ライフサイエンスコーパス: opioid

1 iveness to endogenous EM2 (and perhaps other opioids).

2 sia when administered in combination with an opioid.

3 h is likely due to the release of endogenous opioids.

4 beta-endorphin and are heavily regulated by opioids.

5 The majority of patients were overprescribed opioids.

6 r of days of use of heroin and other illicit opioids.

7 us markers were improved by long-term use of opioids.

8 the reinforcing and addictive properties of opioids.

9 ance to the respiratory depressant effect of opioids.

10 oninstitutionalized adults used prescription opioids; 11.5 million (4.7%) misused them; and 1.9 milli

11 more likely to have filled prescriptions for opioids (49.0% versus 17.2%) and benzodiazepines (52.1%

12 Although prescription opioid abuse shows geographic variation, all physicians

13 es needs Medicaid to address its epidemic of opioid abuse.

14 The cell types and receptors on which opioids act to initiate these maladaptive processes rema

15 the mu opioid receptor (MOR), which mediates opioid actions, have unique pharmacological properties a

16 Postsynaptically, the opioids activate a potassium conductance through the mu-

17 r investigating the neurobiological basis of opioid addiction.

18 ed proteomic approach to show that following opioid administration, peroxiredoxin 6 (PRDX6) is recrui

19 ur interventions with demonstrated efficacy: opioid agonist therapy (OAT), needle and syringe program

20 nd equipment sharing and lower prevalence of opioid agonist therapy were associated with HCV incidenc

21 dependence, and is long-term maintenance of opioid agonist treatment associated with differences in

22 Clinical Question: Are different opioid agonist treatments (eg, methadone vs buprenorphin

23 l buprenorphine-naloxone (BUP-NX), a partial opioid agonist, are pharmacologically and conceptually d

24 Collectively, our data support the idea that opioid agonists can be combined with peripheral MOR anta

25 aling pathways similar to those activated by opioid agonists.

26 Tolerance and OIH counteract opioid analgesia and drive dose escalation.

27 lopment of therapies to maximize and sustain opioid analgesic efficacy.

28 The prescribing of opioid analgesics for pain management-particularly for m

29 orting outcomes of RCT/s comparing 2 or more opioid analgesics for the management of chronic pain wer

30 Prescription opioid analgesics play an important role in the treatmen

31 uropathic pain states that are refractive to opioid analgesics.

32 profen and acetaminophen or with 3 different opioid and acetaminophen combination analgesics.

33 erimentally show that certain variants of mu-opioid and Cholecystokinin-A receptors could lead to alt

34 Here, we compare opioid and dopamine function between two behavioral addi

35 ll other molecular targets tested, including opioid and GABAB receptors.

36 Postoperative pain and consumption of opioids and analgesics.

37 ncrease in overdose deaths from prescription opioids and heroin in the United States over the past 20

38 -established interactions between endogenous opioids and stress.

39 higher comorbidity, and use of prescription opioids and/or benzodiazepines, although the magnitude o

40 MLs have led to substitution of cannabis for opioids, and also possibly for psychiatric medications.

41 lammatory drugs, drugs for neuropathic pain, opioids, and cannabinoids, to physical therapy strategie

42 t patients and carers hold fears relating to opioids, and experience side effects related to their us

43 ing contributes to the decreased efficacy of opioids, and we recently demonstrated that Toll-like rec

44 tems and suggest that administering OT under opioid antagonism may boost the therapeutic efficacy of

45 Extended-release naltrexone (XR-NTX), an opioid antagonist, and sublingual buprenorphine-naloxone

46 sics and mediates the long duration of kappa opioid antidepressants by an uncharacterized, arrestin-i

47 Opioids are increasingly used to manage chronic pain, an

48 Opioids are the gold-standard treatment for severe pain.

49 ns of the N-methyl D-aspartate receptor with opioids at the level of the spinal cord.

50 excessive prescribing that may leave unused opioids available for potential misuse.

51 initiation of nonmedical use of prescription opioids before initiating heroin use increased across ti

52 rons as these neurons produce the endogenous opioid beta-endorphin and are heavily regulated by opioi

53 lerated and produced immediate and sustained opioid blockade and withdrawal suppression.

