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Inward rectifier potassium channels (IK1, Kir) are known to play critical roles in arrhythmogenesis. Thus, how IK1 agonist affects reperfusion arrhythmias needs to be clarified, and its underlying mechanisms should be determined. Reperfusion arrhythmias were modeled by coronary ligation (ischemia, 15 minutes) and release (reperfusion, 15 minutes). Zacopride (1.5-50 μg/kg in vivo, or 0.1-10 μmol/Lex vivo) was applied in the settings of pretreatment (3 minutes before coronary ligation) and posttreatment (5 minutes after coronary ligation). Hypoxia (45 minutes) /reoxygenation (30 minutes) model was established in cultured H9c2 (2-1) cardiomyocytes. Zacopride or KN93 was applied before hypoxia (pretreatment). In the setting of pre- or posttreatment, zacopride at 15 μg/kg in vivo or 1 μmol/Lin vitro exhibited superlative protections on reperfusion arrhythmias or intracellular calcium overload. Western blot data from ex vivo hearts or H9c2 (2-1) cardiomyocytes showed that I/R (H/R) induced the inhibition of Kir2.1 (the dominant subunit of IK1 channel in ventricle), phosphorylation and oxidation of CaMKII, downregulation of SERCA2, phosphorylation of phospholamban (at Thr17), and activation of caspase-3. Zacopride treatment (1 μmol/L) was noted to strikingly restore the expression of Kir2.1 and SERCA2 and decrease the activity of CaMKII, phospholamban, and caspase-3. These effects were largely eliminated by co-application of IK1 blocker BaCl2. CaMKII inhibitor KN93 attenuated calcium overload and p-PLB (Thr17) in an IK1-independent manner. IK1-depedent inhibition of CaMKII activity is found to be a key cardiac salvage signaling under Ca2+ dyshomeostasis and reactive oxygen species (ROS) stress. IK1 might be a novel target for pharmacological conditioning of reperfusion arrhythmia, especially for the application after unpredictable ischemia.

Background: Zacopride, a potent antagonist of 5-HT3 receptors and an agonist of 5-HT4 receptors, is a gastrointestinal prokinetic agent. In a previous study, we discovered that zacopride selectively stimulated the inward rectifier potassium current (IK1) in the rat and that agonizing IK1 prevented or eliminated aconitine-induced arrhythmias in rats. Objective: Our aims were to confirm that the antiarrhythmic effects of zacopride are mediated by selectively enhancing IK1 in rabbits. Methods: The effects of zacopride on the function of the main ion channels were investigated using a whole-cell patch-clamp technique in rabbits. Effects of zacopride on cardiac arrhythmias were also explored experimentally both in vivo and in vitro. Results: Zacopride moderately enhanced cardiac IK1 but had no apparent action on voltage-gated sodium current (INa), L- type calcium current (ICa-L), sodium-calcium exchange current (INa/Ca), transient outward potassium current (Ito), or delayed rectifier potassium current (IK) in rabbits. Zacopride also had a marked antiarrhythmic effect in vivo and in vitro. We proved that the resting membrane potential (RMP) was hyperpolarized in the presence of 1 μmol/L zacopride, and the action potential duration (APD) at 90% repolarization (APD90) was shortened by zacopride (0.1-10 μmol/L) in a concentration- dependent manner. Furthermore, zacopride at 1 μmol/L significantly decreased the incidence of drug-induced early afterdepolarization (EAD) in rabbit ventricular myocytes. Conclusion: Zacopride is a selective agonist of rabbit cardiac IK1 and that IK1 enhancement exerts potential antiarrhythmic effects.

This work investigates the corrosion mechanism of annealed equiatomic AlCoCrFeNi tri-phase alloy in 0.5 M H2SO4 aerated aqueous solution. Experimental results indicate that the B2 matrix is preferentially corroded away while grain-boundary FCC and labyrinth-like BCC endure, consistent with the tendency of formation energy for monolayer hydroxide on the (001) plane of three phases calculated by the first principle based on density function theory. Furthermore, the stable passive current density is related to lower ksp values of Co(OH)3, Fe(OH)3, and Cr(OH)3, while the annealing effect on enhancing corrosion resistance is owing to the more uniformity of passive hydroxide film.

This study is about the manufacturing of a personified automatic robotic lawn mower with image recognition. The system structure is that the platform above the crawler tracks is combined with the lawn mower, steering motor, slide rail, and webcam to achieve the purpose of personification. Crawler tracks with a strong grip and good ability to adapt to terrain are selected as a moving vehicle to simulate human feet. In addition, a lawn mower mechanism is designed to simulate the left and right swing of human mowing to promote efficiency and innovation, and then human eyes are replaced by Webcam to identify obstacles. A human-machine interface is added so that through the mobile phone remote operation, users can choose a slow mode, inching mode, and obstacle avoidance mode on the human-machine interface. When the length of both sides of the rectangular area is input to the program, the automatic robotic lawn mower will complete the instruction according to the specified path. The chip of a Digital Signal Processor (DSP) TMS320F2808 is used as the core controller, and Raspberry Pi is used as image recognition and human-machine interface design. This robot can reduce labor costs and improve the efficiency of mowing by remote control. In addition to the use as an automatic mower on farms, this study concept can also be used in the lawn maintenance of golf courses and school playgrounds.

