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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。

Results Qidan Granules could relieve the pain caused by glacial acetic acid and heat stimuli; significantly inhibit the oxytocin-induced dysmenorrheal in mice; It also showed obvious inhibitory effects on the increased capillary permeability induced by glacial acetic acid, carrageen-induced toe edema in rats and dimethylbenzene-induced ear swelling in mice, and cotton pellet-induced granuloma formation in rats. It could also significantly inhibit oxytocin-induced dysmenorrhea in mice.

结果 奇丹颗粒能明显抑制乙酸和热刺激所致的小鼠疼痛反应;对缩宫素所致实验性痛经小鼠具有良好的镇痛作用,对乙酸所致小鼠腹腔毛细血管通透性增高以及大鼠角叉菜胶足趾肿胀、二甲苯所致小鼠耳廓肿胀、大鼠棉球肉芽肿等急慢性炎症模型均有明显抑制作用。

To observe pharmacological effects of Zangqingguo Houpian on antibacterial effect in vitro,2,4-dinitrophenol induced fever in rats,the croton oil induced swelling in mouse's ear and carrageen induced WBC movement in rat chest,rat granuloma induced by tampon,acetic-acid-induced twisting test in mouse and prednisolone acetate caused immunosuppressive mice.

采用体外抗菌、对2,4-二硝基苯酚所致大鼠发热、巴豆油所致小鼠耳肿胀及角叉菜胶致大鼠胸腔白细胞游走、棉球致大鼠肉芽组织增生、冰醋酸致小鼠疼痛、醋酸泼尼松龙致免疫低下等模型,观察藏青果喉片的药效学作用。

Methods Antipyretic action of CSC was observed on rabbit fever models induced by lipopolysaccharide and rat fever models induced by baker's yeast. Rat models with pedal swelling induced by carrageenin, mouse models with auricle swelling induced by dimethylbenzene and mouse models with celiac capillary hyperpermeability induced by acetic acid were used to observe the anti- inflammatory action of CSC. Its acute toxicity in mice was also evaluated.

方法]采用细菌脂多糖致家兔发热、啤酒酵母致大鼠发热动物模型,观察穿心莲软胶囊的解热作用;采用角叉菜胶致大鼠足肿胀、二甲苯致小鼠耳肿胀和醋酸致小鼠腹腔毛细血管通透性增加的动物模型,观察穿心莲软胶囊的抗炎作用,并对小鼠进行该制剂的急性毒性试验。

PAL activity, chitinase activity, total Polyphenol content and total Flavonoids content in soybean leaves induced by the same crude toxin and race were similar, it stated that the crude toxin is an important factor which can induce resistant substances, but the induced speed and the induced intensity by the crude toxin and conidium were different. Firstly, the induced speed of crude toxin which induced PAL activity and total Flavonoids content of resistant soybean varieties was faster than speed of C.

同一生理小种的粗毒素与灰斑病菌对大豆叶片内PAL活性、总多酚类含量、总黄酮含量以及几丁质酶活性等几种生化指标均表现出相似的诱导作用,由此可推断粗毒素是诱导大豆叶片内的PAL活性、总多酚含量、总黄酮含量以及几丁质酶活性产生变化的主要生物因子,只是二者在对抗性不同的大豆品种的诱导速度及强度上存在一定的差异。

The precipitate in liquor is a common problem in distilleries which have to tackle with and the frequent causations are as follows: floccule induced by three kinds of higher fatty acid ethyl ester and microthermal storage and filtration could prevent it; white flakes of precipitate induced by containers for liquor storage such as aluminous pots which produced alumina and mare nectaris which dissolved into coating and then caused precipitate; precipitate induced by undergrade additives and CP grade or AR grade additives could prevent it; precipitate induced by water quality and strict management of water quality could prevent it; precipitate induced by packing materials and the solution was acid water washing for new bottles and liquor filling after the inner of the bottles was completely dry.

白酒产生混浊沉淀是一普遍问题,常见的有絮状沉淀,主要由3种高级脂肪酸乙酯引起,可于低温贮存过滤;白色片状沉淀,由贮酒容器引起,铝罐贮酒,会产生氧化铝溶入沉淀,最好不用铝罐贮酒;酒海贮酒会溶入涂料,造成沉淀,酒海贮酒不宜过久;由劣质添加剂引起,最好使用CP级或AR级添加剂;水质引起,对水处理应严加管理;包装材料引起,新瓶应用酸性水洗,且须控干水后再灌酒。

