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毒素作用
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  detoxifying function
     Clinical Study on Detoxifying Function of “Renal Failure Granules”in Uremia
     肾衰冲剂对尿毒症毒素作用的临床研究
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  “毒素作用”译为未确定词的双语例句
     After incubated with DT389-IL13 for 48 h, there were 38% (1 × 10-9 mol/L) or 99% (1 × 10-8 mol/L) U251 cells undergoing apoptotic changes, while 3.63% apoptotic cells in control.
     结果 3种检测结果均表明,嵌合毒素DT389-IL13可诱导U251胶质瘤细胞发生凋亡,1×10-9mol/L嵌合毒素作用72 h后亚二倍体细胞百分比为38%,1×10-8mol/L.
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     Compared with Dsg3EC_(1-2), Dsg3EC_(1-2)PE40 markedly inhibited the metabolism and proliferation of T cells from PV patients (P<0.01).
     在重组嵌合毒素作用下,T细胞的增殖、代谢较重组Dsg3EC_(1-2)明显降低,两者间差异有统计学意义(P<0.01)。
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     Result There was no difference between 1.25 nmol/ml FB1 group and blank control group in apoptosis rate. The concentration of 2.5-40 nmol/ml FB1 groups could induce obvious apoptosis and the apoptosis rate increased with the raise of FB1 concentration but 15 nmol/ml FB1 reached the peak.
     结果在1.25nmol/ml的富马毒素作用下凋亡率与空白没有差异,在2.5~40nmol/mlFB1的浓度范围内出现了明显的凋亡,随着富马毒素浓度的增加,体外培养的肝细胞凋亡率增加,且凋亡率在15nmol/ml达到高峰。
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     A typical sub diploid apoptosis peak was demonstrated in lymphocytes treated with DON and AFG 1. A significant dose effect response and time effect correlation could be found between apoptosis rates and mycotoxin concentrations (DON:50~2000 μg/L and AFG 1:3 12~2000 μg/L) and the treated time (DON:2~72 hours and AFG 1:2~24 hours).
     流式细胞术(FCM)检测结果显示,DON、AFG1处理组淋巴细胞出现了典型的亚二倍体凋亡细胞峰,凋亡百分率与毒素作用时间(DON:2~72小时;AFG1:2~24小时)及剂量(DON:50~2000μg/L;AFG1:3.12~2000μg/L)呈正相关关系。
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     A study on The Physiological Mechanism of The Effect of Fusarium solani Toxin on The Soybean Root
     Fusarium solani毒素作用于大豆根部生理机制的研究
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  相似匹配句对
     Mechanisms of the Action of Plant Phototo-xins.
     植物光毒素作用机理
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     Role of phytotoxin in causing plant disease
     病原菌毒素对植物的致病作用
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     Affect of Role Intrusion Detection System
     入侵检测系统的作用
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     Lectins and Toxins
     凝集素和毒素
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     The Function of Capital
     资本金的作用
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  detoxifying function
The liver's detoxifying function has been preserved.
      
Concerning the in vivo function of the enzyme, new findings on the physiological role of D-amino acid oxidase point to a detoxifying function of the enzyme in metabolizing exogenous D-amino acids in animals.
      
Our own results and a literature review led us to reconsider the detoxifying function of MTs in living organisms.
      
This paper deals with the effect of dysentery intoxication on one detoxifying function of the liver-urea formation-in rats.
      
Glutathione-S-transferase activity also decreased, which attests to impaired detoxifying function of the placenta.
      
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The recovery effects of 4-aminopyridine,guanidine,tetraethylammonium andamphotericin B on the neuromuscular transmission blocked by type A botulinumtoxin were investigated at the isolated phrenic diaphragm preparation of rat.Itwas found that the spike of motor nerve terminal abolished by botulinum toxinreappeared after application of 4-aminopyridine(2.5×10~(-6))or guanidine(3 mM)to the bathing medium.The amplitude of the spike as well as that of the endplate potential restored progressively.Consequently,the...

The recovery effects of 4-aminopyridine,guanidine,tetraethylammonium andamphotericin B on the neuromuscular transmission blocked by type A botulinumtoxin were investigated at the isolated phrenic diaphragm preparation of rat.Itwas found that the spike of motor nerve terminal abolished by botulinum toxinreappeared after application of 4-aminopyridine(2.5×10~(-6))or guanidine(3 mM)to the bathing medium.The amplitude of the spike as well as that of the endplate potential restored progressively.Consequently,the contraction of nerve-muscle preparation to indirect stimulus also reappeared.The effect of tetraethylam-monium(3 mM)was similar to that of 4-aminopyridine and guanidine but not sopotent as the latters.Amphotericin B(1×10~(-5)),in the presence of 6 mM of Ca~(++),could increase the mean quantum content of the end plate potential but could notrestore the spike of the nerve terminal abolished by botulinum toxin.

