A fast 600-V Tandem PiN Schottky (TPS) rectifier with ultra-low on-state voltage

The Tandem PiN Schottky (TPS) rectifier features lowly-doped p-layers in both active and termination regions, and is applied in 600-V rating for the first time. In the active region, the Schottky contact is in series connection with a transparent p-layer, leading to a superior forward performance than the conventional diodes. In addition, due to the benefit of moderate hole injection from the p-layer, the TPS offers a better trade-off between the on-state voltage and the switching speed. The active p-layer also helps to stabilise the Schottky contact, and hence the electrical data distributions are more concentrated. Regarding the floating p-layer in the termination region, its purpose is to reduce the peak electric fields, and the TPS demonstrates a high breakdown voltage with a compact termination width, less than 70% of the state-of-the-art devices on the market. Experimental results have shown that the 600-V TPS rectifier has an ultra-low on-state voltage of 0.98 V at 250 A/cm 2, a fast turn-off time of 75 ns by the standard RG1 test (I F=0.5A, I R=1A, and I RR=0.25A) and a breakdown voltage over 720 V. It is noteworthy that the p-layers in the active and termination regions can be formed at no extra cost for the use of self-alignment process. © 2012 IEEE.

A Fully Integrated 900-MHz Passive RFID Transponder Front End With Novel Zero-Threshold RF-DC Rectifier

This paper presents a fully integrated CMOS analog front end for a passive 900-MHz radio-frequency identification (RFID) transponder. The power supply in this front end is generated from the received RF electromagnetic energy by using an RF-dc voltage rectifier. In order to improve the compatibility with standard CMOS technology, Schottky diodes in conventional RF-dc rectifiers are replaced by diode-connected MOS transistors with zero threshold. Meanwhile, theoretical analyses for the proposed rectifier are provided and verified by both simulation and measurement results. The design considerations of the pulsewidth-modulation (PWM) demodulator and the backscatter modulator in the front end are also discussed for low-power applications. The proposed front end is implemented in a 0.35-mu m 2P4M CMOS technology. The whole chip occupies a die area of 490 x 780 mu m(2) and consumes only 2.1 mu W in reading mode under a self-generated 1.5-V supply voltage. The measurement results show that the proposed rectifier can properly operate with a - 14.7-dBm input RF power at a power conversion efficiency of 13.0%. In the proposed RFID applications, this sensitivity corresponds to 10.88-m communication distance at 4-W equivalent isotropically radiated power from a reader base station.

A voltage-adjustable three-phase rectifier with constant power flow

An three phase adjustable output voltage rectifier with constant power flow based on waveform gap patching principle is resented. By patching the gapes in the phase currents in parallel way as well as the ripple of the output voltage in series way, it implements the constant power flow from the three-phase line to the DC output without using any line frequency (and its harmonics) energy storage components. Principally, by treating only 22.4% power of the needed power output, this rectifier can supply constant power flow with adjustable output voltages without bring about any harmonic interferences to the power utility and achieve unite power factor.

Kir2.2 inward rectifier potassium channels are inhibited by an endogenous factor in Xenopus oocytes independently from the action of a mitochondrial uncoupler.

We previously showed inhibition of Kir2 inward rectifier K+ channels expressed in Xenopus oocytes by the mitochondrial agents carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) and sodium azide. Mutagenesis studies suggested that FCCP may act via phosphatidylinositol 4,5-bisphosphate (PIP2) depletion. This mechanism could be reversible in intact cells but not in excised membrane patches which preclude PIP2 regeneration. This prediction was tested by investigating the reversibility of the inhibition of Kir2.2 by FCCP in intact cells and excised patches. We also investigated the effect of FCCP on Kir2.2 expressed in human embryonic kidney (HEK) cells. Kir2.2 current, expressed in Xenopus oocytes, increased in inside-out patches from FCCP-treated and untreated oocytes. The fraction of total current that increased was 0.79?±?0.05 in control and 0.89?±?0.03 in 10 µM FCCP-treated (P?>?.05). Following “run-up,” Kir2.2 current was re-inhibited by “cramming” inside-out patches into oocytes. Therefore, run-up reflected not reversal of inhibition by FCCP, but washout of an endogenous inhibitor. Kir2.2 current recovered in intact oocytes within 26.5 h of FCCP removal. Injection of oocytes with 0.1 U apyrase completely depleted ATP (P?<?.001) but did not inhibit Kir2.2 and inhibited Kir2.1 by 35% (P?<?.05). FCCP only partially reduced [ATP] (P?<?.001), despite inhibiting Kir2.2 by 75% (P?<?.01) but not Kir2.1. FCCP inhibited Kir2.2 expressed in HEK cells. The recovery of Kir2.2 from inhibition by FCCP requires intracellular components, but direct depletion of ATP does not reproduce the differential inhibitory effect of FCCP. Inhibition of Kir2.2 by FCCP is not unique to Xenopus oocytes. J. Cell. Physiol. 219: 8–13, 2009. © 2008 Wiley-Liss, Inc.