The stable clones are further identified by RT-PCR and Western blot; 6 MTT assay is used to investigate the effect of ZNRD1 on the cell growth of cells (AGS, SGC7901, MKN28, NIH3T3, GES-1); 7 Soft agar assay is used to investigate the effect of ZNRD1 on the clonality of cells (AGS, MKN28); 8 Nude mice assay is used to investigate the effect of ZNRD1 on the cell growth of gastric cancer cells (AGS, MKN28); 9 Flow cytometry is used to investigate the effect of ZNRD1 on the cell cycle distribution of cells (AGS, MKN28, NIH3T3, GES-1); 10 Flow cytometry is used to investigate the effect of ZNRD1 on the cell apoptosis of cells (AGS, MKN28, NIH3T3); 11 MTT assay is used to investigate the effect of ZNRD1 on the drug sensitivity of cancer cells (SGC7901, SGC7901/VCR, HL-60, HL-60/VCR) in vitro; 12 SRCA is used to investigate the effect of ZNRD1 on the drug sensitivity of gastric cancer cells (SGC7901, SGC7901/VCR) in vivo; 13 Flow cytometry is used to investigate the effect of ZNRD1 on adriamycin accumulation of cancer cells (SGC7901, SGC7901/VCR, HL-60, HL-60/VCR); 14 Transmission electron microscope is used to investigate the effect of ZNRD1 on the sensitivity of SGC7901 cells towards drug-induced apoptosis; 15 Flow cytometry and DNA ladder assay are used to investigate the effect of ZNRD1 on the sensitivity of cells (SGC7901, SGC7901/VCR, HL-60/VCR) towards drug-induced apoptosis; 16 Microarray is used to investigate the profiling of ZNRD1-responsive genes in gastric cancer cells (AGS, MKN28, SGC7901, SGC7901/VCR); 17 RT-PCR and Western blot are used to identify the results of microarray; 18 Reporter gene assay is used to investigate the effect of ZNRD1 on the transcriptional activity of cyclin D1; 19 Reporter gene assay is used to investigate the effect of ZNRD1 on the transcriptional activity of MDR1; 20 Kinase assay is used to investigate the effect of ZNRD1 on the activity of cyclin E-CDK2 kinase; 21 The antisensenucleic acids of p21 is used to inhibit the expression of p21, and flow cytometry is used to investigate the effect of p21 on ZNRD1-induced cell cycle arrest in gastric cancer cells; 22 The antisensenucleic acids of p27 is used to inhibit the expression of p27, and flow cytometry is used to investigate the effect of p27 on ZNRD1-induced cell cycle arrest in gastric cancer cells; 23 Liposome is used to up-regulate the expression of Skp2, and flow cytometry is used to investigate the effect of Skp2 on ZNRD1-induced cell cycle arrest in gastric cancer cells; 24 Western blot is used to investigate the effect of ZNRD1 on the stability of Skp2 and p27 in gastric cancer cells; 25 MVD assay is used to investigate the effect of ZNRD1 on the angiopoietic activity of gastric cancer cells; 26 ELISA is used to investigate the effect of ZNRD1 on the expression of VEGF165 in gastric cancer cells; 27 The roles of DARPP-32 in MDR of gastric cancer cells are investigated using gene transfection, MTT assay, SRCA, flow cytometry and DNA ladder assay.

