ライフサイエンスコーパス: CBD

1 CBD administration in mice induced G-CSF, CXCL1, and M-C

2 CBD also exerted complex antiinflammatory actions that w

3 CBD and PBD patterns are similarly explained by spatial

4 CBD being a major component of Cannabis, our study indic

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

6 CBD often presents with a 'corticobasal syndrome' includ

7 CBD or vehicle was administered daily throughout the alc

8 CBD showed higher immunosuppressive effects than THC.

9 CBD significantly attenuated the alcohol feeding-induced

10 CBD stones were detected in 22.44% of patients in the in

11 CBD treatment also attenuated the respiratory burst of n

12 CBD was administered 90 min prior to cannabis administra

13 CBD was not a CB1 agonist but inhibited THC-dependent si

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

15 CBD, which alone produced no significant psychoactive or

16 CBD-induced suppressor cells were comprised of CD11b(+)L

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

18 CBD cases (n=152) and 3,311 controls, and 67 CBD cases and 439 controls in a replication stage.

19 either by cAMP binding, which selects for a CBD state devoid of steric clashes with the tetrameric C

20 pants experienced a CHD event, and 225 had a CBD event.

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

22 required for PKA inhibition and activation, CBD-B functions as a "gatekeeper" domain that modulates

23 nactive states independently of the adjacent CBD within a nearly degenerate free energy landscape.

24 n this study, we observed that administering CBD into naive mice triggers robust induction of CD11b(+

25 ly within the CHF-CBD group before and after CBD.

26 made in seven rats before and 6-7 days after CBD and were repeated in seven sham-operated rats.

27 on produces a more sustained hypopnoea after CBD than before, although this change may simply result

28 tes FR and VE in a pH-dependent manner after CBD, consistent with its postulated CCR function.

29 CP55,940 and CBD both signaled through Galpha(s).

30 al surveillance and the diagnosis of BeS and CBD.

31 knowledge about beryllium exposure, BeS, and CBD.

32 affecting the structure of the C-linker and CBD, the nature and extent of these cAMP-dependent chang

33 tudy correlates bona fide changes in PSP and CBD brains with cellular models, identifies drug targets

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

35 f rapamycin (mTOR) were increased in PSP and CBD brains.

36 argets to combat tau accumulation in PSP and CBD.

37 identified as novel drug targets for PSP and CBD.

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

39 that at least three human FABPs bind THC and CBD and demonstrate that THC and CBD inhibit the cellula

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

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

42 ve to the placebo condition, delta-9-THC and CBD had opposite effects on the functional connectivity

43 ind THC and CBD and demonstrate that THC and CBD inhibit the cellular uptake and catabolism of AEA by

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

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

46 ormational selection model in which each apo CBD dynamically samples both active and inactive states

47 P and of cCMP, a partial agonist, to the apo-CBD of HCN4.

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

49 terest due to the antiaromaticity brought by CBD circuits.

50 The latter is contributed by CBD-B and mediates capping of the cAMP bound to CBD-A.

51 nce, whereas this connection was enhanced by CBD.

52 domain that modulates the control exerted by CBD-A.

53 pecies-specific sensitivity to inhibition by CBD.

54 ion insights into motor domain inhibition by CBD.

55 Induction of MDSC by CBD was markedly attenuated in Kit-mutant (Kit(W/W-v)) m

56 as similarly increased in CHF and reduced by CBD (P < 0.05).

57 y was enhanced by delta-9-THC and reduced by CBD.

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

59 Cannabidiol (CBD) is a natural nonpsychotropic cannabinoid from marij

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

61 Cannabidiol (CBD), a constituent of cannabis with few psychoactive ef

62 -Tetrahydrocannabinol (THC) and cannabidiol (CBD) occur naturally in marijuana (Cannabis) and may be

63 rising equal amounts of THC and cannabidiol (CBD)) to mice bearing BRAF wild-type melanoma xenografts

64 drocannabinol (delta-9-THC) and cannabidiol (CBD), the two major derivatives of cannabis sativa, litt

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

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

67 abinol (THC), cannabinol (CBN), cannabidiol (CBD), and the metabolites 11-nor-9-carboxy-Delta(9)-tetr

68 otentially therapeutic compound cannabidiol (CBD).

69 ary nonpsychoactive constituent cannabidiol (CBD).

