ライフサイエンスコーパス: THC

1 THC also increased plasma motilin (P = 0.0021) and decre

2 THC altered functional gene networks related to cell mor

3 THC and CBD doses were 13.75 mg.

4 THC exposure from oil spills might be similarly associat

5 THC exposures were estimated using a job-exposure matrix

6 THC impaired working memory performance (d = 0.65), incr

7 THC increased "liking" (P = 0.031) and "wanting" ratings

8 THC is thought to produce the main psychoactive effects

9 THC was detected on 6 samples out of the 15 collected in

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

11 njections on alternate days denoted as '5X') THC administration on fecal and intestinal tissue metabo

12 y and optogenetics, we examined how Delta(9)-THC alters corticolimbic input to the NAc in rats.

13 evented in DN-DISC1 mice exposed to Delta(9)-THC by simultaneous adolescent treatment with the cycloo

14 pal astrocytes in mice treated with Delta(9)-THC during adolescence.

15 lity could interact with adolescent Delta(9)-THC exposure to impair recognition memory in adulthood.

16 ther, whereas long-term exposure to Delta(9)-THC had no effect on net strength of glutamatergic input

17 Long-term exposure to Delta(9)-THC shifts control of the NAc shell from cortical to lim

18 t the molecular level, DN-DISC1 and Delta(9)-THC synergistically activated the nuclear factor-kappaB-

19 cytes and adolescent treatment with Delta(9)-THC synergistically affected recognition memory in adult

20 a brain reward circuit affected by Delta(9)-THC through modulation of glutamate afferents arising fr

21 We found that long-term exposure to Delta(9)-THC weakens prefrontal cortex glutamate input to the NAc

22 ion of Delta9-tetrahydrocannabinol (Delta(9)-THC), a cannabis constituent and partial agonist of brai

23 n of Delta(9)-tetrahydrocannabinol (Delta(9)-THC), a psychoactive constituent that activates cannabin

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

25 The CBs, Delta(9)-THC, cannabidiol, HU-210, and CP 55,940 caused alcohol-l

26 netic vulnerability could influence Delta(9)-THC-induced signaling in a cell type-specific manner.

27 on within astrocytes can exaggerate Delta(9)-THC-produced cognitive impairments via convergent inflam

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

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

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

31 (-0.34 cm [95% CI, -1.77 to 1.10]; P > .99), THC (0.51 cm [95% CI, -1.01 to 2.02]; P > .99) or THC/CB

32 Consistent with its role as a THC carrier, biotransformation of THC was reduced in pri

33 ients with suspected EVALI reported vaping a THC product, making THC containing e-liquids or oils a k

34 t dosing, surprisingly little is known about THC pharmacology and its effects on behavior and brain a

35 to increased behavioral sensitivity to acute THC exposure during pre-adolescence.

36 We administered THC during an early-middle adolescent window (postnatal

37 at l-theanine pretreatment before adolescent THC exposure is capable of preventing long-term, THC-ind

38 Using a preclinical model of adolescent THC exposure in male rats, we report that l-theanine pre

39 Overall, adolescent THC exposure altered the morphological and transcription

40 t for interpreting results of rat adolescent THC exposure studies, and may lend new insights into how

41 evious evidence demonstrates that adolescent THC exposure induces long-lasting affective and cognitiv

42 malities commonly associated with adolescent THC exposure, further demonstrating functional and long-

43 ng the food image paradigm were higher after THC than after placebo (P = 0.0039).

44 consumed significantly more milkshake after THC than after placebo during oral intake (P = 0.0005),

45 Por hypermethylation was not observed after THC injection or in the subsequent generation.

46 d functional neuroprotective effects against THC-induced developmental neuropathology.

47 periment 1 and voluntarily consumed alcohol, THC edible, or both drugs in Experiment 2.

48 .33 cm [95% CI, 0.80 to 3.86]; P < .001) and THC/CBD-equivalent cannabis (+2.83 cm [95% CI, 1.28 to 4

49 OGTT, HFD-fed rats that co-used alcohol and THC had the lowest insulin levels 75 min after an insuli

50 ndividual and interactive effects of CBD and THC.

51 he SDLP following vaporized THC-dominant and THC/CBD-equivalent cannabis compared with placebo was si

52 or the analysis of THC, CBN, CBD, THC-OH and THC-COOH.

