ライフサイエンスコーパス: CBD

1 CBD abrogated the enhanced intracortical local field pot

2 CBD also showed significant protracted effects on these

3 CBD and PBD patterns are similarly explained by spatial

4 CBD binds at a novel site at the interface of the fenest

5 CBD concentrations in the lymph were 250-fold higher tha

6 CBD had a dose-dependent sedative effect but did not hav

7 CBD may be sourced from cannabis plants but can also be

8 CBD or vehicle was administered daily throughout the alc

9 CBD showed higher immunosuppressive effects than THC.

10 CBD significantly attenuated the alcohol feeding-induced

11 CBD treatment also attenuated the respiratory burst of n

12 CBD was well tolerated, and rates of adverse events were

13 CBD's potential to reduce cue-induced craving and anxiet

14 CBD's reputation as a cure-all puts it in the same class

15 CBD-bound TRPV2 structures revealed that the S4-S5 linke

16 CBD-IL-12 may potentiate CPI immunotherapy for immunolog

17 auopathy and argyrophilic grain disease(10), CBD is characterized by abundant filamentous tau inclusi

18 of a collagen-binding domain fused to IL-12 (CBD-IL-12) in mice bearing aggressive mouse tumours, CBD

19 with the administration of unmodified IL-12, CBD-IL-12 induced sustained intratumoural levels of inte

20 cinoma, n = 15) or nonmalignant (CP, n = 15) CBD stenosis.

21 The core of a CBD filament comprises residues lysine 274 to glutamate

22 s method to study the cAMP binding domain A (CBD-A) of Protein kinase A.

23 Acute CBD administration, in contrast to placebo, significantl

24 However, neither acute CBD nor a 2-week-long course of CBD administered immedia

25 Here, we show that acute CBD (100 mg/kg) treatment attenuated hyperthermia- and a

26 In addition, CBD reduced the drug cue-induced physiological measures

27 the full-length rat TRPV2 channel in apo and CBD-bound states in nanodiscs by cryo-electron microscop

28 Using isothermal titration calorimetry and CBD-mimetic peptides, as well as CaM-agarose affinity pu

29 differentiation between hemp, cannabis, and CBD-rich hemp.

30 r the three major constituents, THC, CBN and CBD.

31 e3 marks in CD4+ T cells from naive, EAE and CBD treated EAE mice by ChIP-seq.

32 fortified or CBD-labeled health products and CBD-associated health claims lacks a rigorous scientific

33 ed with increased ROCK1 and ROCK2 in PSP and CBD brains, whereas experiments in cellular and animal m

34 identified as novel drug targets for PSP and CBD.

35 FTLD pathologies and could separate PSP and CBD.

36 tween tau strains such that only PSP-tau and CBD-tau strains induce astroglial and oligodendroglial t

37 lly relevant brain concentrations of THC and CBD and CAN(THC) administration decreased hippocampal CB

38 THC and CBD doses were 13.75 mg.

39 ology and behavioral interactions of THC and CBD from preclinical and human studies, particularly wit

40 istinct cannabinoid compounds (i.e., THC and CBD).

41 Both THC and CBD, as well as other cannabinoid molecules, are current

42 As CBD's effects do not appear to depend on dopamine recept

43 ace-preference and fear conditioning assays, CBD coadministration reverses these changes by downregul

44 Literature evidence associates CBD with certain semiubiquitous, broadly screened, prima

45 PSP Association, CBD Solutions, Medical Research Council (UK).

46 here were no significant differences between CBD-dominant cannabis and placebo.

47 detailed nature of the interactions between CBD and the NavMs voltage-gated sodium channel, and elec

48 gy to show the functional effects of binding CBD to these channels.

49 NAs and lncRNAs was dramatically affected by CBD.

50 terest due to the antiaromaticity brought by CBD circuits.

51 rn of many EAE-induced genes was reversed by CBD treatment which was consistent with its effect on at

52 moval of CAN(THC) reinforcement (but not CAN(CBD)) resulted in a robust extinction burst and an incre

53 nol-rich (CAN(THC)) or cannabidiol-rich (CAN(CBD)) whole-plant cannabis extracts.

54 ose-poke for discrete puffs of CAN(THC), CAN(CBD), or vehicle (VEH) in daily 1 h sessions.

