ライフサイエンスコーパス: opiate

1 ly restores motivation to self administer an opiate.

2 in adult neurogenesis compared with classic opiates.

3 l, many of these individuals continue to use opiates.

4 going pain that commonly requires the use of opiates.

5 epsis, mechanical ventilation, and sedatives/opiates.

6 patient urine specimens for a broad range of opiates.

7 effect of drug misuse, including the use of opiates.

8 of cell-type-specific plasticity induced by opiates.

9 mediate rewarding and aversive properties of opiates.

10 ith primary dependence on alcohol but not on opiates.

11 s, are important for behavioral responses to opiates.

12 bits biased agonism in response to synthetic opiates.

13 ins (12.8%), sulfonamide antibiotics (7.4%), opiates (6.8%), and nonsteroidal anti-inflammatory drugs

14 Genetic variation may significantly affect opiate absorption, distribution, metabolism, excretion a

15 Opiate abuse and addiction have become a worldwide epide

16 ability to the initiation and maintenance of opiate abuse and is thought to play an important role in

17 Opiate abuse and overdose reached epidemic levels in the

18 Using a well-established murine model of opiate abuse and S. pneumoniae lung infection, we explor

19 is likely to be more productive at reducing opiate abuse related harm.

20 ctional role for impaired Pdyn in the PAC in opiate abuse through activation of the stress and negati

21 tion as reflected by the high comorbidity of opiate abuse with major depressive disorder (MDD).

22 D1 and DLG4 were found to be associated with opiate abuse.

23 singly recognized that stress predisposes to opiate abuse.

24 within these systems in three populations of opiate abusers and controls, totaling 489 individuals fr

25 examined FHC expression and CXCR4 status in opiate abusers and patients with HIV-associated neurocog

26 or amygdala; the correlation was inversed in opiate abusers as compared with controls.

27 Many HIV-infected opiate abusers have increased neuroinflammation that may

28 ns of CXCR4 and exacerbate neuropathology in opiate abusers who are affected by neuroinflammatory/inf

29 n glutamatergic and dopaminergic pathways in opiate abusers.

30 he signal transduction mechanisms underlying opiate actions in the NAc.

31 ly accrued regarding the neurobiology of the opiate-addicted human brain.

32 e mechanism via which this protein modulates opiate addiction and analgesia.

33 Dependence is a hallmark feature of opiate addiction and is defined by the emergence of soma

34 is critical for conferring vulnerability to opiate addiction as reflected by the high comorbidity of

35 Effective medical treatment of opiate addiction is limited by a high relapse rate in ab

36 dent changes in neurons, the role of glia in opiate addiction remains largely unstudied.

37 add support to proposals that treatments for opiate addiction should aim to increase the reward value

38 w the molecular neurobiology and genetics of opiate addiction, including heroin and prescription opio

39 tical need to understand the neurobiology of opiate addiction.

40 n of glutamate-based strategies for treating opiate addiction.

41 activator of G-protein signaling 3 (AGS3) in opiate addiction.

42 vailability reported in alcohol, cocaine and opiate addiction.

43 ming this circuit holds promise for treating opiate addiction.

44 Buprenorphine is used to treat opiate addiction.

45 tes, identifying new therapeutic targets for opiate addictive behaviors.

46 thdrawal and therefore subsequent relapse in opiate addicts.

47 B in rats and mice, we observed that chronic opiate administration activates BDNF-related neuronal pl

48 r benefits that could derive from minimizing opiate administration in critically ill patients, gut hy

49 ficantly decrease days of benzodiazepine and opiate administration, which may improve pediatric inten

50 the apparent tolerance of VTA DA neurons to opiates after chronic exposure.

51 hen P-gp is inhibited, [(11)C]dLop, a potent opiate agonist, enters and becomes trapped in the brain.

52 ard, fMRI, substance use, cocaine, cannabis, opiates, alcohol, nicotine, smokers, gambling, gamblers,

53 ning and addiction, endogenous and exogenous opiates also modulate learning and addiction-related str

54 nicotine, cocaine, amphetamine, Ecstasy, and opiates (among other drugs) produce alterations in neuro

55 However, these mice lack opiate analgesia or withdrawal.

56 dorsal horn, a principal site of action for opiate analgesia.

