TGF-β1/SMAD SIGNALING PATHWAY MEDIATES p53-DEPENDENT APOPTOSIS IN HEPATOMA CELL LINES

Objective To determine whether transforming growth factor betal (TGF-β1)/Smad signaling pathway mediates p53-dependent apoptosis in hepatoma cell lines.Methods Three human hepatic carcinoma cell lines, HepG2, Huh-7, and Hep3B, were used in this study.TGF-β1-induced apoptosis in hepatic carcinoma cell lines was analyzed using TUNEL assay.For identifying the mechanism of apoptosis induced by TGF-β1, cell lines were transfected with a TGF-β1-inducible luciferase reportor plasmid containing Smad4 binding elements.After transfection, cells were treated with TGF-β1, then assayed for luciferase activity.Results The apoptosis rate of HepG2 cell lines (48.51%± 8.21%) was significantly higher than control ( 12.72%±2.18%, P<0.05).But TGF-β1 was not able to induce apoptosis of Huh-7 and Hep3B cell lines.The relative luciferase activity of TGF-β1-treated HepG2 cell lines (4.38) was significantly higher than control (1.00, P< 0.05).But the relative luciferase activity of TGF-β1-treated Huh-7 and Hep3B cell lines less increased compared with control.Conclusions HepG2 cells seem to be highly susceptible to TGF-β1-induced apoptosis compared with Hep3B and Huh-7 cell lines.Smad4 is a central mediator of TGF-β1 signaling transdution pathway.TGF-β1/Smad signaling pathway might mediate p53-dependent apoptosis in hepatoma cell lines.

Single Phase-to-Ground Fault Line Identification and Section Location Method for Non-Effectively Grounded Distribution Systems Based on Signal Injection

A diagnostic signal current trace detecting based single phase-to-ground fault line identifica- tion and section location method for non-effectively grounded distribution systems is presented in this paper.A special diagnostic signal current is injected into the fault distribution system,and then it is detected at the outlet terminals to identify the fault line and at the sectionalizing or branching point along the fault line to locate the fault section.The method has been put into application in actual distribution network and field experience shows that it can identify the fault line and locate the fault section correctly and effectively.

Activation of Sonic Hedgehog Signaling Pathway in S-type Neuroblastoma Cell Lines

The effects of Sonic hedgehog(Shh) signaling pathway activation on S-type neuroblastoma(NB) cell lines and its role in NB tumorigenesis were investigated.Immunohistochemistry was used to detect the expression of Shh pathway components— Patched1(PTCH1) and Gli1 in 40 human primary NB samples.Western blotting and RT-PCR were used to examine the protein expression and mRNA levels of PTCH1 and Gli1 in three kinds of S-type NB cell lines(SK-N-AS,SK-N-SH and SHEP1),respectively.Exogenous Shh was administrated to activate Shh signaling pathway while cyclopamine was used as a selective antagonist of Shh pathway.S-type NB cell lines were treated with different concentrations of Shh or/and cyclopamine for different durations.Cell viability was measured by using MTT method.Apoptosis rate and cell cycle were assayed by flow cytometry.The xenograft experiments were used to evaluate the role of Shh pathway in tumor growth in immunodeficient mice.High-level expression of PTCH1 and Gli1 was detected in both NB samples and S-type NB cell lines.Cyclopamine decreased the survival rate of the three cell lines while Shh increased it,and the inhibition effects of cyclopamine could be partially reversed by shh pre-treatment.Cyclopamine induced the cell apoptosis and the cell cycle arrest in G0/G1 phase,while Shh induced the reverse effects and could partially prevent effects of cyclopamine.Cyclopamine could also inhibit the growth of NB in vivo.Our studies revealed that activation of the Shh pathway is important for survival and proliferation of S-type NB cells in vivo and in vitro through affecting cell apoptosis and cell cycle,suggesting a new therapeutic approach to NB.

Down-regulation and It's Molecular Biology of Nm-23H1 Gene Transfection on PKC Signal Path-way in Human High-metastatic Large Cell Lung Cancer Cell Line L9981

Backgroud and Objective At present, lung cancer has become the most frenquent malignant tumor in China and in the world which its mortality and morbidity is increasing fastest.