55 rogressive ratio schedules compared with CAN(CBD) or VEH, and the number of vapor deliveries positive

56 Cannabidiol (CBD) and (9)-tetrahydrocannabinol (THC) have well docume

57 Cannabidiol (CBD) has been shown by our laboratory to attenuate exper

58 Cannabidiol (CBD) is a non-psychoactive component of marijuana, which

59 Cannabidiol (CBD) is being investigated as a treatment for several me

60 Cannabidiol (CBD), a major phytocannabinoid constituent of cannabis,

61 Cannabidiol (CBD), the non-psychoactive compound isolated from cannab

62 Cannabidiol (CBD), the non-psychotropic therapeutically active ingred

63 -tetrahydrocannabinol (THC) and cannabidiol (CBD) differentially regulate salience attribution and ps

64 tetrahydrocannabinol (THC) and cannabidiol (CBD), have been suggested to have a therapeutic role in

65 -tetrahydrocannabinol (THC) and cannabidiol (CBD).

66 Coupling was partly restored by cannabidiol (CBD).

67 l component of marijuana called cannabidiol (CBD), which possesses promising therapeutic properties f

68 abinol (THC), cannabinol (CBN), cannabidiol (CBD) and in one instance, the metabolite 11-hydroxy-Delt

69 ajor non-intoxicating component cannabidiol (CBD) as a treatment for mental health and neurodevelopme

70 ces a non-psychoactive compound cannabidiol (CBD).

71 al phytocannabinoids, including cannabidiol (CBD), cannabidivarin (CBDV), Delta(9)-tetrahydrocannabiv

72 rmaceutical ingredient (API) is cannabidiol (CBD).

73 on its less intoxicating isomer cannabidiol (CBD).

74 ral concentrations of medicinal cannabidiol (CBD) and terpenoids were not affected by Se.

75 nabinol (THC) and low levels of cannabidiol (CBD) have been shown to underlie neuropsychiatric risks

76 d crash risk, but the effect of cannabidiol (CBD) on driving is unclear.

77 ssential medicinal chemistry of cannabidiol (CBD) provides evidence that the popularization of CBD-fo

78 y investigated the potential of cannabidiol (CBD), a nonintoxicating phytocannabinoid, to reduce cue-

79 There is some evidence that cannabidiol (CBD) can induce cell death and increases the radiosensit

80 Here we show that cannabidiol (CBD) effectively reduced seizures and autistic-like soci

81 imals and humans indicates that cannabidiol (CBD) has antipsychotic properties.

82 a-9 tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabigerol (CBG).

83 (tetrahydrocannabinol, THC; and cannabidiol, CBD), along with real-time ratings of health symptom sev

84 n be used to differentiate between cannabis, CBD-rich plants, and regular hemp.

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

86 e assemblages to quantify the compositional (CBD) and phylogenetic (PBD) beta-diversity of snakes in

87 erties of such conjugated systems containing CBD.

88 On the contrary, CBD should be evaluated for inclusion in long-term storm

89 In contrast, CBD coadministration blocked THC-induced ERK phosphoryla

90 In contrast, CBD potency levels were generally not associated with si

91 ndromes and from studies of over-the-counter CBD products are needed to assess whether the conclusion

92 , and E(T(2)) of benzene and cyclobutadiene (CBD) as excited-state antiaromatic and aromatic archetyp

93 The juxtaposition of fused cyclobutadienoid (CBD) with benzenoid creates intriguing alternating antia

94 es 7 days after the final short-term (3-day) CBD exposure.

95 Beside initiation of death, CBD has been demonstrated as an inducer of autophagy.

96 neurons, while in corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), tau also

97 au filaments from corticobasal degeneration (CBD) human brain tissue.

98 Corticobasal degeneration (CBD) is a neurodegenerative tauopathy-a class of disorde

99 r palsy (PSP) and corticobasal degeneration (CBD) suggest that mitigating pathogenic tau levels is a

100 sy (PSP-tau), and corticobasal degeneration (CBD-tau) patients into different brain regions of female

101 sy [PSP], n = 10; corticobasal degeneration [CBD], n = 10; FTLD-TDP, n = 3; and Pick disease, n = 1).

102 Coastal boulder deposits (CBD) are archives of extreme wave events.

103 n to ask is whether RS can be used to detect CBD and CBG in hemp, as well as enable confirmatory diff

104 nomas: 13 duodenal, 110 ampullary, 43 distal CBD, and 344 PDAC.