57 gnificant amount of postoperative parenteral opiate analgesia.

58 the severity of withdrawal without affecting opiate analgesia.

59 We now describe a potent opiate analgesic lacking the traditional side effects as

60 Because opiate analgesics are highly addictive substances, their

61 cal pain conditions may remain responsive to opiate analgesics for extended periods, but such persist

62 recommended include an opioid-antagonist and opiate analgesics.

63 have been successfully used for treatment of opiate and nicotine addiction, but not for cocaine addic

64 Opiates and acetaminophen are preferred analgesic agents

65 Finally, we examine how opiates and alcohol "break the mold" in terms of BDNF fu

66 ic and sedation therapies are essential, and opiates and benzodiazepines are commonly used.

67 of gene sets previously linked to addiction (opiates and cocaine).

68 Opiates and exogenous cannabinoids, both potent analgesi

69 pothesis of fungibility between prescription opiates and heroin was supported by these analyses.

70 e emerging concept that combined exposure to opiates and human immunodeficiency virus drives enhanced

71 appear to involve the release of endogenous opiates and neurotransmitters, with the signals mediatin

72 These findings reveal that opiates and placebo treatments both influence clinically

73 fects of morphine, a poor muOR-internalizing opiate, and (D-Ala2,MePhe4,Gly-ol5) enkephalin (DAMGO),

74 ancestry was actually smaller among cocaine, opiate, and alcohol addicts (proportion=0.76-0.78) than

75 re [EQ-VAS]), levels of antioxidants, use of opiates, and adverse events.

76 brain neurons to major biological effects of opiates, and also challenge the canonical disinhibition

77 napses in MSNs, as observed with cocaine and opiates, and alter the regulation of corticostriatal pla

78 injuries and cases with chronic exposure to opiates, and analysed the limited associated clinical hi

79 ic brain injury, five cases with exposure to opiates, and three control cases with no known neurologi

80 s were promoted by chronic treatment with an opiate antagonist but suppressed by chronic ethanol feed

81 ages could be reversed by treatment with the opiate antagonist naloxone, the beta-receptor agonist me

82 ch-evoked scratching was inhibited by the mu-opiate antagonist naltrexone.

83 Systemic administration of the opiate antagonist, naloxone, robustly increased LC disch

84 pioid peptides as substrates, but nonpeptide opiate antagonists are excluded.

85 e in the disposition and efficacy of several opiates, antidepressants, statins, and antibiotics.

86 R dopamine neurons likely play a key role in opiate antinociception, potentially via the activation o

87 Opiates are among the most prescribed drugs for pain man

88 Opiates are essential for treating pain, but termination

89 Opiates are potent analgesics but their clinical use is

90 on first-line analgesic (49.1% of patients); opiates are the "second line" in 31.5% of patients; howe

91 Opiates are used extensively to treat chronic pain.

92 Opiates are utilized routinely and effectively as a shor

93 tation due to a lack of cross-tolerance with opiate-based medications.

94 hway and strain optimization to realize full opiate biosynthesis in yeast.

95 K1Rs) have been shown to mediate alcohol and opiate, but not cocaine reward in rodents.

96 fter acute stimulation with opioids and most opiates, but not with morphine.

97 ith human immunodeficiency virus-1 who abuse opiates can have a higher incidence of virus-associated

98 uently named substance, followed by alcohol, opiate, cocaine, oxycodone, and methamphetamine.

99 rmittent exposure to heroin, morphine, other opiates, cocaine, other stimulants, and alcohol in anima

100 t that lack many side-effects of traditional opiates composed, in part, of exon 11-associated truncat

101 uman microglial cells and determined whether opiates converge at this point.

102 By this mechanism, opiates could reduce the neuroprotective functions of CX

103 Chronic opiates decrease the size of VTA dopamine neurons in rod

104 Once opiate dependence and withdrawal has developed, a functi

105 ever, the mechanisms that lead to preventing opiate dependence are still poorly understood.

106 y and induces signs of cellular and physical opiate dependence that endure after the stress.

