ライフサイエンスコーパス: analgesic

1 r pain, and medications (eg, anxiolytics and analgesics).

2 Cebranopadol is known as a highly potent analgesic.

3 for the development of a safe and effective analgesic.

4 one is a strong opioid frequently used as an analgesic.

5 eful strategy for obtaining potent and safer analgesics.

6 S1PR1 antagonists as a class of nonnarcotic analgesics.

7 s a serious adverse event produced by opioid analgesics.

8 erest target for the discovery of non-opioid analgesics.

9 g lead in the development of next generation analgesics.

10 viate OIH, a serious adverse event of opioid analgesics.

11 as a high interest target for developing new analgesics.

12 ds to serve as potential nonaddictive opioid analgesics.

13 quinoline alkaloid (BIA) precursor to opioid analgesics.

14 eptor neurons are attractive targets for new analgesics.

15 fferent opioid and acetaminophen combination analgesics.

16 ic pain states that are refractive to opioid analgesics.

17 hem prime targets for the development of new analgesics.

18 derlie mechanisms of pain suppression by new analgesics.

19 perative pain and consumption of opioids and analgesics.

20 more in patients without a regular need for analgesics.

21 nded include an opioid-antagonist and opiate analgesics.

22 To compare the efficacy of 4 oral analgesics.

23 targeting this system hold promise as novel analgesics.

24 problems are adequately treated with current analgesics.

25 Mg(2+) leads to increased efficacy of opioid analgesics.

26 nistration (FDA) for new approvals of opioid analgesics.

27 been proposed as an improved class of opioid analgesics.

28 ry drugs (NSAIDs) are effective, widely used analgesics.

29 his receptor and improve upon current opioid analgesics.

30 ry was driven by the search for nonaddicting analgesics.

31 tional strategies for screening of potential analgesics.

32 ts who have not responded to oral or topical analgesics.

33 were age 1.014(95% CI: 1.006-1.022), use of analgesics 1.461 (95% CI: 1.060-2.025), and use of herbs

34 to gabapentin and pregabalin, mediating the analgesic action of these drugs against neuropathic pain

35 The 6TM variants are also involved in analgesic action through other drug classes, including d

36 Finally, PCTR1 showed potent analgesic action.

37 spinal-projections from LC neurons can exert analgesic actions, it is not known whether they can act

38 bicyclic core peptidomimetics with promising analgesic activity and reduced abuse liabilities into a

39 y NaV1.7 activation, Pn3a alone displayed no analgesic activity in formalin-, carrageenan- or FCA-ind

40 inil, two wake-promoting agents that have no analgesic activity in rested mice, immediately normalize

41 The analgesic activity is mediated by kappaOR signaling thro

42 A broad lack of analgesic activity was also found for the selective NaV1

43 Contrary to oxycodone, 14u produces analgesic activity with reduced opioid-induced relevant

44 gonism and sigma(1)R antagonism and a potent analgesic activity, comparable to the MOR agonist oxycod

45 R agonism and sigma antagonism) and a potent analgesic activity, comparable to the MOR agonist oxycod

46 Some antithrombotics, antibiotics, opioid analgesics, adrenergics, proton-pump inhibitors, nitrogl

47 unique roles, and whether they may serve an analgesic advantage in providing pain relief without pro

48 s shown that patients may be over-prescribed analgesics after surgery.

49 holinergic effects but that it can act as an analgesic agent as well.

50 indicate that AM1710 is not a broad-spectrum analgesic agent in mice and suggest the need to identify

51 ntinue use of alcohol and smoking and taking analgesic agents (nonsteroidal anti-inflammatory drugs a

52 al anti-inflammatory drugs versus other oral analgesic agents for acute soft tissue injury.

53 core and a decreased or stable use of rescue analgesic agents, as recorded in a daily electronic diar

54 pathways that offer opportunities for novel analgesic alternatives.

55 es, but mu-opioid receptors mediate both the analgesic and addictive effects of opioids.

56 pain medication paracetamol and a promising analgesic and an anti-arthritic medicament itself.