54 ents with non-cancer diagnoses received more opioids (both P < 0.001).

55 otional learning are modulated by endogenous opioids but the cellular basis for this is unknown.

56 ed a novel role of endomorphins by which the opioids can enhance the lactic acid-mediated reflex incr

57 ng and whether they had seen or been offered opioids, cocaine, cannabis, methamphetamine, alcohol, or

58 I2 = 52%) and 6.58 (95% CI, -6.33 to 19.49) opioid consumption at 1 and 2 weeks (P = .32, I2 = 87%),

59 ise had no pain improvement and reduction in opioid consumption: for continuous passive motion, the m

60 sposed, suggesting an important reservoir of opioids contributing to nonmedical use of these products

61 Self-reported opioid craving was initially less with XR-NTX than with

62 the New England region is in the midst of an opioid crisis that has led to a substantial increase in

63 oxycodone in human volunteers diagnosed with opioid dependence (equivalent to moderate-severe opioid

64 rences in efficacy for treating prescription opioid dependence, and is long-term maintenance of opioi

65 associated with a higher risk of subsequent opioid dependency and overdose.

66 METHOD: Participants were 150 opioid-dependent adults randomly assigned 2:1 to one of

67 ould be considered as a treatment option for opioid-dependent individuals.

68 ically worsen pain, and implementation of an opioid detoxification programme.

69 or the first time that endogenously released opioids directly regulate neuronal excitability.

70 tudies reported dose reduction, but rates of opioid discontinuation ranged widely across intervention

71 ive impairment, higher preweaning mean daily opioid dose, longer duration of sedation, receipt of thr

72 Higher opioid doses correlated with death in a monotonically in

73 fects of early-life experience on later-life opioid drug-taking.

74 Thirty-two studies investigating 10 opioid drugs fulfilled the eligibility criteria.

75 formulation, CAM2038, to block euphorigenic opioid effects and suppress opioid withdrawal in non-tre

76 Amid the current opioid epidemic in the United States, the enhanced recov

77 isks of HIV transmission associated with the opioid epidemic make cost-effective programs for people

78 he legal status of marijuana, addressing the opioid epidemic, insurance coverage of substance use dis

79 er-regulatory mechanisms, neuroinflammation, opioid facilitation, and interactions of the N-methyl D-

80 e resulted from increases in prescription of opioids for management of acute and chronic pain.

81 Randomisation was stratified by use of opioids for prostate cancer-related pain at screening, d

82 s; and availability of analgesics, including opioids, for pain relief.

83 nhibited by agonists of the Gi-coupled micro opioid, GABA-B and NPY receptors.

84 We propose that opioid genes are regulated as interconnected components

85 We demonstrated that expression patterns of opioid genes highly correlate within and across function

86 Intra- and interregional coregulation of opioid genes: broken symmetry in spinal circuits.

87 polyneuropathy who were receiving long-term opioids had multiple functional status markers that were

88 to severe pain in SCD is mostly reliant upon opioids; however, long-term use of opioids is associated

89 fects of ibudilast on the abuse potential of opioids in humans are largely unknown.

90 id use disorder, and had used non-prescribed opioids in the past 30 days.

91 weeks of gestation) who had been exposed to opioids in utero and who had signs of the neonatal absti

92 control, and 16% to 29% of patients reported opioid-induced adverse effects.

93 s in adults with chronic non-cancer pain and opioid-induced constipation.

94 the role of heat-shock protein 90 (Hsp90) in opioid-induced MOR signaling and pain, which has only be

95 revious results showing antagonistic galanin-opioid interactions and offers a new therapeutic target

96 Diversion of prescription opioids is a major contributor to the rising mortality f

97 Tolerance to the analgesic effects of opioids is a major problem in chronic pain management.

98 iant upon opioids; however, long-term use of opioids is associated with multiple side effects.

