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   5 '-primer 在 精神病学 分类中 的翻译结果: 查询用时:0.023秒
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-primer
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  “5 '-primer”译为未确定词的双语例句
    Methods: Genomic DNA was deaminated by sodium bisulfite,two sets of PCR primers which are specific to unmethylated and methylated DNA respectively ,were used to amplify the target regions of FMR1 and XIST.
    方法:用亚硫酸氢钠和对苯二酚对基因组DNA进行脱氨基修饰。 以修饰后的DNA为模板,用两对不同的引物:1对甲基化特异性引物和1对非甲基化特异性引物扩增FMR1基因(CGG)n重复序列区、FMR1和XIST基因的启动子区。
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    Methods The gene frequency of HLA DR2,DRB1*04 and DRB1*09 were detected separately by using sequence special primer polymerase chain reaction(PCR SSP) in 44 SAD patients and 45 healthy control subjects.
    正常对照组45例(中山大学附属第二医院保健科体检的自愿健康老年人),男14例,女31例,年龄61~88岁。 采用序列特异性引物聚合酶链反应(PCR-SSP)技术分别测定44例SAD患者(SAD组)和45例正常老年人(对照组)的HLA-DR2,DRB1*04,DRB1*09基因频率。
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    The sequences of the(α2 MG) PCR primer was 5` CTG AAG AAT TAT CCC TGA AC 3`and 5` TGG TTC CTG CCA TAT CGC TC 3`,the total reaction volume was 50 μL,The cycling parameters was indicated as below:94 ℃5 min,each circle was 94 ℃1 min,50 ℃30 s,72 ℃30 s,35 circles,and extend 72 ℃7 min. α2 MG after amplification was 910 bp.
    扩增A2M目的基因引物序列为:5`-CTGAAGAATTATCCCTGAAAC-3`和5`-TGGTTCCTGCCATATCGCTC-3`,PCR总反应体积50μL; 预变性94℃5min后,变性94℃1min,退火50℃30s,延伸72℃30s,35个循环后延伸72℃7min,扩增得到的A2M基因大小为910bp。
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    Methods Forty patients were diagnosed as narcolepsy based on clinical characteristics,routine examination,and multiple sleep latency tests (MSLT). All patients were checked for HLA-DRB1*15 low resolution,DRB1*15 and DQB1*6 high resolution by PCR/SSP(sequence specific primers),and gene frequencies of these alleles were compared with those in control group.
    方法 对 4 0例临床表现和各项检查、多次小睡潜伏时间试验 (MSLT)均符合发作性睡病诊断标准的患者 ,用序列特异性引物体外基因扩增 (PCR SSP)方法进行HLA DRB1 15低分辨、DRB1 15及DQB1 6高分辨测定基因型 ,并和 91例正常对照组进行比较。
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    METHODS: DNA fragment encoding Aβ_ 42 gene w as obtained from Tg2576 mice genome by PCR technique and the signal peptide of I gG к light chain was fused to N-terminal of the Aβ_ 42 gene by primer ext ension.
    方法:PCR法从Tg2576转基因鼠基因组DNA中扩增人Aβ42基因片段; 在Aβ42基因的5′端引物延伸连接IgGк轻链信号肽序列;
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  -primer
It also does not require 5'-primer extensions and finally delivers an expression clone for the preparation of untagged protein in less than a week.
      


The deposition of β-amyloid protein (β-AP) in the brain is the causative agent of Alzh-eimer's pathology. β-AP is a peptide product of the β-amyloid precursor protein (β-APP).Due to alternative splicing, there are several mRNA variants of β-APP. β-APP695, β-APP751 and P-APP770 are the main three which are different in the absence or presence of the Kunitz pro-tease inhibitor domain(KPI). RT-PCR with a pair of primers for the flank sequences of KPI can give rise to three cDNA variants corresponding to p-APP695,...

The deposition of β-amyloid protein (β-AP) in the brain is the causative agent of Alzh-eimer's pathology. β-AP is a peptide product of the β-amyloid precursor protein (β-APP).Due to alternative splicing, there are several mRNA variants of β-APP. β-APP695, β-APP751 and P-APP770 are the main three which are different in the absence or presence of the Kunitz pro-tease inhibitor domain(KPI). RT-PCR with a pair of primers for the flank sequences of KPI can give rise to three cDNA variants corresponding to p-APP695, β-APP751 and 3-APP770. In embryo rat's brain there is no detectable β-APPmRNA, whereas in the cerebral cortex and hippocampus of six-month-old rat the β-APP695 mRNA existed predominantly. In the neuro-blastoma cell line C 6 cells, p-APP695, β-APP751 and β-APP770 all appeared and the β-APP770 mRNA was the main one.

