Distributed amplifier of L-type network with 2-μm GaAs HBT process

The characteristic impedances of L-type and T-type networks are first investigated for a distributed amplifier design.The analysis shows that the L-type network has better frequency characteristics than the T-type one.A distribution amplifier based on the L-type network is implemented with the 2-μm GaAs HBT（heterojunction-bipolar transistor） process of WIN semiconductors.The measurement result presents excellent bandwidth performance and gives a gain of 5.5 dB with a gain flatness of ±1dB over a frequency range from 3 to 18 GHz.The return losses S11 and S22 are below-10dB in the designed frequency range.The output 1-dB compression point at 5 GHz is 13.3 dBm.The chip area is 0.95 mm2 and the power dissipation is 95 mW under a 3.5 V supply.

Experimental Study on Hydrodynamics of L-type Podded Propulsor in Straight-ahead Motion and Off-Design Conditions

Experimental tests were conducted to evaluate the hydrodynamic performance of an L-type podded propulsor in straight-ahead motion and off-design conditions using an open-water measuring instrument developed by the authors for podded propulsors, a ship model towing tank, and under water particle image velocimetry （PIV） measurement systems. Under the three types of conditions, the main parameters of an L-type podded propulsor were measured, including the propeller thrust and torque, as well as the thrust, side force, and moment of the whole pod unit.In addition, the flow field on the section between the propeller and the strut was analyzed. Experimental results demonstrate that the dynamic azimuthing rate and direction and the turning direction affect the forces on the propeller and the whole pod unit. Forces are asymmetrically distributed between the left and right azimuthing directions because of the effect of propeller rotation. The findings of this study provide a foundation for further research on L-type podded propulsors.

Effects of Tiaomaiyin and Its Disassembled Prescription on Expression of L-type Calcium Channel β2 Subunit in Rat Model of Tachyarrhythmia

[Objectives] To study the effects of Tiaomaiyin and its disassembled prescription on expression of L-type calcium channel β2 subunit in rat model of tachyarrhythmia. [Methods] Sixty Wistar rats were randomly divided into model group,Tiaomaiyin prescription group( whole prescription group),main efficacy group of removing heat to cool blood( blood cooling group),and auxiliary drug efficacy group of benefiting qi and nourishing heart( qi benefiting group),auxiliary efficacy group of promoting flow of qi and blood circulation( qi flow promoting group),and amiodarone group( western medicine group). Aconitine was given 7 d after the intragastric administration of the corresponding drugs,and the time of occurrence of arrhythmia in each group was observed. The left ventricular myocardium was subjected to reverse transcription-polymerase chain reaction and Western blotting. [Results] The ventricular premature beats( VPB) time in the whole prescription group and western medicine group was significantly longer than that in the model group. Ventricular tachycardia( VT),ventricular fibrillation( VF),and cardiac arrest( CA) were longer in the whole prescription group,blood cooling group,and western medicine group. The mRNA and protein expression of L-type calcium channel β2 subunit in the whole prescription group,blood cooling group and western medicine group were significantly decreased. [Conclusions] Tiaomaiyin whole prescription group and blood cooling group can reduce the occurrence time of tachyarrhythmia and reduce the expression of LTCC β2 in myocardium.

Antiepileptic Drug-Induced Apoptosis Was Prevented by L-Type Calcium Channel Activator in Cultured Rat Cortical Cells