105 ith cancers of the duodenum, ampulla, distal CBD, or pancreas, respectively (P = .01), indicating a s

106 ancers were intestinal type, and most distal CBD tumors were PB type (86.0% [37 of 43]).

107 testinal-type duodenal, ampullary, or distal CBD adenocarcinomas had longer median overall survival t

108 with PB-type duodenal, ampullary, or distal CBD adenocarcinomas have survival similar to those with

109 nating from the duodenum, ampulla, or distal CBD with those having pancreatic ductal adenocarcinoma (

110 FF motif in the first Ca(2+) binding domain (CBD) 1 in NCX1.

111 domain of MSL2, named Clamp-binding domain (CBD) directly interacts with the N-terminal zinc-finger

112 on did not require the cargo-binding domain (CBD) of TNPO3, which typically mediates nuclear entry fo

113 by WzmWzt via a carbohydrate-binding domain (CBD) that extends its nucleotide-binding domain (NBD).

114 hin a predicted BdALMT12 CaM-binding domain (CBD), also decreased the channels' ability to activate.

115 domain (AID) and calmodulin-binding domain (CBD), which block the catalytic center and a conserved s

116 main mapped to the chromatin binding domain (CBD).

117 psids, enzymes, and a chitin binding domain (CBD).

118 -type V domains and a chitin-binding domain (CBD).

119 uncated C-terminal cell wall binding domain (CBD).

120 ) residue in the chromophore-binding domain (CBD, composed of a PAS and a GAF domain).

121 Participants vaporized THC-dominant, CBD-dominant, THC/CBD-equivalent, and placebo cannabis.

122 While THC is an illicit drug, CBD and CBG are legal substances that have a variety of

123 The treatment of common bile duct (CBD) disorders, such as biliary atresia or ischemic stri

124 for diagnosis of malignant common bile duct (CBD) stenoses are complex and lack accuracy.

125 The role of common bile duct (CBD) stenting in the establishment of bile stream in the

126 duodenum, ampulla, distal common bile duct (CBD), or head of the pancreas.

127 Thermal conditions best explain CBD and PBD of snakes for the whole AF, whereas water-re

128 ic strategy allows facile access to extended CBD-fused pi-systems with tunable local antiaromaticity

129 Finally, CBD-tau- and PSP-tau-injected mice showed spatiotemporal

130 ntially overlapping mechanisms of action for CBD in these disorders and indicate the need for further

131 outcome of limited PS combined with EPBD for CBD stone removal in patients with difficult biliary can

132 scopic papillary balloon dilation (EPBD) for CBD stone removal in patients with difficult biliary can

133 graphy at university hospitals in Europe for CBD stenosis of malignant (pancreatic cancer, n = 20 or

134 novel insight into a possible mechanism for CBD interactions with sodium channels.

135 V, 4 ng/mL for CBG and THCV, and 7 ng/mL for CBD.

136 also recently proposed as a target site for CBD.

137 However, the effect size for CBD-dominant cannabis may not have excluded clinically i

138 he structures and PTMs of tau filaments from CBD and Alzheimer's disease, it is found that ubiquitina

139 and mass spectrometry of tau filaments from CBD reveal that this conformer is heavily decorated with

140 Furthermore, CBD enhanced the pro-apoptotic activities of JNK1/2 and

141 Furthermore, CBD improved alcohol-induced hepatic metabolic dysregula

142 Furthermore, CBD-IL-12 potently synergized with CPI to eradicate larg

143 olycyclic conjugated hydrocarbons with fused CBD.

144 Across groups, CBD increased subcortical, but decreased cortical, Glx.

145 followed by (Z)-1,1,2,3,4-penta-CBD and hexa-CBD.

146 Cannabis tissue containing low CBD over high CBD.

147 ificial diet (AD), larvae reared on the high CBD diet suffer significantly reduced growth and increas

148 While the larva avoided the high CBD diet, we investigated detrimental effects of CBD in

149 trations after administration of the highest CBD dose (800 mg).

150 molecular mechanism that may account for how CBD functionally mitigates the neuropsychiatric side eff

151 However, CBD, like all natural cannabinoids, is a controlled subs

152 We previously demonstrated that human CBD and PSP tauopathy lysates (CBD-tau and PSP-tau) cont

153 s can produce all the features of imbricated CBD.

154 odestly affected the levels of cell death in CBD- or CBD/gamma-irradiated 3D GBM cultures.

