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To match the key features of light-emitting diode (LED) lighting source and further save power, LED lighting driver also requires long life, while maintaining high efficiency, high power factor, pulse-width modulation dimming and low cost. However, a typical LED lighting driver has the following drawbacks: (i) utilise bulky electrolytic capacitor as storage capacitor with short lifetime; (ii) employ a low-frequency diode bridge as the rectifier cell; and (iii) engage multiple stages cascade structure for multiple LED strings. To overcome the aforementioned shortages, this study proposed a bridgeless electrolytic capacitor-less AC/DC converter for offline LED lighting application. In the proposed converter, the conventional diode rectified bridge is replaced by Totem-pole bridgeless configuration for reducing the number of semiconductors in the line-current path. Meanwhile, the valley-fill circuit is introduced to further reduce the capacitor size. As comparison to its counterpart, the proposed circuit requires only one quarter of the capacitor energy when considering the energy amount (CV2) as the capacitor sizing criterion. Furthermore, the isolation type of the studied circuit is compatible with Twin-Bus configuration for achieving higher overall system efficiency. Finally, the experimental results, taken from a laboratory prototype rated at 50 W, are presented to verify the effectiveness of the proposed converter.

Gemcitabine is an antineoplastic drug commonly used in the treatment of several types of cancers including pancreatic cancer and non–small cell lung cancer. Although gemcitabine-induced cardiotoxicity is widely recognized, the exact mechanism of cardiac dysfunction causing arrhythmias remains unclear. The objective of this study was to electrophysiologically evaluate the proarrhythmic cardiotoxicity of gemcitabine focusing on the human rapid delayed rectifier potassium channel, hERG channel. In heterologous hERG expressing HEK293 cells (hERG-HEK cells), hERG channel current ( I hERG ) was reduced by gemcitabine when applied for 24 h but not immediately after the application. Gemcitabine modified the activation gating properties of the hERG channel toward the hyperpolarization direction, while inactivation, deactivation or reactivation gating properties were unaffected by gemcitabine. When gemcitabine was applied to hERG-HEK cells in combined with tunicamycin, an inhibitor of N-acetylglucosamine phosphotransferase, gemcitabine was unable to reduce I hERG or shift the activation properties toward the hyperpolarization direction. While a mannosidase I inhibitor kifunensine alone reduced I hERG and the reduction was even larger in combined with gemcitabine, kifunensine was without effect on I hERG when hERG-HEK cells were pretreated with gemcitabine for 24 h. In addition, gemcitabine down-regulated fluorescence intensity for hERG potassium channel protein in rat neonatal cardiomyocyte, although hERG mRNA was unchanged. Our results suggest the possible mechanism of arrhythmias caused by gemcitabine revealing a down-regulation of I hERG through the post-translational glycosylation disruption possibly at the early phase of hERG channel glycosylation in the endoplasmic reticulum that alters the electrical excitability of cells.

The proliferation of smart devices increases the demand for energy-efficient, battery-free technologies essential for sustaining IoT devices in Industry 4.0 and 5G networks, which require zero maintenance and sustainable operation. Integrating radio frequency (RF) energy harvesting with IoT and 5G technologies enables real-time data acquisition, reduces maintenance costs, and enhances productivity, supporting a carbon-free future. This survey reviews the challenges and advancements in RF energy harvesting, focusing on far-field wireless power transfer and powering low-energy devices. It examines miniaturization, circular polarization, fabrication challenges, and efficiency using the metamaterial-inspired antenna, concentrating on improving diode nonlinearity design. This study analyzes key components such as rectifiers, impedance matching networks, and antennas, and evaluates their applications in biomedical and IoT devices. The review concludes with future directions to increase bandwidth, improve power conversion efficiency, and optimize RF energy harvesting system designs.

