ライフサイエンスコーパス: cocaine abuse

1 tial therapeutic utility in the treatment of cocaine abuse.

2 reatments (behavioral and pharmacologic) for cocaine abuse.

3 r an effective strategy for the treatment of cocaine abuse.

4 potential agents for the pharmacotherapy of cocaine abuse.

5 ns as potential therapy for the treatment of cocaine abuse.

6 dictive or withdrawal states associated with cocaine abuse.

7 3R-selective antagonists to clinical use for cocaine abuse.

8 te to these long-term neural consequences of cocaine abuse.

9 B gene products as important determinants of cocaine abuse.

10 cept of dopamine system involvement in human cocaine abuse.

11 humans and the dysregulation is enhanced by cocaine abuse.

12 sporter with a postulated therapeutic use in cocaine abuse.

13 try of the brain are associated with chronic cocaine abuse.

14 linical utility, especially for treatment of cocaine abuse.

15 in the setting of cocaine detoxification or cocaine abuse.

16 tion would reduce both cigarette smoking and cocaine abuse.

17 ment of active vaccines for the treatment of cocaine abuse.

18 t the SHR phenotype models comorbid ADHD and cocaine abuse.

19 rapy would reduce both cigarette smoking and cocaine abuse.

20 t did not have an impact on vulnerability to cocaine abuse.

21 accumbens in an adult mouse model of chronic cocaine abuse.

22 e adhesion and trafficking is exacerbated by cocaine abuse.

23 sent with these conditions in the setting of cocaine abuse.

24 AMPA receptors as promising targets against cocaine abuse.

25 on is associated with high susceptibility to cocaine abuse.

26 e mechanisms in a search for medications for cocaine abuse.

27 plicated in stress responses and stress with cocaine abuse.

28 rther support for the dopamine hypothesis of cocaine abuse.

29 necessary for a pharmacotherapy for treating cocaine abuse.

30 al pharmacotherapeutics for the treatment of cocaine abuse.

31 alues for confirmative conclusions regarding cocaine abuse.

32 el approach toward designing medications for cocaine abuse.

33 om which to design potential medications for cocaine abuse.

34 nd increased oxidative stress resulting from cocaine abuse.

35 ne and as a potential therapeutic target for cocaine abuse.

36 s to discover pharmacological treatments for cocaine abuse.

37 roteins that is excessively exacerbated with cocaine abuse.

38 lutamatergic neurotransmission in relapse to cocaine abuse.

39 ght be targeted as a potential treatment for cocaine abuse.

40 ld be used as a maintenance therapy to treat cocaine abuse.

41 ram to develop site-specific medications for cocaine abuse, a series of 2-(aminomethyl)-3-phenylbicyc

42 for long-acting agents for the treatment of cocaine abuse, a series of optically pure hydroxylated d

43 conditions, commonly associated with chronic cocaine abuse, altered BLA-to-mPFC synaptic transmission

44 ne (DA) D2/D3 receptors and vulnerability to cocaine abuse, although most research has used males.

45 indicate that HS is a resilience factor for cocaine abuse and a novel therapeutic target for the tre

46 r-based vaccine may be effective in treating cocaine abuse and addiction.

47 Cocaine abuse and attention deficit/hyperactivity disord

48 tors that may be useful for the treatment of cocaine abuse and certain neurological disorders.

49 Cocaine abuse and dependence is a major public health pr

50 ines progress being made in the treatment of cocaine abuse and dependence, with a particular focus on

51 anism of HIV associated neuropathogenesis in cocaine abuse and how it accelerates the energy sensor A

52 y to establish a causal relationship between cocaine abuse and lower VMAT2.

53 potential probes for the pharmacotherapy of cocaine abuse and may also open new avenues for the char

54 the development of a pharmacotherapeutic for cocaine abuse and other disorders affecting the dopamine

55 With 2 exceptions (cocaine abuse and stimulant dependence), twin resemblanc

56 er understand the role of serotonin (5HT) in cocaine abuse and treatment, we examined the effects of

57 urrently being evaluated in animal models of cocaine abuse and will provide an important tool with wh

58 mine storage vesicles in response to chronic cocaine abuse and/or a loss of dopaminergic terminals.

59 (CUs) (52 with cocaine dependence and 3 with cocaine abuse) and 56 healthy individuals serving as con

60 tral to understanding DA function in health, cocaine abuse, and disease.

61 essential neuromodulatory roles of TAAR 1 on cocaine abuse, and suggest that TAAR 1 may represent a n

62 al avenue for developing new medications for cocaine abuse, and support the hypothesis that neuron-gl

63 Nicotine dependence and cocaine abuse are major public health problems, and most

64 Nicotine dependence and cocaine abuse are major public health problems, and most

65 oing mouse studies of a proposed therapy for cocaine abuse based on viral gene transfer of butyrylcho

66 e may not be useful for treatment of ongoing cocaine abuse but may be useful in relapse prevention.

67 ies of a biological therapeutic for treating cocaine abuse but requires additional development to imp

68 therapy may offer a promising means to treat cocaine abuse by aiding in the prevention of relapse.

69 Cocaine abuse can result in stroke, neuroischemia, and c

70 ural and declarative memory functioning in a cocaine-abusing cohort in the 45-day period following us

71 of nasal mucus as a biological specimen for cocaine abuse confirmation has been proposed as an alter

72 Comorbidities between cocaine abuse, depression, and anxiety support the devel

73 Cocaine abuse disrupts dopamine system function, and red

74 ous administration more closely mimics human cocaine abuse during pregnancy.

