ライフサイエンスコーパス: general anesthetic

1 wakefulness despite continuous exposure to a general anesthetic.

2 dies, we consider its use justified in every general anesthetic.

3 Propofol is the most widely used injectable general anesthetic.

4 ternal rotation while the patient received a general anesthetic.

5 ring imaging; one was imaged with the use of general anesthetic.

6 ery, compared with 76% of patients who had a general anesthetic.

7 sary for its anesthetic potency in vivo as a general anesthetic.

8 and eliminate perioperative risks related to general anesthetic.

9 dentified 1-aminoanthracene as a fluorescent general anesthetic.

10 ric ligand-gated ion channels are targets of general anesthetics.

11 re modulated by clinically relevant doses of general anesthetics.

12 e currents elicited by GABA, similar to many general anesthetics.

13 ls) in the thalamus are cellular targets for general anesthetics.

14 o nervous system function and the actions of general anesthetics.

15 physical stimuli in the presence of inhaled general anesthetics.

16 family believed to be the protein target for general anesthetics.

17 -Rs) have been proposed as a target for many general anesthetics.

18 The GABAA receptor is a target of many general anesthetics.

19 binding and function by the intravenous (IV) general anesthetics.

20 are potential targets for a wide variety of general anesthetics.

21 ors are targets for allosteric modulation by general anesthetics.

22 anges in r infinity in response to the three general anesthetics.

23 s of ethanol and the motor ataxic effects of general anesthetics.

24 to components of high and low sensitivity to general anesthetics.

25 endogenous and synthetic neurosteroids, and general anesthetics.

26 explain the mechanisms of action of certain general anesthetics.

27 and-gated ion channels are also inhibited by general anesthetics.

28 argets for the neurophysiological actions of general anesthetics.

29 thetics, indicating some selectivity amongst general anesthetics.

30 o the mammalian brain, are major targets for general anesthetics.

31 tion and are targeted by benzodiazepines and general anesthetics.

32 local anesthetics is very similar to that of general anesthetics.

33 n of the electronic structure of proteins by general anesthetics.

34 eptors play a crucial role in the actions of general anesthetics.

35 ent functional targets for some neurosteroid general anesthetics.

36 roach to investigate molecular mechanisms of general anesthetics.

37 tes for a variety of therapeutics, including general anesthetics.

38 tein kinase C (PKC) activity is modulated by general anesthetics.

39 ction, we synthesized a novel photoactivable general anesthetic, 3-(2-hydroxyethyl)-3-n-pentyldiaziri

40 e various targets and putative mechanisms of general anesthetics across biology and identify key subs

41 We review the behavioral endpoints of general anesthetics across species and propose the isola

42 s or lipids are the primary target sites for general anesthetic action has engendered considerable de

43 The structural bases of general anesthetic action on a neuronal K(+) channel wer

44 n of the study is that a leading element for general anesthetic action on proteins is to disrupt the

45 ficulties of locating the molecular sites of general anesthetic action, we synthesized a novel photoa

46 ptors, an effect that has been implicated in general anesthetic action.

47 a framework to study the structural basis of general anesthetic action.

48 in-vivo research on molecular mechanisms of general anesthetics' actions.

49 phenyl-propionamide exhibited excellent oral general anesthetic activity and appears devoid of signif

50 d neuronal AChRs, which have no demonstrable general anesthetic activity in vivo.

51 This partitioning correlated with general anesthetic activity of this class of compounds.

52 ed a novel class of compounds that have oral general anesthetic activity, potent anticonvulsant activ

53 Propofol, a widely used intravenous general anesthetic, acts at anesthetic concentrations as

54 It remains unclear whether general anesthetics affect brain dynamics similarly in a

55 All currently used general anesthetic agents have either NMDA receptor-bloc

56 Halogenated inhaled general anesthetic agents modulate voltage-gated ion cha

57 Many general anesthetic agents regulate voltage-gated Na(+) (

58 Therefore, we propose that amphiphilic general anesthetic agents such as 1-alkanols may modulat

59 The general anesthetic alcohols, butanol and octanol, furthe

60 ase Cdelta, and studied its interaction with general anesthetic alcohols.

61 gated the effects of a clinical neurosteroid general anesthetic, allopregnanolone, believed to occupy

62 Both volatile and intravenous general anesthetics allosterically enhance gamma-aminobu

63 General anesthetics allosterically modulate the activity

64 e whether receptor modulation by intravenous general anesthetics also was affected by these point mut

65 (+)-azietomidate is a potent stereoselective general anesthetic and an effective photolabel.