Experimental data have shown that antiepileptic drugs cause neurodegeneration in developing rats. Valproate (VPA) is the drug of choice in primary generalized epilepsies, and carbamazepine (CBZ) is one of the most prescribed drugs in partial seizures. These drugs block sodium channels, thereby reducing sustained repetitive neuronal firing. The intracellular mechanisms whereby AEDs induce neuronal cell death are unclear. We examined whether AEDs induce apoptotic cell death in cultured cortical cells and whether calcium ions are involved in the AED-induced cell death. VPA and CBZ increased apoptotic cell death and induced morphological changes that were characterized by cell shrinkage and nuclear condensation or fragmentation. Incubation of cortical cultures with VPA or CBZ decreased phospho-Akt levels. CBZ decreased the intracellular calcium levels. On the other hand, FPL64176, an L-type calcium channel activator, increased the intracellular calcium levels and prevented the AED-induced apoptosis. Glycogen synthase kinase-3 inhibitors, such as alsterpaullone and azakenpaullone, prevented the AED-induced apoptosis. These results suggest that intracellular calcium level changes are associated with AEDs and apoptosis and that the activation of glycogen synthase kinase-3 is involved in the death of rat cortical neurons.

The Effect of Extrogenous Phosphocreatine on L-type Calcium Current in Ischemic Guinea Pig Ventricular Myocytes

Objectives Heart failure （HF） is one of the most common outcome for all kinds of heart diseases, the effects of energetic therapy on HF remains controversial, especially to ischemic HF. The aim of this study was to explore the effect of exogenous phosphocreatine with different concentration on L-type calcium（I Cc-L） current in ischemic ventricular myocytes of guinea pig and to investigate its underlying electrophysiological mechanism for the treatment of ischemic HF. Methods Single ventricular myocytes were isolated enzymatically from left ventricle of guinea pig. Peak I Ca-L current were recorded using patch clamp techniques in the whole-cell configuration when myocytes had been superfused with normal Tyrode solution, simple ischemic solution, ischemic solution containing phosphocreatine with different concentration for 10 minutes respectively. Results Peak I Ca-L current density of myocytes superfused with simple simulated ischemic solution was remarkably inhibited by 80.6 ± 5.2% compared with myocytes superfused with normal Tyrode solution（P〈0.05）. Ischemic solution containing phosphocreatine of 5, 10, 20, 30mmol/L inhibited Peak I Ca-L current density by （53.8±6.7）%, （41.8 ± 8.2）%, （38.1±7.4）%, （36.6±9.7）% respectively. There was no statistical significance among phosphocreation of 10, 20, 30 mmol / L. Conclusions Extrogenous phosphocreatine could reverse the inhibition of I Ca-L current under ischemic condition, which could be the ionic basis for the treatment of ischemic heart failure. 0-10 mmol/L phosphocreatine exerted significant dose-effect relationship which no longer existed as concentration more than 10 mmol/L. It is supposed that phosphocreatine increased I Ca-L current by many pathways rather than simple substrate for ATP synthesis.

基于STAR-CCM+仿真软件的双体船水动力性能分析

以某双体船为研究对象,基于STAR-CCM+仿真软件,按网格无关性验证和时间步长无关性验证的要求,对双船体船静水阻力进行数值方法验证,证明数值计算结果的准确性。对不同片体间距、不同片体形态和不同斜向航行角度等工况进行数值计算,分析双体船水动力性能。计算结果表明:在双体船直航时,在片体间距比为0.2、弗劳德数为0.4的工况条件下,与同一航速的其他工况条件相比静水具有明显的骤升现象,且总阻力系数达最大值14.56×10^(-3);在片体外旋转2°时,与其他旋转角度相比阻力值最小。研究发现,无论是在直航还是斜向航行的情况下,双体船的总阻力系数均呈现先升后降的趋势,说明该船型在处于高速航行状态时具有一定的优越性。

Amlodipine inhibits the proliferation and migration of esophageal carcinoma cells through the induction of endoplasmic reticulum stress

