ライフサイエンスコーパス: propofol

1 t on ischemia-reperfusion injury compared to propofol.

2 photoactive analog of the general anesthetic propofol.

3 pass under total anesthesia with intravenous propofol.

4 involvement of this pocket in the actions of propofol.

5 Continuous sedation with dexmedetomidine or propofol.

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

7 care patients who receive dexmedetomidine or propofol.

8 care patients receiving dexmedetomidine and propofol.

9 s of consciousness induced by the anesthetic propofol.

10 er general anaesthesia or deep sedation with propofol.

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

12 n the high-dose group compared with low-dose propofol.

13 te binding sites for the opposing effects of propofol.

14 eversed by the positive allosteric modulator propofol.

15 n of and emergence from unconsciousness with propofol.

16 in the crystal structure of GLIC with bound propofol.

17 f the intravenous anesthetics, etomidate and propofol.

18 odel dynamics in a manner similar to that of propofol.

19 ERK1/2, were also competitively inhibited by propofol.

20 nd potentiated by the intravenous anesthetic propofol.

21 n of alpha1beta2gamma2 receptors by GABA and propofol.

22 this site explain the complex modulation by propofol.

23 079 cavity is a positive modulatory site for propofol.

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

25 ered the molecular targets of isoflurane and propofol.

26 After this first acquisition, propofol (0.22 mg kg(-1) min(-1)) was combined with keta

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

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

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

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

31 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

32 ; 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

33 pe nAChR by use of a photoreactive analog of propofol, 2-isopropyl-5-[3-(trifluoromethyl)-3H-diazirin

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

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

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

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

38 Propofol, a general anesthetic that binds to GABAAR inte

39 Propofol, a sedative and anesthetic drug was chosen as a

40 Propofol acceleration of T254C modification suggests tha

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

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

43 Propofol acts as a positive allosteric modulator of gamm

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

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

46 Deep sedation with propofol, administered by anaesthesia personnel, can be

47 ist during wakefulness and with two doses of propofol, administered by Target Control Infusion, deter

48 Propofol administration is often contraindicated in pati

49 The enhancement in the transport of propofol after complexation was found to be due to multi

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

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

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

53 rivative carrying ionizable groups to render propofol amenable to iontophoresis.

54 Propofol, an intravenous anesthetic, is a positive modul

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

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

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

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

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

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

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

62 eatment period, each animal was sedated with propofol and administered a bolus of fenfluramine (5 mg/

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

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

65 Propofol and dexmedetomidine were the most commonly rest

66 Potentiation of GABA-evoked currents by propofol and etomidate and the lack of inhibition of cur

67 Thus, propofol and isoflurane decrease force development by di

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

69 Both propofol and isoflurane dose dependently depressed force

70 Both propofol and isoflurane increased autophagy induction (P

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

72 For propofol and natural sleep, these changes occur first in

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

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

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

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

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

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

79 , including volatile anesthetics, etomidate, propofol, and barbiturates.

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

81 ight sedation, minimized benzodiazepines and propofol, and decreased the need for physical restraints

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

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

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

85 highlighting the advantages and benefits of propofol anesthesia for both flexible and rigid bronchos

86 Propofol anesthesia is widely used in surgery and in int

87 Propofol anesthesia reduces the V(T) of (11)C-PBR28 by a

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

89 ET studies using (11)C-PBR28 and concomitant propofol anesthesia, as would be required in impaired po

90 enesis compared with animals without delayed propofol anesthesia.

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

92 Dexmedetomidine and propofol are commonly used sedatives in neurocritical ca

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

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

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

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

97 95-200 min) compared with those receiving IV propofol at 215 minutes (150-280 min) (p < 0.001).