57 SzV-1287 exerts potent analgesic and anti-inflammatory actions in chronic arthr

58 ecent years, especially with regard to their analgesic and anti-inflammatory actions.

59 tic approach as Ms 9a-1 produces significant analgesic and anti-inflammatory effects in mice models o

60 Evaluation of analgesic and anti-inflammatory properties revealed simi

61 Kappa opioid receptor (KOR) agonists produce analgesic and anti-pruritic effects, but their clinical

62 as menthol has been used for centuries as an analgesic and anti-pruritic, these findings support the

63 found that in CD-1 mice nalfurafine produced analgesic and anti-scratch effects dose-dependently, lik

64 Acetaminophen (paracetamol) is a widely used analgesic and antipyretic drug with only incompletely un

65 of circulating acetaminophen (a widely used analgesic and antipyretic) in saliva and sweat, using a

66 g whether sleep disruption alters morphine's analgesic and hedonic properties.

67 expressed in primary sensory neurons in the analgesic and hyperalgesic effects produced by systemic

68 strong evidence of dysregulation of our main analgesic and limbic systems in chronic TMD pain.

69 iac surgery and may be affected by choice of analgesic and sedative.

70 n whether AM1710 behaves as a broad-spectrum analgesic and/or suppresses the development of opioid to

71 pioid receptor, the primary target of opioid analgesics and abused drugs.

72 Regular or frequent use of analgesics and acute antimigraine drugs can increase the

73 t to the clinical community: anticoagulants, analgesics and buffers.

74 of low-dose opioids combined with nonopioid analgesics and in the treatment of opioid use disorder a

75 ts the therapeutic efficacy of morphine-like analgesics and mediates the long duration of kappa opioi

76 nd depression, employment status, and use of analgesics and nonsteroidal anti-inflammatory drugs at 1

77 The use of analgesics and sedatives was assessed daily.

78 Age, use of analgesics and use of herbs increase the risk, albeit mi

79 eful strategy for obtaining potent and safer analgesics and were the basis for the selection of 14u a

80 re admitted to the ICU and administered with analgesics and/or sedatives.

81 onist distinguished for its neuroprotective, analgesic, and anti-inflammatory properties in numerous

82 med enough THC to trigger acute hypothermia, analgesic, and locomotor responses, and that 15 days of

83 nd consists of adequate fluid resuscitation, analgesics, and monitoring.

84 th hip or knee OA, inadequate response to OA analgesics, and no radiographic evidence of prespecified

85 oped chronic abdominal pain requiring strong analgesics, and one in five suffered from severe abdomin

86 of chronic pain is poorly managed by current analgesics, and there is a need for new classes of drugs

87 ith various biological activities, including analgesic, anti-inflammatory, anti-HIV, antidiabetic, an

88 U50,488H-induced aversion, without affecting analgesic, anti-scratch, and sedative effects and motor

89 erent therapeutic classes (i.e. antibiotics, analgesics, anti-inflammatories, cardiovascular agents,

90 Treatment usually involves analgesics, anti-inflammatory drugs, and supportive care

91 insulin secretion and has potent anorectic, analgesic, anxiolytic and antidepressive-like effects in

92 Opioid analgesics are powerful pain relievers; however, over ti

93 Opioids serve a vital role in the current analgesic array of treatment options.

94 le personalized dosing and monitoring of the analgesic as well as quick diagnostics of possible overd

95 al evidence still supports the use of opioid analgesics as the gold standard to treat cancer-related

96 e points: 1) before surgery 2) first dose of analgesic at home, 3) 24 hours postoperatively, and 4) 7

97 Opioids are some of the most potent analgesics available.

98 Opiates are potent analgesics but their clinical use is limited by side eff

99 lycine transporter 2, GlyT2, show promise as analgesics, but may be limited by their toxicity through

100 ily, are under active investigation as novel analgesics, but their modes of signaling are less well c

101 Opioids are very effective analgesics, but they are also highly addictive.

102 esses pain in part by activating supraspinal analgesic circuits.

103 low back pain (66.2% vs 50.0%; P = 0.04) and analgesic consumption (30.9% vs 15.5%; P = 0.03) after 6

104 Analgesic consumption was generally parallel to pain per

105 operties, and suggests a novel direction for analgesic development.

