ライフサイエンスコーパス: analgesia

1 ssion, a phenomenon known as "stress-induced analgesia".

2 s and diminish cooling-mediated pain relief (analgesia).

3 anisms underlying exercised-induced pain and analgesia.

4 nfusion failed to reverse meditation-induced analgesia.

5 protein muOR signalling is thought to confer analgesia.

6 ficantly reduces the need for periprocedural analgesia.

7 ental absence and use of continuous sedation/analgesia.

8 anted delta, kappa1, and alpha2 actions from analgesia.

9 fect of active drug interfering with placebo analgesia.

10 the weak-opioid group, because of inadequate analgesia.

11 after correcting for modeled placebo-related analgesia.

12 patients diminishes modeled placebo-related analgesia.

13 heat perception, cold hyperalgesia, and cold analgesia.

14 eling of euphoria, anxiolysis, sedation, and analgesia.

15 gonist, bicuculline, disrupted A3AR-mediated analgesia.

16 gnificantly increased and prolonged morphine analgesia.

17 is both necessary and sufficient for IBNtxA analgesia.

18 related to pain were not affected by placebo analgesia.

19 d their activation there produces meaningful analgesia.

20 with GPR55 signaling in the PAG may promote analgesia.

21 lop new and safe approaches for sedation and analgesia.

22 horn, a principal site of action for opiate analgesia.

23 ecover faster and require less postoperative analgesia.

24 care unit (ICU) are often given sedation or analgesia.

25 ne (DA), opioid) related to pain and placebo analgesia.

26 ntness (p < 0.001) ratings more than placebo analgesia.

27 IL-1beta experienced less endogenous opioid analgesia.

28 ief is mechanistically distinct from placebo analgesia.

29 elective NaV1.7 inhibitors produced profound analgesia.

30 ntly increased doses of standard opioids for analgesia.

31 ts compared with patients receiving systemic analgesia.

32 transduction role for P450 enzymes in micro analgesia.

33 beta in the NAc without diminishing morphine analgesia.

34 icients) significantly predicted conditioned analgesia.

35 0 activity in opioid-mediated stress-induced analgesia.

36 t response, without reducing opioid-mediated analgesia.

37 in swim-induced, but not restraint-induced, analgesia.

38 this protein modulates opiate addiction and analgesia.

39 ress response that results in stress-induced analgesia.

40 dulation were closely involved in predicting analgesia.

41 n, and schizophrenia, as well as in pain and analgesia.

42 s the activity of these neurons and produces analgesia.

43 R can modulate side effects without altering analgesia.

44 rimary outcome evaluated was intra-operative analgesia.

45 e than males to produce comparable levels of analgesia.

46 erity of withdrawal without affecting opiate analgesia.

47 ub of key brainstem structures to endogenous analgesia.

48 brainstem structure implicated in endogenous analgesia.

49 nsively in humans for general anesthesia and analgesia.

50 n shown to be effective adjuncts to narcotic analgesia.

51 te a biological brake to opioid drug-induced analgesia.

52 e veteran population affects intra-operative analgesia.

53 n smoke inhalation under deep anesthesia and analgesia.

54 ia, 5236 (58.2%) with specific preprocedural analgesia.

55 echanisms promoting pain vs. those dampening analgesia.

56 in nociceptors might enable ligand-dependent analgesia.

57 vs 1.2 +/- 0.2, p = 0.006) and required less analgesia (0% vs 10%, p = 0.03) immediately after PLB in

58 41.3% (95% CI, 33.7%-48.9%) received opioid analgesia (20.7% [95% CI, 5.3%-36.0%] of black patients

59 0), but the NSAID group required more rescue analgesia (26.3% vs 38.1%; rate ratio, 2.1; 95% CI, 1.3-

60 he risk of death was decreased with epidural analgesia (3.1% vs 4.9%; odds ratio, 0.60; 95% confidenc

61 e and avoidance learning [2], and endogenous analgesia [3].

62 2379 (26.4%) were performed with continuous analgesia, 5236 (58.2%) with specific preprocedural anal

63 vs 14.4%; P < 0.001), and patient-controlled analgesia (56.5% vs 22.8%; P < 0.001).

