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methods the rats
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  方法实验
     Methods The rats were randomly divided into normal control group(N),sham operation group(SO),common bile duct ligation group(CBDL) and CBDL3d,CBDL7d and CBDL11d groups.
     方法实验大鼠分为正常对照组(Norm control,N组),假手术组(Shamoperation,SO组),胆总管结扎组(Common bile duct ligation,CBDL组)。 其中CBDL组又分为CB-DL3d、CBDL7d、CBDL11d三亚组。
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     Methods The rats were divided into the normal control group, model group and treatment group Ⅰ and Ⅱ.
     方法实验分正常对照组,模型组,治疗Ⅰ、Ⅱ组。
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     Methods The rats were divided into four groups as group A: male group, group B: OVX group, group C: female control group (false operative group), group D: OVX+E2 group.
     方法实验分为四组:A 组:雄性组,B 组:卵巢去势组(OVX 组),C组:雌性对照组(假手术组),D 组:给予17β-雌二醇的卵巢去势组(OVX+E_2组)。
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     Methods: The rats were infused with the drug doses of 20.4 g/kg,10.2 g/kg and 3.4g/kg,and observed for 3 months in the experimental group. Then the observation was kept for 2 weeks after the drug was stopped.
     方法:实验组大鼠灌服金花舒肤胶囊高、中、低剂量(分别为20.4 g/kg1、0.2 g/kg和3.4 g/kg),连续观察3个月,停药后,继续观察2周;
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     METHODS: The rats were divided into four groups:control,lipopolysaccharide(LPS),CCK-8 and CCK-8+LPS.
     方法 :实验分对照组、脂多糖 (LPS)组、CCK组及CCK +LPS组 ;
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  “methods the rats”译为未确定词的双语例句
     MATERIAL AND METHODS: The rats were induced by azo dye DAB,the mRNA expression of three isoforms(CYP2D1、CYP2D2and CYP2D4)were detected by quantitative RT-PCR,then PCR products were sequenced and analyzed.
     材料与方法:用DAB诱导大鼠形成肝癌,RT_PCR定量分析CYP2D1、CYP2D2和CYP2D4mRNA在肝脏中的表达水平,并对各PCR产物测序分析,观察是否有点突变。
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     Methods The rats were randomly divided into AD group 〔injection of 2 μl (10 μl) Aβ_(25~35)〕 and menstruum group (injection of 2 μl physiological saline).
     方法将大鼠随机分为2组:AD模型组、溶媒体组,在双侧海马分别注射2μl(10μg)Aβ25~35、2μl生理盐水;
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     METHODS: The rats in the pentobarbital group and ketamine group were subjected to 40 mg/kg pentobarbital and 60 mg/kg ketamine by abdominal anaesthesia, respectively.
     方法:戊巴比妥组和氯胺酮组大鼠分别以戊巴比妥40mg/kg,氯胺酮60mg/kg腹腔麻醉。
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     Methods the rats were given once aday for 12 weeks with the doses of 25g kg、12.5g /kg、6.25g /kg.
     方法分别以25g/kg、12.5g/kg、6.25g/kg的剂量给大鼠注射,连续给药12周,1d/次。
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     METHODS: The rats in shenxian tang 30, 15, 7.5 (g/kg·d) groups were by gavage given shenxian tang, respectively in doses 20, 10 and 5 time that for adult person per kilogram body quality, or 30, 15, 7.5 g/(kg·d).
     方法:参仙汤30,15,7.5g/(kg·d)剂量组分别按成人每公斤体质量剂量的20,10,5倍给予参仙汤灌胃,剂量分别为生药30,15,7.5g/(kg·d);
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     METHODS E.
     方法采用ipE.
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     Methods.
     方法:
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     Methods: The
     定性鉴别方法为马氏距离与限定值相比较。
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     Methods The E.
     方法 选用Westphal热酚法提纯E .
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     All rats
     ②手术对照组:给大鼠施予与实验组大鼠相同
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Objectlve To study the influence of hypoxia/reoxygenation on the production and release of nitric oxide (NO) , lactate dehydrogenase CLDH) and creatine kinase (CPK ) from cultured newborn rat car- diomyocytes. Methods The rats were divided into four groups : control , hypoxia/reoxy-genation , heat shock pretreated , dexamethasone pretreated. Results After 3 hours of hypoxia and 30 minutes of re- oxygenation , the content of NO in the supernatent of cardiomyocytes increased significantly ( P < 0....

Objectlve To study the influence of hypoxia/reoxygenation on the production and release of nitric oxide (NO) , lactate dehydrogenase CLDH) and creatine kinase (CPK ) from cultured newborn rat car- diomyocytes. Methods The rats were divided into four groups : control , hypoxia/reoxy-genation , heat shock pretreated , dexamethasone pretreated. Results After 3 hours of hypoxia and 30 minutes of re- oxygenation , the content of NO in the supernatent of cardiomyocytes increased significantly ( P < 0. 05) , which was accompanied by an increase in the release of LDH and CPK (P<0. 001 , P<0. 001 respectively ). When pretreated by the heat shock (expcaed to 42 ℃ for 1 hour and then allowed to re- cover for 24 hours) or by applying dexamethasone at the onset of hypoxia , the production and release of NO , LDH , CPK decreased markedly (P< 0. 05 ) . Conclusions Exceasive release of NO may play an important role in the reperfusion injury of cardiomyocytes. Heat shock seems to provide protection for cardiomyacytes from hypoxia /reoxygenation injury. The mechanism may be related to the inhibition of excessive release of No from the cardiomyocytes,