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). The smallest channel length for our 2D material nanochannel FETs was approximately 30 nm. The modified molecular configuration for charge induced in the nanochannel of the MoS

Biomass energy is considered a clean and sustainable energy source that can reduce the amount of greenhouse gases. Among the different varieties of biomass, the algae can provide a number of different biofuel sources and reduce carbon dioxide (CO2) emissions. Botryococcus braunii is especially rich in lipids, which can be converted into bioenergy, but it typically grows more slowly. The aim of this study was to optimize the cultivation conditions in order to obtain high growth rates, biomass productivity, and lipid productivity. The effects of illumination and CO2 were studied in 21-day intervals. The cultured B. braunii in this work reached the maximum specific growth rate of 0.553 d−1, and can tolerate CO2 concentrations of up to 10%. An illumination intensity of 6000 lux was identified as the optimum for both biomass and lipid productivities. Compared to the results of other studies, the major components of fatty acid methyl esters (FAMEs) obtained in this study had shorter carbon chains. The percentage of C14:0 and C16:0 in the FAMEs was greater than 70%, indicating potential applications for biojet fuel.

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 N2-based plasma enhanced atomic layer deposition (PEALD) and shown a refractive index of 1.94 at 633 nm of wavelength. Prior to deposit AlN on III-nitrides, the H2/NH3 plasma pre-treatment led to remove the native gallium oxide. The X-ray photoelectron spectroscopy (XPS) spectroscopy confirmed that the native oxide can be effectively decomposed by hydrogen plasma. Following the in situ ALD-AlN passivation, the surface traps can be eliminated and corresponding to a 22.1% of current collapse with quiescent drain bias (V DSQ) at 40 V. Furthermore, the high temperature measurement exhibited a shift-free threshold voltage (V th), corresponding to a 40.2% of current collapse at 150 °C. The thermal stable HEMT enabled a breakdown voltage (BV) to 687 V at high temperature, promising a good thermal reliability under high power operation.

An inductively coupled plasma (ICP) process was used to synthesize transition metal dichalcogenides (TMDs) through a plasma-assisted selenization process of metal oxide (MOx) at a temperature as low as 250 °C. In comparison with other CVD processes, the use of ICP facilitates the decomposition of the precursors at low temperatures. Therefore, the temperature required for the formation of TMDs can be drastically reduced. WSe2 was chosen as a model material system due to its technological importance as a p-type inorganic semiconductor with an excellent hole mobility. Large-area synthesis of WSe2 on polyimide (30 × 40 cm2) flexible substrates and 8 in. silicon wafers with good uniformity was demonstrated at the formation temperature of 250 °C confirmed by Raman and X-ray photoelectron (XPS) spectroscopy. Furthermore, by controlling different H2/N2 ratios, hybrid WOx/WSe2 films can be formed at the formation temperature of 250 °C confirmed by TEM and XPS. Remarkably, hybrid films composed of partially reduced...

Intracellular Ca2+ overload, prolongation of the action potential duration (APD), and downregulation of inward rectifier potassium (IK1) channel are hallmarks of electrical remodeling in cardiac hypertrophy and heart failure (HF). We hypothesized that enhancement of IK1 currents is a compensation for IK1 deficit and a novel modulation for cardiac Ca2+ homeostasis and pathological remodeling. In adult Sprague-Dawley (SD) rats in vivo, cardiac hypertrophy was induced by isoproterenol (Iso) injection (i.p., 3 mg/kg/d) for 3, 10, and 30 days. Neonatal rat ventricular myocytes (NRVMs) were isolated from 1 to 3 days SD rat pups and treated with 1 μmol/L Iso for 24 h in vitro. The effects of zacopride, a selective IK1/Kir2.1 channel agonist, on cardiac remodeling/hypertrophy were observed in the settings of 15 μg/kg in vivo and 1 μmol/L in vitro. After exposing to Iso for 3 days and 10 days, rat hearts showed distinct concentric hypertrophy and fibrosis and enhanced pumping function (P < 0.01 or P < 0.05), then progressed to dilatation and dysfunction post 30 days. Compared with the age-matched control, cardiomyocytes exhibited higher cytosolic Ca2+ (P < 0.01 or P < 0.05) and lower SR Ca2+ content (P < 0.01 or P < 0.05) all through 3, 10, and 30 days of Iso infusion. The expressions of Kir2.1 and SERCA2 were downregulated, while p-CaMKII, p-RyR2, and cleaved caspase-3 were upregulated. Iso-induced electrophysiological abnormalities were also manifested with resting potential (RP) depolarization (P < 0.01), APD prolongation (P < 0.01) in adult cardiomyocytes, and calcium overload in cultured NRVMs (P < 0.01). Zacopride treatment effectively retarded myocardial hypertrophy and fibrosis, preserved the expression of Kir2.1 and some key players in Ca2+ homeostasis, normalized the RP (P < 0.05), and abbreviated APD (P < 0.01), thus lowered cytosolic [Ca2 +]i (P < 0.01 or P < 0.05). IK1channel blocker BaCl2 or chloroquine largely reversed the cardioprotection of zacopride. We conclude that cardiac electrical remodeling is concurrent with structural remodeling. By enhancing cardiac IK1, zacopride prevents Iso-induced electrical remodeling around intracellular Ca2+ overload, thereby attenuates cardiac structural disorder and dysfunction. Early electrical interventions may provide protection on cardiac remodeling.