99 eries of small molecules targeting the kappa-opioid (KOP) receptor featuring a diphenethylamine scaff

100 tment of postoperative pain; however, unused opioids may be diverted for nonmedical use and contribut

101 howed that electrotherapy reduced the use of opioids (mean difference, -3.50; 95% CI, -5.90 to -1.10

102 al cell activation in rodents, and may alter opioid-mediated effects, including analgesia and withdra

103 al administration of naloxone, suggesting an opioid-mediated mechanism; pharmacological and genetic d

104 on of CIN firing with the mu/delta selective opioid [Met(5)]enkephalin (1 mum) decreased spontaneous

105 of the patient as to the mechanisms by which opioids might paradoxically worsen pain, and implementat

106 Opioid misuse is at historically high levels in the Unit

107 problems may be associated with prescription opioid misuse.

108 Opioids modulate the tumor microenvironment with potenti

109 Subset analysis of the 5756 (75.2%) opioid-naive patients showed the majority received >200

110 (OME), should be prescribed at discharge in opioid-naive patients.

111 , opioid users (compared with those who were opioid-naive) had 9.2% higher costs [95% confidence inte

112 number of pills that would fully supply the opioid needs of 80% of patients undergoing each operatio

113 cal trial completion rate, the proportion of opioid-negative urine drug tests, and number of days of

114 c regulation of selective neural circuits by opioid neurohormones.-

115 iny projection neurons (SPNs) co-release the opioid neuropeptide dynorphin, which acts at presynaptic

116 ysiologically relevant target for endogenous opioid neurotransmitters and analgesics, has been a majo

117 Although morphine and other opioids offer dramatic and impressive relief of pain, th

118 Postoperative prescription opioids often go unused, unlocked, and undisposed, sugge

119 of two hedonic hotspots in cortex, where mu opioid or orexin stimulations enhance the hedonic impact

120 en administered with subtherapeutic doses of opioids or the enkephalinase inhibitor thiorphan, these

121 ds and outcomes of in-hospital postoperative opioid overdose (OD) and identify predictors of postoper

122 e of administration and dosing for suspected opioid overdose in out-of-hospital settings on mortality

123 The ongoing epidemics of opioid overdose raises an urgent need for effective anti

124 Naloxone is effective for reversing opioid overdose, but optimal strategies for out-of-hospi

125 decision analytical Markov model to simulate opioid overdose, HIV incidence, overdose-related deaths,

126 at of intramuscular naloxone for reversal of opioid overdose, with no difference in adverse events.

127 jor contributor to the rising mortality from opioid overdoses.

128 The primary outcome-opioid oversupply-was defined as the number of patients

129 Most patients stopped or used no opioids owing to adequate pain control, and 16% to 29% o

130 Opioid peptide genes, compared with their receptor genes

131 There was a wide variation in the number of opioid pills prescribed to patients undergoing the same

132 Compared with non-users, patients using opioids preoperatively were more likely to have a longer

133 Among them, 502 patients (21%) used opioids preoperatively.

134 ans as being high-intensity or low-intensity opioid prescribers according to relative quartiles of pr

135 These data will guide practices to optimize opioid prescribing after surgery.

136 were associated with a higher likelihood of opioid prescription at discharge.

137 2.9 [13.3] years), 18338 (54.3%) received an opioid prescription at discharge.

138 of patients had a chronic (>/=90-day supply) opioid prescription each year, in 2010 usually for hydro

139 rsistent opioid use, which was defined as an opioid prescription fulfillment between 90 and 180 days

140 Causal relationships cannot be inferred, and opioid prescription may be an illness marker.

141 Opioid prescription was confirmed from Part D prescripti

142 nown regarding outcomes associated with ESRD opioid prescription.

143 els were used to determine the predictors of opioid prescription.

144 However, the use of opioid prescriptions in trauma patients at hospital disc

145 er of patients with either filled but unused opioid prescriptions or unfilled opioid prescriptions.

146 herapy, defined by 1 or multiple consecutive opioid prescriptions resulting in 90 continuous days or

147 The mean number of opioid prescriptions written annually by ophthalmologist

148 The 6 states with the highest volume of opioid prescriptions written annually per ophthalmologis

149 ions written; and geographic distribution of opioid prescriptions written per ophthalmologist.

150 but unused opioid prescriptions or unfilled opioid prescriptions.

151 t controls the surface delivery of the delta opioid receptor (deltaR).