BACKGROUND L-type calcium channels are the only protein channels sensitive to calcium channel blockers,and are expressed in various cancer types.The Cancer Genome Atlas database shows that the mRNA levels of multiple L-type calcium channel subunits in esophageal squamous cell carcinoma tumor tissue are significantly higher than those in normal esophageal epithelial tissue.Therefore,we hypothesized that amlodipine,a long-acting dihydropyridine L-type calcium channel blocker,may inhibit the occurrence and development of esophageal cancer(EC).AIM To investigate the inhibitory effects of amlodipine on EC through endoplasmic reticulum(ER)stress.METHODS Cav1.3 protein expression levels in 50 pairs of EC tissues and corresponding paracancerous tissues were examined.Subsequently,the inhibitory effects of amlodipine on proliferation and migration of EC cells in vitro were detected using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and Transwell assays.In vivo experiments were performed using murine xenograft model.To elucidate the underlying mechanisms,in vitro cell studies were performed to confirm that ER stress plays a role in inhibition proliferation and migration of EC cells treated with amlodipine.RESULTS The expression level of Cav1.3 in esophageal carcinoma was 1.6 times higher than that in paracancerous tissues.Amlodipine treatment decreased the viability of esophageal carcinoma cells in a dose-and time-dependent manner.In vivo animal experiments also clearly indicated that amlodipine inhibited the growth of EC tumors in mice.Additionally,amlodipine reduces the migration of tumor cells by inhibiting epithelial-mesenchymal transition(EMT).Mechanistic studies have demonstrated that amlodipine induces ER stress-mediated apoptosis and suppresses EMT.Moreover,amlodipine-induced autophagy was characterized by an increase in autophagy lysosomes and the accumulation of light chain 3B protein.The combination of amlodipine with the ER stress inhibitor 4-phenylbutyric acid further confirmed the role of the ER stress response in amlodipine-induced apoptosis,EMT,and autophagy.Furthermore,blocking autophagy increases the ratio of apoptosis and migration.CONCLUSION Collectively,we demonstrate for the first time that amlodipine promotes apoptosis,induces autophagy,and inhibits migration through ER stress,thereby exerting anti-tumor effects in EC.

Quantitative proteomics analysis reveals the pathogenesis of obstructed defecation syndrome caused by abnormal expression of dystrophin

BACKGROUND Obstructed defecation syndrome(ODS)represents the most prevalent form of chronic constipation,affecting a diverse patient population,leading to numerous complications,and imposing a significant burden on healthcare resources.Most ODS patients have insufficient rectal propulsion,but the exact mechanism underlying the pathogenesis of ODS remains unclear.AIM To explore the molecular mechanism underlying the pathogenesis of ODS.METHODS A total of 30 pairs of rectal samples were collected from patients with ODS(ODS group)or grade IV prolapsed hemorrhoids without constipation(control group)for quantitative proteomic and bioinformatic analysis.Subsequently,50 pairs of paraffin-embedded rectal specimens were selected for immunohistochemistry and immunofluorescence studies to validate the analysis results.Human intestinal smooth cell contractile function experiments and electrophysiological experiments were conducted to verify the physiological functions of target proteins.Cellular ultrastructure was detected using transmission electron microscopy.RESULTS In comparison to the control group,the expression level of dystrophin(DMD)in rectal specimens from ODS patients was markedly reduced.This finding was corroborated using immunohistochemistry and immunofluorescence techniques.The diminished expression of DMD compromised the contractile function of intestinal smooth muscle cells.At the molecular level,nucleoporin protein 153 and L-type voltage-gated calcium channel were found to be overexpressed in intestinal smooth muscle cells exhibiting downregulated DMD expression.Electrophysiological experiments confirmed an excessive influx of calcium ions into these cells.Moreover,vacuolar-like structures which may be associated with excessive calcium influx were observed in the cells by transmission electron microscopy.CONCLUSION Decreased DMD expression in intestinal smooth muscle may upregulate L-type voltage-gated calcium channel expression,leading to excessive calcium influx which may cause a decrease in rectal propulsion,thereby contributing to the pathogenesis of ODS.

