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   p 15 genes 的翻译结果: 查询用时:0.185秒
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p genes
相关语句
  p15基因
     The homozygous deletion and protein expression of p16 and p15 genes in hydatidiform mole were significantly higher than that in the chorion of early gestation( χ 2=11.152,14.388;P <0.05).
     葡萄胎中p16、p15基因及蛋白表达缺失率均高于早孕绒毛组织,差异有显著性(χ2=11.152、14.388,P<0.05)。
短句来源
     Homozygous Deletion of p16 and p15 Genes in Cervical Carcinoma and Clinical Significance
     p16及p15基因在子宫颈癌中的纯合性缺失及其临床意义
短句来源
     EXPRESSION OF P16 AND P15 GENES IN GESTATIONAL TROPHOBLASTIC TUMORS AND ITS CLINICAL SIGNIFICANCE
     P16、P15基因在妊娠性滋养细胞肿瘤中的表达及其意义
短句来源
     Deletions and aberrant transcription of p16 and p15 genes in childhood acute lymphoblastic leukemia
     小儿急性淋巴细胞白血病p16和p15基因缺失与转录异常的研究
短句来源
     Homozygous deletion of p16 and p15 genes in laryngeal squamous cell carcinoma
     喉癌p16、p15基因纯合性缺失的研究
短句来源
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  “p 15 genes”译为未确定词的双语例句
     Deletion and Methylation ofp16 / p15 Genes Analysis in Adult Acute Myeloid Leukemia
     成人急性髓性白血病中p16/p15缺失与甲基化
短句来源
     Genomic Instability and Alterations of K-ras and P15 Genes in Transformed 16HBE Cells by Nickel Sulfate
     硫酸镍诱导16HBE细胞恶变过程中的K-ras、P15基因的改变及基因组不稳定性分析
短句来源
     A study of the expression of p27 and p15 genes and the correlation between them in astrocytomas
     星形细胞瘤中p15与p27基因的表达及相关性研究
短句来源
     Co-negative expressions of p16 and p15 genes and protein in hydatidiform mole which had become invasive or choriocarcinoma were higher than in other cases( χ 2=4.675,P <0.05).
     葡萄胎恶变组P16、P15 蛋白表达联合阴性率高于无恶变组(χ2 = 4.675, P<0.05);
短句来源
     The homozygous deletion of P16 and P15 genes play an important role in the genesis and development of trophoblastic neoplasm, and in related to the grading, FIGOstage and prognosis.
     4.妊娠滋养细胞肿瘤中,P16、P15蛋白表达缺失与肿瘤的临床分期、预后明显相关,有望成为该组肿瘤的检测指标。
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  相似匹配句对
     15. C.
     15.高颊秽蝇C.
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     15P.
     第Ⅱ组:15号秀珍菇、日本秀珍菇、美味侧耳;
短句来源
     (p 15;?)
     (P15;?)
短句来源
     15 and E.
     15和E .
短句来源
     cytoskeleton genes ;
     细胞骨架相关基因;
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  p genes
Both cell lines showed homozygous deletion of the representative tumor suppressor p16 and p15 genes, but no p53 gene alteration.
      
Among the lines, three lines had mutations in codon 12 in K-ras, two lines harbored p53 mutations within the DNA-binding domain; two lines had homozygous deletions in both p16 and p15 genes; and one line had a missense mutation.
      
Methylation of p16 and/or p15 genes was detected in 15 HLs.
      
Hypermethylation of p16 and p15 genes and RB protein expression in acute leukemia.
      


A survey of the distribution of ABO,P and Rh blood groups was made among960 primary and middle school students of Tujia Minority in Luota,Xiche andMiaoshi Communes in Longshan county.Slide method was used for the identificationof ABO and P blood groups and direct bromelin method,for Rh blood group.Thedistribution of ABO blood group system in The Minority of Tujia is shown inTable 1.The sequence of the frequencies of phenotypes is A>O>B,AB.As for thegene frequencies,the sequence is O>A>B.In view of...

A survey of the distribution of ABO,P and Rh blood groups was made among960 primary and middle school students of Tujia Minority in Luota,Xiche andMiaoshi Communes in Longshan county.Slide method was used for the identificationof ABO and P blood groups and direct bromelin method,for Rh blood group.Thedistribution of ABO blood group system in The Minority of Tujia is shown inTable 1.The sequence of the frequencies of phenotypes is A>O>B,AB.As for thegene frequencies,the sequence is O>A>B.In view of the frequencies of the pheno-types of P blood group system,P_1 is much more frequent than P_2(Table 2),on thecontrary,the gene frequency P(gene of P_2)is higher than P(gene of P_1)(Table 4).As for the Rh blood group,among 930 investigated individuals,we found only8 phenotypes.The sequence of the frequencies of these phenotypes is CCDee>CcDE>ccDE>CcDee>CCDE>ccDee>CCdE and ccdee(Table 3).The rate of Rh posi-tive is 99.78% and Rh negative,0.22%.The sequence of frequencies of Rh genecomplexes is R' R~e>r>R~o>R~z,while r,r'and r~y are zero(Table 4).Detailedcomparisons are made between our results and those reported by the Shanghai Inst-itute of Biological Products(Table 5 to 8).The probable reason why the frequencyof the phenotype P_1 is much higher than P_2 while the gene frequency is quite thecontrary is discussed in thits paper.