155 Clinical outcomes including success rates in CBD stones clearance, incidence of pancreatitis, perfora

156 cription factors may play important roles in CBD mediated immune modulation.

157 autophagic flux to 2D GBM cultures increased CBD-induced cell death, presenting proof for the protect

158 Hospital in Qom, Iran with multiple or large CBD stones (above three or larger than 15 mm) received s

159 e towards the Cannabis tissue containing low CBD over high CBD.

160 Contrasted to the performance on low CBD-infused artificial diet (AD), larvae reared on the h

161 ed that human CBD and PSP tauopathy lysates (CBD-tau and PSP-tau) contain distinct tau strains that p

162 e best distinguished patients with malignant CBD from controls in the discovery cohort.

163 in bile samples from patients with malignant CBD stenoses than controls or nonmalignant CBD stenoses

164 a levels) after a single oral dose of 600 mg CBD or placebo.

165 eatment for patients with large and multiple CBD stones.

166 der to reduce the size of large and multiple CBD stones.

167 ered artificial ducts can replace the native CBD, with no evidence of cholestasis or occlusion of the

168 on correct: nfvPPA-PSP, 98% [80-100]; nfvPPA-CBD, 81% [65-98]; P = .08) were found in the nfvPPA-CBD

169 n [IQR] score: nfvPPA-PSP, 19 [3-28]; nfvPPA-CBD, 4 [0-16]; P = .04), and relatively selective white

170 ian [IQR] score: nfvPPA-PSP, 4 [2-7]; nfvPPA-CBD, 0 [0-4]; P = .02), depression (Geriatric Depression

171 % [65-98]; P = .08) were found in the nfvPPA-CBD group.

172 ld discriminated malignant from nonmalignant CBD stenoses with 100% accuracy.

173 uld discriminate malignant from nonmalignant CBD stenoses.

174 t CBD stenoses than controls or nonmalignant CBD stenoses (2.41 x 10(15) vs 1.60 x 10(14) nanoparticl

175 ween patients with malignant vs nonmalignant CBD stenosis with 100% accuracy.

176 with malignant vs patients with nonmalignant CBD stenoses with 63.3% diagnostic accuracy.

177 cm [95% CI, 1.28 to 4.39]; P < .001) but not CBD-dominant cannabis (-0.05 cm [95% CI, -1.49 to 1.39];

178 Notably, CBD treatment significantly improved ethanol-intoxicated

179 s a modular and efficient synthesis of novel CBD-containing acene analogues, dinaphthobenzo[1,2:4,5]d

180 arieties that would produce large amounts of CBD and CBG.

181 idiol (H2CBD), a fully synthetic analogue of CBD that is prepared from inexpensive, non-cannabis deri

182 f MAPT (the tau gene) is present in cases of CBD at a higher frequency than in controls(4,5), and gen

183 either acute CBD nor a 2-week-long course of CBD administered immediately after a kindling protocol c

184 es of CBD, as well as precise definitions of CBD-containing substances and products, distilled to rev

185 thus help guide the rational development of CBD as a treatment for AS.

186 tology, astrocytic plaques are diagnostic of CBD(7,8); by SDS-PAGE, so too are detergent-insoluble, 3

187 r, most studies have tested only one dose of CBD in combination with one dose of oral THC, making it

188 Treatment with lower doses of CBD also improved autistic-like social interaction defic

189 reduced hyperalgesia, with a trend effect of CBD, and no effect of morphine.

190 ors assessed the safety and effectiveness of CBD in patients with schizophrenia.

191 and meta-analysis of the adverse effects of CBD across all medical indications.

192 onsecutive daily administrations) effects of CBD administration (400 or 800 mg, once daily for 3 cons

193 ng the individual and interactive effects of CBD and THC.

194 PR55, suggesting that therapeutic effects of CBD are mediated through this lipid-activated G protein-

195 diet, we investigated detrimental effects of CBD in the insects' diet.

196 ls, a better understanding of the effects of CBD on brain would be desirable.

197 The beneficial effects of CBD on inhibitory neurotransmission were mimicked and oc

198 Herein, we investigated the effects of CBD on liver injury induced by chronic plus binge alcoho

199 This includes effects of CBD on THC-induced anxiety, psychosis, and cognitive def

200 Our results do not speak to the efficacy of CBD.

201 Here, we found that inactivation of CBD or CXC individually only modestly affected recruitme

202 In the detection and resultant management of CBD stones for the majority of patients undergoing lapar

203 A decision tree model of CBD exploration was developed to determine the optimal d

204 gests that one aspect of the polypharmacy of CBD is that it modulates brain excitatory glutamate and

205 provides evidence that the popularization of CBD-fortified or CBD-labeled health products and CBD-ass

206 he putative antipsychotic-like properties of CBD in the mesolimbic circuitry.

