Modeling of Gate Tunneling Current for Nanoscale MOSFETs with High-k Gate Stacks

A quantum model based on solutions to the Schrodinger-Poisson equations is developed to investigate the device behavior related togate tunneling current for nanoscale MOSFETs with high-k gate stacks. This model can model various MOS device structures with combinations of high-k dielectric materials and multilayer gate stacks,revealing quantum effects on the device performance. Comparisons are made for gate current behavior between nMOSFET and pMOSFET high- k gate stack structures. The results presented are consistent with experimental data, whereas a new finding for an optimum nitrogen content in HfSiON gate dielectric requires further experimental verifications.

Gate Current for MOSFETs with High k Dielectric Materials

The MOSFET gate currents of high k gate dielectrics due to direct tunneling are investigated by using a new direct tunneling current model developed.The model includes both the inversion layer quantization effect with finite barrier height and the polysilicon depletion effect.The impacts of dielectric constant and conduction band offset as well as the band gap on the gate current are discussed.The results indicate that the gate dielectric materials with higher dielectric constant,larger conduction band offset and the larger band gap are necessary to reduce the gate current.The calculated results can be used as a guide to select the appropriate high k gate dielectric materials for MOSFETs.

Two outward potassium current types are expressed during the neural differentiation of neural stem cells

The electrophysiological properties of potassium ion channels are regarded as a basic index for determining the functional differentiation of neural stem cells. In this study, neural stem cells from the hippocampus of newborn rats were induced to differentiate with neurotrophic growth factor, and the electrophysiological properties of the voltage-gated potassium ion channels were observed. Immunofluorescence staining showed that the rapidly proliferating neural stem cells formed spheres in vitro that expressed high levels of nestin. The differentiated neurons were shown to express neuron-specific enolase. Flow cytometric analysis revealed that the neural stem cells were actively dividing and the percentage of cells in the S ＋ G2/M phase was high. However, the ratio of cells in the S ＋ G2/M phase decreased obviously as differentiation proceeded. Whole-cell patch-clamp re- cordings revealed apparent changes in potassium ion currents as the neurons differentiated. The potassium ion currents consisted of one transient outward potassium ion current and one delayed rectifier potassium ion current, which were blocked by 4-aminopyridine and tetraethylammonium, respectively. The experimental findings indicate that neural stem cells from newborn rat hippo- campus could be cultured and induced to differentiate into functional neurons under defined condi- tions in vitro. The differentiated neurons expressed two types of outward potassium ion cur＇ents similar to those of mature neurons in vivo.

Effects of Volsartan on Transmural Heterogeneous Changes of Transient Outward Potassium Currents in Hypertrophic Cardiomyocytes in Rabbits

The transmural heterogeneous changes of transient outward potassium currents (Ito) in rabbit hypertrophic cardiaomyocytes and the effects of long-term prophylactic treatment with volsartan were investigated. Rabbits were divided into hypertrophy group (left ventricular hypertrophy induced by partial ligation of abdominal aorta), vol-treated group (volsartan was administrated after the ligation), and control group (sham operated). Myocytes were isolated by a two-step enzymatical method. The sub-endocardial (Endo) and sub-epicardium (Epi) tissues were separated from midmyocardium (Mid) with a razor. Whole-cell patch-clamp technique was used to record potassium currents. The results showed that membrane capacitance was larger in hypertrophic cells than those in control and vol-treated cells (P<0.01 vs control cells, n=30). The densities of Ito in hypertrophic cells were reduced by sub-epicardium (Epi) (27.8±2.9) %, midmyocardium (Mid) (41.0±4.7) %, and sub-endocardium (Endo) (20.3±3.4) % compared with those in control cells. The decrease of Ito density was more pronounced in Mid than in Epi and Endo (P<0.01 vs Epi or Endo). There were no significant differences in Ito densities between vol-treated group and control group in three layers separately. In conclusion, volsartan can inhibit the transmural heterogeneous changes of Ito in left ventricular hypertrophic cardiomyocytes in rabbit.

Silencing gamma-aminobutyric acid A receptor alpha 1 subunit expression and outward potassium current in developing cortical neurons

We used RNA interference （RNAi） to disrupt synthesis of the cortical neuronal y-aminobutyric acid A receptor （GABAAR） al in rats during development, and measured outward K＋ currents during neuronal electrical activity using whole-cell patch-clamp techniques. Three pairs of small interfering RNA （siRNA） for GABAAR al subunit were designed using OligoEngine RNAi software. This siRNA was found to effectively inhibited GABAAR al mRNA expression in cortical neuronal culture in vitro, but did not significantly affect neuronal survival. Outward K^currents were decreased, indicating that GABAAR al subunits in developing neurons participate in neuronal function by regulating outward K＋ current.

