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Objective To study antiradiation and antifatigue effects of a soft capsule mainly composed of cistanche,acanthopanax senticosus and jujube. Methods The mice were divided into four groups and then orally given soft capsule at doses of 0 .0g/kg.bw, 0.18g/kg.bw, 0.36g/kg.bw, 1.08g/kg.bw for a successive period of 30 days.The burden-swimming time , hepatic glycogen, serum urea nitrogen, lactic dehydrogenase of mice were observed. The mice were divided into four groups and then was orally given soft capsule at doses of 0 .0g/kg.bw, 0.18g/kg.bw, 0.36g/kg.bw, 1.08g/kg.bw for a succession of 21 days.

设立3个实验组，每天分别以0.18、0.36和1.08g/kg·bw剂量的软胶囊给小鼠灌胃一次，同时设立空白对照组，连续灌胃30d后，测定小鼠的负重游泳时间、肝糖原含量、运动后血清尿素水平、血乳酸曲线下面积等指标，以测定其抗疲劳作用；每天以上述剂量给小鼠灌胃，同时设立一个辐射对照组，连续灌胃21d后，不同指标选择不同的照射剂量，各组均以同一剂量γ射线全身照射一次，照射后继续给予样品。

At 4th week, the percentages of Clara cells over bronchiolar epithelial cells were similar between groups. At 24th week, the percentages of Clara cells were reduced in mice exposed to TCDD, NNK, CSC, or TCDD+CSC exposure, but not in mice exposed to TCDD+1 mg NNK. Thus, these findings suggested that TCDD, NNK, CSC, or TCDD+CSC exposure injuried Clara cells to lose CCSP protein in mice lung.

在A/J mice 4周实验组中，TCDD或NNK各实验组Clara cell的数目(26.6%-34.3%)与控制组(34.2%)比较，并没有明显的差异；反观A/J mice 24周实验组中，除了TCDD+NNK (1 mg)实验组外，其他各实验组Clara cell的数目与控制组(55.9%)比较明显下降11.7%-41.4%，显示暴露NNK、TCDD、CSC或TCDD+CSC皆会伤害Clara cell，暗示Clara cell对这些环境毒物比其他呼吸道上皮细胞敏感。

Methods 60 female mice were randomly divided into 4 groups (n=15):Mice in normal control group received subcutaneous injection of normal saline and mice in the other 3 groups received cervicodorsal injection of D-galactose[1000 mg/(kg1·d)] for 42 d to establish subacute aging model.

60只雌性昆明种小鼠，随机分为4组(n=15)：正常对照组皮下注射生理盐水；其余3组每日颈背部皮下注射 D-半乳糖[1000 mg/] 造成小鼠衰老模型，同时各组分别灌胃生理盐水、枸杞多糖[200 mg/]、丹参酮[1 500 mg/]。42 d后，测定小鼠背部皮肤组织匀浆中超氧化物歧化酶活力、过氧化脂质代谢产物丙二醛含量和皮肤羟脯氨酸含量。

In Rh2＋DDP group 1000uM cisplatine and 100uM gensenoside Rh2 were injected to nude mice by abdomen. Growth status of tumors were observed. Diameter of tumors were measured. After 60 days,〓Tc-MIBI were injected from vein of nude mice tail to perform SPECT exam and calculate the value R of the tumors. Later the nude mice were killed.

将A549DDP细胞和A549细胞分别种植于裸鼠皮下，种植A549细胞的裸鼠为A549组，种植A549DDP细胞的裸鼠分对照组、DDP组和Rh2+DDP组，每组4只裸鼠。A549组和对照组的裸鼠腹腔注射生理盐水，DDP组裸鼠腹腔注射低效浓度的顺铂；Rh2+DDP组裸鼠腹腔注射低效浓度的顺铂及无毒浓度的Rh2。

In the experiment, 98 KunMing mice were randomly divided into 2 groups, which were normal mice group and immunosuppressive mice group. Each group included: commonly cribble group, ultra-fine powder group and normal saline group.

本试验将98只昆系小鼠随机平均分为2组，为正常组和免疫抑制模型组，每组各设粗粉组、微粉组和生理盐水对照组，粗粉和微粉各设低、中、高三个剂量组。

MethodsThe model of cerebral ischemia and anoxia in mice was established by decollation and ligating common bicarotid artery the effect of BVF on the survival time of the mice,and the time of catching their breath after mice decollated,and mouse brain capillary vessel permeability were observed.

方法采用小鼠断头、结扎双侧颈总动脉等脑缺血缺氧模型，观察苦菜总黄酮对脑缺血缺氧小鼠存活时间、断头小鼠喘息时间及脑毛细血管通透的影响

Methods The model of cerebral ischemia and anoxia in mice was established by decollation and ligating common bicarotid artery the effect of BVF on the survival time of the mice,and the time of catching their breath after mice decollated,and mouse brain capillary vessel permeability were observed.

采用小鼠断头、结扎双侧颈总动脉等脑缺血缺氧模型，观察苦菜总黄酮对脑缺血缺氧小鼠存活时间、断头小鼠喘息时间及脑毛细血管通透的影响；TBA法、NBT法测定小鼠脑缺血缺氧后脑组织MDA含量和SOD活性。

ResultsBVF could remarkably lengthen the survival time of cerebral ischemia and anoxia mice, and the time of catching their breath after mice decollated,could evidently decrease mouse brain capillary vessel permeability and the content of MDA, increase activity of SOD in the brain tissues of cerebral ischemia and anoxia mice.