207 published medicinal chemistry properties of CBD, as well as precise definitions of CBD-containing su

208 pERK1-2 blocked the inhibitory properties of CBD.

209 To investigate the defensive role of CBD, a feeding preference assay was performed with tobac

210 In contrast, co-treatment of CBD-targeted cells with inhibitors of PI3K-AKT-NF-kappaB

211 entific basis for increased medicinal use of CBD.

212 has sparked great interest in other uses of CBD, in ethical drugs and botanical supplements as well

213 systematic investigation of the viability of CBD as a psychiatric pharmacotherapy.

214 ived standard endoscopic therapies with only CBD stenting (group A).

215 affected the levels of cell death in CBD- or CBD/gamma-irradiated 3D GBM cultures.

216 that the popularization of CBD-fortified or CBD-labeled health products and CBD-associated health cl

217 morphine developed after 1 week while THC or CBD reduced allodynia over three weeks.

218 aucoma" AND "marijuana" or "cannabinoid" or "CBD." The top 20 Google search and YouTube results for e

219 r tetra-CBDs followed by (Z)-1,1,2,3,4-penta-CBD and hexa-CBD.

220 d trials examined the role of pharmaceutical CBD or medicinal cannabis.

221 Under placebo CBD conditions, active cannabis (1) was self-administere

222 Compared with placebo, CBD was associated with an increased likelihood of withd

223 eted an additional session to measure plasma CBD concentrations after administration of the highest C

224 Seven days post-CBD, blood gases and ventilation in 21% O2 were normal,

225 MS-IT-TOF technology, to detect and quantify CBD, CBDV, Delta(9)-THCV, and CBG in biological matrices

226 Up to 1.6 micromoles of rcSso7d-CBD was found to adsorb per gram of cellulose, yielding

227 These rcSso7d-CBD fusion proteins were solubly expressed and purified

228 ia were randomized in a 1:1 ratio to receive CBD (1000 mg/day; N=43) or placebo (N=45) alongside thei

229 Patients who received CBD also showed greater improvements that fell short of

230 pression of JNK activation partially reduced CBD-induced cell death in 3D GBM cultures.

231 Across regions, CBD increased GABA+ in controls, but decreased GABA+ in

232 le site by either of two inhibitory regions, CBD and LAVP, which block substrate access to the substr

233 The Convention on Biological Diversity's (CBD's) post-2020 global biodiversity framework and targe

234 nal flortaucipir uptake was able to separate CBD and PSP.

235 ide critical preclinical evidence supporting CBD treatment of seizures and alleviation of EEG abnorma

236 rences in tau strain potency between AD-tau, CBD-tau, and PSP-tau in non-Tg mice.

237 In summary, this study demonstrates that CBD suppresses inflammation through multiple mechanisms,

238 We also provide evidence that CBD alleviates alcohol-induced stress; consequently, imp

239 s observed in AS model mice, indicating that CBD administration could also help normalize the EEG def

240 This means that CBD, even when containing megagravel, cannot be used as

241 Specifically, we report that CBD can attenuate both behavioral and dopaminergic neuro

242 We further report that CBD controls downstream phosphorylation of the mTOR/p70S

243 ic archetypes, respectively, and reveal that CBD fulfills the criteria on the state ordering for a si

244 We show that CBD interacts with TRPV2 through a hydrophobic pocket lo

245 These findings suggest that CBD has beneficial effects in patients with schizophreni

246 lable data from clinical trials suggest that CBD is well tolerated and has relatively few serious adv

247 iffered in individual genes, suggesting that CBD may modulate gene expression by altering histone met

248 Unlike Delta(9)-tetrahydrocannabinol (THC), CBD does not act through the cannabinoid type 1 (CB1) re

249 tic nerve injury, which was reversed by THC, CBD, and morphine.

250 cm [95% CI, 0.80 to 3.86]; P < .001) and THC/CBD-equivalent cannabis (+2.83 cm [95% CI, 1.28 to 4.39]

251 DLP following vaporized THC-dominant and THC/CBD-equivalent cannabis compared with placebo was signif

252 ts vaporized THC-dominant, CBD-dominant, THC/CBD-equivalent, and placebo cannabis.

