ライフサイエンスコーパス: propofol

1 s under different anaesthetics (ketamine and propofol).

2 sthetics, except for a high concentration of propofol.

3 nd potentiated by the intravenous anesthetic propofol.

4 rformed in mice, with or without exposure to propofol.

5 of InsP3R-1 were treated with isoflurane or propofol.

6 for the inhibitory effects of isoflurane and propofol.

7 n of alpha1beta2gamma2 receptors by GABA and propofol.

8 this site explain the complex modulation by propofol.

9 079 cavity is a positive modulatory site for propofol.

10 loop D was impeded by GABA but unaffected by propofol.

11 ered the molecular targets of isoflurane and propofol.

12 t on ischemia-reperfusion injury compared to propofol.

13 photoactive analog of the general anesthetic propofol.

14 pass under total anesthesia with intravenous propofol.

15 involvement of this pocket in the actions of propofol.

16 Continuous sedation with dexmedetomidine or propofol.

17 care patients who receive dexmedetomidine or propofol.

18 arked contrast to the hemodynamic effects of propofol.

19 allosteric modulators, such as A-967079 and propofol.

20 and partially recovered direct activation by propofol.

21 ive effect at the myocardium is inhibited by propofol.

22 sedation were obtained during sedation with propofol.

23 oncentrations of etomidate, R-mTFD-MPAB, and propofol.

24 eptor activity is only weakly potentiated by propofol.

25 as they are progressively anesthetized with propofol.

26 with a potency slightly greater than that of propofol.

27 Propofol (1 mum), which potentiates sub-maximal but not

28 ed with Krebs-Henseleit buffer alone or with propofol (10 uM).

29 10.1) months; p = 0.54) or overall survival (propofol: 17.4 (95% CI 14.0-20.7) vs. volatiles: 16.9 (9

30 Midazolam (48%) and propofol (19%) were reported as the most frequently used

31 infusion, sedative doses remained unchanged (propofol 2.6 +/- 1.2 vs 2.6 +/- 1.2 mg/kg/hr; p = 0.23 a

32 ventilated pig under continuous intravenous propofol (2,6-diisopropylphenol, narcotic drug) infusion

33 Here, we use a photoreactive analog of propofol (2-isopropyl-5-[3-(trifluoromethyl)-3H-diazirin

34 OR, 6.5; 95% CI, 2.5-15.2) and ketamine and propofol (2.1%; OR, 4.4; 95% CI, 2.3-8.7) had the highes

35 ; OR, 4.0; 95% CI, 1.8-8.1) and ketamine and propofol (2.5%; OR, 2.2; 95% CI, 1.2-3.8) had the highes

36 dependently depressed force from low doses (propofol, 27 +/- 6 muM; isoflurane, 1.0 +/- 0.1%) to mod

37 investigated the dose-dependent influence of propofol (36 or 72 mg/kg/hr) either during controlled co

38 dexmedetomidine group received supplemental propofol (64% of patients), midazolam (3%), or both (7%)

39 g again to 0.42 +/- 0.36 mug/kg/min while on propofol 8 hours after stopping dexmedetomidine (p < 0.0

40 tenance was performed with sevoflurane 3% or propofol 8 to 10 mg/kg per hr until pneumonectomy was do

41 ce-free (volatiles: 8.0 (95% CI 6.5-9.8) vs. propofol: 8.4 (95% CI 7.9-10.1) months; p = 0.54) or ove

42 isoflurane, 1.0 +/- 0.1%) to moderate doses (propofol, 87 +/- 4 muM; isoflurane, 3.0 +/- 0.25%), with

43 Propofol, a general anesthetic that binds to GABAAR inte

44 o the thalamus may be a critical part of how propofol accomplishes its effects, including unconscious

45 In addition to inducing anesthesia, propofol activates a key component of the pain pathway,

46 identified two binding domains through which propofol acts on the GABAA receptor.

47 Short exposure to propofol adequately activated InsP3-1 to provide suffici

48 he awake state) significantly decreased with propofol administration (P < 0.05, two group test of coh

49 While confirming alpha-power increases with propofol administration both in thalamus and cortex, we

50 Likewise, propofol administration resulted in decreased phase ampl

51 n of GABA by the drug pair of alfaxalone and propofol agree very well with predictions.

