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cytidine -triphosphate
相关语句
  三磷酸胞苷
     The Process Research for Cytidine 5'-Triphosphate Separation and Purification by Ion Exchange Resin
     离子交换法分离纯化5’-三磷酸胞苷的研究
短句来源
  相似匹配句对
     Purification of Cytidine Triphosphate
     胞苷三磷酸的分离纯化
短句来源
     (5) C.
     ( 5 )短脚锦鸡儿C .
短句来源
     (5).
     6ml及玻璃体腔内填充0.5~3m!
短句来源
     Photophosphorylation preparation of cytidine triphosphate
     胞嘧啶核苷三磷酸的光合合成
短句来源
     The Process Research for Cytidine 5'-Triphosphate Separation and Purification by Ion Exchange Resin
     离子交换法分离纯化5’-三磷酸胞苷的研究
短句来源
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  cytidine -triphosphate
The kinetics and cytidine 5'-triphosphate (CTP) feedback inhibition of CTP synthetase in wild-type and four mutants of Chinese hamster V79 cells have been studied.
      
The kinetics and feedback inhibition of cytidine 5'-triphosphate synthetase in wild-type and mutant Chinese hamster cells
      
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.
      
Pleiotropic mutants of Chinese hamster cells with altered cytidine 5'-triphosphate synthetase
      
cepacia cytidine 5'-triphosphate (CTP) inhibited the activity of aspartate transcarbamylase.
      
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In order to study the effect of argipressin(4—8)(AVP 4—8 ) on the mRNA level and activity of cytidine triphosphate: phosphocholine cytidylyltransferase(CCT) in rat hippocampal neurons, and elucidate its possible mechanism. Rat hippocampal neurons treated with AVP 4—8 or actinomycin D were incubated with different time periods. The mRNA level of CCT was detected using RT PCR plus Southern blot, CCT activity was determined by measuring the rate of incorporation of [ 14 C] phosphocholine...

In order to study the effect of argipressin(4—8)(AVP 4—8 ) on the mRNA level and activity of cytidine triphosphate: phosphocholine cytidylyltransferase(CCT) in rat hippocampal neurons, and elucidate its possible mechanism. Rat hippocampal neurons treated with AVP 4—8 or actinomycin D were incubated with different time periods. The mRNA level of CCT was detected using RT PCR plus Southern blot, CCT activity was determined by measuring the rate of incorporation of [ 14 C] phosphocholine into cytidine diphosphate choline(CDP choline). It was found that AVP 4—8 could upregulate the CCT mRNA in rat hippocampal neurons. ZDC(C)PR, the antagonist of AVP 4—8 , could greatly inhibit this upregulation. Using actinomycin D to inhibite the eucaryotic transcription, it was found that the halflife of CCT mRNA could be prolonged by coincubation with AVP 4—8 . Meanwhile, AVP 4—8 could also increase CCT activity in rat hippocampal neurons. These results demonstrated that AVP 4—8 upregulated CCT mRNA level and its activity through stabilizing the CCT mRNA in rat hippocampal neurons.

为了研究精氨酸加压素C端片断 4~ 8(AVP4~ 8)对大鼠海马神经元中胞苷三磷酸 :磷酸胆碱胞苷转移酶 (CCT)的mRNA水平和酶活性的影响及其作用机制。将大鼠海马神经元用不同药物处理一定时间后 ,用RT PCR结合Southern杂交的方法测定CCT的mRNA水平 ,用测定胞苷二磷酸胆碱中 [14 C]的参入率来确定CCT活性。结果表明 :AVP4~ 8能上调海马神经元内CCT的mRNA水平 ,AVP4~ 8的拮抗剂ZDC(C)PR对此有抑制作用 ,当用放线菌素D中止基因转录 ,发现用AVP4~ 8共处理的细胞 ,比单独用放线菌素D处理的细胞 ,其CCTmRNA的半衰期较长 ;AVP4~ 8处理后 ,神经元内CCT的酶活性也有一定程度的上升。由此得出结论 :AVP4~ 8通过提高神经元内CCTmRNA的稳定性 ,提高了CCTmRNA的水平 ,进而影响了胞内CCT的酶活性。

Objective: To compare the efficacy and safety of disodium cytidine triphosphate and cerebrolysin in treatment of acute cerebral vascular disease. Method: Patients with acute cerebral vascular disease were divided into two groups, which were given disodium cytidine triphosphate and cerebrolysin, respectively. Results: The effective rate was 74. 2% in cytridini triphosphatis group and 50.9% in disodium cytidine triphosphate. The incidence rates of side effect of both groups...

Objective: To compare the efficacy and safety of disodium cytidine triphosphate and cerebrolysin in treatment of acute cerebral vascular disease. Method: Patients with acute cerebral vascular disease were divided into two groups, which were given disodium cytidine triphosphate and cerebrolysin, respectively. Results: The effective rate was 74. 2% in cytridini triphosphatis group and 50.9% in disodium cytidine triphosphate. The incidence rates of side effect of both groups were 13.3% and 19.0%, respectively. There was a significant difference between groups. Conclusion: Disodum cytidine triphosphate is safe and effective in treatment of acute cerebral vascular disease.

