ライフサイエンスコーパス: LSD

1 LSD affinity, in contrast, was unaffected by either muta

2 LSD also increased global integration by inflating the l

3 LSD altered sensorimotor gating in a human model of psyc

4 LSD catalyzes a double-bond cleavage reaction that is cl

5 LSD dissociates exceptionally slow from both 5-HT2BR and

6 LSD has profound modulatory effects on consciousness and

7 LSD induces profound psychedelic effects, including chan

8 LSD may alter meaningfulness by increasing activity in c

9 LSD significantly increased blood pressure, heart rate,

10 LSD therapies for systemic diseases have been developed,

11 LSD's marked effects on the visual cortex did not signif

12 LSD-positive human urine specimens from LSD users were a

13 LSDs mainly stem from deficiencies in lysosomal enzymes,

14 inding of 5-HT(1a) receptors as well as 125I-LSD-labeled binding of 5-HT(2a) receptors were evaluated

15 Autoradiographic analysis of 125I-LSD-labeled 5-HT(2a) receptor binding revealed no signif

16 f binding sites with high affinity for [125I]LSD that correspond to 5-HT5A receptors and that are con

17 raphy with 3H-lysergic acid diethylamide (3H-LSD), 3H-8-hydroxy-2-[di-N-propylamine] tetralin (3H-8-O

18 on in 5-HT receptor binding measured with 3H-LSD was observed between midgestation and infancy, and b

19 using [3H]-lysergic acid diethylamide ([3H]-LSD) binding to cell membranes of human embryonic kidney

20 k order of affinity for displacement of [3H]-LSD from the cloned human 5-HT7 receptor was: methiothep

21 methyltransferase, 22 JmjC demethylase and 4 LSD demethylase genes in F. vesca.

22 the mobility of this lid greatly accelerates LSD's binding kinetics and selectively dampens LSD-media

23 conformational rearrangements to accommodate LSD, providing a structural explanation for the conforma

24 ealed marked changes in brain activity after LSD that correlated strongly with its characteristic psy

25 o the full agonist 5-HT, the partial agonist LSD, and the inverse agonist Ketanserin.

26 Moreover, all LSD cells studied show extraordinary sensitivity to bref

27 s of DARPP-32, the effects of D-amphetamine, LSD, and PCP on two behavioral parameters-sensorimotor g

28 alidated the interaction between miR-137 and LSD-1.

29 Moreover, DOI and LSD showed similarities in the transcriptome fingerprint

30 to neurodegeneration and tissue injury, and LSD defects in immune cells may not preclude an appropri

31 hedelic substances: psilocybin, ketamine and LSD.

32 While lisuride and LSD both act at 2AR expressed by cortex neurons to regul

33 chondrial and lysosomal pathways in NBIA and LSD, respectively, and with Parkinson's disease represen

34 By studying wild-type and LSD mice at diverse time-points after HCT, we showed the

35 In animals, LSD disrupts prepulse inhibition (PPI) of the acoustic s

36 t associated with the development of another LSD, Tay-Sachs disease, thus suggesting general applicab

37 The mucopolysaccharidoses (MPS) are LSDs defined by the storage of glycosaminoglycans.

38 orders and alcohol dependence, drugs such as LSD showed initial therapeutic promise before prohibitiv

39 amphetamine), serotonergic agonists (such as LSD), and glutamatergic antagonists (such as PCP) all in

40 xicating properties of hallucinogens such as LSD.

41 y of the distributions were observed between LSDs and NLSDs.

42 Both LSD and efavirenz reduce ambulation in a novel open-fiel

43 The drug discrimination data in both LSD- and DOI-trained rats paralleled the binding data us

44 netic memory, and that erasure of H3K4me2 by LSD/KDM1 in the germline prevents the inappropriate tran

45 thers, openness, and trust were increased by LSD.

46 The predominant effects induced by LSD included visual hallucinations, audiovisual synesthe

47 Adverse effects produced by LSD completely subsided within 72 hours.

48 cortex neurons to regulate phospholipase C, LSD responses also involve pertussis toxin-sensitive het

49 Augmenting cellular LSDs that affect PLIN2 associations with these proteins,

50 ent of Gaucher disease (GD), the most common LSD.

