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Passive transfer of sera from mice immunized with expressed G1 and G2 conferred partial protection or prolongation of time to death from fatal hantaan virus infection in infant mice which challenged with hantaan virus at 10LD50. The spleen cells from mice immunized with G1, G2and NP can protect or prolongate the lifetime of infant mice infected with lethal dose (10LD50 or 40LD50) hantaan virus.

将重组G1、G2和NP免疫小鼠的血清和脾细胞注入汉滩病毒致死性感染的乳小鼠体内,发现G1、G2的免疫血清和G1、G2及NP免疫脾细胞对乳鼠有保护作用,同时在一组试验中观察到G1的脾细胞可显著缩短乳鼠的存活时间。

It was found that during all three stages, the expression levels of Dnmt1 mRNA in the epithelial cells of the pregnant mice were significantly lower than those in the pseudopregnant mice (P.05), and the level of Dnmt1 protein expression in the pregnant mice was significantly decreased as compared with that in pseudopregnant mice at the 4-cell stage.

结果 Dnmt1蛋白主要表达于上皮层;妊娠组小鼠各期Dnmt1 mRNA表达水平均显著性低于同期假孕组(P.05),妊娠组4细胞期Dnmt1蛋白表达水平显著性低于同期假孕组(P.05)。

The results of flow cytometry in normal, B27 single transgenic mice and B27/hβ〓m double transgenic mice were 0.63%, 7. 87% and 35. 87% respectively. B27 antigen was also expressed in the cell surface and cytoplasm of colon, skin, testis and eyes of the double transgenic mice by the detection of immunohistochemistry, which was evident on the cell surface. 8 double transgenic mice bearing high copy (7 males, 1 female) developed spontaneous alopecia, psoriasiform dermatosis, joint swelling and nail changes in the rear paw.

免疫组化检测可见转基因小鼠的结肠、皮肤、睾丸和眼睛组织的细胞膜和细胞浆均有B27抗原的存在,尤以细胞膜明显。21只B27/h〓转基因阳性鼠中有8只出现脱毛和皮肤的银屑病样改变,同时伴有后肢的关节肿胀和趾甲变化。8只小鼠均为高拷贝,其中雄性7只,雌性1只。

It is estimated that there are about 40,000 functional genes.In order to understand those genes related to human diseases and the novel functional genes, the genetic manipulated mice including transgenic mice and knockout mice have been generated to facilitate the purpose.This transgenic core has been collaborated with industrial and research institutes for years, and has built up competitive know-how for transgenic mice, embryo cryopreservation, and pathogen free rederivation.

小鼠长期以来即为研究人类疾病最佳动物模式,2001年美国赛洛因公司已将小鼠129的两个品系之基因序列解码完成提供付费使用,2003年小鼠B6的基因序列也被Mouse Genomic DNA Sequencing Consortium解码完成,预估约有4万个功能基因,随著基因操控技术的成熟,制造出各种带不同基因缺陷的模式动物供生物医学研究已非难事。

Results Protein oxidation and lipid oxidation decreased significantly in HO-2 knockout mice at 72 h compared with that of wild-type mice. Striatal cell viability increased significantly in knockout mice at 72 h compared with that of wild-type mice.

结果 与野生型相比,基因(HO-2)敲除小鼠纹状体内蛋白和脂类的氧化作用显著降低,而纹状体细胞的存活率显著增加;HO-1的表达在两种小鼠注射前后没有明显差异。

NOD/SCID (non-obese diabetic/severe combined immunodeficient) mice are immunodeficient mice which are generated by backcrossing severe combined immunodeficient mice with non-obese diabetic mice strains.

NOD/SCID(非肥胖糖尿病/重症联合免疫缺陷)小鼠是在SCID小鼠的基础上与非肥胖性糖尿病小鼠品系回交的免疫缺陷鼠。

During the first two weeks after birth, the growth performances were not significant between the mutant mice and the normal ones, but after that, the mutant mice grew much slower. The differences were significant in the indexes of eyes, lungs, thymuses, and adrenal glands between the genders. At the same time, the differences were significant in the organ indexes, such as lungs, adrenal glands, uterine and testicles between the normal phenotype mutant mice and the abnormal ones. And these two kinds of mice showed different amount of hemoglobin and red blood cell.

