应用时域积分方程法分析复杂细线导体瞬态响应

应用时域积分方程法(time domain integral equation,TDIE)分析细线导体的瞬态响应,将矩量法与时间步进算法相结合,提出了一种新的TDIE求解方法。该方法以导体段的轴向电流为变量,选用分段线性函数为基函数,采用分域匹配法构造线性方程组,形成一个不随时间变化的系数矩阵,从而避免了时间步进过程中的矩阵求逆运算,极大地提高了运算效率。选用分域匹配法,空间步长可以适当加大,与常用的点匹配法相比,采用更少的分段数,就可以获得同样高的计算精度。此外,作为一种直接时域方法,该方法可以在充分完善地考虑集中参数源和负载的基础上高效快速分析复杂结构导体的瞬态早时响应。将该文计算方法与频域矩量法和多导体传输线方法针对同一个算例进行计算,结果均一致,从而验证了该文方法的正确性。最后,应用所提方法分析了变电站内开关操作时,母线上的瞬态电磁响应。

高速铁路桥面10kV电缆雷击过电压的仿真分析

研究雷击高速铁路供电系统时在桥面贯穿电缆上产生的过电压的特性时,研究方法主要分为两部分:第一部分为计算雷击在电缆铠层上产生的过电压波形,由于高速铁路导体结构为地上地下共存,所以建立了一种可以考虑任意结构细线导体的改进的回路电流法对之进行求解,并且对该方法的基本原理以及优缺点进行了描述;第二部分为仿真电缆上的雷击过电压暂态,计算中,首先将铠层电位强制为第一部分计算得到的电位波形,然后应用EMTP中的JMarti模型,计算不同电缆端接方式下电缆各层的电位波形。计算结果表明,当铠层正确接地时,虽然电缆各导体上的绝对电位很高,但相邻导体之间的电位差却很低,一般不会超过电缆的耐受电压。但是,如果铠层未能良好接地,则雷击将在电缆上产生非常高的电位差,足以造成电缆损坏。

Glycyrrhizin attenuates HMGB1-induced hepatocyte apoptosis by inhibiting the p38-dependent mitochondrial pathway

AIM： To examine how High-mobility group box I （HMGB1） regulates hepatocyte apoptosis and, furthermore, to determine whether glycyrrhizin （GL）, a known HMGB1 inhibitor, prevents HMGBl-induced hepatocyte apoptosis.

Alisol B acetate induces apoptosis of SGC7901 cells via mitochondrial and phosphatidylinositol 3-kinases/Akt signaling pathways

AIM： To examine the effect of alisol B acetate on the growth of human gastric cancer cell line SGC7901 and its possible mechanism of action.METHODS： The cytotoxic effect of alisol B acetate on SGC7901 cells was measured by 3-（4,5-dimethylthiazol- 2-yl）-2,5-diphenyltetrazolium bromide （MI-I-） assay. Phase-contrast and electron microscopy were used to observe the morphological changes. Cell cycle and mitochondrial transmembrane potential （A^Pm） were determined by flow cytometry. Western blotting was used to detect the expression of apoptosis-regulated gene Bcl-2, Bax, Apaf-1, caspase-3, caspase-9, Akt, P-Akt and phosphatidylinositol 3-kinases （PI3K）.RESULTS： Alisol B acetate inhibited the proliferation of SGC7901 cell line in a time- and dose-dependent manner. PI staining showed that alisol B acetate can change the cell cycle distribution of SGC7901, increase the proportion of cells in G0-G1 phase and decrease the proportion of S phase cells and G2-M phase cells. Alisol B acetate at a concentration of 30 pmol/L induced apoptosis after 24, 48 and 72 h incubation, with occurrence rates of apoptotic cells of 4.36%, 14.42% and 21.16%, respectively. Phase-contrast and electron microscopy revealed that the nuclear fragmentation and chromosomal condensed, cells shrank and attachment loss appeared in the SGC7901 treated with alisol B acetate. Apoptosis of SGC7901 cells was associated with cell cycle arrest, caspase-3 and caspase-9 activation, loss of mitochondrial membrane potential and up-regulation of the ratio of Bax/Bcl-2 and inhibition of the PI3K/Akt.CONCLUSION： Alisol B acetate exhibits an antiproliferative effect in SGC7901 cells by inducing apoptosis. Apoptosis of SGC7901 cells involves mitochondria-caspase and PI3K/Akt dependent pathways.

