ライフサイエンスコーパス: THC

1 THC administration to pregnant mice in a restricted time

2 THC and alcohol use were quantified as average exposure

3 THC and CP55,940 promoted CB1 internalization and decrea

4 THC exposure increased the likelihood of acquiring the n

5 THC is thought to produce the main psychoactive effects

6 THC was significantly higher among Hispanics than for wh

7 THC was significantly higher for Hispanics than whites (

8 THC-COOH was rapidly removed from both deionized (DI) wa

9 oil concentration range of 0.2-5.5 mg.L(-1) (THC, C5-C36) after which they were subjected to a 25-day

10 e-experienced male cynomolgus monkeys (N=4), THC SA was examined under a second-order schedule of rei

11 l effects of marijuana (0.00, 1.98, or 3.56% THC) to dronabinol (0, 10, or 20 mg).

12 o capsules and smoked active marijuana (5.6% THC) at six timepoints.

13 ave now synthesized a series of (-)-Delta(8)-THC analogues encompassing a carboxyester group within t

14 the 2'-position on a series of (-)-Delta(8)-THC analogues.

15 yl)phe nol], and HU-210 [11-hydroxy-Delta(8)-THC-dimethylheptyl] were biased toward cAMP inhibition.

16 smoked cannabis (0.01 (inactive), 5.30-5.80% THC).

17 where Delta(9)-tetrahydrocannabinol (Delta(9)THC) is metabolized to only one major active metabolite,

18 , and efficacy greater than those of Delta(9)THC.

19 Delta(9)-THC (0.03 mg/kg) reduced evoked power during 40 Hz stimu

20 Delta(9)-THC (0.03 mg/kg) reduced intertrial coherence (ITC) in t

21 ing which they received intravenous Delta(9)-THC (placebo, .015 and .03 mg/kg) in a double-blind, ran

22 ing which they received intravenous Delta(9)-THC (placebo, 0.015, and 0.03 mg/kg) in a double-blind,

23 ocannabinol (THC), 11-nor-9-carboxy-Delta(9)-THC (THC-COOH) and 11-hidroxy-Delta(9)-THC (THC-OH) in m

24 ta(9)-THC (THC-COOH) and 11-hidroxy-Delta(9)-THC (THC-OH) in milk, liver and hemp seeds based on liqu

25 nt users of cannabis showed blunted Delta(9)-THC effects on ITC and evoked power.

26 ocampal neurons induced by repeated Delta(9)-THC exposures.

27 id plaques and neurodegeneration by Delta(9)-THC in Alzheimer's disease animals are retained in the p

28 Delta(9)-THC increased neural noise in a dose-related manner.

29 at produced psychosis-like effects, Delta(9)-THC increased neural noise in humans in a dose-dependent

30 The acute, dose-related effects of Delta(9)-THC on Lempel-Ziv complexity and signal power were studi

31 In addition, Delta(9)-THC reduced total signal power during both active drug c

32 Both AM1710 and Delta(9)-THC suppressed established paclitaxel-induced allodynia

33 ord following 7 d of treatment with Delta(9)-THC was absent in S426A/S430A mutants.

34 h as Delta(9)-tetrahydrocannabinol (Delta(9)-THC) can produce tolerance, physical withdrawal, and unw

35 ts of Delta-9-tetrahydrocannabinol (Delta(9)-THC) on the auditory steady-state response (ASSR) were s

36 tered delta-9-tetrahydrocannabinol (Delta(9)-THC), have delayed tolerance to Delta(9)-THC, and showed

37 L., Delta(9)-tetrahydrocannabinol (Delta(9)-THC), led to the identification of at least 100 addition

38 ast, Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the major psychoactive component of cannabis, prod

39 ts of delta-9-tetrahydrocannabinol (Delta(9)-THC), the principal active constituent of cannabis.

40 nist Delta(9)-tetrahydrocannabinol (Delta(9)-THC).

41 for predicting the binding modes of Delta(9)-THC, and endogenous and synthetic cannabinoids.

