ライフサイエンスコーパス: cocaine addict

1 ortem in the nucleus accumbens of male human cocaine addicts.

2 may reduce cue-induced relapse in abstinent cocaine addicts.

3 remediating deficits of cognitive control in cocaine addicts.

4 lds the potential to reduce relapse in human cocaine addicts.

5 ing cue-induced cocaine craving in abstinent cocaine addicts.

6 ts are determinants of relapse in recovering cocaine addicts.

7 nsistent with brain-imaging studies of human cocaine addicts.

8 mmetry in control subjects was absent in the cocaine addicts.

9 reatment of cue-induced relapse in drug-free cocaine addicts.

10 one concentrations in pregnant opiate and/or cocaine addicts.

11 cingulate and low frontal lobe activation in cocaine addicts.

12 ization therapies for cue-induced relapse in cocaine addicts.

13 In cocaine addicts, amygdala volume did not correlate with

14 ortem hippocampus of eight alcoholics, eight cocaine addicts and eight controls.

15 al nuclei isolated from post-mortem dlPFC of cocaine addicts and healthy controls.

16 Brain activity was measured in cocaine addicts and healthy subjects by functional magne

17 tomography (PET) to compare the responses of cocaine addicts and normal controls to intravenous methy

18 ampal gene expression changes common to both cocaine-addicted and alcoholic individuals that may refl

19 the cognitive and olfactory deficits seen in cocaine addicts, and further suggest that adult-generate

20 s increase the risk of relapse in recovering cocaine addicts are not well understood.

21 xcitability, or sensitization, is present in cocaine addicts as a consequence of repeated cocaine use

22 llowing cocaine exposure are responsible for cocaine-addicted behaviors, the underlying molecular mec

23 ostasis is a key adaptation occurring in the cocaine-addicted brain, but the effect of cocaine on the

24 ortant contributors to relapse in recovering cocaine addicts, but the mechanisms by which they influe

25 thy controls, we hypothesized and found that cocaine-addicted carriers of a 9R-allele exhibited highe

26 Clinical observations imply that female cocaine addicts experience enhanced relapse vulnerabilit

27 ral and neurochemical processes occurring in cocaine-addicted humans [1].

28 uding self-administration, and in the NAc of cocaine-addicted humans.

29 ls testing positive for cocaine in urine, 26 cocaine addicted individuals testing negative for cocain

30 Sixteen cocaine addicted individuals testing positive for cocain

31 d behavioral dependent variables in 73 human cocaine-addicted individuals and 47 healthy controls, we

32 e demonstrate fMRI response to drug words in cocaine-addicted individuals in mesencephalic regions as

33 nd that D2 receptor dysfunction in abstinent cocaine addicts may, in part, be determined by premorbid

34 However, to procure such drugs as cocaine, addicts often require considerable ingenuity an

35 lutamate-glutamine levels in the striatum of cocaine-addicted participants (n = 15) compared with hea

36 Here we report on impairments in cocaine-addicted patients to act purposefully toward a g

37 ted in 1986 that cue-induced drug craving in cocaine addicts progressively increases over the first s

38 these findings to previous studies in human cocaine addicts strongly suggest that the increased dens

39 as increased in several brain regions of the cocaine addicts studied 1-4 days after their last use of

40 olic responses (marker of brain function) of cocaine-addicted subjects (n = 21) and controls (n = 15)

41 e volumes of the amygdala and hippocampus in cocaine-addicted subjects and matched healthy controls a

42 The cocaine-addicted subjects demonstrated bilateral activat

43 y heightened activation with procaine in the cocaine-addicted subjects is similar to the pattern of i

44 The findings for the cocaine-addicted subjects may thus represent evidence of

45 with salience attribution and motivation) in cocaine-addicted subjects may underlie the strong emotio

46 by intravenous methylphenidate (a drug that cocaine-addicted subjects report to be similar to cocain

47 After receiving placebo, the cocaine-addicted subjects showed markedly lower rCBF in

48 We tested eighteen cocaine-addicted subjects using positron emission tomogr

49 of DeltaFosB and CaMKII in the NAc of human cocaine addicts, suggesting possible targets for future

50 nce) showed expression changes in alcoholics/cocaine addicts; these factors included genes involved i

51 Following the scans, the cocaine-addicted volunteers performed cocaine self-admin

52 s also precipitates drug-seeking behavior in cocaine addicts, we also postulated that cocaine manifes

53 Cocaine addicts were randomized to receive vigabatrin 30

54 that specific brain regions become active in cocaine addicts when they are exposed to cocaine stimuli