64 s in pain response ("offset-analgesia"; mean analgesia: 85%, n = 20 subjects).

65 We induced placebo analgesia, a phenomenon specifically modulating the firs

66 Observations: Regional analgesia, acetaminophen, nonsteroidal anti-inflammatory

67 care for supportive care and pain management-analgesia, adjunct therapies, radiotherapy, surgery, sys

68 Receipt of analgesia administration (any and opioid) by race.

69 gnificant differences in the overall rate of analgesia administration by race.

70 rics, and racial disparities with respect to analgesia administration exist.

71 d the frequency of both opioid and nonopioid analgesia administration using complex survey weighting.

72 hippocampus gyrus connectivity predicts drug analgesia after correcting for modeled placebo-related a

73 inoid receptors mediate acute anxiolysis and analgesia after running.

74 This procedure induced significantly more analgesia after sham or real acupuncture on the test sit

75 ration of analgesia, and specifically opioid analgesia, after adjusting for important demographic and

76 system contributes not only to acetaminophen analgesia against acute pain but also against inflammato

77 Time of onset of analgesia, akinesia, and intraoperative pain, if any, wa

78 direction: participants experiencing placebo analgesia also reported decreased empathy for pain, and

79 roduce their effects (loss of consciousness, analgesia, amnesia, and immobility) remain an unsolved m

80 opioid antagonist naltrexone blocked placebo analgesia and also resulted in a corresponding "normaliz

81 physiological effects of opioids, including analgesia and dependence.

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

83 Use of patient-controlled narcotic analgesia and duration of use decreased (63.2% of patien

84 ectively preserving the efficacy of morphine analgesia and eliminating tolerance.

85 analgesia reduces pain, as shown in placebo analgesia and expectancy modulations during drug adminis

86 .6%) patients had pain requiring intravenous analgesia and Fc-SEMS had to be removed because of unbea

87 gical changes that lead to the experience of analgesia and improvements in emotional state.

88 radoxical behavioural responses: early-phase analgesia and late-phase mechanical allodynia which requ

89 ve recently developed, alongside appropriate analgesia and monitoring.

90 f of the population, reported higher placebo analgesia and more positive affective states immediately

91 Drug reduction for sedation and analgesia and non-pharmacological approaches are recomme

92 e evidence for an interaction between opioid analgesia and opioid rewarding, which may have implicati

93 The Opiates produce analgesia and other adverse effects through activation o

94 article reviews mechanisms underlying opioid analgesia and other opioid actions.

95 nd evaluation of a chemical probe exhibiting analgesia and reduced opioid-induced side effects.

96 at end of life, specifically in relation to analgesia and related medicines (for side-effect managem

97 many opiate-like behavioral effects such as analgesia and reward, it does not lead to tolerance or w

98 d in pediatric intensive care unit (ICU) for analgesia and sedation.

99 domain of the CaMKI enzyme produces thermal analgesia and shifts the operating range for nocifensive

100 gents and analgesics; length of sedation and analgesia and total doses of sedatives and analgesics.

101 may alter opioid-mediated effects, including analgesia and withdrawal symptoms.

102 hat underlie both their therapeutic effects (analgesia) and their adverse effects (addiction and over

103 ssment score), interventions (e.g., sedation/analgesia), and ICU characteristics (e.g., size).

104 y genes known to be involved in nociception, analgesia, and antidepressant drug actions.

105 ciceptive afferents could be used to produce analgesia, and if so, how.

106 RGS9-2 complexes negatively control morphine analgesia, and promote the development of morphine toler

107 cally involved in the modulation of pain and analgesia, and represent a candidate mechanism for the d

108 tors curtail immune-driven peripheral opioid analgesia, and sigma-1 antagonism produces local opioid

109 inistered intraoperatively for postoperative analgesia, and some evidence suggests that ketamine prev

110 ial differences in overall administration of analgesia, and specifically opioid analgesia, after adju

111 port showed decreased empathy during placebo analgesia, and this was mirrored by reduced amplitudes o

112 ions as well as considerations for sedation, analgesia, anticoagulation, and prognostication.