53 the chemical reaction between target THC and THC specific antibody to a measure signal output related

54 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

55 ould produce very little (below 0.3%) if any THC to make their cultivation legal.

56 We assessed the relationship between THC exposure during the response and cleanup of the Deep

57 ve regions mediated the relationship between THC+ status and WM performance.

58 of the developmental transcriptomes between THC- and vehicle-exposed rats.

59 In contrast, CBD coadministration blocked THC-induced ERK phosphorylation, and prevented THC-induc

60 dition, pretreatment with l-theanine blocked THC-induced downregulation of local GSK-3 (glycogen synt

61 Salivary THC levels are correlated to blood THC levels making it a non-invasive medium for rapid THC

62 vaporizing the mixture, as a hydrogen bonded THC/VEA complex linked by the THC hydroxyl and VEA carbo

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

64 and 225 cell-type-specific genes affected by THC administration, including those genes involving in i

65 inct transcriptomic sub-clusters affected by THC in major immune cell types where THC perturbed cell-

66 onses to milkshake intake were attenuated by THC during both oral (P = 0.0002) and intragastric (P =

67 SDLP was significantly increased by THC-dominant cannabis (+2.33 cm [95% CI, 0.80 to 3.86];

68 y sensitive to developmental perturbation by THC.

69 sciatic nerve injury, which was reversed by THC, CBD, and morphine.

70 CAN(THC) maintained higher response rates under fixed ratio

71 brain concentrations of THC and CBD and CAN(THC) administration decreased hippocampal CB1 receptor b

72 Removal of CAN(THC) reinforcement (but not CAN(CBD)) resulted in a robu

73 ained to nose-poke for discrete puffs of CAN(THC), CAN(CBD), or vehicle (VEH) in daily 1 h sessions.

74 ized Delta(9)-tetrahydrocannabinol-rich (CAN(THC)) or cannabidiol-rich (CAN(CBD)) whole-plant cannabi

75 bolites (11-hydroxy-THC and 11-nor-9-carboxy-THC) in blood and brain following acute injection (0.5 o

76 GC-MS/MS for the analysis of THC, CBN, CBD, THC-OH and THC-COOH.

77 gnatures of CBG, cannabigerolic acid (CBGA), THC, delta-9-tetrahydrocannabinolic acid (THCA), CBD, an

78 Moreover, transient on-chip THC treatment also decreased spontaneous firing in these

79 This study determined if chronic THC exposure alters sperm DNA methylation (DNAm) and if

80 measure the total hemoglobin concentration (THC) and scattering properties of epithelial tissues wit

81 d positive for the three major constituents, THC, CBN and CBD.

82 In contrast, THC exposure disrupted the normal developmental process

83 These findings implicate GLUT1 as a Delta9-THC target and provide a potential mechanism for the fet

84 Although Delta9-THC administration reduced the activation of several spl

85 Thus, chronic occupancy of CB1Rs by Delta9-THC during adolescence may competitively decrease the fu

86 2.27-times higher increase following Delta9-THC administration.

87 E19.5 placentas from Delta9-THC-exposed pregnancies exhibited a phenotype characteri

88 Gestational Delta9-THC exposure resulted in pups born with symmetrical feta

89 0.040) were associated with a higher Delta9-THC-induced Glx increase.

90 nabinoid receptor agonists, including Delta9-THC, on inflammation and organ injury in endotoxemic mic

91 mine, in rats, the impact of maternal Delta9-THC exposure on fetal development, neonatal outcomes, an

92 mediate the central neural effects of Delta9-THC and endocannabinoids that regulate NMDA receptor-dep

93 Administration of Delta9-THC caused a dramatic early upregulation of plasma IL-10

94 The anti-inflammatory effects of Delta9-THC in endotoxemic mice were reversed by a cannabinoid r

95 ns resulting from excessive intake of Delta9-THC in the increasingly available marijuana products use

96 d to placebo, acute administration of Delta9-THC significantly increased Glutamate (Glu) + Glutamine

97 ets, the anti-inflammatory effects of Delta9-THC were preserved in splenectomized endotoxemic mice.

98 ive to the psychotomimetic effects of Delta9-THC, individuals who developed transient psychotic-like

99 njection (i.p.) of vehicle control or Delta9-THC (3 mg/kg) from embryonic (E)6.5 through 22.