66 thesized that nitrous oxide, an inhalational general anesthetic and N-methyl-D-aspartate receptor ant

67 yloxy)allopregnanolone (F(4)N(3)Bzoxy-AP), a general anesthetic and photoreactive allopregnanolone an

68 R)-mediated inhibition is a property of most general anesthetics and a candidate for a molecular mech

69 to low-affinity neurological agents such as general anesthetics and alcohols.

70 arget for many therapeutic agents, including general anesthetics and benzodiazepines, which enhance r

71 the target of allosteric modulators such as general anesthetics and ethanol and is a major locus for

72 a major target of many drugs including some general anesthetics and ethanol.

73 pnosis (unconsciousness) which is induced by general anesthetics and ethanol.

74 ptor is an important target for a variety of general anesthetics and for benzodiazepines such as diaz

75 ules are "on-pathway" targets for anthracene general anesthetics and may also represent functional ta

76 r the noxious and vasorelaxant properties of general anesthetics and may prove useful in understandin

77 General anesthetics and neuromuscular blockers are used

78 er rationalizes clinical observations in how general anesthetics and neuromuscular blockers interact.

79 the underlying mechanisms for the action of general anesthetics and possibly of other low-affinity d

80 fects of a broad range of chemically diverse general anesthetics and related nonanesthetics on lipid

81 General anesthetics and sedatives are used in millions o

82 es and molecular mechanisms in between small general anesthetics and the more complex molecular toxin

83 as the link between the unspecific action of general anesthetics and toxins with their highly specifi

84 the importance of structural fitting between general anesthetics and yet-unidentified hydrophobic pro

85 logy to other relevant channels sensitive to general anesthetics and, as shown here, to barbiturates,

86 pe devices, requiring invasive surgery under general anesthetic, and percutaneous lead-type devices,

87 abolish the modulatory activity of specific general anesthetics, and that molecular volume is a key

88 pparent need, at least at the present, for a general anesthetic; and the increased cost because of ex

89 General anesthetics are a class of drugs whose mode of a

90 General anesthetics are both neuroprotective and neuroto

91 ere has been no empirical demonstration that general anesthetics are capable of functional quantum in

92 General anesthetics are known to cause depression of the

93 Although general anesthetics are known to modulate the activity o

94 frequent use across many clinical settings, general anesthetics are medications with lethal side eff

95 General anesthetics are routinely used in clinical pract

96 Other general anesthetics are thought to act by one of two mec

97 General anesthetics are thought to depress the central n

98 tein that has been proposed to interact with general anesthetics at its cysteine-rich diacylglycerol/

99 reveal the potential binding mode of noxious general anesthetics at TRPA1.

100 We show here that general anesthetics, barbiturates, and local anesthetics

101 Propofol and other intravenous general anesthetics bind at the betaM3-alphaM1 subunit i

102 he proposal that these structurally distinct general anesthetics bind to sites in GABA(A)Rs in the tr

103 General anesthetic binding sites are distinct from the G

104 us but pharmacologically distinct classes of general anesthetic binding sites in the alpha1beta3gamma

105 To locate general anesthetic binding sites on ligand-gated ion cha

106 mportance of polar interactions for volatile general anesthetic binding, and suggest that hydrogen bo

107 nfrequent event (approximately 1 : 2000-3000 general anesthetics), but its impact on individual patie

108 tylcholine receptors (nAChRs) are targets of general anesthetics, but functional sensitivity to anest

109 d-gated ion channels (pLGICs) are targets of general anesthetics, but molecular mechanisms underlying

110 Cys-loop receptors are molecular targets of general anesthetics, but the knowledge of anesthetic bin

111 hannels are modulated by halogenated inhaled general anesthetics, but the underlying molecular mechan

112 ously shown that recognition of inhalational general anesthetics by the model protein apoferritin clo

113 odents, and sub-human primates suggests that general anesthetics can be neurotoxic to the developing

114 Multiple lines of evidence demonstrate that general anesthetics can co-opt the neural circuits regul

115 General anesthetics cause a profound loss of behavioral

116 How general anesthetics cause loss of consciousness is unkno

117 General anesthetics cause sedation, hypnosis, and immobi

118 understanding of the mechanisms of action of general anesthetics, coincident with progress in structu

119 volatile anesthetic sevoflurane is a common general anesthetic derived from ether as a prototype.

