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1  carcinogenesis in CFI mice treated with 1,2-dimethylhydrazine.
2 nificantly decreased by EGF and increased by dimethylhydrazine.
3 s no qualitative interaction between EGF and dimethylhydrazine.
4 ion in wild type (WT) animals exposed to 1,2-dimethylhydrazine, a known colon and liver carcinogen; h
5 e by addition of Bu(t)-bpy to 1 prior to 1,1-dimethylhydrazine addition, which provided Ti(eta(1)-NNM
6  were four groups: vehicle alone, EGF alone, dimethylhydrazine alone, and dimethylhydrazine followed
7                  After administration of 1,2-dimethylhydrazine and DSS, invasive carcinomas were obse
8 OM) and dextran sodium sulfate (DSS), or 1,2-dimethylhydrazine and DSS, to induce colorectal tumors.
9 nesis, female CF1 mice were administered 1,2-dimethylhydrazine and then fed an essentially sphingolip
10 late-replete control animals did not receive dimethylhydrazine and were fed the 0- and 8-mg folate di
11  investigated the distribution of ACF in the dimethylhydrazine (DMH) model of colonic carcinogenesis
12 6J x UL53-3) F(1) mice were treated with 1,2-dimethylhydrazine (DMH), a colon carcinogen.
13                                      The 1,2-dimethylhydrazine (DMH)-induced colon carcinoma model wa
14 ficient environment in all tissues where 1,2-dimethylhydrazine exerts its damage.
15 one, EGF alone, dimethylhydrazine alone, and dimethylhydrazine followed by EGF infusion.
16 ission are modified by the pretreatment with dimethylhydrazine for 16 weeks, dimethylhydrazine was th
17       A protocol using the aluminum amide of dimethylhydrazine for opening and cleavage of a [1,4]-di
18                                  Importantly dimethylhydrazine had no significant effect on crypt cel
19 alloamination/cyclization of unsaturated N,N-dimethylhydrazines has been extended to the use of 1,2-d
20 tic syntheses of ammonia, silylamine and N,N-dimethylhydrazine have been accomplished from the corres
21 is further supported by the observation that dimethylhydrazine increases crypt fission in crypts of n
22 sceptibility of Vparp-/- and Tep1-/- mice to dimethylhydrazine-induced colon tumorigenesis and uretha
23                               In this model, dimethylhydrazine induces exon-specific p53 hypomethylat
24  without calcium or tocopherol, was given to dimethylhydrazine-initiated rats (47% meat diet for 100
25        This study investigated the effect of dimethylhydrazine on DNA methylation of the colonic p53
26  week for 2 weeks or 20 mg/kg body weight of dimethylhydrazine once a week for 10 weeks and were anal
27 a catalyst for hydroaminations involving 1,1-dimethylhydrazine resulted in only a few turnovers under
28 its conversion to CH(4) and N(2), and of 1,1-dimethylhydrazine to CH(2)=O, CH(4), and N(2).
29 p53 hypomethylation was observed only in the dimethylhydrazine-treated folate-depleted rats compared
30 0.025% and 0.1% of the diet (AIN 76A) to 1,2-dimethylhydrazine-treated mice, there were significant r
31 cant p53 hypomethylation was observed in all dimethylhydrazine-treated rats relative to controls (P <
32 ciency enhances colorectal carcinogenesis in dimethylhydrazine-treated rats.
33            Five weeks after diet initiation, dimethylhydrazine was injected weekly for fifteen weeks.
34 eatment with dimethylhydrazine for 16 weeks, dimethylhydrazine was then discontinued for 8 weeks, fol
35       In the case of methylhydrazine and 1,1-dimethylhydrazine, we propose that the inactive methylhy
36 effects of epidermal growth factor (EGF) and dimethylhydrazine, which are both known to stimulate cry

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