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体内诱导
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  induced in vivo
     STUDY OF THE ANTITUMOR IMMUNE RESPONSES INDUCED in vivo BY ANTI-IDIOTYPIC VACCINE OF OVARIAN CANCER (6B11mGM)
     卵巢癌抗独特型疫苗(6B11mGM)动物体内诱导抗肿瘤免疫应答的实验研究
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     Peripheral circulating CD1α dendritic cells were induced in vivo by IFN-α application in patients with chronic hepatitis B
     干扰素-α对慢性乙型肝炎患者CD1α树突状细胞的体内诱导作用
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     Conclusion Specific CTL response can be induced in vivo by OVA 257-264-β 2m fusion protein.
     结论 OVA2 57 2 64 β 2m的表达产物 ,可有效的在体内诱导特异性CTL应答。
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  in vivo induction
     The Experimental Study on the in Vivo Induction of the Cytotoxicityof Killer Cells by Tumor Cells Transfected with TNF-aGene
     TNF基因转染的肿瘤细胞体内诱导免疫细胞杀伤活性的研究
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     Studies on the in vivo induction of differentiation of the erythroleukemia cells by the antigenpulsed dendritic cells modified with GMCSF gene
     GM-CSF基因修饰、抗原预激的树突状细胞体内诱导白血病细胞分化的实验研究
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     THEEXPERIMENTALTUDY ON THE IN VIVO INDUCTION OF
     白细胞介素4基因转移的肿瘤细胞体内诱导杀伤细胞活性及细胞因子产生的实验研究
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     In vivo induction of interferon γ like activity from Ctenopharyngodon idellus by phytoagglutinin
     草鱼γ样干扰素的体内诱导
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  “体内诱导”译为未确定词的双语例句
     Conclusion:Aβ25-35 can induce apoptosis of rat's hippocampal neurons in vivo.
     结论:Aβ25-35可在体内诱导大鼠海马神经元凋亡。
短句来源
     CELL MEDIATED IMMUNE RESPONSE TO H1N1 AND H3N2 INFLUENZA VIRUS IN MICE
     甲1(H1N1)和甲3(H3N2)型流感病毒在小鼠体内诱导细胞免疫反应的研究
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     Results At the dose of 5 mg/kg and 1 mg/kg,As 2O 3 induced apoptosis in nasopharyngeal carcinoma cells.
     结果 :As2 O3腹腔注射 1mg/kg和 5mg/kg均能在小鼠体内诱导鼻咽癌细胞凋亡。
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     Methods SLE-like syndrome in(C57BL/6×BALB/c)F1mice was induced by intravenous injection of lymphocytes from BALB/c parental mice.
     方法将亲代BALB/c鼠淋巴细胞经静脉途径输入到(C57BL/6×BALB/c)F1小鼠体内,诱导成狼疮鼠模型。
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     Objective To evaluate the immunogenicity of recombinant fowl-pox virus vUTAL3CP1 co-expressing P1-2A gene and 3C~(pro) gene of foot-and-mouth disease virus(FMDV) and DNA vaccine plasmid pVIRIL18P1 co-expressing P1-2A gene and pig IL-18 gene in pigs.
     目的评价本课题组构建的共表达FMDV衣壳蛋白前体P1-2A基因以及免疫辅助基因的重组鸡痘病毒vUTAL3CP1和重组DNA疫苗pVIRIL18P1在猪体内诱导特异性体液免疫和细胞免疫的能力。
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  induced in vivo
It was suggested that loss of ovarian function induced in vivo osteoblast lineage increased IL-6 mRNA expression.
      
We conclude that the modified nick translation assay is sensitive enough to detect SSB induced in vivo by exposure to a genotoxic agent and could therefore be used in biological monitoring at the workplace.
      
Amylin-induced in vivo insulin resistance in conscious rats: the liver is more sensitive to amylin than peripheral tissues
      
We conclude that: (1) the migration and maturation of cytotoxic T cells can be induced in vivo by IEC and (2) IEC may contribute to the increased severity of intestinal rejection through interaction with macrophages.
      
In rats chronically treated with clozapine, tyrosine depletion attenuates the clozapine-induced in vivo increase in prefrontal c
      
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  in vivo induction
The cells carrying the mutant alleles have impaired tumorigenicity compared with their progenitors due to in vivo induction of a cytotoxic T-cell response specific for tum - antigens.
      
These results indicate that LC 9018-induced Ia-positive macrophages, which first encounter a tumor antigen in the peritoneal cavity, play an important role in the in vivo induction of tumor specific T cell-mediated antitumor immunity.
      
These results indicate that augmentation of in vivo induction of certain kinds of antitumor cells does not necessarily result in a beneficial augmentation of the host's ability to resist tumor growth.
      
