ライフサイエンスコーパス: EtOH

1 EtOH (11-66 mM) also decreased current-evoked spike firi

2 EtOH (66 mM) had no effect on AMPA-mediated EPSCs but de

3 EtOH also inhibited the effects of nicotine at presynapt

4 EtOH and ButOH increase erythema as a function of skin b

5 EtOH gave virtually no enhancement of mIPSCs.

6 EtOH increased the holding current of voltage-clamped ne

7 EtOH ingestion for 8 weeks significantly (1.8-fold) up-r

8 EtOH inhibition of spike firing was prevented by the GAB

9 EtOH provides an example of an immunomodulatory drug tha

10 EtOH-induced increases in corticosterone require CRF act

11 EtOH-treated larvae develop hepatomegaly and steatosis a

12 ectrocatalytic production of hydrogen in 1/1 EtOH/H2O.

13 ing thiones were 116.8 and 109.6 kJ.mol(-1) (EtOH, 78 degrees C), respectively.

14 ts obtained by SFE at 25MPa pressure and 10% EtOH/water (v/v) mixture as a co-solvent contained 24.58

15 nnel patch clamp analysis confirm that 0.16% EtOH increased ENaC activity in rat alveolar cells.

16 ere resistant to steatosis in response to 2% EtOH, and the expression of many Srebp target genes are

17 H)4(H2O)2] (7), [Mn6O2(Et-sao)6{O2CPh(Me)2}2(EtOH)6] (8), [Mn6O2(Et-sao)6(O2C11H15)2(EtOH)6] (9), [Mn

18 )2}2(EtOH)6] (8), [Mn6O2(Et-sao)6(O2C11H15)2(EtOH)6] (9), [Mn6O2(Me-sao)6(O2C-th)2(EtOH)4(H2O)2] (10)

19 (H2O)2] (11), and [Mn6O2(Et-sao)6(O2C12H17)2(EtOH)4(H2O)2] (12) (Et-saoH2 = 2-hydroxypropiophenone ox

20 ces the complex [MnIII6O2(Et-sao)6(O2CCMe3)2(EtOH)5] (2) that displays an S = 7 ground state with Uef

21 Ph3)2(EtOH)4] (2), [Mn6O2(Et-sao)6(O2CCMe3)2(EtOH)5] (3), [Mn6O2(Et-sao)6(O2CPh2OPh)2(EtOH)4] (4), [M

22 e of the complexes [Mn6O2(Me-sao)6(O2CCPh3)2(EtOH)4] (2), [Mn6O2(Et-sao)6(O2CCMe3)2(EtOH)5] (3), [Mn6

23 CPhBr)2(EtOH)6] (6), [Mn6O2(Et-sao)6(O2CPh)2(EtOH)4(H2O)2] (7), [Mn6O2(Et-sao)6{O2CPh(Me)2}2(EtOH)6]

24 3)2(EtOH)5] (3), [Mn6O2(Et-sao)6(O2CPh2OPh)2(EtOH)4] (4), [Mn6O2(Et-sao)6(O2CPh4OPh)2(EtOH)4(H2O)2] (

25 h)2(EtOH)4] (4), [Mn6O2(Et-sao)6(O2CPh4OPh)2(EtOH)4(H2O)2] (5), [Mn6O2(Me-sao)6(O2CPhBr)2(EtOH)6] (6)

26 EtOH)4(H2O)2] (5), [Mn6O2(Me-sao)6(O2CPhBr)2(EtOH)6] (6), [Mn6O2(Et-sao)6(O2CPh)2(EtOH)4(H2O)2] (7),

27 tOH)4(H2O)2] (10), [Mn6O2(Et-sao)6(O2CPhMe)2(EtOH)4(H2O)2] (11), and [Mn6O2(Et-sao)6(O2C12H17)2(EtOH)

28 1H15)2(EtOH)6] (9), [Mn6O2(Me-sao)6(O2C-th)2(EtOH)4(H2O)2] (10), [Mn6O2(Et-sao)6(O2CPhMe)2(EtOH)4(H2O

29 BZDH)(2)] (4), [Cu(dipsH)(2)(2-MeOHBZDH)(2)].EtOH (5), [Cu(sal)(phen)] (6), [Cu(dips)(phen)].H(2)O (7

30 imately 250 g) were gavaged with 5 ml of 20% EtOH 4 h before approximately 12.5% total body surface a

31 nate-cyclodextrin conjugate (SIM-ALN-CD); 3) EtOH alone; 4) ALN-CD alone; or 5) no injections.