42 (9)-THC), have delayed tolerance to Delta(9)-THC, and showed increased dependence for Delta(9)-THC.

43 In contrast to Delta(9)-THC, chronic administration of AM1710 did not engage CB1

44 disorganization symptoms induced by Delta(9)-THC, which was independent of total signal power.

45 Delta(9)-THC-induced downregulation of CB1R in the spinal cord wa

46 oise were related with increases in Delta(9)-THC-induced psychosis-like symptoms but not negative-lik

47 the prototypic classic cannabinoid Delta(9)-THC.

48 total scores under the influence of Delta(9)-THC.

49 e to the psychotomimetic effects of Delta(9)-THC.

50 and showed increased dependence for Delta(9)-THC.

51 rt, following an oral dose of either delta-9-THC (10 mg) or placebo, while they performed a fear-proc

52 ntially modulated by single doses of delta-9-THC and CBD and that this relates to the processing of s

53 Relative to the placebo condition, delta-9-THC and CBD had opposite effects on the functional conne

54 frontal connectivity was enhanced by delta-9-THC and reduced by CBD.

55 modulation of amygdalar function by delta-9-THC and the extent of these effects are related to local

56 Relative to the placebo condition, delta-9-THC induced anxiety and modulated right amygdala activat

57 Delta-9-THC reduced fronto-striatal connectivity, which was rela

58 ve found that chronic treatment with delta-9-THC selectively decreases dendritic morphology and spine

59 nce of delta-9-tetrahydrocannabinol (delta-9-THC) and cannabidiol (CBD), the two major derivatives of

60 cts of delta-9-tetrahydrocannabinol (delta-9-THC), the main psychoactive ingredient of cannabis, on a

61 RI) following oral administration of delta-9-THC, CBD, or a placebo capsule.

62 were extracted, using either 1% citric acid (THC) or water (THW), had a good foaming capacity (32-36%

63 al phenolics (TP) and hydroxycinnamic acids (THC).

64 Acute THC administration causes increased dopamine release and

65 In addition, THC administration induced an increase in seizure suscep

66 In addition, THC treatment also caused alternative promoter usage and

67 eys trained to intravenously self-administer THC.

68 that induction of BDNF following adolescence THC exposure may serve as a homeostatic response geared

69 2-AG, AEA, THC, and WIN55,212-2 also activated Galpha(q)-dependent

70 ntly correlated with lower performance after THC.

71 In this system, 2-AG, THC, and CP55,940 were more potent mediators of arrestin

72 cket may accommodate the cannabinoid agonist THC.

73 c Meridional Overturning Circulation (AMOC), THC, and climatic shifts by contributing a component of

74 mproved cell viability, whereas CP55,940 and THC displayed beta-arrestin1 bias and reduced CB1 protei

75 icits in cerebellar function in Cb1(-/-) and THC-withdrawn mice.

76 Recent reports suggest that CBD and THC elevate the levels of the endocannabinoid anandamide

77 ndividual and interactive effects of CBD and THC.

78 ydrocannabinol (THC), cannabidiol (CBD), and THC+CBD (1:1), and compared between wild-type and HD cel

79 Here we compare attenuation of nicotine and THC reinforcement and reinstatement in squirrel monkeys

80 d AM4113 reduced two effects of nicotine and THC that play major roles in tobacco and marijuana depen

81 ng and abuse-related effects of nicotine and THC, but their clinical use is hindered by potentially s

82 NMOG and THC emissions displayed a pronounced minimum with midlev

83 fects of CP 55 940 (1.0-10 mug/kg, i.v.) and THC (3.0-300 mug/kg, i.v.) on food-maintained responding

84 We evaluated the impact of topically applied THC on DNFB-mediated allergic contact dermatitis in wild

85 noids that are beta-arrestin-biased--such as THC found at high levels in modern varieties of marijuan

86 of naturally occurring CB1 ligands, such as THC, and synthetic cannabinoids.