152 Activation of the delta-opioid receptor (DOR) produces similar analgesia with re

153 or insula with a downregulation of the kappa opioid receptor (Kappa), as well as decreased DNA methyl

154 promoted phosphorylation of the mouse kappa opioid receptor (KOPR) at residues S356, T357, T363, and

155 Administration of the kappa-opioid receptor (KOR) antagonist JDTic (30 mg/kg, i.p.)

156 Administration of a kappa-opioid receptor (KOR) antagonist reduced stress effects

157 The kappa-opioid receptor (KOR) has emerged as a promising target

158 ositive allosteric modulator (PAM) of the mu-opioid receptor (micro-OR).

159 Functional selectivity at the micro opioid receptor (microR), a prototypical G-protein-coupl

160 e tyrosine kinase, c-Src, participates in mu opioid receptor (MOP) mediated inhibition in sensory neu

161 The mu-opioid receptor (MOPr) is a clinically important G prote

162 there was no difference in the ability of mu-opioid receptor (MOR) agonists to inhibit sIPSCs in POMC

163 effects of the systemic administration of mu-opioid receptor (MOR) agonists.

164 report convergent evidence for decreased mu-opioid receptor (MOR) function in the female rat LC.

165 in 2 [EM2; the highly specific endogenous mu-opioid receptor (MOR) ligand] induces antinociception th

166 SIGNIFICANCE STATEMENT: The mu-opioid receptor (MOR) localized in the ventral tegmental

167 ivate a potassium conductance through the mu-opioid receptor (MOR), suggesting for the first time tha

168 Splice variants of the mu opioid receptor (MOR), which mediates opioid actions, ha

169 that tianeptine is a full agonist at the mu opioid receptor (MOR).

170 ity on the A-ring in its activity as a kappa-opioid receptor agonist.

171 aversion induced by thermal pain or a kappa opioid receptor agonist.

172 lpiperazines 4 and 5 were reported to be pan opioid receptor antagonists, while 6 was a MOR agonist.

173 G, BED patients show widespread losses of mu-opioid receptor availability together with presynaptic d

174 peroxiredoxin 6 (PRDX6) is recruited to the opioid receptor complex by c-Jun N-terminal kinase (JNK)

175 Extensive 3' alternative splicing of the mu opioid receptor gene OPRM1 creates multiple C-terminal s

176 te analgesic tolerance to morphine and kappa opioid receptor inactivation in vivo.

177 or sufentanil when given the preferential mu-opioid receptor inverse agonist naloxone, suggesting the

178 We used PET and the mu-opioid-receptor (MOR)-specific ligand [(11)C]carfentanil

179 tressful experiences potently activate kappa opioid receptors (kappaORs).

180 e dynorphin, which acts at presynaptic kappa-opioid receptors (KORs) on dopaminergic afferents and ca

181 f acute physical exercise on the cerebral mu-opioid receptors (MOR) of 22 healthy recreationally acti

182 Mu opioid receptors (MORs) are central to pain control, dru

183 We found that mu opioid receptors (MORs) expressed by primary afferent no

184 Activation of somatic mu-opioid receptors (MORs) in hypothalamic proopiomelanocor

185 oncomitant opioid release could downregulate opioid receptors and promote the development of obesity.

186 First, Dbx1 preBotC neurons express kappa-opioid receptors in addition to mu-opioid receptors that

187 The activation of opioid receptors in peripheral inflamed tissue can reduc

188 naloxone, suggesting the participation of mu-opioid receptors in the reinforcing properties of sufent

189 systemic side effects, targeting peripheral opioid receptors is an attractive alternative treatment

190 Inactivation of opioid receptors limits the therapeutic efficacy of morp

191 The activation of central mu-opioid receptors related to CXCL1-CXCR2 signaling plays

192 ess kappa-opioid receptors in addition to mu-opioid receptors that heretofore have been associated wi

193 hormones (estrogen and progesterone), delta-opioid receptors, and T cells of the adaptive immune sys

194 rs of G protein-coupled receptors, including opioid receptors, have been proposed as possible therape

195 is is consistent with nalmefene's actions on opioid receptors, which modulate the mesolimbic dopamine

196 genetic data suggest the importance of delta-opioid receptors.

197 f hyperalgesia include activation of bimodal opioid regulatory systems, counter-regulatory mechanisms

198 represents a novel approach for influencing opioid reinforcement.