113 rences between groups in nasogastric output; analgesia, antiemetic, or fluid requirement; complicatio

114 While epidural analgesia appears to be safe, it comes with higher hospi

115 After adoption of the multimodal analgesia approach for a colorectal ERAS pathway, most p

116 groups, respectively, were given sedation or analgesia as a continuous infusion, intermittent doses,

117 ting in rostral ventromedial medulla promote analgesia associated with exercise.

118 prostaglandin E synthase 1 (mPGES-1) confers analgesia, attenuates atherogenesis, and fails to accele

119 s, induced JF-NP-26-mediated light-dependent analgesia both in neuropathic and in acute/tonic inflamm

120 While anti-NGF antibodies have demonstrated analgesia both preclinically and in patients, the mechan

121 ls of acute nociceptive pain, indicated that analgesia by acetaminophen involves an indirect activati

122 n important site of the cannabinoid-mediated analgesia by acetaminophen.

123 Neurotensin exerts potent analgesia by acting at both NTS1 and NTS2 receptors, whe

124 and sigma-1 antagonism produces local opioid analgesia by enhancing the action of EOPs of immune orig

125 tudy was to study the tolerability of opioid analgesia by performing a network meta-analysis (NMA) of

126 Here, we show that pregnancy analgesia can produce a complete cessation of chronic pa

127 no significant effect on orthodontic pain or analgesia consumption during initial alignment with fixe

128 6764 (75.2%) heelsticks were performed with analgesia (continuous and/or specific).

129 The intensity and duration of on-demand analgesia could be adjusted by varying the intensity and

130 ortion of care periods with optimal sedation-analgesia, defined as being free from excessive sedation

131 imination of RGS7 enhanced reward, increased analgesia, delayed tolerance, and heightened withdrawal

132 To characterize sedation, analgesia, delirium, and mobilization practices in patie

133 Such analgesia depends on nuclear CMK-1 signaling, while cyto

134 o develop a mechanism-based understanding of analgesia devoid of the influence of anesthetics or rest

135 Epidural analgesia did not affect the incidence of respiratory fa

136 Importance: Epidural analgesia (EA) is used as an adjunct procedure for posto

137 nful electrical stimulation in mediating the analgesia effect of BreEStim.

138 stent nociception, producing a phenomenon of analgesia-enhanced opioid reward.

139 ptor antagonist, interferes with acupuncture analgesia, even at a low dose.

140 Brain mu opioid receptors mediate analgesia evoked either by exogenous agents (e.g. morphi

141 st that T cells are a mediator of the opioid analgesia exhibited during pregnancy.SIGNIFICANCE STATEM

142 tal cases performed with or without epidural analgesia for cancer, diverticular disease, and benign p

143 ng questions concerning the use of nonopioid analgesia for stronger cancer pain.

144 ated with the lack of specific preprocedural analgesia for this procedure.

145 of NPFF2-R as it relates to opioid-mediated analgesia, for further exploration of NPFF1-R, or for me

146 By subtracting away linearly modeled placebo analgesia from duloxetine response, we uncovered in 6/19

147 uishing the pathways involved in MOR-induced analgesia from its side effects.

148 ewer complications in the patient-controlled analgesia group compared with epidural analgesia (odds r

149 or patients in the epidural and conventional analgesia groups.

150 This pregnancy-related analgesia has been demonstrated for acute pain in rats.

151 M splice variant, mMOR-1G, can rescue IBNtxA analgesia in a mu-opioid receptor-deficient mouse that l

152 mm visual-analogue scale) and intake of oral analgesia in a questionnaire, following appliance-placem

153 >/= 24 hours postoperatively) with systemic analgesia in adults having surgery under general anesthe

154 neurons suppresses nociception and promotes analgesia in an animal model of inflammatory pain.

155 nto the spinal cord and dramatically reduces analgesia in both female and male Nav1.7-null mutant mic

156 n distributed brain regions predicts placebo analgesia in chronic back pain patients.

157 s demonstrated superiority over conventional analgesia in controlling pain.