51 reported by 33% of the sample, most commonly LSD (lysergic acid diethylamide), amphetamines, Ecstasy

52 We compare LSDs and nonlysosomal storage diseases (NLSDs) in terms

53 As a consequence, LSD chondrocytes fail to properly secrete collagens, the

54 D's binding kinetics and selectively dampens LSD-mediated beta-arrestin2 recruitment.

55 d that the mRNA level of H3K4me2 demethylase LSD/KDM1, spr-5, was significantly reduced in the F0 exp

56 ry of a lysine-specific histone demethylase (LSD 1).

57 T (CoREST), and lysine-specific demethylase (LSD) 1.

58 ibition of the lysine-specific demethylases (LSDs or KDM1s) and JmjC families of N-methyl-lysine deme

59 and morphological changes during developing LSDs that are extremely critical for many metabolic proc

60 ared (FTIR) spectrometer: low-sulfur diesel (LSD), ultralow-sulfur diesel (ULSD), and a blend of 20%

61 an-biodiesel process, and low-sulfur diesel (LSD).

62 Rats placed on low salt diet (LSD) or normal salt diet (NSD) were treated with cyclosp

63 ce subjected to 7 days of a low sodium diet (LSD) containing 0.01% Na(+) , a normal sodium diet (NSD)

64 e coordinated response to a low-sodium diet (LSD).

65 hedelics such as lysergic acid diethylamide (LSD) and dissociative drugs such as phencyclidine (PCP)

66 se of ayahuasca, lysergic acid diethylamide (LSD) and magic mushrooms; demographics, current well-bei

67 f (3)H-labeled d-lysergic acid diethylamide (LSD) binding to recombinant human 5-hydroxytryptamine 6

68 nterest in using lysergic acid diethylamide (LSD) in clinical psychiatric research and practice.

69 Lysergic acid diethylamide (LSD) is a non-selective serotonin-receptor agonist that

70 Lysergic acid diethylamide (LSD) is the prototypical psychedelic drug, but its effec

71 e the effects of lysergic acid diethylamide (LSD) on the human brain but the underlying dynamics are

72 tamine (DOI) and lysergic acid diethylamide (LSD) stimulated a head-twitch behavioral response that w

73 ing the ergoline lysergic acid diethylamide (LSD), and a series of substituted tryptamine and pheneth

74 tor ligands like lysergic acid diethylamide (LSD), in which the amine nitrogen is embedded in a heter

75 psilocybin, and lysergic acid diethylamide (LSD), profoundly affect perception, cognition, and mood.

76 The hallucinogen lysergic acid diethylamide (LSD; 0.1 mg/kg, i.p.) caused a time-dependent increase i

77 ite of action of lysergic acid diethylamine (LSD), appears to dominate efavirenz's behavioral profile

78 allucinogenic agent, N,N-diethyllysergamide, LSD-25.

79 hat toxic lipids relevant to three different LSDs disrupt multiple lysosomal and other cellular funct

80 lar to bacterial lignostilbene dioxygenases (LSD).

81 nation assay in rats trained to discriminate LSD from saline, and failed to substitute, a result typi

82 otent to LSD in rats trained to discriminate LSD from saline.

83 drug-lever responding in rats discriminating LSD from saline, and this effect is abolished by selecti

84 (SP), goat pox (GP), and lumpy skin disease (LSD), caused by capripoxviruses (CaPVs), are economicall

85 ) deficits due to lysosomal storage disease (LSD mice).

86 manifestations of lysosomal storage disease (LSD) are a significant health problem for affected patie

87 bbe disease) is a lysosomal storage disease (LSD) caused by a deficiency in galactocerebrosidase (GAL

88 neurodegenerative lysosomal storage disease (LSD) caused by a deficiency in palmitoyl protein thioest

89 GD was the first lysosomal storage disease (LSD) for which enzyme therapy became available, and alth

90 neurodegenerative lysosomal storage disease (LSD) that has no effective treatment.