This study develops a three-finger robotic hand with seven degrees of freedom (DOF), which integrates the design and testing of mechanical fingers and modular force sensors. The design concept, the test data and advantages of the pressure/shear force sensor are mentioned in detail. Finally, the force sensors are embedded into several portions of the fingers which are leveraged to feedback for controlling the grasping action to adapt to more types of workpieces. In the future, we will balance the volume and sensitivity of the pressure/shear sensor and combine ROS to expand the applications of this robotic hand.

This paper propose a method which uses the CNN-LSTM speech recognition as a basis to convert the input of user's speech signal into text, and combine the CKIP system to break sentence or phrases into words and calculate Valence-Arousal values by the method of vector-based in the last. We calculate Valence-Arousal values with vector-based method and three lexicons which is emotional, degree and negative lexicon respectively for words and phrases. If the input is not exist in three lexicons, we will use the OOV(Out-of-Vocabulary) function to solve the problem. The OOV function not only solve the problem but also is helpful for Valence-Arousal values calculation. Because the sentence is consists of many modifiers and words, the system will have calculation deviation. In order to improve the accuracy of values, we use the way of detecting modifiers again and implement in OOV function to reach the goal. Finally, the system will output the Valence-Arousal values and present on the chart.

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. To achieve this goal, we used a copolymer containing phosphorylcholine groups. An in-depth physicochemical characterization revealed not only the controlled presence of the copolymer in the membrane but also that bicontinuous membranes could be formed. Membrane hydrophilicity was greatly improved, resulting in the mitigation of a variety of biofoulants: the attachment of Stenotrophomonas maltophilia, Streptococcus mutans, and platelets was reduced by 99.9, 99.9, and 98.9%, respectively. Besides, despite incubation in a plasma platelet-poor medium, rich in plasma proteins, a flux recovery ratio of 75% could be measured while it was only 40% with a hydrophilic commercial membrane of similar structure and physical properties. Similarly, the zwitterionic membrane severely mitigated biofouling by microalgae during their harvesting. All in all, the material/process combination presented in this work leads to antibiofouling porous membranes with a large span of potential biomedically and biologically related applications.

Intracellular Ca2+ overload, prolongation of the action potential duration (APD), and downregulation of inward rectifier potassium (IK1) channel are hallmarks of electrical remodeling in cardiac hypertrophy and heart failure (HF). We hypothesized that enhancement of IK1 currents is a compensation for IK1 deficit and a novel modulation for cardiac Ca2+ homeostasis and pathological remodeling. In adult Sprague-Dawley (SD) rats in vivo, cardiac hypertrophy was induced by isoproterenol (Iso) injection (i.p., 3 mg/kg/d) for 3, 10, and 30 days. Neonatal rat ventricular myocytes (NRVMs) were isolated from 1 to 3 days SD rat pups and treated with 1 μmol/L Iso for 24 h in vitro. The effects of zacopride, a selective IK1/Kir2.1 channel agonist, on cardiac remodeling/hypertrophy were observed in the settings of 15 μg/kg in vivo and 1 μmol/L in vitro. After exposing to Iso for 3 days and 10 days, rat hearts showed distinct concentric hypertrophy and fibrosis and enhanced pumping function (P < 0.01 or P < 0.05), then progressed to dilatation and dysfunction post 30 days. Compared with the age-matched control, cardiomyocytes exhibited higher cytosolic Ca2+ (P < 0.01 or P < 0.05) and lower SR Ca2+ content (P < 0.01 or P < 0.05) all through 3, 10, and 30 days of Iso infusion. The expressions of Kir2.1 and SERCA2 were downregulated, while p-CaMKII, p-RyR2, and cleaved caspase-3 were upregulated. Iso-induced electrophysiological abnormalities were also manifested with resting potential (RP) depolarization (P < 0.01), APD prolongation (P < 0.01) in adult cardiomyocytes, and calcium overload in cultured NRVMs (P < 0.01). Zacopride treatment effectively retarded myocardial hypertrophy and fibrosis, preserved the expression of Kir2.1 and some key players in Ca2+ homeostasis, normalized the RP (P < 0.05), and abbreviated APD (P < 0.01), thus lowered cytosolic [Ca2 +]i (P < 0.01 or P < 0.05). IK1channel blocker BaCl2 or chloroquine largely reversed the cardioprotection of zacopride. We conclude that cardiac electrical remodeling is concurrent with structural remodeling. By enhancing cardiac IK1, zacopride prevents Iso-induced electrical remodeling around intracellular Ca2+ overload, thereby attenuates cardiac structural disorder and dysfunction. Early electrical interventions may provide protection on cardiac remodeling.