52 e presence of combinations of GABA, taurine, propofol, allopregnanolone and/or the inhibitory steroid

53 Rather, we propose that a transient propofol allosteric site forms when the motor head binds

54 Compared with ketamine alone, propofol alone (3.7%; odds ratio [OR], 5.6; 95% CI, 2.3-

55 advisory resulted in providers discontinuing propofol an average of 16.6 hours (95% CI, 4.8-28.3) soo

56 Propofol, an intravenous anesthetic, is a positive modul

57 n rat olfactory cortices is uninterrupted by propofol, an intravenous general anesthetic with putativ

58 Propofol anaesthesia resulted in local power increases a

59 Signals were acquired during induction of propofol anaesthesia while subjects were resting.

60 e functional MRI data from awake volunteers, propofol-anaesthetised volunteers, and patients with dis

61 id haemorrhage in the gyrencephalic brain of propofol-anaesthetized juvenile swine using subdural ele

62 3)H]R-mTFD-MPAB to identify para-substituted propofol analogs and other drugs that bind selectively t

63 vation by propofol are likely steric because propofol analogs with less bulky ortho substituents acti

64 med this by introducing a hydrogen bond-null propofol analogue as a protecting ligand for targeted-AB

65 s 925 (interquartile range, 512-3274) in the propofol and 1097 (interquartile range, 540-2633) in the

66 There were 4 mortalities (8.3%) in the propofol and 2 (4.0%) in the sevoflurane group.

67 ier lipophilic substitutions [4-(tert-butyl)-propofol and 4-(hydroxyl(phenyl)methyl)-propofol] bind w

68 Propofol and 4-chloro-propofol bind with 5-fold selectiv

69 with recombinant human SIRT2 determined that propofol and [(3)H]AziPm only bind specifically and comp

70 reflexes) under dexmedetomidine, compared to propofol and alfaxalone.

71 with stable hydrogen bonds observed between propofol and alpha/beta cavity residues but not gamma ca

72 on with current intravenous sedation agents (propofol and benzodiazepines).

73 Propofol and dexmedetomidine had the highest bladder pre

74 Thus, propofol and isoflurane decrease force development by di

75 ons in both intact and skinned preparations, propofol and isoflurane depressed maximum Ca(2+)-activat

76 Both propofol and isoflurane dose dependently depressed force

77 Both propofol and isoflurane increased autophagy induction (P

78 Propofol and ketamine were selected due to their differe

79 esia induced by intraperitoneal injection of propofol and maintained by inhalation of sevoflurane for

80 These results suggest that propofol and other common anesthetics, such as etomidate

81 is observation is important as sedation with propofol and other compounds with GABA receptor activity

82 e, the results indicate that the anesthetics propofol and pentobarbital interact with partially share

83 esidues were probed on channel activation by propofol and pentobarbital.

84 o the number of functional binding sites for propofol and the energetic contributions stemming from p

85 individual differences in susceptibility to propofol and track drug exposure.

86 no conscious experience after emergence from propofol and xenon anesthesia, whereas after ketamine th

87 Sedation was switched back to propofol, and a final set of measurements was obtained a

88 ine, risperidone, ketamine, dexmedetomidine, propofol, and clonidine) reduced the risk of delirium (r

89 rom enteral nutrition, parenteral nutrition, propofol, and dextrose containing fluids were collected

90 altered the maximum level of enhancement by propofol, and the M3 A288I substitution abolished propof

91 Time to induction was shortest with propofol, and time to recovery was shortest with dexmede

92 pharmacokinetic (PK) monitoring of ketamine, propofol, and valproic acid, and their metabolites was a

93 for the residues of 5-LOX in the vicinity of propofol, and we evaluated the functional role of these

94 Loss of cardioprotection by RIPC during propofol anesthesia depends on inhibition of release of

95 Propofol anesthesia is widely used in surgery and in int

96 rtical activation with low complexity during propofol anesthesia, a high-amplitude EEG slow wave corr

97 neural activity, delineates wakefulness from propofol anesthesia, NREM and REM sleep.

