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1 ula on the dorsolateral prefrontal cortex in cocaine users.
2 Is within the drug-cue processing network in cocaine users.
3 ications for the male descendants of chronic cocaine users.
4 nd decreases daytime sleepiness in abstinent cocaine users.
5 l on sleep and daytime sleepiness in chronic cocaine users.
6 tion may underlie compulsive drug seeking in cocaine users.
7 yet been evaluated in general populations of cocaine users.
8 to the dopamine transporter (DAT) in chronic cocaine users.
9 trates as naturally evocative stimuli in the cocaine users.
10 ions with projections to the frontal lobe in cocaine users.
11 y (BA 10), but this pattern did not exist in cocaine users.
12 hrine transporter function in active chronic cocaine users.
13 n was significantly reduced by 22% in active cocaine users (0.109 +/- 0.017 min-1), as compared to no
14 oung asymptomatic and abstinent (> 5 months) cocaine users (34 male and 30 female) and 58 healthy com
15                                        Among cocaine users, 34 of 112 (30.4%) had CAAs compared with
16 neural response differences among 42 current cocaine users, 35 former cocaine users, and 47 healthy s
17 infarction was common in both groups (45% of cocaine users, 38% of control patients).
18 quent history of myocardial infarction among cocaine users, 48% had nonobstructive coronary artery di
19 ional cocaine-word Stroop to 27 recreational cocaine users, 50 stimulant-dependent individuals, and 5
20 ned from heroin and 52% (3941/7636) of crack cocaine users abstained from crack cocaine.
21  outcome, where former compared with current cocaine users activated ventral tegmental area more robu
22 tylcholine and nitroprusside in 10 long-term cocaine users and 13 control subjects of similar age who
23                                      Sixteen cocaine users and 16 controls completed a similar intera
24                           Forty male regular cocaine users and 51 male control subjects underwent a f
25                       In study I, 80 regular cocaine users and 63 healthy controls completed an inter
26  protein was tested in striatal samples from cocaine users and age-, sex-, and postmortem interval-ma
27  postmortem neuropathological specimens from cocaine users and age-matched drug-free control subjects
28 king did not explain the differences between cocaine users and control subjects.
29 n, there was no difference (p = 0.2) between cocaine users and control subjects.
30  to compare periodontal status between crack cocaine users and crack cocaine non-users and investigat
31 s in the frontal cortex and striatum of nine cocaine users and nine matched control subjects who had
32 mparison brain regions of 14 detoxified male cocaine users and six cocaine-naive comparison subjects
33 t robust reduction observed to date in human cocaine users and the first to involve mechanisms other
34 human subjects who had been ethanol users or cocaine users and then compared to those of a matched gr
35 es among 42 current cocaine users, 35 former cocaine users, and 47 healthy subjects who also complete
36 lusion, basic social interaction deficits in cocaine users as observed here may arise from altered so
37 fmol bound/microg protein (SD = 2.8) for the cocaine users but only 6.0 (SD = 1.7) for the comparison
38                                           In cocaine users, but not in control subjects, skin conduct
39 DAT binding sites were markedly increased in cocaine users, but, paradoxically, medial DAT messenger
40 e investigated basal social gaze behavior in cocaine users by applying behavioral, psychophysiologica
41 ether these data suggest that, when engaged, cocaine users can mobilize their executive control syste
42 l complex were elevated threefold in chronic cocaine users compared with normal age-matched subjects.
43 or psychosocial treatment in heroin or crack cocaine users compared with users of both drugs.
44 rticipants included 56 non-treatment-seeking cocaine users (CUs) (52 with cocaine dependence and 3 wi
45  pure recreational users (RCU) and dependent cocaine users (DCU) display alterations of PPI, startle
46                                              Cocaine users display a wide range of cognitive impairme
47                                              Cocaine users displayed a marked reduction in VMAT2 immu
48           In response to social interaction, cocaine users displayed decreased activation of the medi
49 ts without ulcers to report sex with a crack cocaine user, exchange of money or drugs for sex, and mu
50                During the cocaine video, the cocaine users experienced craving and showed a pattern o
51                    Relative to the controls, cocaine users had a lower ventral striatal BOLD response
52                                          The cocaine users had significantly lower dopamine levels an
53             The present results confirm that cocaine users have a high number of dopamine transporter
54 al brain activity and associated behavior in cocaine users; however, the neural systems-level effects
55 triatal connectivity is disrupted in chronic cocaine users in a baseline (resting) state.