In medium-voltage medium- and high-power converters, it is of great importance to reach high-quality waveforms with low switching frequency. In active rectifiers, both converter's ac-side harmonics and grid preexisting distortions affect the quality of the input current, which according to the existing standards is restricted from both the individual harmonics amplitude and total harmonic distortion point of view. The well known selective harmonic elimination pulse-width modulation technique is able to completely eliminate certain harmonics from the ac-side voltage of the converter, and as a result increases the quality of the input current. In this study, an optimal selective harmonic elimination control strategy is introduced for cascaded H-bridge (CHB) rectifiers. By fully manipulating the ac-side waveform of the rectifier, maximum number of harmonics is eliminated for a specific number of switching transitions. Moreover, this method can be easily extended for any number of H-bridge cells and it uses only one lookup table for the whole interval of modulation index. Also using an effective voltage balancing technique, dc-link voltages are balanced to the reference value and the rectifier does not encounter any difficulty under equal or non-equal loads conditions. Using this method, the size of the bulky line-side filters can be reduced which leads to lower overall cost of implementation. To prove the feasibility of the proposed scheme, simulation and experimental results for a seven-level CHB-based rectifier are reported.

Sour taste is detected by a subset of taste cells on the tongue and palate epithelium that respond to acids with trains of action potentials. Entry of protons through a Zn²⁺-sensitive proton conductance that is specific to sour taste cells has been shown to be the initial event in sour taste transduction. Whether this conductance acts in concert with other channels sensitive to changes in intracellular pH, however, is not known. Here, we show that intracellular acidification generates excitatory responses in sour taste cells, which can be attributed to block of a resting K⁺ current. We identify KIR2.1 as the acid-sensitive K⁺ channel in sour taste cells using pharmacological and RNA expression profiling and confirm its contribution to sour taste with tissue-specific knockout of the Kcnj2 gene. Surprisingly, acid sensitivity is not conferred on sour taste cells by the specific expression of KIR2.1, but by the relatively small magnitude of the current, which makes the cells exquisitely sensitive to changes in intracellular pH. Consistent with a role of the K⁺ current in amplifying the sensory response, entry of protons through the Zn²⁺-sensitive conductance produces a transient block of the KIR2.1 current. The identification in sour taste cells of an acid-sensitive K⁺ channel suggests a mechanism for amplification of sour taste and may explain why weak acids that produce intracellular acidification, such as acetic acid, taste more sour than strong acids.

Background: Artemisinin (ART) is an anti-malarial agent reported to influence endocrine function. Methods: Effects of ART on ionic currents and action potentials (APs) in pituitary tumor (GH 3 ) cells were evaluated by patch clamp techniques. Results: ART inhibited the amplitude of delayed-rectifier K + current (I K(DR) ) in response to membrane depolarization and accelerated the process of current inactivation. It exerted an inhibitory effect on I K(DR) with an IC 50 value of 11.2 µM and enhanced I K(DR) inactivation with a K D value of 14.7 µM. The steady-state inactivation curve of I K(DR) was shifted to hyperpolarization by 10 mV. Pretreatment of chlorotoxin (1 µM) or iloprost (100 nM) did not alter the magnitude of ART-induced inhibition of I K(DR) in GH 3 cells. ART also decreased the peak amplitude of voltage-gated Na + current (I Na ) with a concentration-dependent slowing in inactivation rate. Application of KMUP-1, an inhibitor of late I Na , was effective at reversing ART-induced prolongation in inactivation time constant of I Na . Under current-clamp recordings, ART alone reduced the amplitude of APs and prolonged the duration of APs. Conclusion: Under ART exposure, the inhibitory actions on both I K(DR) and I Na could be a potential mechanisms through which this drug influences membrane excitability of endocrine or neuroendocrine cells appearing in vivo.

