ライフサイエンスコーパス: general anesthetic

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

2 Propofol is the most widely used injectable general anesthetic.

3 ternal rotation while the patient received a general anesthetic.

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

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

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

7 and eliminate perioperative risks related to general anesthetic.

8 dentified 1-aminoanthracene as a fluorescent general anesthetic.

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

10 re modulated by clinically relevant doses of general anesthetics.

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

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

13 physical stimuli in the presence of inhaled general anesthetics.

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

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

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

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

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

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

20 ors are targets for allosteric modulation by general anesthetics.

21 tion and are targeted by benzodiazepines and 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 local anesthetics is very similar to that of general anesthetics.

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

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

28 ent functional targets for some neurosteroid general anesthetics.

29 roach to investigate molecular mechanisms of general anesthetics.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 The general anesthetic alcohols, butanol and octanol, furthe

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

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

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

53 General anesthetics allosterically modulate the activity

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 General anesthetics and sedatives are used in millions o

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

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

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

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

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

74 General anesthetics are both neuroprotective and neuroto

75 General anesthetics are known to cause depression of the

76 Although general anesthetics are known to modulate the activity o

77 General anesthetics are routinely used in clinical pract

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

79 General anesthetics are thought to depress the central n

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

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

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

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

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

85 General anesthetic binding sites are distinct from the G

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

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

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

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

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

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

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

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

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

95 How general anesthetics cause loss of consciousness is unkno

96 General anesthetics cause sedation, hypnosis, and immobi

97 A widely used general anesthetic directly depolarizes sleep-promoting

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

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

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

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

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

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

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

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

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

107 The potent general anesthetic etomidate produces its effects by enh

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

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

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

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

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

113 General anesthetics exert many of their CNS actions by b

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

115 General anesthetics exert their effects on the central n

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

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

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

119 General anesthetics (GAs) are central nervous system dep

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

121 General anesthetics (GAs) have transformed surgery throu

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

123 The general anesthetic halothane is reported here to have ve

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

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

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

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

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

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

130 General anesthetics have been a mainstay of surgical pra

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

132 General anesthetics have been reported to alter the func

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

134 Inhalational general anesthetics have recently been shown to inhibit

135 General anesthetics have revolutionized medicine by faci

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

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

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

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

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

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

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

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

144 Most general anesthetics including long chain aliphatic alcoh

145 General anesthetics, including etomidate, act by binding

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 General anesthetics may control cell survival via their

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

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

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

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

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

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

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

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

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

175 General anesthetics often interact more strongly with si

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 General anesthetic photolabels have been instrumental in

191 General anesthetics produce neurotoxicity and enduring c

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

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

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

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

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

197 The general anesthetic propofol was also tested in homomeric

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 General anesthetics suppress cerebral metabolism signifi

215 General anesthetics suppress CNS activity by modulating

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 Classes of general anesthetics with distinct clinical profiles appe

245 )-1H-imidazole-5-carboxylate are both potent general anesthetics with half-effective anesthetic conce

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

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

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