100 6J male mice that received vehicle or Delta9-THC in escalating doses (2.5-10 mg/kg/ip) through adoles

101 idation or blockade of other putative Delta9-THC receptors, including cannabinoid receptor type 2, TR

102 L-PFC of adult mice that had received Delta9-THC only during adolescence showed a significant (1) dec

103 ison with vehicle, the mice receiving Delta9-THC showed a hyperpolarized resting membrane potential,

104 ponents, Delta9-tetrahydrocannabinol (Delta9-THC) and cannabidiol, are increasingly being used to tre

105 sure to delta-9-tetrahydrocannabinol (Delta9-THC), the major psychoactive compound in marijuana.

106 how that (-)- 9-tetrahydrocannabinol (Delta9-THC), the major psychoactive ingredient in cannabis, cau

107 istered delta-9-tetrahydrocannabinol (Delta9-THC; 1.19 mg/2 ml), the key psychoactive ingredient in c

108 These results indicate that Delta9-THC potently induces IL-10, while reducing proinflammato

109 derived suppressive cells mediate the Delta9-THC-induced early rise in circulating IL-10.

110 In conclusion, maternal exposure to Delta9-THC effectively compromised fetal growth, which may be a

111 ceptor (GR) expression in response to Delta9-THC exposure.

112 ipants vaporized THC-dominant, CBD-dominant, THC/CBD-equivalent, and placebo cannabis.

113 dolescent rats of both sexes consumed enough THC to trigger acute hypothermia, analgesic, and locomot

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

115 We also evaluated THC effects on behavioral assays of anxiety, locomotion,

116 Finally, THC-exposed and control adult male rats were mated with

117 denoted here as '1X') and short -term (five THC injections on alternate days denoted as '5X') THC ad

118 Affinity biosensing is leveraged for THC biomarker detection through the chemical reaction be

119 side-stream cannabis vapor are positive for THC at quantifiable levels.

120 vely, these data position FABP1 as a hepatic THC transport protein and a critical mediator of cannabi

121 vidence demonstrates that cannabis with high THC concentrations and negligible cannabidiol concentrat

122 Across product characteristics, only higher THC levels were independently associated with greater sy

123 atin by rats and used it to study if and how THC consumption during adolescence impacts adult behavio

124 studies, and may lend new insights into how THC impacts the brain in a sex-dependent manner.

125 Exposure to total hydrocarbons (THC) and volatile organic compounds from air pollution i

126 its main first-pass metabolites (11-hydroxy-THC and 11-nor-9-carboxy-THC) in blood and brain followi

127 ation in the bioactive metabolite 11-hydroxy-THC.

128 ious work, we find marked sex differences in THC metabolism, including a female-specific elevation in

129 of chromatin- and dendrite-related genes in THC-treated animals.

130 e in most countries, and its conversion into THC can be easily performed using common chemicals.

131 c profiling provides important insights into THC's acute effects on immune function that may have imp

132 erted by any reasonable synthetic route into THC, and thus has the potential to act as a safe, noncon

133 models are required to properly investigate THC effects in adolescents.

134 and dark cycles, with animals consuming less THC-gelatin than the other gelatin groups.

135 he risk difference for highest versus lowest THC level was 10 excess cases per 1,000 workers.

136 EVALI reported vaping a THC product, making THC containing e-liquids or oils a key focus on the ongo

137 tances of cannabis use and carefully matched THC-naive controls.

138 Maximum THC levels of >=0.30 parts per million (ppm) were associ

139 g as a critical neural nexus point mediating THC-induced affective disturbances and suggest a potenti

140 olunteer showed low levels of the metabolite THC-OH.

141 ng of CB(2)R transmembrane region 5 mimicked THC effects.

142 rt task", 90 trials) after administration of THC (7.5 and/or 15 mg oral) or placebo.

143 eir wild-type littermates, administration of THC to male and female FABP1-KO mice potentiated the phy

144 dures, and then GC-MS/MS for the analysis of THC, CBN, CBD, THC-OH and THC-COOH.

145 and distribution in blood and brain, and of THC effects upon behavior and neural activity in adolesc

146 tability and the electrochemical behavior of THC immunoassay in varying salivary pH buffers.

147 designed to investigate possible benefits of THC for women with endometriosis.