目的 探讨热休克预处理对心肌细胞保护作用的机理。方法作者在培养的新生大鼠心肌细胞的模型上,观察缺氧、复氧对培养心肌细胞产生和释放一氧化氮(NO)、乳酸脱氢酶(LDH)和磷酸肌酸激酶(CPK)的影响。实验共分为4组:1.对照组;2.损伤组(加无糖无氧Hank's液,充入氮气以置换瓶内空气);3.热休克处理组(细胞培养瓶放入42℃水浴箱中孵育1小时);4.地塞米松组(在无氧Hank's液中加入地塞米松)。结果培养心肌细胞缺氧3小时、复氧30分钟后NO的产生显著增加,CPK、LDH的释放也显著升高。热休克(细胞在42℃水浴1小时,恢复24小时)或地塞米松(10mol/L)预处理可显著减少心肌细胞NO、LDH和CPK的产生和释放。结论提示心肌细胞在缺氧、复氧过程中产生的大量NO对培养心肌细胞是有毒的。热休克预处理对缺氧、复氧损伤的培养心肌细胞的保护作用与抑制过量NO的产生有关。

Objectives: To study the gonadotoxicity of high energy shock wave in male. Design: Experimental study in rat. Setting: Laboratory in Department of Urology, Guangxi Medical University. Methods: The rat testes were exposed to high energy shock wave at 19kV and 1 000 impacts with frequency rate of 1/sec. The treated animals and controls were killed at the same day of impact given and in 1,2,4,8 and 16 days after treatment. Morphologic and functional examination of changes in the testes of controls...

Objectives: To study the gonadotoxicity of high energy shock wave in male. Design: Experimental study in rat. Setting: Laboratory in Department of Urology, Guangxi Medical University. Methods: The rat testes were exposed to high energy shock wave at 19kV and 1 000 impacts with frequency rate of 1/sec. The treated animals and controls were killed at the same day of impact given and in 1,2,4,8 and 16 days after treatment. Morphologic and functional examination of changes in the testes of controls and treated rats. Results: Angiectasis and congestion and focal hemorrhage in the testicular tissue, as well as mitochondrial swell, reduction or disappearance of mitochondrial cristae and degranulation of rough endoplasmic reticulum in spermatocytes were found within three weeks after treatment. There was no statistically significant difference in the pregnancy rate or fetus numbers and weight in female rats mated with treated male rats compared with the control group after three weeks'gestation. FSH, progesterone and testosterone in serum were not change significantly. Conclusions: The rat testes appear to be functionally resistant to the shock wave energy levels used in this experiment, although there were temporary inflammatory reaction and histologic changes in testicular tissue.

用JDPN-IV型体外震波碎石机直接冲击Wistar大鼠的睾丸,观察高能震波对雄性动物的生殖毒性作用。结果发现,单次高能震波冲击Wistar大鼠睾丸3周内,睾丸组织出现炎性损伤性改变,包括毛细血管充血及瘀血(58%)、局部出血(42%)、精母细胞线粒体浊肿、嵴减少或消失(42%),粗面内质网颗粒减少或脱颗粒(33%)。但是,受高能震波冲击睾丸的雄性Wistar大鼠与同龄母鼠配对同笼饲养后,其配对母鼠的受孕率、平均胚胎数、平均胎重与对照组比较无显著性差异,血清睾酮、孕酮及卵泡刺激素水平也无显著性改变。本研究结果表明,单次高能震波冲击大鼠睾丸会造成睾丸组织的炎性损伤性改变,但并不造成雄鼠生育能力的明显下降。

Purposes: To examine the effects of Ca2+ and ketamine on Ca2+/CaM PK Ⅱ activity under a condition of hypoxic state in vitro. Methods: The rat hippocampal slice was developed as a model for investigating the above effects. Results: (1) Ca2+/CaM PK Ⅱ activity decreased gradually with increasing hypoxic time in culture medium with or without Ca2+ (1.3 mmol/L), with the decrease much more pronounced in the former case. (2) The inhibition of the enzyme activity induced by either hypoxia could be antagonized...

Purposes: To examine the effects of Ca2+ and ketamine on Ca2+/CaM PK Ⅱ activity under a condition of hypoxic state in vitro. Methods: The rat hippocampal slice was developed as a model for investigating the above effects. Results: (1) Ca2+/CaM PK Ⅱ activity decreased gradually with increasing hypoxic time in culture medium with or without Ca2+ (1.3 mmol/L), with the decrease much more pronounced in the former case. (2) The inhibition of the enzyme activity induced by either hypoxia could be antagonized markedly by pretreatment with ketamine, showing that the hypoxia-induced inhibition of enzyme activity is mediated by NMDA receptor. Conclution: The brain hypoxia-induced inhibition of the enzyme activity is mediated by the following pathway: NMDA receptor→Ca2+→Ca2+ target enzyme.

目的研究Ca2+和氯胺酮对海马脑片Ca2+/CaMPKⅡ活性的影响。方法采用大鼠海马脑片体外缺氢模型进行实验,结果(1)有钙或无钙培养时,酶活性随缺氧时间的延长均下降,但前者比后者酶活性下降更显著,提示外Ca2+在神经元缺氧损伤中起重要作用;(2)氯胺酮对缺氧所诱导的酶活性抑制均有明显的拮抗作用,说明脑缺氧引起酶活性下降与NMDA受体介导有关。结论脑缺氧时该酶活性的抑制与下列通路有关:NMDA受体→Ca2+→Ca2+靶酶。

 
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