In this work, we use thermal-ALD to prepare ferroelectric HfZrO 2 (HZO) thin film with thickness from 3 to 7 nm for the NC-FinFET's gate stack. The subthreshold swing (SS) was as low as 5 mV/dec (SSmin) over 4 orders of I D . Lower thermal budget process, CO 2 far-infrared laser activation and 400°C Ni silicide are employed in the 2-level metal backend integration for maintaining the orthorhombic phase in HZO thin film and minimizing the hysteresis in IV. NC-FinFET inverter has 77% higher voltage gain compared to FinFET-inverter employing HfO 2 gate dielectric. NC-FinFET ring oscillator exhibit small speed and power advantages over FinFET oscillator. For the first time, NC-FET cut-off frequency (F t ) frequency is measured, 23.1 GHz or 23% higher than the control FET Ft. NC-FinFET SRAM was observed to exhibit large noise margin.

Unlike previous studies, this paper empirically investigates the impact of urbanization on energy consumption and CO 2 emissions with consideration of provincial differences. The results show the following: (1) Urbanization increases energy consumption and CO 2 emissions in China, but it is not the most outstanding contributor to the increases. (2) Significant differences exist between provinces in terms of the impact of urbanization on energy consumption and CO 2 emissions. The distribution of urbanization strongly and relatively strongly affects energy consumption in regions with high-urbanization areas but also those with low-urbanization areas. Meanwhile, urbanization strongly and relatively strongly affects the regional CO 2 emissions in northern China, where the major coal production areas, characterized by an energy-guzzling heavy industry base, are located. (3) Some evidence supports the arguments of urban environmental transition theory. Cities at a post-industrial stage (such as Beijing and Shanghai) experience a large effect from urbanization because of higher energy consumption in private residential and public service sectors, while in western and central China, the impact of urbanization can be associated with industrial development, which is characterized by low energy efficiency, high energy consumption and high emissions. In eastern China, the coexistence of light industrial structures and rapid urbanization has led to a smaller impact from urbanization on energy consumption and CO 2 emissions than in the other two regions.

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). The smallest channel length for our 2D material nanochannel FETs was approximately 30 nm. The modified molecular configuration for charge induced in the nanochannel of the MoS2 FET can be tuned by applying an up-gate voltage pulse, which can vary the channel conductance to exhibit memory states. Through controlling the amounts of triggered molecules through either different gate voltage pulses or gate duration time, multilevel states were obtained in the molecular memory. These new molecular memory transistors exhibited an erase/program ratio of more than three orders of current magnitude and high sensitivity, of a few picoamperes, at the current level. Reproducible operation and four-level states with stable retention and endurance were achieved. We believe this prototype device has potential for use in future memory devices.

Aims Arrhythmogenesis of chronic myocardial infarction (MI) is associated with the prolongation of action potential, reduction of inward rectifier potassium (IK1, Kir) channels and hyper-activity of Calcium/calmodulin-dependent kinase II (CaMKII) in cardiomyocytes. Zacopride, a selective IK1 agonist, was applied to clarify the cardioprotection of IK1 agonism via a CaMKII signaling on arrhythmias post-MI. Methods Male SD rats were implanted wireless transmitter in the abdominal cavity and subjected to left main coronary artery ligation or sham operation. The telemetric ECGs were monitored per day throughout 4 weeks. At the endpoint, isoproterenol (1.28 mg/kg, i.v.) was administered for provocation test. The expressions of Kir2.1 (dominant subunit of IK1 in ventricle) and CaMKII were detected by Western-blotting. Key findings In the telemetric rats post-MI, zacopride significantly reduced the episodes of atrioventricular conduction block (AVB), premature ventricular contraction (PVC), ventricular tachycardia (VT) and ventricular fibrillation (VF), without significant effect on superventricular premature contraction (SPVC). In provocation test, zacopride suppressed the onset of ventricular arrhythmias in conscious PMI or sham rats. The expression of Kir2.1 was significantly downregulated and p-CaMKII was upregulated post-MI, whereas both were restored by zacopride treatment. Significance IK1/Kir2.1 might be an attractive target for pharmacological controlling of lethal arrhythmias post MI.

2,6-Di(9H-carbazol-9-yl)pyridine (DiCP) was synthesized and its corresponding homopolymer (PDiCP) and copolymers (P(DiCP-co-CPDT), P(DiCP-co-CPDT2), P(DiCP-co-CPDTK), and P(DiCP-co-CPDTK2)) were synthesized electrochemically. The anodic copolymer with DiCP:cyclopentadithiophene ketone (CPDTK) = 1:1 feed molar ratio showed high transmittance change (&Delta, T%) and colouration efficiency (&eta, ), which were measured as 39.5% and 184.1 cm2 C&minus, 1 at 1037 nm, respectively. Electrochromic devices (ECDs) were composed of PDiCP, P(DiCP-co-CPDT), P(DiCP-co-CPDT2), P(DiCP-co-CPDTK), and P(DiCP-co-CPDTK2) as anodically-colouring polymers, and poly(3,4-ethylenedioxythiophene)-poly(styrene sulfonic acid) (PEDOT-PSS) as cathodically-colouring polymers. P(DiCP-co-CPDTK)/PEDOT-PSS ECD showed light silverish-yellow at 0.0 V, light grey at 0.7 V, grey at 1.3 V, light greyish blue at 1.7 V, and greyish blue at 2.0 V. Moreover, P(DiCP-co-CPDTK)/PEDOT-PSS ECD presented high &Delta, T (38.2%) and high &eta, (633.8 cm2 C&minus, 1) at 635 nm.