87 lta(9)-tetrahydrocannabinol derivatives (azo-THCs) from a central building block 3-Br-THC.

88 As such, azo-THCs enable CB1-mediated optical control of inwardly rec

89 Associations between THC use and progression to significant fibrosis were ass

90 we show that at least three human FABPs bind THC and CBD and demonstrate that THC and CBD inhibit the

91 Both THC and CBD, as well as other cannabinoid molecules, are

92 azo-THCs) from a central building block 3-Br-THC.

93 ressions of many transcripts were altered by THC in both total lymph node cells and CD4(+) T cells.

94 tion and acetylation regions were altered by THC.

95 dissociate the cognitive deficits induced by THC from its beneficial antinociceptive properties.

96 te strand of CD27 and Appbp2 were induced by THC.

97 ariants that are differentially regulated by THC in super antigen-activated lymph node cells and CD4(

98 own to induce apoptosis, was up-regulated by THC.

99 d miR-374b/421 cluster was down-regulated by THC.

100 ic features was not altered significantly by THC, suggesting that THC activates the expression of a s

101 o major metabolites of THC, 11-nor-9-carboxy-THC and 11-hydroxy-THC, in active users and particularly

102 Acute and chronic THC intake produces a spectrum of biological effects ran

103 Here, we show that chronic THC administration to SIV-infected macaques induced an a

104 ption of the ocean thermohaline circulation (THC) system during the MPT between marine isotope stages

105 changes in global thermohaline circulation (THC).

106 inpatient morality and total hospital costs (THC).

107 ghtly correlated with total hemocyte counts (THCs) and can be manipulated by raising or lowering THC.

108 Cumulative THC use was not associated with fibrosis progression (HR

109 Chronic Delta9-THC administration to uninfected macaques significantly

110 Cannabinoids including Delta9-THC attenuated intestinal inflammation in mouse colitis

111 e if the anti-inflammatory effects of Delta9-THC involved differential microRNA (miRNA) modulation, w

112 tine of uninfected macaques receiving Delta9-THC (n=3) and SIV-infected macaques administered either

113 ues with Delta9-tetrahydrocannabinol (Delta9-THC) increased survival and decreased viral replication

114 ation of Delta9-tetrahydrocannabinol (Delta9-THC) inhibited viral replication and intestinal inflamma

115 table reader system and smartphone to detect THC in saliva using competitive assays.

116 roach for the synthesis of 1,3-disubstituted THCs.

117 ls, Somerset, NJ, USA), Marinol (dronabinol; THC; AbbVie, Inc., North Chicago, IL, USA), and Sativex

118 r with distinct cannabinoid compounds (i.e., THC and CBD).

119 The identity of embryonic THC neuronal targets was determined by a Cre-mediated, l

120 e model based on host (DISC1) X environment (THC administration) interaction, we aimed at studying th

121 food samples obtaining positive results for THC in hemp seeds (average 0.82mugg(-1)) and three brand

122 This work facilitates on-site screening for THC and shows potential for testing of other small molec

123 emonstrate that parental history of germline THC exposure affects the molecular characteristics of th

124 adult offspring as a consequence of germline THC exposure.

125 d is characterized by continued weak glacial THC.

126 y-Delta(9)-tetrahydrocannabinol glucuronide (THC-COO-glu).

127 Furthermore, compared to the VEH/SIV group, THC selectively upregulated the expression of miR-10a, m

128 itrogen oxides (NOx), and total hydrocarbon (THC) decrease by 60%-70% from 2010 to 2030, as older veh

129 her alcohol fuels, while total hydrocarbons (THC) and nitrogen oxides (NOx) did not show strong fuel

130 ne organic gases (NMOG), total hydrocarbons (THC), methane, ethene, acetaldehyde, formaldehyde, ethan

131 riteria pollutants, NO2, total hydrocarbons (THC), n-alkanes, branched alkanes, saturated cycloalkane

132 of THC, 11-nor-9-carboxy-THC and 11-hydroxy-THC, in active users and particularly in people exposed

133 e from 65% in vehicle-exposed rats to 94% in THC-exposed rats.