Effects of WIN 55,212-2 on I_K Current in Cultured Trigeminal Ganglion Neurons of Rat

Summary: To investigate the effects of WIN 55,212-2 on I K in cultured rat trigeminal ganglion (TG) neurons, whole-cell patch clamp techniques were used to record the I K before and after WIN 55,212-2 perfusion at different concentrations. 30 μmol/L WIN 55,212-2 markedly (35 7 %± 7 3 %, P<0.01, n=8) inhibited I K currents, and the currents were partially recovered after washing. 30 μmol/L WIN 55,212-2 also induced a significant depolarizing shift in conductance-voltage parameters (control: V 0 5=10 43 ± 4.25 mV, k=16 27±3 86; WIN 55,212-2: V 0.5=24.71±3.91 mV, k =16.69±2.75; n = 8, P<0.01 for V 0.5). 0.01 μmol/L WIN 55,212-2 slightly (27.0 %± 7.9 %, P<0.05, n=7) increased I K currents, but had no significant change in conductance–voltage parameters (control: V 0.5=10.74±5.27 mV, k=17.33±2.96; WIN 55,212-2: V 0.5=11.06±2.05 mV, k=19.69±6.60; n=7, P>0.05 for V 0.5 and k). These results suggested that WIN 55,212-2 has dual action, which might be through different receptors.

Effects of Atractylodes Macrocephala on the Cytomembrane Ca^(2+)-activated K^+ Currents in Cells of Human Pregnant Myometrial Smooth Muscles

The study examined the inhibitory effect of Atractylodes macrocephala （AM） on the uterine contraction during premature delivery and explored its electrophysiological mechanism by studying the effects of AM on the Ca^2＋-activated K^＋ currents of pregnant human myometrial smooth muscle cells with or without the treatment with intedeukin-6. Single cells were acutely isolated from pregnant human myometrial smooth muscles. Whole-cell Ca^2＋-activated K^＋ currents were recorded by using an Axopatchl-D amplifier. The cells were divided into three groups： group A in which AM was added into perfusate, group B, in which interleukin-6 was added into perfusate） and group C in which AM was added into perfusate after addition of interleukin-6. IL-6 10 ng/mL inhibited BKca by 36.9%±13.7% as compared with control （P〈0.01）. AM at 2 mg/mL raised BKca by 36.7%±22.6% or 45.2%±13.7% with or without the treatment of IL-6, respectively （P〈0.01）. It is concluded that AM was able to enhance the BKca of pregnant human myometrial smooth muscle cells treated or untreated with interleukin-6 and its effect on the BKca IL-treated cells was stronger that its effect on BKca of untreated cells. Our results suggested that AM can help to maintain the membrane potentials and the resting status of pregnant human myometrial smooth muscle cells.

Effects of sodium ferulate on the ultrarapid delayed rectifier K^+ current in human atrial myocytes

Objective：To study the effects of sodium ferulate on the ultrarapid delayed rectifier K^＋ current（IKur） in human atrial myocytes. Methods：Human atrial myocytes were isolated by enzyme dispersion method. IKur, in human atrial myocytes were recorded by using the whole cell patch clamp. The changes of IKur were compared in the absence and the presence of sodium ferulate. Results：There was no effect of 0.4 g/L sodium ferulate on I-V relation of IKur. However, 0.4 g/L sodium ferulate inhibited IKur to some degrees at each test pulse. The current densities of IKur at ＋60 mV decreased from 4.997 ± 0.35 PA/PF to 3.331 ± 0.26 PA/PF（n = 6, P 〈 0.05）. The inhibitory effect was concentration-dependent. IC50 was（0.41 ±0.03）g/L and the Hill coefficient was 0.95 ± 0.05. Conclusion：Sodium ferulate as a potassium channel blocker can inhibit IKur in human atrial myocytes effectively.