91 ease, a prevalent lysosomal storage disease (LSD), is caused by insufficient activity of acid beta-gl

92 Lysosomal storage diseases (LSD) are metabolic disorders characterized by accumulati

93 For most lysosomal storage diseases (LSDs) affecting the CNS, there is currently no cure.

94 common for other lysosomal storage diseases (LSDs) and whether BK channel agonists rescue abnormal ly

95 Lysosomal storage diseases (LSDs) are a class of metabolic disorders caused by mutat

96 Lysosomal storage diseases (LSDs) are a family of disorders that result from inherit

97 Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by d

98 Lysosomal storage diseases (LSDs) are monogenic disorders of metabolism caused by de

99 presence of four lysosomal storage diseases (LSDs) at increased frequency in the Ashkenazi Jewish pop

100 Lysosomal storage diseases (LSDs) represent a significant portion of inborn metaboli

101 Lysosomal storage diseases (LSDs), as a group, are among the most common inherited d

102 dysfunction and lysosomal storage diseases (LSDs), but the mechanisms by which lysosomes acquire and

103 eutic agents for lysosomal storage diseases (LSDs), inherited metabolic disorders caused by defects i

104 d in a number of lysosomal storage diseases (LSDs).

105 dysfunction and lysosomal storage diseases (LSDs).

106 o five different lysosomal storage diseases (LSDs): MPSI, MPSIIIB, MPSVII, Niemann-Pick type A/B, and

107 osomal recessive lysosomal storage disorder (LSD) caused by deficiency of the lysosomal enzyme acid a

108 inflammation in the lipid storage disorder (LSD) Niemann-Pick C (NPC), we deleted the macrophage inf

109 n's disease and lysosomal storage disorders (LSD) with the common theme being a combined lysosomal-mi

110 ases, including lysosomal storage disorders (LSD).

111 o virtually all lysosomal storage disorders (LSDs) and to common neurodegenerative diseases like Alzh

112 n 50 hereditary lysosomal storage disorders (LSDs) are currently described.

113 urodegenerative lysosomal storage disorders (LSDs) are severe and untreatable, and mechanisms underly

114 lable for other lysosomal storage disorders (LSDs) but none of these highly expensive treatments has

115 ment option for lysosomal storage disorders (LSDs) caused by deficiencies of soluble lysosomal enzyme

116 an 40 different lysosomal storage disorders (LSDs) cumulatively affect one in 5000 live births, and i

117 Lysosomal storage disorders (LSDs) occur at a frequency of 1 in every 5,000 live birt

118 In lysosomal storage disorders (LSDs), a number of highly prevalent alleles have missens

119 ases, including lysosomal storage disorders (LSDs), for which hematopoietic cell transplantation (HCT

120 bone growth in lysosomal storage disorders (LSDs).

121 majority of >50 lysosomal storage disorders (LSDs).

122 ent epitopes were identified in two distinct LSD disease models, implying a unique vascular signature

123 We also found that DOI, LSD, and LHM each induced distinct transcriptome fingerp

124 usly described large T stabilization domain (LSD) loop that binds E3 ligases, such as Fbw7.

125 d by sT through its LT-stabilization domain (LSD).

126 R Ca(2+) or blocking IP3Rs caused a dramatic LSD-like lysosome storage phenotype.

127 LIN2 associates with lipid storage droplets (LSDs), but other functions of PLIN2 remain unclear.

128 n addition to marked hallucinogenic effects, LSD exerts methylenedioxymethamphetamine-like empathogen

129 ssays in rats trained to discriminate either LSD or DOI from saline were employed to assess the hallu

130 As expected, LSD did not alter measured GFR and increased the abundan

131 ation in moisture (LSD<1.33), dietary fibre (LSD<0.15) and total sugar (LSD<0.09) were found to be in

132 repeated-measures ANOVA, and post hoc Fisher LSD tests revealed significant (P < or = 0.05, 0.01) dif

133 ng; and provides a molecular explanation for LSD's actions at human serotonin receptors.