120 A widely used general anesthetic directly depolarizes sleep-promoting

121 General anesthetics disrupt brain network dynamics throu

122 es an unprecedented opportunity for studying general anesthetic distribution in vivo at the cellular

123 Propofol, like most general anesthetic drugs, can induce both behavioral and

124 Common clinical general anesthetic drugs, such as propofol and isofluran

125 General anesthetics during surgery are presumed to block

126 ically used barbiturate, thiopental, and its general anesthetic EC(50) approaches those for propofol

127 on of VLPO neurons sensitizes animals to the general anesthetic effects of isoflurane, but that the s

128 onset, depth, or recovery from isoflurane's general anesthetic effects.

129 channels, two derivatives of the intravenous general anesthetic etomidate (2-ethyl 1-(phenylethyl)-1H

130 oactivable derivative of the stereoselective general anesthetic etomidate (R-(2-ethyl 1-(phenylethyl)

131 nical concentrations, the potent intravenous general anesthetic etomidate enhances gamma-aminobutyric

132 Photoreactive derivatives of the general anesthetic etomidate have been developed to iden

133 The potent general anesthetic etomidate produces its effects by enh

134 zietomidate is a photoreactive analog of the general anesthetic etomidate that acts as a nicotinic ac

135 hese signatures will be recapitulated by the general anesthetic etomidate, if the electrocortical eff

136 argeting a site overlapping with that of the general anesthetic etomidate.

137 ts showed that the degree of potentiation by general anesthetics (etomidate, propofol, and isoflurane

138 (isoflurane, desflurane) and i.v. (propofol) general anesthetics excite peripheral sensory nerves to

139 General anesthetics exert many of their CNS actions by b

140 There is a distinct possibility that general anesthetics exert their action on the postsynapt

141 General anesthetics exert their effects on the central n

142 the relative lifelong risks and benefits of general anesthetic exposure should be considered when re

143 d 26 (59%) underwent a procedure while under general anesthetic for diagnostic purposes.

144 Despite widespread use of volatile general anesthetics for well over a century, the mechani

145 related to network function and suggest that general anesthetics - from single cells to complex brain

146 How different types of general anesthetics (GAs) affect the hippocampus, a brai

147 General anesthetics (GAs) are central nervous system dep

148 ing literature supports the idea that common general anesthetics (GAs) cause long-term cognitive chan

149 Lengthy use of general anesthetics (GAs) causes neurobehavioral deficit

150 General anesthetics (GAs) exert their effects through en

151 General anesthetics (GAs) have transformed surgery throu

152 Several general anesthetics (GAs) produce pain or irritation upo

153 The use of inhalation general anesthetic gases has led to contamination of the

154 The general anesthetic halothane is reported here to have ve

155 emarkably, binding of ligands, including the general anesthetic halothane shifts the population to th

156 omain with designed cavities for binding the general anesthetic halothane.

157 f this study was to investigate effects of a general anesthetic, halothane, on membrane and synaptic

158 We tested the ability of the general anesthetic, halothane, to affect either the inhi

159 ic reticulum membrane were used to study two general anesthetics: halothane, a halogenated two-carbon

160 The low affinity of general anesthetics has complicated the search for the l

161 Ketamine, a general anesthetic, has rapid and sustained antidepressa

162 General anesthetics have been a mainstay of surgical pra

163 PURPOSE OF REVIEW: Although general anesthetics have been provided effectively for m

164 General anesthetics have been reported to alter the func

165 We conclude that general anesthetics have minimal effects on bilayer prop

166 Inhalational general anesthetics have recently been shown to inhibit

167 General anesthetics have revolutionized medicine by faci

168 erlying the therapeutic and toxic actions of general anesthetics helps us reframe the 'art' of anesth

169 The effects of the general anesthetics hexanol, halothane, and diethyl ethe

170 prolongs the primary pharmacologic effect of general anesthetics in a behavioral phenotype we termed

171 cond class of intersubunit binding sites for general anesthetics in the alpha1beta3gamma2 GABAAR tran

172 ct classes of intersubunit-binding sites for general anesthetics in the GABAAR transmembrane domain.

173 oteins are likely to be occupied by volatile general anesthetics in vivo.

174 ribe the properties of bromoform acting as a general anesthetic (in Rana temporaria tadpoles) and as

175 Previous studies show that general anesthetics including isoflurane activate VLPO n

176 Most general anesthetics including long chain aliphatic alcoh

177 General anesthetics, including etomidate, act by binding

178 ptor is an important target for a variety of general anesthetics, including halogenated ethers such a

179 nsmitter receptors, are the targets for many general anesthetics, including volatile anesthetics, eto

180 This treatment allowed the general anesthetic infusions to be weaned with resolutio

181 We show that both noxious and non-noxious general anesthetics inhibit agonist-evoked transient rec

182 soflurane and sevoflurane, two commonly used general anesthetics, inhibit c-Fos expression in orexine