应用杂交瘤技术制备ZNRD1的首个单克隆抗体;2)利用RT-PCR、Western blot和免疫组化检测ZNRD1在胃癌组织、胃炎组织、正常胃上皮组织、胃癌细胞和正常胃组织上皮细胞中的表达;3)构建ZNRD1的小干扰RNA载体,并测序鉴定;4)利用脂质体将ZNRD1的真核表达载体及其空载体转染胃癌细胞(AGS、SGC7901、MKN28)和小鼠成纤维细胞(NIH3T3),G418筛选后进行鉴定;5)利用脂质体将ZNRD1的小干扰RNA载体及其空载体转染药敏胃癌细胞(SGC7901)、正常胃组织上皮细胞(GES-1)、对长春新碱耐药的胃癌细胞(SGC7901/VCR)、药敏白血病细胞(HL-60)、对长春新碱耐药的白血病细胞(HL-60/VCR),G418筛选后进行鉴定;6)利用MTT实验检测ZNRD1高/低表达对细胞(AGS、SGC7901、MKN28、NIH3T3、GES-1)生长的影响;7)通过软琼脂克隆形成实验检测上调ZNRD1对AGS、MKN28细胞克隆形成能力的影响;8)通过裸鼠成瘤实验检测上调ZNRD1对AGS、MKN28细胞体内成瘤性的影响;9)通过流式细胞仪分析ZNRD1高/低表达对细胞(AGS、MKN28、NIH3T3、GES-1)的细胞周期的影响;10)通过流式细胞仪分析上调ZNRD1对细胞(AGS、MKN28、NIH3T3)的凋亡的影响;11)通过MTT实验检测ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR、HL-60、HL-60/VCR)体外药物敏感性的影响;12)通过肾包膜下移植法检测ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR)体内药物敏感性的影响;13)通过流式细胞仪分析ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR、HL-60、HL-60/VCR)内阿霉素蓄积和泵出的影响;14)通过透射电镜检测上调ZNRD1对SGC7901细胞凋亡敏感性的影响;15)通过流式细胞仪和DNA梯度试验检测ZNRD1高/低表达对细胞(SGC7901、SGC7901/VCR、HL-60)凋亡敏感性的影响;16)通过基因芯片检测ZNRD1高/低表达对胃癌细胞内基因表达谱的影响;17)利用RT-PCR、Western blot对基因芯片的结果进行鉴定;18)利用报告基因实验检测ZNRD1对cyclin D1的启动子活性的调节作用;19)利用报告基因实验检测ZNRD1高/低表达对MDR1的启动子活性的调节作用;20)利用激酶试验检测ZNRD1对cyclin E-CDK2 激酶活力的影响;21)利用反义核酸技术抑制p21的表达;通过流式细胞仪检测抑制p21对ZNRD1介导的细胞周期阻滞的影响;22)利用反义核酸技术抑制p27的表达;通过流式细胞仪检测抑制p27对ZNRD1介导的细胞周期阻滞的影响;23)利用脂质体转染法上调Skp2的表达;通过流式细胞仪检测上调Skp2对ZNRD1介导的细胞周期阻滞的影响;24)利用Western blot检测ZNRD1对p27和Skp2的蛋白稳定性的影响;25)利用微血管密度实验检测ZNRD1对AGS、MKN28细胞裸鼠移植瘤微血管形成的影响;26)利用ELISA检测ZNRD1对AGS、MKN28细胞培养上清和移植瘤匀浆中VEGF165含量的影响;27)利用脂质体转染法、MTT实验、肾包膜下移植法、流式细胞仪和DNA梯度试验检测新耐药相关分子DARPP-32对细胞(SGC7901、SGC7901/VCR、对阿霉素耐药的胃癌细胞SGC7901/ADR)多药耐药表型的影响;利用脂质体转染法和MTT实验检测下调ZNRD1对DARPP-32介导的胃癌多药耐药的调控作用。

Methods the models of xylene-induced ear edema in mice, hind paw edema induced with carrageen in rats, granuloma induced with cotton ball in rats, and capillary permeability increase induced with acetic acid in mice were used to observe the anti-inflammatory effects.

目的 研究岗梅水提取物的抗炎作用。方法采用二甲苯致小鼠耳廓肿胀法、角叉菜胶致大鼠足跖肿胀法、大鼠棉球肉芽肿法和醋酸致小鼠毛细血管通透性增高法观察岗梅水提取物的抗炎作用。

Result: Xinhuang Tablet had very significant inhibition on acute and chronic inflammation in model of ear edema induced by croton oil in mice, paw swelling induced by carrageenin in rats, granuloma induced by cotton pellet in rats and very significant analgesic effect on thermal and chemical stimulation in model of writhing body response induced by acetic acid in mice and tail flicking in rats.And at the same doses, Xinhuang Tablet hadn't significant difference from ig administration.

结果:新癀片外涂给药对小鼠耳肿、大鼠角叉菜胶足肿、棉球肉芽肿等急、慢性炎症有非常显著的抑制作用;对大、小鼠水浴甩尾、小鼠醋酸扭体等温热刺激、化学刺激引起的疼痛有非常显著的镇痛作用,且在相同剂量下,外涂给药和ig给药的作用无明显差异。

The time-domain response of the induced currents on a scattering object irradiated by a plane wave with a Gaussian pulse in time is expanded as an associate Hermite series in this paper. Using the isomorphism of the associate Hermite function and its Fourier transform, the frequency-domain information can be obtained similarly to the time-domain expansion. According to the corresponding relation between time-domain analysis and frequency-domain analysis, and using the early-time response and the low-frequency information of the induced currents, the non-known coefficients in the expansion series can be decided. The entire responses of the induced currents on the scattering object in both time and frequency domains can be obtained at one time by simultaneous extrapolation computation using both the early-time response and the low-frequency information of the induced currents.

摘要首先根据散射体在高斯脉冲平面波激励下感应电流的能量几乎全部集中在时间轴和频率轴上的有限范围内,该文将时域响应展开为系数待定的连带Hermite级数的叠加,并根据连带Hermite函数的傅里叶变换的自反性,得到与时域响应形式类似的频域响应;然后利用时域方法和频域方法分别计算散射体上感应电流的早时响应和低频信息;最后经过时域和频域联合外推计算,由早时响应和低频信息确定时域和频域响应的待定系数,从而获得了整个时域和频域的完全响应。

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