134 non-coding RNAs was dramatically altered in THC-treated mice.

135 55,212-2 self-administration was enhanced in THC-exposed rats relative to vehicle-exposed controls.

136 t a role for differential miRNA induction in THC-mediated suppression of intestinal inflammation.

137 essed, miRNA-690 was highly overexpressed in THC-MDSCs ( approximately 16-fold).

138 rebellar molecular layer plays a key role in THC-induced cerebellar deficits.

139 ly, miR-99b was significantly upregulated in THC-treated SIV-infected macaques and confirmed to direc

140 CBD was not a CB1 agonist but inhibited THC-dependent signaling (THC+CBD).

141 nd can be manipulated by raising or lowering THC.

142 heme, we have optimized the assay to measure THC in the range from 0 to 50 ng/mL, covering most cutof

143 Measured THC emissions from most vehicles stayed below the legal

144 Next, THC was administered daily to monkeys until tolerance de

145 le range, 6-17) years, 324 (56%) reported no THC use, 141 (25%) less than weekly use, 70 (12%) weekly

146 and model specific; emission trends for NOx, THC, and NMOG will not be the same for all FFVs.

147 chanism of the anti-inflammatory activity of THC and the role of CB1 and CB2 receptors.

148 Whether the immunomodulatory activity of THC is mediated by epigenetic regulation has not been in

149 tory preparation comprising equal amounts of THC and cannabidiol (CBD)) to mice bearing BRAF wild-typ

150 sensitive enough to detect trace amounts of THC in oral fluids.

151 However, the cutoff concentration of THC that causes impairment is still controversial, and c

152 ) than cannabis with lower concentrations of THC.

153 ped for the synthesis of novel conjugates of THC with alanine (2a), isoleucine (2b), proline (2c), va

154 Consequences of THC exposure were reminiscent of those elicited by CB1 r

155 All the derivatives of THC exhibited more potent anti-microbial activity than T

156 al experiments in rats, URB694 was devoid of THC-like or nicotine-like interoceptive effects under dr

157 t rats were treated with increasing doses of THC (or its vehicle) twice/day for 11 consecutive days (

158 technology to examine the in vivo effect of THC on global histone methylation in lymph node cells of

159 Electrophysiological effect of THC was evaluated using acute hippocampal slices, and hi

160 in the beneficial antinociceptive effects of THC and its detrimental amnesic properties.

161 Many of the reinforcing effects of THC are mediated by the dopamine system.

162 findings suggest that persistent effects of THC on cognitive abilities are more evident when exposur

163 We studied long-term effects of THC on fibrosis progression in women coinfected with hum

164 tudy was therefore to examine the effects of THC on frontolimbic activation and functional connectivi

165 and animal studies concerning the effects of THC on the dopamine system.

166 Relative to the acute effects of THC on working memory at the beginning of the study, nei

167 We found that specific effects of THC such as memory deficits, anxiolytic-like effects, an

168 rest in harnessing the beneficial effects of THC.

169 h potentiation of the reinforcing effects of THC.

170 ith antagonism of the reinforcing effects of THC.

171 chanism involved in the rewarding effects of THC.

172 ates the behavioral and cognitive effects of THC.

173 rm and developmental dopaminergic effects of THC.

174 ver-expression of BDNF in the hippocampus of THC-treated DN-DISC1 mice prevented the impairment in re

175 ugal connectivity, we analyzed the impact of THC exposure on cortical projection neuron development.

176 pharmacology and behavioral interactions of THC and CBD from preclinical and human studies, particul

177 NOX4+ epithelial cells in the intestines of THC-treated SIV-infected macaques.

178 to the effects of high circulating levels of THC, and 2) associated either with greater levels of can

179 n kinetics of the main urinary metabolite of THC, 11-nor-9-carboxy-Delta(9)-tetrahydrocannabinol (THC

180 and cannabinol, and two major metabolites of THC, 11-nor-9-carboxy-THC and 11-hydroxy-THC, in active

181 nor tolerance was evident after 6 months of THC exposure.