253 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) condition

254 ith THC-dominant cannabis, 21.09 cm with THC/CBD-equivalent cannabis, and 18.28 cm with placebo canna

255 ith THC-dominant cannabis, 20.59 cm with THC/CBD-equivalent cannabis, and 19.37 cm with placebo canna

256 delta-9-tetrahydrocannabinolic acid (THCA), CBD, and cannabidiolic acid (CBDA) that can be used for

257 The CBD dimer is oriented perpendicularly to the NBDs and it

258 Conserved loops at the CBD dimer interface straddle a conserved peripheral NBD

259 mendations, which are primarily aimed at the CBD post-2020 process, include moving from separate soci

260 nfirmed the physical interaction between the CBD and CaM.

261 s of adverse events were similar between the CBD and placebo groups.

262 atment, compared with the placebo group, the CBD group had lower levels of positive psychotic symptom

263 The SDLP did not differ significantly in the CBD (-0.34 cm [95% CI, -1.77 to 1.10]; P > .99), THC (0.

264 The ability of the CBD to bind to the surfaces of yeast cells was found to

265 also features strong antiaromaticity of the CBD units, as revealed by nucleus-independent chemical s

266 Gag nuclear entry does not require the CBD of TNPO3.

267 ssing, whose divergent C terminus shares the CBD common to all isoforms, but lacks the AID.

268 cAMP binding stabilizes the CBD-A against a denaturing force, and increases the fold

269 nd topographic conditions in structuring the CBD and PBD of snake assemblages, and determine the exte

270 Electrophysiology results revealed that the CBD-treated ganglia had delayed but much larger response

271 inhibitory segment (AIS), located within the CBD, is progressively removed by Ca(2+) and Ca(2+)/CaM,

272 Thus, CBD may have therapeutic potential in the treatment of a

273 Thus, CBD modulates glutamate-GABA systems, but prefrontal-GAB

274 as found to have effectiveness comparable to CBD both for decreasing the number and reducing the seve

275 BA pathways in ASD mean that the response to CBD in people with and without ASD may be not be the sam

276 Adding UDCA to CBD stenting, due to decrease in the stone size and subs

277 ect of adding Ursodeoxycholic acid (UDCA) to CBD stenting alone in order to reduce the size of large

278 2) in mice bearing aggressive mouse tumours, CBD-IL-12 accumulates in the tumour stroma due to expose

279 ved standard endoscopic therapies and UDCA + CBD stenting (group B) and controls only received standa

280 two-month period were assessed in the UDCA + CBD stenting group.

281 plays a critical role in channel gating upon CBD binding.

282 limited to childhood epilepsy studies, where CBD may have interacted with other medications such as c

283 (NGS)-based approaches to determine whether CBD would alter genome-wide histone modification and gen

284 esent study, we address the question whether CBD simultaneously induces a protective effect in GBM by

285 To test whether CBD 'shifts' glutamate and GABA levels; and to examine p

286 Studies conflict as to whether CBD attenuates or exacerbates the behavioral and cogniti

287 s and suggest a potential mechanism by which CBD may counteract the psychotomimetic and psychotropic

288 However, the mechanisms by which CBD mitigates the side effects of THC have not been iden

289 ronal and molecular mechanisms through which CBD may exert these effects are entirely unknown.

290 main psychoactive effects of cannabis, while CBD does not appear to have similar effects.

291 sy, the only adverse outcome associated with CBD treatment was diarrhoea (OR 5.03, 95% CI: 1.44-17.61

292 wing consumption, the SDLP was 19.03 cm with CBD-dominant cannabis, 19.88 cm with THC-dominant cannab

293 wing consumption, the SDLP was 18.21 cm with CBD-dominant cannabis, 20.59 cm with THC-dominant cannab

294 nd autistic-like behaviors linked to DS with CBD.

295 ed from the brains of three individuals with CBD.

296 Ten patients with CBD obstruction due to biliary stones were included as c

297 Pharmaceutical THC (with or without CBD) did not significantly affect any other primary outc

298 Pharmaceutical THC (with or without CBD) improved anxiety symptoms among individuals with ot

299 nce that pharmaceutical THC (with or without CBD) leads to a small improvement in symptoms of anxiety

300 Pharmaceutical THC (with or without CBD) worsened negative symptoms of psychosis in a single