107 the thalamus to nucleus accumbens circuit to opiate dependence, and suggests that reprogramming this

108 Chronic opiate use induces opiate dependence, which is characterized by extremely u

109 in synaptic transmission thought to underlie opiate dependence.

110 This study suggests that patients with opiate dependency on MMT exhibit abnormal brain activati

111 n impairment among drug users in general and opiate dependent individuals in particular is not fully

112 Stimulation of endogenous opiate-dependent pathways, manipulation of epithelial io

113 eural responses to reward and loss events in opiate-dependent patients receiving methadone maintenanc

114 s necessary for both the establishment of an opiate-dependent state and aversive withdrawal motivatio

115 d CaMKIIalpha signaling, specifically in the opiate-dependent/withdrawn state, demonstrating function

116 The employee acknowledged parenteral opiate diversion.

117 Both may be associated with sedative or opiate doses and pharmacokinetic or pharmacogenetic vari

118 ogression to AIDS dementia is accelerated in opiate drug abusers.

119 on and progression to HAD are accelerated in opiate drug abusers.

120 dicted that a detailed molecular analysis of opiate drug actions would someday lead to better treatme

121 Placebo treatments and opiate drugs are thought to have common effects on the o

122 neous determination of these three important opiate drugs based on their direct electrochemical oxida

123 While the abuse of opiate drugs continues to rise, the neuroadaptations tha

124 (PS) is that injury complicates the study of opiate drugs like morphine.

125 KEY POINTS: Both endogenous opioids and opiate drugs of abuse modulate learning of habitual and

126 2 signaling in mediating neuroadaptations to opiate drugs of abuse.

127 fects of endogenous opioid neuropeptides and opiate drugs such as morphine.

128 replacing illicit drug use with long-acting opiate drugs.

129 f critical features affecting the actions of opiate drugs.

130 uronal populations that mediate the distinct opiate effects remain elusive.

131 Several paradoxical observations related to opiate effects were noted when micro-opioid receptors we

132 -methyltransferase, cytochrome P450 2D6) and opiate effects, more recent studies have begun to assess

133 e used to investigate the cellular basis for opiate-enhanced human immunodeficiency virus neurotoxici

134 in defining the location and degree to which opiates exacerbate the synaptodendritic injury commonly

135 spontaneously during withdrawal from chronic opiate exposure - in contrast to withdrawal from acute d

136 However, following chronic opiate exposure and withdrawal, intra-BLA reward memory

137 ence of anxiety during withdrawal from acute opiate exposure begins with activation of VTA mesolimbic

138 , but not disinhibit, DA cells after chronic opiate exposure may contribute to long-term negative aff

139 tegmental area (VTA) in response to chronic opiate exposure, which was mediated by specific epigenet

140 t not to inhibit, VTA DA cells after chronic opiate exposure.

141 ory mechanisms within the BLA, controlled by opiate-exposure state.

142 n of opiate reward memories as a function of opiate-exposure state.

143 The clinical efficacy of opiates for pain control is severely limited by analgesi

144 ent style are postulated to contribute to mu-opiate functioning.

145 Pain scores in the opiate group (n = 150) vs the NSAID group (n = 144) were

146 failure occurred in 30 patients (20%) in the opiate group and 33 (23%) in the NSAID group, meeting cr

147 Opiates have long been used as analgesics to relieve pai

148 man opioid receptor ligands mimics exogenous opiates, highlighting the utility of this model for diss

149 ne pain includes nonsteroidal analgesics and opiates; however, long-term use of these drugs is common

150 In contrast, a commercial broad opiate immunoassay technique (CEDIA) achieved 65% qualit

151 The PSi opiate immunosensor achieved 96% concordance with liquid

152 tical screening capability of label-free PSi opiate immunosensors in authentic patient samples and is

153 ribing of both acetaminophen/paracetamol and opiates in 97% of patients and gabapentin in 45% of pati

154 In light of the increasing long-term use of opiates in chronic pain, in principle, the tapentadol co

155 ay have therapeutic potential as adjuncts to opiates in relieving suffering from chronic pain.