In vivo induction of HLA molecules in patients with myeloproliferative syndrome during IFNα treatment
      
In vivo induction of the growth associated protein GAP43/B-50 in rat astrocytes following transient middle cerebral artery occlu
      
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In a previous paper we have shown that the high molecular weight RNAs isolated from the substrate and the hormonal induced rat livers were capable of inducing tryptophan pyrrolase (TP). In the present investigation, it was found that during the substrate and the hormanal induction of TP, ~(32)P pulse-labeled RNAs formed. The pattern of changes in the radio-specific activity of the pulse-labelling (Na_2H~(32)PO_4 injected 20 min. before sacrifice of the animals) in RNAs isolated from the rat livers in each case...

In a previous paper we have shown that the high molecular weight RNAs isolated from the substrate and the hormonal induced rat livers were capable of inducing tryptophan pyrrolase (TP). In the present investigation, it was found that during the substrate and the hormanal induction of TP, ~(32)P pulse-labeled RNAs formed. The pattern of changes in the radio-specific activity of the pulse-labelling (Na_2H~(32)PO_4 injected 20 min. before sacrifice of the animals) in RNAs isolated from the rat livers in each case was parallel to that in the inductive activities for TP by these RNAs. The formation of the pulse-labeled RNAs was inhibited by actinomycin K_2. However, changes in the radio-specific activity of the ~(32)P long term-labeled RNAs (Na_2H~(32)PO_4 injected 2 hours before sacrifice of the animals) were quite different from those observed for the pulse-labeled RNAs. Furthermore, the RNAs isolated from both the substrate and the hormonal induced animals at the time corresponding to the high radio-specific activity of the long term-labeled RNAs showed no significant difference in stimulating TP activity from that of the normal RNA.

本实验观察到在大鼠肝色氨酸吡咯酶的激素和底物诱导过程中都有~(32)P快速标记RNA的出现,它们在氢可地松诱导2小时和在色氨酸诱导3.5小时的比放射性较对照RNA者分别增加100%和60%左右。~(32)P长期标记高聚RNA的变化与快速标记RNA者显然不同,在激素诱导4~6小时和在底物诱导10小时的比放射性始有增高。激素和底物诱导后不同时间提取的~(32)P快速标记RNA的放射性动态变化与其相应RNA诱导TP活性的动态变化呈平行关系,而从~(32)P长期标记活性最高时提取的高聚RNA刺激TP的活力与正常鼠肝RNA刺激TP的活力无显著差别,激素和底物诱导过程中~(32)P快速标记RNA的生成为放线菌素K_2所抑制。去肾上腺大鼠底物诱导2小时和3.5小时也出现~(32)P快速标记RNA,其生成也为放线菌素K_2所抑制。自去肾上腺大鼠底物诱导3.5小时提取的RNA对TP的诱导活性高于相应的正常鼠肝RNA。以上结果说明,在TP的激素和底物诱导过程中所生成的具有体内诱导TP功能的高聚RNA,可能是一种“特异的mRNA”。

Two strains of influenza A viruses, A/Hong Kong/123/77 ( A/HK ) ( HlNl )and A/Queensland/6/72 ( A/Qld ) ( H3N2 )and the two cold-adap-ted(ca ) reassortants which posses the surface antigens of these strains, CR35 and CR6 respectively, were compared for thier ability to induce primary cyto-toxic T cell(Tc ) responses in mice.When similar doses ( IO or IO3 HAU ) of each virus were injected i.v.into mice and the spleens tested for Tc activity 6 days later, both A/Qld and CR6 were about IOO-fold higher in inducing...

Two strains of influenza A viruses, A/Hong Kong/123/77 ( A/HK ) ( HlNl )and A/Queensland/6/72 ( A/Qld ) ( H3N2 )and the two cold-adap-ted(ca ) reassortants which posses the surface antigens of these strains, CR35 and CR6 respectively, were compared for thier ability to induce primary cyto-toxic T cell(Tc ) responses in mice.When similar doses ( IO or IO3 HAU ) of each virus were injected i.v.into mice and the spleens tested for Tc activity 6 days later, both A/Qld and CR6 were about IOO-fold higher in inducing a primary Tc responses than A/HK or CR35, The use of the two reassortant viruses which contain gene coding for identical internal proteins shows conclusively that tha surface protiens determine the magnitude of the primary Tc response under these circumstances, Whether the hemagglutinin and neuramini-dase are equally important remains to be determined.These strains were also tested for thier ability to sensitize mice for a secondary Tc response challenged with a distantly related A strains virus A/Shearwater (A/SW)/77 ( H6N5 ) .If mice were primed with a low dose ( IO4 E-ID50 )of these viruses ,A/Qld and CR6 were more effective than A/HK or CR35 at sensitizing for a secondary Tc response when challenged with A/S-W, but if larger doses were given either i.n. (IO6 EID50 ) or i.v. (IO3HAU) all viruses sensitized the mice equally well, despite the fact that A/SW gave a poor primary Tc response in mice.We also disscussed that probably Tc cells recognized internal virus determinants on the membrane of infected target cells.