158 Racial disparities in use of analgesia in emergency departments have been previously

159 Finally, compound 6 produces potent analgesia in experimental models of acute and persistent

160 vated peripheral opioid receptors to produce analgesia in inflamed rat paws without major side effect

161 The use of epidural analgesia in laparoscopic colorectal surgery has demonst

162 The perioperative use of epidural analgesia in laparoscopic colorectal surgery is limited

163 Here, we analyzed acetaminophen analgesia in mice of either sex with inflammatory pain a

164 Intraplantar injection of PD-L1 evoked analgesia in naive mice via PD-1, whereas PD-L1 neutrali

165 investigated the current use of sedation or analgesia in neonatal ICUs (NICUs) in European countries

166 xperiments confirmed the absence of morphine analgesia in Null mice.

167 he mu-opioid receptor can support functional analgesia in Oprm1-deficent animals.

168 t mMOR-1G restored IBNtxA, but not morphine, analgesia in Oprm1-deficient animals.

169 hort study of the management of sedation and analgesia in patients in NICUs.

170 MP 32 mg daily did not provide additional analgesia in patients with cancer receiving opioids, but

171 in GABAA receptor signaling modulate opioid analgesia in persistent inflammation.

172 rats, i.v. ANG2002 induced a dose-dependent analgesia in the formalin model of persistent pain.

173 etic blockade are effective alternatives for analgesia in this population.

174 ffer the first example of optical control of analgesia in vivo using a photocaged mGlu5 receptor nega

175 on of persistent nociception, we showed that analgesia induced by either morphine or the nonsteroid a

176 correlation between PTSD and intra-operative analgesia, intra-operative time, and anesthesia type for

177 nt exercise protocols, show exercise-induced analgesia involves activation of central inhibitory path

178 al insensitivity to pain (CIP) or congenital analgesia is a rare monogenic hereditary condition.

179 ression and brain metastases, where improved analgesia is a secondary benefit.

180 Placebo analgesia is an indicator of how efficiently the brain t

181 ent models of neuropathic pain and that A3AR analgesia is independent of adenosine A1 or A2A unwanted

182 Although morphine analgesia is independent of these 6TM mu receptor isofor

183 unknown whether mindfulness-meditation-based analgesia is mediated by endogenous opioids.

184 ains unknown if mindfulness-meditation-based analgesia is mediated by opioids, an important considera

185 However, animal studies indicate that PAG analgesia is mediated largely via caudal brainstem struc

186 Multimodal analgesia is readily available and the evidence is stron

187 This pregnancy-related analgesia is reversible by intrathecal administration of

188 PP scores in arthritic rats, suggesting that analgesia itself had a rewarding effect.

189 esia (TEA) to intravenous patient-controlled analgesia (IV-PCA) for pain control over the first 48 ho

190 The mechanisms underlying capsaicin-induced analgesia likely involve reversible ablation of nocicept

191 Despite their role in analgesia, loss of the 6TM variants were not involved wi

192 d large decrements in pain response ("offset-analgesia"; mean analgesia: 85%, n = 20 subjects).

193 In addition to analgesia, modulatory effects of EA on spinal sympatheti

194 (N = 106) or intravenous patient-controlled analgesia (N = 34).

195 al direct current stimulation (tDCS)-induced analgesia, neuromodulation occurs through a top-down pro

196 of oral FDC drugs in four therapeutic areas: analgesia (non-steroidal anti-inflammatory drugs [NSAIDs

197 including selective application of regional analgesia, non-narcotic medications, and complimentary a

198 ave not yet fully recapitulated the dramatic analgesia observed in Nav1.7-null subjects.

199 olled analgesia group compared with epidural analgesia (odds ratio, 1.97; 95% CI, 1.10-3.53; P = .02)

200 Analgesia of 11, 22, and 26 was evaluated in the mouse f

201 those, 56.8% (95% CI, 49.8%-63.9%) received analgesia of any type; 41.3% (95% CI, 33.7%-48.9%) recei

202 d painful thermal stimuli following hypnotic analgesia on their own hand, but also when they viewed p

203 her acquisition or extinction of conditioned analgesia or hyperalgesia.

