ライフサイエンスコーパス: morphine

1 ot change a second (decreased sensitivity to morphine).

2 ing by mu-opioid receptor agonists DAMGO and morphine.

3 ioid neuronal adaptations that are seen with morphine.

4 near-maximal respiratory depressant doses of morphine.

5 respiratory rate depression at all doses of morphine.

6 n, and in measures of long-term tolerance to morphine.

7 ndence and rewarding actions associated with morphine.

8 IV-infected macaques under conditioning with morphine.

9 ly antagonized the antinociception effect of morphine.

10 the infection risk between other opioids and morphine.

11 ssion in the ventral striatum is affected by morphine.

12 rally active with similar in vivo potency to morphine.

13 that are triggered by chronic treatment with morphine.

14 tribute to the sexually dimorphic effects of morphine.

15 mmatory response to prolonged treatment with morphine.

16 ases in response to a single dose of 1 mg/kg morphine.

17 with a trend effect of CBD, and no effect of morphine.

18 ad no effect on rate following high doses of morphine.

19 liability, and respiratory depression versus morphine.

20 ogenetically-driven immobility is blocked by morphine.

21 te following administration of high doses of morphine.

22 exhibits a higher acute toxic potential than morphine.

23 injury, which was reversed by THC, CBD, and morphine.

24 session 1, participants received intravenous morphine (10 mg/70 kg) in the clinic to ensure tolerabil

25 8360 (0.1 mg/kg per day i.p. x 12 days) with morphine (10 mg/kg per day x 12 days) blocked morphine t

26 icantly shorter with buprenorphine than with morphine (15 days vs. 28 days), as was the median length

27 tions of morphine, the two main metabolites, morphine-3-glucuronide and morphine-6-glucuronide, were

28 n of Arg259 with Leu resulted in the loss of morphine, 4-methylumbelliferone, and zidovudine glucuron

29 Lidocaine (5 mg/L), flunixin (8 mg/L) and morphine (48 mg/L) prevented the associated reduction in

30 Intrathecal application of morphine (5 ng/50 mul) significantly reduced Adelta- and

31 main metabolites, morphine-3-glucuronide and morphine-6-glucuronide, were quantified by high-performa

32 R4) as a promising pharmacological target in morphine abstinence.

33 behavioral effects of VU0155041 treatment in morphine abstinent mice were correlated with restored ex

34 xiety and blunted locomotor sensitization in morphine abstinent mice.

35 We found that DAMGO, but not morphine, activates Ras-related C3 botulinum toxin subst

36 lta(9)-tetrahydrocannabinol, cannabidiol, or morphine ad libitum.

37 ound that in a subpopulation of SIV-infected morphine addicted macaques, the presence of drugs of abu

38 ciency virus (SIV) infections in control and morphine-addicted macaques, we found that two of the mos

39 genetic risk identified the enrichment terms morphine addiction and retrograde endocannabinoid signal

40 t offer a novel therapeutic intervention for morphine addiction.

41 ucible SIV reservoir in lymph nodes (LNs) of morphine administered RMs.

42 Further, chronic morphine administration increases the numbers of circula

43 esults suggest that probiotic therapy during morphine administration may be a promising, safe, and in

44 study the effects of smoke exposure, chronic morphine administration, and HIV infection using the NSG

45 high-gamma-frequency activity with repeated morphine administration.

46 tical models that incorporate the effects of morphine-altered antibody responses on HIV/SIV dynamics.

47 Using our model, we quantified how morphine alters virus-specific antibody responses, and h

48 demonstrate that sleep disruption diminishes morphine analgesia and modulates reward processing.

49 demonstrate that sleep disruption attenuates morphine analgesia in humans and suggest that sleep dist

50 (+)-1 significantly increased and prolonged morphine analgesia in vivo.

51 Morphine analgesia was diminished threefold under FA, re

52 VEGFR-2 inhibition also attenuated morphine analgesic tolerance in rats.

53 The mechanism underlying morphine analgesic tolerance still remains unresolved.

54 We show that morphine analgesic tolerance was significantly attenuate

55 can be targeted to blunt the development of morphine analgesic tolerance, without affecting normal P

56 mice with naive fecal microbiota reinstated morphine analgesic tolerance.