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. In particular, the selenization/sulfurization at low temperature leads to poor crystallinity films with poor electrical performance, hindering its practical development. A common approach to improve the quality of the selenized/sulfurized films is by further increasing the process temperature, thus requiring additional transfer in order to explore the electrical properties. Here, we show that by finely tuning the quality of the predeposited oxide the selenization/sulfurization temperature can be largely decreased, avoiding major substrate damage and allowing direct device fabrication. The direct relationship between the role of selecting different metal oxides prepared by e-beam evaporation and reactive sputtering and their oxygen deficiency/vacancy leading to quality influence of TMDCs was investigated in detail. Because of its outstanding physical properties, the formation of tungsten diselenide (WSe2) from the reduction of tungsten oxide (WO x) was chosen as a model for proof of concept. By optimizing the process parameters and the selection of metal oxides, layered WSe2 films with controlled atomic thickness can be demonstrated. Interestingly, the domain size and electrical properties of the layered WSe2 films are highly affected by the quality of the metal oxides, for which the layered WSe2 film with small domains exhibits a metallic behavior and the layered WSe2 films with larger domains provides clear semiconducting behavior. Finally, an 8'' wafer scale-layered WSe2 film was demonstrated, giving a step forward in the development of 2D TMDC electronics in the industry.

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/Kir2.1 channels, prevents and cures acute ischemic arrhythmias. To test this viewpoint, adult Sprague-Dawley (SD) rats were subjected to MI by ligating the left main coronary artery. The antiarrhythmic effects of zacopride (i.v. infusion) were observed in the settings of pre-treatment (zacopride given 3 min prior to coronary occlusion), post-treatment (zacopride given 3 min after coronary occlusion) and therapeutic treatment (zacopride given 30 s after the onset of the first sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) post MI). In all the three treatment modes, zacopride (15 μg/kg) inhibited MI-induced ventricular tachyarrhythmias, as shown by significant decreases in the premature ventricular contraction (PVC) and the duration and incidence of VT or VF. In Langendorff perfused rat hearts, the antiarrhythmic effect of 1 μmol/L zacopride were reversed by 1 μmol/L BaCl2, a blocker of IK1 channel. Patch clamp results in freshly isolated rat ventricular myocytes indicated that zacopride activated the IK1 channel and thereby reversed hypoxia-induced RMP depolarization and action potential duration (APD) prolongation. In addition, zacopride (1 μmol/L) suppressed hypoxia- or isoproterenol- induced delayed afterdepolarizations (DADs). In Kir2.x transfected Chinese hamster ovary (CHO) cells, zacopride activated the Kir2.1 homomeric channel but not the Kir2.2 or Kir2.3 channels. These results support our hypothesis that moderately enhancing IK1/Kir2.1 currents as by zacopride rescues ischemia- and hypoxia- induced RMP depolarization, and thereby prevents and cures acute ischemic arrhythmias. This study brings a new viewpoint to antiarrhythmic theories and provides a promising target for the treatment of acute ischemic arrhythmias.

An atomic-scale numerical study of Si contact with transition metal dichalcogenides (TMD) semiconductor materials is proposed by first-principles simulation for the first time. The monolayer MoS 2 channel can be operated as both of n- and p-type FET by properly doping Si S/D to adjust the TMD channel potential. The gradient MoS x junction of dichalcogenide vacancies enables Si-MoS 2 contact resistance lower than 100Ω-μm for interface Schottky barrier height reduction. The compact Si-MoS 2 interface study can potentially provide monolayer TMD contact design guideline for the sub-5 nm TMD FET fabrication technology.

A U-shape MoS 2 pMOSFET with 10nm channel and poly-Si source/drain is demonstrated. The fabrication process is simple. Because the Si S/D serves as the nucleation seed for CVD MoS 2 deposition, thin MoS 2 is well deposited in the channel region any where over the fully scale oxide coated Si wafer. This is a big step forward toward a low cost multi-layer stacked TMD IC technology.

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. By using the whole-cell patch clamp technique, it was found that zacopride (0.1-10 μmole/L) dose dependently enhanced the IK1 current in isolated rat cardiomyocytes, had no effects on other ion channels, transporters, or pumps. At the same dosage range, zacopride hyperpolarized the resting potential and shortened the action potential duration. When applied at the optimal dose of 1.0 μmole/L, zacopride could prevent or eliminate aconitine induced after depolarization and triggered activity in isolated cardiomyocytes. In a rat model of aconitine-induced arrhythmias both ex vivo and in vivo, zacopride (1.0 μmole/L or 25 μg/kg, respectively) treatment apparently protected the heart from ventricular tachyarrhythmias, which compares favorably with 7.5 mg/kg of lidocaine, a classical aconitine antidote. In conclusion, zacopride was found to be a selective IK1 agonist, and agonizing IK1 could prevent or eliminate aconitine-induced arrhythmias in the rat.

