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model of diabetic
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  糖尿病模型
     The model of diabetic rat: 2%STZ injection into abdomen by 60mg/kg, blood suger is higher than 16. 7mmol/L ,feed for 6 weeks, becomes the model of chronic diabetic rats. Induction of focal cerebral infarction with an filament.
     糖尿病模型的制作,用2%STZ按60mg/kg体重腹腔注射,血糖达到16.7mmol/L以上为成功,饲养6周,可以作为慢性糖尿病大鼠模型。
短句来源
     Methods The model of diabetic SD rat was established.
     方法建立SD大鼠糖尿病模型
短句来源
     Methods Rat model of diabetic mellitus was established by interperitoneal injection of streptozotocin (50 mg/kg) . Renal damages and changes of endothelin (ET) in urine and renal tissues were observed at 12 weeks after the induction of diabetic mellitus and after treatment with rhein (70 mg/kg).
     方法 采用链脲佐菌素 (STZ)诱导大鼠糖尿病模型 ,观察 12周时肾脏损害和尿、肾脏组织内皮素 (ET)的变化 ,以及经大黄酸 ( 70mg/kg)治疗后的变化。
短句来源
     Methods:The model of diabetic rats induced by alloxan was used. Diabetic rats were fed by silkworm cocoon with low(3.75g dry weight/kg/d)and high(18.75g dry weight/kg/d)dosages for30days.
     方法 :采用四氧嘧啶诱发SD大鼠糖尿病模型 ,蚕茧以18 75g干重/(kg·d)和3 75g干重/(kg·d)灌胃糖尿病模型大鼠30d。
短句来源
     To construct the experimental animal model by receiving an intraperitoneal injection streptozotocin (STZ) When the blood sugar of the rats was higher than 16.7mmol/L and kept at least 5 days, the animal model of diabetic rat should have been established.
     通过腹腔注射链尿佐菌素(streptozotocin,STZ)复制大鼠糖尿病模型。 当大鼠血糖值大于16.7mmol/L并持续至少5天,表明糖尿病动物模型己建立。
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  “model of diabetic”译为未确定词的双语例句
     Expression Level of Cubilin in the Rat Model of Diabetic Nephropathy
     Cubilin在糖尿病肾病大鼠模型的表达变化
短句来源
     Method: The rats model of diabetic mellitus (DM) was produced by intraperitoneal injection of 50 mg·kg-1 streptozocin (STZ) after nephrectomy. The diabetic rats were assigned to diabetic rat (DM) group, calcium dobesilate treatment (R) group(100 mg·kg-1· d-1 )and controlled (C) group.
     方法:左肾切除后单次腹腔注射50mg·kg-1链脲佐菌素制备糖尿病大鼠模型,糖尿病大鼠随机分成糖尿病组、羟苯磺酸钙治疗组(100 mg·kg-1·d-1)和正常对照组。
短句来源
     Methods: Wistar rats, weight 160~200g, were assayed for the serum CGRP content in diabetic rats and the quantity of uric micro-albumin in 24h at the 6th,8th,10th,12th and 14th weeks after they were made the model of diabetic rats.
     方法:Wistar大鼠,体重160~200g,于造成糖尿病大鼠模型后第6、8、10、12、14周测定血浆中的CGRP和24h尿微量白蛋白。
短句来源
     Methods: SHR were induced by strepozotocin to establish animal model of diabetic rats with hypertension (SHRDM).
     方法 :STZ诱导SHR大鼠建立SHRDM实验动物模型 ,。
短句来源
     RESULTS:In rats' model of diabetic,the pretreatment plasma and renal level of ATⅡ and ETⅠ were significantly increased and the expression of renal TGFβ 1 was obviously strengthened in comparison with nomal rats (P<0.05) and after treatment with benazepril,the level of ATⅡ, ET significantly deceased and the expression of TGFβ 1 was weakened.
     结果 :糖尿病大鼠AT Ⅱ ,ET 1明显升高 ,TGF β1表达增强 ,贝那普利治疗后AT Ⅱ ,ET 1显著下降 ,TGF β1表达减弱 ,肾脏肥大减轻 ,尿蛋白减少。
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  相似匹配句对
     model.
     模型。
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     Model.
     模型的适用范围。
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     -of-detail model.
     例如地形场景需要建立地形模型;
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     _n of the model.
     同时讨论了该模型中? _n项的某些性质.
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     Diabetic Neuropathy
     糖尿病神经病变
短句来源
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  model of diabetic
Our present study is based on the overall hypothesis that regulatory proteins, in addition to contractile protein, myosin contribute to altered cardiac contractile performance in the rat model of diabetic cardiomyopathy.
      