156 silicon (PSi) photonic sensor for detecting opiates in urine.

157 nd investigated main behavioral responses to opiates, including motivation to obtain heroin and palat

158 ional side effects associated with classical opiates, including respiratory depression, significant c

159 ther tVTA neurons participate in the loss of opiate-induced disinhibition of VTA DA neurons observed

160 re system and successfully recapitulated the opiate-induced homeostatic adaptation in electrical acti

161 channel-NMDAR feedback loop plays a role in opiate-induced impairment of hippocampal plasticity and

162 ing AMPA receptors (AMPARs), are involved in opiate-induced neuronal and behavioral plasticity, altho

163 ors (AMPARs), are believed to be involved in opiate-induced neuronal and behavioral plasticity, altho

164 -null background, restores opiate reward and opiate-induced striatal dopamine release and partially r

165 Chronic exposure to opiates induces plasticity in dopaminergic neurons of th

166 Opioids and opiates inhibit gastrointestinal functions via mu, delta

167 cked micro-opioid receptors, indicating that opiate interactions with human immunodeficiency virus co

168 increase in the availability of prescription opiates is fuelling a rise in addiction nationally, draw

169 stingly, while tianeptine also produces many opiate-like behavioral effects such as analgesia and rew

170 uprenorphine (BUP) are widely prescribed for opiate maintenance therapy.

171 ovide insight into a mechanism through which opiates may elicit inappropriate desire resulting in the

172 s at supply-based reductions in prescription opiates may reduce harm, but addicted individuals may sw

173 zepines (mean, 0.253 vs 0.177; P = .007) and opiates (mean, 2.18 vs 1.79; P < .001).

174 Morphine and other opiates mediate their effects through activation of the

175 Abuse of heroin and prescription opiate medications has grown to disturbing levels.

176 Although the long-acting opiate methadone is commonly used to treat drug addictio

177 Together, these results demonstrate that opiates modulate nociception in Caenorhabditis elegans t

178 ty to oxycodone, in addition to other common opiates, morphine, morphine-3-glucuronide, 6-acetyl morp

179 e further report that CB1-mediated intra-PLC opiate motivational signaling is mediated through a mu-o

180 odulated podocyte expression of SDCM through opiate mu (MOR) and kappa (KOR) receptors.

181 ein that controls the function of monoamine, opiate, muscarinic, and other G protein-coupled receptor

182 4F chest tube and were randomized to receive opiates (n = 103) vs NSAIDs (n = 103), and those not und

183 eurons inhibited VTA DA neurons similarly in opiate-naive and long-term withdrawn rats.

184 TA inactivation increased VTA DA activity in opiate-naive rats, but not in withdrawn rats, resembling

185 a D1-mediated ERK-dependent mechanism in the opiate-naive state, but switches to a D2-mediated CaMKII

186 Thus, in the opiate-naive state, intra-BLA D1 transmission is require

187 -BLA ERK1/2 signaling only in the previously opiate-naive state.

188 16.5 million people worldwide illicitly use opiates, of whom 4 million use raw opium.

189 Conversely, the effects of opiates on different components of the stress axis can i

190 Cocaine, opiates, opioids, amphetamines, benzodiazepines and seve

191 s in psychopathology; e.g., binge eating and opiate or alcohol abuse, disorders in which muORs and ab

192 primary (unconditioned) stimulus (i.e., the opiate or the stimulant) and likely reflect mechanisms e

193 is that changes in the rates of Prescription Opiate Overdoses (POD) are correlated with changes in th

194 to these drugs and changing the geography of opiate overdoses.

195 n, successful detection of a commonly abused opiate, oxycodone, resulted in 100% qualitative agreemen

196 er relationships, access to social services, opiate pain medications, and acute symptoms motivated ca

197 Effective and safe doses of opiate painkillers, like morphine, can be limited by res

198 We provide a current review of opiate pharmacogenetics.

199 Patients were least likely to abandon opiate prescriptions.

200 The Opiates produce analgesia and other adverse effects thro

201 In the natural killer (NK) cells, delta-opiate receptor (DOR) and mu-opioid receptor (MOR) inter

202 ther hallucinogens and consistent with kappa opiate receptor agonism.