β-淀粉样蛋白(β-AP)是阿尔茨海默氏病(Alzheimer’s disease)病人老年斑的主要成分,它是β-淀粉样前体蛋白(β-APP)剪切后的产物。β-APP基因在体内存在β-APP_(695),β-APP_(751)β-APP_(770)。等几种主要的转录物,它们的区别在于Kunize丝氨酸蛋白酶抑制区(KDI)编码序列的存在和缺失。通过RT-PCR技术,用针对KPI编码区两侧序列的一种特异性引物可由总RNA样品中扩增出反映以上三种转录物的cDNA片段。实验表明,胎鼠脑组织中未检测到β-APPmRNA;6月龄大鼠海马组织,大脑皮层中只检测到β-APP_(695);在神经胶质瘤细胞系C6中存在β-APP_(695),β-APP_(751),β-APP_(770),其中β-APP_(770)占优势。

Objective and Methods: According to the cDNA sequence of human amyloid precusor protein (APP), gene, a pair of specific primer were designed to detect the expression of APP gene in noneuronal, neuron like and neuronal cell lines by RT PCR. Results: No amplification products was observed in noneuronal wild COS 7 cells, but we can detect the expression of APP gene in COS 7 cell transfected with human APP gene, neuron like wild PC12 cells and human neuroblastoma SH SY5Y cells. Conclusion: Specifically...

Objective and Methods: According to the cDNA sequence of human amyloid precusor protein (APP), gene, a pair of specific primer were designed to detect the expression of APP gene in noneuronal, neuron like and neuronal cell lines by RT PCR. Results: No amplification products was observed in noneuronal wild COS 7 cells, but we can detect the expression of APP gene in COS 7 cell transfected with human APP gene, neuron like wild PC12 cells and human neuroblastoma SH SY5Y cells. Conclusion: Specifically designed primer and RT PCR can be used to assay the level of human APP gene in neuron like and neuronal cell lines.

目的与方法:根据人淀粉样前体蛋白(amyloidprecursorprotein,APP)基因cDNA序列设计的引物,提取总RNA,利用RTPCR方法检测非神经、类神经及神经细胞系APP基因的表达。结果:利用专门设计的引物不能检测野生型COS7细胞中APP基因的表达,但可以检测转染人APP基因的非神经元类COS7细胞,类神经元的野生型PC12及人神经母细胞瘤细胞SHSY5Y细胞中APP基因的表达。结论:利用特异设计的人APP基因引物及RTPCR方法可以检测类神经及神经细胞系APP基因的表达

To investigate the distribution of apolipoprotein E(apo E)genotypes and to explore the role of apo E in pathogenesis of Alzheimer′s disease(AD).apo E genotype was studied with polymorase chain reaction and restriction fragment length polymorphism(PCR RFLP).The apo E exon 4 gene was cloned into pUC18,Primer 1 was used to sequence the pUC apo E.The frequencies of apo E exon 4 detected were as follows :AD(n=42)ε 2/2=0,ε 2/3=0 048,ε 2/4=0 024,ε 3/3=0 524,ε 3/4=0 381,ε 4/4=0 024;Controls(n=108)ε...

To investigate the distribution of apolipoprotein E(apo E)genotypes and to explore the role of apo E in pathogenesis of Alzheimer′s disease(AD).apo E genotype was studied with polymorase chain reaction and restriction fragment length polymorphism(PCR RFLP).The apo E exon 4 gene was cloned into pUC18,Primer 1 was used to sequence the pUC apo E.The frequencies of apo E exon 4 detected were as follows :AD(n=42)ε 2/2=0,ε 2/3=0 048,ε 2/4=0 024,ε 3/3=0 524,ε 3/4=0 381,ε 4/4=0 024;Controls(n=108)ε 2/2=0 009,ε 2/3=0 130,ε 2/4=0 028,ε 3/3=0 667,ε 3/4=0 157,ε 4/4=0 009,the frequencies of ε 3/4 genotype and ε 4 allele in AD were significantly higher than in age matched controls(P<0 05,P<0 01).The apo E ε 4 allele was associated with a tripling of the risk for AD compared with no ε 4 allele(odd ratio 2 932,95%CI 1 379 6 226).Serum apo AI level in AD was higher than that in age matched healthy control,but the concentration of TC,Trig,Lp(a),HDL C,LDL C and apo B was not significantly different compared AD with controls.The results suggests that apo E ε 4 allele was significantly associated with AD and apo E ε 4 allele may be a risk factor in the pathogenesis of AD.

探讨了载脂蛋白E (apoE)外显子 4基因多态性与Alzheimer′s病的关系。应用聚合酶链式反应扩增apoE外显子 4基因片段 ,对扩增片段用HhaⅠ酶切消化后进行基因分型 ,并用DNA测序技术对分型结果予以证实。Alzheimer′s病组与年龄匹配对照组在apoE外显子 4ε3/4基因型频率和ε4等位基因频率分布上的差异有显著性 (χ2 =8 91,P <0 0 5 ;χ2 =9 49,P<0 0 1) ,Alzheimer′s病组血清apoAⅠ水平显著高于对照组 (P <0 0 5 ) ,而TC、Trig、Lp (a) ,HDL C、LDL C、apoB两组间没有显著性差异 ,有apoEε 4等位基因个体患Alzheimer′s病风险为无ε 4个体的 3倍 ,比值比 (OR)为 2 932。总之 ,apoEε 4等位基因与Alzheimer′s病显著性相关 ,apoEε 4可能是Alzheimer′s病发病的危险因素。

 
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