199 The primary outcome was time to opioid relapse post-release in the community confirmed b

200 We aimed to estimate the difference in opioid relapse-free survival between XR-NTX and BUP-NX.

201 nceptually distinct interventions to prevent opioid relapse.

202 Persons dying of opioid-related causes, particularly those who were diagn

203 tudy analyzed health service patterns before opioid-related death among nonelderly individuals in the

204 The study group included 13,089 opioid-related deaths partitioned by presence or absence

205 iverted for nonmedical use and contribute to opioid-related injuries and deaths.

206 Given the epidemic of opioid-related morbidity and mortality, it is critical t

207 hy to test whether feeding triggers cerebral opioid release and whether this response is associated w

208 een proposed that overeating and concomitant opioid release could downregulate opioid receptors and p

209 anil to quantify laughter-induced endogenous opioid release in 12 healthy males.

210 resolved whether feeding leads to endogenous opioid release in humans.

211 asurable sensations and triggered endogenous opioid release in thalamus, caudate nucleus, and anterio

212 Feeding-triggered opioid release thus also reflects metabolic and homeosta

213 ese observations, consistent with endogenous opioid release, highlight the role of the mu-opioid syst

214 Opioid, serotonin and NMDA mechanisms acting in rostral

215 different effects on protein expression and opioid signaling in each line, suggesting that cell mode

216 ticle was to outline important components of opioid-sparing analgesic regimens.

217 reliable antinociceptive effects, and offer opioid-sparing antinociceptive effects in myriad preclin

218 Opioid stimulation of JNK also inactivates dopamine D2 r

219 include needle and syringe programmes (NSP), opioid substitution therapy (OST), HIV counselling and t

220 injection equipment, HIV testing, linkage to opioid substitution treatment (OST) programs and HIV car

221 opioid release, highlight the role of the mu-opioid system in mediating affective responses to high-i

222 The endogenous opioid system supports a multitude of functions related

223 ch was partially dependent on the endogenous opioid system.

224 a regulatory relationship between the OT and opioid systems and suggest that administering OT under o

225 d their receptors functionally interact with opioid systems within the NAc to support reward, most li

226 Of all the opioid tablets obtained by surgical patients, 42% to 71%

227 d with differences in efficacy compared with opioid taper or psychological treatments alone?

228 f the pharmacology and behavioral effects of opioids that underlie both their therapeutic effects (an

229 Prevalence of long-term opioid therapy among patients with polyneuropathy and co

230 in, and 12 patients (60%) no longer required opioid therapy at a median follow-up period of 6 months.

231 However, long-term opioid therapy did not improve functional status but rat

232 Long-term opioid therapy, defined by 1 or multiple consecutive opi

233 tly leads to decisions about using long-term opioid therapy.

234 al status among patients receiving long-term opioid therapy.

235 ta to inform surgeons on the optimal dose of opioids to prescribe after common general surgical proce

236 ses its application to 3 patients prescribed opioids to treat chronic pain.

237 Opioid tolerance and the potential for addiction is a si

238 d influence disease-specific decisions about opioid treatment.

239 ssociated with increased incident nonmedical opioid use (adjusted odds ratio=2.99, 95% CI=1.63-5.47)

240 Preoperative opioid use (binary exposure variable) was retrospectivel

241 .004; I2 = 17%) and that acupuncture delayed opioid use (mean difference, 46.17; 95% CI, 20.84 to 71.

242 h increased incident nonmedical prescription opioid use (odds ratio=5.78, 95% CI=4.23-7.90) and opioi

243 To determine the incidence of new persistent opioid use after minor and major surgical procedures.

244 To quantify the prevalence of long-term opioid use among patients with polyneuropathy and to ass

245 ve 1 (2001-2002) and nonmedical prescription opioid use and prescription opioid use disorder at wave

246 rate or more severe pain and with nonmedical opioid use at wave 1.

247 use (odds ratio=5.78, 95% CI=4.23-7.90) and opioid use disorder (odds ratio=7.76, 95% CI=4.95-12.16)

248 Opioid use disorder (OUD) frequently begins in adolescen

249 n of medication-assisted treatment (MAT) for opioid use disorder (OUD) in U.S. primary care settings

250 is an efficacious, widely used treatment for opioid use disorder (OUD).

