investigated in isolated rat ventricular myocytes. After loading myocytes with Fura-2/AM, electrically triggered Ca(2+) transient and cell shortening in single myocyte were measured simultaneously using ion imaging system with charge-coupled device (CCD) camera.

[Action of AMP579 and adenosine on potassium or sodium ionic channels in isolated rat and guinea pig ventricular myocytes].

Aim: To study the effect of AMP579 and adenosine on potassium ionic (K+) or sodium ionic (Na+) channels and to elucidate ionic mechanisms underlying negative inotropic and antiarrhythmic effects of AMP579 and adenosine.

Methods: Ionic channel currents of rat and guinea pig ventricular myocytes were recorded by patch clamp technique in whole-cell configuration.

Results: Adenosine showed a stronger activating effect on transient outward K+ current (I(to)) than AMP579, EC50 of adenosine and AMP579 were 2.

[Effects of neuropeptide Y on ion channels in ventricular myocytes].

Neuropeptide Y (NPY) co-exists with norepinephrine (NE) in sympathetic terminals, and is the most abundant neuropeptide in myocardium. Many studies have focused on the effects of NE on ion channels in cardiac myocytes and its physiological significance has been elucidated relatively profoundly. There have been few investigations, however, on the physiological significance of NPY in myocardium.

Effects of AMP579 and adenosine on L-type Ca2+ current in isolated rat ventricular myocytes.

Aim: To compare the effects of AMP579 and adenosine on L-type Ca2+ current (I(Ca-L)) in rat ventricular myocytes and explore the mechanism by which AMP579 acts on I(Ca-L).

Methods: I(Ca-L) was recorded by patch-clamp technique in whole-cell configuration.

Results: Adenosine (10 nmol/L to 50 micromol/L) showed no effect on basal I(Ca-L), but it inhibited the I(Ca-L) induced by isoproterenol 10 nmol/L in a concentration-dependent manner with the IC(50) of 13.