183 rongly suggest that halogenated inhalational general anesthetics interact with gates and pore regions

184 The molecular basis of general anesthetic interactions with GABA(A) receptors i

185 be beyond a year of age in a facility with a general anesthetic is at the discretion of the ophthalmo

186 A common endpoint of general anesthetics is behavioral unresponsiveness, whic

187 e that the inhibition of K-Shaw2 channels by general anesthetics is governed by interactions between

188 tween cardiac and skeletal SR in response to general anesthetics is not due to the presence of phosph

189 The detailed action mechanism of volatile general anesthetics is still unknown despite their effec

190 in the VLPO are directly depolarized by the general anesthetic isoflurane and hyperpolarized by nore

191 We also showed that the general anesthetic isoflurane, and to a lesser extent pr

192 mulations in the presence and absence of the general anesthetic isoflurane.

193 likely role of pore block inhibition by the general anesthetics isoflurane and propofol of the proka

194 his, we exposed mouse pups to a prototypical general anesthetic, isoflurane (ISO, 1.5% for 3 hr), at

195 investigated the effects of the most common general anesthetic, isoflurane, on time perception and t

196 cess pathways for the commonly used volatile general anesthetic, isoflurane.

197 In the process of developing safer general anesthetics, isomers of anesthetic ethers and ba

198 The general anesthetic ketamine has been repurposed by physi

199 itive modulation by volatile and intravenous general anesthetics may be quite distinct.

200 General anesthetics may control cell survival via their

201 rt for the theory that structurally distinct general anesthetics may occupy the same domains on prote

202 ggesting that the binding sites of local and general anesthetics may overlap.

203 uoromethyldiazirine-containing derivative of general anesthetic mephobarbital, separated the racemic

204 ese results indicate that several classes of general anesthetics modulate etomidate binding to the GA

205 ty, which can accommodate a variety of small general anesthetic molecules.

206 Because of their roles as general anesthetics, n-alcohols are perhaps the best-stu

207 Here, two photoactivable general anesthetics, n-octan-1-ol geometric isomers bear

208 The general anesthetics, nitrous oxide (N(2)O) and ketamine,

209 were marked differences in the responses to general anesthetics of the TPA decay between cardiac and

210 General anesthetics often interact more strongly with si

211 The effects of general anesthetics on apoptosis and autophagy are close

212 The effects of these general anesthetics on Ca-ATPase activity were similar i

213 focuses on the utilization of the effects of general anesthetics on cerebral metabolism as revealed b

214 Thus the effect of n-alkanols and general anesthetics on changes in the amount of water th

215 To locate the binding sites of general anesthetics on ligand-gated ion channels, two de

216 may contribute to the presynaptic effects of general anesthetics on nerve terminal excitability and n

217 The cellular effects of n-alkanols and general anesthetics on PKC-mediated processes will there

218 general implication for inhibitory action of general anesthetics on pLGICs.

219 was recently postulated that the effects of general anesthetics on protein global dynamics might und

220 We studied the effects of representative general anesthetics on voltage-gated Na+ currents (INa)

221 o be involved in the behavioral responses to general anesthetics or pentobarbital.

222 It binds a diverse range of general anesthetics over a large potency range, displays

223 smitter GABA, allosteric ligands such as the general anesthetics pentobarbital and etomidate can acti

224 sing density functional theory, we show that general anesthetics perturb and extend the highest occup

225 General anesthetic photolabels have been instrumental in

226 General anesthetics produce neurotoxicity and enduring c

227 All currently available general anesthetics produce potentially deadly side effe

228 As), the original and still most widely used general anesthetics, produce anesthesia by ill-defined m

229 family of ubiquitous substances that display general anesthetic properties in accordance to their deg

230 recently published crystal structure of the general anesthetic propofol bound to Gloeobacter violace

231 Recent data reveal that the general anesthetic propofol gives rise to a frontal alph

232 cacies of bicuculline and gabazine using the general anesthetic propofol to directly activate GABAA r

233 The general anesthetic propofol was also tested in homomeric

234 pofol (aziPm), a photoreactive analog of the general anesthetic propofol.

235 pofol (AziPm) is a photoactive analog of the general anesthetic propofol.

236 rsubunit transmembrane sites targeted by the general anesthetics propofol and etomidate.