182 the first time an in-source rearrangement of THC was observed and characterized in this paper, thus c

183 Radical-scavenging activities (RSA) of THC, zingerone and their quinoline derivatives were eval

184 l factors that may enhance intravenous SA of THC and the cannabinoid receptor (CBR) agonist CP 55 940

185 or para position of the phenol structure of THC-COOH was confirmed by detection of monochlorinated b

186 During this study, formation of THCs was realized to be a reason for the yield loss in c

187 hydroxy-Delta(9)-tetrahydrocannabinol (11-OH-THC), and 11-nor-9-carboxy-Delta(9)-tetrahydrocannabinol

188 This includes effects of CBD on THC-induced anxiety, psychosis, and cognitive deficits.

189 Only THC correlated with antiglucosidase activity (R(2) = 0.8

190 dministered either vehicle (VEH/SIV; n=4) or THC (THC/SIV; n=4).

191 e cognitive performance, received vehicle or THC intravenously 5 days/week for 6 months.

192 of CBD in combination with one dose of oral THC, making it difficult to assess the nature of this in

193 On the molecular level, parental THC exposure was associated with changes in the mRNA exp

194 s analysis compared 16 animals with parental THC exposure and 16 without to characterize relevant sys

195 ated regions (DMRs) associated with parental THC exposure in F1 adults, each represented by multiple

196 cognitive reappraisal, relative to placebo, THC increased amygdala activation and reduced amygdala a

197 Because of its immune-inhibitory potential, THC and related cannabinoids are being considered for th

198 ates underlying the consequences of prenatal THC exposure remain unknown.

199 Atg7, but not Beclin-1 or Ambra1, prevented THC-induced autophagy and cell death in vitro.

200 n addition to automatic emotional processes, THC affects frontolimbic functioning during cognitive re

201 tions about the safety profile of regimented THC intake.

202 er a second-order schedule of reinforcement; THC functioned as reinforcer in two monkeys.

203 exposed control animals, those with repeated THC exposure had a blunted trajectory of accuracy improv

204 In a separate set of animals given the same THC (or vehicle) treatment regimen, electrophysiological

205 onist but inhibited THC-dependent signaling (THC+CBD).

206 the physiological consequence of subchronic THC intake on eyeblink reflexes, a fundamental neuronal

207 ts ingested either an oral dose of synthetic THC (n=41) or placebo (n=37) before completion of an emo

208 g cannabinoids, Delta9-tetrahidrocannabinol (THC), 11-nor-9-carboxy-Delta(9)-THC (THC-COOH) and 11-hi

209 (9) -Tetrahydrocannabinol (THC), the active constituent of Cannabis sativa, exerts

210 nistration of Delta(9)-tetrahydrocannabinol (THC) alters threat perception and enhances the suppressi

211 choactive compound (9)-tetrahydrocannabinol (THC) and a decrease of the potentially therapeutic compo

212 Delta(9)-Tetrahydrocannabinol (THC) and cannabidiol (CBD) occur naturally in marijuana

213 is, including Delta(9)-tetrahydrocannabinol (THC) and cannabidiol (CBD).

214 nabidiol (CBD) and (9)-tetrahydrocannabinol (THC) have well documented immunomodulatory effects in vi

215 r exposure to Delta(9)-tetrahydrocannabinol (THC) in adolescent rats might enhance reinforcing effect

216 in aspects of Delta(9)-tetrahydrocannabinol (THC) intoxication.

217 reatment with Delta(9)-Tetrahydrocannabinol (THC) resulted in the activation of autophagy, loss of ce

218 o)cannabinoid Delta(9)-tetrahydrocannabinol (THC)(1).