Distinct protein kinase C isozymes mediates inhibitory effects of different G-protein coupled receptors on cardiac rapidly activating delayed rectifier K ~ current

Aim Evidence has shown that stimulation of alA-adrenorecetors receptor （alA-AR） or angiotensin II type 1 receptor （AT1R） acutely down-regulates the rapid component of the delayed rectifier K ＋ current （IKr） via protein kinase C （PKC）. This study was designed to investigate which PKC isozymes mediate down-regulations of IKr by alA-AR and AT1R. Method The whole-cell patch-clamp technique was used to record IKr in native cardio- myocytes and in human embryonic kidney （HEK） 293 cells co-transfected with human ether-a-go-go related gene （hERG） encoding α-subunit of IKr and human alA-AR or AT1R gene. Result In isolated guinea-pig ventricular cardiomyocytes the inhibitory action of Ang II on IKr was little affected by Go6976 （selectively inhibiting PKCα, β and γ） and Go6983 （selectively inhibiting PKCα, β, γ , δ, and ζ）, but was significantly antagonized by an inter- nal dialysis with PKCe-selective inhibitory peptide εV1 -2. In contrast, the inhibitory action of alA-AR agonist A61603 on IKr was remarkably attenuated by Go6976 or Go6983, but not affected by peptide εV1 -2. Moreover, specific PKC-selective inhibitory peptide antagonized the effect of A61603. The results suggested that PKCe and PKCα isoform respectively mediated the inhibitory effect of AT1R and a1A-AR. In heterologous expression system, both PKCα and e-selective activator peptides down regulated hERG current with different manner. PKCα activator peptide shifted the activation curve of the channel to the right, but PKCe-selective activator peptide did not. Simi- larly, A61603 shifted the activation curve to the right, whereas Ang Ⅱ had no effect. In addition, both A61603 and PKCα activator peptide showed inhibitory action on bERG A PKC current （an bERG mutant in which 17 of the 18 ROSITE-predicted PKC acceptor serines/threonines were changed to alanine） with a similar potency to wild type bERG current. But, both Ang Ⅱ and PKCe-selective activator peptide exhibited no effects on bERG △ PKC cur- rent. The results indicated that PKCα and PKCe isoforms down-regulated bERG current through different mecha- nism. Conclusion PKCα and PKCe isoform respectively mediates the inhibition on IKr by stimulation of AT1R and alA-AR via different molecular mechanism.

基于改进k-means算法的科研仪器机时智能计算系统

传统的机时统计常使用人工,不仅效率低,而且成本相对较大,因此在传统的机时计算的基础上提出一种基于改进k均值聚类算法的科研仪器机时智能计算系统。通过对仪器机时电流数据的聚类分析,完成对仪器机时的计算和统计,同时将传统k均值聚类算法进行改进,提升其系统机时计算的准确性。结果表明,使用改进k均值聚类算法后的机时系统在仪器的机时计算中表现更为优异,计算的时间与正常运行时间相同,能够在一定程度上达到0误差标准。由此可见,使用改进聚类算法进行仪器的机时统计能够提升机时计算结果的准确性。

Stress-induced leakage current characteristics of PMOS fabricated by a new multi-deposition multi-annealing technique with full gate last process

In the process of high-k films fabrication, a novel multi deposition multi annealing （MDMA） technique is introduced to replace simple post deposition annealing. The leakage current decreases with the increase of the post deposition annealing （PDA） times. The equivalent oxide thickness （EOT） decreases when the annealing time（s） change from 1 to 2. Furthermore, the characteristics of SILC （stress-induced leakage current） for an ultra-thin SiO2/HfO2 gate dielectric stack are studied systematically. The increase of the PDA time（s） from 1 to 2 can decrease the defect and defect generation rate in the HK layer. However, increasing the PDA times to 4 and 7 may introduce too much oxygen, therefore the type of oxygen vacancy changes.

基于k值调制三电平Boost PFC变换器的变占空比控制

随着国家大力发展城市轨道交通,不间断电源(uninterruptible power supply,UPS)系统作为关键供电装置,具有重要的研究意义和价值。为了满足相关电能质量法规的要求,集成功率因数校正(power factor correction,PFC)输入级是保证轨道交通基础设施设备供电的UPS系统的重要要求。三电平Boost PFC在采用传统载波调制时,在一定的输入电压范围内输入电流始终为零,导致变换器功率因数校正效果较差。因此,提出一种基于k值调制的变占空比控制的方法,不仅可以解决高输入电压下传统载波调制存在的问题,且可进一步抑制输入电流的畸变从而提高输入电流波形质量。首先介绍了这种k值调制方法,分析了其原理以及k值对变换器功率因数和电感电流有效值的影响。在此基础上,结合电压平衡策略对k值进行优化,解决直流侧输出电容电压上下不均衡问题。最后,针对高输入电压下输入电流仍然严重畸变的问题,提出一种基于k值调制的可变占空比控制方法,分析了变占空比控制对变换器功率因数、输出功率、电压纹波以及电感电流峰值的影响。最后通过仿真和搭建小功率实验平台,验证了所提控制方法的正确性和有效性。