237 nd directly activating concentrations of the general anesthetics propofol, pentobarbital, and isoflur

238 We propose that liquid general anesthetics provide an experimental tool for low

239 tation, this response pattern is mimicked by general anesthetics, questioning to what extent the hypo

240 The site(s) of action of the volatile general anesthetics remain(s) controversial, but evidenc

241 e conclude that the inhibition of K-Shaw2 by general anesthetics results from allosteric interactions

242 However, the general anesthetics retained the ability to directly ope

243 The mechanisms whereby volatile general anesthetics reversibly alter protein function in

244 teric modulators (PAMs) of GABA(A)Rs such as general anesthetics, sedatives, antiepileptics, and anxi

245 ence is presented that binding of the modern general anesthetic sevoflurane to the hydrophobic core o

246 ess despite continuous administration of the general anesthetic sevoflurane.

247 (d) approximately 0.1 mM, for binding to the general anesthetic site in horse spleen apoferritin (HSA

248 sthetics (VAs), such as isoflurane, induce a general anesthetic state by binding to specific targets

249 usal relationship between LC-NE activity and general anesthetic state under isoflurane.

250 C) modulates arousal and may have effects on general anesthetic state.

251 on channels as potential facilitators of the general anesthetic state.

252 General anesthetics, such as chloroform, isoflurane, die

253 The GABA(A) receptor is a target of many general anesthetics, such as propofol.

254 prokaryotic pLGIC homologue, is inhibited by general anesthetics, suggesting anesthetics stabilize a

255 General anesthetics suppress cerebral metabolism signifi

256 General anesthetics suppress CNS activity by modulating

257 uded that they are very competitive with the general anesthetic techniques that are frequently employ

258 they have been shown to be sensitive to all general anesthetics tested thus far.

259 Etomidate is a potent general anesthetic that acts as an allosteric co-agonist

260 Thus, 3-diazirinyloctanol is a novel general anesthetic that acts on, and can be photoincorpo

261 Propofol is an intravenous general anesthetic that alters neuronal excitability by

262 Propofol, a general anesthetic that binds to GABAAR intersubunit sit

263 ital; 'GABAergic agents') and to ketamine, a general anesthetic that does not affect GABA(A) receptor

264 se results indicate R-(-)-14 is a functional general anesthetic that is well-suited for identifying b

265 diterbutylphenol, two structural analogs of general anesthetics that are hydrophobic but have no ane

266 e increases in r infinity in response to the general anesthetics that resemble those in cardiac SR.

267 nts (e.g., anxiolytics, anticonvulsants, and general anesthetics) that act as positive allosteric mod

268 ndered immobile and unresponsive by sleep or general anesthetics, their brains do not shut off - they

269 For many general anesthetics, their molecular basis of action inv

270 Propofol is a widely used general anesthetic to induce and maintain anesthesia, an

271 Propofol is the most widely used i.v. general anesthetic to induce and maintain anesthesia.

272 It is concluded that the ability of general anesthetics to interact with amphipathic residue

273 The effects of propofol, a short-acting general anesthetic, upon cell growth and Ca(2+) signalin

274 ome alterations appear to be specific to the general anesthetic used, while others probably reflect c

275 Etomidate, one of the most potent general anesthetics used clinically, acts at micromolar

276 The molecular mechanisms whereby volatile general anesthetics (VAs) disrupt behavior remain undefi

277 For volatile general anesthetics (VAs), indirect evidence for both li

278 fly became the world's most popular volatile general anesthetic (VGA) before being abandoned because

279 hysiological evidence indicates that certain general anesthetics, volatile anesthetics in particular,

280 ing 3-mL blood sample that was taken while a general anesthetic was administered.

281 ed ion channel for etomidate, an intravenous general anesthetic, we photolabeled nicotinic acetylchol

282 ss of consciousness and analgesia induced by general anesthetics, we examined the patterns of express

283 l (GLIC), which is sensitive to a variety of general anesthetics, we performed multiple molecular dyn

284 that the specific dynamics effects caused by general anesthetics were not shared by nonanesthetic mol

285 Long-chain alkanols are general anesthetics which can also act as uncharged nonc

286 d the effects of isoflurane, a commonly-used general anesthetic, which was delivered to newborn rabbi

287 Studies indicate that a variety of general anesthetics, which act primarily as gamma-amino-

288 is uninterrupted by propofol, an intravenous general anesthetic with putative actions on the inhibito

289 Classes of general anesthetics with distinct clinical profiles appe

290 )-1H-imidazole-5-carboxylate are both potent general anesthetics with half-effective anesthetic conce

291 , we show that interaction of n-alkanols and general anesthetics with PKCalpha results in dramaticall

292 Although interactions of general anesthetics with soluble proteins have been stud

293 study reveals a structural mechanism for how general anesthetics work on excitatory nicotinic recepto

294 General anesthetics work through a variety of molecular

295 We show that the general anesthetics xenon, sulfur hexafluoride, nitrous