57 ad received more sedatives, whereas doses of morphine and antipsychotics were equal.

58 development of antinociceptive tolerance to morphine and attenuated morphine-induced physical depend

59 ) allowed best discriminating between 4-week morphine and cocaine abstinence in the nucleus accumbens

60 he long-term transcriptional consequences of morphine and cocaine exposure, we identified the metabot

61 3,000 THIQ alkaloids, including the opioids morphine and codeine.

62 abilized by phosphorylated muOR bound to the morphine and D-Ala(2), N-MePhe(4), Gly-ol]-enkephalin (D

63 hat underlie the spatiotemporal signaling of morphine and DAMGO.

64 Opioids, such as morphine and fentanyl, are widely used for the treatment

65 dy sought to explore the association between morphine and ischemic events in 5,438 patients treated w

66 a better understanding of the disposition of morphine and its metabolites in critically ill children

67 predictors of pharmacokinetic parameters of morphine and its metabolites.

68 tion and blocks acute analgesic tolerance to morphine and kappa opioid receptor inactivation in vivo.

69 gnificant pharmacodynamic difference between morphine and methadone that is determined entirely by he

70 he fastest- and slowest-reacting pollutants (morphine and methamphetamine, respectively) were always

71 Therefore, morphine and naloxone promote neurogenesis in a receptor

72 The abilities of morphine and naloxone to facilitate neurogenesis were al

73 When two opioids, morphine and naloxone, were used during the early stage

74 toward opioids screening is demonstrated for morphine and norfentanyl.

75 he development of tolerance and addiction to morphine and other drugs of abuse, understanding the mol

76 Morphine and other opioids are commonly used to treat pa

77 Although morphine and other opioids offer dramatic and impressive

78 reactions (n = 10) then received intravenous morphine and placebo (saline) sessions, in counterbalanc

79 ivate the dopaminergic system as compared to morphine and predicted a dissociation of therapeutic ver

80 alogous data obtained for the classic opioid morphine and the G protein-biased ligand TRV130.

81 Opium alkaloids such as morphine and thebaine occur in the latex of Papaver somn

82 t pharmacokinetics and efficacy of tramadol, morphine, and codeine.

83 t) in response to an intravenous infusion of morphine, and its relationship with morphine-induced sub

84 the suprachiasmatic nucleus to a low dose of morphine, and showed the bidirectional effect of morphin

85 Our results show that smoke, morphine, and the combination promotes the decline in CD

86 press withdrawal, but produces and maintains morphine antinociceptive tolerance.

87 g in the vHip-mPFC connection contributes to morphine-associated and normal memory, largely depending

88 Mechanistic studies have shown that morphine blunts the antiplatelet effects of oral adenosi

89 Morphine, buprenorphine, and oxycodone prescribing rates

90 expression in the caudate putamen and NAc of morphine, but not cocaine, abstinent mice.

91 uring the late stage of NSC differentiation, morphine, but not naloxone, inhibited neurogenesis via t

92 e and safe doses of opiate painkillers, like morphine, can be limited by respiratory depression.

93 ical opioid analgesics, such as fentanyl and morphine, can produce hyperalgesia and chronification of

94 Morphine caused an acute increase in the slope and ampli

95 simulated photolysis of the pharmaceuticals morphine, codeine, and methamphetamine and, for context,

96 etermine the content of six opium alkaloids (morphine, codeine, thebaine, noscapine, papaverine and n

97 ele exhibited lower sensitivity to DAMGO and morphine compared with major allele carriers (112A/A).

98 Following chronic treatment with morphine, compound 101 was less effective at blocking ac

99 udies, 4 (V2a) significantly prevented acute morphine-conditioned place preference (CPP) and stress-i

100 The median difference in morphine consumption between the PCM + IBU group vs PCM

101 cetamol plus ibuprofen significantly reduced morphine consumption compared with paracetamol alone in

102 Two co-primary outcomes: 24-hour morphine consumption using patient-controlled analgesia

103 Median 24-hour morphine consumption was 20 mg (99.6% CI, 0-148) in the

104 The difference in morphine consumption was not statistically significant f

105 motion (ROM) in postoperative 5 days; reduce morphine consumption, achieve earlier straight leg raisi

106 involved in the acquisition and retrieval of morphine contextual memory, and DA signaling in the vHip

107 red for the acquisition and retrieval of the morphine contextual memory, respectively.