251 g, alcohol, and behavioral problems, and, in opioid use disorder analyses, nonmedical opioid use.

252 cal prescription opioid use and prescription opioid use disorder at wave 2 (2004-2005) of the Nationa

253 l disorders in the last year of life, though opioid use disorder diagnoses near the time of death wer

254 the last 30 days of life, while diagnoses of opioid use disorder during this period were uncommon in

255 of the nearly 2.4 million Americans with an opioid use disorder received treatment in 2015.

256 tandard of care for patients presenting with opioid use disorder to California's publicly funded trea

257 he observed standard of care (54.3% initiate opioid use disorder treatment with medically managed wit

258 id dependence (equivalent to moderate-severe opioid use disorder).

259 ociated with increased incident prescription opioid use disorder, although the association fell short

260 and Statistical Manual of Mental Disorders-5 opioid use disorder, and had used non-prescribed opioids

261 presenting for publicly funded treatment of opioid use disorder.

262 new therapeutic target for the treatment of opioid use disorder.

263 use; of these, 16.7% reported a prescription opioid use disorder.

264 adjusted odds ratio=2.62, 95% CI=1.86-3.69; opioid use disorder: adjusted odds ratio=2.18, 95% CI=1.

265 t of office-based buprenorphine treatment of opioid use disorders, the nature of what constitutes app

266 y of an effective heroin vaccine in treating opioid use disorders.

267 t is critical to understand how preoperative opioid use impacts surgical outcomes.

268 stitutionalized adults reported prescription opioid use in 2015, with substantial numbers reporting m

269 independently associated with new persistent opioid use included preoperative tobacco use (adjusted o

270 The extent to which chronic opioid use influences postoperative outcomes following e

271 To examine the extent to which preoperative opioid use is correlated with healthcare utilization and

272 y and mortality associated with prescription opioid use is escalating in the United States.

273 used to determine the effect of preoperative opioid use on postoperative healthcare utilization (leng

274 New persistent opioid use represents a common but previously underappre

275 tratified participants by treatment site and opioid use severity and used a web-based permuted block

276 Understanding the association of long-term opioid use with functional status, adverse outcomes, and

277 y and to assess the association of long-term opioid use with functional status, adverse outcomes, and

278 Among adults with prescription opioid use, 12.5% reported misuse; of these, 16.7% repor

279 ely diagnosed, given the current epidemic of opioid use, it is likely to be under-recognised.

280 To estimate the prevalence of prescription opioid use, misuse, and use disorders and motivations fo

281 ssa or suprapubic site-specific pain scores, opioid use, recovery parameters, or complications.

282 The primary outcome was new persistent opioid use, which was defined as an opioid prescription

283 s resulting in 90 continuous days or more of opioid use.

284 ist of scheduled narcotics was used to query opioid use.

285 in opioid use disorder analyses, nonmedical opioid use.

286 cluding those for ambulation, nutrition, and opioid use.

287 to identify risk factors for new persistent opioid use.

288 t for background characteristics (nonmedical opioid use: adjusted odds ratio=2.62, 95% CI=1.86-3.69;

289 After covariate adjustment, opioid users (compared with those who were opioid-naive)

290 gly used to manage chronic pain, and chronic opioid users are challenging to care for perioperatively

291 ervised withdrawal (ie, detoxification) from opioids using clonidine or buprenorphine hydrochloride i

292 were not controlled with the maximum dose of opioid were treated with adjunctive phenobarbital.

293 of patients reported that their prescription opioids were not stored in locked containers.

294 In both males and females, spontaneous opioid withdrawal altered glucose metabolism in regions

295 However, the underlying metabolic effects of opioid withdrawal and replacement have not been examined

296 ock euphorigenic opioid effects and suppress opioid withdrawal in non-treatment-seeking individuals w

297 l analog scale (eg, high and desire to use), opioid withdrawal scales, and physiological and pharmaco

298 and comparable to buprenorphine in reducing opioid withdrawal symptoms during a residential tapering

299 ination of tramadol ER as a method to manage opioid withdrawal symptoms.

300 tched control animals undergoing spontaneous opioid withdrawal, male animals treated with methadone e