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1 tients (10 slow, 26 intermediate, and 7 fast metabolizers).
2 phenotype (extensive, intermediate, and poor metabolizers).
3 ely to experience drug toxicity than a rapid metabolizer.
4  to affect pulmonary function in inefficient metabolizers.
5 ed and used to determine proportions of slow metabolizers.
6 life was 2.7 times greater in slow vs normal metabolizers.
7 , intermediate, normal, or ultrarapid CYP2D6 metabolizers.
8 , intermediate, normal, or ultrarapid CYP2D6 metabolizers.
9 pine, by 12% (95% CI, 3%-22%) in CYP3A5 poor metabolizers.
10 fee intake in the entire group or among fast metabolizers.
11 with LENS would predominantly be CYP2B6 slow metabolizers.
12 gher prevalence of poor cytochrome P450 2C19 metabolizers.
13 ng individuals who are at risk of being poor metabolizers.
14  belonging to the group of intermediate/poor metabolizers.
15  of the RUT-positive patients were extensive metabolizers.
16 d to identify participants as normal or slow metabolizers.
17 with severity of nicotine dependence in slow metabolizers.
18 zers, but depends on nicotine dose in normal metabolizers.
19  to smoking cues in normal and slow nicotine metabolizers.
20 therapy, with increased quit rates in slower metabolizers.
21 95% CI, 1.42 to 14.37) for ultrarapid CYP2D6 metabolizers.
22 concentrations observed in human CYP2D6 poor metabolizers.
23  12% (95% CI, 4%-20%) in CYP2C9 intermediate metabolizers, 12% (95% CI, 2%-24%) in CYP2C19 intermedia
24 46% (95% CI, 33%-61%) in CYP2C9 intermediate metabolizers, 20% (95% CI, 17%-30%) in CYP2C19 intermedi
25 aving option over DPYD intermediate and poor metabolizers (43 individuals) with mean QALYs of 4.18 (9
26                               DPYD extensive metabolizers (528 individuals) had greater effectiveness
27 nosis for breast cancer compared with normal metabolizers after receiving a standard dose of tamoxife
28                            Only slow ethanol metabolizers (alcohol dehydrogenase alleles [ADH1B*1] ca
29    Heterozygosity for the most frequent poor metabolizer allele (CYP2D6*4) was not associated with in
30                        Homozygosity for poor metabolizer alleles was found to be associated with AS.
31   Treatment-seeking smokers (N = 69; 30 slow metabolizers and 39 normal metabolizers) completed a vis
32 individuals predicted to be CYP2C9 extensive metabolizers and 8.7% of those predicted to be intermedi
33 over an otherwise stable community of public-metabolizers and cheats.
34  consortia has allowed uncultured syntrophic metabolizers and methanogens to be optimally grown and s
35  owing to the reduced growth rate of private-metabolizers and population bottlenecks that are frequen
36 12% (95% CI, 2%-24%) in CYP2C19 intermediate metabolizers, and 20% (95% CI, 2%-41%) in CYP2C19 poor m
37 0% (95% CI, 17%-30%) in CYP2C19 intermediate metabolizers, and 39% (95% CI, 24%-56%) in CYP2C19 poor
38 rs, and 20% (95% CI, 2%-41%) in CYP2C19 poor metabolizers; and for carbamazepine, by 12% (95% CI, 3%-
39               In contrast, ultrarapid CYP2D6 metabolizers are at risk for exaggerated response with p
40 dwater and wastewater treatment), syntrophic metabolizers are known to play an important role.
41                                  Poor CYP2D6 metabolizers are likely to experience an impaired respon
42 lects primarily non-nicotine effects in slow metabolizers, but depends on nicotine dose in normal met
43 egories was possible, and (3) 3 patients per metabolizer category were available.
44  (N = 69; 30 slow metabolizers and 39 normal metabolizers) completed a visual cue reactivity task dur
45                       Identification of fast metabolizers could be a strategy to improve graft surviv
46 eight gain among CYP2B6 slow or intermediate metabolizers could explain the increased weight gain on
47                              In STRIDE, slow metabolizer CYP2B6 and NAT2 genotypes were each associat
48 ma appears confined to individuals with slow metabolizer (CYP2C9*3) genotypes.
49 zers (defined as AS = 0.25-0.75) than normal metabolizer (defined as AS = 1-2) patients (1.44 vs. 0.2
50 os were significantly higher in intermediate metabolizers (defined as AS = 0.25-0.75) than normal met
51 ignificant interaction (n=5), and convergent metabolizers did have a significant interaction (n=15).
52                                    Divergent metabolizers did not have significant interaction (n=5),
53                                       Public-metabolizers digest resources externally, private-metabo
54                                         Poor metabolizers, either genotypic or due to phenocopying, a
55          We classified patients as extensive metabolizers (EM) or reduced metabolizers (RM) based on
56        Patients found to be CYP2D6 extensive metabolizers (EM) remained on 20 mg and those found to b
57                                         Slow metabolizers exhibited greater reductions in cravings af
58 -brain analysis, normal (compared with slow) metabolizers exhibited heightened abstinence-induced neu
59 compared between faster versus slower CYP2A6 metabolizers for the PWS signals in survival analyses.
