Jun Li

Jun Li的基本解释

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[人名]李军

与Jun Li相关的网络例句 [注：此内容来源于网络，仅供参考]

Results are as followed:1 Exposure of HELF cells to BP caused c-Jun activation,and increased the activity of MAPK,PI-3K,p53 and cyclin D1 pathway.2 BP-induced c-Jun activation was inhibited by dominant negative mutants of extracellular signal-regulated protein kinase or c-Jun NH_2-terminal kinase,but not by p38,impling that JNK and ERK pathways medicate c-Jun activation induced by BP.3 Overexpression of dominant-negative mutants PI-3K and Akt potently blocked phosphorylations of c-Jun and ERK,but not JNK in response to BP,suggesting that PI-3K/Akt pathway positively regulates BP-induced c-Jun activation through ERK.4 Inhibition of p53 by its chemical or molecular inhibitor markedly increased the phosphorylation levels of c-Jun,Akt and ERK upon BP stimulation,indicating that p53 negatively medicates BP-induced c-Jun activation through PI-3K/Akt/ERK pathway.5 The cell lines expressed TAM67 exhibits no significant affecting normal cell growth properties.6 TAM67 was able to significantly block G_1-S transition and subsequent cell proliferation,suggesting that c-Jun is essential for cell cycle alternations elicited by BP.7 Overexpression of TAM67 impaired BP-induced cyclin D1 activation,decreasing expression of E2F1 and pRb,indicating that c-Jun participates in the modulation of BP-induced activation of cyclin D1/pRb/E2F1 pathway.8 Stably expression of TAM67 led to the increases in the expression levels of p53 and p21,elevating phosphorylation level of p53,clearly indicating that c-Jun regulates p53/p21 pathway activation induced by BRCollectively,PI3K/Akt/ERK pathway mediated BP-induced c-Jun activation through p53-dependent mechanism.

结果显示：1BP刺激细胞可促进c-Jun活化，并伴随着MAPK、PI-3K、p53和cyclinD1通路各组成成分的活性增强。2利用MAPK通路的显性失活突变体分别阻断细胞外信号调节激酶和c-Jun氨基末端激酶活性，均可明显抑制BP诱导的c-Jun活化，但阻断p38活性对BP引起的c-Jun活化无明显影响，提示JNK和ERK通路参与调控BP诱导的c-Jun活化。3过表达PI-3K和Akt的显性失活突变体也可显著抑制BP诱导的c-Jun活化，并降低磷酸化ERK的表达水平，但对磷酸化JNK的表达水平无明显影响，说明PI-3K/Akt通路通过ERK正性调控了BP诱导的c-Jun活化。4p53的化学/分子抑制剂能使BP作用的细胞内c-Jun活性明显增加，并同时诱导Akt和ERK的磷酸化水平的升高，表明p53可通过PI-3K/Akt/ERK通路对BP诱导的c-Jun活化进行负性调控。5随后观察转染细胞的生长情况，发现TAM67对细胞正常生长和形态无明显影响。6稳定表达TAM67可有效抑制BP诱导的S期细胞数的增加，提示c-Jun在BP致细胞周期改变的过程中发挥了重要作用。7TAM67过表达能够抑制BP诱导的cyclin D1活化，降低磷酸化Rb以及E2F1蛋白表达水平，表明c-Jun参与调控BP诱导的cyclin D1/Rb/E2F1通路的活化。8过表达TAM67可使BP刺激的细胞中p53、p21总蛋白以及p53磷酸化的表达水平明显升高，可见c-Jun也参与调控BP诱导的p53/p21通路活化。

They are the Tang firewood Jun, Song firewood Jun as breasts, Yuan and Ming dynasties of coal Transitional Jun Porcelain, Charcoal-Broiled Qing Jun, and the contemporary straight Yan Jun, and down draft Jun, and Jun Porcelain-free sagger, Coal burning Drawer Jun, and gas mixture burning Jun, natural gas Jun Porcelain.

它们分别是唐代柴烧钧窑、宋代双乳状柴烧钧窑、元明时期柴煤过渡时期钧窑、清代炭烧钧窑、当代直焰钧窑、倒焰钧窑、无匣钵钧窑、煤烧抽屉式钧窑、煤气混合烧钧窑、天然气钧窑。

Pristine Li-Al LDHs are synthesized by hydrothermal process in different reaction conditions by varying the aging time for 1 and 24 hours. Both the Li-Al layered double hydroxides (abbreviated as Li-Al LDH1 and Li-Al LDH24 for aging time 1 hour and 24 hours, respectively) were modified by using sulphanilic acid sodium salt hydrate, modified agent to form modified Li-Al LDH1-SAS and Li-Al LDH24-SAS. The morphology of the pristine layered double hydroxides are investigated by using wide angle X-rays diffraction, scanning electron microscopy and particle size analyzer which indicates that the crystallinity and aspect ratio is increased with increasing the aging time from 1 hour to 24 hours. The particle size of Li-Al LDH24 and Li-Al LDH1 are found to be ~1000 nm and ~250 nm, respectively. Both the pristine and modified LDHs are characterized by XRD, FTIR spectra and thermogravimetric analysis.

本研究目的在於改变长晶时间的长短，合成出同径大小的Li-Al LDHs，再经由改质剂sulphanilic acid sodium salt hydrate将Li-Al LDHs无机层材表面有机官能化制备出改质型Li-Al LDHs-SAS，於是进一步藉由扫描式电子显微镜、射径仪和穿透式电子显微镜等仪器分别观察LDHs改质前和改质后其主层结构型态上的变化；从中可以发现Li-Al LDHs随著长晶时间的增加其径有随之增大的趋势，但经有机化改质后其径会由於改质环境的影响明显低许多，针对此现象本实验将未改质和改质后之Li-Al人工无机层材制备成复材进一步探讨其在热性质和难燃特性上的为表现。

与Jun Li相关的网络解释 [注：此内容来源于网络，仅供参考]

Euphemia Li Britannia：由菲米娅.Li.布里塔尼亚

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