共调查了土家族青年学生960人的 ABO、P 及 Rh 等血型系统,结果表明在 ABO 血型系统中,表现型频率的次序为 A>O>B>AB 型,而基因频率的次序为 O 基因>A 基因>B 基因。P 血型的表现型频率,P_1远高于 P_2,但其基因频率却相反,P_2高于 P_1。在我们调查的930例 Rh 血型中各表现型频率的次序为 CCDee>CcDE>ccDE>CeDee>CCDE>ccDee>CCdE 及 ccdee·Rh阳性占99.78%,Rh 阴性仅占0.22%。基因频率的次序为 R~1>R~2>r>R~0>R~z·r′、r″及置 r~y 为O。我们将调查结果与上海生物制品研究所血型组的调查结果作了较详尽的比较,并指出土家族与各民族间某一血型的表现型分布上的差别以及基因频率的差别的显著性基本上一致,但也有个别不尽相同的情况。此外,本文还讨论了土家族 P 血型 P_1远多于 P_2而 P_1基因频率反较 P_2为小的可能原因。

In order to test the promoter function of two HBV DNA fragments, a soluble cell-free system extracted from Hela celis was used. In the in viiro transcriptional system using the 1.4kb DNA fragment as the templa-te, there were two RNA products whose transcriptional initiation sites were supposed to be at nucleotide 276±5% and 821±5% respectively on the HBV map. The first transcriptional initiation site is identical to the one that is directed by the HBV C gene promoter known before.The rela-tionship between...

In order to test the promoter function of two HBV DNA fragments, a soluble cell-free system extracted from Hela celis was used. In the in viiro transcriptional system using the 1.4kb DNA fragment as the templa-te, there were two RNA products whose transcriptional initiation sites were supposed to be at nucleotide 276±5% and 821±5% respectively on the HBV map. The first transcriptional initiation site is identical to the one that is directed by the HBV C gene promoter known before.The rela-tionship between the location of the second initiation site and the gene open reading frame suggests that the promoter may direct the synthesis of P gene mRNA.The 0.8kb DNA fragment starts from the core structure gene, not in-cluding the regulating sequence. Deducing from the 708±5% nt-long RNA product, the transcriptional initiation site is 588 + 5% on the HBV DNA map. Associated with this RNA start site, there is an ATG codon at po-sition 677 downstream, suggsting that the ATG codon may be a start site of a new open reading frame.

自adr亚型乙型肝炎病毒DNA重组质粒中获得两个DNA片段,用体外转录方法研究启动子的位点。其中1.4kb片段有两个转录产物,其转录起始点分别位于乙型肝炎病毒DNA序列的276±5%位和821±5%位,第一个转录起始点与已报道的乙型肝炎病毒核心抗原基因上游启动子位置一致,第二个转录起始点在888位P基因的起始密码子上游。0.8kb片段自校心抗原结构基因起始密码子ATG以下的序列开始,不含有已知的调控序列,其708±5%核苷酸长的RNA产物,根据其长度计算共转录起始点位于乙型肝炎病毒DNA序列588±5%位,与此位置相关的下游ATG密码子位于677位。

The autho rs found that rhizomania resistant charac tor was controlled by two pairs of dominant genes by our observing on the resistance of differ rent original materials, their cross progenies and test cross progenies to the disease in the breeding of rhizomania resistance. The gene types and genetic niodel of sugarbeet (Beta vulgaris) rhizomania resistance were infered acco rding to the result. Let us assume that"P" and "R"represent the two pairs domnant genes, so the RRPP for immune...

The autho rs found that rhizomania resistant charac tor was controlled by two pairs of dominant genes by our observing on the resistance of differ rent original materials, their cross progenies and test cross progenies to the disease in the breeding of rhizomania resistance. The gene types and genetic niodel of sugarbeet (Beta vulgaris) rhizomania resistance were infered acco rding to the result. Let us assume that"P" and "R"represent the two pairs domnant genes, so the RRPP for immune type; RrPP, RRPp for disease resistanc e typel RrPp, RRpp, rrPP for disease tolerant type Ⅰ; Rrpp, rrp for disease tolerant typeⅡ and rrpp for sensitive type.The cultivated sugarbeet has lost a pair of the dominant gene in their cultivating process. If the sugarbeet lost the "p", we obtain only the stock of disease tolerant type, but it is not possible get the stocks of disease resistant and immune types in our selecting works.However, we wi1l get the disease resistant or immune type, after the sugarbeet will pick up the lost"P"gene by crossing with their ancestors.

在从事甜菜抗丛根病育种工作中,通过对各类育种材料的抗病性观察,及对其互交和测交后代的调查,发现甜菜的抗丛根病性是由两对显性基因控制的。经过一步分析,提出了甜菜抗丛根病的基因型和遗传模式。假定以“R”和“P”代表这两对显性基因,免疫型为RPRP;抗病型为RPRp、RPrP耐病Ⅰ型为RPrp、RpRp、rPrP;耐病Ⅱ型为Rprp、rPrP;敏感型为rprp。推测:糖用甜菜在驯化过程中,丢失了其中的一对显性基因,假设丢失的“P”,那么,只有耐病Ⅰ型(RpRp)、耐病Ⅱ型(Rprp)和敏感型(rprp)。这样,采用选择的方法,只能选育出耐病型品种,不可能选育出抗病型和免疫型的品种。只有通过与其祖先杂交,将丢失的“P”基因找回来,才能育成抗病型和免疫型品种。

 
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