106 onist/delta-opioid receptor (DOR) antagonist analgesic devoid of tolerance or dependence in mice (AAH

107 inal pain were defined as those using strong analgesics, diagnosed with chronic pain, or referred to

108 in vitro, subcutaneous administration of an analgesic dose of fentanyl (30 mug/kg, s.c.) was perform

109 dy demonstrate that the administration of an analgesic dose of ketamine does not compromise tolerance

110 (APAP) is widely used as an antifebrile and analgesic drug at recommended doses, whereas an overdose

111 At least 2 different nonopioid analgesic drug classes (cyclooxygenase inhibitors, aceta

112 Importantly, the number of nonopioid analgesic drug classes administered during surgery predi

113 a key target for the spicy taste sensor and analgesic drug development.

114 sodium channel is therefore a key target for analgesic drug development.

115 nd hospital stays, and doses of sedative and analgesic drugs administered were recorded.

116 The attrition of novel analgesic drugs in the clinic can be attributed in the m

117 act of laboratory procedures and efficacy of analgesic drugs in the model species, the zebrafish.

118 ugh to require increased use of sedative and analgesic drugs, and is among the events that predict cl

119 essential for the action of a novel class of analgesic drugs, including 3-iodobenzoyl-6beta-naltrexam

120 rgets for antiepileptic, antiarrhythmic, and analgesic drugs.

121 and mediate the effects of the most powerful analgesic drugs.

122 for developing future resting-state-targeted analgesic drugs.

123 stem, suggesting that at least part of their analgesic effect might be of central origin.

124 The analgesic effect of intrathecally administered morphine

125 n, produced strong aversion and canceled the analgesic effect of low-dose ketamine.

126 diurnal variation in the reward behavior or analgesic effect of opioid administration.

127 limbs, but corpus callosotomy eliminated the analgesic effect that was ipsilateral, but not contralat

128 o their anti-inflammatory, anti-pyretic, and analgesic effect.

129 gesting that signaling mechanisms regulating analgesic effectiveness of intrathecally applied EM2 als

130 ticals, opioids differ in their rewarding or analgesic effects depending on when they are applied.

131 Notably, AOC3 inhibitors provoked analgesic effects in inflammatory pain models in vivo, s

132 e rotarod test and statistically significant analgesic effects in the formalin test for acute inflamm

133 of Fcgr1 in sensory neurons produced similar analgesic effects in these models.

134 y self-reported pain intensity, and that the analgesic effects of a competing task were influenced by

135 binoid signaling is also responsible for the analgesic effects of acetaminophen against inflammatory

136 The analgesic effects of BMAs are modest, and they should no

137 This nAChR is a candidate for the analgesic effects of nicotine as well as the frog toxin

138 The powerful analgesic effects of opioid drugs have captivated the in

139 Tolerance to the analgesic effects of opioids is a major problem in chron

140 e (including drug craving), reinforcing, and analgesic effects of oxycodone in human volunteers diagn

141 Finally, exendin-4 did not alter the analgesic effects of oxycodone, suggesting that activati

142 opioid use disorders and it may enhance the analgesic effects of oxycodone.

143 lectroacupuncture of the acupoints generated analgesic effects on MO-induced visceral hypersensitivit

144 lation in primary sensory neurons diminishes analgesic effects produced by systemic and intrathecal o

145 Cannabis elicits its mood-enhancing and analgesic effects through the cannabinoid receptor 1 (CB

146 Each pathway would produce analgesic effects.

147 of acetaminophen appears to further enhance analgesic efficacy and potentially reduce the need for o

148 ily dose-equivalent of 3 mg/kg, 12 exhibited analgesic efficacy comparable to dose of 10 mg/kg of 1 i

149 There is evidence that its analgesic efficacy might be modified by variants of the

150 r, clinical data have yet to demonstrate the analgesic efficacy of inhibitors of endocannabinoid-regu

151 rget engagement of new drugs and predict the analgesic efficacy of new drugs.