结果:B6-Co小鼠不育率22%、平均产仔数5.62±2.55只、离乳成活率56.59±41.22显著低于正常的B6小鼠,而胎间隔29.50±10.50天比正常B6小鼠短。B6-Co小鼠出生后2周内生长发育与正常B6小鼠基本一致,2周后,其生长发育慢于正常B6小鼠。B6-Co小鼠雌雄间的眼球、肺、胸腺、肾上腺的脏器指数差异有统计学意义。B6-Co表型异常小鼠与B6-Co表型正常小鼠相比,肺、肾上腺、子宫、睾丸的脏器系数差异有统计学意义。B6-Co小鼠表型异常小鼠在血红蛋白和红细胞数量上异于B6-Co表型正常小鼠。

The fusion DNA fragments of ag85b-mpb64 and ag85b-mpb64-esat-6 were obtained by PCR andSOE technique. Various DNA vaccines were constructed with the pcDNA3.1: fusion of two genes, and of three genes, bivalent combinations and trivalent combinations(pCA+pCM+pCE6). BALB/c mice were vaccinated with this DNA vaccines.The mice injected withBCG were positive control and the mice injected with pCDNA3.1 and PBS were negative control.The mice were immunized 3 times with 2-wk intervals. The animals in group BCG were only inoculatedsubcutaneously with 1×10~6 CFU BCG at initial vaccination. The serum IgG titers and IgG isotype weredetermined using iELISA coated with M. bovis PPD and rMAE protein expressed and depurated inprokaryotic expression system every week.

同样,利用PCR和SOE技术,获得牛分枝杆菌mpb64-ag85b和mpb64-ag85b-esat-6融合基因,以pCDNA3.1为载体构建了牛分枝杆菌多价组合和多基因融合DNA疫苗:二基因融合(pCDNA3.1-MPB64-Ag85B,简称pCMA)和三基因融合(pCDNA3.1-MPB64-Ag85B-ESAT-6,简称pCMAE)DNA疫苗;二价组合和三价组合(pCA+pCM+pCE6)DNA疫苗,免疫BALB/c小鼠,以牛分枝杆菌BCG免疫组为阳性对照,以pCDNA3.1及PBS免疫组为阴性对照,共免疫3次,每次间隔2周,BCG组仅初免时皮下免疫1次。1免后每周,以原核表达纯化的重组MPB64-Ag85B-ESAT-6蛋白和牛分枝杆菌PPD为包被抗原,以间接ELISA方法检测血清IgG水平及lgG亚类。

Methods The nude mice tumors were formed by injection of human ovarian cancer cell line AO and AO/HSV1-tkc (AO cells carried with HSV1-tk gene which was constructed in China) subcutaneously, and then were transplanted to the omentum of nude mice. The filter-passing culture fluid of VPC/HSV1-tkc was injected daily into the peritoneum of the nude mice in the group of in vivo. Finally, all of the three groups of nude mice accepted the treatment of GCV.

先将人卵巢癌细胞AO及携有HSV1-tk基因的AO细胞(AO/HSV1-tkc)注射于裸鼠皮下,形成肿瘤后再移植于裸鼠网膜,并以病毒生产细胞(VPC/HSV1-tkc)的培养液对AO网膜移植瘤进行体内转染,然后以GCV对体外AO/HSV1-tkc转移的肿瘤及经体内转染的AO肿瘤进行治疗。

Moreover, in order to make clear whether IV infection touches off the cause and its pathogenesis of artherosclerosis inflammatory reaction. The study also uses IV of type A1 and A3 to infect repeatedly Jimpy mice with E gene defect, to observe AS histology change of Jimpy mice aorta and detect the change of IV antibody and inflammatory reaction medium (eg.TNF-α, IL-1) in Jimpy mice serum and express of monocyte chemotactic factor( MCF-1) and nuclear factor kB in Jimpy mice aorta tissue .

另外,为了弄清流感病毒感染是否是触发动脉粥样硬化炎症反应的发生原因及其机理,本研究还用A1、A3型流感病毒反复感染载脂蛋白E基因缺陷小鼠,观察小鼠主动脉的动脉粥样硬化组织学改变,并检测小鼠血清中流感病毒抗体、炎症反应介质(如TNF-a、IL-1等)变化情况以及小鼠主动脉组织中的单核细胞趋化因子-1(MCP-1)和核转录因子kB表达情况。

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The Best Laid Plans Of Mice And Marionettes
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