219 iol (CBD) and Delta(9)-tetrahydrocannabinol (THC)) on arrestin2-, Galpha(i/o)-, Gbetagamma-, Galpha(s

220 pal target of Delta(9)-tetrahydrocannabinol (THC), a psychoactive chemical from Cannabis sativa with

221 in marijuana, Delta(9)-tetrahydrocannabinol (THC), and its metabolites are emerging organic contamina

222 A), CP55,940, Delta(9)-tetrahydrocannabinol (THC), cannabidiol (CBD), and THC+CBD (1:1), and compared

223 ocannabinoids Delta(9)-tetrahydrocannabinol (THC), cannabidiol, cannabichromene, and cannabinol is pr

224 nd mapping of Delta(9)-tetrahydrocannabinol (THC), cannabinol (CBN), cannabidiol (CBD), and the metab

225 Unlike Delta(9)-tetrahydrocannabinol (THC), CBD does not act through the cannabinoid type 1 (C

226 in marijuana, Delta(9)-tetrahydrocannabinol (THC), has also been shown to mediate potent anti-inflamm

227 of marijuana, Delta(9)-tetrahydrocannabinol (THC), is a signaling network that modulates a diverse ra

228 t exposure to Delta(9)-tetrahydrocannabinol (THC), the main psychoactive component of cannabis, resul

229 t exposure to Delta(9)-tetrahydrocannabinol (THC), the main psychoactive component of marijuana (Cann

230 he effects of Delta(9)-tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, are

231 acco, and (-)-Delta(9)-tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, play

232 ain target of Delta(9)-tetrahydrocannabinol (THC), the most prominent psychoactive compound of mariju

233 ng effects of Delta(9)-tetrahydrocannabinol (THC), the primary active ingredient in marijuana, as ass

234 in cannabis, Delta(9)-tetrahydrocannabinol (THC), was isolated in the mid-1960s, but the cannabinoid

235 tentiation by Delta(9)-tetrahydrocannabinol (THC).

236 nor-9-carboxy-Delta(9)-tetrahydrocannabinol (THC-COOH) with chlorine.

237 nor-9-carboxy-Delta(9)-tetrahydrocannabinol (THC-COOH), 11-hydroxy-Delta(9)-tetrahydrocannabinol (11-

238 Delta-9-tetrahydrocannabinol (THC) is the primary psychoactive component of cannabis.

239 f cannabinoids delta-9-tetrahydrocannabinol (THC) or anandamide in squirrel monkeys.

240 ve ingredient, delta-9-tetrahydrocannabinol (THC), to be more harmful (in terms of causing the main r

241 ogenously administered tetrahydrocannabinol (THC), the primary CB found in marijuana.

242 rocannabinol (HHC) and tetrahydrocannabinol (THC) analogues in which a seven atom long side chain, wi

243 , heroin, codeine, and tetrahydrocannabinol (THC) and their major human metabolites.

244 s tetryl, cocaine, and tetrahydrocannabinol (THC), have been successfully detected.

245 , heroin, codeine, and tetrahydrocannabinol (THC).

246 tal transfer of Delta9-tetrahydrocannabinol (THC) during pregnancy has the potential to interfere wit

247 e, cocaine, and Delta9-tetrahydrocannabinol (THC) from a single blood spot.

248 nine-normalized Delta9-tetrahydrocannabinol (THC) levels.

249 abinoid agonist Delta9-tetrahydrocannabinol (THC) on executive function in 20 healthy volunteers, usi

250 ted exposure to Delta9-tetrahydrocannabinol (THC) on performance of spatial and object working memory

251 ptors (CB1R) by delta9-tetrahydrocannabinol (THC) produces a variety of negative effects with major c

252 ysis of urinary Delta9-tetrahydrocannabinol (THC), cannabidiol and cannabinol, and two major metaboli

253 Delta9-Tetrahydrocannabinol (THC), which is the main bioactive component in marijuana

254 1-nor-9-carboxy-Delta9-tetrahydrocannabinol (THC-COOH) were shown to be strongly correlated to NH4-N.

255 sychoactive substance, tetrahydrocannabinol (THC).

