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The etiology and pathogenesis is not very clear,may be due to excessive mechanical load or unbalanced distribution of cartilage wear,and then chondrocyte metabolic changes.Cell release a variety of catabolic enzymes that lead to aggrecan degradation,collagen network useless and cartilage unhomogeneity.

整合素作为细胞表面受体使整合素在细胞跨膜信号传递中起一定的作用,并且参与细胞的多种生理功能,如细胞的生长、发育、分化、凋亡等,同时参与多种病理过程,如淋巴细胞向炎症部位的聚集及肿瘤细胞的浸润等[2]。

We conclude that Di-Darg Tang and Vaccaria seed is well tolerated , safe ,and effective ; The test shows that those herbs are more sensitive on Myoma cell , Bcl-2 protein can repress Myoma cell by apoptosis.

子宫肌瘤细胞半致死量浓度(IC50)之测定,较正常子宫细胞低,显示些中药对子宫肌瘤细胞较为敏感,应可经由细胞凋亡的途径,而抑制子宫肌瘤细胞生长。

We conclude that Di-Darg Tang and Vaccaria seed is well tolerated , safe ,and effective ; The test shows that those herbs are more sensitive on Myoma cell , Bcl-2 protein can repress Myoma cell by apoptosis.

子宫肌瘤细胞半致死量浓度(IC50)之测定,较正常子宫细胞为低,显示这些中药对子宫肌瘤细胞较为敏感,应可经由细胞凋亡的途径,而抑制子宫肌瘤细胞生长。51-论文-网-欢迎您

One hand mechanical obstruct led to the increase of veinous resistance and the obstacle of microcirculation, the other hand the adhesive PMN was activated in excess, the white blood cells released a lot of enzymes, in which PMN-elastase can decompose the components of cell and many albumens, inclusive of immunoglobulin、alexin and fibrication. These components induced the injury of the pancreatic capillary vessels and cell and lysosome enzy made the tissue protein hydrolyze and produced unsaturated fatty acids, which destroyed the structure and function of cellar membrane. The inflammatory cellar factors activate other immunocytes to produce the injury and necrosis of tissue, which aggravated the pathological injury and led to shock、pyaemia and MODS. So ICAM-1 and LFA-1 played an important role in SAP. Frossard found that the expression of ICAM-1 in the rat model, especially in serum、pancreas and lung. All these showed ICAM-1 is an important factor in AP and concomitant lung injury.

胰腺小叶组织局部血管EC首先被激活,ICAM-1表达升高,与被激活的PMN表面表达的LFA-1相结合,&PMN-EC&相互作用加剧,一方面机械性阻塞毛细血管导致静脉阻力增加、微循环障碍;另一方面粘附的PMN过度吞噬或激活,当白细胞吞噬的颗粒不能被封闭隔离,连同细胞内的酶被释放出来,其中的PMN-elastase能够降解细胞基质中各种成分,水解多种蛋白,加重胰腺的毛细血管内皮细胞和腺泡的损伤;释放的溶酶体酶使组织蛋白水解,产生的不饱和脂肪酸引发脂质过氧化方应,破坏细胞膜的结构和功能;释放的炎性细胞因子,激发其他的免疫细胞的功能,导致进一步的组织损伤和坏死,加重SAP的病理损伤,最终导致休克、脓毒血症及多器官功能障碍等严重后果。

Results IL-6R immunoreactive cells were observed in the anterior of optical area,the ventromedial nucleus,the periventricular nucleus and arcurate nucleus of the hypothalamus.The strongly stained cells are concentrated in the granule cell layer of the dentdate gyrus and the pyramidal cells of the CA1-CA2 fields of the hippocampus.IL-6R positive cells are also detected in the cortex, the ventromedial nucleus of the thalamus,bed nu stria,olfaltory tubercle.

结果 IL-6R 免疫反应性细胞主要分布在下丘脑的视前区、腹内侧核、室旁核和弓状核;在海马, IL-6R 阳性细胞呈强阳性,密集分布于齿状回颗粒细胞层和 CA1~ CA2锥体细胞层;在大脑皮层、嗅结节、丘脑腹内侧核、终纹床核等处也有 IL-6R 阳性细胞

The study ~s conducted to elucidate the mechanism by which the expression of adhesion molecules on human endothelial cells ~s up-regulatecL Methods Human endothelial cells derived fium umbilical venisQ-IUVEC were coincubated in viny whh native human sennn albtuiiin, HSA modified v~ith advanced glycation end products or RPMI-1640 culture medium. The expression of adhesion molecule intereellular adhesion molecule-l(7ICAM-l), vascular cell adhesion molecule-l and E-selectin was determined by irnrnunofluorescen staining and flow cytometer analysis.