Role of the STAT3/survivin signaling pathway in the EML4-ALK-positive lung adenocarcinoma cell line H2228 before and after crizotinib-induced resistance

Objective This study investigated the role of the STAT3/survivin signaling pathway in the EML4-ALK–positive lung adenocarcinoma cell line H2228 before and after crizotinib-induced resistance. The mechanism of resistance was studied. Methods Cell viability was determined using the MTT assay. Crizotinib-induced apoptosis in H2228 and H2228 crizotinib-resistant cells treated with the indicated doses of crizotinib was measured at different times(24 h, 48 h, 72 h) using flow cytometry. The levels of p-ALK, ALK, p-STAT3, STAT3, and survivin after treatment of cells with 0, 0.3, and 1 μM crizotinib for 72 h were determined using Western blot analysis. DNA sequencing was used to identify mutations in H2228 crizotinib-resistant cells. Results The crizotinib IC50 values in H2228 and H2228 crizotinib-resistant cells at 72 h were 334.5 n M and 3418 n M, respectively. The resistance index of H2228 crizotinib-resistant cells was 10.20. Crizotinib induced apoptosis in H2228 cells and reduced the levels of p-ALK, p-STAT3, and survivin. In contrast, no changes in the levels of p-ALK, p-STAT3, and survivin were observed in H2228 crizotinib-resistant cells. The mutations 2067G→A and 2182G→C in EML4-ALK were present in the H2228 crizotinib-resistant cells. Conclusion Crizotinib decreased the viability of H2228 cells in a dose- and time-dependent manner. In the STAT3/survivin pathway, downregulation of p-ALK, p-STAT3, and survivin might contribute to crizotinib-induced apoptosis in H2228 cells. However, the STAT3/survivin pathway in H2228 crizotinib-resistant cells was unaffected by crizotinib treatment. Acquired resistance in H2228 cells might be related to ALK mutations.

基于窄带频谱分析的电力线载波通信干扰过滤技术

电力线路载波通信受到背景噪声、脉冲噪声等方面干扰因素影响,导致通信信号质量下降,为此提出一种基于窄带频谱分析的通信干扰过滤技术。首先构建近似模型分析通信信号特征,利用马尔可夫链模拟信道上脉冲噪声状态。然后基于窄带频谱分析算法,在信号频谱周期图下,利用正交数据窗分离直接频谱,筛选估计方差以避免频谱泄漏事件的发生。利用傅里叶变换计算特征频谱,估计信号能量的集中特性,分析通信信号,平衡信号振幅和干扰抑制。最后通过时频峰值实施干扰滤波,有效保证电力线载波通信信号质量。经过实验数据分析证明,所提技术的载波干扰幅值最小值为1.1 dB,载波通信信号误码率平均值为1.9%,方法耗时平均值为3.8 s。

基于稀疏编码的复杂机械振动信号盲分离方法

复杂机械振动信号激励源较多,故源信号之间互为相关源,且较难满足统计独立特性,导致传统盲源分离方法分离效果不佳。对此,提出一种基于信号稀疏编码的机械振动信号盲分离方法。盲源分离的关键在于对混合矩阵的精确估计,然而机械振源中相关成分的存在严重影响混合矩阵的估计。对此,首先对观测信号进行短时傅里叶变换,增加信号稀疏性;然后利用稀疏编码筛选出具备直线聚类特性的时频观测点,利用K均值(K-means)聚类法找到聚类中心;最后利用所提筛选规则找到估计的混合矩阵,重构出源信号。通过对往复压缩机故障数据的分析,验证了所提方法有效性。

区域轨道交通跨线站配线方案研究

“四网融合”发展背景下,区域轨道交通网络化运营成为重要发展趋势,而跨线站则是实现不同轨道交通线路互联互通的关键节点,因此有必要对跨线站设计进行探究。从优化车站运输组织出发,对跨线站配线方案进行研究,为实际配线布设提供参考。首先,以跨线运营模式为研究对象,根据跨线前后信号制式异同,将跨线分为同信号制式跨线和跨信号制式跨线,分析两种跨线模式列车作业种类及流程,并研究两种模式下行车组织、承载客流形式、应急管理等因素对于车站配线设置的相关需求。之后,结合配线需求,针对同信号制式和跨信号制式跨线站,分别提出了配线布置原则。最后,基于布置原则,在进一步分析两种跨线站列车作业特征基础上,研究并提出适用于不同车站构型、不同客流特征的典型配线设置方法,并进一步考虑运输组织适应性、建筑规模、工程量等因素提出适应不同实际运营场景的建议方案。通过研究,对于同信号制式跨线站,建议以在发车端设单渡线、交叉渡线等配线为主;对于跨信号制式跨线站,结合当前技术条件建议增设到发线,并根据实际需求设置折返线等其他配线。