152 hermore, although RGS9-2 does not affect the analgesic efficacy of oxycodone or the expression of phy

153 oaddition, with the aim of improving in vivo analgesic efficacy versus DPDPE.

154 recruitment of beta-arrestin-2 could provide analgesic efficacy with fewer side-effects.

155 evaluation of risk of developing pain and of analgesic efficacy.

156 of therapies to maximize and sustain opioid analgesic efficacy.

157 influence of low-dose ketamine, one of three analgesics employed in the pre-hospital setting by the U

158 risk of developing OUD and receiving opioid analgesics, even after accounting for comorbidities and

159 on that specific receptors for morphine-like analgesics exist, the search for endogenous ligands for

160 onal design of proteins that bind the potent analgesic fentanyl.

161 nvision a class of non-opioid nAChR-targeted analgesics for chronic pain.

162 ioids such as oxycodone are highly effective analgesics for clinical pain management, but their misus

163 l incision or positioning that required oral analgesics for longer than 3-4 days after surgery (five

164 The prescribing of opioid analgesics for pain management-particularly for manageme

165 ciceptor signaling to the brain and serve as analgesics for persistent pain.

166 Opioids are commonly used as analgesics for severe pain, but their addictive potentia

167 outcomes of RCT/s comparing 2 or more opioid analgesics for the management of chronic pain were obtai

168 nee osteoarthritis (OA) have been limited to analgesics, glucocorticoids, hyaluronic acid (HA) and a

169 Development of an efficacious, non-addicting analgesic has been challenging.

170 Frequent use of analgesics has been associated with a higher risk of hea

171 for endogenous opioid neurotransmitters and analgesics, has been a major focus for drug discovery in

172 Efforts to improve safety of u-opioid analgesics have focused on agonists that show signaling

173 harmaceutical development pipeline lacks new analgesics, health-care professionals, patients and medi

174 otinic acetylcholine receptor (nAChR) and is analgesic in animal models of pain.

175 RGS proteins modulate the efficacy of opioid analgesics in a brain region- and agonist-selective fash

176 rmacological profile against existing opioid analgesics in assays not confounded by limited signal wi

177 c intractable insomnia where the traditional analgesics in PCA were replaced with dexmedetomidine (De

178 on to being on average inferior to NSAIDs as analgesics in postsurgical dental pain, opioids produce

179 dequate staffing ratios; and availability of analgesics, including opioids, for pain relief.

180 ng, and usually refractory to treatment with analgesics, including opioids.

181 om animal and human studies indicates opioid analgesics increase susceptibility to infections, it is

182 tiation, 97% respondents administer sedative/analgesic infusions, and the sedation target was "sedate

183 st day and the first week after surgery, the analgesic intake and the modified early-wound healing in

184 Patients reported their worst pain score and analgesic intake at baseline and days 10 and 42 after tr

185 ween the two methods in reported pain level, analgesic intake, and MEHI.

186 Pain ratings disclosed the anticipated analgesic interaction between task difficulty and pain i

187 Identification of non-narcotic analgesics is of paramount importance.

188 compounds from the literature, including the analgesic lidocaine, the Dess-Martin periodinane oxidati

189 Such peripheral opioid analgesics may represent alternatives to presently avail

190 tterns and the mobilization of a new type of analgesic mechanism within this early temporal nocicepti

191 It is increasingly appreciated that common analgesic mechanisms for these treatments depend on neur

192 We further distinguish the analgesic mechanisms of regenerative therapies from thos

193 Low dose ketamine is an effective analgesic medication.

194 edications (OR = 0.28, P < .001), non-opioid analgesic medications (OR = 0.21, P = .002), anti-hyperl

195 ns with resistant symptoms or intolerance to analgesic medications.

196 no patient called after discharge to request analgesic medications.

197 gement, the opportunity to deliver effective analgesic medicines targeting Na(V)1.7 endures.

198 ement consists of education and reassurance, analgesic medicines, non-pharmacological therapies, and

199 hibitors of this Na(+) ion channel target as analgesic medicines.

200 s have prompted investigation of alternative analgesic methods in this patient population.