比较了甲型流感病毒A/HK/123/77(H1N1)和A/Qld/6/72(H3N2)及其具有相应表面抗原的两个冷适应基因重分配株(Cold-Adapted Reassortant)的子代毒株CR35和CR6,在小鼠体内诱导初次细胞毒性T细胞(简称Tc)反应的能力。静脉注射相同剂量病毒后第6天,甲3型A/QLd和CR6所诱导的脾细胞Tc活性均比甲1型A/HK和CR35者高100倍。编码内部蛋白的基因相同而表面抗原的基因不同的CR6与CR35所诱导的Tc活性也不同,说明了表面抗原决定着初次Tc反应的强度。用无关的流感病毒A/SW/72(H6N5)攻击已用低剂量(10~4EID_(?))病毒致敏的小鼠表明,对A/Qld和CR6致敏者所诱导的第二次Tc活性,比A/HK和CR3S致敏者的稍高;但对用大剂量病毒致敏者,则均能产生同样好的第二次Tc活性。对Tc识别感染靶细胞上的病毒成份进行了讨论。

dbcAMP was injected i. p. into four U_(14) ascitic tumor bearing mice on 3,4,5,6 and 7 days after inoculation of tumor cells. The ascites was aspirated 0.5-1 hour after last injection. For scanning electron microscopy, the tumor cells, washed twice in Hanks solution, were fixed in glutaraldehyde and OsO_4, dehydrated with ethyl alcohol and dried with camphene. For flow microcytometric analysis, the treated tumor cells were fixed in 70% cold ethyl alcohol and stained with propidium iodide. Under SEM, the untreated...

dbcAMP was injected i. p. into four U_(14) ascitic tumor bearing mice on 3,4,5,6 and 7 days after inoculation of tumor cells. The ascites was aspirated 0.5-1 hour after last injection. For scanning electron microscopy, the tumor cells, washed twice in Hanks solution, were fixed in glutaraldehyde and OsO_4, dehydrated with ethyl alcohol and dried with camphene. For flow microcytometric analysis, the treated tumor cells were fixed in 70% cold ethyl alcohol and stained with propidium iodide. Under SEM, the untreated tumor cells were large, spherical, and uniform in size with numerous long thin microvilli on the cell surface. A few barely visible minute protrusions were present on the microvilli and cell membrane. The great majority of treated tumor cells became smaller and variable in size, with shortened microvilli which reduced in number and even disappeared in some area. Many granular protrusions, larger than that of the control, were clearly observed on the cell membrane and microvilli. The result of flow microcytometric analysis showed that the DNA histogram and cell cycle profile from dbcAMP treated cells have no significant difference from the untreated controls, so it is evident that morphologic changes resulted from dbcAMP were not caused by cell cycle alteration. The morphogenesis of microvilli and cell membrane changes in dbcAMP treated cells is not clear. The relation of these configurations to differentiation of malignant tumor cells is discussed.

本文根据扫描电镜观察,报告了dbcAMP引起小鼠U_(14)腹水瘤细胞微绒毛和质膜表面的细微形态变化。U_(14)腹水瘤的多数细胞体积大,大小相近,表面有许多细长微绒毛;微绒毛表面和微绒毛间细胞质膜表面,仅见很细微的点状微突。腹腔内注射dbcAMP的U_(14)腹水瘤,85%以上的细胞体积缩小,大小不等,表面微绒毛缩短且减少。在没有微绒毛的部位,细胞质膜表面有许多颗粒状微突起,较对照组明显易见。微绒毛表面也有与之大小类似的微突起,使微绒毛表面凹凸不平。流式细胞光度计分析结果表明,在本文实验条件下,dbcAMP未引起U_(14)腹水瘤细胞周期的变化,细胞膜表面和微绒毛的变化,也不单纯是细胞周期中微绒毛数量和分布的改变。因此作者认为,这些变化不是通过改变细胞周期引起的。 cAMP引起微绒毛退缩的机制不详。至于微绒毛间的颗粒状微突起是微绒毛退缩的遗迹,抑或是由cAMP引起,尚待研究。cAMP引起瘤细胞表面形态的变化,进一步证明了cAMP在小鼠体内诱导恶性细胞分化的作用。

 
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