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While the TCR engagement with specific antigen, the administration of CTLA-4Ig can induce T cell anergy in vitro or tolerance in vivo.

在TCR识别外来抗原的同时给予可溶性CTLA-4,在体外可诱导T细胞无应答,在体内则可诱导特异性免疫耐受。

The apical buds and axillary buds of Dracaena cambodiana Pierre ex Gagnep. were inoculated on MS medium containing 1 mg/L BA, 0.1 mg/L NAA, 100 mg/L PVP and 30 g/L sucrose for inducing shoots. After cultured for 40~50 d, the shoots bourgeoned. They were then transferred onto MS medium supplemented with 2 mg/L BA, 0.5 mg/L KT and 30 g/L sucrose for inducing clustered buds. After 25~10 d, the clustered buds formed. The proliferation rate of the clustered buds was 300%~500% per month.

以海南龙血树的顶芽和侧芽作为外植体,把其接种于MS+BA 1 mg/L+NAA0.1 mg/L+PVP100 mg/L+蔗糖30 g/L培养基上培养40~50 d可诱导其腋芽萌发,再把萌发后所形成的新芽切割下来接种于MS+BA 2mg/L+KT 0.5 mg/L+蔗糖30 g/L的培养基上培养25~30 d可诱导形成丛生芽,丛生芽在继代培养过程中每25~30 d可增殖3~5倍。

RESULTS:(1)NO production and iNOS mRNA expression induced by LPS and TNF α was blocked by pyrrolidine dithiocarbamate or N-acetylcysteine.(2)LPS and TNF α triggered the activation and translocation of NF κ B, and PDTC or NAC inhibited the activation of NF κ B induced by LPS and TNF α.

结果:抗氧化剂可阻断内皮细胞培养体系LPS和TNFα诱导的NO生成及iNOS mRNA的表达;LPS和TNFα可诱导大鼠肺微血管内皮细胞NFκB的激活并可被抗氧化剂阻断。

Results showed that green firm callus and rooting were obtained with treatments of NAA 0.5-3.0mg/L, in which the NAA 0.5mg/L treatment appeared the optimal rooting result of 90%. White loose callus was obtained with treatment of 2,4-D0.1-3.0 mg/L.Callus can not be induced by adding BA solely at 0.5-3.0mg/L. There appeared bud redifferentiation only when appropriate concentration of combined BA,NAA and 2,4-D were applied.

结果表明:单独加入NAA0.5~3.0mg/L可诱导出绿色致密的愈伤组织,并再生出根,其中NAA0.5mg/L处理生根率最高,达90%;单独加入2,4-D0.1-3.0mg/L可诱导出白色疏松的愈伤组织;单独使用BA0.5—3.0mg/L不能诱导出愈伤组织;BA与NAA或2,4-D只有在适当的质量浓度范围内配合使用才能分化出芽,芽分化率最高的处理为BA3.0mg/L+NAA0.5mg/L,分化率为30%。

Results The levels of HSP 70 mRNA and HSP 70 protein expression were significantly different among the 5 groups. Ketamine induced marked HSP 70 mRNA and HSP 70 protein expression in the posterior cingulated cortex. Propofol itself did not induce HSP 70 gene expression in this brain region. Propofol significantly inhibited ketamine-induced HSP 70 mRNA and HSP 70 protein expression in the posterior cingulate cortex in a dose-dependent manner.

结果氯胺酮可明显诱导HSP70 mRNA与HSP70蛋白在大鼠后扣带回皮质区的表达;异丙酚自身不能诱导HSP70基因的表达;预先给予异丙酚可显著抑制氯胺酮诱导的HSP70 mRNA和HSP70蛋白在这一区域的表达,且抑制效应呈剂量依赖性。

In fundic strips, ghrelin and GHRP-6 could decrease the on-response induced relaxation and increase off-response induced contraction of the muscle, with the effect of Ghrelin obviously stronger than that of GHRP-6.L-NNA could increase the effects of Ghrelin and GHRP-6-induced muscle contraction, and L-AA could decrease their effects.

在胃底部,Ghrelin和GHRP-6可使开电刺激诱导的平滑肌舒张活动减弱,断电刺激诱导的肌条收缩活动增强,且Ghrelin作用明显强于GHRP-6.L-NNA可显著增强Ghrelin和GHRP-6的促平滑肌收缩效应,但L-AA可显著减弱该作用。

No callus could be induced from leaf or petiole explants of varieties F30 and Ⅱ cultured on MS medium if supplemented alone with 6-bezyladenine (6-BA) or thidiazuron, or kinetin. However, the calli were induced on MS medium containing 2.0 mg L-1 6-BA and 0.5 mg L-1 NAA (α-naphthaleneacetic acid), and the calli derived from petioles of variety Ⅱ could produce redifferentiated shoots, but of variety F30 could not. The later could only produce shoots directly from the base of the petioles.