By using sidewall electrode technology, both record small functional TiO 2 selection device (1 × 5 nm2) and HfO 2 based RRAM device (1 × 3 nm2) were for the first time successfully demonstrated in this work, improving the understanding of the switching mechanism in an ultra-small, functional resistive random access memory (RRAM) device. The tunneling based low temperature back-end selection devices show high driving current density of > 10 MA/cm2 and selectivity of > 103. The pulse driven cycle endurance of sub-5nm selection device and RRAM device reaches 106 and 103, respectively. Well controlled TiO 2 barrier produced with conformal plasma oxidation exhibits tight uniformity. The 1 × 3 nm2 RRAM device exhibited an excellent performance, featuring a large on/off verified window (>100), and reasonable reliability (stress time > 103 s). Furthermore, the 1 × 3 nm2 RRAM device exhibited distinctive unipolar behavior when a high voltage and rapid switching operation (7 V, 50 ns) were applied. We also study on double oxide layer device and propose a physical mechanism picture to compare with previous study. This technology demonstrates the potential of future atomic-scale memories.

Stackable 3DFETs such as FinFET using hybrid Si/MoS 2 channels were developed using a fully CMOS-compatible process. Adding several molecular layers (3–16 layers) of the transition-metal dichalcogenide (TMD), MoS 2 to Si fin and nanowire resulted in improved (+25%) I on,n of the FinFET and nanowire FET (NWFET). The PFETs also operated effectively and the N/P device V th are low and matched perfectly. The proposed heterogeneous Si/TMD 3DFETs can be useful in future electronics.

Aim: To compare the effects of AMP579 and adenosine on L-type Ca 2+ 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 umol/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 13.06 umol/L. Similar to adenosine, AMP579 also showed an inhibitory effect on the I Ca-L induced by isoproterenol. AMP579 and adenosine (both in 10 umol/L) suppressed isoproterenol-induced I Ca-L by 11.1% and 5.2%, respectively. In addition, AMP579 had a direct inhibitory effect on basal I Ca-L in a concentration-dependent manner with IC 50 (1.17 mumol/L). PD116948 (30 mumol/L), an adenosine A1 receptor blocker, showed no action on the inhibitory effect of AMP579 on basal I Ca-L . However, GF109203X (0.4 mumol/L), a special protein kinase C (PKC) blocker, could abolish the inhibitory effect of AMP579 on basal I Ca-L . So the inhibitory effect of AMP579 on basal ICa-L was induced through activating PKC, but not linked to adenosine A 1 receptor. Conclusion: AMP579 shows a stronger inhibitory effect than adenosine on the I Ca-L induced by isoproterenol. AMP579 also has a strong inhibitory effect on basal ICa-L in rat ventricular myocytes. Activation of PKC is involved in the inhibitory effect of AMP579 on basal I Ca-L at downstream-mechanism.

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. Cardiac remodeling was induced through coronary ligation-induced myocardial infarction (MI) in male Sprague-Dawley rats. Zacopride (15 µg/kg) was administered (intraperitoneally) daily for 28 days after MI to determine whether it could attenuate MI-induced cardiac remodeling. A 4-week treatment with zacopride attenuated post-MI cardiac remodeling, as shown by the reduced left ventricular end-diastolic dimension and left ventricular end-systolic dimension and the increased ejection fraction and fractional shortening in zacopride-treated animals compared with animals treated with vehicle (all P < 0.05). Furthermore, zacopride significantly decreased myocardial collagen deposition, cardiomyocyte hypertrophy, the plasma level of brain natriuretic peptide, and cardiomyocyte ultrastructural injury. Zacopride also upregulated the expression of the IK1 channel protein and downregulated the expression of phosphorylated p70S6 kinase (p-p70S6K) and mTOR. These beneficial effects of zacopride were partially abolished by the IK1 channel blocker chloroquine. We conclude that the activation of IK1 channel by zacopride attenuates post-MI cardiac remodeling by suppressing mTOR-p70S6 kinase signaling.

A sidewall electrode technology was successfully developed for the first time in this study, improving the understanding of the working mechanism in an ultra small, functional HfO 2 -based resistive random access memory (RRAM) device (100), and reasonable reliability (stress time > 10 3 s, 2 × 10 4 h at 250 °C). Furthermore, the 1 × 3 nm 2 RRAM device exhibited distinctive unipolar behavior when a high voltage and rapid switching operation (7 V, 50 ns) were applied, and a switching mechanism model is proposed.

Carbon nanofibers (CNFs) with diameter ∼66 nm have been synthesized from coronene by low-temperature (∼45 °C) vacuum sublimation without the aid of a catalyst. Our method makes use of the property of polycyclic aromatic hydrocarbon (PAH) molecules, which can self-assemble into columnar aggregates. This polycyclic aromatic hydrocarbon-carbon nanofibers (PAH-CNFs) reveal much better thermal stability than commercial carbon nanotubes and exhibit field-emission characteristics with the onset of an electric field of 5.4 V/μm and field enhancement factor of 1326 cm−1 for 100 μm interelectrode distance. The relative high thermal stability and easier process open up a possibility to fabricate large-scale field-emission devices in an efficient way and to provide a broad range of applications in nanoscience and technology.

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. Furthermore, the article discusses the role of I(K1) in ventricular excitability and arrhythmogenesis and explores the possibility of modulating I(K1) as an antiarrhythmic mechanism. In fact, both blocking and enhancing I(K1) could be antiarrhythmic, but have proarrhythmic potential at the same time. Action potential duration (APD) prolongation has been accepted as an important antiarrhythmic strategy with some evidence in animal models of arrhythmogenesis that I(K1) blockade can prolongate APD and be antiarrhythmic. However, the potential of I(K1) blockade has not resulted in the development of specific I(K1) blockers used clinically. Safety concerns are probably the main reason, and the therapeutic potential for I(K1) blockers seems somewhat small. On the contrary, the up to date reports indicate that moderately activating I(K1) and hyperpolarizing the RP which has been depolarized by pathologic injury are to be feasible and effective to alleviate some kinds of ventricular arrhythmias.