108 f Oprm1 circular RNA (circRNA) expression by morphine, coupled with the high abundance and existence

109 Morphine-CPP acquisition increased the activity of the D

110 stress-induced reinstatement of extinguished morphine-CPP in mouse models of opioid reward and relaps

111 Morphine-CPP reinstatement was associated with the D2R-m

112 After US, subjects receiving morphine demonstrated significantly longer HWL compared

113 e facilitated morphine tolerance and reduced morphine dependence without affecting morphine reward.

114 igher in the CD11b+ microglia/macrophages in morphine dependent RMs.

115 In this study, we used morphine dependent SIVmac251 infected rhesus macaque (RM

116 Herein, we developed a morphine dependent SIVmac251 infected Rhesus macaque (RM

117 f changes in FOS correlation networks in the morphine-dependent state.

118 expression in mice that are morphine-naive, morphine-dependent, or have undergone 4 wk of withdrawal

119 brain structures that respond differently to morphine depending on the time of its administration.

120 elective MOR agonists including fentanyl and morphine derivatives are limited clinically due to high

121 sciatic nerve injury model, but tolerance to morphine developed after 1 week while THC or CBD reduced

122 However, the subjective effects of morphine did not show a simple pattern of correlation wi

123 l compartments for metabolites best describe morphine disposition in this population.

124 eta and a significant rightward shift in the morphine dose-response curve.

125 hine) than for the high floodplain (5.6% for morphine) due to greater water exchange relative to chan

126 number of items prescribed, costs, and oral morphine equivalency to account for variation in strengt

127 After correcting for total oral morphine equivalency, the increase was 127% (from 190 00

128 opioid prescribing at discharge [median oral morphine equivalent (OME)] were performed at the special

129 tity of opioid prescribed (converted to oral morphine equivalent [OME]), and opioid prescription refi

130 Each 25-mg increase in morphine equivalent daily dose was associated with an 11

131 rescription fills and trajectories of opioid morphine equivalent dose (MED) prescribed during the 12-

132 Median daily oral morphine equivalent dose was 31 mg (18-54).

133 Median daily oral morphine equivalent dose was 31mg (18-54).

134 daily doses of opioids (>=50 vs <50 mg oral morphine equivalent) had an increased risk of new persis

135 alog scale (VAS) and opioid dose (milligrams morphine equivalent/day, MME/day) were compared at 12 mo

136 unt of opioid prescribed increased: 150 oral morphine equivalents (OME) for low-intensity, 225 OME fo

137 opioids prescriptions were converted to oral morphine equivalents (OME).

138 tion within 30 days postoperatively [in oral morphine equivalents (OME)].

139 hospital length of stay (LOS), and parental morphine equivalents (PMEs) on the day of surgery and on

140 RE 32.0%->POST 20.0%), opioid use by 19 oral morphine equivalents daily (95% CI 1-36; PRE 101->POST 8

141 an difference, -3.50; 95% CI, -5.90 to -1.10 morphine equivalents in milligrams per kilogram per 48 h

142 Surgical patients' mean total oral morphine equivalents per prescription increased from 240

143 Median total oral morphine equivalents prescribed was 600 mg (equivalent t

144 95% CI, -0.71 to 0.15); median opioid use in morphine equivalents was 50 mg (IQR, 18-122 mg) and 58 m

145 sion, diabetes, use of opioids, and specific morphine equivalents).

146 scribed opioids ranged from 34.4 to 212.3 mg morphine equivalents.

147 e was self-reported total opioid use in oral morphine equivalents.

148 through analgesia (median, 322.5 vs 405.3 ug morphine equivalents; difference, -83 [95% CI, -154 to -

149 Morphine exerts its rewarding actions, at least in part,

150 e, whereas both intermittent and interrupted morphine exposure caused long-lasting psychomotor sensit

151 Continuous morphine exposure caused tolerance to the psychomotor-ac

152 The interruption of continuous morphine exposure exacerbated drug-evoked transcriptiona

153 Chronic morphine exposure in mice increased brain circOprm1e2.3

154 Finally, the combination of smoke and morphine exposure induces microglial activation followin

155 Similar to murine morphine exposure models, opioid agonist use was associa

156 ss the combined effects of smoke and chronic morphine exposure on the inflammation associated with HI

157 ocomotor sensitization caused by interrupted morphine exposure was accompanied by enhanced dopamine s

158 We then interrupted continuous morphine exposure with either naloxone-precipitated or s

159 ve undergone 4 wk of withdrawal from chronic morphine exposure, relative to saline-exposed controls.