将品种F30和Ⅱ的叶片和带叶叶柄接种到含不同浓度单一细胞分裂素(6-BA、TDZ、KT)的MS培养基上培养,均未能诱导出愈伤组织,而在含2.0mgL-1 6-BA+0.5mgL-1 NAA的培养基上可以诱导出愈伤组织,且由品种Ⅱ叶柄诱导产生的愈伤组织可再分化出芽,品种F30诱导的愈伤组织却不能分化,但在其叶柄基部可直接出芽。

Based on these results and inferred to related reports from other labratories, it was possible to make some analyses and conclusions or inferrences:(1) CD〓AK with tumoricidal activity were induced and expanded in number througth costimulation of PBMC with anti-CD〓 McAb . and r IL-2 ;(2) CD〓AK induced and expanded in such manner did exibit more potent proliferation·ability and cytotoxicity which maintained for lonser time than those of LAK cells, thus CD〓AK was a new variety of antitumor effector cells worth to be explored;(3) CD〓AK could mediate MHC nonrestricted cytotoxicity and kill tumor target cells through inducing necrosis and apoptosis;(4) Normal mature lymphocytes of PBMC could be induced to proliferate and /or to die from apoptosis when they were costimulated by anti-CD〓McAb and rIL-2. Both proliferation and apoptosis were existing in the same cultivation system sugsesting that the presence of rIL- 2 might provide some accessary signals for apoptosis.

以这些结果为基础并参考其它有关文献可能做出如下分析与结论或推论:(1)用抗CD〓单抗和rIL-2共刺激外周血单个核细胞能诱生扩增出具有杀瘤活性的CD〓AK细胞,(2)与LAK相比,用这种方法诱生扩增的CD〓AK增殖能力强、细胞毒活性强而且维持时间长;CD〓AK是一类值得开发的抗瘤效应细胞;(3)CD〓AK能够介导MHC非限制性细胞毒活性,可以通过诱导靶细胞坏死和/或凋亡杀伤肿瘤细胞;(4)正常外周血单个核细胞中的成熟淋巴细胞在受到抗CD〓单抗和rIL-2共同刺激后既可诱导增殖也可诱导凋亡,两者并存于同一体系,推测rIL-2的存在可能为细胞凋亡提供一些辅助信号。

With the inducing time prolonged, the amount of fusion protein increased, and the highest content amounted to 39. 14% of total protein. Different temperature (15℃, 25℃ and 37℃) could induce expression of fusion protein, and the higher inducing temperature was, the more total fusion protein and soluble fusion protein was produced. Most fusion protein was expressed in the cytoplasm and was soluble, a little of fusion protein was expressed in periplasm or expressed as inclusion bodies, and no fusion protein was found in culture. Furthermore, the results of in vitro enzymatic reaction suggested that the fusion protein could catalyze the methylation of theobromine.

随着诱导时间的延长,表达的融合蛋白产量逐渐增加,表达蛋白总量最高可达到菌体总蛋白的39.14%;在15℃、25℃和37℃三个不同的诱导温度下,均能诱导产生融合蛋白,而且产生的融合蛋白的总量及其可溶性部分所占比例均随诱导温度升高而增加;在菌体的各个部位中,融合蛋白主要在细胞质中以可溶的形式进行表达,有少量在外周质中表达或以包含体形式在细胞质中表达。

RESULTS ① TLSFJM could induce apoptosis of PHA plus IL-2-activated mouse thymo cytes;② TLSFJM could induce apoptosis of alloantigen activated human pe ripheral blood mononuclear cells and hold the cell cycle at G1 phase;③ TLSFJM neither influenced the CD25 expression nor induced apoptosis of PMA activated human PBMC .

结果 TLSFJM 在体外可诱导PHA/IL-2活化的小鼠胸腺细胞的凋亡。 TLSFJM 在体外可诱导alloantigen活化的人外周血单个核细胞的凋亡,且把细胞周期阻遏在G1期。 TLSFJM 对PMA诱导的人PBMC活化抗原CD25的表达无明显影响,也不引起凋亡。

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