Transition metal dichalcogenides (TMDs) receive a significant attention due to its intriguing properties for fundamental research and potential for application in electronics, catalysis, optoelectronics, and so on. In this work, we focus on growth of PtSe2 because of its chemical activity, small band gap and low resistivity. Recently, Yeliang Wang et al. 1 demonstrate single layer of PtSe2 by single crystal Pt substrate and selenization with 270 ºC. Despite in this case, the electrical properties of PtSe2 monolayer cannot be exploited due to the underneath Pt. It should be pointed that the synthesis temperature of PtSe2 is much lower compared with other TMDs such as MoS2 and WSe2. Besides, the electrical performance of PtSe2 is different from the other TMDs. Theoretical calculations of the band structure of PtSe2 shows large changes in the bandgap going from 1.3eV at the monolayer to 0.3 eV on bilayer and is expected a semi-metallic behavior at multiple PtSe2 monolayers. However, no experimental demonstration of the electrical properties has been explored so far. In our work, we try to grow PtSe2 by the plasma assisted selenization process. First, we deposit Pt metal on Si substrate by DC sputtering process within 5 nm thickness. After Pt deposition, we apply plasma assisted selenization to form a few PtSe2 monolayers at a temperature below 200 oC. Material characterization based on TEM, XPS and Raman analysis was applied to investigate the quality and the plasma effect on the resulting PtSe2 film. Moreover, we experimentally demonstrate the semiconducting properties of PtSe2and demonstrate the potential as a channel material for MOSFET applications. References 1. Wang Y., et al. Monolayer PtSe(2), a New Semiconducting Transition-Metal-Dichalcogenide, Epitaxially Grown by Direct Selenization of Pt. Nano Lett 15, 4013-4018 (2015).

Ordered nanodot arrays of titanium oxides were prepared from TiN/Al films on the silicon substrate by electrochemical anodization of a TiN layer using a nanoporous anodic aluminum oxide film as the template. The microstructure of the nanodot arrays was studied by transmission electron microscopy and scanning electron microscopy, and the chemical composition of nanodots was analyzed by electron energy loss spectroscopy. The as-prepared nanodots are basically composed of amorphous TiOx with a hexagonal arrangement and an average diameter of about 60 nm. Using this approach, it is expected that nanodot arrays of various oxide semiconductors can be achieved.

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. Whole-cell patch clamp technique was used to study the change of Na(+)-Ca(2+) exchange current (I(Na/Ca)) in adult rat cardiomyocytes. To evaluate the functional specificity of this antibody, its effects on L-type Ca(2+) current (I(Ca,L)), voltage-gated Na(+) current (I(Na)) and delayed rectifier K(+) current (I(K)) were also observed. The amino acid sequences of α-1(117-137) in NCX and residues 1 076-1 096 within L-type Ca(2+) channel were compared using EMBOSS Pairwise Alignment Algorithms. The results showed that outward and inward I(Na/Ca) were decreased by the antibody against α-1(117-137) dose-dependently in the concentration range from 10 to 160 nmol/L, with IC(50) values of 18.9 nmol/L and 22.4 nmol/L, respectively. Meanwhile, the antibody also decreased I(Ca,L) in a concentration-dependent manner with IC(50) of 22.7 nmol/L. No obvious effects of the antibody on I(Na) and I(K) were observed. Moreover, comparison of the amino acid sequences showed there was 23.8% sequence similarity between NCX α-1(117-137) and residues 1 076-1 096 within L-type Ca(2+) channel. These results suggest that antibody against α-1(117-137) is a blocking antibody to NCX and can also decrease I(Ca,L) in a concentration-dependent manner, while it does not have obvious effects on I(Na) and I(K).

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). Hearts from male Wistar rats (260–320 g) were divided into five groups and perfused in Langendorff mode. Ventricular myocytes were enzymatically isolated from male Wistar rats. Whole-cell voltage-clamping technique was used to test the Na+–Ca2+ exchange (NCE) current (I NCX); Calcium transients and cell shortening provoked by field stimulation or using calcium current command waveform were observed synchronously with an ionic imaging system. DOF (0.03–1.0 μM) increased left ventricular function in isolated rat hearts in a concentration-dependent manner. DOF (0.03–1.0 μM) also concentration-dependently increased both inward and outward I NCX in isolated rat ventricular cells. The EC50 values of DOF were 0.149 μM for the inward I NCX and 0.249 μM for outward I NCX, respectively. DOF 0.2 μM significantly enhanced Ca2+ transient and cell shortening in single rat ventricular myocytes driven by field electric stimulation. When the patch clamp system was connected to the ionic imaging system, Ca2+ current (I Ca), Ca2+ transient and cell shortening amplitude in a same cell were recorded synchronously. Application of DOF 0.2 μM had no effect on I Ca, but significantly increased Ca2+ transient and cell shortening. NCX inhibitor KB-R7943 0.6 μM significantly depressed the effects of DOF on Ca2+ transient and cell shortening. We conclude that DOF enhanced contractility of rat ventricular myocytes. The enhancement of NCE may be involved in the positive inotropic action of DOF.