75 ssion analysis revealed that the alcohol and cocaine abuse group had a higher likelihood of associate

76 Cocaine abuse has been implicated in multiple cardiovasc

77 Maternal cocaine abuse has several deleterious effects in the new

78 he benztropine analogues in animal models of cocaine abuse has suggested that these two classes of tr

79 Cocaine abuse hastens the neurodegeneration often associ

80 tly used pharmacological agents for treating cocaine abuse have proved inadequate, leaving few treatm

81 parison of their effects in animal models of cocaine abuse have provided insight into the complex rel

82 imen consistent with exposure to the drug by cocaine-abusing HIV-infected patients to determine the e

83 iated with HIV-1 infection is exacerbated in cocaine-abusing, HIV+ individuals.

84 nced HIV-1 infection is often exacerbated in cocaine-abusing, HIV-infected patients.

85 s have confirmed this observation in chronic cocaine-abusing humans.

86 extension, microglial activation in chronic cocaine-abusing humans.

87 tial therapeutic option for the treatment of cocaine abuse in humans.

88 phenidate, does not enhance vulnerability to cocaine abuse in SHR and may represent an important alte

89 have therefore been optimized for assessing cocaine abuse in urine by monitoring the fluorescence qu

90 actors for psychostimulant, amphetamine, and cocaine abuse include dopamine (DA) receptor polymorphis

91 Cocaine abuse increases the risk of life-threatening neu

92 One aspect of immunopharmacotherapy for cocaine abuse involves the use of a catalytic monoclonal

93 Cocaine abuse is a large social and economic problem tha

94 Cocaine abuse is a major medical and public health conce

95 Cocaine abuse is a world-wide public health and social p

96 Cocaine abuse is frequently associated with cerebrovascu

97 Except where otherwise indicated, the term cocaine abuse is used in this article in a generic sense

98 on of alpha-synuclein protein with long-term cocaine abuse may put addicts at increased risk for deve

99 ain metabolism were significantly greater in cocaine-abusing (mean = 21%, SD = 13%) than in compariso

100 rther design of new leads for development of cocaine abuse medication as well as certain neurological

101 esign of the new leads in the discovery of a cocaine abuse medication.

102 sidered as lead structures in the search for cocaine abuse medications.

103 oholics, either exclusively (n = 10) or with cocaine abuse (n = 30), and a matched comparison group o

104 Cocaine abuse occurs in 40% to 60% of patients entering

105 e (N = 38), alcohol abuse only (N = 38), and cocaine abuse only (N = 25)--consecutively admitted to a

106 ulomatosis, natural killer/T-cell lymphomas, cocaine abuse, or infections.

107 al mechanisms for white matter disruption in cocaine abuse patients is complicated by polydrug use an

108 Previous studies from human cocaine abuse patients show disruption of white matter a

109 e to the cerebrovascular insults observed in cocaine-abused patients.

110 Eighty-nine cocaine-abusing patients underwent 2 weeks of substance

111 h may be exploited toward the discovery of a cocaine-abuse pharmacotherapeutic.

112 d suggests JHW007 as a lead for discovery of cocaine-abuse pharmacotherapeutics.

113 ogs and may be used in future drug design of cocaine abuse pharmacotherapies.

114 e had limited success in clinical trials for cocaine abuse, possibly due to neurobiological changes t

115 onin-1B receptors (5-HT(1B)Rs) in modulating cocaine abuse-related behaviors has been controversial d

116 esolimbic 5-HT(1B)Rs differentially modulate cocaine abuse-related behaviors, with a facilitative inf

117 ms for mediating serotonergic attenuation of cocaine abuse-related neurochemical and behavioral effec

118 Cocaine abuse remains a public health concern for which

119 Chronic cocaine abuse remains a serious and costly public health

120 Future studies on the effects of cocaine abuse should control for the effects of gender-s

121 Cocaine abuse significantly increases the risk of ischem

122 Thirteen current cocaine-abusing subjects and 14 comparison subjects were

123 s striatal dopamine transporter levels in 28 cocaine-abusing subjects and 24 comparison subjects matc

124 in striatal V3" values in acutely abstinent cocaine-abusing subjects relative to comparison subjects

125 The enhanced sensitivity to lorazepam in cocaine-abusing subjects suggests disruption of GABA pat

126 administration were significantly higher in cocaine-abusing subjects than in comparison subjects, th

127 vations in striatal dopamine transporters in cocaine-abusing subjects than noted in previous postmort

128 Lorazepam-induced sleepiness in cocaine-abusing subjects was intense and was significant

129 ered in acutely (96 hours or less) abstinent cocaine-abusing subjects, as suggested by postmortem stu

130 oncentrations in comparison subjects than in cocaine-abusing subjects, lorazepam-induced decrements i

131 ed responses to sedative hypnotics in active cocaine-abusing subjects.

132 uthors hypothesized GABA-ergic disruption in cocaine-abusing subjects.

133 he preparation of potential extended-release cocaine-abuse therapeutic agents afforded a series of co

134 fication and formulation as extended-release cocaine-abuse therapeutic agents.

135 a new target for medication development for cocaine abuse treatment.

136 hese compounds may provide leads for a novel cocaine-abuse treatment.

137 cocaine and the ultimate identification of a cocaine-abuse treatment.

138 ere diagnostic for assigning subjects to the cocaine-abusing vs control cohort.

139 ], 3.24-7.55), but not with ischemic stroke; cocaine abuse was associated with hemorrhagic (OR, 2.33;

140 ytosis caused by levamisole exposure through cocaine abuse was first described in 2009.

141 Amphetamine, but not cocaine, abuse was associated with a higher risk of deat

142 Using a rodent model of cocaine abuse, we found long-lasting, possibly permanent

143 nts that might be useful in the treatment of cocaine abuse, we have chosen to re-explore a class of m

144 T2 findings and attribute VMAT2 reduction to cocaine abuse, we imaged four rhesus monkeys with [(11)C