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1 phenotype (extensive, intermediate, and poor metabolizers).
2 ely to experience drug toxicity than a rapid metabolizer.
3 d to identify participants as normal or slow metabolizers.
4 with severity of nicotine dependence in slow metabolizers.
5  to smoking cues in normal and slow nicotine metabolizers.
6 therapy, with increased quit rates in slower metabolizers.
7 concentrations observed in human CYP2D6 poor metabolizers.
8 zers, but depends on nicotine dose in normal metabolizers.
9                            Only slow ethanol metabolizers (alcohol dehydrogenase alleles [ADH1B*1] ca
10    Heterozygosity for the most frequent poor metabolizer allele (CYP2D6*4) was not associated with in
11                        Homozygosity for poor metabolizer alleles was found to be associated with AS.
12   Treatment-seeking smokers (N = 69; 30 slow metabolizers and 39 normal metabolizers) completed a vis
13 individuals predicted to be CYP2C9 extensive metabolizers and 8.7% of those predicted to be intermedi
14  consortia has allowed uncultured syntrophic metabolizers and methanogens to be optimally grown and s
15 dwater and wastewater treatment), syntrophic metabolizers are known to play an important role.
16 lects primarily non-nicotine effects in slow metabolizers, but depends on nicotine dose in normal met
17  (N = 69; 30 slow metabolizers and 39 normal metabolizers) completed a visual cue reactivity task dur
18                              In STRIDE, slow metabolizer CYP2B6 and NAT2 genotypes were each associat
19 ma appears confined to individuals with slow metabolizer (CYP2C9*3) genotypes.
20 ignificant interaction (n=5), and convergent metabolizers did have a significant interaction (n=15).
21                                    Divergent metabolizers did not have significant interaction (n=5),
22                                         Poor metabolizers, either genotypic or due to phenocopying, a
23          We classified patients as extensive metabolizers (EM) or reduced metabolizers (RM) based on
24        Patients found to be CYP2D6 extensive metabolizers (EM) remained on 20 mg and those found to b
25                                         Slow metabolizers exhibited greater reductions in cravings af
26 -brain analysis, normal (compared with slow) metabolizers exhibited heightened abstinence-induced neu
27 o 55 years, homozygous for CYP2C19 extensive metabolizer genotype, confined, standardized diet) was c
28 20 to 53 years; homozygous CYP2C19 extensive metabolizer genotype; no nicotine for 6 weeks, prescript
29                        Individuals with slow metabolizer genotypes in both genes had markedly elevate
30                                         Slow-metabolizer genotypes were associated with increased cen
31 py in 58% with CYP2B6 and 93% with NAT2 slow metabolizer genotypes.
32 ed 10 extensive, 17 intermediate, and 7 slow metabolizer genotypes.
33    Smokers in the first NMR quartile (slower metabolizers) had lower Fagerstrom Test for Nicotine Dep
34 tions in cravings after scanning than normal metabolizers; however, craving was unrelated to nAChR av
35 om NADH are present in almost all syntrophic metabolizers, implicating their critical role in syntrop
36 eponema succinifaciens, a known carbohydrate metabolizer in swine.
37 gradation remain unknown for many syntrophic metabolizers, including strain UI.
38 r' or 'high-responsive' person, and the slow metabolizer is often more likely to experience drug toxi
39                                Considering 3 metabolizer levels (extensive, intermediate and slow), s
40                                       Normal metabolizers may benefit from adjunctive behavioral smok
41 ed closure times seen in extensive and rapid metabolizers (n = 16; p = 0.001).
42 slow metabolizers (NMR < 0.26) and 12 normal metabolizers (NMR >/= 0.26)-underwent 2-(18)F-FA-PET bra
43                  Twenty-four smokers-12 slow metabolizers (NMR < 0.26) and 12 normal metabolizers (NM
44 YP2C19 allele carriers, but only 20% of poor metabolizers of clopidogrel had an escalation in the dos
45 their antiplatelet therapy, only 20% of poor metabolizers of clopidogrel had their antiplatelet thera
46 n treatment response between slow and normal metabolizers of nicotine.
47  species more widely, may be relatively poor metabolizers of penta-BDEs.
48 tion of cytochrome P450 enzymes, the primary metabolizers of xenobiotics in humans.
49 the recommended dose of a drug than a 'rapid metabolizer' or 'high-responsive' person, and the slow m
50 erences are often more than tenfold; a 'slow metabolizer' or 'low-responsive' individual might theref
51 y was significantly reduced in slow nicotine metabolizers (P = 0.04).
52 d hemoglobin A1c) compared with fast ethanol metabolizers (persons homozygous for ADH1B*2).
53 urrently used as biomarker to predict CYP2D6 metabolizer phenotype.
54 er a wide spectrum of different human CYP2D6 metabolizer phenotypes.
55 ative affect in the whole sample, but normal metabolizers reported greater reductions of craving and
56 , smokers in the fourth NMR quartile (faster metabolizers) reported greater craving for cigarettes fo
57 ts as extensive metabolizers (EM) or reduced metabolizers (RM) based on CYP2C19 genotype and evaluate
58  Patients with KCNH2 risk genotypes and slow metabolizer status (approximately 7% of patients) showed
59     There was no association between CYP2C19 metabolizer status (EM vs. RM) and the primary composite
60                                         Slow metabolizer status and gene variants in KCNH2 associated
61                                      CYP2C19 metabolizer status is not associated with the composite
62 risperidone compared with patients with fast metabolizer status or without the KCNH2 risk genotypes.
63 tion in cigarettes, but that irrespective of metabolizer status, reductions to <0.763 mg/cigarette ma
64 atings depend on nicotine dose regardless of metabolizer status.
65 hosting diverse syntrophic aromatic compound metabolizers (Syntrophus, Syntrophorhabdus, Pelotomaculu
66 inished effectiveness of clopidogrel in poor metabolizers, those having 2 loss-of-function alleles, h
67 els (extensive, intermediate and slow), slow metabolizers were at increased risk.
68 unced when extreme groups of slow and normal metabolizers were examined.
69 e found to be intermediate (IM) or poor (PM) metabolizers were increased to 40 mg daily.
70  those predicted to be intermediate and poor metabolizers were VKORC1 p.D36Y carriers who require mar
71 ductions of craving and withdrawal than slow metabolizers, with dose-dependent effects.
72   They suggest that normal and slow nicotine metabolizers would respond differently to nicotine reduc

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