基于PI3K/Akt/p53信号通路探讨白花蛇舌草乙酸乙酯萃取物诱导急性髓系白血病细胞凋亡的作用

目的通过评估白花蛇舌草乙酸乙酯萃取物(EAEHDW)对磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)/p53信号通路传导调节作用,探讨其抑制急性髓系白血病M2型(AML-M2)细胞株Kasumi-1增殖及诱导凋亡的机制。方法利用乙酸乙酯从白花蛇舌草中萃取制备得到EAEHDW,高效液相色谱串联质谱装置检测样品纯度。设置空白组,将浓度分别为0.02 mg/mL、0.04 mg/mL、0.06 mg/mL、0.08 mg/mL、0.10 mg/mL的EAEHDW加入对数生长期的Kasumi-1细胞株,采用MTT法检测不同浓度EAEHDW作用不同时间后Kasumi-1细胞存活率,采用Annexin V/PI流式细胞术检测不同浓度EAEHDW作用24 h后Kasumi-1细胞凋亡情况,采用Western blot法检测不同浓度EAEHDW(0.02 mg/mL、0.04 mg/mL、0.06 mg/mL)作用24 h后Kasumi-1细胞中含半胱氨酸的天冬氨酸蛋白水解酶(Caspase)家族蛋白及PI3K/Akt/p53信号传导通路蛋白表达情况。结果不同浓度的EAEHDW干预后,细胞存活率较空白组明显降低,细胞凋亡率较空白组明显升高,且细胞存活率随着作用时间的延长和药物浓度的增加而下降越明显,细胞凋亡率随着药物浓度的增加而升高越明显,差异均有统计学意义(P均<0.05);不同浓度的EAEHDW作用于Kasumi-1细胞后,细胞中多聚ADP核糖聚合酶(PARP)、Caspase-3、Caspase-8、Caspase-9、细胞色素C(Cyto-C)、p53蛋白相对表达量均明显升高(P均<0.05),Akt、磷酸化Akt(p-Akt)、鼠双微染色体2(MDM2)、磷酸化MDM2(p-MDM2)蛋白相对表达量均明显降低(P均<0.05)。结论EAEHDW可明显抑制髓系白血病Kasumi-1细胞增殖并诱导其凋亡,其机制可能与影响Caspase家族蛋白表达和抑制PI3K/Akt/p53信号通路导致p53激活有关。

Alterations and Its Mechanisms of Wnt Signal Pathway in Human High-matastatatic Large Cell Lung Cancer Cell Line L9981 by Transfecting with Nm23-H1 Gene

Backgroud and Objective Tumor metastasis is not only the malignant marker and characteristics of lung cancer, but also the main cause of failure to cure and lose their life of the

基于单矢量水听器的水中目标高分辨线谱增强方法

微弱信号检测一直是被动声呐系统远程探测面临的技术挑战。为了解决水下微弱信号条件下,即低信噪比(SNR)情况下,目标线谱检测难点问题,本文基于单矢量水听器信号接收,提出一种水下目标声压振速频域解卷积联合(CPVD)处理方法,可以实现线谱增强以及提高频域分辨率。采用单矢量水听器接收,保证声呐系统体积小,同时利用其具有指向性这一特点,可以抑制噪声,提高信号增益。在此基础上,通过CPVD算法对水中微弱信号进行线谱增强,实现有效检测。本文提出的方法克服了一些增强算法以及功率谱分析算法需要一定的先验知识以及频域线谱分辨率较低的缺点,从仿真分析和海试数据处理结果可以看出:本文所提出的基于单矢量水听器的水下目标线谱增强算法在低SNR条件下提高频率分辨率方面具有优势,为被动声呐系统微弱信号下的线谱检测提供有效算法。