134 The new analogue substituted fully for LSD in drug discrimination studies and was 5-fold more p

135 of geographic distribution was observed for LSD versus NLSD mutations-with some being more common in

136 Although 1 fully substituted for LSD in the DD assays (ED50 = 33.5 mumol/kg), neither 8 n

137 For example, 7b substituted for LSD in the drug discrimination assay with an ED50 of 61

138 Neither 3a nor 3b substituted for LSD or DOI up to doses of 50 micromol/kg.

139 5 mumol/kg), neither 8 nor 9 substituted for LSD, with just 50% of the rats administered 8 selecting

140 epresent the principal molecular targets for LSD-like hallucinogens and atypical antipsychotic drugs.

141 present a potential therapeutic approach for LSDs.

142 lls as a potentially universal biomarker for LSDs.

143 in rats trained to discriminate saline from LSD tartrate (0.08 mg/kg) and for the ability to displac

144 in rats trained to discriminate saline from LSD tartrate (0.08 mg/kg).

145 in rats trained to discriminate saline from LSD tartrate (0.08 mg/kg).

146 LSD-positive human urine specimens from LSD users were also analyzed.

147 The prototypical hallucinogen LSD acts via serotonin receptors, and here we describe t

148 zetidine gave a lysergamide with the highest LSD-like behavioral activity in the rat two lever drug d

149 eline by 105+/-14 nM (p<0.05, ANOVA post hoc LSD test).

150 e observed to significantly (ANOVA, post hoc LSD) increase versus vehicle treated animals (saline 1 m

151 e determined through examination of [(125)I] LSD binding, protein expression (by use of Western blott

152 uthors observed significantly higher [(125)I]LSD binding in the prefrontal cortex and greater protein

153 M3 expression) failed to alter adiposity in LSD animals.

154 and protein expressions at 7 and 28 days in LSD rats.

155 nner for treating the global CNS deficits in LSD patients.

156 leads to a blockage of the autophagy flux in LSD chondrocytes.

157 ified AAVs expressing the enzymes lacking in LSD mice reconstituted enzyme activity throughout the br

158 the systemic nature of lipid perturbation in LSD.

159 By comparison, 1a fully substituted in LSD-trained rats.

160 ife" of lysosomes in the normal state and in LSDs.

161 characteristic feature of affected cells in LSDs.

162 eutic target to rescue enzyme homeostasis in LSDs.

163 ulation to rescue destabilizing mutations in LSDs.

164 despread cellular perturbations occurring in LSDs, how they might be linked and interventions that ma

165 ion, in modulating lysosomal proteostasis in LSDs.

166 disease processes and treatment response in LSDs.

167 oop to correct abnormal lysosomal storage in LSDs.

168 gonists rescue abnormal lysosomal storage in LSDs.

169 the diverse pathogenic mechanisms at work in LSDs.

170 s that will be most effective for individual LSDs.

171 otype in that some 5-HT(2A)R agonists induce LSD-like hallucinations, while others lack this psychoac

172 The fact that the naphthofurans lack LSD-like activity suggests that they do not bind to the

173 ip or with refinery fractions of ULSD, low- (LSD), and high sulfur diesel (HSD) and monitored for sul

174 channels underlies the pathogenesis of many LSDs and possibly that of metabolic and common neurodege

175 (LSD<0.05), while the variation in moisture (LSD<1.33), dietary fibre (LSD<0.15) and total sugar (LSD

176 eins (VCAM1 and MCP1) were found in multiple LSDs.

177 titute the transforming activity of a mutant LSD sT protein.

178 PPT1, cause a devastating neurodegenerative LSD, INCL.

179 L) is the most devastating neurodegenerative LSD, which is caused by inactivating mutations in the pa

180 rophy (MLD), a progressive neurodegenerative LSD.

181 mon (one in 12,500 births) neurodegenerative LSDs.

182 the most common childhood neurodegenerative LSDs.

183 neurodegenerative and non-neurodegenerative LSDs and suggest that the beneficial effects of chemical

184 neurodegenerative and non-neurodegenerative LSDs.

185 neurodegenerative and non-neurodegenerative LSDs.