Results described here support previous evidence that increased basement membrane collagen synthesis occurs in thedb/db model of diabetic nephropathy.
      
Results described here support previous evidence that increased basement membrane collagen synthesis occurs in thedb/db model of diabetic nephropathy.
      
? Background: No satisfactory primate model of diabetic retinopathy has been produced.
      
The dog may prove to be another useful spontaneous model of diabetic neuropathy.
      
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While sympathetic efferents and prostaglandins (PGs) play an important role inhyperalgesia of partial injury of peripheral nerves and inflammation, whether these arealso involved in diabetic hyperalgesia is unknown. With intraperitoneal injection of 6-hydroxydopamine (6-OHDA) to eliminate effects of sympathetic postganglionic neurons (SPGNs) terminals, a model of diabetic rats with infused 6-OHDA could be set upby injection of streptozotocin (STZ). Nociceptive paw-withdrawal threshold (NPWT)and tail flick...

While sympathetic efferents and prostaglandins (PGs) play an important role inhyperalgesia of partial injury of peripheral nerves and inflammation, whether these arealso involved in diabetic hyperalgesia is unknown. With intraperitoneal injection of 6-hydroxydopamine (6-OHDA) to eliminate effects of sympathetic postganglionic neurons (SPGNs) terminals, a model of diabetic rats with infused 6-OHDA could be set upby injection of streptozotocin (STZ). Nociceptive paw-withdrawal threshold (NPWT)and tail flick latency (TFL) in 6-OHDA/diabetic rats were not changed significantly inthe following four weeks. However, in diabetic group rats, pain threshold was decreased significantly and accompanied by development of hyperalgesia. NPWT was significantly decreased with noradrenaline (NA) in diabetic hyperalgesic rats and increased with phentolamine or yohimbine, but not by prazocin. In the control rats,NPWT are not changed significantly by NA or phentolamine, and in 6-OHDA/diabeticrats, neither NA nor phentolamine also affected on NPWT significantly. However,NPWT may be significantly decreased by PGEI, PGE2 and PGD2 in both the controland the diabetic hyperalgesic rats. The above results suggested that SPGNs terminals areinvolved in hyperalgesia of diabetic rats, NA accelerated synthesis of PGs and releasedby way of presynaptic effect on a2-adrenergic receptors at the SPGNs terminals, PGs,in turn, directly acted on the primary afferent nociceptors, producing hyperalgesia.

交感传出和前列腺素(PGs)在周围神经不全损伤和炎症所引起的痛过敏中起重要作用,它们对糖尿病性痛过敏的影响尚不清楚。本工作先给大鼠腹腔注射6-羟多巴胺(6-OHDA)损毁交感节后神经元(SPGNS)末梢后,再给予链脲佐菌素(STZ)以建立6-OHDA糖尿病大鼠模型,在连续4周的观察中这组大鼠伤害性爪回缩阈值(NPWT)和甩尾反射潜伏期(TFL)没有明显变化,而糖尿病组大鼠的痛阈显著降低,并伴有痛过敏。皮内注射NA可使糖尿病痛过敏大鼠的NPWT显著降低,酚妥拉明或育亨宾能使它们的NPWT明显升高,而哌唑嗪则不影响其NPWT。去甲肾上腺素(NA)和酚妥拉明不影响对照组大鼠的NPWT。给6-OHDA糖尿病组大鼠皮内注射NA或酚妥拉明都不能明显改变大鼠的NPWT。PGE1,PGE2和PGD2能使对照组和糖尿病组大鼠的NPWT均明显降低、结果提示,SPGNs末梢参与糖尿病大鼠的痛过敏,NA作用于SPGNs末梢的突触前α2-受体,刺激SPGNs末梢合成和释放PGs增多,后者作用于初级传入伤害感受器,引起大鼠产生痛过敏。

