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The key to using aberrant energy metabolism as a way to enhance site affinity that specifically targets the cancerous tumor cells' microenvironment that produces measurable tumor selective alkalinization involves administering an alkaline composition that has little toxicity to normal healthy viable cells which preferentially targets and elevates the pH level of the tumor micro-environment, thus causing the non-viability and apoptosis of tumor cells.

可使用异常能量新城代谢来提高癌瘤位置的亲和力,使癌瘤进行具有可测性、可选性的碱化,从而专门改变癌瘤细胞的微环境。其关键在于使用一种对正常健康活性细胞无毒性的碱性制剂,能优先提高癌瘤微环境的pH水平,从而使癌瘤细胞不具有生存能力,促使其凋亡。

The theory is cell kinetics and mechanism of drugs.

主要是根据细胞动力学原理和药物的作用机理分析,如果把药物集中应用,一方面只是一过性的杀灭增殖期的白血病细胞,对静止期细胞影响不大,另一方面对正常细胞造成较大损伤,而如果药物作用于几个细胞增殖周期,对白血病细胞进行几个循环的打击,会清除更多白血病细胞,而对正常细胞损伤较小。

SW620/pRETRO-On-TRAIL cells become round and small,dioptre of ellsbroken cells increase.

用相差显微镜观察细胞形态发现,SW620/pRETRO-On-TRAIL细胞经四环素诱导后,变圆变小,贴壁性差,折光性强,细胞碎片增多。

Microinjection was used to inject the sperm-like cells into oocytes and enucleate oocytes to observe the development situation of zygotes. Results The proportions of sperm-like cells induced by the three methods were 5.9%,1.6%,0.35% respectively.

但在体外研究SSCs诱导精子的很少,某些雄性性原细胞可以直接分化成精原细胞[6],这提示具有一少部分雄性性原细胞维持在干细胞状态。

Eosinophile, mast cell , basophils, lymphocyte and many kinds of cytokine are involved in this inflammation.

是以气道高反应性和慢性气道炎症为特征的变态反应性疾病,是由嗜酸性粒细胞、肥大细胞、T淋巴细胞等多种炎症细胞和细胞因子参与的气道慢性炎症。

ResultsMacroscopic examination showed no excrescence,thrombus formation,arm fractures and corrosion.The devices were covered with collagen fibrosis and discrete endocardial cells,apparent inflammatory infiltration in the devices and around the devices 1 month after implantation.The implants were nearly endothelialized,while the inflammatory reaction relieved gradually,with myocardial cells ingrowth at the edges of the device 3 months after implantation.The devices were completely covered with endocardium and fibrous tissue.Moreover,endothelial cells could be found on the smooth microscrew adaptor.The inflammatory reaction diminished with a few chronic inflammatory cells existing.Neovascularization and lymphatic vessels ingrowth could be observed 6 months after implantation.

结果所有封堵装置表面均没有发现赘生物、血栓形成、支架发生断裂及被腐蚀;术后1个月,封堵装置表面被胶原纤维和散在内皮细胞所覆盖,大量炎症细胞浸润,封堵装置边缘有小灶性炎症细胞浸润;术后3个月,封堵装置表面几乎被内皮细胞所覆盖,炎症细胞较1个月时明显减少,封堵装置内见纤维化,封堵装置边缘心肌细胞浸入;术后6个月,封堵装置表面完全被心内膜和纤维组织所覆盖,伞尖表面光滑并有内皮细胞上爬,炎症反应明显消散,但仍有少量慢性炎症细胞存在,装置内有新生的血管、淋巴管长入。

Results: The coelomocyte could be divided into 7 types: large grained cell, small granular cell, large hyaline leucocyte, small hyaline leucocyte, lanceolate cell, facultative cell and bacillary flutter. The concentration range of the coelomocyte was 5.62~10.00×10^6/ml. In the observation of phagocytize, pseudopod were obviously found and the phagocytic power was strong in the small granular cell.

结果:观察发现罗氏海盘车的体腔细胞可分成:大颗粒细胞、小颗粒细胞、大透明细胞、小透明细胞、柳叶形细胞、兼性大细胞和杆状颤动体;体腔细胞的浓度范围是:5.62~10.00×10^6个/mL。

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。

Result 1 Magnetic nanoparticles, magnetic nanoparticles modified with antisense oligodeoxynucleotide of human telomerase reverse transcriptase induced HL-60 tumor cells to apoptosis, we could see typical morphologic change of apoptosis cells: karyopyknosis, chromation"s condensing and aggregation in nuclear, forming crescent-shaped or annulus structures to lean on edge of cell nucleus"s membrane and posing apoptosis body by Atomic Force Microscope, Fluorescence microscope, transmission electron Microscope 2 There was a significant difference compared with control group(p.01), inhibition ratio had significant positive correlation with medication dosage and time ;during 0.8-8μM dosage amplitude, inhibition ratio accrescenced by dosages increasing. However, the inhibition ratio would decrease when dosage over 8-80μM.

结果 1 磁性纳米粒子、修饰有端粒酶反义寡核苷酸的磁性纳米粒子诱导HL-60细胞发生凋亡,原子力显微镜、光学显微镜、荧光显微镜和透射电镜下均观察到HL-60细胞呈现典型的凋亡细胞的形态变化:细胞核固缩,核内染色质浓缩、凝聚、形成新月形或环状结构紧靠在细胞核膜边缘,并形成凋亡小体。2 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子对HL-60肿瘤细胞的生长和增殖有明显的抑制作用,与对照组相比有显著性差异(p<0.01),在剂量为0.8-8μmol/L范围内,抑制率随剂量的增加而增加,当剂量超过8μmol/L时,抑制率反而下降;3 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子可增强p53基因的表达活性,引起DNA降解损伤,反向调节细胞周期活动,促使细胞从G0期进入G1期,抑制肿瘤细胞的生长。4 修饰有端粒酶反义寡聚脱氧核苷酸的量子点能通过内吞作用进入HL-60肿瘤细胞的细胞核,可以在细胞内进行定位和促进HL-60肿瘤细胞的凋亡。

The results indicated that the typical apoptosis was induced by PRRSV in lungs and uteri. The ultrastructural changes showed different characterizations at different stages of the infection. During the early stage from 8th h to day 3 postinfection,the apoptosis cells shrank,the cytoplasm concentrated,the chromatin condensed,the kernel disaggregated and the endoplasmic reticulum dilated. During the middle stage from day 5 to day 9 postinfection,the apoptosis cells evidently shrank,the cell membranes protu berated,the plastosome manifolded,and apoptosis bodies were found. During the last stage from day 10 upwards postinfection,the apoptosis bodies degenerated and disappeared,and no inflammation occurred. Few apoptosis cells were necrotic.

结果表明,PRRSV可诱导宿主肺和子宫发生典型的细胞凋亡,表现为细胞的超微形态结构随着病毒感染进程出现不同的特征性变化,早期(感染后第8 h至第3 d)凋亡细胞多表现为细胞体积缩小,细胞质密度增强,染色质浓缩,核仁解体,内质网扩张;中期(感染后第5 d至第9 d)凋亡细胞体积显著缩小,细胞膜突起,线粒体增多,有凋亡小体形成;晚期(感染后第10 d以后)凋亡细胞形态多表现为凋亡小体降解和消失,少数凋亡细胞在凋亡晚期表现为坏死细胞。

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