分离正常人脐静脉内皮细胞,将晚期糖基化终产物修饰的人血清白蛋白、人血清白蛋白以及RPMI-1640完全培养基与HUVEC在体外共同培养,用荧光单克隆抗体染色,流式细胞仪定量检测内皮细胞表面细胞间粘附分子-1(ICAM-1)、血管细胞间粘附分子-1(VCAM-1)、E-选择素的表达。

The iso-electric point of was 4.8-5.2. The amino acid analysis indicated that the recombinant protein is non- N-glycosylated.The ability of 0.5 ug/m rhsTRAIL to induce apoptosis of liver cancer cells SMMC7721 and BEL 7402 could be visioned morphologically. This was further verified by Electrical microscope observision of induced SMMC7721 cells and agarose gel electrophoresis of apoptosis DNA. MTT test results also showed that 0.01 u g/ml purified rhsTRAIL has strong effect to induce apoptosis of SMMC7721 cell.

形态学上观察了rhsTRAIL对肝癌细胞SMMC7721和BEL7402的诱导凋亡活性,发现rhsTRAIL在0.5μg/ml时显示了很好的诱导凋亡活性,并通过电镜观察rhsTRAIL诱导后的SMMC7721细胞,证实了凋亡;同时提取凋亡细胞DNA,进行琼脂糖电泳分析,在分子水平证明凋亡;最后利用SMMC7721细胞分组加入纯化后的rhsTRAIL蛋白,结果显示纯化蛋白含量在0.01μg/ml时细胞就呈现了诱导凋亡活性。

In summary, the BRD7 gene acted as a candidate of tumor suppressor gene with NPC. The overexpression of BRD7 can partly reverse malignant phenotype of NPC cell line. The suppression effect of BRD7 on NPC tumorigenesis my be achieved by recognizing acetylated histone peptide through their motif-bromodomain, then modulating gene transcription by taking part in histone acetylating and chromosome remodeling, finally influencing signal-transduction pathways.

综上所述,BRD7基因作为一个重要的鼻咽癌抑瘤基因侯选者,在鼻咽癌细胞中的过表达后,可导致鼻咽癌细胞 HNE蛋白质表达谱发生改变,逆转其恶性表型,其作用机理可能是:BRD7基因通过其功能域彭聪硕士学位论文10Bromodomain与乙酚化的组蛋白特异性结合,参于染色体的乙酚化,染色质的组装,从而影响基因转录的调控,最终影响细胞内的信号传导通路并实现对细胞周期的调控,从而发挥抑制鼻咽癌细胞生长的作用。

After maturation with the stimulation of LPS, apophyses became obviously increased by SEM scanning; the expression percentages of 33D1 and CD11c exceeded 80% by immunofluorescence staining and those of CD86 and MHCⅡwere 99.0% and 32.5%; MLR showed that mature BMDCs could better stimulate the proliferation of homologous T cells.

以LPS刺激成熟后,扫描电镜发现细胞突起更加明显,免疫荧光发现表达33D1和CD11c的细胞数均达到80%以上;流式细胞术检测CD86和MHCⅡ的细胞表达率分别为99.0%和32.5%;混合淋巴细胞反应提示成熟的BMDCs能明显刺激同源T细胞的增殖。

As exposed to optics microscope and inverted microscope,compared to control,SW480 cells with Giemsa staining that treated with the H2RA(cimetidine、nizatidine) took on malignance declining as crimpled firstly,cellular bulk and heteromorphism dimimished,the amount of rounded cell manifolded,nucleolus bulk lessened,dyeing thin,the amount of nucleolus decreased,partial cell organs manifest side-gathering phenomenon on chromatin,and the link between SW480 cell is loosened , subsequently partial rounded cell is floated.When the H2RA(cimetidine 40μM、nizatidine 20μM) against SW480 cells after 3 day,SW480 cells change roundly,nucleolus smashed,shrinking nucleolus came into being,and part of those not adhibited cell wall.

在光镜和倒置相差显微镜下,与对照组相比,经姬姆萨染色观察,西咪替丁、尼扎替丁处理的SW480细胞,先发生皱缩,体积变小,异形性减少,细胞变圆数目增多,细胞核变小,染色变淡,核仁数量减少,部分可见染色质边集现象;细胞间连接疏松,随后部分变圆细胞浮起。40μM西咪替丁及20μM尼扎替丁连续处理3天后,SW480细胞全部变圆,细胞核碎裂,固缩微核形成,部分不再贴壁。

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