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1  risk ratios (RRs) comparing rapid with slow acetylators.
2 nt GSTP1 allele, or women who were slow NAT2 acetylators.
3 AT2*4) and slow (NAT2*5, NAT2*6, and NAT2*7) acetylators.
4 k is pronounced among slow rather than rapid acetylators.
5 5.13) for recurrent loss compared with rapid acetylators.
6 ors and reduce treatment failure among rapid acetylators.
7 th 3-fold more adducts in slow than in rapid acetylators.
8  15 were genotypic NAT2 slow or intermediate acetylators.
9 % 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.
10 ve confirmed that N-acetyl transferase2 slow acetylator and glutathione S-transferase Mu null genotyp
11 eractions between N-acetyl transferase2 slow acetylator and smoking.
12  Thirteen randomized studies with 1631 rapid acetylators and 1751 slow acetylators met inclusion and
13 ance was 2.2 times higher among intermediate acetylators and 3.8 times higher among rapid acetylators
14 to reduce isoniazid toxicity among slow NAT2 acetylators and reduce treatment failure among rapid ace
15 acetylators and 3.8 times higher among rapid acetylators, compared with slow acetylators (P < 0.0001)
16 antly higher (2-3-fold) in rapid versus slow acetylator congenic hamsters in both cecum (P = 0.0352)
17 the cecums and colons of both rapid and slow acetylator congenic hamsters treated with 3,2' -dimethyl
18 cinogenesis, were measured in rapid and slow acetylator congenic Syrian hamsters administered 3,2' -d
19                                     For slow acetylators, current smoking and smoking in the distant
20 ncer among postmenopausal women who are slow acetylators, demonstrate heterogeneity in response to ca
21 meat intake with cancer risk among NAT rapid acetylators, especially among men 60 years old or older.
22 .82.73/H-Patr) and slow (Bio.82.73/ H-Pat(s) acetylator female Syrian hamsters congenic at the NAT2 l
23               Among those men who were rapid acetylators for both NAT1 and NAT2, consumption of >1 se
24                                     The slow acetylator frequency for N-acetyltransferase 2 for spora
25 gen, to investigate the specific role of the acetylator genotype (NAT2) in colon carcinogenesis.
26  expression differed significantly with NAT2 acetylator genotype (p < 0.0001).
27     We found an association between the slow acetylator genotype for N-acetyltransferase 2 and famili
28                                     The slow acetylator genotype for N-acetyltransferase 2 was more c
29 ll risk of bladder cancer, and the NAT2 slow-acetylator genotype increases risk particularly among ci
30 idemiological studies that suggest the rapid acetylator genotype is associated with higher risk of co
31                                          INH acetylator genotypes were determined and urine tested fo
32                           Subjects with slow acetylator genotypes were found to be at twofold increas
33 rapid or intermediate acetylators, NAT2 slow acetylators had an increased overall risk of bladder can
34 The common rapid (NAT2*4) and slow (NAT2*5B) acetylator human NAT2 alleles were also characterized fo
35  a higher incidence of colon cancer in rapid acetylator individuals.
36 ere acetylated among slow, as well as rapid, acetylators (mean +/- SD 95 +/- 1.9% vs. 97 +/- 1.6%, re
37 learance rates were lowest in predicted slow acetylators (median 14.5 L/h), moderate in intermediate
38  (median 14.5 L/h), moderate in intermediate acetylators (median 40.3 L/h), and highest in fast acety
39 ators (median 40.3 L/h), and highest in fast acetylators (median 53.0 L/h).
40 es with 1631 rapid acetylators and 1751 slow acetylators met inclusion and exclusion criteria.
41 2; n = 121 [78%]), and occurred in NAT2 slow acetylators (n = 62 [61%]).
42                          Phenotypically slow acetylators (N-acetyltransferase 2 index <0.37) had an o
43 hepatocytes of rapid, intermediate, and slow acetylator NAT2 genotypes.
44 sent, a CYP1A1 variant allele, and the rapid-acetylator NAT2 imputed phenotype was associated with in
45 drazine drugs and carcinogens, but predicted acetylator NAT2 phenotypes were not associated with insu
46     Compared with NAT2 rapid or intermediate acetylators, NAT2 slow acetylators had an increased over
47  among rapid acetylators, compared with slow acetylators (P < 0.0001).
48 response was found for pack-years among slow acetylators (p < 0.01) but not among rapid acetylators (
49 w acetylators (p < 0.01) but not among rapid acetylators (p = 0.06).
50 ein expression, but that mechanisms for slow acetylator phenotype differ for NAT2 alleles that do not
51                Different mechanisms for slow acetylator phenotype in humans are consistent with multi
52 two-compartment model with an effect of NAT2 acetylator phenotype on clearance.
53                                    NAT2 slow acetylator phenotype(s) infer a consistent and robust in
54  in humans are consistent with multiple slow acetylator phenotypes.
55 uman populations are divided into three NAT2 acetylator phenotypes: slow, rapid and intermediate.
56 We investigated the effects of Ahr locus and acetylator polymorphisms on 32P-postlabeled IQ/DNA adduc
57  proportions of slow, intermediate, and fast acetylators predicted by a conventional 6-SNP NAT2 panel
58 rse pharmacokinetic sampling, and tested the acetylator prediction algorithm accuracy against estimat
59  use, and TB drug metabolism variables (NAT2 acetylator profiles).
60  slow and intermediate N-acetyltransferase 2 acetylators, respectively.
61 ntified as slow, intermediate, and rapid INH acetylators, respectively.
62                                  Among rapid acetylators, smoking was not associated with increased b
63 NAT2 genotypes conferring intermediate/rapid acetylator status (OR = 1.6, 95% CI: 1.0, 2.7).
64 re was no evidence of an interaction between acetylator status and INH treatment with respect to ELIS
65                           Finally, isoniazid acetylator status determined by N-acetyltransferase type
66  of isoniazid based on N-acetyltransferase 2 acetylator status may help patients attain effective exp
67  that N-acetyltransferase 2 gene (NAT2) slow acetylator status was the best independent predictor of
68 y virus (HIV)-related severity and isoniazid acetylator status.
69 95 percent CI: 1.7, 6.1) compared with rapid acetylators that smoked (OR = 1.4; 95 percent CI: 0.7, 2
70 aled gene-environment interaction among slow acetylators that smoked (OR = 3.2; 95 percent CI: 1.7, 6
71 Rapid acetylators were more likely than slow acetylators to have microbiological failure (RR, 2.0; 95
72 the 48 patients with tuberculosis, predicted acetylator types were 27 (56.2%) slow, 16 (33.3%) interm
73                                         Fast acetylators underperformed even at 15 mg/kg.
74                                        Rapid acetylators were more likely than slow acetylators to ha
75 consisting of DNA-damaging agents and mutp53 acetylators, which is currently being pursued clinically
76 le EBA, except against a subset of slow NAT2 acetylators (who experienced the highest concentrations)