98 Infarct size with control plasma from propofol anesthetized rats was 59% (58-64%) (Prop-Con).

99 igates the influence of delayed single-bolus propofol applications at the peak of p75 neurotrophin re

100 Isoflurane and propofol are known to depress cardiac contraction, but t

101 ta3(Y143W) and beta3(Q224W) on activation by propofol are likely steric because propofol analogs with

102 ent sleep (NREM) and general anesthesia with propofol are prominent states of reduced arousal linked

103 induced by the commonly used anesthetic drug propofol are synchronized between the thalamus and the m

104 In the propofol arm, 11 patients (23%) experienced early allogr

105 e to within-subject state changes induced by propofol as well as sevoflurane, such that individuals s

106 the cortical recording site, we investigated propofol-associated changes in thalamic and cortical loc

107 95-200 min) compared with those receiving IV propofol at 215 minutes (150-280 min) (p < 0.001).

108 rane increased the activation of TLR9, while propofol attenuated it.

109 Propofol attenuated the production of 5-lipoxygenase (5-

110 OX-transfected human embryonic kidney cells, propofol attenuated the production of 5-LOX-related AA d

111 Finally, propofol attenuated the sevoflurane-induced increase in

112 beling of myofilament proteins with meta-Azi-propofol (AziPm) and Azi-isoflurane (Azi-iso) and molecu

113 meta-Azi-propofol (AziPm) is a photoactive analog of the general

114 Using meta-azi-propofol (AziPm), we photolabeled stable 5-LOX protein,

115 Propofol-based sedation may increase hemodynamic instabi

116 ecular modeling predicts that isoflurane and propofol bind to this pocket by forming H-bond and halog

117 Propofol and 4-chloro-propofol bind with 5-fold selectivity to beta (+), while

118 tyl)-propofol and 4-(hydroxyl(phenyl)methyl)-propofol] bind with ~10-fold higher affinity to beta (-)

119 Two propofol binding pockets were identified near the active

120 GABA(A) receptor postulated a high-affinity propofol binding site in a hydrophobic pocket in the mid

121 Residues that line the propofol binding site on SIRT2 contact the sirtuin co-su

122 Specific propofol binding sites have been mapped using photoaffin

123 erturbation calculations predicted selective propofol binding to interfacial sites, with higher affin

124 nd the energetic contributions stemming from propofol binding to the individual sites.

125 r affinity-based protein profiling (ABPP) of propofol-binding proteins in their native state within m

126 zirin-3-yl]phenol ([(3)H]AziPm)) to identify propofol-binding sites in heterologously expressed human

127 Intravenous anesthetic propofol binds to 5-lipoxygenase and attenuates leukotri

128 We deduce that 4-benzoyl-propofol binds with >100-fold higher affinity to the gam

129 aled that the response time of the developed propofol biosensors was 25s.

130 Deltapressure was greatest with propofol, bladder capacity was highest with alpha-chlora

131 Sedation by IV propofol bolus application delayed after controlled cort

132 ing the scenario of continuous monitoring of propofol, both in PBS and in undiluted human serum, to d

133 Propofol bound to the TLR9 antagonist binding site.

134 tency activation by GABA and potentiation by propofol but impaired direct activation by higher propof

135 , and beta3(T266) residues in the actions of propofol but not pentobarbital in beta3 receptors.

136 In addition, propofol, but not ketamine, triggered a large reduction

137 idence indicates that even brief exposure to propofol can substantially increase host susceptibility

138 of the ML-based model to correctly classify propofol concentration in the therapeutic range between

139 nt, the methods employed for detecting blood propofol concentrations in hospitals comprise high-perfo

140 was characterized for the rapid detection of propofol concentrations.

141 fol but impaired direct activation by higher propofol concentrations.

142 Recipients were randomly assigned to propofol (control group) or sevoflurane anesthesia.

143 Propofol damaged mitochondria and decreased cytosolic AT

144 Here we apply photoaffinity labeling using a propofol derivative, meta-azipropofol, for direct identi

145 tert-butylphenol (2,6-DTBP), a nonanesthetic propofol derivative, reverses inflammation-mediated disi

146 tosyl-monopalmitin, N-methylalanine, and two propofol derivatives.

147 aesthesia-analgesia (paravertebral block and propofol) did not reduce breast cancer recurrence after

148 oform, isoflurane, diethyl ether, xenon, and propofol, disrupt lipid rafts and activate PLD2.