203 others have used intrathecal fentanyl, a mu-opiate receptor agonist, in humans to reduce the input f

204 ecretogogues, and peripherally restricted mu-opiate receptor antagonists, the latter a major advance

205 Cannabinoid, dopamine (DA), and opiate receptor pathways play integrative roles in emoti

206 mic morphine exposure requires a decrease in opiate receptor stimulation in the VTA and can be reliev

207 One gene, OPRL1, encoding an opiate receptor, displayed extremely efficient levels of

208 eceptor-dependent reward pathway, or a kappa-opiate receptor-dependent aversion pathway, directly wit

209 ivational signaling is mediated through a mu-opiate receptor-dependent reward pathway, or a kappa-opi

210 (SA)-a highly selective agonist at the kappa opiate receptor-is believed to be one of the most potent

211 nervated by the orexin neurons express kappa opiate receptors, the main receptor for dynorphin.

212 t this trapping was not caused by binding to opiate receptors, we examined whether [(11)C]dLop, a wea

213 recent developments in our understanding of opiate receptors.

214 s are mediated by endogenous opioid systems, opiate regulation of pair bond maintenance has never bee

215 an important structure for the processing of opiate-related associative memories and is functionally

216 e, intra-BLA D1 transmission is required for opiate-related memory formation.

217 ceptor substrates functionally interact with opiate-related motivational processing circuits, particu

218 armacogenetic data make it evident that many opiate-related phenomena are influenced by genetics.

219 eroin addiction is treated successfully with opiate replacement strategies but relapse and switch to

220 ferent also contribute to the development of opiate resistance, we used a recently developed model of

221 nt acute pain can undergo a transition to an opiate-resistant chronic pain state that becomes a much

222 rs that heretofore have been associated with opiate respiratory depression, which may have clinical a

223 t is well accepted that glia are critical to opiate responses.

224 Use of NSAIDs vs opiates resulted in no significant difference in pain sc

225 n an otherwise MOR-null background, restores opiate reward and opiate-induced striatal dopamine relea

226 e role of intra-mPFC CB1 transmission during opiate reward learning.

227 Opiate reward memories are powerful triggers for compuls

228 ors independently modulates the formation of opiate reward memories as a function of opiate-exposure

229 ined with molecular analyses, we report that opiate reward memory acquisition requires intra-BLA ERK1

230 , VTA plasticity was associated with altered opiate reward, as sexually experienced males did not for

231 ect-pathway neurons is sufficient to support opiate reward-driven behaviors and provides a new inters

232 atal sites, is needed for the restoration of opiate reward.

233 allenge the canonical disinhibition model of opiate reward.

234 transmission in the modulation of behavioral opiate-reward processing is not currently known.

235 emories are powerful triggers for compulsive opiate-seeking behaviors.

236 humans to reduce the input from type III-IV opiate-sensitive muscle afferents.

237 n 100% qualitative agreement between the PSi opiate sensor and LC-MS/MS.

238 ing the utility of this model for dissecting opiate signaling in mammals.

239 that this model may be useful for dissecting opiate signaling in mammals.

240 ion to modulate the motivational salience of opiates similarly operates through a D1-mediated ERK-dep

241 on interventions such as needle exchange and opiate substitution therapy (OST) alone.

242 Interventions such as opiate substitution therapy (OST) and high-coverage need

243 g interaction studies between ART, DAAs, and opiate substitution therapy must be expedited.

244 We included 198 patients in opiate substitution therapy, who fulfilled indications f

245 lack of evidence, trial data have shown that opiate substitution treatments reduce substance misuse r

246 maceutical value, including most notably the opiates such as codeine and morphine.

247 but addicted individuals may switch to other opiates such as heroin.

248 Variability of morphine detection as a model opiate target was <9% both within-run and between-day at

249 ) results on samples that underwent standard opiate testing (n = 50).

250 ethanol, Delta(9)-tetrahydrocannabinol, and opiates; the antipsychotic drug, haloperidol; juvenile e

251 ential for treating pain, but termination of opiate therapy can cause a debilitating withdrawal syndr

252 lie the development of cellular tolerance to opiate therapy.