60 fold difference in AUC between slow and fast metabolizers for the same dose.
61 s, and 39% (95% CI, 24%-56%) in CYP2C19 poor metabolizers; for valproate, by 12% (95% CI, 4%-20%) in
62  with weight gain (P = .009), with extensive metabolizers gaining the most weight, and with changes i
63 o 55 years, homozygous for CYP2C19 extensive metabolizer genotype, confined, standardized diet) was c
64 that LENS is associated with the CYP2B6 slow metabolizer genotype, with a median efavirenz plasma con
65 20 to 53 years; homozygous CYP2C19 extensive metabolizer genotype; no nicotine for 6 weeks, prescript
66                        Individuals with slow metabolizer genotypes in both genes had markedly elevate
67  DXA from baseline to week 48 between CYP2B6 metabolizer genotypes in the efavirenz arm, and with the
68                                         Slow-metabolizer genotypes were associated with increased cen
69 py in 58% with CYP2B6 and 93% with NAT2 slow metabolizer genotypes.
70 ed 10 extensive, 17 intermediate, and 7 slow metabolizer genotypes.
71 e observational cohort (n = 61), CYP2B6 slow metabolizers had greater weight gain after switch (P = .
72 the observational cohort (N=61), CYP2B6 slow metabolizers had greater weight gain after switch (p=0.0
73                               Slow efavirenz metabolizers had increased risk of hepatotoxicity.
74 linical trials cohort (n = 462), CYP2B6 slow metabolizers had lesser weight gain at week 48 among par
75  clinical trials cohort (N=462), CYP2B6 slow metabolizers had lesser weight gain at week 48 among par
76    Smokers in the first NMR quartile (slower metabolizers) had lower Fagerstrom Test for Nicotine Dep
77 tions in cravings after scanning than normal metabolizers; however, craving was unrelated to nAChR av
78 izer (NM) phenotype, 35% had an intermediate metabolizer (IM) phenotype, 5% had a poor metabolizer (P
79 om NADH are present in almost all syntrophic metabolizers, implicating their critical role in syntrop
80 eponema succinifaciens, a known carbohydrate metabolizer in swine.
81 as to determine the frequency of CYP2B6 slow metabolizers in participants with LENS.
82 ht gain was similar between CYP2B6 extensive metabolizers in the efavirenz arm and in the dolutegravi
83  Weight gain was similar in CYP2B6 extensive metabolizers in the efavirenz arm and in the dolutegravi
84 gradation remain unknown for many syntrophic metabolizers, including strain UI.
85 olizers digest resources externally, private-metabolizers internalize resources before digestion, and
86 d ecological experiments reveal that private-metabolizers invade and take over an otherwise stable co
87 r' or 'high-responsive' person, and the slow metabolizer is often more likely to experience drug toxi
88                                Considering 3 metabolizer levels (extensive, intermediate and slow), s
89      Genetic polymorphisms of CYP2C19, a PPI metabolizer may also affect eradication.
90  pulmonary function, and inefficient arsenic metabolizers may be at increased risk.
91                                       Normal metabolizers may benefit from adjunctive behavioral smok
92 ed closure times seen in extensive and rapid metabolizers (n = 16; p = 0.001).
93 le phenotype was predicted, 58% had a normal metabolizer (NM) phenotype, 35% had an intermediate meta
94 slow metabolizers (NMR < 0.26) and 12 normal metabolizers (NMR >/= 0.26)-underwent 2-(18)F-FA-PET bra
95                  Twenty-four smokers-12 slow metabolizers (NMR < 0.26) and 12 normal metabolizers (NM
96 YP2C19 allele carriers, but only 20% of poor metabolizers of clopidogrel had an escalation in the dos
97 their antiplatelet therapy, only 20% of poor metabolizers of clopidogrel had their antiplatelet thera
98 n treatment response between slow and normal metabolizers of nicotine.
99  species more widely, may be relatively poor metabolizers of penta-BDEs.
100              Both poor and ultrarapid CYP2D6 metabolizers of tamoxifen have a worse prognosis for bre
101 e (MRC) of Alphaproteobacteria as the likely metabolizers of TMA and provide genomic evidence that th
102 tion of cytochrome P450 enzymes, the primary metabolizers of xenobiotics in humans.
103 the recommended dose of a drug than a 'rapid metabolizer' or 'high-responsive' person, and the slow m
104 erences are often more than tenfold; a 'slow metabolizer' or 'low-responsive' individual might theref
105 y was significantly reduced in slow nicotine metabolizers (P = 0.04).
106 d hemoglobin A1c) compared with fast ethanol metabolizers (persons homozygous for ADH1B*2).
107 urrently used as biomarker to predict CYP2D6 metabolizer phenotype.
