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Bax相关的网络例句
与 Bax 相关的网络例句 [注:此内容来源于网络,仅供参考]

Results 2 ClAdo and 2 CldAdo had different cytotoxicities on the cells, while 2' dAdo had no cytotoxicity on the cells. 2 CldAdo blocked the cell growth at the phase of S and G2/M, while 2 ClAdo at the phase of G0/G1. 2 CldAdo mainly induced cell necrosis, while 2 ClAdo induced both cell necrosis and apoptosis. Down regulated Bcl 2 expression and up regulated p53 and Bax expression were associated with 2 ClAdo, while 2 CldAdo down regulated Bcl 2 expression and up regulated mildly p53 expression without any effect on Bax expression.

结果 2 ClAdo、2 CldAdo对所研究的细胞均有程度不等的毒性;2' dAdo对各细胞生长、增殖均无明显抑制(c=100 μmol/L即30 μg/mL内);2 CldAdo明显阻断细胞于S、G2/M期,2 ClAdo阻断细胞于G0/G1期;2 CldAdo 致细胞坏死为主,2 ClAdo 既致细胞坏死又诱导凋亡;2 ClAdo 下调Bcl 2,上调P53、Bax蛋白表达;2 CldAdo小幅上调P53、小幅下调Bcl 2,不影响Bax蛋白表达。

To produce the scientific evidence for developing and manufacturing new antitumor drugs.Methods: 1 The inhibitory effect on cell growth of Hela was measured by MTT assay in treated or untreated groups (3.125, 6.25, 12.5, 25, 50μg/ml TAM and control) for three different treatment times (24h, 48h and 72h).2 Apoptosis and cell cycle were measured by FCM in four experimental groups (0, 4, 16, 40μg/ml TAM) for 48h.3 Adopting Wright and Giemse's staining to observe the morphology of Hela cells which treated with 40μg/ml TAM.4 Using invasion experiment to detect the Hela cells'invasive abilities which treated with 40μg/ml TAM.5 The protein expressional levels of P-ERK, ERK, C-myc and Cyclin D1 in Hela cells untreated or treated with 4, 16, 40μg/ml TAM for 24h were measured by Western blot.6 Expression of anti-apoptotic gene bcl-2, apoptotic gene bax and MMP-9 in Hela cells of four experimental groups (0, 4, 16, 40μg/ml TAM for 24h), were observed by revers transcription PCR.7 The protein expression of P-ERK, ERK, Bcl-2 and Bax in Hela cells treated with 40μg/ml TAM for 24h observed by laser scanning microscopes.

1采用四甲基偶氮唑蓝法检测不同浓度北豆根总碱(3.125、6.25、12.5、25、50μg/ml)处理不同时间(24、48和72小时)对Hela细胞增殖反应的抑制作用。2采用流式细胞技术(flow cytometry,FCM)检测不同浓度北豆根总碱(0、4、16、40μg/ml)作用48小时,对Hela细胞凋亡及周期变化的影响。3瑞氏-姬姆萨染色后显微镜观察北豆根总碱(0、40μg/ml)作用24小时后Hela细胞形态学变化。4采用Transwell小室法检测北豆根总碱(0、40μg/ml)作用24小时后对Hela细胞侵袭性的影响。5采用免疫印迹方法检测不同浓度北豆根总碱(0、4、16、40μg/ml)作用24小时后,Hela细胞中磷酸化ERK、ERK、C-myc、CyclinD1的表达变化。6采用逆转录-聚合酶链反应(revers transcription PCR,RT-PCR)半定量检测北豆根总碱(0、4、16、40μg/ml)作用24小时,Hela细胞抗凋亡基因bcl-2、促凋亡基因bax、基质金属蛋白酶-9(MMP-9)的表达变化。7应用激光共聚焦显微镜(laser scanning microscope,LSM)观察北豆根总碱(0、40μg/ml)作用24小时后,Hela细胞内P-ERK、ERK、Bcl-2、Bax蛋白的表达变化。

Immunohistochemistry for Bax: Bax expression was detected in germ cell cytoplasm cytoplasm and nucleus of seminiferous tubule theca cell, obviously spermatocyte.

免疫组化观察Bax的表达情况:Bax表达见于生精细胞的胞质和胞核,以精母细胞为主。

Objectives: To observe apoptosis and the expression of bcl-2、bax protein in the peri -hematomal brain region of Intracerebral Hemorrhage patients; so as to investigate into the relationship among neural apoptosis、the expression of Bcl-2、Bax pro -tein and Sthenia ZHENG、Protration ZHENG,as well as the relationship among apoptosis、hematoma volume and the scores of nervous impairment, to inquir the eff -ect of apoptosis in delayed neural injury following ICH and then to provide the mole -cular biology standard for the microcosmic syndrome differentiation with TCM to quest for new treatment.