Inward rectifier potassium channels in the HL-1 cardiomyocyte-derived cell line.

HL-1 is a line of immortalized cells of cardiomyocyte origin that are a useful complement to native cardiomyocytes in studies of cardiac gene regulation. Several types of ion channel have been identified in these cells, but not the physiologically important inward rectifier K(+) channels. Our aim was to identify and characterize inward rectifier K(+) channels in HL-1 cells. External Ba(2+) (100?µM) inhibited 44?±?0.05% (mean?±?s.e.m., n?=?11) of inward current in whole-cell patch-clamp recordings. The reversal potential of the Ba(2+)-sensitive current shifted with external [K(+)] as expected for K(+)-selective channels. The slope conductance of the inward Ba(2+)-sensitive current increased with external [K(+)]. The apparent Kd for Ba(2+) was voltage dependent, ranging from 15?µM at -150 ?mV to 148?µM at -75 ?mV in 120 ?mM external K(+). This current was insensitive to 10?µM glybenclamide. A component of whole-cell current was sensitive to 150?µM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), although it did not correspond to the Ba(2+)-sensitive component. The effect of external 1 mM Cs(+) was similar to that of Ba(2+). Polymerase chain reaction using HL-1 cDNA as template and primers specific for the cardiac inward rectifier K(ir)2.1 produced a fragment of the expected size that was confirmed to be K(ir)2.1 by DNA sequencing. In conclusion, HL-1 cells express a current that is characteristic of cardiac inward rectifier K(+) channels, and express K(ir)2.1 mRNA. This cell line may have use as a system for studying inward rectifier gene regulation in a cardiomyocyte phenotype.

Altered stress stimulation of inward rectifier potassium channels in Andersen-Tawil syndrome

Inward rectifier potassium channels of the Kir2 subfamily are important determinants of the electrical activity of brain and muscle cells. Genetic mutations in Kir2.1 associate with Andersen-Tawil syndrome (ATS), a familial disorder leading to stress-triggered periodic paralysis and ventricular arrhythmia. To identify the molecular mechanisms of this stress trigger, we analyze Kir channel function and localization electrophysiologically and by time-resolved confocal microscopy. Furthermore, we employ a mathematical model of muscular membrane potential. We identify a novel corticoid signaling pathway that, when activated by glucocorticoids, leads to enrichment of Kir2 channels in the plasma membranes of mammalian cell lines and isolated cardiac and skeletal muscle cells. We further demonstrate that activation of this pathway can either partly restore (40% of cases) or further impair (20% of cases) the function of mutant ATS channels, depending on the particular Kir2.1 mutation. This means that glucocorticoid treatment might either alleviate or deteriorate symptoms of ATS depending on the patient's individual Kir2.1 genotype. Thus, our findings provide a possible explanation for the contradictory effects of glucocorticoid treatment on symptoms in patients with ATS and may open new pathways for the design of personalized medicines in ATS therapy. © FASEB.

A novel dual-fluorescence strategy for functionally validating microRNA targets in 3-prime untranslated regions: regulation of the inward rectifier potassium channel Kir2.1 by miR-212.

Gene targeting by microRNAs is important in health and disease. We developed a functional assay for identifying microRNA targets and applied it to the K+ channel Kir2.1 (KCNJ2) which is dysregulated in cardiac and vascular disorders. The 3'UTR was inserted downstream of the mCherry red fluorescent protein coding sequence in a mammalian expression plasmid. MicroRNA sequences were inserted into the pSM30 expression vector which provides enhanced green fluorescent protein as an indicator of microRNA expression. HEK293 cells were co-transfected with the mCherry-3'UTR plasmid and a pSM30-based plasmid with a microRNA insert. The principle of the assay is that functional targeting of the 3'UTR by the microRNA results in a decrease in the red/green fluorescence intensity ratio as determined by automated image analysis. The method was validated with miR-1, a known downregulator of Kir2.1 expression, and was used to investigate targeting of the Kir2.1 3'UTR by miR-212. Red/green ratio was lower in miR-212-expressing cells compared to non-targeting controls, an effect that was attenuated by mutating the predicted target site. MiR-212 also reduced inward rectifier current and Kir2.1 protein in HeLa cells. This novel assay has several advantages over traditional luciferase-based assays including larger sample size, amenability to time course studies and adaptability to high-throughput screening.