Remdesivir (RDV, GS-5734), a broad-spectrum antiviral drug in the class of nucleotide analogs, has been particularly tailored for treatment of coronavirus infections. However, to which extent RDV is able to modify various types of membrane ion currents remains largely uncertain. In this study, we hence intended to explore the possible perturbations of RDV on ionic currents endogenous in pituitary GH cells and Jurkat T-lymphocytes. The whole-cell current recordings of ours disclosed that upon membrane depolarization in GH cells the exposure to RDV concentration-dependently depressed the peak or late components of elicitation with effective IC values of 10.1 or 2.8 μM, respectively; meanwhile, the value of dissociation constant of RDV-induced blockage of on the basis of the first-order reaction was yielded to be 3.04 μM. Upon the existence of RDV, the steady-state inactivation curve of was established in the RDV presence; moreover, the recovery became slowed. However, RDV-induced blockage of failed to be overcome by further addition of either α,β-methylene ATP or cyclopentyl-1,3-dipropylxanthine. The RDV addition also lessened the strength of M-type K current with the IC value of 2.5 μM. The magnitude of voltage hysteresis of elicited by long-lasting triangular ramp pulse was diminished by adding RDV. Membrane electroporation-induced current in response to large hyperpolarization was enhanced, with an EC value of 5.8 μM. Likewise, in Jurkat T-lymphocytes, adding RDV declined amplitude concomitantly with the raised rate of current inactivation applied by step depolarization. Therefore, in terms of the RDV molecule, there appears to be an unintended activity of the prodrug on ion channels. Its inhibition of both and occurring in a non-genomic fashion might provide additional but important mechanisms through which cellular functions are seriously perturbed.

The rodent granular retrosplenial cortex (GRS) is reciprocally connected with the hippocampus. It is part of several networks implicated in spatial learning and memory, and is known to contain head-direction cells. There are, however, few specifics concerning the mechanisms and microcircuitry underlying its involvement in spatial and mnemonic functions. In this report, we set out to characterize intrinsic properties of a distinctive population of small pyramidal neurons in layer 2 of rat GRS. These neurons, as well as those in adjoining layer 3, were found to exhibit a late-spiking (LS) firing property. We established by multiple criteria that the LS property is a consequence of delayed rectifier and A-type potassium channels. These were identified as Kv1.1, Kv1.4 and Kv4.3 by Genechip analysis, in situ hybridization, single-cell reverse transcriptase-polymerase chain reaction, and pharmacological blockade. The LS property might facilitate comparison or integration of synaptic inputs during an interval delay, consistent with the proposed role of the GRS in memory-related processes.

The Kir3.1 K + channel participates in heart rate control and neuronal excitability through G‐protein and lipid signaling pathways. Expression in Escherichia coli has been achieved by replacing three fourths of the transmembrane pore with the pore of a prokaryotic Kir channel, leaving the cytoplasmic pore and membrane interfacial regions of Kir3.1 origin. Two structures were determined at 2.2 Å. The selectivity filter is identical to the Streptomyces lividans K + channel within error of measurement (r.m.s.d.<0.2 Å), suggesting that K + selectivity requires extreme conservation of three‐dimensional structure. Multiple K + ions reside within the pore and help to explain voltage‐dependent Mg 2+ and polyamine blockade and strong rectification. Two constrictions, at the inner helix bundle and at the apex of the cytoplasmic pore, may function as gates: in one structure the apex is open and in the other, it is closed. Gating of the apex is mediated by rigid‐body movements of the cytoplasmic pore subunits. Phosphatidylinositol 4,5‐biphosphate‐interacting residues suggest a possible mechanism by which the signaling lipid regulates the cytoplasmic pore.

Protein–lipid interactions are a key element of the function of many integral membrane proteins. These potential interactions should be considered alongside the complexity and diversity of membrane lipid composition. Inward rectifier potassium channel (Kir) Kir2.2 has multiple interactions with plasma membrane lipids: Phosphatidylinositol (4, 5)-bisphosphate (PIP₂) activates the channel; a secondary anionic lipid site has been identified, which augments the activation by PIP₂; and cholesterol inhibits the channel. Molecular dynamics simulations are used to characterize in molecular detail the protein–lipid interactions of Kir2.2 in a model of the complex plasma membrane. Kir2.2 has been simulated with multiple, functionally important lipid species. From our simulations we show that PIP₂ interacts most tightly at the crystallographic interaction sites, outcompeting other lipid species at this site. Phosphatidylserine (PS) interacts at the previously identified secondary anionic lipid interaction site, in a PIP2 concentration-dependent manner. There is interplay between these anionic lipids: PS interactions are diminished when PIP₂ is not present in the membrane, underlining the need to consider multiple lipid species when investigating protein–lipid interactions.