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

71 40), and two phytocannabinoids (cannabidiol (CBD) and Delta(9)-tetrahydrocannabinol (THC)) on arresti

72 cannabis-derived phytochemical, cannabidiol (CBD), has been shown to have pharmacotherapeutic efficac

73 abinoid of Cannabis sativa, (-)-cannabidiol (CBD), on human sebaceous gland function and determined t

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

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

76 (9)-tetrahydrocannabinol (THC), cannabidiol (CBD), and THC+CBD (1:1), and compared between wild-type

77 We hypothesized that denervation of the CB (CBD) chemoreceptors would reduce SNA, reduce apnoea and

78 vents h(-1) CHF, 108 +/- 48 events h(-1) CHF-CBD, P < 0.05).

79 HF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD).

80 am 0.79 +/- 0.06), and was attenuated in CHF-CBD animals (0.59 +/- 0.05) (P < 0.05 for all comparison

81 was increased in CHF-sham and reduced in CHF-CBD animals (213 +/- 58 events h(-1) CHF, 108 +/- 48 eve

82 .05), and this increase was not found in CHF-CBD animals (25 +/- 1% max, P < 0.05 vs. CHF-sham).

83 eased in CHF-sham animals and reduced in CHF-CBD animals (P < 0.05).

84 e augmented in CHF-sham and abolished in CHF-CBD animals.

85 2% reduction from pre-pace, P < 0.05) in CHF-CBD compared to CHF-sham rabbits.

86 were observed longitudinally within the CHF-CBD group before and after CBD.

87 m); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD).

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

89 In conclusion, CBD is effective in reducing RSNA, SRC and arrhythmia in

90 In patients with pathologically confirmed CBD, accuracy of diagnosis was similar under the new and

91 erties of such conjugated systems containing CBD.

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

93 r palsy (PSP) and corticobasal degeneration (CBD) are neurodegenerative four-repeat tauopathies with

94 Corticobasal degeneration (CBD) is a complex neurodegenerative disorder.

95 Corticobasal degeneration (CBD) is a neurodegenerative disorder affecting movement

96 ar palsy (PSP) or corticobasal degeneration (CBD) proved by autopsy.

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

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

99 Carotid body denervation (CBD) causes hypoventilation and increases the arterial P

100 e demonstrate that dehydroxylcannabidiol (DH-CBD), a nonpsychoactive cannabinoid, can rescue GlyR fun

101 Consistent with this idea, DH-CBD selectively rescues impaired presynaptic GlyR activi

102 Homomeric mutants are more sensitive to DH-CBD than are heteromers, suggesting presynaptic GlyRs as

103 Chronic beryllium disease (CBD) is a granulomatous lung disease characterized by th

104 Susceptibility to chronic beryllium disease (CBD) is linked to certain HLA-DP molecules, including HL

105 , are at risk for chronic beryllium disease (CBD), a debilitating inflammatory lung condition caused

106 ization (BeS) and chronic beryllium disease (CBD).

107 isease (CHD) and/or cerebrovascular disease (CBD) events in a large cohort of elderly men.

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

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

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

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

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

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

114 al-scale within a central business district (CBD).

115 006, the Convention on Biological Diversity (CBD) has driven MPA establishment, with 193 parties comm

116 Nations Convention on Biological Diversity (CBD), address major causes of biodiversity loss in part

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

118 mational changes of the cAMP-binding domain (CBD) have been previously mapped, only limited informati

119 connects a more distal cAMP-binding domain (CBD) to the inner pore.

120 l secretion signal, a chitin-binding domain (CBD), a fluorescent protein and a cleavage site to relea

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

122 g to a C-terminal Ca(2+)-CaM binding domain (CBD).

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

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

125 MP binds to two tandem cAMP-binding domains (CBD-A and -B) within the regulatory subunit of PKA (R),

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

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

128 ) can result in failure of common bile duct (CBD) stone removal and pancreatitis.

129 suggesting a stone in the common bile duct (CBD), but these factors are not highly sensitive or spec

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

131 abilizes the active conformation within each CBD and inter-CBD contacts, which require both cAMP and

132 proliferative, and antiinflammatory effects, CBD has potential as a promising therapeutic agent for t

133 reconstitution of the full-length endolysin-CBD complex with free CBD.

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

135 derived T cell lines from HLA-DP2-expressing CBD patients contained an expansion of Be-responsive Vbe

136 epertoire in the lungs of HLA-DP2-expressing CBD patients using promiscuous Valpha-chain pairing to r

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

138 re, we show that in contrast to rodent FAAH, CBD does not inhibit the enzymatic actions of human FAAH

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

140 rease in circulating AEA in humans following CBD consumption.