160 lieves long-term deleterious consequences of morphine exposure.

161 ids with known immunosuppressive properties (morphine, fentanyl, methadone) to the infection risk amo

162 We exposed male and female mice to morphine for one week, with administration patterns that

163 Since the isolation of morphine from the opium poppy over 200 years ago, the mo

164 and zidovudine glucuronidation activity, but morphine glucosidation was preserved.

165 An investigation of UGT2B7-catalyzed morphine glycosidation indicated that glucuronidation is

166 ne group and in 7 of 30 infants (23%) in the morphine group (P=0.36).

167 silon) in common, whereas systemic high-dose morphine (HDM)-induced analgesia and priming are neither

168 In contrast, high-dose morphine (HDM, 3 mg/kg) increased nociceptive threshold

169 e of prescription and illegal opioids (e.g., morphine, heroin) has led to major problems with addicti

170 se to cocaine, amphetamine, methamphetamine, morphine, heroin, nicotine, or alcohol seeking, as asses

171 cord enhanced the antinociceptive effects of morphine in mice.

172 loped as an antinociceptive agent similar to morphine in rodents.

173 ors 17-AAG or KU-32 amplified the effects of morphine in suppressing sensitivity to both thermal and

174 tribute to the sexually dimorphic effects of morphine in the rat.SIGNIFICANCE STATEMENT We demonstrat

175 rimary striatal neurons treated with chronic morphine in vitro.

176 ivo) but not upon direct exposure of glia to morphine (in vitro).

177 Morphine increased dopamine transients in the NAc, but d

178 In contrast, 10-minute exposure to DAMGO or morphine increased the fraction of immobile FLAG-MORs.

179 Instead, high doses of morphine increased the occurrence of apnoeas.

180 In contrast, morphine increased the proximity of the MOR to desmosoma

181 The results show that chronic treatment with morphine induced heterologous adaptations in kinase regu

182 y reduced gut bacteria and prevented chronic morphine induced increases in gut permeability, colonic

183 Rats then underwent morphine-induced (10 mg/kg) conditioned-place-preference

184 ed inhibition of neuronal firing to modulate morphine-induced analgesia, reward, and withdrawal.

185 vicious cycle of chronic morphine tolerance: morphine-induced gut dysbiosis leads to gut barrier disr

186 rons in adult mice did not affect general or morphine-induced locomotor activity, but markedly increa

187 In Gpr88 knockout mice, morphine-induced locomotor sensitization, withdrawal and

188 eatment of cells with convallatoxin enhanced morphine-induced MOR endocytosis through an adaptor prot

189 P2)/clathrin-dependent mechanism, attenuated morphine-induced phosphorylation of MOR, and diminished

190 ceptive tolerance to morphine and attenuated morphine-induced physical dependence.

191 usion of morphine, and its relationship with morphine-induced subjective effects, in healthy, nondepe

192 We show that withdrawal from morphine induces long-term synaptic facilitation in lami

193 also found that the combination of smoke and morphine inhibited the expression of IL-1alpha, IL-4 and

194 circuit activation, VTA gene expression, and morphine intake.

195 Morphine is a unique opioid analgesic that activates the

196 preclinical and clinical studies report that morphine is less efficacious in females compared to male

197 Morphine is one of the most widely used drugs for the tr

198 OIH and priming induced by systemic low-dose morphine (LDM) share action at Toll-like receptor 4 (TLR

199 OIH and priming induced by systemic low-dose morphine (LDM, 0.03 mg/kg).

200 oids in poppy seeds were mainly based on the morphine level, whereas other opium alkaloids thereunder

201 receptors limits the therapeutic efficacy of morphine-like analgesics and mediates the long duration

202 he demonstration that specific receptors for morphine-like analgesics exist, the search for endogenou