148 role as a THC carrier, biotransformation of THC was reduced in primary hepatocytes obtained from FAB

149 cologically relevant brain concentrations of THC and CBD and CAN(THC) administration decreased hippoc

150 ) than cannabis with lower concentrations of THC.

151 Thus, voluntary oral consumption of THC during adolescence is associated with sex-dependent

152 h by measuring voluntary oral consumption of THC-containing gelatin by rats and used it to study if a

153 ectrochemical biosensor for the detection of THC in saliva as a marijuana roadside DUI test with a lo

154 l-Theanine prevented the development of THC-induced behavioral aberrations, blocked cortical dow

155 to report a long-term impact of one dose of THC on the functional activation of the threat extinctio

156 three main goals: (1) quantify the effect of THC on visual working memory in a well-powered sample, (

157 size on power to detect the acute effect of THC on working memory.

158 ly little empirical support for an effect of THC or cannabis on working memory.

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

160 t is difficult to distinguish the effects of THC from those of coexisting factors.

161 s by which CBD mitigates the side effects of THC have not been identified.

162 reat extinction learning, and the effects of THC on extinction memory retention when assessed 1 day a

163 tigates the neuropsychiatric side effects of THC.

164 the physiological and behavioral effects of THC.

165 ates the behavioral and cognitive effects of THC.

166 hotomimetic and psychotropic side effects of THC.SIGNIFICANCE STATEMENT Strains of marijuana with hig

167 nt analysis further supports the findings of THC's common and cell-type-specific effects on immune re

168 nd-held platform for rapid identification of THC in saliva samples obtained from human subjects.

169 urther investigating the long-term impact of THC on threat and anxiety circuitry.

170 st study of the persistent health impacts of THC exposure during oil spill work, and results support

171 siological tools to examine the influence of THC on the mechanisms of conditioned threat extinction l

172 show here that intraperitoneal injection of THC in C57BL/6 mice modulates metabolic profiles that ha

173 , we conducted a systematic investigation of THC pharmacokinetics, metabolism and distribution in blo

174 The observed reaction kinetics for loss of THC on glass and cotton surfaces are consistent with a r

175 The mechanisms of THC's effects on gene expression in human immune cells r

176 rate that FABP1 accommodates one molecule of THC within its ligand binding pocket.

177 icipants were randomized to take one pill of THC or placebo (PBO) 2-h before threat extinction learni

178 .95) was employed to predict the presence of THC in human saliva.

179 We determined the pharmacokinetic profile of THC and its main first-pass metabolites (11-hydroxy-THC

180 that FABP1-KO mice exhibit reduced rates of THC biotransformation.

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

182 The low volatility of THC and its oxidation products suggest that their contri

183 0.51 cm [95% CI, -1.01 to 2.02]; P > .99) or THC/CBD (1.22 cm [95% CI, -0.29 to 2.72]; P = .20) condi

184 alcohol after receiving subcutaneous oil or THC injections in Experiment 1 and voluntarily consumed

185 Another cohort was injected with vehicle or THC, and sperm DNAm was analyzed.

186 calorie food images were acquired after oral THC or placebo administration.

187 tion was confirmed (p < 0.05) following oral THC administration for cytochrome P450 oxidoreductase (P

188 Epoxide, dicarbonyl, and secondary ozonide THC reaction products were detected from both pure THC a

189 Pharmaceutical THC (with or without CBD) did not significantly affect a

190 Pharmaceutical THC (with or without CBD) improved anxiety symptoms amon

191 Pharmaceutical THC (with or without CBD) worsened negative symptoms of

192 ery low quality evidence that pharmaceutical THC (with or without CBD) leads to a small improvement i

193 deliveries positively correlated with plasma THC concentrations.

194 es: low potency (THC <10%) and high potency (THC >=10%).

195 rticipants into two categories: low potency (THC <10%) and high potency (THC >=10%).

196 C-induced ERK phosphorylation, and prevented THC-induced behavioral and neural abnormalities.

197 ntervention strategies capable of preventing THC-induced neuropathological adaptations.

198 action products were detected from both pure THC and cannabis experiments, with the product ratios de

199 ls making it a non-invasive medium for rapid THC testing.

