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uridine -triphosphate utp
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  uridine -triphosphate utp
RNA synthesis was established by incorporation of [3H]-uridine5'-triphosphate (UTP) into the nuclear RNA.
      
The enzymes of the wild type and three of the four mutants exhibited positive cooperativity with the substrate uridine 5'-triphosphate (UTP).
      
The cytidine 5'-triphosphate (CTP) and deoxycytidine 5'-triphosphate (dCTP) pools in the mutants were expanded, but the uridine 5'-triphosphate (UTP) pool either decreased or remained unchanged relative to the wild-type level.
      
In the pyrimidine biosynthetic pathway, CTP synthetase catalyses the conversion of uridine 5'-triphosphate (UTP) to cytidine 5'-triphosphate (CTP).
      
The nucleotide uridine 5'-triphosphate (UTP) had similar effects on [Ca2+]i although the plateau level of the [Ca2+]i response was higher with this P2Y agonist.
      
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AIM: To study the electrophysiologic effects of uridine triphosphate (UTP) on the guinea pig papillary muscles in vitro and purinoceptors related with the action of UTP. METHODS: Intracellular microelectrode method was used to record action potentials (AP) in guinea pig papillary muscles. RESULTS: UTP, adenosine triphosphate (ATP), and adenosine diphosphate (ADP) prolonged the action potential duration (APD) concentration-dependent-ly in guinea pig papillary muscles. The potency...

AIM: To study the electrophysiologic effects of uridine triphosphate (UTP) on the guinea pig papillary muscles in vitro and purinoceptors related with the action of UTP. METHODS: Intracellular microelectrode method was used to record action potentials (AP) in guinea pig papillary muscles. RESULTS: UTP, adenosine triphosphate (ATP), and adenosine diphosphate (ADP) prolonged the action potential duration (APD) concentration-dependent-ly in guinea pig papillary muscles. The potency order was UTP = ATP > ADP. There was cross-desensitization between the response to ATP and that to UTP, and neither Ado nor α, β-MeATP caused great change in AP of (he papillary muscles. The prolongation of APD by UTP was not affected by sustained perfusion with amino-phylline. As an osmotic pressure control equivalent to UTP 3 mmol/L, ceftriaxonum 3 mmol/L or NaCl 9 mmol/L induced a marked but slight prolongation of APD. CONCLUSION: UTP produced APD prolongation through specific and nonspecific actions, and the specific response to UTP was mediated by P2Y2 purinoceptors.

目的:研究尿苷三磷酸(UTP)对豚鼠乳头状肌的电生理作用,及UIP作用的相关受体。方法:利用细胞内微电极技术记录豚鼠乳头状肌跨膜电位。结果:UTP、ATP和ADP均可浓度依赖性延长豚鼠乳头状肌动作电位时程(APD)。激动剂的效应强度序列为UTP=ATP>ADP,且UTP和ATP的作用存在交叉脱敏现象。Adenosine(Ado)和α,β-methyleneATP(α,β-MeATP)对豚鼠乳头状肌动作电位各参数均无影响,氨茶碱持续灌流亦不影响UTP的作用。与UTP 3mmol/L等渗的ceftriaxonum(3mmol/L)或NaCl(9mmol/L)可显著但轻微地延长APD。结论:UTP延长豚鼠乳头状肌APD的作用由特异性和非特异性两种作用组成,前者与P2Y_2受体有关。

Aim To study the effects of adenosine triphosphate(ATP) on the proliferation of Chinese esophageal carcinoma Eca-109 and hepatoma SMMC-7721 cells.Methods MTT assay was used to determine the inhibition of the proliferation of the two cultured tumor cell 1ines in vitro by ATP,adenosine(ADO) and uridine triphosphate(UTP).Morphological changes of the two cell lines induced by ATP were observed under light microscope.Results ATP(0.03~0.3 mmol·L~(-1)) and ADO(0.1~0.3 mmol·L~(1)) had inhibitory...