149 ough-max PAC, which is associated with lower propofol dose, or peak-max PAC, associated with higher d

150 Our analyses indicate that propofol dramatically restricted the size and duration o

151 ssistance (AA) to achieve deep sedation with propofol during colonoscopy has significantly increased

152 aumatic brain injury, rats were sedated with propofol either during or 2 hours after experimental tra

153 The anesthetic propofol elicits many different spectral properties on t

154 Propofol enhanced pro-brain-derived neurotrophic factor/

155 Instead, these data suggest that propofol enhancement and inhibition are mediated by bind

156 fol, and the M3 A288I substitution abolished propofol enhancement.

157 Propofol, etomidate, and barbiturate anesthetics are all

158 ABA and clinically used GABAergic modulators propofol, etomidate, or pentobarbital or the steroid alp

159 for enhancement of steady-state currents by propofol, etomidate, pentobarbital, or alphaxalone were

160 Propofol-evoked currents mediated by alpha1(T47R)beta2ga

161 GABA-, THIP- and propofol-evoked currents mediated by alpha1(T47R)beta2ga

162 Propofol exposure increased neutrophilic infiltrates int

163 aster extubation times in comparison with IV propofol for patient undergoing coronary artery bypass g

164 pendent sustained alpha critically relies on propofol GABAA potentiation to alter the intrinsic spind

165 volatile (isoflurane, desflurane) and i.v. (propofol) general anesthetics excite peripheral sensory

166 182 minutes (140-255 min) in comparison with propofol group at 291 minutes (210-420 min) (p < 0.001).

167 he acetaminophen-dexmedetomidine and placebo-propofol groups (24% and 23%) had hypotension.

168 he placebo-dexmedetomidine and acetaminophen-propofol groups (46% and 45%) and 7 in the acetaminophen

169 ith effective removal of non-entrapped drug (propofol >95% reduction of non-entrapped drug present) o

170 Patients receiving dexmedetomidine vs propofol had no significant difference in delirium (17%

171 impaired stabilization of the open state by propofol, i.e., reduced gating efficacy.

172 The T266W mutation removed activation by propofol in beta3 homomeric receptors; however, this mut

173 significantly more lung metastasis than with propofol in both syngeneic murine 4T1 and xenograft huma

174 r the electrical detection of the anesthetic propofol in human plasma samples for clinical diagnoses.

175 g the loss of consciousness (LOC) induced by propofol in nonhuman primates.

176 per protocol and time to discontinuation of propofol in the setting of triglyceride and/or lipase le

177 Propofol in total intravenous anesthesia is widely used

178 Mutations of the conserved proline and propofol increase desensitization.

179 he conserved M1 proline, and the anaesthetic propofol, increase a rate constant for desensitization.

180 h of the four sites affected the response to propofol, indicating that each of the four sites is func

181 cytoprotection, while prolonged exposure to propofol induced cell apoptosis via impairment of autoph

182 he cortex at specific frequency bands during propofol-induced anaesthesia and modelling work suggests

183 imb RIPC performed while patients were under propofol-induced anesthesia did not show a relevant bene

184 n for states with lower conscious level like propofol-induced anesthesia.

185 and the thalamus is a critical component of propofol-induced cortical spectral phenomena.

186 Our results show that propofol-induced LOC is accompanied by spatiotemporally

187 We demonstrate that propofol-induced LOC is accompanied by spatiotemporally

188 coherence but in support of the theory that propofol-induced loss of consciousness is associated wit

189 is implies the thalamus may be the source of propofol-induced PAC.

190 state fMRI as well as two distinct levels of propofol-induced sedation.

191 of high-density EEG during patient-titrated propofol-induced sedation.

192 d intracortical neuronal dynamics leading to propofol-induced unconsciousness by recording single-neu

193 al neuronal dynamics during transitions from propofol-induced unconsciousness into consciousness by d

194 ved in the human electroencephalogram during propofol-induced unconsciousness.

195 The gamma-aminobutyric acid modulator propofol induces neuronal cell death in healthy immature

196 nd breathing pattern were also influenced by propofol infusion to an extent that varied with the dept

197 Propofol infusion was gradually increased while auditory

198 Propofol infusion was titrated to maintain stable vital

199 ted in a single allosteric protein site, and propofol inhibited [(3)H]AziPm photolabeling of this sit

200 disrupted by the M3 G329I substitution, both propofol inhibition and enhancement of GluCls were sever

201 dicated pore block as a likely mechanism for propofol inhibition at high concentrations.