高速双体船兴波阻力的数值计算

本文以理想流体的势流理论为基础，建立高速双体船的数学模型。由于双体船每一片体长宽比Ｌ／Ｂ很大，兴波接近于线性理论，计算时在船体表面及自由表面布置Ｒａｎｋｉｎｅ源，采用线性自由表面条件，对片体方尾后自由表面作特殊边界处理［３］，从理论上预报了高速双体船在不同Ｆｒｏｕｄｅ数，不同片体间距船宽比时，船体周围的流场分布，船体内、外侧表面的波形。

Mechanisms of Cyclovirobuxine D on APD Prolongation in Rat Ventricular Myocytes

Aim To study the effects of cyclovirobuxine D on inward rectifier K^- current(I_(k1) ) > transient outward K^+ current (I_(to)), L-type Ca^(2+) current (I_(Ca-L)), and actionpotential duration (APD) in isolated rat ventricular myocytes. Methods The whole cell patch-clamptechniques were used to study the changes of I_(k1), I_(to), I_(Ca-L) and APD in rat ventricularmyocytes. Results Cyclovirobuxine D (1-10 μmol·L^(-1)) significantly prolonged APD_(50) andAPD_(90) in isolated rat ventricular myocytes. Resting potential (RP) was decreased by 10μmol·L^(-1) of cyclovirobuxine D. Cyclovirobuxine D significantly decreased both inward andoutward components of I_(k1) . At - 100 mV, 1 and 10 μmol·L^(-1) of cyclovirobuxine D decreasedI_(k1), density from (-8.0+- 1.1) pA/pF to ( - 4.1 +- 0.7) pA/pF and ( - 3.4 +- 0.8) pA/pF,respectively, whereas at - 30 mV, I-(k1) density was decreased from (1.10 +-0.24) pA/pF to (0.61+-0.18) pA/pF and (0.36+- 0.11) pA/pF, respectively. 1_(to) was markedly inhibited bycyclovirobuxine D from the test potential of 0 mV to + 60 mV. At + 40 mV, 1 and 10μmol·L^(-1) ofcyclovirobuxine D decreased I_(to) density from (8.9+- 2.0) pA/pF to (5.5 +- 1.2) pA/pF and (4.9+-0.9) pA/pF, respectively. Cyclovirobuxine D inhibited I_(Ca-L) in a concentration-dependentmanner. At 10 mV, 1 and 10μmol·L^(-1) of cyclovirobuxine D decreased I_(Ca-L) density from ( - 9.9+- 1.8) pA/pF to ( - 6.4 +- 1.4) pA/pF and (-4.2+-0.6) pA/pF, respectively. ConclusionCyclovirobuxine D significantly prolonged APD and inhibited I_(k1), I_(to), and I_(Ca-L) in ratventricular myocytes. The inhibitory effects of cyclovirobuxine D on _(k1) and I_(to) are majormolecular mechanisms of APD prolongation in rat.

五体船波浪中运动与增阻的主片体协同优化研究

以波浪中的运动和增阻为目标,进行了五体船主体型线、片体主尺度和布置的协同优化。解决了型线自动变换、参数化自动建模及计算网格合并等关键技术,实现了五体船全船的自动建模。利用ISIGHT进行建模与水动力计算的集成,建立了主片体协同多目标优化系统。运用遗传算法进行多目标优化,结果表明优化后五体船运动和增阻都有所改善,并对非规则波中的情况进行了一定的探讨。

带片体的滑行艇高速航行纵稳性研究

为研究片体布置对滑行艇高速航行纵稳性的影响,本文对单体艇进行了静水拖曳试验,采用有限体积法结合SST k-ω湍流模型,利用重叠网格技术对模型周围绕流场进行了数值模拟,计算值与试验值对比验证了该方法的有效性;利用全因子设计空间采样法和数值手段,对带片体的三体艇高速航行发生海豚运动时的运动响应和水动力特性进行计算,分析了片体纵垂向位置对单体艇高速航行纵稳性的影响。结果表明:增设片体可以一定程度上延缓滑行艇海豚运动的发生,提高其最大航速;片体纵向靠近艇重心或适当靠后、垂向增加浸深均可一定程度上提高滑行艇的纵稳性,优选出具备较好纵稳性能的片体纵垂向位置a=0.2L_(m),c=30 mm,为滑行艇高速航行时片体的布置提供设计参考。