Outer membrane VDAC1 controls permeability transition of the inner mitochondrial membrane in cellulo during stress-induced apoptosis

Voltage-dependent anion channel （VDAC）I is the main channel of the mitochondrial outer membrane （MOM） and it has been proposed to be part of the permeability transition pore （PTP）, a putative multiprotein complex candidate agent of the mitochondrial permeability transition （MPT）. Working at the single live cell level, we found that overexpression of VDAC1 triggers MPT at the mitochondrial inner membrane （MIM）. Conversely, silencing VDAC1 ex- pression results in the inhibition of MPT caused by selenite-induced oxidative stress. This MOM-MIM crosstalk was modulated by Cyclosporin A and mitochondrial Cyclophilin D, but not by Bcl-2 and BcI-XL, indicative of PTP operation. VDAC1-dependent MPT engages a positive feedback loop involving reactive oxygen species and p38-MAPK, and secondarily triggers a canonical apoptotic response including Bax activation, cytochrome e release and caspase 3 activation. Our data thus support a model of the PTP complex involving VDAC1 at the MOM, and indicate that VDACl-dependent MPT is an upstream mechanism playing a causal role in oxidative stress-induced apoptosis.

Effects of α-mangostin on apoptosis induction of human colon cancer

AIM:To investigate the effect of α-mangostin on the growth and apoptosis induction of human colon cancer cells.METHODS:The three colorectal adenocarcinoma cell lines tested (COLO 205,MIP-101 and SW 620) were treated with α-mangostin to determine the effect on cell proliferation by MTT assay,cell morphology,chromatin condensation,cell cycle analysis,DNA fragmentation,phosphatidylserine exposure and changing of mitochondrial membrane potential.The molecular mechanisms of α-mangostin mediated apoptosis were further investigated by Western blotting analysis including activation of caspase cascade,cytochrome c release,Bax,Bid,p53 and Bcl-2 modifying factor.RESULTS:The highest inhibitory effect of α-mangostin on cell proliferation of COLO 205,MIP-101 and SW 620 were 9.74 ± 0.85 μg/mL,11.35 ± 1.12 μg/mL and 19.6 ± 1.53 μg/mL,respectively.Further study showed that α-mangostin induced apoptotic cell death in COLO 205 cells as indicated by membrane blebbing,chromatin condensation,DNA fragmentation,cell cycle analysis,sub-G1 peak (P < 0.05) and phosphatidylserine exposure.The executioner caspase,caspase-3,the initiator caspase,caspase-8,and caspase-9 were expressed upon treatment with α-mangostin.Further studies of apoptotic proteins were determined by Western blotting analysis showing increased mitochondrial cytochrome c release,Bax,p53 and Bmf as well as reduced mitochondrial membrane potential (P < 0.05).In addition,up-regulation of tBid and Fas were evident upon treatment with α-mangostin (P < 0.01).CONCLUSION:α-Mangostin may be effective as an anti-cancer agent that induced apoptotic cell death in COLO 205 via a link between extrinsic and intrinsic pathways.

The mitochondrial serine protease HtrA2/Omi cleaves RIP1 during apoptosis of Ba/F3 cells induced by growth factor withdrawal

Interleukin-3 （IL-3） deprivation of the mouse pro-B cell line Ba/F3 induces cell death that is abrogated by B-cell lymphoma 2 （Bcl-2） overexpression, but remains unaffected by the pan-caspase inhibitor carbobenzoxy-valyl-analyl- aspartyl-[O-methyl]-fluoromethylketone （zVAD-fmk）. IL-3 withdrawal causes receptor-interacting protein （RIP）I cleavage into C-terminal fragments of 30 and 25 kDa, and only cleavage leading to the former was prevented by zVAD-fmk, siRNA experiments demonstrated that generation of the 25-kDa fragment was due to a Bcl-2-modulated release of the mitochondrial serine protease high temperature requirement protein A2 （HtrA2）/Omi. Accordingly, recombinant HtrA2/Omi efficiently cleaved mouse RIP1 in vitro, generating fragments matching those observed in IL-3-deprived Ba/F3 cells. The HtrA2/Omi cleavage site in mouse RIP1 was mapped to the intermediate domain and the corresponding N- and C-terminal fragments were impaired in their ability to activate nuclear factor-r,B, c-Jun N-terminal kinase and p38 mitogen-activated protein kinase. Interestingly, knockdown of HtrA2/Omi afforded pro- tection against IL-3 withdrawal-induced death in the presence of zVAD-fmk, demonstrating a role for HtrA2/Omi in caspase-independent cell death during growth factor withdrawal by cleaving RIP1.

