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停滞细胞
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  “停滞细胞”译为未确定词的双语例句
     [Results] AngⅡ stimulation enhanced the positive cell number of β-gal stained HUVEC, depressed cell proliferation, and increased the protein expression of P16, at the same time, stimulated cells produced less NO and more.
     结果给予AngⅡ后,β-gal染色阳性细胞数增加,细胞向G0-G1期停滞,细胞p16蛋白表达增高,出现衰老的特征性改变;
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     TGF β induces growth arrest in various cell types, including lung epithelial cells, and expression of a wide array of proteins, some of which are deposited in the lung extracellular matrix.
     TGF-β诱导不同类型停滞细胞 (包括肺上皮细胞 )的生长和一批蛋白的表达 ,其中一些蛋白沉积于肺泡外基质中
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     Conclusion:FFAs could inhibit proliferation of rat Mesangial cells in vitro by arresting cells growth in G1 phase.
     结论:游离脂肪酸可通过停滞细胞生长于G1期,抑制大鼠肾小球系膜细胞的生长增殖。
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  相似匹配句对
     Tom Clancys Splinter Cell
     细胞分裂
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     SPLINTER CELL
     分裂细胞
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     Cell cycle analysis revealed the percentages of G1 phase cells were increased, that of G2/M and S phase decreased linearly with the increase of concentrations of gentamicin.
     庆大霉素致细胞周期停滞于G1期。
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     But the LDH activity was not significantly altered in the treatment with 50 μmol·L -1 NPPB. Flow cytometry experiments showed that 50 and 25 μmol·L -1 NPPB arrested ( 84.2±2.4)% and (80.8±2.9)% of cells at G0/G1 stage, versus (70.5±1.4)% of control cells.
     NPPB使细胞周期停滞在G0/G1期。
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  arresting cell
High salt culture conditions suppress proliferation of rat C6 glioma cell by arresting cell-cycle progression at S-phase
      
Copper inhibited growth of cells, most probably either by arresting cell division or by penetrating inside the cell and affecting metabolism.
      
However, arresting cell proliferation after 2 days in culture by reducing the FCS concentration to 0.01% induced the expression of the sustained VACC the next day.
      
Anti-apoptotic genes, bag-1 and bcl-2, enabled hybridoma cells to survive under treatment for arresting cell cycle
      
Lycopene induces apoptosis in immortalized fibroblasts exposed to tobacco smoke condensate through arresting cell cycle and down
      
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Objective To explore the possibility of using Vpr as a biological agent for anticancer therapy.Methods A HIV-1 wild type Vpr and a mutant vprX gene were expressed and tested in a cervical cancer HeLa cell line.The ability of Vpr to induce cell cycle G2 arrest and cell death was measured by flow cytometric analysis.Nuclear localization of Vpr was visualized by fluorescent light emitted from the green fluorescent protein (GFP)-Vpr fusion protein.Results Consistent with early reports,Vpr,not VprX,induced G2...

Objective To explore the possibility of using Vpr as a biological agent for anticancer therapy.Methods A HIV-1 wild type Vpr and a mutant vprX gene were expressed and tested in a cervical cancer HeLa cell line.The ability of Vpr to induce cell cycle G2 arrest and cell death was measured by flow cytometric analysis.Nuclear localization of Vpr was visualized by fluorescent light emitted from the green fluorescent protein (GFP)-Vpr fusion protein.Results Consistent with early reports,Vpr,not VprX,induced G2 arrest.However,both Vpr and VprX were able to induce cell death in HeLa cells.We also demonstrated that the nuclear localization of Vpr could be determined by using a GFP-Vpr fusion protein.Conclusion This is the first report documenting in mammalian cells that G2 arrest and cell death induced by Vpr are two independent functions.The unique biological properties of Vpr shown in cervical cancer cells suggest that Vpr may be a useful biological agent for anti-cancer therapy.

目的 通过研究HIV - 1Vpr基因在宫颈癌细胞HeLa中诱导细胞周期G2停滞、细胞致死效应及其核定位功能 ,探讨将Vpr用于肿瘤治疗的可能性。方法 用脂质体转染的方法 ,将携带Vpr或其突变体VprX基因的质粒转入HeLa细胞内 ,用流式细胞仪分析Vpr诱导的G2停滞和细胞致死性 ;用荧光显微镜观察GFP -Vpr融合蛋白的荧光确定其核定位功能。结果 Vpr具有核定位功能。Vpr和VprX蛋白都具有细胞致死性 ,但是VprX蛋白不能使细胞停滞到G2期。结论 首次报道了Vpr的G2期停滞和细胞致死功能在哺乳动物细胞中是互相独立的。Vpr在肿瘤治疗中有很大的潜力

Lung development begins with the outgrowth of paired lung buds from the foregut endoderm that invade the surrounding mesodermal mesenchyme in a genetically predetermined pattern of branching morphogenesis and lung specific cell differentiation. It is likely that cell differentiation of the respiratory epithelium is influenced by complex cell cell interactions and autocrine, paracrine and humoral signals which influence the expression of transcription factors in foregut tissues. which influence the expression...