186 Administration of LSD to healthy subjects produced pronounced alterations

187 tures for millennia [1]; however, because of LSD's unique potency and the timing of its discovery (co

188 In the case of LSD, the NH3 emissions were elevated, and in the case of

189 mized and evaluated for the determination of LSD, its analogs, and metabolites in spiked human urine

190 In addition, the stimulatory effect of LSD on exploratory activity was attenuated in 5A-KO mice

191 The subjective effects of LSD are fully blocked by a 5-HT2A receptor antagonist.

192 est that some of the psychotropic effects of LSD may be mediated by 5-HT5A receptors.

193 Here we studied the effects of LSD on intrinsic functional connectivity within the huma

194 ver, no data are available on the effects of LSD on PPI in humans.

195 s on the subjective and autonomic effects of LSD, and its endocrine effects are unknown.

196 LSD indicates that the N,N-diethyl groups of LSD optimally bind when they are oriented in a conformat

197 many of the cardiovascular manifestations of LSD.

198 y thus reveals an unexpected binding mode of LSD; illuminates key features of its kinetics, stereoche

199 inster (spin) mutants, a Drosophila model of LSD-like neurodegeneration.

200 In mouse models of LSD, normalization of mTORC1 signaling or stimulation of

201 n reduced expression of the worm ortholog of LSD-1 (T08D10.2), a histone demethylase; knockdown by RN

202 Concentrations as low as 2.5 ppt of LSD and several of its analogs were detected in spiked h

203 uperimposable upon, the A, B, and C rings of LSD.

204 nation for the conformational selectivity of LSD's key diethylamide moiety.

205 acker et al. report the crystal structure of LSD in complex with one of its major targets in the brai

206 nd here we describe the crystal structure of LSD in complex with the human serotonin receptor 5-HT2B.

207 T(2A) receptors, which is also the target of LSD-like drugs.

208 of screens that was most similar to that of LSD itself.

209 ntal metrics studied are lower than those of LSD and comparable to soybean biodiesel.

210 an model of psychosis, supporting the use of LSD in translational psychiatric research.

211 More than 60% of LSDs have CNS involvement.

212 mplex strategies for metabolic correction of LSDs.

213 There are many recognized forms of LSDs and, although individually rare, their combined pre

214 sses are also cytoprotective in all forms of LSDs studied.

215 K agonist, NS1619 and NS11021 in a number of LSDs including NPC1, mild cases of mucolipidosis type IV

216 Over two-thirds of LSDs involve central nervous system (CNS) dysfunction (p

217 hyma and thus hinders effective treatment of LSDs with CNS involvement.

218 therapeutic approaches for the treatment of LSDs.

219 hat AP-5 deficiency represents a new type of LSDs.

220 ts in vitro transforming activity depends on LSD interactions rather than PP2A targeting.

221 After the first English language report on LSD in 1950, psychedelics enjoyed a short-lived relation

222 hylamines cannot be directly superimposed on LSD in a common binding orientation for these two chemic

223 ins and in mouse models representing 6 other LSDs.

224 oach for the treatment of MPS IIIA and other LSDs with CNS involvement.

225 ikely improve therapeutic efficacy for other LSDs with complex pathological and clinical presentation

226 dysregulate lysosomal acidification in other LSDs and common neurodegenerative diseases.

227 The target tissues in other LSDs receive much lower doses of enzyme and intravenous

228 ed with ENT3 mutations and potentially other LSDs.

229 assay approach can be used for several other LSDs and genetic disorders, especially those that rely o

230 Compared with placebo, LSD decreased PPI.

231 bind to 5-HT2 receptor subtypes and possess LSD-like behavioral effects.

232 also suggest that both 1 and 3 would possess LSD-like psychopharmacology in humans.

233 (MPSVII, Sly syndrome), develop progressive LSD unless provided with GUSB early in life.

234 pe IIIA (MPS IIIA) is an autosomic recessive LSD caused by a deficiency in sulfamidase, a sulfatase i

235 reported to delay neuronal loss in Sandhoff LSD mice by inhibiting macrophage infiltration.

236 In a controlled clinical setting, LSD can be used safely, but it produces significant symp

237 ution, in the Ashkenazi population, of seven LSD and seven NLSD mutations.