204 Phenomena such as placebo analgesia or pain relief through distraction highlight t

205 However, these mice lack opiate analgesia or withdrawal.

206 was associated with intraoperative epidural analgesia (OR = 1.07, P = 0.019).

207 use of continuous or intermittent sedation, analgesia, or neuromuscular blockers, pain assessments,

208 he effect of intervention was independent of analgesia (P = 0.883).

209 1.50 minutes to the first patient-controlled analgesia; P < .001; I2 = 19%).

210 nvestigated this issue within an attentional analgesia paradigm with brainstem-optimized fMRI and ana

211 understanding of the degree of variation in analgesia practice and patient-reported pain between hos

212 to characterize patient-reported outcomes of analgesia practices in a population-based surgical colla

213 Wide variations in sedation and analgesia practices occur between NICUs and countries.

214 agement requires dissemination of multimodal analgesia practices.

215 However, around the clock analgesia prescription did not guarantee administration.

216 TOR-negative regulator TSC2 reduced morphine analgesia, produced pain hypersensitivity, and increased

217 f daily sedation interruption and a sedation/analgesia protocol was reported by 51% and 39%, respecti

218 cation has the potential to improve sedation-analgesia quality and patient safety in mechanically ven

219 The sedation-analgesia quality data feedback did not improve quality

220 tion programme; regular feedback of sedation-analgesia quality data; and use of a novel sedation-moni

221 on alone (two ICUs), education plus sedation-analgesia quality feedback (two ICUs), education plus RI

222 Providing sedation-analgesia quality feedback to ICUs did not appear to imp

223 By contrast, sedation-analgesia quality feedback was poorly understood and tho

224 We assessed patients' sedation-analgesia quality for each 12 h period of nursing care,

225 The RI monitoring seemed to improve sedation-analgesia quality, but inconsistent adoption by bedside

226 not seem to alter other measures of sedation-analgesia quality.

227 three interventions to improve sedation and analgesia quality: an online education programme; regula

228 rception of pain, whereas the expectation of analgesia reduces pain, as shown in placebo analgesia an

229 der general anesthesia, concomitant epidural analgesia reduces postoperative mortality and improves a

230 to patient and surgeon success, the optimal analgesia regimen in HPB surgery remains controversial.

231 may represent mechanistic probes to explore analgesia-related biological receptors.

232 some forms of opioid-mediated stress-induced analgesia require brain neuronal P450 activity.

233 significant difference in the pain score and analgesia requirement one hour after the procedure, the

234 widely-used models of opioid stress-induced analgesia (restraint and warm water swim) were studied i

235 ent signaling contributes to nociception and analgesia, reward-related behavior, mood, cognition, and

236 Intersubject analgesia scores correlated to activity within a distinc

237 e showed highly attenuated restraint-induced analgesia, showing a critical role for neuronal P450s in

238 Epidural analgesia significantly decreased the risk of atrial fib

239 However, black patients received opioid analgesia significantly less frequently than white patie

240 delta or mu opioid receptor agonist-mediated analgesia specifically in the spared nerve injury (SNI)

241 mized trial was to compare thoracic epidural analgesia (TEA) to intravenous patient-controlled analge

242 oderate pain were less likely to receive any analgesia than white patients (adjusted odds ratio = 0.1

243 rs also mediate some forms of stress-induced analgesia, the present studies assessed the significance

244 lthough, most heelsticks were performed with analgesia, this was not systematic.

245 ional control of hnRNP K in morphine-induced analgesia through activation of MOR.

246 Here we show that inducing analgesia through hypnosis leads to decreased responses

247 and suggest strategies for producing thermal analgesia through the regulation of CaMKI-dependent sign

248 approach: we used the phenomenon of placebo analgesia to experimentally reduce the first-hand experi

249 emains controversial whether adding epidural analgesia to general anesthesia decreases postoperative

250 READD activation produced a ligand-dependent analgesia to heat in vivo and a decrease in neuronal fir

251 ominis plane (TAP) block provides 12-24 h of analgesia to the parietal peritoneum and abdominal wall,

252 k of the spinal nerve roots provides similar analgesia to thoracic epidural without the risk of hypot

253 ive signaling, which may also enhance opioid analgesia, to help to alleviate the enormous burden of p

254 ed behavior and a battery of tests to assess analgesia, tolerance, and physical dependence to morphin

255 cing behaviors to morphine without affecting analgesia, tolerance, and withdrawal.