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

142 combined with EPBD is safe and effective for CBD stone removal in patients with difficult biliary can

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

144 underwent limited PS combined with EPBD for CBD stone removal, and these 58 patients were included i

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

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

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

148 Of the 12 patients who were positive for CBD stones by EUS, nine had successful ERCP, one failed

149 full-length endolysin-CBD complex with free CBD.

150 eful for differentiating underlying PSP from CBD pathology during life.

151 Furthermore, CBD improved alcohol-induced hepatic metabolic dysregula

152 Furthermore, CBD-MDSC suppressed LPS-induced acute inflammatory respo

153 olycyclic conjugated hydrocarbons with fused CBD.

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

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

156 gests a pathogenic role for these T cells in CBD.

157 ct a genome-wide association study (GWAS) in CBD cases (n=152) and 3,311 controls, and 67 CBD cases a

158 eneration of a common antigen specificity in CBD.

159 rcapnia (3-6% FiCO2 ) increased FR and VT in CBD rats (n = 4).

160 ctive conformation within each CBD and inter-CBD contacts, which require both cAMP and W260.

161 The inter-CBD interface is dispensable for intra-CBD conformationa

162 inter-CBD interface is dispensable for intra-CBD conformational selection, but is indispensable for f

163 Lastly, CBD enhanced the transcriptional activity of peroxisome

164 e of destabilizing the intramolecular linker/CBD interactions in R.

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

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

167 e progression (from BeS to CBD, or from mild CBD to more severe CBD).

168 structural transition for the apo-monomeric CBD occurs through a manifold of pathways that are more

169 We demonstrate that Intra-NASh CBD attenuates AMPH-induced sensitization, both in terms

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

171 We identify new CBD susceptibility loci and show that CBD and PSP share

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

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

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

175 fy differences between nfvPPA-PSP and nfvPPA-CBD both at presentation and longitudinally.

176 [20%]; 1 of 5 left-handed [20%]; and nfvPPA-CBD group: mean [IQR] age, 65 [54-81] years; 3 of 9 male

177 % [65-98]; P = .08) were found in the nfvPPA-CBD group.

178 clinical diversity of CBD and mimicry by non-CBD pathologies hinders accurate diagnosis.

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

180 uld discriminate malignant from nonmalignant CBD stenoses.

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

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

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

184 e neurodegenerative pathologies that are not CBD.

185 CP55,940, but not CBD, activated downstream Galpha(s) pathways via CB1 tar

186 te predict an increased risk of CHD, but not CBD, events in elderly men.

187 ata shed light on the mechanism of action of CBD in modulating the endocannabinoid tone in vivo and m

188 ular analyses to characterize the actions of CBD directly in the nucleus accumbens shell (NASh), a br

189 Administration of CBD to cultured human sebocytes and human skin organ cul

190 Testing for association of CBD with top progressive supranuclear palsy (PSP) GWAS s

191 opancreatography (ERCP) for the detection of CBD stones in all patients.

192 s significantly associated with detection of CBD stones in patients who underwent EUS > 7 days after

193 ccurate diagnostic tool for the detection of CBD stones, and can prevent the unnecessary use of ERCP.

194 100% and specificity of 80% for detection of CBD stones.

195 tive than clinical signs in the diagnosis of CBD.

196 n accurate ante mortem clinical diagnosis of CBD.

197 matory response in the lung is diagnostic of CBD.

198 The clinical diversity of CBD and mimicry by non-CBD pathologies hinders accurate

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

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

201 Effect of CBD on naive immune system is not precisely understood.

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

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

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

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

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

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

208 l data outlining the therapeutic efficacy of CBD for the treatment of motivational disorders such as

209 For those 18 patients without evidence of CBD stones by EUS, no false-negative case was noted duri

210 nnabis ratings did not vary as a function of CBD dose relative to placebo capsules.

211 oratory study was to assess the influence of CBD (0, 200, 400, 800 mg, p.o.) pretreatment on the rein

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

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

214 roadens the recognised clinical phenotype of CBD but does not sufficiently improve the specificity of

215 provide a good prediction of the presence of CBD stones, even in patients who fulfill the criteria fo

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

217 lly significant association with the risk of CBD events.

218 cy is critical to explain the sensitivity of CBD-B to weak interactions with C and its high affinity

219 pose that the region immediately upstream of CBD is an autoinhibitory domain that maintains the close

220 entific basis for increased medicinal use of CBD.

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

222 postmortem pathological diagnosis of PSP or CBD.