238 In several LSDs, cells of the reticuloendothelial (RE) system are t

239 ly, autophagy, which is increased in several LSDs, is responsive to dietary intervention and is reduc

240 Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiolog

241 reveal shared principles relevant to several LSDs, in which diverse cellular and biochemical disrupti

242 peutic benefits in a mouse model of a severe LSD.

243 and Fe; most of which varied significantly (LSD<0.05) among the genotypes.

244 ontents were found to be vary significantly (LSD<0.05), while the variation in moisture (LSD<1.33), d

245 ed as small-molecule chaperones for specific LSDs.

246 lly distinguished by mutagenesis from MCV sT LSD-dependent 4E-BP1 hyperphosphorylation and viral DNA

247 Mutating the sT LSD decreases LT protein levels and eliminates synergism

248 mg to 37.77 mg per 100g edible strawberries (LSD<0.060).

249 omized, placebo-controlled, crossover study, LSD (200 mug) and placebo were administered to 16 health

250 ), dietary fibre (LSD<0.15) and total sugar (LSD<0.09) were found to be insignificant among the genot

251 c treatment was evaluated in 1 of the tested LSD mouse models.

252 ion model that was slightly more potent than LSD itself.

253 activity but about 10-fold less potent than LSD.

254 sent results provide the first evidence that LSD selectively expands global connectivity in the brain

255 We found that LSD alters the energy and the power of individual harmon

256 ntly published by and in Nature, reveal that LSD 1's specificity and activity is in fact regulated by

257 They showed that LSD 1, a nuclear amine oxidase homolog, is a bona fide h

258 cular dynamics (MD) simulations suggest that LSD's slow binding kinetics may be due to a "lid" formed

259 SH immunoreactivity was more than double the LSD value.

260 In the case of the LSD and ULSD fuels, the SCR system also significantly re

261 alidated this metric in a mouse model of the LSD Niemann-Pick type C1 disease (NPC1) and in a prospec

262 is uniquely comprehensive examination of the LSD state represents an important advance in scientific

263 In contrast, in PC2(-/-) mice, MAP on the LSD was not greater than in wild-type mice, but plasma g

264 enerally marked nervous tissue damage in the LSDs here evaluated.

265 5000 live births, and in the majority of the LSDs, neurodegeneration is a prominent feature.

266 rrected the impaired Ca(2+) release in these LSDs and successfully rescued the abnormal lysosomal sto

267 ated Ca(2+) release was compromised in these LSDs.

268 Thus, LSDs can be characterized as diseases of deficiency as w

269 diction, as (R)-2 proved to be equipotent to LSD in rats trained to discriminate LSD from saline.

270 ysergamide with pharmacology most similar to LSD indicates that the N,N-diethyl groups of LSD optimal

271 Similar to LSD, efavirenz induces head-twitch responses in wild-typ

272 In order to more successfully treat LSDs, a shift in focus towards a combination therapy may

273 uction or methanogenesis rates between ULSD, LSD, and HSD.

274 crease in global connectivity observed under LSD correlated with subjective reports of "ego dissoluti

275 the active repertoire of brain states under LSD closely follows power-laws indicating a re-organizat

276 two-lever drug discrimination paradigm using LSD- and DOI-trained rats.

277 two-lever drug discrimination paradigm using LSD-trained rats, was attenuated or abolished for all of

278 ice, HSD for 1 week did not alter MAP versus LSD mice, but plasma gamma-MSH immunoreactivity was more

279 When LSD (10 microM) was directly applied to the PFC by rever

280 ly, we hypothesized that cells affected with LSD have increased energy expenditure for biosynthesis b

281 he effect of the HSD (8% NaCl) compared with LSD (0.07%) on mean arterial pressure (MAP) in mice with

282 avioral effect in rodents is consistent with LSD-like activity mediated via the 5-HT(2A) receptor.

283 on the first modern brain imaging study with LSD and three separate clinical trials of psilocybin for

284 lactosialidosis and possibly for others with LSDs that primarily involve the RE system.

285 The relatively small number of patients with LSDs and lack of validated biomarkers are substantial ch

286 ic phenotype in nonneuropathic patients with LSDs.