98 , avermectin Ba1, baclofen, isoguvacine, and propofol, at 1 or 10 muM, providing an in vitro system f

99 We investigated the effects of propofol, at a dose that produced mild sedation without

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

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

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

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

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

105 Propofol, AziPm, etomidate, and R-mTFD-MPAB each inhibit

106 hese results establish that AziPm as well as propofol bind to the homologous intersubunit sites in th

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

108 ion of T254C (intrasubunit), indicating that propofol binding induces structural rearrangements in th

109 Two propofol binding pockets were identified near the active

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

111 ify for the first time a single intrasubunit propofol binding site in the nAChR transmembrane domain

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

113 Specific propofol binding sites have been mapped using photoaffin

114 Here, we characterize propofol binding sites in a muscle-type nAChR by use of

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

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

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

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

119 Identifying the location of propofol-binding sites is necessary to understand its me

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

121 GLIC closed channel homology model suggests propofol binds to intersubunit sites in the TMD in the r

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

123 Sedation by IV propofol bolus application delayed after controlled cort

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

125 -propofol solution enhanced the transport of propofol by an additional fourfold.

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

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

128 was characterized for the rapid detection of propofol concentrations.

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

130 Propofol damaged mitochondria and decreased cytosolic AT

131 Propofol decreased V(T), which corrects for any alterati

132 rature on the use of general anaesthesia and propofol deep sedation for patients undergoing endoscopi

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

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

135 heterogeneity of barbiturate, etomidate, and propofol derivatives is accommodated by varying selectiv

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

137 Propofol did not alter superoxide generation or elastase

138 ification suggests that in the resting state propofol does not bind in the TMD intrasubunit cavity as

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

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

141 effective for patients and endoscopists than propofol during endoscopic oesophageal interventions?

142 Application of propofol during trauma induction afforded a significant

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

144 The anesthetic propofol elicits many different spectral properties on t

145 Propofol enhanced pro-brain-derived neurotrophic factor/

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

147 Evidence suggests that propofol enhancement of anion-selective pLGICs is mediat

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

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

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

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

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

153 Propofol exposure increased neutrophilic infiltrates int

154 Common drugs implicated included propofol, fentanyl, metoprolol, lorazepam, hydralazine,

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

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

157 trocorticography during gradual induction of propofol general anesthesia in humans, we discovered a r

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

159 182 minutes (140-255 min) in comparison with propofol group at 291 minutes (210-420 min) (p < 0.001).

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

161 atched ICU population, patients treated with propofol had a reduced risk of mortality and had both an

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

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

164 itive to mutations that reduce the action of propofol in both receptors.

165 The force trajectory generated by propofol in each subunit over the course of a simulation

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

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

168 Propofol in total intravenous anesthesia is widely used

169 tion of meta-azipropofol, a potent analog of propofol, in Xenopus laevis tadpoles.

170 Mutations of the conserved proline and propofol increase desensitization.

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

172 In these animals, propofol increased mortality rate and impaired neurologi

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

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

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

176 First, we find that propofol-induced anesthesia does not bear differently on

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

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

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

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

181 These findings suggest that propofol-induced loss of consciousness is mainly tied to

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

183 functional connectivity during wakefulness, propofol-induced sedation and loss of consciousness, and

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

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

186 ults provide insights into the mechanisms of propofol-induced unconsciousness, establish EEG signatur

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

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

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

190 Propofol infusion was titrated to maintain stable vital

191 The propofol-inhibitable [(3)H]AziPm photolabeling in the GA

192 There was also propofol-inhibitable [(3)H]AziPm photolabeling of beta3M

193 ntified by protein microsequencing, we found propofol-inhibitable photolabeling of amino acids in the

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

195 Consistent with the hypothesis, propofol inhibited the binding of N-formyl-Nle-Leu-Phe-N

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

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

198 2 +/- 48 muM, providing the first example of propofol inhibition of an anion-selective pLGIC.

199 ding site between adjacent subunits, whereas propofol inhibition of cation-selective pLGICs occurs vi

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

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

202 We conclude that propofol inhibits the mammalian deacetylase SIRT2 throug

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

204 Propofol is a sedative and anesthetic agent that can bot

205 Propofol is an intravenous anesthetic that produces its

206 Propofol is an intravenous general anesthetic that alter

207 Propofol is commonly used as sedative in newborns and ch

208 Propofol is known to increase GABAA inhibition and decre

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

210 Propofol is primarily an anaesthetic agent, but its use

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

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

213 n we adjust it to reflect two key actions of propofol: its potentiation of GABA and its reduction of

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

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

216 flammatory processes, our data indicate that propofol may have therapeutic potential to attenuate neu

217 The results show that propofol may prevent or limit reparative processes in th

218 c increase in the duration of etomidate- and propofol-mediated hypnosis.