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

201 Remarkably, THC consumption by adolescent male rats and not female r

202 Salivary THC levels are correlated to blood THC levels making it

203 we investigated the effects of acute (single THC injection denoted here as '1X') and short -term (fiv

204 Strikingly, THC also inhibits the development of endometrial cysts.

205 nce is the underlying mechanisms surrounding THC's therapeutic effects and the role of gut metabolite

206 through the chemical reaction between target THC and THC specific antibody to a measure signal output

207 lutamine, is capable of preventing long-term THC side effects.

208 exposure is capable of preventing long-term, THC-induced dysregulation of both PFC and VTA DAergic ac

209 erve injury, and by the last day of testing, THC significantly reduced hyperalgesia, with a trend eff

210 e urine drug screen for tetrahydocannabinol (THC+ status), the principal psychoactive constituent in

211 ned, including delta-9 tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabigerol (CBG).

212 entrations of Delta(9) tetrahydrocannabinol (THC) or cannabidiol.

213 e cannabinoid Delta(9)-tetrahydrocannabinol (THC) disrupts HER2-CB(2)R complexes by selectively bindi

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

215 centration of Delta(9)-tetrahydrocannabinol (THC) in the different types of cannabis available across

216 Delta(9)-tetrahydrocannabinol (THC) is the intoxicating constituent of cannabis and is

217 s reaction of Delta(9)-tetrahydrocannabinol (THC), a major component of cannabis smoke, with ozone wa

218 t exposure to Delta(9)-tetrahydrocannabinol (THC), a psychoactive component of cannabis, on the morph

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

220 ds, including Delta(9)-tetrahydrocannabinol (THC), are metabolized and inactivated by cytochrome P450

221 orporation of Delta(9)-tetrahydrocannabinol (THC), cannabinol (CBN), cannabidiol (CBD) and in one ins

222 ive component Delta(9)-tetrahydrocannabinol (THC), impairs working memory, i.e., the ability to tempo

223 ic effects of Delta(9)-tetrahydrocannabinol (THC), many studies have concentrated on its less intoxic

224 f alcohol and Delta(9)-tetrahydrocannabinol (THC), the main psychoactive constituent of cannabis, aff

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

226 offspring of Delta(9)-tetrahydrocannabinol (THC)-exposed dams, a rat PCE model, exhibit extensive mo

227 hoactive drug Delta(9)-tetrahydrocannabinol (THC).

228 te 11-hydroxy-Delta(9)-tetrahydrocannabinol (THC-OH).

229 tocannabinoids Delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) differentially regulate salie

230 high levels of delta-9-tetrahydrocannabinol (THC) and low levels of cannabidiol (CBD) have been shown

231 Delta-9-tetrahydrocannabinol (THC) is known to modulate immune response in peripheral

232 nt exposure to Delta-9-tetrahydrocannabinol (THC) is linked to elevated neuropsychiatric risk and ind

233 Delta-9-tetrahydrocannabinol (THC) is the primary psychoactive compound in Cannabis, w

234 the effects of Delta-9-tetrahydrocannabinol (THC) on brain structure.

235 e cannabinoid, Delta-9-tetrahydrocannabinol (THC), cerebral organoids exhibited reduced neuronal matu

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

237 es to minimize Delta-9-tetrahydrocannabinol (THC)-induced neuropathology.

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

239 c derivatives, such as tetrahydrocannabinol (THC) and cannabidiol (CBD), have been suggested to have

240 psychoactive compound tetrahydrocannabinol (THC) in marijuana.

241 d durability of Delta9-tetrahydrocannabinol (THC) impact on threat processing in humans are not fully

242 ted exposure to Delta9-tetrahydrocannabinol (THC) in a mouse model of surgically-induced endometriosi

243 ayed effects of Delta9-tetrahydrocannabinol (THC) intoxication on susceptibility to false memory in 6

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

245 effect of oral Delta9-tetrahydrocannabinol (THC) on subjective and metabolic hormone responses to vi

246 0 (94%) had detectable tetrahydrocannabinol (THC) or its metabolites in BAL fluid or had reported vap

247 gher concentrations of tetrahydrocannabinol (THC).

248 on effects of paternal tetrahydrocannabinol (THC) exposure prior to reproduction.