56                   More than three fourths of cocaine users in the United States are exposed to levami
57 anatomical circuitry; instead, unique to the cocaine user is the ability of learned, drug-related cue
58                    The hypothesis that human cocaine users lose vesicular monoamine transporter (VMAT
59                                        Human cocaine users lose VMAT2 protein, which might reflect da
60 levels of impulsive choice observed in human cocaine users may be due in part to long-term effects of
61 ]DTBZ binding was significantly lower in the cocaine users (mean = 330 nCi/mg, SD = 42) than in the c
62  sensitivity to aversive conditioned cues in cocaine users might be a risk factor for stress-relief c
63 92 (n = 1382) and all hyperthermia deaths of cocaine users (n = 10) were used to identify a maximum d
64 lected during autopsy examination from human cocaine users (n = 34) and from age-, sex-, and race-mat
65         To address these issues, experienced cocaine users (N=17) and comparison subjects (N=14) unde
66   Subjects included 64 non-treatment-seeking cocaine users (NTSCUs) and 67 healthy control subjects a
67       After withdrawal from cocaine, chronic cocaine users often experience persistent reduction in t
68                              Further, in the cocaine users only, these increased drug-related mesence
69 al words, activated the mesencephalon in the cocaine users only.
70                                           In cocaine users, PPI was positively correlated with cumula
71                      Whereas the majority of cocaine users quit as they experience the negative conse
72 ul NOGOs and errors of commission in chronic cocaine users relative to cocaine-naive controls.
73                               Both groups of cocaine users scored higher than control subjects on imp
74 fferent eye-contact conditions revealed that cocaine users show diminished emotional engagement in so
75                                      Current cocaine users show little evidence of cognitive impairme
76                 During cocaine-cue exposure, cocaine users showed a particular feed-forward effective
77 contrary to the effects of the cocaine film, cocaine users showed a smaller response than the compari
78                                              Cocaine users showed hyperresponsiveness of the amygdala
79                               Active chronic cocaine users showed small areas of abnormal blood flow
80 ng to the serotonin transporter was lower in cocaine users than in comparison subjects.
81 lcholine infusion was significantly lower in cocaine users than in control subjects (p = 0.02).
82 ites were significantly more numerous in the cocaine users: the mean Bmax value was 9.0 fmol bound/mi
83 we investigated the prevalence of CAAs among cocaine users undergoing coronary angiography.
84 he cocaine film (population specificity) and cocaine users viewing the nature film (content specifici
85                  The prevalence of CAA among cocaine users was higher than expected (30.4%), given su
86       After observing CAAs in multiple young cocaine users, we investigated the prevalence of CAAs am
87      The increased protein levels in chronic cocaine users were accompanied by changes in the express
88          AMs from marijuana smokers and from cocaine users were also severely limited in their abilit
89                      Compared with nonusers, cocaine users were more likely to be male (87% vs 67%, P
90 le volunteers and nine female active chronic cocaine users were studied.
91                                              Cocaine users were young (mean age, 44 years), predomina
92 se that showed significant activation in the cocaine users when viewing the cocaine film.
93 mine uptake sites in the striatum of chronic cocaine users, which might contribute to cocaine withdra
94 cocaine film than during the sex film in the cocaine users, which suggests that cocaine cues activate
95  mol/liter), we studied a second group of 10 cocaine users with angiographically normal or near-norma
96 osis, all of which have been demonstrated in cocaine users with myocardial infarction.
97       This diagnosis should be considered in cocaine users with severe chest pain.
98                                    Long-term cocaine users with the low-repeat MAOA allele have enhan

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