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

220 reatment with continuously infused sedation (propofol, midazolam, or lorazepam).

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

225 us dexmedetomidine (n = 1), midazolam versus propofol (n = 1), and lorazepam versus propofol (n = 1).

226 ersus propofol (n = 1), and lorazepam versus propofol (n = 1).

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

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

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

230 a control arm to account for the effects of propofol on brain measurements of TSPO.

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

232 e compound was found to mimic the actions of propofol on GLIC and GABA(A), and to be sensitive to mut

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

234 care therapy with the widely used anesthetic propofol on recovery from acute traumatic brain injury.

235 egenerative or neuroprotective properties of propofol on the developing brain.

236 nd interventions than ketamine combined with propofol or fentanyl.

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

238 esthesia, in whom no sensitization to either propofol or its lipid vehicle was confirmed.

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

240 ior to a 3h exposure to isoflurane, control, propofol, or 10% intralipid.

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

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

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

244 Propofol potentiated maximal GABA-evoked currents mediat

245 Use of dexmedetomidine or propofol rather than a benzodiazepine sedation strategy

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

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

248 Propofol reduced the respiratory drive, while breathing

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

250 However, the mechanism of propofol remains to be established.

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

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

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

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

255 ed 4-6 hours after surgery in the ICU during propofol sedation and mechanical ventilation.

256 Propofol sedation at 24 hours after traumatic brain inju

257 In pressure support ventilation, deep propofol sedation increased asynchronies, while light se

258 The acceptance level among patients after propofol sedation is high.

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

260 the physiologic effects of varying depths of propofol sedation on patient-ventilator interaction and

261 Propofol sedation reduced populations of effector phagoc

262 s undergoing esophagogastroduodenoscopy with propofol sedation was conducted between January 2009 and

263 n, melatonin, lower levels of intraoperative propofol sedation, and a single dose of ketamine during

264 haracterise changes in brain networks during propofol sedation.

265 f 404 upper endoscopies were performed under propofol sedation.

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

267 Propofol significantly increased peak and integrated cal

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

269 In this study, we showed that propofol significantly reduced superoxide generation, el

270 Propofol slowed the rate of modification of L240C (inter

271 cation of iontophoresis (0.5mA/cm(2)) to SCD-propofol solution enhanced the transport of propofol by

272 idine sedation compared to the standard used propofol TCI sedation during endoscopic oesophageal inte

273 Comparison of propofol to midazolam and lorazepam in adult ICU patient

274 d Drug Administration approval to administer propofol to patients undergoing ERCP and other endoscopi

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

276 Propofol toxicity was abolished both by pharmacologic in

277 rment in locomotive activity was observed in propofol treated adolescent animals at P30.

278 ospital mortality was statistically lower in propofol-treated patients as compared with midazolam- or

279 lysis for 28-day ICU time period showed that propofol-treated patients had a statistically higher pro

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

281 We characterized the EEG response to propofol using a two-dimensional linear compartment mode

282 When propofol was coadministered with vancomycin prophylaxis,

283 Propofol was complexed with sulfobutyl ether-beta-cyclod

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

285 g the controlled cortical impact injury, and propofol was given after an awake phase.

286 Propofol was given to 16 of 21 (76%) of early goal-direc

287 Propofol was safely administered for procedural sedation

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

289 The GABAergic anesthetics pentobarbital and propofol were also effective.

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

291 of 342 patients (105 dexmedetomidine and 237 propofol) were included in the analysis, with 190 matche

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

293 hus contortus AVR-14B GluCl was inhibited by propofol with an IC50 value of 252 +/- 48 muM, providing

294 The phase solubility studies of propofol with SCD revealed an AL type curve indicating a

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