201 Worldwide, the use of prescription opioid analgesics more than doubled between 2001 and 2013, with

202 inophen and other potentially opioid-sparing analgesics, on the incidence of postoperative delirium i

203 NSAIDs have analgesic, opioid-sparing, and anti-inflammatory effects

204 ence was observed regarding the days free of analgesics or sedatives, the duration of night sleep, an

205 laws experienced slower increases in opioid analgesic overdose mortality.

206 n endocrine disruptor as reported for fellow analgesics paracetamol and aspirin.

207 Lipidised analgesic peptide prodrugs self-assemble into peptide na

208 phenotype, an assertion consistent with the analgesic pharmacology seen in this animal.

209 Prescription opioid analgesics play an important role in the treatment of po

210 Published research on prescribed opioid analgesic (POA) use during pregnancy and birth outcomes

211 Currently available analgesics poorly serve individuals suffering from chron

212 ve the mu opioid receptor but that have high analgesic potency and low risk of adverse effects, parti

213 Both analogs also exhibited good analgesic potency in the CFA inflammatory-pain model wit

214 ion of EOPs of immune origin, maximizing the analgesic potential of immune cells that naturally accum

215 mediated neuronal activation, revealing the analgesic potential of macitentan.

216 Given its analgesic properties and milder undesired effects than m

217 stin scaffolding proteins could preserve the analgesic properties of MOR agonists while avoiding cert

218 rts have focused on trying to dissociate the analgesic properties of opioids from their undesirable s

219 rther, the efficacy of a range of drugs with analgesic properties to identify efficacy of these agent

220 e mesolimbic system but still possess strong analgesic properties.

221 his review discusses the development of the "analgesic" receptor concept, the demonstration that such

222 To the extent that nonopioid analgesics reduce opioid consumption, they may decrease

223 opioid interventions as part of a multimodal analgesics regimen for effective pain management after t

224 stitute the major component of perioperative analgesic regimens for surgery in general, a variety of

225 cts on other cancer types and to personalize analgesic regimens in patients with cancer for optimal o

226 Furthermore, it is prudent to use multimodal analgesic regimens to reduce reliance on opioids during

227 tline important components of opioid-sparing analgesic regimens.

228 ly, with implications for personalization of analgesic regimens.

229 eneficial and harmful effects of 4 nonopioid analgesics regimens.

230 Two compounds (13l and 11b) showed analgesic response in tail flick test which was blocked

231 Acetaminophen (APAP) is a commonly used analgesic responsible for more than half of acute liver

232 g represent a novel mechanism for modulating analgesic responsiveness to endogenous EM2 (and perhaps

233 dentified molecular mechanism underlying the analgesic role of SGCs offers new approaches for reversi

234 atory agents, junctional protein regulators, analgesics, secretagogues, and serotonin antagonists hav

235 ceptor agonists, currently in development as analgesics, should be considered as relapse prevention m

236 tively modulates the actions of other opioid analgesics, such as fentanyl and methadone.

237 ANCE STATEMENT Commonly used clinical opioid analgesics, such as fentanyl and morphine, can produce h

238 ain conditions, are emerging as non-narcotic analgesics, supporting the repurposing of fingolimod for

239 d that, when controlling for prematurity and analgesics, supportive experiences (e.g., breastfeeding,

240 The pain and analgesic systems are complex, and the actions of system

241 e or hip and inadequate response to standard analgesics, tanezumab, compared with placebo, resulted i

242 itical limitation in developing deltaR as an analgesic target, however, is that deltaR agonists show

243 proved drug suitable for use as an effective analgesic targeting mPGES-1.

244 eptive neurons, identifying them as putative analgesic targets.

245 Morphine is a unique opioid analgesic that activates the mu-opioid receptor (MOR) wi

246 Ketamine is a valuable anaesthetic and analgesic that in recent years has gained notoriety as a

247 ion is often required and, in the absence of analgesics that are at least as effective but safer, NSA

248 pidemic levels, the identification of opioid analgesics that lack abuse potential may provide a path

249 abuse potential compared with current opioid analgesics that target the mu opioid receptor.

250 ion hold in providing new and transformative analgesic therapies for the treatment of chronic pain.