Aim: The aim of the present study was to investigate the effect of the antibody against alpha-2 repeat on Na + -Ca 2+ exchanger (NCX) current (I Na /Ca). To evaluate the functional specificity of this antibody, its effects on L-type Ca 2+ 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. Results: The antibody against alpha-2 repeat augmented both the outward and inward Na + -Ca 2+ exchanger current concentration-dependently, with EC50 values of 27.9 nmol/L and 24.7 nmol/L, respectively. Meanwhile, the antibody could also increase I Ca,L in a concentration-dependent manner with the EC50 of 33.6 nmol/L. Effects of the antibody on I Na and I K were not observed in the present study. Conclusion: The present results suggest that antibody against alpha-2 repeat is a stimulating antibody to NCX and could also increase I Ca,L in a concentration-dependent manner, but did not have an obvious effect on I Na and I K .

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 (46.13±4.12)% and (36.53±10.57)%, respectively. SNC162 at 1×10(-4) mol/L inhibited the current density of I(Ca-L) from (8.98±0.40) pA/pF to (4.84±0.44) pA/pF (P0.01, n=5) and inhibited that of I(to) from (18.69±2.42) pA/pF to (11.73±1.67) pA/pF (P0.01, n=5). Furthermore, the effects of naltrindole, a highly selective antagonist of δ-opioid receptors, on I(Ca-L) and I(to) were also observed. The results showed that naltrindole alone had no effects on I(Ca-L) and I(to), while it abolished the inhibitory effects of SNC162 on I(Ca-L) and I(to). In conclusion, SNC162 concentration-dependently inhibited I(Ca-L) and I(to) in rat ventricular myocytes via activation of the δ-opioid receptors, which may be a fundamental mechanism underlying the antiarrhythmic effect of activating δ-opioid receptors.

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. According to the similarity analysis between AdipoR-1 and AdipoR-2 by Clustal W, a 16-amino acid polypeptide was designed as the antigen corresponding to AdipoR-1. To ensure the specificity of the polypeptide antigen, similarity search was run in the protein databases such as SWISS-PROT, PDB and Prosite databases. The polypeptide synthesized by solid-phase synthesis was used as immunogen to immunize rats to obtain anti-mouse AdipoR-1 polyclonal antibodies, the specificity and titer of which was identified by Western blot and indirect ELISA. The antibodies were applied to detect the AdipoR-1 expression in the muscle tissue in normal and cholesterolemic mice. The results from bioinformatics analysis showed that the similarity of amino acid sequences between AdipoR-1 and AdipoR-2 in mouse was 66%, and the designed polypeptide antigen corresponding to AdipoR-1 exhibited excellent immunogenicity (score=3.1). Using the polypeptide as antigen for immunization, anti-mouse AdipoR-1 polyclonal antibodies with high titer and good specificity were obtained. The results of Western blot demonstrated that there was no statistical difference in AdipoR-1 expression in muscle tissue between normal (1.80±0.06) and cholesterolemic mice (1.71±0.11). These results suggest that the antigen epitopes of mouse AdipoR-1 are well predicted by bioinformatics analysis, and successful preparation of the specific anti-AdipoR-1 polyclonal antibodies provides a useful tool for identification and further functional study of AdipoR-1.

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. CCh (100 mumol/L) increased I(Na/Ca) in forward mode from (1.18 +/- 0.57) pA/pF in the control group to (1.65 +/- 0.52) pA/pF (P0.01) and that in reverse mode from (1.11 +/- 0.49) pA/pF in the control group to (1.53 +/- 0.52) pA/pF (P0.01), respectively. CCh had no effect on I(Ca,L). The stimulatory effect of CCh on I(Na/Ca) was blocked by application of atropine, a non-selective M muscarinic receptor antagonist, and methoctramine, a selective M(2) muscarinic receptor antagonist. CCh (100 mumol/L) increased cell shortening from (3.00 +/- 0.67) mum in the control group to (3.55 +/- 1.21) mum. Ca(2+) transient was also increased from 203.8 +/- 50.0 in the control group to 234.8 +/- 64.3 in 100 mumol/L CCh group. KB-R7943, a selective inhibitor of reverse mode Na(+)/Ca(2+) exchange, did not change the baseline level of cell shortening and Ca(2+) transient, while completely abolished CCh-induced increments of both Ca(2+) transient and cell shortening. CCh increased cell shortening and Ca(2+) transient in the presence of nicardipine, indicating that the positive inotropic effect of CCh was through activation of Na(+)/Ca(2+) exchange. Calcium sensitivity was not changed by CCh. Both atropine and methoctramine abolished the positive inotropic effects of CCh, demonstrating that CCh induced positive inotropism via the M(2) muscarinic receptor. The results suggest that CCh increases cell contraction and Ca(2+) transient in rat ventricular myocytes. This positive inotropic effect of CCh is through activation of reverse mode Na(+)/Ca(2+) exchange, and M(2) receptors are involved in mediating CCh-induced contraction.