方法采用小鼠断头、结扎双侧颈总动脉等脑缺血缺氧模型，观察苦菜总黄酮对脑缺血缺氧小鼠存活时间、断头小鼠喘息时间及脑毛细血管通透的影响；TBA法、NBT法测定小鼠脑缺血缺氧后脑组织MDA含量和SOD活性。

ResultsBVF could remarkably lengthen the survival time of cerebral ischemia and anoxia mice, and the time of catching their breath after mice decollated,could evidently decrease mouse brain capillary vessel permeability and the content of MDA, increase activity of SOD in the brain tissues of cerebral ischemia and anoxia mice.

结果苦菜总黄酮能显著延长小鼠存活时间、喘息时间，能显著降低缺血缺氧小鼠脑毛细血管的通透性，能显著降低脑组织MDA含量，能显著提高脑组织SOD活性。

Results: Tyroserleutide can significantly increase the life span of H22 tumor-bearing mice by 50-70% in dosages of 20ug/kg/d-80ug/kg/d,specially the high dosage of 80ug/ml can significantly increase the life span by 69.24%; Tyroserleutide can inhibit the growth of transplanted hepatocellular tumor BEL-7402 in nude mice,the rate of tumor inhibition was25-50% in dosages of 40-320ug/ml ,the inhibition rate of 160ng/ml was 44.03%; Tyroserleutide could inhibit the growth of H22 and BEL-7402 tumor in a dose-dependent manner. Simultaneously, tumoricidal activity of tyroserleutide against BEL-7402 cell line in vitro was observed hinger when compared with the control group(P.05).The inhibition effect of 72hrs was higher than 24hrs,48hrs,96hrs.And specially the high dosage of 160ug/ml can significantly inhibit growth of tumor cell by 19.36%. Tyroserleutide can activated PEM and marked enhance cytotoxicity andphagocytosis functions in vitro and in vivo. The OD values of cytotoxicity were observed hinger when compared with the control group(P.05).The cytotoxicity of macrophages activated by tyroserleutide against BEL-7402 and B16-F10 was 35.58%,61.2% in vitro and21.39%,47.63% in vivo. The cytotoxicity rate of nude mice PEM was 32.86%,73.07% in vivo. Furthermore, tyroserleutide alone could stimulated the production of IL-1B TNF- a and NO by M . Tyroserleutide and LPS could synergistically activated M producing more cytotoxicity effectors. Conclusion: Tyroserleutide had inhibition functions against hepatoma carcinoma .Its possible mechanisms were related to the affect that Tyroserleutide could inhibit tumor cell directively and induce tumor cells apoptosis or death effectively.

结果：酪丝亮肽能显著延长腹水型肝癌H_(22)小鼠的生存时间，给药剂量为80μg／kg／d时疗效最显著，达到69.24％，在20μg／kg／d-80μg／kg／d剂量范围内生命延长率为50-70％，给药剂量与荷瘤鼠生存时间呈现一定量效关系；酪丝亮肽能显著抑制人肝癌BEL-7402移植瘤裸鼠的肿瘤生长，给药剂量为160μg／kg／d时疗效最显著，抑制率为44.03％，并且在40-320μg／kg／d剂量范围内抑制率为25-50％，给药剂量与肿瘤抑制率呈现一定量效关系；酪丝亮肽体外对人肝癌BEL-7402细胞生长有一定的抑制作用，在作用72hrs时各浓度酪丝亮肽对肿瘤细胞的抑制作用较24hrs、48hrs、96hrs明显，其中浓度为100μg／ml时抑制率达19.36％；酪丝亮肽体内外均能增强小鼠腹腔巨噬细胞对肿瘤细胞的杀伤：体外作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强，与效应细胞对照组相比有显著性差异(P＜0.05)杀伤率分别达到35.58％、61.2％；体内作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强，与生理盐水对照组相比有显著性差异(P 。05)，杀伤率分别达到21.39%、47.63%；裸鼠腹腔巨噬细胞经酪丝亮肤作用后对BEL一7402、B 16一F10杀伤功能明显增强，与生理盐水对照组相比有显著性差异(P.05)，最高杀伤率分别达到32.86%、73.07%；酪丝亮肤能增强单核巨噬细胞系统的吞噬功能，吞噬指数与生理盐水组比较有显著性差异(P.05)；酪丝亮肤体外作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO，与效应细胞对照组相比有显著性差异(P.05)；酪丝亮肤体内作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO，与生理盐水对照组相比有显著性差异(P.05)；酪丝亮肤能促进鼠巨噬细胞株R戌W264.7分泌合成IL一1p和NO，IL一1日、NO水平分别在酪丝亮肤作用24hrs、12hrs时达到高峰，酪丝亮肤单独应用能提高巨噬细胞的分泌合成功能，而且酪丝亮肤能与LPS协同作用刺激巨噬细胞的细胞毒效应分子分泌合成。

According to my definition, the Manchurian Candidate is an experimentally created dissociative identity disorder that meets the following four criteria

根据我的定义，满州候选人是一个创造分离身份混乱的实验，它符合下述的4条标准

I'd be chuffed to play at a World Cup, but I have many years ahead of me in the game so I hope to have more opportunities.

我会chuffed发挥在世界杯，但我有很多年的比赛在我前面，所以我希望有更多的机会。