202 We have recently discovered that propofol inhibits conventional kinesin-1 KIF5B and kines

203 on of acetylated alpha-tubulin revealed that propofol inhibits enzymatic function.

204 Furthermore, propofol inhibits rodent but not human TRPA1.

205 We conclude that propofol inhibits the mammalian deacetylase SIRT2 throug

206 ic alpha1beta3 receptors can be activated by propofol interactions with beta3-beta3, alpha1-beta3, an

207 The intravenous anesthetic propofol is a full agonist (maximal P(Open,peak) = 0.99)

208 Propofol is a sedative and anesthetic agent that can bot

209 Propofol is an intravenous anesthetic that produces its

210 Direct and continuous monitoring of propofol is crucial in the development of automatic syst

211 Propofol is known to increase GABAA inhibition and decre

212 The lack of a velocity effect suggests that propofol is not binding at the ATP site or allosteric si

213 Propofol is suggested to be an inhibiting factor of card

214 Propofol is the most widely used i.v. general anesthetic

215 effects on consciousness (ketamine, but not propofol, is known to induce an unusual state known as "

216 hythm under GABAA potentiation such as under propofol, its hyperpolarization may determine whether a

217 here were 2,250 propofol-midazolam and 1,054 propofol-lorazepam matched patients.

218 otrophin receptor becomes down-regulated and propofol loses its neurotoxic effect.

219 in turn could render the brain sensitive to propofol-mediated neurotoxicity.

220 r primary sedative or to receive usual care (propofol, midazolam, or other sedatives).

221 There were 2,250 propofol-midazolam and 1,054 propofol-lorazepam matched

222 This suggests that propofol might influence cellular events that are regula

223 We considered this idea by testing propofol modulation of homomeric human glycine receptors

224 ts regarding their relative contributions to propofol modulation.

225 performance in the separation and sensing of propofol molecules in the human plasma samples.

226 Ninety-eight recipients were randomized to propofol (n = 48) or sevoflurane (n = 50).

227 esthesia and postoperative sedation using IV propofol (n = 74) or inhaled volatile (isoflurane or sev

228 taminophen and propofol: n = 31; placebo and propofol: n = 30).

229 d dexmedetomidine: n = 30; acetaminophen and propofol: n = 31; placebo and propofol: n = 30).

230 beta (-) and gamma (+)/beta (-) pockets, and propofol occupies all four.

231 f 5-LOX, and examined the binding site(s) of propofol on 5-LOX.

232 m was tested with the compartmental model of propofol on a database of 59 subjects.

233 To establish the influence of propofol on endogenous neurogenesis and functional recov

234 eukotriene (LT)B4, we examined the effect of propofol on LTB4 production in vivo and in vitro Cecal l

235 s versus total-intravenous anaesthesia using propofol) on recurrence-free and overall survival in gli

236 val agents (dexmedetomidine, alfaxalone, and propofol) on urodynamic (Deltapressure, bladder capacity

237 For dexmedetomidine vs propofol, only breakthrough analgesia was significantly

238 e subjects were randomized to receive either propofol or dexmedetomidine until unresponsiveness.

239 scheduled IV acetaminophen, combined with IV propofol or dexmedetomidine, reduced in-hospital deliriu

240 nd interventions than ketamine combined with propofol or fentanyl.

241 th Krebs-Henseleit solution, with or without propofol or isoflurane.

242 ctivation using the agonist pair of GABA and propofol or potentiation of responses to a low concentra

243 esthesia-analgesia (paravertebral blocks and propofol) or general anaesthesia (sevoflurane) and opioi

244 GABA or beta-alanine, the allosteric agonist propofol, or combinations of GABA, propofol, pentobarbit

245 al functionally equivalent binding sites for propofol, other than those modified by substitutions at

246 e-4-sulfonic acid) and/or allosteric agents (propofol, pentobarbital, and several neuroactive steroid

247 c agonist propofol, or combinations of GABA, propofol, pentobarbital, and the steroid allopregnanolon

248 transmitter GABA and the allosteric agonists propofol, pentobarbital, or alfaxalone can be understood

249 y with the allosterically acting anesthetics propofol, pentobarbital, or alfaxalone.