203 Specifically, the binding of morphine, methadone, and cocaine to antimorphine, antime

204 g cutoffs based on days supplied (DS), total morphine milligram equivalents (MME) dispensed, and quan

205 Opioids were converted to Morphine Milligram Equivalents (MME).

206 opioid and calculated days' supply and daily morphine milligram equivalents (MMEs) from 1 year prior

207 Opioid prescription, dosage thresholds (morphine milligram equivalents [MME] of >=50/day and >=9

208 Of those who started on high dose (120-199 morphine milligram equivalents [MME]/day) or very high d

209 rates of high-dose opioid use (average >= 90 morphine milligram equivalents daily).

210 There was a major reduction in morphine milligram equivalents in the ERAS group whether

211 Morphine milligram equivalents of 50 or greater per day

212 more than a 3-day supply or for a dose of 50 morphine milligram equivalents per day or higher) persis

213 Prevention (CDC)-recommended threshold of 90 morphine milligram equivalents per day, little is known

214 e than 7 days (median ARI, 4.5%), and higher morphine milligram equivalents per day.

215 Morphine milligram equivalents were separately calculate

216 first 72 hours after surgery as measured by morphine milligram equivalents when liposomal bupivacain

217 we compared FOS expression in mice that are morphine-naive, morphine-dependent, or have undergone 4

218 , suggesting that MOR mediates the effect of morphine on NSC neuronal differentiation and maturation.

219 hine, and showed the bidirectional effect of morphine on pERK1/2 and pGSK3beta levels in the suprachi

220 MOR activation by morphine or [d-Ala(2),N-MePhe(4), Gly-ol]enkephalin (DAM

221 hed unexposed group although no reduction in morphine or benzodiazepine coadministration was observed

222 We also blocked tolerance by administering morphine or fentanyl with the PDGFR-beta inhibitor imati

223 g receptor internalization induced by either morphine or fentanyl.

224 in after double-blind injection of .08 mg/kg morphine or placebo.

225 RMs on a morphine (or saline control) regimen were infected with

226 nificant withdrawal effects than naloxone in morphine-pelleted mice.

227 THC also potentiates salience attribution in morphine place-preference and fear conditioning assays,

228 results suggest that in the proposed model, morphine plays a differential role in SIV reservoirs by

229 SR-17018 in morphine-tolerant mice restores morphine potency and efficacy, whereas the onset of opio

230 ptors as a key mechanistic step required for morphine potentiation of P2X7R function.

231 Remarkably, systemically administered morphine potently inhibited acute thermal and mechanical

232 Morphine primarily binds to the mu opioid receptor, a pr

233 Morphine produced marked subjective and physiological ef

234 All samples contained morphine ranging from 0.2 to 240mg/kg.

235 Morphine remains one of the most widely prescribed opioi

236 ot males (95% CI - 0.10, 0.11), administered morphine reported increased negative drug effects compar

237 The results show that chronic treatment with morphine results in a surprising and heterologous adapta

238 ficacy values at MOR better or comparable to morphine, retained their DOR-antagonist properties, and

239 PVT->CeA activity associates morphine reward to the environment, whereas transient in

240 educed morphine dependence without affecting morphine reward.

241 by examining whether sleep disruption alters morphine's analgesic and hedonic properties.

242 , safe, and inexpensive treatment to prolong morphine's efficacy and attenuate analgesic tolerance.

243 f the animals five weeks post-infection, and morphine/saline administration continued until the end o

244 We show that rat morphine self-administration (MSA), a paradigm that effe

245 onvallatoxin are potentially therapeutic for morphine side effects and open a new avenue to study MOR

246 on plakoglobin or desmocolin-1, switched the morphine spatiotemporal signaling profile to mimic that

247 Morphine stimulation of MOR activates a Galpha(i/o)-Gbet

248 ater for the low floodplain (e.g., 18.8% for morphine) than for the high floodplain (5.6% for morphin

249 ve animals, following chronic treatment with morphine, the acute kinase-dependent desensitization of

250 Concentrations of morphine, the two main metabolites, morphine-3-glucuroni

251 We used DO mice treated with morphine to map quantitative trait loci for respiratory

252 Acute convallatoxin administration reversed morphine tolerance and dependence in morphine-tolerant m

253 iated truncation in mE4M-B6 mice facilitated morphine tolerance and reduced morphine dependence witho

254 the exon 7-associated truncation diminished morphine tolerance and reward without altering physical

255 treatment with chronic convallatoxin reduced morphine tolerance in animal models of acute thermal pai

256 in the development, but not maintenance, of morphine tolerance in male rats.