目的:本课题旨在对脑出血患者血肿周围组织细胞凋亡和凋亡调控基因Bcl -2、Bax表达情况的观察。探讨中医出血中风闭脱证与细胞凋亡及Bcl-2、Bax表达的关系,及细胞凋亡与出血量、临床神经功能缺损积分的关系,从而探讨细胞凋亡在脑出血后继发性神经细胞损伤中的作用,为中医微观辨证提供分子生物学水平的依据,为探索中西医结合治疗脑出血的新途径提供理论指导。

The experiments showed a significant increase in Bax mRNA levels (P.01) in neurons cultured at severe hypoxia condition compared with those cultured at normoxia. In hypoxia groups, tolbutamide increased Bax mRNA expression (P.05), while diazoxide reduced it (n=5 for each).

缺氧+二氮嗪组中基因Bax的mRNA表达水平与单纯缺氧组相比下降(P.01),缺氧+甲苯磺丁脲组中基因Bax的mRNA表达水平相对于单纯缺氧组也有提高(P.05)。

The percent of atresic follicular increase with dosage rising (P.05).The result of expression of Bax and Bcl-2 showed that the Bax expressed widely in every groups, and it enhanced with dosage, there is extreme significant difference between experiment group and control group (P.01),there is not difference between withdrawal 48 hours and 96 hours.

免疫组化法检测Bax和Bcl-2蛋白表达,结果Bax在各组普遍表达,并随镉剂量的加大而表达增强,实验组与对照组间差异极显著(P.01),48h与96h两时间段间无差异;Bcl-2则普遍表达较弱或不表达,各组间无显著性差异。

Group 1 had increased bcl-2 and bax protein expression in hippocampal CA1 region at 6 hafter CPB ( bcl-2, 0.18 ± 0.05 versus 0.09 ± 0.01; P = 0.02; bax , 0.20 ± 0.06 versus 0.04 ± 0.02; P = 0.01; Group 1 versus Group 2, respectively).

CPB 后6h ,组1大鼠海马 CA1区 bcl-2和 bax 的蛋白表达增加(组1比组2: bcl-2,0.18 ± 0.05比0.09 ± 0.01, P = 0.02; bax ,0.20 ± 0.06比0.04 ± 0.02, P = 0.01)。

The results showed: there is the apoptosis of the myocardial cells during the period of I/R. The further study showed that there is the express of Bcl-2, Bax and Fas in the model of the cultured myocardial cells which were treated with ischemia-reperfusion The express of Bax, Fas proteins increase obviously. The overexpress of Bcl-2 is weak positive which shows that there is certain relationship between the apoptosis of the myocardial cells and the higher express of Fas and the ratio descent of the Bcl-2/Bax.

结果表明:在I/R过程中确有心肌细胞凋亡现象,而且进一步研究发现在培养的心肌细胞缺血-再灌注的模型中均见Bcl-2、Bax、Fas的表达,Bax、Fas蛋白的过度表达明显增加,Bcl-2的过度表达仅呈弱阳性,表明心肌细胞的凋亡与Fas的高表达,Bcl-2/Bax的比例下调有一定的必然联系。

Our study shows that Bax ,the protein of accelerating apoptosis, may participate in the proliferation and regression of hemangioma. 2 The expression of TGFβ1 in the involuting phase was higher than in the proliferative phase, the difference was statistically significant, p<0.01. 3 This shows that Bax and TGFβ1 may be the important factors which cause the apoptosis of hemangioma and accelerate its regression as well.

1 Bax在血管瘤增生晚期开始表达,至退化期Bax的表达达到高峰,提示Bax这种促进细胞凋亡的蛋白参与血管瘤的增生与退化过程。2 TGFβ1在血管瘤退化期的表达高于增生期,差异有统计学意义,p<0.01.3 提示Bax与TGFβ1可能是引起血管瘤凋亡,进而促进其退化的重要因素。

With an increase in Bcl-2 protein, more Bax homodimers were separated and conjugated with Bcl-2 protein to form more stable Bcl-2/Bax heterodimers than Bax homodimers, which'neutralize'apoptosis induction of Bax protein.

随着Bcl-2蛋白增多,越来越多的Bax蛋白同源二聚体被分开,与Bcl-2蛋白结合形成比Bax-Bax蛋白更稳定的Bcl-2-Bax蛋白杂二聚体,从而&中和&Bax蛋白的诱导细胞调亡作用。

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