Aim To study the effects of adenosine triphosphate(ATP) on the proliferation of Chinese esophageal carcinoma Eca-109 and hepatoma SMMC-7721 cells.Methods MTT assay was used to determine the inhibition of the proliferation of the two cultured tumor cell 1ines in vitro by ATP,adenosine(ADO) and uridine triphosphate(UTP).Morphological changes of the two cell lines induced by ATP were observed under light microscope.Results ATP(0.03~0.3 mmol·L~(-1)) and ADO(0.1~0.3 mmol·L~(1)) had inhibitory effects on Eca-109 and SMMC-7721 cells concentration-dependently,and the inhibition by ATP was stronger than that by ADO in both cell lines.For Eca-109 cell line,the maximal inhibition rate of the proliferation by ATP and ADO was 86.36% and 29.88%,and the IC_(50) was 0.056 and 0.823 mmol·L~(-1),respectively.For SMMC-7721 cell line,the maximal inhibition rate of the proliferation by ATP and ADO was 82.06% and 52.84%,and the IC_(50) was 0.218 and 0.517 mmol·L~(-1),respectively.UTP had a very weak inhibitory effect on Eca-109 cell line,with the maximal inhibition rate of 18.27%,and did not significantly affect SMMC-7721 cell line.Exposed to higher concentration(0.3 mmol·L~(-1)) of ATP for 72 h,SMMC-7721 cells displayed morphological changes of apoptosis,but Eca-109 cells did not show the characteristics of apoptosis markedly.Conclusion ATP has a strong inhibitory effect on the proliferation of Eca-109 cell line,which is mainly induced by ATP per se,and a metabolite ADO also has weaker effects.For SMMC-7721 cell line,however,ATP inhibits the cell proliferation mainly via its degradation to ADO.

目的研究三磷酸腺苷(ATP)对人食管癌细胞株Eca-109和人肝癌细胞株SMMC-7721细胞增殖的影响。方法采用MTT法测定ATP、腺苷(ADO)和三磷酸尿苷(UTP)抑制肿瘤细胞增殖的作用,W rights-G iem sa染色观察细胞形态学的改变。结果ATP(0.03~0.3 mmol.L-1)和ADO(0.1~0.3 mmol.L-1)可不同程度地抑制Eca-109和SMMC-7721的增殖,ATP对两株肿瘤细胞增殖的抑制作用均强于ADO。ATP和ADO对Eca-109细胞的最大抑制率分别为86.36%和29.88%,IC50分别为0.056和0.823 mmol.L-1;对SMMC-7721细胞的最大抑制率分别为82.06%和52.84%,IC50分别为0.218和0.517 mmol.L-1。UTP对Eca-109细胞有很弱的抑制增殖作用,最大抑制率仅为18.27%;对SMMC-7721无抗增殖作用。两株细胞经高浓度(0.3 mmol.L-1)ATP处理后,部分SMMC-7721细胞形态出现了明显的凋亡特征,而Eca-109细胞凋亡特征不明显。结论ATP具有较强的抗Eca-109细胞增殖作用,其抗...

目的研究三磷酸腺苷(ATP)对人食管癌细胞株Eca-109和人肝癌细胞株SMMC-7721细胞增殖的影响。方法采用MTT法测定ATP、腺苷(ADO)和三磷酸尿苷(UTP)抑制肿瘤细胞增殖的作用,W rights-G iem sa染色观察细胞形态学的改变。结果ATP(0.03~0.3 mmol.L-1)和ADO(0.1~0.3 mmol.L-1)可不同程度地抑制Eca-109和SMMC-7721的增殖,ATP对两株肿瘤细胞增殖的抑制作用均强于ADO。ATP和ADO对Eca-109细胞的最大抑制率分别为86.36%和29.88%,IC50分别为0.056和0.823 mmol.L-1;对SMMC-7721细胞的最大抑制率分别为82.06%和52.84%,IC50分别为0.218和0.517 mmol.L-1。UTP对Eca-109细胞有很弱的抑制增殖作用,最大抑制率仅为18.27%;对SMMC-7721无抗增殖作用。两株细胞经高浓度(0.3 mmol.L-1)ATP处理后,部分SMMC-7721细胞形态出现了明显的凋亡特征,而Eca-109细胞凋亡特征不明显。结论ATP具有较强的抗Eca-109细胞增殖作用,其抗增殖作用主要由ATP自身所致,代谢产物ADO也具有一定的作用;而对于SMMC-7721细胞,ATP可能较大程度地通过降解为ADO而发挥抗增殖作用。

 
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