Fault Identification of Power Grid Based on Wide-Area Differential Current and K-Means Clustering

A new method of fault domain identification is proposed based on K-means clustering analysis theories using the wide-area information of power grid. In the method, the node Intelligent Electronic Device (IED) associated domain is defined, and the relationship of positive sequence current fault component for the association domain boundaries is sought, then the conception of positive sequence fault component differential current for node IED association domains is introduced. The information of the positive sequence fault component differential current gathered by node IEDs is selected as the object of K-means clustering. The node IEDs of fault associated domains can be classified into one category, and the node IEDs of non-fault associated domains are classified into another category. With the fault area minimum principle, the group of node IEDs about fault associated domains can be obtained. The overlap of fault associated domains for different nodes is the fault area. A large number of simulations show that the algorithm proposed can identify fault domains with high accuracy and no influence by the operating mode of the system and topological changes.

基于并行k-means聚类的配电网台区无功补偿模块化控制方法

配电网台区无功补偿过程中受到配电线损谐波影响,出现电流、电压不平衡而无法抑制无功电流、电压的问题。为了实现配电网台区无功补偿,结合并行k-means聚类算法提出配电网台区无功补偿模块化控制方法。构建模块化多电平换流器稳定无功补偿控制结构,结合k-means聚类算法归一化计算配电网线损率,避免无功补偿谐波增大而导致电压不平衡,有助于保持无功补偿控制稳定性。采用k-means聚类算法对多个样本分类处理,并将中心样本数据作为聚类中心。结合配电网运行状态,计算电流平衡度,筛选出最佳状态下智能电流控制开关分布状态,改变电流输入和输出的选相,控制无功补偿电流值,保持配电网内部的电流平衡。构建电压正、负序分量变换矩阵,控制目标有功、无功电压。通过引入非闭环控制结构,对实际运行过程中出现的扰动及时纠正,使电压在额定电压调节范围内稳定波动,保持配电网内部电压平衡。由实验结果可知,该方法补偿后无功电流、电压为0,配电网台区主要为有功电流、电压,说明使用该方法能够瞬时抑制无功电流,达到理想补偿效果。

KCNE2对Kv4.3通道功能的调节作用

目的研究KCNE2对人类心肌细胞瞬间外向钾电流的主要α亚基-Kv4.3功能的调节。方法通过基因转染技术将Kv4.3或Kv4.3与KCNE2cDNA转入COS-7细胞株,采用膜片钳全细胞记录方式记录通道电流。结果KCNE2对Kv4.3功能有明显调控作用:减小Kv4.3通道电流密度;Kv4.3单独表达组通道电流密度为375.13±112.87pA/pF(n=11),KCNE2与Kv4.3共表达组电流密度为152.96±33.71pA/pF(n=16);减慢Kv4.3通道激活和衰减,在+60mV电压刺激下通道激活达峰值的时间由4.82±0.32ms(n=11)延长至20.41±2.13ms(n=16),P<0.05;通道电压依赖性失活发生正向移位,半数失活电压由-53.62±1.24mV(n=8)移至-46.58±1.6mV(n=10);通道从失活中恢复的速度加快,恢复时间常数由193.43±17.98ms缩短137.71±18.29ms,(n=7,P<0.05)。结论KCNE2可能作为人类心肌细胞膜Kv4.3钾离子通道一个重要的辅助亚基-β亚基参与Ito通道功能的调节。

蝎毒素BmkTXKβ对家兔心房肌细胞瞬间外向钾电流的抑制作用

为研究蝎毒素BmkTXKβ对家兔心房肌细胞瞬间外向钾电流 (Ito)的影响 ,采用全细胞膜片钳技术记录应用BmkTXKβ前后的Ito电流 .结果显示BmkTXKβ (1μmol/L)使心房肌细胞Ito (刺激电压为 +5 0mV)从(13 6 3± 0 87)pA/ pF减少到 (7 98± 0 78) pA/pF ,抑制率为 4 1 4 % (n =16 ,P <0 0 0 1) .冲洗后 ,Ito部分恢复至 (11 18± 0 82 ) pA/pF (n =6 ,P <0 0 1,与给药后比较 ) .在 0 0 1～ 10 0 μmol/L范围内BmkTXKβ呈浓度依赖性地抑制Ito,IC50 的均值为 0 95 μmol/L (n =10 ,P <0 0 1) ,但无频率依赖性 (n =6 ,P >0 0 5 ) .1μmol/L的BmkTXKβ可使Ito通道的失活动力学曲线明显左移 ,V1/ 2 分别为 (- 2 3 6± 2 7)mV和 (- 35 3± 3 6 )mV(n =8,P <0 0 5 ) ,曲线斜率基本不变 .同时可使Ito通道的恢复过程明显减慢 ,恢复曲线右移 ,τ值从 (5 1 2±8 5 )ms延长至 (93 5± 13 4 )ms (n =9,P <0 0 1) ,但不影响其激活过程 .据此推断BmkTXKβ对家兔心房肌细胞Ito具有显著的抑制作用 ,主要作用于失活过程 。