目的:评价三磷酸胞苷二钠的安全性和有效性,并与脑活素比较。方法:236例急性脑血管疾病患者随机分成两组,使用三磷酸胞苷二钠和脑活素进行治疗。结果:治疗组和对照组有效率分别为74.2%和50.9%,两者有显著性差异。不良反应率分别为13.3%和19.0%。结论:三磷酸胞苷二钠是治疗急性脑血管病安全有效的药物。

Objective This is a study on the level of molecular biology to clarify the possible mechanism of delayed neural death after traumatic brain injury(TBI) and to probe into the influences of motor function of cytidine triphosphate(CTP) on rats after brain trauma. Method The model of severe closed traumatic brain injury (TBI) was established according to the method created by Marmarou in 1994. 300 Wistar rats were divided randomly into TBI group (n=96), CTP treating group and sham operation group,...

Objective This is a study on the level of molecular biology to clarify the possible mechanism of delayed neural death after traumatic brain injury(TBI) and to probe into the influences of motor function of cytidine triphosphate(CTP) on rats after brain trauma. Method The model of severe closed traumatic brain injury (TBI) was established according to the method created by Marmarou in 1994. 300 Wistar rats were divided randomly into TBI group (n=96), CTP treating group and sham operation group, and each of these three groups was divided into 8 subgroups, namely, 3, 6, 12, 24, 48, 72, 168 and 336 hours. At the same time, the rest 12 rats were taken as the normal group for comparison. The CTP treating group after injury were treated with injection of CTP (30mg/(kg·d)) in peritoneum; the TBI group, the sham operation group and the normal group were treated with normal saline for comparison at the same time and all were killed at each time point. Another 48 rats were divided randomly into 4 groups, namely, brain injury group, CTP treating group, sham operation group and the normal group, and their motor dysfuction was evaluated using Neurological Severity Score (NSS). The methods such as immunohistochemistry, TUNEL and NSS were used to dynamically observe the pathological changes in cortex of rats,the expression of P53 protein and the motor function after TBI. Results The increased expression of P53 protein and neural apoptosis showed up in cortex and motor dysfunction occurred after TBI. Conclusion The increased expression of P53 protein may bring about nerve cell apoptosis after TBI. Motor dysfunction is the inevitable outcome of nerve cell apoptosis in cortex. CTP can reduce P53 protein expression and nerve cell apoptosis, and it can improve motor function.

目的 在分子生物学水平进一步研究颅脑创伤后神经细胞延迟性死亡的机制 ,并探讨美洛宁对大鼠脑创伤后运动功能障碍的影响。方法 采用 Marm arou的方法建立大鼠重型闭合性颅脑创伤模型。将 Wistar大鼠3 0 0只随机分为脑创伤组、美洛宁治疗组、假手术组 ,每组又分别再分为伤后 3、6、12、2 4、48、72、168及 3 3 6h等 8个时相组 ,每时相组各 12只 ,剩余 12只作为正常对照组。美洛宁治疗组经致伤后 ,给予腹腔注射美洛宁〔3 0 m g/ ( kg·d)〕,直至各时相点处死 ;脑创伤组、假手术组及正常对照组在相同时间给予等量的生理盐水腹腔注射作为对照。另取 48只大鼠随机分为脑创伤组、美洛宁治疗组、假手术组及正常对照组 ,进行神经损伤严重性评分 ( NSS)测试。采用免疫组织化学、原位细胞凋亡检测及 NSS测试等方法 ,动态观察大鼠颅脑创伤后顶叶皮质的组织病理改变 ,P5 3蛋白的表达情况以及运动功能的改变。结果 脑创伤后顶叶皮质出现 P5 3蛋白表达增加并出现神经细胞凋亡及运动功能障碍。美洛宁治疗组伤后皮质神经细胞 P5 3蛋白表达高峰较创伤组明显下调 ,凋亡阳性细胞密度亦较创伤组有...

目的 在分子生物学水平进一步研究颅脑创伤后神经细胞延迟性死亡的机制 ,并探讨美洛宁对大鼠脑创伤后运动功能障碍的影响。方法 采用 Marm arou的方法建立大鼠重型闭合性颅脑创伤模型。将 Wistar大鼠3 0 0只随机分为脑创伤组、美洛宁治疗组、假手术组 ,每组又分别再分为伤后 3、6、12、2 4、48、72、168及 3 3 6h等 8个时相组 ,每时相组各 12只 ,剩余 12只作为正常对照组。美洛宁治疗组经致伤后 ,给予腹腔注射美洛宁〔3 0 m g/ ( kg·d)〕,直至各时相点处死 ;脑创伤组、假手术组及正常对照组在相同时间给予等量的生理盐水腹腔注射作为对照。另取 48只大鼠随机分为脑创伤组、美洛宁治疗组、假手术组及正常对照组 ,进行神经损伤严重性评分 ( NSS)测试。采用免疫组织化学、原位细胞凋亡检测及 NSS测试等方法 ,动态观察大鼠颅脑创伤后顶叶皮质的组织病理改变 ,P5 3蛋白的表达情况以及运动功能的改变。结果 脑创伤后顶叶皮质出现 P5 3蛋白表达增加并出现神经细胞凋亡及运动功能障碍。美洛宁治疗组伤后皮质神经细胞 P5 3蛋白表达高峰较创伤组明显下调 ,凋亡阳性细胞密度亦较创伤组有所下调 ,运动功能改善。结论 脑创伤后 P5 3蛋白表达增加可造成伤后神经细胞凋亡 ,伤后运动功能障碍是皮质神经细胞凋亡的必

 
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