Effects of chemical sympathectomy On the diabetic hyperalgesia of rats were observed.First intral eritoneally injecting 6-hydroxydopamine (6-OHDA) to eliminate effects of sympathetic postganglionic neurons(SPGNs), then injecting streptozotocin(STZ),the model of diabetic rats with 6-OHDA was set up. This group of rats had no abnormal expression in behaviour and their nociceptive paw-with-drawal threshold (NPWT) and tail flick latency(TFL)did not change significantly for continuous six weeks.However,after...

Effects of chemical sympathectomy On the diabetic hyperalgesia of rats were observed.First intral eritoneally injecting 6-hydroxydopamine (6-OHDA) to eliminate effects of sympathetic postganglionic neurons(SPGNs), then injecting streptozotocin(STZ),the model of diabetic rats with 6-OHDA was set up. This group of rats had no abnormal expression in behaviour and their nociceptive paw-with-drawal threshold (NPWT) and tail flick latency(TFL)did not change significantly for continuous six weeks.However,after the group of diabetic were intraperitoneally injected with STZ, their behavioral expressionwas abnormal, at the time of first week after the experiment, TFL was significantly reduced, at the time of second week, NPWT was decreased obviously.The results suggest that SPGNs play an important role in the diabetic hyperalgesia of rats.

观察了交感传出在大鼠糖尿病痛过敏中的作用。先给大鼠腹腔注射6-羟多巴胺(6-OHDA)损毁交感节后神经元(SPGNs)末梢后,再给予链脲佐菌素(STZ)建立6-OHDA糖尿病大鼠模型。在连续6周的观察中,发现这组大鼠在行为上没有反常表现,它们的伤害性爪回缩阈值(NPWT)和甩尾反射潜伏期(TFU)也没有显著变化,而糖尿病组大鼠在腹腔注射STZ后,在行为上出现反常表现,实验至第1周时,TFL显著缩短,第2周时,NPWT明显降低。结果提示SPGNs在大鼠糖尿病痛过敏中起重要的作用。

Objective:To investigate the influence of diabeteson the function and morphology of Leydig cells.Methods:The model of diabetic rat was induced by STZ. Two months later, the diabetic rats were sacrificed. Serum testosterone level and hCG binding site of testicular tissue were measured, the morphology of Leydig cells was observed with light and electron microscopy.Results:The serum testosterone level and hCG binding sites of diabetic rats were significantly lower than those of normal rats (P<0.01)....

Objective:To investigate the influence of diabeteson the function and morphology of Leydig cells.Methods:The model of diabetic rat was induced by STZ. Two months later, the diabetic rats were sacrificed. Serum testosterone level and hCG binding site of testicular tissue were measured, the morphology of Leydig cells was observed with light and electron microscopy.Results:The serum testosterone level and hCG binding sites of diabetic rats were significantly lower than those of normal rats (P<0.01). The morphologocal changes of Leydig cells consisted of cell shrinkage severe mitochondrion and endoplasmic reticulum vacuolization.Conclusions:Diabetes could impaire the function and structure of Leydig cells.

目的:了解糖尿病对睾丸间质细胞(Leydig细胞)功能和形态的影响。方法:用链脲佐菌素诱导制成糖尿病大鼠模型,2个月后处死大鼠,测定血清睾酮及睾丸组织hCG结合位点,并用光镜和电镜作了睾丸形态学观察。结果:糖尿病大鼠的血清睾酮水平及睾丸组织的hCG结合位点水平明显低于正常对照组(P<0.01);糖尿病大鼠Leydig细胞萎缩,内质网、线粒体等细胞器空泡样变。结论:糖尿病可使Leydig细胞功能降低,结构变性。

 
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