108 nantly CYP2C19 metabolized, enhanced vs poor metabolizer phenotypes were associated with a 2.52-fold
109 er a wide spectrum of different human CYP2D6 metabolizer phenotypes.
110 after referred to as phenotypic intermediate metabolizers [pIMs] or phenotypic poor metabolizers [pPM
111 te metabolizer (IM) phenotype, 5% had a poor metabolizer (PM) phenotype, and 2% had an ultrametaboliz
112 l or high CYP2D6 activity (phenotypic normal metabolizers [pNMs] and phenotypic ultrarapid metabolize
113 diate metabolizers [pIMs] or phenotypic poor metabolizers [pPMs]) had experienced pain-related ED vis
114 etabolizers [pNMs] and phenotypic ultrarapid metabolizers [pUMs]) (2.1% vs 1.8%; inverse probability-
115 stribution of fiber, protein, and amino acid metabolizers, reflected by higher detection of metabolit
116 ative affect in the whole sample, but normal metabolizers reported greater reductions of craving and
117 , smokers in the fourth NMR quartile (faster metabolizers) reported greater craving for cigarettes fo
118 5% among CYP2B6 normal and slow/intermediate metabolizers, respectively.
119 ts as extensive metabolizers (EM) or reduced metabolizers (RM) based on CYP2C19 genotype and evaluate
120       PS strain was enriched with propionate metabolizers, selenate reducers, and xylan, chitin, and
121  Patients with KCNH2 risk genotypes and slow metabolizer status (approximately 7% of patients) showed
122     There was no association between CYP2C19 metabolizer status (EM vs. RM) and the primary composite
123 -shaped association was found between CYP2D6 metabolizer status and breast cancer-specific mortality,
124                                         Slow metabolizer status and gene variants in KCNH2 associated
125     This study aims to investigate if CYP2D6 metabolizer status is associated with tamoxifen-related
126                                      CYP2C19 metabolizer status is not associated with the composite
127 risperidone compared with patients with fast metabolizer status or without the KCNH2 risk genotypes.
128 otic resistance nor CYP2C19 and CYP3A5 rapid metabolizer status was associated with eradication failu
129                      We investigated whether metabolizer status was associated with tamoxifen discont
130                  Additionally, faster CYP2A6 metabolizer status was associated with younger age of di
131 tion in cigarettes, but that irrespective of metabolizer status, reductions to <0.763 mg/cigarette ma
132 ticipants, and determine their antipsychotic metabolizer status.
133 atings depend on nicotine dose regardless of metabolizer status.
134 d as phenotypic normal, and not intermediate metabolizers, suggesting that phenotype classification i
135 n was enriched with sulfur oxidizers, sulfur metabolizers, sulfate reducers and naphthalene and aroma
136 hosting diverse syntrophic aromatic compound metabolizers (Syntrophus, Syntrophorhabdus, Pelotomaculu
137 inished effectiveness of clopidogrel in poor metabolizers, those having 2 loss-of-function alleles, h
138 (p > 0.05), while the cost of DPYD extensive metabolizers was significantly lower (p < 0.01) compared
139  intermediate, normal, and ultrarapid CYP2D6 metabolizers were -0.8 cm(2), -4.5 cm(2), -4.1 cm(2), an
140 , intermediate, normal and ultrarapid CYP2D6 metabolizers were 0.18 ng/ml, 0.38 ng/ml, 0.56 ng/ml and
141  intermediate, normal, and ultrarapid CYP2D6 metabolizers were 25.7%, 23.6%, 28.6%, and 44.4%, respec
142  intermediate, normal, and ultrarapid CYP2D6 metabolizers were 7.1%, 7.6%, 6.7%, and 18.8%, respectiv
143 els (extensive, intermediate and slow), slow metabolizers were at increased risk.
144 id-producers, mucin-degraders, and bile acid-metabolizers were consistently associated with reduced r
145                                         Fast metabolizers were defined by a C/D ratio < 1.05.
146 unced when extreme groups of slow and normal metabolizers were examined.
147 e found to be intermediate (IM) or poor (PM) metabolizers were increased to 40 mg daily.
148                            Ultrarapid CYP2D6 metabolizers were more likely than other groups to repor
149  those predicted to be intermediate and poor metabolizers were VKORC1 p.D36Y carriers who require mar
150 P = .001) increased significantly among slow metabolizers who consumed more than 3 cups per day.
151 nsider alternative treatment in CYP2C19 poor metabolizers who might receive clopidogrel and to identi
152                                         Slow metabolizers will experience more prolonged subtherapeut
153 AT2*14, but not NAT2*7, were found to be low metabolizers with high sensitivity to APA.
154 s were successfully genotyped as slow CYP2B6 metabolizers, with 6 participants additionally having CY
155 ductions of craving and withdrawal than slow metabolizers, with dose-dependent effects.
156   They suggest that normal and slow nicotine metabolizers would respond differently to nicotine reduc

 
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