Progress of CACNA1S Gene and Hypokalemic Periodic Paralysis

CACNA1 S gene is the gene encoding L-type calcium channel αa-subunit. CACNA1 S gene mutations can cause hypokalemic periodic pa- ralysis （HOKPP）. The related research speculated that CACNA1 S gene was the candidate genes which affect meat quality traits. In the present ar- ticle, the biological characteristics of CACNA1 S gene, structure, genetic diseases and the research development were respectively reviewed so as to provide a reference for further research.

小水面双体船水动力性能预报的数值研究

文章以Wigley船型为研究对象,验证不同参数对波浪增阻的影响。通过对比研究在相似波浪条件迎浪航行工况下,肥大船型与瘦长船型的阻力性能的差异。另外,考虑片体间距对波浪增阻的影响,发现在一定的范围内片体间距越小,片体间干扰作用对阻力性能的不利影响越明显。

机器人智能焊接技术在甲板片体框架结构上的应用

针对甲板片体框架结构特点和机器人智能化焊接工艺要求,在合理的甲板片体分段划分基础上,综合运用机器人智能控制、离线编程、焊接工艺数据库和视觉识别等技术,完善机器人焊接作业流程,优化机器人焊接分段作业顺序,提高机器人焊接可达性,可进一步提高甲板片体框架结构机器人智能焊接技术应用水平。

基于遗传算法的五体船片体布局多目标优化研究

尝试并实现了iSIGHT优化软件与水动力计算软件HydroSTAR的集成优化,以五体船在波浪中的运动响应及增阻为目标函数,对片体布局作了多目标优化研究.运动计算采用三维频域面元法,增阻计算应用了近场压力积分方程,优化算法采用NSGA-II遗传算法,结果给出了Pareto解,还进行了DOE试验设计分析,为五体船片体布局设计提供参考.

Geochronology and geochemistry of Late Carboniferous dykes in the Aqishan-Yamansu belt,eastern Tianshan:Evidence for a post-collisional slab breakoff

With aim of providing constraints on the Late Paleozoic tectonic evolution of the southern Central Asian Orogenic Belt(CAOB),an integrated study was conducted on the geochronological and geochemical data for dioritic,granitic and diabase dykes from the Aqishan-Yamansu belt in the eastern Tianshan,NW China.Zircon U-Pb dating indicates that the dioritic and granitic dykes were both emplaced in the Late Carboniferous(~311 Ma and^315 Ma).The dioritic dykes show adakitic characteristics and have high Na2 O and positiveεHf(t)values(+12 to+17),which suggest an origin from partial melts of a subducted oceanic slab.The granitic dykes have high SiO2 and K2 O contents and are characterized by en riched light rare earth elements(LREE)and slightly flat heavy rare earth elements(HREE),with negative Eu and Nb-Ta-Ti anomalies.These dykes are alkali-calcic and show geochemical features of highly fractionated Itype granites.Their positiveεHf(t)values(+16 to+17)suggest that they were derived from a juvenile accreted oceanic crustal sou rce.The coeval diabase dykes have low SiO2 and K2 O contents but high TiO2,MgO and Mg#(54-59).They are enriched in LREE and show characteristics of enriched mid-ocean ridge basalts(E-MORB).The relatively high Ba/Th,slightly low Th/Ta ratios,and negative Nb-Ta anomalies imply a mantle source metasomatised by slab-derived fluids.Thus,these basic dykes were generated likely by partial melting of the upwelling asthenosphere mantle with a slight influence of slab-derived fluids.Therefore,we suggest that the formation of these Late Carboniferous dykes were triggered by a post-collisional slab breakoff and the Aqishan-Yamansu belt was a continental arc formed by southdipping subduction of the Kangguer oceanic plate.

