ライフサイエンスコーパス: acetylator

1 AT2*4) and slow (NAT2*5, NAT2*6, and NAT2*7) acetylators.

2 k is pronounced among slow rather than rapid acetylators.

3 5.13) for recurrent loss compared with rapid acetylators.

4 th 3-fold more adducts in slow than in rapid acetylators.

5 risk ratios (RRs) comparing rapid with slow acetylators.

6 nt GSTP1 allele, or women who were slow NAT2 acetylators.

7 % CI, 1.3-1.6; P = 1.9 x 10(-14)), NAT2 slow acetylator and bladder cancer (OR, 1.46; 95% CI, 1.26-1.

8 ve confirmed that N-acetyl transferase2 slow acetylator and glutathione S-transferase Mu null genotyp

9 eractions between N-acetyl transferase2 slow acetylator and smoking.

10 Thirteen randomized studies with 1631 rapid acetylators and 1751 slow acetylators met inclusion and

11 antly higher (2-3-fold) in rapid versus slow acetylator congenic hamsters in both cecum (P = 0.0352)

12 the cecums and colons of both rapid and slow acetylator congenic hamsters treated with 3,2' -dimethyl

13 cinogenesis, were measured in rapid and slow acetylator congenic Syrian hamsters administered 3,2' -d

14 For slow acetylators, current smoking and smoking in the distant

15 ncer among postmenopausal women who are slow acetylators, demonstrate heterogeneity in response to ca

16 meat intake with cancer risk among NAT rapid acetylators, especially among men 60 years old or older.

17 .82.73/H-Patr) and slow (Bio.82.73/ H-Pat(s) acetylator female Syrian hamsters congenic at the NAT2 l

18 Among those men who were rapid acetylators for both NAT1 and NAT2, consumption of >1 se

19 The slow acetylator frequency for N-acetyltransferase 2 for spora

20 gen, to investigate the specific role of the acetylator genotype (NAT2) in colon carcinogenesis.

21 We found an association between the slow acetylator genotype for N-acetyltransferase 2 and famili

22 The slow acetylator genotype for N-acetyltransferase 2 was more c

23 ll risk of bladder cancer, and the NAT2 slow-acetylator genotype increases risk particularly among ci

24 idemiological studies that suggest the rapid acetylator genotype is associated with higher risk of co

25 INH acetylator genotypes were determined and urine tested fo

26 Subjects with slow acetylator genotypes were found to be at twofold increas

27 rapid or intermediate acetylators, NAT2 slow acetylators had an increased overall risk of bladder can

28 The common rapid (NAT2*4) and slow (NAT2*5B) acetylator human NAT2 alleles were also characterized fo

29 a higher incidence of colon cancer in rapid acetylator individuals.

30 ere acetylated among slow, as well as rapid, acetylators (mean +/- SD 95 +/- 1.9% vs. 97 +/- 1.6%, re

31 es with 1631 rapid acetylators and 1751 slow acetylators met inclusion and exclusion criteria.

32 Phenotypically slow acetylators (N-acetyltransferase 2 index <0.37) had an o

33 sent, a CYP1A1 variant allele, and the rapid-acetylator NAT2 imputed phenotype was associated with in

34 drazine drugs and carcinogens, but predicted acetylator NAT2 phenotypes were not associated with insu

35 Compared with NAT2 rapid or intermediate acetylators, NAT2 slow acetylators had an increased over

36 response was found for pack-years among slow acetylators (p < 0.01) but not among rapid acetylators (

37 w acetylators (p < 0.01) but not among rapid acetylators (p = 0.06).

38 ein expression, but that mechanisms for slow acetylator phenotype differ for NAT2 alleles that do not

39 Different mechanisms for slow acetylator phenotype in humans are consistent with multi

40 NAT2 slow acetylator phenotype(s) infer a consistent and robust in

41 in humans are consistent with multiple slow acetylator phenotypes.

42 uman populations are divided into three NAT2 acetylator phenotypes: slow, rapid and intermediate.

43 We investigated the effects of Ahr locus and acetylator polymorphisms on 32P-postlabeled IQ/DNA adduc

44 Among rapid acetylators, smoking was not associated with increased b

45 NAT2 genotypes conferring intermediate/rapid acetylator status (OR = 1.6, 95% CI: 1.0, 2.7).

46 re was no evidence of an interaction between acetylator status and INH treatment with respect to ELIS

47 Finally, isoniazid acetylator status determined by N-acetyltransferase type

48 95 percent CI: 1.7, 6.1) compared with rapid acetylators that smoked (OR = 1.4; 95 percent CI: 0.7, 2

49 aled gene-environment interaction among slow acetylators that smoked (OR = 3.2; 95 percent CI: 1.7, 6

50 Rapid acetylators were more likely than slow acetylators to have microbiological failure (RR, 2.0; 95

51 Rapid acetylators were more likely than slow acetylators to ha