256 .56]), anxiety (-0.68 [-0.95 to -0.41]), and analgesia use (-0.37 [-0.54 to -0.20]), and increased pa

257 the GABA inhibitory system to A3AR-mediated analgesia using well-characterized mouse and rat models

258 e efficacious for the affective component of analgesia versus the reflexive component and is devoid o

259 ropic P2X receptors while adenosine mediates analgesia via activation of metabotropic P1 receptors.

260 ipating NICUs, the median use of sedation or analgesia was 89.3% (70.0-100) for neonates in the TV gr

261 The use of patient-controlled analgesia was also reduced among patients who received l

262 On case-matched analysis, epidural analgesia was associated with a longer hospital stay by

263 In contrast, placebo analgesia was associated with activation of the dorsolat

264 In contrast, placebo analgesia was associated with decreased pain-related bra

265 Following qualitative assessment, epidural analgesia was associated with faster return of gut funct

266 e model, the increased lack of preprocedural analgesia was associated with female sex, term birth, hi

267 Furthermore, A3AR-mediated analgesia was associated with reductions in CCI-related

268 Inhibition of morphine analgesia was equivalent when tested in knock-in and wil

269 Analgesia was induced by building positive expectations

270 Morphine analgesia was not altered, and neither was physical depe

271 Sham mindfulness meditation-induced analgesia was not correlated with significant neural act

272 rmal and mechanical pain thresholds in vivo; analgesia was observed for 3 days after a single systemi

273 During the baseline period, optimal sedation-analgesia was present for 5150 (56%) care periods.

274 However, warm water swim-induced analgesia was unchanged in Null vs. control mice.

275 Epidural analgesia was used in 4102 cases (2.14%).

276 Antinociception (analgesia) was measured as the latency to remove the tai

277 To identify their involvement in endogenous analgesia, we used brainstem optimized, whole-brain imag

278 effects of vasopressin on expectancy-induced analgesia were significantly larger than those observed

279 rials (9044 patients, 4525 received epidural analgesia) were eligible.

280 NT provides strong analgesia when administered directly into the brain; how

281 estricted NaV1.7 inhibitors can only produce analgesia when administered in combination with an opioi

282 reverse morphine-induced, centrally mediated analgesia when given intravenously.

283 Children receive more analgesia when ordered around the clock compared to as r

284 re the need for periinterventional on-demand analgesia when water for injection (WFI) was replaced wi

285 spatially specific, as is evident in placebo analgesia, which can be limited to the location at which

286 tant) pregnant mice do not exhibit pregnancy analgesia, which can be rescued with the adoptive transf

287 al using a well-established model of placebo analgesia while controlling for sex differences.

288 g tolerance and may prolong effective opioid analgesia while reducing opioid dependence.

289 d no improvement in overall optimal sedation-analgesia with education (OR 1.13 [95% CI 0.86-1.48]), b

290 FST provides analgesia with modest to moderate increased risk of lowe

291 oximately half of the participants exhibited analgesia with placebo treatment.

292 systems have been developed to provide rapid analgesia with potent opioid drugs such as fentanyl.

293 nce by the neuromodulatory process to induce analgesia with potential relevance for patient stratific

294 delta-opioid receptor (DOR) produces similar analgesia with reduced side effects.

295 significant improvement in optimal sedation-analgesia with RI monitoring (odds ratio [OR] 1.44 [95%

296 domized controlled trials comparing epidural analgesia (with local anesthetics, lasting for >/= 24 ho

297 s for a brainstem triumvirate in attentional analgesia: with the PAG activated by attentional load; s

298 benzoyl-6beta-naltrexamide) mediate a potent analgesia without many undesirable effects.

299 the mechanisms of electroacupuncture induced analgesia would benefit chronic pain conditions such as

300 However, it remains unclear whether opioid analgesia would enhance the opioid rewarding effect ther