Exogenous phosphatidylethanolamine induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway

AIM: To investigate the signaling pathways implicated in phosphatidylethanolamine (PE)-induced apoptosis of human hepatoma HepG2 cells. METHODS: Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell cycle, apoptosis and mitochondrial transmembrane potential (ΔΨm) were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS: PE inhibited the growth of HepG2 cells in a doseand timedependent manner. It did notaffect the cell cycle, but induced apoptosis. PE significantly decreased ΔΨm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a doseand time-dependent manner. CONCLUSION: Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.

Curcumin induces apoptosis through the mitochondria-mediated apoptotic pathway in HT-29 cells

Objective： To investigate the effects of curcumin on release of cytochrome c and expressions of Bcl-2, Bax, Bad, Bcl-xL, caspase-3, poly ADP-ribose polymerase （PARP）, and survivin of HT-29 cells. Methods： HT-29 cells were treated with curcumin （0-80 μmol/L） for 24 h. The release of cytochrome c from the mitochondria and the apoptosis-related proteins Bax, Bcl-2, Bcl-xL, Bad, caspase-3, PARP, and survivin were determined by Western blot analysis and their mRNA expressions by reverse transcriptase-polymerase chain reaction （RT-PCR）. Results： Curcumin significantly induced the growth inhibition and apoptosis of HT-29 cells. A decrease in expressions of Bcl-2, Bcl-xL and survivin was observed after exposure to 10-80 μmol/L curcumin, while the levels of Bax and Bad increased in the curcumin-treated cells. Curcumin also induced the release of cyto- chrome c, the activation ofcaspase-3, and the cleavage of PARP in a dose-dependent manner. Conclusion： These data suggest that curcumin induced the HT-29 cell apoptosis possibly via the mitoehondria-mediated pathway.

The impact of X-rays on the expressions of miR-130a/miR-25 and its potential role in the enhanced metastasis of A549 cell lines in vitro induced by X-rays

We aimed to investigate the impact of X-rays on miR-130a and miR-25 expressions of A549 cell lines and to understand the mechanism of miR-130a and miR-25 on the regulation of invasion and metastasis of A549 cell lines. Human adenocarcinoma cells of the line A549 were cultured and radiated by X-rays at the absorbed doses of 2 and 4, respectively by linear accelerator. Transwell invasion and migration assay were employed to exam the metastasis ability of A549 cells post X-rays irradiation. Both the miRNA and mRNA were extracted from A549 cells at different time points post radiation. The expressions of miR-130a and miR-25, as well as the expressions of VEGF and CCR-7 mRNAs, were detected in A549 cells with 2 and 4 Gy X-rays radiation, respectively by real time PCR. Results were statistically analyzed by SAS 8.2 software, which showed that the invasiveness of A549 cells post 2 and 4 Gy X-rays increased significantly compared with that of untreated A549 cells (the migration cell numbers are 20, 48 and 62 in Group 0, 2 and 4 Gy X-rays, respectively). Furthermore, the expressions of miR-130a and miR-25 also increased significantly at the time-points of 1, 2, 4, and 8 h post radiation, and began to decrease to the control level at 12 h post radiation. VEGF and CCR-7 mRNAs were detected to be up-regulated 18 h post radiation and remained at a high level till 72 h post radiation. The expression of VEGF mRNA has a close correlation with that of CCR-7 mRNA, and the expression of miR-130a also has a correlation with that of VEGF and CCR-7mRNAs. It is concluded that the metastasis of A549 cells in vitro could be promoted by X-rays, and miR-130a might play a role in the metastasis of A549 cells via regulating the expressions of VEGF and CCR-7 mRNAs.