256 Marijuana (hereafter "tetrahydrocannabinol [THC]") use has been associated with liver fibrosis progr

257 s, indolotropones, and tetrahydrocarbazoles (THCs) have been reported.

258 ted more potent anti-microbial activity than THC against Bacillus cereus, Staphylococcus aureus, Esch

259 showed higher immunosuppressive effects than THC.

260 ntiated hGlyR-alpha1 at a level greater than THC at 1 muM.

261 FABPs bind THC and CBD and demonstrate that THC and CBD inhibit the cellular uptake and catabolism o

262 We found that THC (1) inhibited the production of IFNgamma by T cells,

263 It was found that THC left firing rate unaltered and only slightly reduced

264 Our results indicate that THC exposure elicits deficits in exploratory activity an

265 They revealed that THC served to functionally isolate CA1 from CA3 by reduc

266 Our results showed that THC treatment leads to the association of active histone

267 Neurophysiological data showed that THC-exposed rats displayed a reduced capacity for WIN55,

268 Preliminary evidence shows that THC exacerbates, whereas CBD protects from, such harmful

269 Collectively, our findings suggest that THC activates noncanonical autophagy-mediated apoptosis

270 ltered significantly by THC, suggesting that THC activates the expression of a subset of genes while

271 le regulation to metabolism, suggesting that THC had a pleiotropic effect on gene expression in immun

272 t study demonstrates for the first time that THC may modulate immune response through epigenetic regu

273 abinol (THC), 11-nor-9-carboxy-Delta(9)-THC (THC-COOH) and 11-hidroxy-Delta(9)-THC (THC-OH) in milk,

274 -THC (THC-COOH) and 11-hidroxy-Delta(9)-THC (THC-OH) in milk, liver and hemp seeds based on liquid ch

275 stered either vehicle (VEH/SIV; n=4) or THC (THC/SIV; n=4).

276 a mechanism may play a critical role in the THC-mediated switch from Th1 to Th2.

277 oup compared to none showing decrease in the THC/SIV group.

278 ly, NIDA's varieties contain only 27% of the THC levels and as much as 11-23 times the Cannabinol (CB

279 uced a significant shift to the right of the THC self-administration dose-response curves, consistent

280 detected in VEH/SIV macaques compared to the THC/SIV group.

281 ster group at strategic positions within the THC structure.

282 inflammatory miRNA expression contributes to THC-mediated suppression of gastrointestinal inflammatio

283 cetylation patterns in such cells exposed to THC or vehicle.

284 ese findings-that early, passive exposure to THC can produce lasting alterations of the reward system

285 ndings demonstrate that prenatal exposure to THC has long-lasting deleterious consequences in the adu

286 of memory impairments caused by exposure to THC.

287 blation, and CB1-null mice were resistant to THC-induced alterations.

288 The BDNF surge in response to THC is perturbed in the presence of mutant DISC1, sugges

289 CB1-null mice and restored susceptibility to THC-induced motor alterations.

290 offspring that were themselves unexposed to THC displayed increased work effort to self-administer h

291 g individual differences in vulnerability to THC SA may lead to novel treatment strategies for mariju

292 When THC SA was reexamined, it functioned as a reinforcer in

293 ed as a reinforcer in three monkeys, whereas THC (0.01-10 mug/kg) did not have reinforcing effects in

294 rior studies, however, have examined whether THC also affects volitional forms of emotion processing

295 ying the pathobiological basis through which THC exposure elicits psychiatric manifestations.

296 While THC and its derivatives have garnered notoriety in the e

297 h were 250-fold higher than in plasma, while THC concentrations in the lymph were 100-fold higher tha

298 ive-DISC1 (DN-DISC1) mice were injected with THC (10 mg/kg) or vehicle for 10 days during mid-adolesc

299 Maternal treatment with THC or the synthetic CB1R agonist WIN55,212-2 (WIN) prod

300 is large cohort of HIV/HCV-coinfected women, THC was not associated with progression to significant l