249 effects of exposure to tetrahydrocannabinol (THC) and nicotine on DNA methylation in rat sperm at gen

250 ort a history of using tetrahydrocannabinol (THC)-containing e-cigarette or vaping products; approxim

251 cannabinoid contents (tetrahydrocannabinol, THC; and cannabidiol, CBD), along with real-time ratings

252 ncentrations of Delta-9-tetrahydrocannabiol (THC), decreases in cannabidiol, or both, have occurred.

253 showed higher immunosuppressive effects than THC.

254 We demonstrate that THC induces cognitive and affective abnormalities resemb

255 This letter demonstrates that THC and VEA exist in the unvaped e-liquids, vaped e-liqu

256 We found that THC administration increased amygdala and ventromedial p

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

258 ults are consistent with the hypothesis that THC administration alters host metabolism by targeting t

259 Thus, our findings indicate that THC does impair visual working memory, and that this imp

260 Our data indicate that THC-rich cannabis vapor has reinforcing properties that

261 e cell transcriptome mapping, we report that THC acutely alters gene expression in 15,973 blood cells

262 These results suggest that THC and alcohol co-exposure can distinctly alter the phy

263 These results support that THC alters DNAm in sperm and that route of exposure can

264 FC co-expression networks common to both the THC-treated animals and patients with schizophrenia were

265 ydrogen bonded THC/VEA complex linked by the THC hydroxyl and VEA carbonyl groups.

266 etention was tested 24 h after learning, the THC group exhibited lower SCRs to the extinguished cue w

267 ention was tested 1 week after learning, the THC group exhibited significantly decreased responses to

268 nfirmed the successful immobilization of the THC immobilization assay on the biosensing platform.

269 or vaping products; approximately 50% of the THC-containing vaping products examined by the Food and

270 and globally connected tool to quantify the THC and scattering properties of tissues in vivo.

271 hemp, a variety of Cannabis sativa with the THC concentration below 0.3%.

272 The THCs of the three oral mucosa tissues are significantly

273 tor responses, and that 15 days of access to THC-gelatin in adolescence resulted in the down-regulati

274 bind to FABP1 with comparable affinities to THC, our results further suggest that FABP1 could serve

275 al methylation in sperm from rats exposed to THC via injection as well as those exposed to nicotine.

276 equencing data from sperm of rats exposed to THC via oral gavage showed that seven neurodevelopmental

277 se data indicate that volitional exposure to THC-rich cannabis vapor has bona fide reinforcing proper

278 (DA) pathway are particularly susceptible to THC-induced pathologic alterations, including dysregulat

279 .88 [0.29-1.46]; p=0.0003) and lower urinary THC-COOH concentrations (mean 657.92 ng/mL [95% CI 381.6

280 atment) self-reported cannabis use and urine THC-COOH concentrations in the intention-to-treat popula

281 abolites in BAL fluid or had reported vaping THC products in the 90 days before the onset of illness.

282 driving tests, the SDLP following vaporized THC-dominant and THC/CBD-equivalent cannabis compared wi

283 Participants vaporized THC-dominant, CBD-dominant, THC/CBD-equivalent, and plac

284 Remarkably, whereas intra-vHipp THC also potentiates salience attribution in morphine pl

285 Dawley rats, we demonstrate that intra-vHipp THC strongly increases ventral tegmental area (VTA) DA n

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

287 cted by THC in major immune cell types where THC perturbed cell-type-specific intracellular gene expr

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

289 While THC is an illicit drug, CBD and CBG are legal substances

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

291 nce to morphine developed after 1 week while THC or CBD reduced allodynia over three weeks.

292 d exposure to even low doses of alcohol with THC, HU-210, or CP 55,940 caused a greater incidence of

293 cm with CBD-dominant cannabis, 19.88 cm with THC-dominant cannabis, 20.59 cm with THC/CBD-equivalent

294 cm with CBD-dominant cannabis, 20.59 cm with THC-dominant cannabis, 21.09 cm with THC/CBD-equivalent

295 cm with THC-dominant cannabis, 21.09 cm with THC/CBD-equivalent cannabis, and 18.28 cm with placebo c

296 cm with THC-dominant cannabis, 20.59 cm with THC/CBD-equivalent cannabis, and 19.37 cm with placebo c

297 Adult male rats underwent oral gavage with THC or vehicle control.

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

299 and control adult male rats were mated with THC-naive females.

300 Interestingly, daily treatments with THC (2 mg/kg) alleviate mechanical hypersensitivity and