223 Further, the effect of oral CBD on smoked cannabis administration is unknown.

224 These findings suggest that oral CBD does not reduce the reinforcing, physiological, or p

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

226 e prototypical member of the RPC (RING, PHD, CBD) family of ubiquitin-ligases, characterized by the p

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

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

229 In the absence of cAMP, the most populated CBD state leads to steric clashes with the activated or

230 diagnostic criteria of probable or possible CBD, demonstrating that the new criteria lacks the neces

231 Post-CBD, RTN inhibition reduced FR and VE in proportion to a

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

233 ion produced a more sustained hypopnoea post-CBD than before; in hyperoxia, the responses were identi

234 iteria: 9/19 (47%) met criteria for probable CBD at presentation, 13/19 (68%) at last clinical assess

235 nuclear palsy/corticobasal degeneration (PSP/CBD) or multiple-system atrophy (MSA) by PET and clinica

236 ortality was significantly increased for PSP/CBD (HR=5.2) and MSA (HR=5.6) classified by PET, but for

237 MSA (HR=5.6) classified by PET, but for PSP/CBD only when diagnosed by clinical follow-up (HR=4.5).

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

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

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

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

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

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

244 BeS to CBD, or from mild CBD to more severe CBD).

245 sham CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD).

246 n three groups of animals: (1) sham CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); and (3) CH

247 ithm for the evaluation of clinically silent CBD stones during routine cholecystectomy is unclear.

248 cell line and local drug deposition in swine CBD tissues.

249 a higher average drug deposit dose in swine CBD walls with intrabiliary RF hyperthermia than without

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

251 sebaceous gland function and determined that CBD behaves as a highly effective sebostatic agent.

252 We found that CBD-B plays an essential role in R-C interaction and pro

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

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

255 fy new CBD susceptibility loci and show that CBD and PSP share a genetic risk factor other than MAPT

256 Recent reports suggest that CBD and THC elevate the levels of the endocannabinoid an

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

258 Together, the results suggest that CBD may induce activation of PPAR-gamma in mast cells le

259 Preliminary evidence suggests that CBD-B dynamics are critical for its gatekeeper function.

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

261 cannabinol (THC), cannabidiol (CBD), and THC+CBD (1:1), and compared between wild-type and HD cells.

262 t but inhibited THC-dependent signaling (THC+CBD).

263 ollowing oral administration of delta-9-THC, CBD, or a placebo capsule.

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

265 We found that alpha1(IV)NC1 binds the CBD of MMP-2 and forming a stable complex that prevents

266 athways become disallowed, pre-confining the CBD conformational ensemble to a tetramer-compatible sta

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

268 ranulocytic amoebocytes; the function of the CBD is not understood.

269 P799L are located immediate upstream of the CBD.

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

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

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

273 n where MPAs should be placed to support the CBD's overall goal to avert biodiversity loss.

274 Our data indicate that the CBD exists in a dynamic two-state equilibrium, whose pos

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

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

277 Thus, CBD, by creating a new antigen by indirectly modifying t

278 The determinants of progression from BeS to CBD are uncertain, but higher exposures and the presence

279 can detect disease progression (from BeS to CBD, or from mild CBD to more severe CBD).

280 nd adjacent detachable Ca(2+)-CaM binding to CBD sterically interferes with this autoinhibition.

281 the first C-subunit prior to the binding to CBD-A.

282 -B and mediates capping of the cAMP bound to CBD-A.

283 bacterium Lactococcus lactis, the truncated CBD is also produced, showing that the alternative start

284 The truncated CBD is produced through an internal translation start si

285 evidence shows that THC exacerbates, whereas CBD protects from, such harmful effects.

286 accumbens as a critical brain region whereby CBD can produce effects similar to antipsychotic medicat

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

288 However, the mechanisms by which CBD may produce antipsychotic effects are entirely unkno

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

290 e molecular signaling pathways through which CBD may functionally reduce schizophrenia-like neuropsyc

291 While CBD-A in RIalpha is required for PKA inhibition and acti

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

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

294 s typically administered when a patient with CBD exhibits evidence of significant lung function abnor

295 In addition, patients with CBD may present with aphasia or behavioural change.

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

297 iteria were more common in the patients with CBD pathology (n=19) than without (n=14).

298 llowing difficulty; atrophy in patients with CBD spread anteriorly in prefrontal regions consistent w

299 occludes C-subunit recognition sites within CBD-A.

300 nts with a corticobasal syndrome but without CBD pathology all (14/14) met the new diagnostic criteri