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The results shown that:(1) Bufo raddei Strauch tadpole was capable of lens regeneration, which originated from the epithelial cells at dorsal iris margin by depigmentation.(2) Depigmentation of Bufo raddei Strauch during lens regeneration was by two methods: First, pigment granules initially dispersed all over the cytoplasm were moved towards the periphery of the cell, and then were directly taken up by the amoeboid cells. Second, pigment granules in a cell were first crowded in a mass, surrounded by a membranous structure in the cytoplasm, which were eventually discharged as a mass from the cell.

结果表明:花背蟾蜍蝌蚪(1)具有晶状体再生的能力,其晶状体的再生来源于虹膜背缘的上皮细胞;(2)虹膜背缘去色素是转分化的前提,主要有两种方式:一种也是最主要的方式是在晶状体被摘除后虹膜外侧产生巨噬细胞,巨噬细胞吞噬虹膜色素上皮细胞中的色素颗粒;另一种方式是虹膜色素上皮细胞自身释放色素颗粒;(3)电镜观察发现虹膜色素上皮细胞转分化过程中线粒体有明显变化,核糖体增多,粗面内质网增多,晶状体纤维分化过程中细胞核逐渐凝聚。

High concentration of amylin is responsible for the prevention of rise of Ca++ inside the islet B-cells and /or the decrease of cAMP content which is one of the causes that bring about the decreased release of insulin.

高浓度的胰淀素抑制了胰岛细胞内Ca++升高和/或细胞内cAMP形成,可能是胰岛素分泌减少的原因之一。

Methods RGD peptide were through direct covalent linkage attached on micro-channel surface with 1-ethyl-3- 3-dimethylaminopropyl carbodiimide hydrochloride and N-hydroxysuccinimide to A549 cells.

方法采用化学共价连接的方法固定RGD多肽,建立由流体控制系统、免疫反应系统构成的细胞识别芯片系统,用于细胞的筛选/捕获;选用不同密度的细胞进行进样试验,考察不同细胞密度对通道内细胞数量的影响,并讨论不同的孵育时间对细胞捕获的影响。

Methods RGD peptide were through direct covalent linkage attached on micro-channel surface with 1-ethyl-3- 1 3-dimethylaminopropyl carbodiimide hydrochloride and N- hydroxysuccinimide to A549 cells.

采用化学共价连接的方法固定RGD多肽,建立南流体控制系统、免疫反应系统构成的细胞识别芯片系统,用于细胞的筛选/捕获;选用不同密度的细胞进行进样试验,考察不同细胞密度对通道内细胞数量的影响,并讨论不同的孵育时间对细胞捕获的影响。

Two cases were isointense or hypointense signal on T1WI and heterogeneous hyperintense signal on T2WI and T2WI STIR. Conclusion Enhanced CT clearly showed calcification and blood supply of the tumor while MRI showed small hemorrhage, cystis foci, necrosis and central stellate scar of the tumor. MRI can provide more useful information in detecting chromophobe cell renal carcinoma.

结论肾脏嫌色细胞癌属少血供肿瘤,CT能清晰显示肿瘤内钙化灶和血供情况,而MRI容易检出肿瘤内小出血灶、囊变坏死灶以及中央星状瘢痕,可对肾脏嫌色细胞癌的诊断提供更多更有价值的信息。

Methods Westernblot was employed to detect the intracellular expressions of caspase-9, hTERT, Bcl-2 and Bax, and mitochondrial and cytoplastic cytochrome C in HepG2 cells transfected by pSliencer 3.1-H1 neo-shTERT.

收集第20代hTERT基因RNAi真核表达载体论定转染细胞、对照细胞及未转染HepG2细饱,采用Western blot检测线粒体,胞质细胞色素C的表达及细胞内caspase-9、Bcl-2、Bax和hTERT的表达。

It is well known that retinal pigment epithelial cells are predominant proliferative cells in PVR which is an excessively wound healing response occurring after RPE cell wounding. The activated RPE cells migrate from their normal, sessile state to vitreous and onto both surfaces of the retina, in which they begin to dedifferentiate, migrate, proliferate, change phenotype and secrete ECM.

既往研究证明视网膜色素上皮(retinal pigmentepithelial,RPE)细胞是参与PVR的主要细胞,PVR是视网膜脱离后RPE细胞损伤的一种自我修复过程,是一种过度的眼内创伤修复反应;RPE细胞在正常位置上处于静止状态,而在某些病理条件下,如视网膜裂孔形成和视网膜脱离后,RPE细胞脱离原位,开始去分化、移行、增生、发生表型转化并分泌胶原等ECM,最终在视网膜前后表面和玻璃体内形成具有收缩能力的增生膜,造成牵拉性视网膜脱离。

After contact with xeno-target cells, the cytotoxicity of natural killer cells and the secretion of cytokines are related to the ratio of effecter cells and target cells.

NK细胞与异种靶细胞接触后,其杀伤活性和细胞因子的分泌水平与效靶细胞的比例在一定范围内呈正相关。

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。

In this study, oral tolerance was induced by tube-feeding transgenic mice with 0.5mg/day OVA protein daily, simultaneously sensitized by OVA protein with aluminum hydroxide. Oral-administered OVA protein (0.5mg/day for 5 or 10 consecutive days) resulted in significant lowered airway hypersensitivity as well as reduced inflammative cells infiltration, titer of serum OVA-specific IgE, IL-5 secretion in bronchoalveolar lavage fluid, and IL-4 secretion in splenocyte.

首先,本实验於小鼠中成功诱发了呼吸道过敏、大量OVA特异性IgE抗体生成、及嗜酸性白血球不正常聚集等现象;致敏前,同以连续管餵小鼠OVA抗原(0.5mg/day) 5天或10天后,结果显示皆能缓和呼吸道阻力、减低肺部发炎细胞浸润现象、降低血清中OVA特异性IgE抗体的生成量、也减少肺部冲洗液及脾脏细胞内第二型辅助T细胞(type II helper T cell, Th2)细胞激素的分泌(IL-4、IL-5)。

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