有氧运动抑制衰老大鼠脑动脉平滑肌STOC/BK_(Ca)功能下调

目的探讨有氧运动训练对衰老大鼠脑动脉平滑肌细胞全细胞K＋电流、自发瞬时外向电流及大电导钙激活钾通道生物物理特性的影响。方法 19~21月龄雄性Wistar大鼠12只（老年组）,随机分为安静组和有氧运动组,并选用2月龄Wistar大鼠安静处理作为青年对照组。12周后取脑动脉,急性分离动脉平滑肌细胞。分别采用膜片钳全细胞模式、穿孔膜片钳模式和单通道内面向外模式观察运动对全细胞K＋电流、自发瞬时外向电流和大电导钙激活钾通道门控特性的影响。结果安静组全细胞K＋电流密度及对Iberiotoxin敏感性降低;安静组自发瞬时外向电流幅值降低,频率无明显变化;安静组大电导钙激活钾通道平均开放概率和平均开放时间显著低于青年对照组,而平均关闭时间高于青年对照组;电压依赖性和钙敏感性亦显著下降;与安静组相比,有氧运动可以增加全细胞K＋电流密度、自发瞬时外向电流幅值及大电导钙激活钾通道平均开放概率、电压依赖性和钙敏感性来实现对大鼠脑动脉平滑肌自发瞬时外向电流/大电导钙激活钾通道功能的保护作用。结论长期规律有氧运动可以减弱衰老所致的大鼠脑动脉平滑肌细胞大电导钙激活钾通道功能下调,这可能是有氧运动改善衰老动脉功能的重要机制之一。

白花前胡甲素对豚鼠单一心室肌细胞Ⅰ_K通道作用机制的初步探讨

目的通过比较白花前胡甲素（Pd－Ia）与异丙肾上腺素对豚鼠单一心室肌细胞迟发性外向钾电流（IK）的影响，初步探讨Pd－Ia开放钾通道作用的可能机制。方法；应用全细胞膜片钳制技术。结果与结论：Pd－Ia对IK通道作用的最大效应与异丙肾上腺素相近，均使IK增加2～2．5倍，对IK的激活动力学过程均无明显影响，而且两药的作用不具有相加性。另外，乙酰胆碱对Pd－Ia增加IK作用的影响也与对异丙肾上腺素的影响相似，提示Pd－Ia对IK的作用可能是通过激活PKA而产生的。其确切机制还有待进一步实验研究。

ABA对拟南芥los5-1突变体及其野生型保卫细胞质膜内向K^+通道的调节

以拟南芥(Arabidopsis thaliana)ABA缺失突变体los5-1及其相应野生型为材料,用细胞质膜钙离子通道的抑制剂LaCl3和细胞内钙离子的螯合剂EGTA处理,运用膜片钳技术探讨在ABA调节突变体和相应野生型保卫细胞质膜内向K+电流过程中Ca2+的作用.实验结果表明ABA均可以明显抑制拟南芥C24野生型及其突变体los5-1保卫细胞原生质体的内向K+电流,而且ABA对los5-1突变体及其相应野生型保卫细胞质膜内向K+通道的调节具有不同的Ca2+依赖性,说明ABA对突变体和野生型的K+通道的调节可能通过不同的信号转导机制.

Na^+和Ca^(2+)对拟南芥根原生质体质膜内向K^+通道电流的影响

以拟南芥 ArabidopsisthalianaColumbia 根为材料,利用膜片钳技术测定其根细胞原生质体质膜内向K+电流,并对Na+对其K+电流的影响进行了初步研究,发现Na+可明显抑制拟南芥根细胞原生质体的内向K+电流,外施Ca2+可缓解Na+对内向K+电流的抑制.说明Ca2+参与了质膜上K+通道对K+/Na+的选择性吸收的调节,从而使植物适应盐胁迫.