Hydrogen sulfide-induced enhancement of gastric fundus smooth muscle tone is mediated by voltagedependent potassium and calcium channels in mice

AIM:To investigate the effect of hydrogen sulfide(H2S)on smooth muscle motility in the gastric fundus.METHODS:The expression of cystathionineβ-synthase(CBS)and cystathionineγ-lyase(CSE)in cultured smooth muscle cells from the gastric fundus was examined by the immunocytochemistry technique.The tension of the gastric fundus smooth muscle was recorded by an isometric force transducer under the condition of isometric contraction with each end of the smooth muscle strip tied with a silk thread.Intracellular recording was used to identify whether hydrogen sulfide affects the resting membrane potential of the gastric fundus in vitro.Cells were freshly separated from the gastric fundus of mice using a variety of enzyme digestion methods and whole-cell patch-clamp technique was used to find the effects of hydrogen sulfide on voltage-dependent potassium channel and calcium channel.Calcium imaging with fura-3AM loading was used to investigate the mechanism by which hydrogen sulfide regulates gastric fundus motility in cultured smooth muscle cells.RESULTS:We found that both CBS and CSE were expressed in the cul tured smooth muscle cel ls from the gastric fundus and that H2S increased the smooth muscle tension of the gastric fundus in mice at low concentrations.In addition,nicardipine and aminooxyacetic acid(AOAA),a CBS inhibitor,reduced the tension,whereas Nω-nitro-L-arginine methyl ester,a nonspecific nitric oxide synthase,increased the tension.The AOAA-induced relaxation was significantly recovered by H2S,and the Na HS-induced increase in tonic contraction was blocked by 5 mmol/L4-aminopyridine and 1μmol/L nicardipine.Na HS significantly depolarized the membrane potential and inhibited the voltage-dependent potassium currents.Moreover,Na HS increased L-type Ca2+currents and caused an elevation in intracellular calcium([Ca2+]i).CONCLUSION:These findings suggest that H2S may be an excitatory modulator in the gastric fundus in mice.The excitatory effect is mediated by voltagedependent potassium and L-type calcium channels.

青藏铁路L型挡土墙土压力的试验与分析(英文)

Considering the only retaining structure L-type retaining wall used in Golmud-Lhasa sectionofQinghai-Tibet Railway, the earth pressure and frost-heavingforce was tested in a frost-thaw circle for one year, and several different analysis models were studied.Comparedwith site test and theory analysis, it was found that the actual earth pressure is much larger than the designedearth pressure. Hence, a revised analysis model of earth pressure is put forward, which could include another possible force except slide triangle or frost heaving force. The model in this paper is only consider the thrust force other than failure sliding wedge.This model could be used as reference for the design and construction of similar projects.

Diabetes-induced changes in cardiac voltage-gated ion channels

Diabetes mellitus affects the heart through various mechanisms such as microvascular defects,metabolic abnormalities,autonomic dysfunction and incompatible immune response.Furthermore,it can also cause functional and structural changes in the myocardium by a disease known as diabetic cardiomyopathy(DCM)in the absence of coronary artery disease.As DCM progresses it causes electrical remodeling of the heart,left ventricular dysfunction and heart failure.Electrophysiological changes in the diabetic heart contribute significantly to the incidence of arrhythmias and sudden cardiac death in diabetes mellitus patients.In recent studies,significant changes in repolarizing K+currents,Na+currents and L-type Ca^(2+)currents along with impaired Ca^(2+ )homeostasis and defective contractile function have been identified in the diabetic heart.In addition,insulin levels and other trophic factors change significantly to maintain the ionic channel expression in diabetic patients.There are many diagnostic tools and management options for DCM,but it is difficult to detect its development and to effectively prevent its progress.In this review,diabetes-associated alterations in voltage-sensitive cardiac ion channels are comprehensively assessed to understand their potential role in the pathophysiology and pathogenesis of DCM.