257 orphine (10 mg/kg per day x 12 days) blocked morphine tolerance in WT but not in CB2KO mice.

258 MORs specifically in nociceptors eliminated morphine tolerance, OIH and pronociceptive synaptic long

259 n of proinflammatory cytokines, which drives morphine tolerance.

260 role of miRNAs and Oprm1 splice variants in morphine tolerance.

261 We hypothesize a vicious cycle of chronic morphine tolerance: morphine-induced gut dysbiosis leads

262 activity of NM0127 and NM0127 was active in morphine tolerant animals.

263 vel in Be(2)C cells and the brainstem of the morphine tolerant mice, contributing to the decreased ex

264 Interestingly, substitution with SR-17018 in morphine-tolerant mice restores morphine potency and eff

265 eversed morphine tolerance and dependence in morphine-tolerant mice.

266 Serum from morphine-treated (1 or 10 mg/kg, i.p. every 12 h) or sal

267 nternalization in tissue from both naive and morphine-treated animals, suggesting that GRK2/3 remaine

268 However, in slices taken from morphine-treated animals, the combination of these block

269 by compound 101 in slices from naive but not morphine-treated animals.

270 n of MOR in brain slices from drug-naive and morphine-treated animals.

271 of the somatostatin receptor in slices from morphine-treated animals.

272 mmunities, attenuated analgesic tolerance in morphine-treated mice.

273 that were isolated from mice with long-term morphine treatment (in vivo) but not upon direct exposur

274 inus is differentially modulated by repeated morphine treatment and has no bearing on normal P2X7R fu

275 s also detected in the cultured rat NSCs and morphine treatment in vitro increases NSC neuronal diffe

276 Chronic morphine treatment significantly increased the miR-378-3

277 After chronic morphine treatment, alanine mutations in the sequence be

278 te desensitization was present after chronic morphine treatment, but the sensitivity to morphine was

279 upregulated in the VTA by chronic cocaine or morphine treatment, positioning SGK1 as a critical media

280 Additionally, chronic morphine treatment-induced hyperalgesia was absent in Op

281 s the same phenomenon after a short in vitro morphine treatment.

282 Reduction in morphine use of 0.25 mug/kg/hr (95% CI, -0.68 to 1.18 mu

283 In patients treated with clopidogrel, morphine use was associated with higher rates of the 4-w

284 one users had a lower rate of infection than morphine users (aIRR:0.73 [CI: 0.60-0.89]).

285 ndividual long-acting opioids to long-acting morphine users (considered the prototypical immunosuppre

286 We randomized 100 healthy adults to receive morphine versus placebo after two nights of undisturbed

287 algesic effect of intrathecally administered morphine was also profoundly reduced in Oprm1-cKO mice.

288 oncomitantly with clopidogrel pre-treatment, morphine was associated with higher rates of ischemic ev

289 In patients not treated with clopidogrel, morphine was not associated with either the 4-way endpoi

290 c morphine treatment, but the sensitivity to morphine was not changed.

291 nflammation related to prolonged exposure to morphine was significantly attenuated by carbenoxolone (

292 ssion induced by an anti-nociceptive dose of morphine was significantly attenuated following deletion

293 ate glucuronyl transferase 2B7 metabolism of morphine were identified.

294 aine, 3,4-methylenedioxymethamphetamine, and morphine) were also tested to explore the possibility of

295 nce to the psychomotor-activating effects of morphine, whereas both intermittent and interrupted morp

296 mmon side effects of opioid agonists such as morphine, which acts at mu-opioid receptors.

297 ere suppressed by the MOR agonists DAMGO and morphine, which caused a shift in the excitatory/inhibit

298 We induced tolerance with either morphine, which did not cause MOR internalization, or fe

299 th of hospital stay than treatment with oral morphine, with similar rates of adverse events.

300 facilitation and ameliorated the sequelae of morphine withdrawal.