250 d a significant infarct size reduction under propofol perfusion (Pento-RIPC: 34% [30-42%] vs Pento-Co

251 ic also significantly reduced intraoperative propofol (pooled SMD -0.72 [95% CI -1.01 to -0.43], P <

252 Propofol potentiated maximal GABA-evoked currents mediat

253 barbital (Pento, 40 mg/kg body weight/hr) or propofol (Prop, 12 mg/kg body weight/hr), respectively.

254 Both GABA and the allosteric agonist propofol reduced MTSEA modification of alpha1(D43C)beta2

255 Both GABA and the allosteric agonist propofol reduced MTSEA modification of Cys43 and Cys47.

256 Propofol reduced the respiratory drive, while breathing

257 a2gamma2 receptors, where only GABA, but not propofol, reduced MTSEA modification.

258 ide and lipase level monitoring and mitigate propofol-related hazardous conditions.

259 otocol compliance and may mitigate potential propofol-related hazardous conditions.

260 evels of sedation with the anaesthetic agent propofol, replicating our results in two separate datase

261 additional doses of fentanyl, midazolam, and propofol required for CAE were 0.05, 1.9 and 36.3 mg.

262 ificantly from the UC group in the amount of propofol required to reach moderate sedation.

263 Infusion of propofol resulted in 1) aggravation of neurologic dysfun

264 he anaesthetics phenobarbital, etomidate and propofol reveal both distinct and common transmembrane b

265 gait analysis was significantly impaired in propofol-sedated animals.

266 This study provides first evidence that propofol sedation after acute brain lesions can have a d

267 Propofol sedation at 24 hours after traumatic brain inju

268 Here, we delineate the impact of propofol sedation on MRSA bloodstream infections in mice

269 Propofol sedation reduced populations of effector phagoc

270 haracterise changes in brain networks during propofol sedation.

271 f 404 upper endoscopies were performed under propofol sedation.

272 drogen bonding is a key component leading to propofol-selective binding within GABAA receptor subunit

273 Propofol significantly increased peak and integrated cal

274 data indicate that short-term sedation with propofol significantly increases the severity of bloodst

275 ssibility of continuous online monitoring of propofol since polymerization of the surface produces se

276 stoperative sedation with dexmedetomidine or propofol starting at chest closure and continued for up

277 vels of sedation and serum concentrations of propofol, supporting the hypothesis that consciousness i

278 ing paravertebral blocks and the anaesthetic propofol than with general anaesthesia with the volatile

279 Similar to R-mTFD-MPAB and propofol, these drugs bind in the presence of GABA with

280 ing, which compensates the fouling effect of propofol through machine learning (ML) model.

281 comparable level of sedation, switching from propofol to dexmedetomidine resulted in a reduction of c

282 to SIRT2, specific binding of [(3)H]AziPm or propofol to recombinant human SIRT1 was not observed.

283 hypothesis that switching from sedation with propofol to the alpha-2 agonist dexmedetomidine may decr

284 Propofol toxicity was abolished both by pharmacologic in

285 Sleep was induced with propofol under light sedation (bispectral index 70-75),

286 a sedative for intubation, with midazolam or propofol use as the reference.

287 When propofol was coadministered with vancomycin prophylaxis,

288 The passive permeation flux of propofol was enhanced by fourfold due to complexation wi

289 Propofol was then replaced by dexmedetomidine and a seco

290 kg per hr until pneumonectomy was done; then propofol was used for all animals.

291 The GABAergic anesthetics pentobarbital and propofol were also effective.

292 us reports, brief periods of anesthesia with propofol were sufficient to significantly increase bacte

293 ently generating the sustained alpha seen in propofol, which may then be relayed to cortex and expres

294 Propofol, which reduces neuronal activation, was used to

295 This first multicenter trial comparing propofol with sevoflurane anesthesia in liver transplant

296 of sites appeared to differ in affinity for propofol, with the site affected by M286W having about a

297 ively abolishes activation by isoflurane and propofol without affecting actions of A-967079 or the ag

298 ce decreases 40-60% with EC50 values <100 nM propofol without an effect on velocity.

299 Based on these results, we hypothesized that propofol would directly affect 5-LOX function.

300 sessing consciousness during anesthesia with propofol, xenon, and ketamine, independent of behavioral