既有线信号系统智能运维平台建设思考

信号系统作为保障城市轨道交通列车运行的重要系统,其制式日新月异,同时信号设备种类也变得更加庞杂,这就对信号系统的运维保障提出了更高要求。传统的维护方式已经不能满足当前的运营生产需求,通过对既有线路信号系统智能运维平台建设的思考,提供一种通过建设智能运维平台,解决既有线信号系统维护困难的方法。

电子纺织品用纺织信号传输线的研究进展

归纳现有纺织信号传输线的研究现状,介绍不同信号用纺织传输线及其制备方法,概述现阶段有关传输线在不同环境条件中的性能研究,总结其未来发展趋势,以期为今后研发可穿戴设备用纺织信号传输线提供方向。

线路阻抗对构网变流器降阶模型精度影响及次同步振荡分析

在大部分关于构网变流器(GFM)次同步振荡稳定性的研究中,GFM通常被简化为只含有功率外环的三阶模型,这种降阶方法虽然简便,但其精确度会受到线路阻抗特征的影响,因此需要对GFM降阶模型适用性问题展开讨论,并提出更加精准的降阶模型。分析电网线路阻抗特征变化对降阶模型精度的影响,结果表明线路阻感比变化或短路比变化时三阶模型不能精确反映系统特性的变化,会对系统稳定性产生错误判断,其原因在于线路阻抗参数会影响电压环与功率环的耦合特性,2个控制环路均会对GFM次同步振荡稳定性产生影响。提出一种更加准确的包含电压环的降阶模型,可以精确表征线路阻抗特征变化对系统特性的影响,更加适合复杂电网下GFM的稳定性分析。基于MATLAB/Simulink仿真验证了理论分析的正确性及所提模型的有效性。

苏州轨道交通双线贯通车站信号系统改造方案研究与实现

以苏州轨道交通11号线与苏州轨道交通3号线贯通改造工程为例,研究隶属于苏州轨道交通11号线的接口车站——唯亭站的信号系统改造方案。基于11号线唯亭站站场的变化,设计信号平面布置图,包含两线信号系统边界的重新划分、轨旁设备拆除与新增后的重新布置等;为实现两线列车以CBTC模式跨线运营,贯通改造采用并行冗余协议技术实现LTE与WLAN的车地无线双制式贯通;两线接口由继电接口改为CBTC邻站网络接口。并且对改造工程中其他既有站小交路运营数据的配置和相关影响项点,以及改造的工序逐个进行说明。该改造方案对后续类似的地铁改造项目有一定参考意义。

中低速磁浮线信号系统测速方案分析

中低速磁悬浮车辆和轨道构造与普通轮轨交通系统存在本质差异,传统的测速方案不再适用于中低速磁悬浮交通系统,需要重新构建新型测速方式,对中低速磁浮线信号系统五种测速方式的测速原理、测速精度、工程运用、工程造价等进行分析,提出中低速磁浮线信号系统测速合理化建议。

基于声音特征的隧道衬砌空洞识别方法研究

目前隧道衬砌空洞检测以人工敲击判断为主,检测过程中由于受到检测人员水平、注意力等主观因素影响,检测结果存在较大不确定性,因此有必要研制一种智能化的检测装置实现空洞自动识别。文章开展了衬砌空洞敲击回声智能识别算法研究,通过提取隧道衬砌冲击回波的梅尔倒谱系数(Mel Frequency Cepstral Coefficient,MFCC)作为特征,针对敲击回声脉冲信号长度不一的特点,提出了变帧长MFCC优化算法,并面向小样本条件,建立了支持向量机(Support Vector Machine,SVM)的识别模型。试验结果表明,该模型对衬砌空洞识别准确率可达89.9%。

高速PCB传输线信号完整性设计要点研究

为了解决高密度、集成化高速PCB中传输线因走线空间有限,走线设计不当所带来的信号完整性问题,采用理论分析、经验值设计、仿真分析的手段对8层高速PCB设计进行研究.分析高速PCB走线设计对传输线反射、串扰等信号完整性问题的影响.在PCB布线完成后,通过SI⁃wave软件仿真对PCB传输线线宽、线间距和阻抗值大小对信号完整性的影响进行研究,验证设计经验值3 W间距和50Ω阻抗的可靠性.指导PCB信号走线设计,达到信号的完整性,以期为实际工程实践应用提供参考和借鉴.