Lung development begins with the outgrowth of paired lung buds from the foregut endoderm that invade the surrounding mesodermal mesenchyme in a genetically predetermined pattern of branching morphogenesis and lung specific cell differentiation. It is likely that cell differentiation of the respiratory epithelium is influenced by complex cell cell interactions and autocrine, paracrine and humoral signals which influence the expression of transcription factors in foregut tissues. which influence the expression of transcription factors in foregut tissues. Several families of transcription factors play critical roles in lung morphogenesis and gene expression, including the homeodomain protein thyroid transcription factor 1 (TTF 1), the winged helix family member hepatocyte nuclear factor 3β (HNF 3β) and zinc finger transcription factors of the Gli family. Growth factor β (TGF β) family peptides regulate cell growth, differentiation and tissue morphogenesis through autocrine/paracrine signaling mechanisms. TGF β induces growth arrest in various cell types, including lung epithelial cells, and expression of a wide array of proteins, some of which are deposited in the lung extracellular matrix.

哺乳动物肺的发育起始于从前肠内胚层发育而来的成对肺芽突起 ,它以分支形态发生和肺特异性细胞分化的遗传预定模式侵入周围的中胚层间质。呼吸上皮细胞的分化很可能受复杂的细胞 -细胞间相互作用的影响 ,并且受影响前肠组织中转录因子表达的自分泌、旁分泌和体液信号的影响。在肺形态发生和基因表达中 ,若干个转录因子家族起关键作用 ,包括同源 [异型 ]域蛋白甲状腺转录因子 - 1 (TTF- 1 ) ,翼状 -螺旋家族成员肝细胞核因子 - 3β(HNF- 3β)和 GIi家族中的锌指转录因子。 TGF-β诱导不同类型停滞细胞 (包括肺上皮细胞 )的生长和一批蛋白的表达 ,其中一些蛋白沉积于肺泡外基质中

Objective To investigate whether p53 pathway participates in the effect of emodin on vascular smooth muscle cell proliferation.Methods The effects of emodin on vascular smooth muscle cell proliferation were evaluated by cell count, senescent-associated β-galactosidase staining, and annexin V staining. DNA synthesis was determeined by ~3H-thymidine corporation, cell cycle was analyzed by FACS, the p53 protein level was measured by Western blot and cDNA expression array technology was used to demonstrate the effect...

Objective To investigate whether p53 pathway participates in the effect of emodin on vascular smooth muscle cell proliferation.Methods The effects of emodin on vascular smooth muscle cell proliferation were evaluated by cell count, senescent-associated β-galactosidase staining, and annexin V staining. DNA synthesis was determeined by ~3H-thymidine corporation, cell cycle was analyzed by FACS, the p53 protein level was measured by Western blot and cDNA expression array technology was used to demonstrate the effect of emodin on the simultaneous expression of a large number of genes in cultured vascular smooth muscle cells.Results Emodin at 1.6-3.1 μg/ml inhibited VSMC growth, at 6.3-12.5 μg/mlpromoted VSMC aging and induced VSMC apoptosis at 25.0 μg/ml 24 hours after exposure. Unscheduled DNA synthesis, which was a sensitive indicator for DNA injury, was observed in VSMC following 24 hours emodin exposure. The mRNA and protein levels of p53 were up-regulated in a concentration-dependent manner. Proliferation/carcinogenesis-related genes were down-regulated and other genes related to cell senescence, apoptosis, and DNA damage/repair were up-regulated in VSMC after exposure to emodin for 24 hours. Emodin readily permeated VSMC membrane and mostly located in the cytoplasm and few of them in the nucleus.Conclusions The p53 pathway in VSMC was activated post emodin exposure in a concentration-dependent manner and which might be responsible for the observed antiproliferative effects of emodin in vascular smooth muscle cells.

目的探讨p53途径在大黄素抑制血管平滑肌细胞增殖作用中的地位。方法通过细胞计数、老化相关β-半乳糖苷酶染色、AnnexinV标记等方法观察大黄素抑制血管平滑肌细胞增殖的特点。3H-胸苷掺入法测定DNA合成、流式细胞仪了解细胞周期变化、Westernblot检测p53蛋白表达变化、基因芯片观察mRNA表达水平。结果(1)1·6~3·1μg/ml大黄素延缓细胞生长,6·3~12·5μg/ml大黄素促进细胞老化,25·0μg/ml大黄素则可显著诱导细胞凋亡。(2)大黄素干预24h后,出现非计划性DNA合成现象,这是DNA损伤的敏感性标志。p53基因和蛋白表达水平呈大黄素浓度依赖性上调。除了细胞增殖基因表达下调,其他基因表达均上调,如细胞老化基因、细胞凋亡基因、DNA损伤修复基因。(3)大黄素能够迅速渗透进入细胞,在细胞内的分布具有明显的选择性,绝大多数以颗粒形态分布于细胞胞浆中,细胞核中也有少量分布。结论大黄素通过损伤DNA激活p53途径。随着大黄素浓度升高,p53途径激活程度也随之增强并产生多种细胞增殖抑制效应,即生长停滞、细胞老化和细胞凋亡。

 
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