253 developed for analyzing naturally occurring opiates, this is the first detailed ion mobility study o

254 of classical EGFR transactivation may enable opiates to diminish neurite outgrowth and synapse format

255 A DA circuit could be an important factor in opiate tolerance and addiction.

256 hese systems, which could solve the issue of opiate tolerance and improve quality of life in oral can

257 s, but not in withdrawn rats, resembling the opiate tolerance effect in DA cells.

258 rrelations with heroin use history and acute opiate toxicology.

259 use in the past month was assessed using the Opiate Treatment Index.

260 Upon discovering that chronic opiate treatment of rats down-regulates thrombospondin 1

261 Postoperative opiate usage was converted to morphine equivalent daily

262 Pain Questionnaire (SF-MPQ), and concurrent opiate usage.

263 [IQR], 3 [2-5] and 3 [1-5.5], respectively), opiate use after discharge (median [IQR], 6.7 [5-10] and

264 Antepartum maternal opiate use also increased from 1.19 (95% CI, 1.01-1.35)

265 ciated with coalescence of symptoms, chronic opiate use and more severe disease as characterized by l

266 of life were similar between groups, as was opiate use and number of hospital admissions and outpati

267 are available for the incidence of maternal opiate use at the time of delivery or NAS.

268 ime to initiation of cytotoxic chemotherapy, opiate use for cancer-related pain, prostate-specific an

269 Patient-reported outcomes and total opiate use further supported the benefit of TEA on patie

270 Withdrawal is therefore a key determinant of opiate use in dependent individuals, yet its underlying

271 ncrease in the incidence of NAS and maternal opiate use in the United States was observed, as well as

272 Chronic opiate use induces opiate dependence, which is character

273 For this group with chronic opiate use prior to surgery, change in morphine equivale

274 The historical patterns of opiate use show that sources and methods of access great

275 Chronic opiate use was less frequent in the pediatric-onset grou

276 NAS and maternal opiate use were described as an annual frequency per 100

277 COME MEASURES: Incidence of NAS and maternal opiate use, and related hospital charges.

278 plus prednisone on overall survival, time to opiate use, and use of other subsequent therapies.

279 mpact traumatic brain injury or a history of opiate use, did not have any astroglial scarring in the

280 harges for mothers diagnosed with antepartum opiate use, within data sets including 784,191 to 1.1 mi

281 drawal syndrome primarily caused by maternal opiate use.

282 l alterations produced in neurons by chronic opiate use.

283 Opiates were the first drugs shown to negatively impact

284 onally regulates the motivational valence of opiates; whereas CB1 activation switched morphine reward

285 Most pain remains treated by opiates, which have significant side effects that limit

286 Conditioned opiate withdrawal contributes to relapse in addicts and

287 A brief comment as to sedative and opiate withdrawal follows.

288 Protracted opiate withdrawal is accompanied by altered responsivene

289 contribute to somatic and affective signs of opiate withdrawal is not fully understood.

290 f phase (taper, post taper) for the Clinical Opiate Withdrawal Scale (COWS) score (taper mean, 5.19 [

291 .23]; F2,170 = 3.6, P = .03) and Subjective Opiate Withdrawal Scale (SOWS) score (taper mean,8.81 [S

292 001) and suppression of withdrawal (Clinical Opiate Withdrawal Scale, CAM2038, 24 mg: effect size, 0.

293 nogenic alkaloid proposed as a treatment for opiate withdrawal, has been shown to inhibit serotonin t

294 LC discharge rate in a manner suggestive of opiate withdrawal, selectively in stressed rats when adm

295 icts and can be studied in rats by using the opiate withdrawal-induced conditioned place aversion (OW

296 was accompanied by behavioral signs of mild opiate withdrawal.

297 1 (Panx1) channel as a therapeutic target in opiate withdrawal.

298 ve symptoms in two different mouse models of opiate withdrawal.

299 n long-term negative affective states during opiate withdrawal.

300 ucleus accumbens mediating the expression of opiate-withdrawal-induced physical signs and aversive me