A型肉毒杆菌毒素中毒大白鼠的膈神经膈肌标本,随着毒素作用的发展,细胞外记录的神经末梢动作电位与终板电位的平均振幅逐渐下降,直至完全消失,神经冲动不再能到达神经末梢。4-氨基吡啶、盐酸胍可恢复运动神经末梢传导冲动的能力,增加终板电位的量子含量,解除肉毒素产生的传递阻遏,恢复肌肉对间接刺激的收缩反应,而二性霉素对末梢电活动已消失的接头则无恢复作用。在上述资料基础上,对内毒素的作用机制和4-氨基吡啶等的抗肉毒效应进行了讨论。

The postsynaptic response was recorded from the sixth abdominal ganglion of the cockroach Periplaneata futiginosa with the sucrose-gap technique and the actions of thio-cyclam hydrogen oxalate and a-bungarotoxin (a-bgt) were studied. The results are summarized as follows.1. The excitatory postsynaptic potential (EPSP) was considerably suppressed by thiocyclam hydrogen oxalate at concentrations above 1×10-5M which seemed to be the threshold concentration for the suppressive action when applied on the presynaptic...

The postsynaptic response was recorded from the sixth abdominal ganglion of the cockroach Periplaneata futiginosa with the sucrose-gap technique and the actions of thio-cyclam hydrogen oxalate and a-bungarotoxin (a-bgt) were studied. The results are summarized as follows.1. The excitatory postsynaptic potential (EPSP) was considerably suppressed by thiocyclam hydrogen oxalate at concentrations above 1×10-5M which seemed to be the threshold concentration for the suppressive action when applied on the presynaptic (cercal) nerve.2. When a-bgt was applied to the sixth abdominal ganglion, the EPSP was progressively reduced in amplitude, due to the occupation of acetylcholine receptor by a-bgt. The axon conduction and resting potentials were not affected by thiocyclam hydrogen oxalate or a-bgt. Thus it appears that these two drugs are similar in their mode of action.3. It was seen that thiocyclam hydrogen oxalate frequently induced the bursts of the spontaneous EPSP. The amplitude and frequency of the discharges gradually increased to form spikes and finally the discharges were suppressed.

用电生理糖间隙法研究杀虫环对黑胸大蠊神经突触传递的作用,并以α-银环蛇毒素作比较。结果证明:1)杀虫环阈浓度1×10~(-5)M即显著地抑制兴奋性突触后电位(EPSP)。作用开始使之阈值递增,此时只有增加刺激强度方可诱出EPSP。2)(虫非)蠊第Ⅵ腹神经节是胆碱能的。已知突触后阻遏剂如α-银环蛇毒素的作用是N型乙酰胆碱受体(n-AchR)的专一性配基,与杀虫环阻遏神经突触的传递颇为相似,二者均不影响突触后神经元的静息电位和动作电位的传导;而杀虫环对非胆磁能的神经肌肉接头则无影响。3)自发突触后电位随杀虫环处理时间的不同而变化。开始自发释放电位的振幅、频率逐渐增加,继之产生持续期较长的阵发性高频发放,以后又逐渐消失。

THe effect of membrane toxin-c (MT-C) on Ca++ -binding and transport in rat liver mitochondria has been studied.The Ca++-binding capacity to the rat liver mitochondria is lowered to an extent of 50% at a concentration of 7. 14 nmole MT-C/ mg mitochondrial protein. Linear relationship has been observed on Scatchard plots of Ca++-binding in the presence of MT-C (Kd: 48.2 uM; number of Ca++-binding sites. 341 nmol/ nag mho.), i. e., MT-C inhibited the high-affinity Ca++-binding sites, but did not interfere with...

THe effect of membrane toxin-c (MT-C) on Ca++ -binding and transport in rat liver mitochondria has been studied.The Ca++-binding capacity to the rat liver mitochondria is lowered to an extent of 50% at a concentration of 7. 14 nmole MT-C/ mg mitochondrial protein. Linear relationship has been observed on Scatchard plots of Ca++-binding in the presence of MT-C (Kd: 48.2 uM; number of Ca++-binding sites. 341 nmol/ nag mho.), i. e., MT-C inhibited the high-affinity Ca++-binding sites, but did not interfere with the low-affinity Ca++-binding sites. Our result suggest that the site of action of MT-C on rat liver mitochondria can be mainly ascribed to the high affinity site of Ca++-binding on the inner membrane.

本文探讨膜毒素对鼠肝线粒体Ca~(++)传递和Ca~(++)结合亲和力的影响。当膜毒素的浓度为7.14毫微克分子/毫克线粒体蛋白时,处理过的线粒体传递Ca~(++)能力下降至原来一半左右。本实验做Ca~(++)结合膜毒素处理线粒体的Scatchard图呈直线(K_d=48.2μM,结合Ca~(++)数目N=341毫微克分子/毫克线粒体蛋白)。就是说,膜毒素抑制线粒体高亲和力Ca~(++)结合部位,而不影响低亲和力Ca~(++)结合部位。我们认为膜毒素作用位点在于线粒体高亲和力Ca~(++)结合部位。

 
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