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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.
10 Heterozygosity for the most frequent poor metabolizer allele (CYP2D6*4) was not associated with in
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
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
20 ignificant interaction (n=5), and convergent metabolizers did have a significant interaction (n=15).
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
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
38 r' or 'high-responsive' person, and the slow metabolizer is often more likely to experience drug toxi
42 slow metabolizers (NMR < 0.26) and 12 normal metabolizers (NMR >/= 0.26)-underwent 2-(18)F-FA-PET bra
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
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
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
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
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
70 those predicted to be intermediate and poor metabolizers were VKORC1 p.D36Y carriers who require mar
72 They suggest that normal and slow nicotine metabolizers would respond differently to nicotine reduc
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