251 ch, making it an attractive target for novel analgesic therapies(2).

252 se sleep disturbances should be mitigated by analgesic therapy.

253 have not demonstrated a beneficial effect of analgesic therapy; this is despite owner-reported improv

254 The choice of analgesic to treat acute pain in the emergency departmen

255 e dilemma of prescribing opioid or nonopioid analgesics to chronic pain patients; however, the impact

256 of low-dose opioids combined with nonopioid analgesics to treat pain and opioid use disorders.

257 eceptor (MOR), the primary target for opioid analgesics, to define a signaling pathway that dynamical

258 ned with peripheral MOR antagonists to limit analgesic tolerance and OIH.

259 cal use is limited by side effects including analgesic tolerance and opioid-induced hyperalgesia (OIH

260 ions have detrimental side effects including analgesic tolerance and opioid-induced hyperalgesia (OIH

261 wever, over time, pain control diminishes as analgesic tolerance develops.

262 with these bacterial communities, attenuated analgesic tolerance in morphine-treated mice.

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

264 d-induced analgesia is strongly enhanced and analgesic tolerance is greatly diminished.

265 The mechanism underlying morphine analgesic tolerance still remains unresolved.

266 eptor G-protein association and blocks acute analgesic tolerance to morphine and kappa opioid recepto

267 Classically, it was thought that analgesic tolerance to opioids was caused by desensitiza

268 We show that morphine analgesic tolerance was significantly attenuated in germ

269 eir impact is truncated by loss of efficacy (analgesic tolerance).

270 Prolonged exposure to opioids results in analgesic tolerance, drug overdose, and death.

271 argeted to blunt the development of morphine analgesic tolerance, without affecting normal P2X7 recep

272 fectiveness is limited by the development of analgesic tolerance.

273 to prolong morphine's efficacy and attenuate analgesic tolerance.

274 h naive fecal microbiota reinstated morphine analgesic tolerance.

275 proposal that sustained MOR signaling caused analgesic tolerance.

276 ically underlies the development of morphine analgesic tolerance.SIGNIFICANCE STATEMENT Controlling p

277 onism is on the verge of becoming a powerful analgesic treatment for numerous conditions, including o

278 search and the development and assessment of analgesic treatment strategies.

279 Risk factors were preoperative use of strong analgesics, unemployment, postoperative complications, a

280 tigated the relationship between duration of analgesic use and self-reported hearing loss among 55,85

281 MIS is associated with decreased analgesic use, shorter length of stay, and faster postop

282 macological interventions to decrease opioid analgesics use, as they have significant adverse effects

283 The number of adjunct analgesics used postoperatively was greater in the ERAS

284 ricyclic antidepressant drugs are first line analgesics used to treat SCI-induced neuropathic pain, b

285 d before discharge, and receipt of nonopioid analgesics varied substantially.

286 B(2) receptor (CB(2)) agonists are potential analgesics void of psychotropic effects.

287 Preoperative use of strong analgesics was a risk factor for chronic abdominal pain

288 oth short-term and longer-term use of opioid analgesics were associated with hip fracture events.

289 the opioid crisis, we need to discover novel analgesics whose mechanisms do not involve the mu opioid

290 and this enhanced pain may be reduced not by analgesics, whose effectiveness is reduced, but by incre

291 ochloride extended-release (ER), an approved analgesic with opioid and nonopioid mechanisms of action

292 among patients initiating long-acting opioid analgesics with and without previously reported immunosu

293 The development of novel analgesics with improved safety profiles to combat the o

294 k for further optimization of fentanyl-based analgesics with improved safety profiles.

295 tensive research efforts, the development of analgesics with reduced adverse effects remains a signif

296 ed the promise of these ligands as effective analgesics with reduced liability for adverse effects.

297 ntagonist ligands may emerge as novel opioid analgesics with reduced side effects.

298 ective Na(v)1.7 antagonist should provide an analgesic without abuse liability and an improved side-e

299 the mu-opioid receptor would be an effective analgesic without the accompanying adverse effects assoc

300 Tramadol is one of the most commonly used analgesics worldwide, classified as having a low abuse p