32 of the profenal substrates with SsADH in 5% EtOH/phosphate buffer, pH 9, with catalytic NADH at 80 d

33 timum conditions of the extraction, i.e. 70% EtOH, 30mL/g, APD of 0.22W/mL, AED of 450J/mL are able t

34 combination of 5 min of bead beating in 70% EtOH followed by a 10-min room temperature incubation pe

35 resting fluorescence properties (Phi = 0.79, EtOH; Stoke's shift 113 nm).

36 ve optimum conditions of MAE obtained at 80% EtOH, 50mL/g, APD of 0.35W/mL, AED of 250J/mL can be use

37 y can be collected in a 1-mL fraction of 90% EtOH/0.9N HCl after removal of (68)Ge-breakthrough in a

38 Here we demonstrate that after acute EtOH intoxication and CIE, upregulation of hippocampal a

39 r levels, DHM (1 muM) antagonized both acute EtOH-induced potentiation of GABA(A)Rs and EtOH exposure

40 One-dose and two-dose acute EtOH treatments produced temporal plastic changes in EtO

41 a model of fluid redistribution during acute EtOH intoxication and recovery to account for rapid vent

42 vidence indicates that withdrawal from acute EtOH and chronic intermittent EtOH (CIE) results in decr

43 synaptic and postsynaptic GABA(A)Rs to acute EtOH and, most importantly, increases in GABA(A)R alpha4

44 rease in ROS production in response to acute EtOH exposure.

45 A)-R plasticity in response to in vivo acute EtOH, we measured early time changes in GABA(A)-R subuni

46 Overall, these results suggest that acutely, EtOH may reduce lOFC function via a glycine receptor dep

47 seen with both gavaged and self-administered EtOH, although the magnitude of DPDPE-induced inhibition

48 After EtOH exposure, cells produce excessive reactive oxygen s

49 L)-23 enhances PP cell IL-17 and IL-22 after EtOH and burn injury.

50 ed the decrease in IL-17 but not IL-22 after EtOH exposure and burn injury.

51 ibition persisted for at least 14 days after EtOH access was terminated.

52 rea of hippocampal slices obtained 1 h after EtOH intoxication (5 g/kg, gavage), revealed decreases i

53 ng reflex was decreased at 12 and 24 h after EtOH intoxication, respectively, suggesting functional G

54 to EtOH (60 mM) for 30 min showed, 1 h after EtOH withdrawal, a 50% decrease in basal I(tonic) magnit

55 4 GABA(A)R subunits as early as 20 min after EtOH exposure and reduced alpha5-containing GABA(A)Rs at

56 also was internalized during 5-15 min after EtOH exposure, while phosphorylation of beta3 was increa

57 f T cell IL-2 and IFN-gamma production after EtOH and burn injury.

58 e T cell IL-2 and IFN-gamma production after EtOH and burn injury.

59 minished IL-2 and IFN-gamma production after EtOH plus burn injury resulted from a decrease in IL-12.

60 Alcohol (EtOH) intoxication causes changes in the rodent brain ga

61 Alcohol (EtOH) intoxication is a risk factor for increased morbid

62 recent findings indicate that acute alcohol (EtOH) intoxication exacerbates postburn intestinal and l

63 erbal medicines, counteracted acute alcohol (EtOH) intoxication, and also withdrawal signs in rats in

64 e of an enhanced motivation to seek alcohol (EtOH).

65 eprotected under mild conditions (aq ammonia-EtOH, rt).

66 observation was supported in VA-13 cells, an EtOH-metabolizing human hepatoma cell line, which displa

67 In rats fed an EtOH diet, exposure to cigarette smoke increased ER stre

68 awley rats were fed isocaloric amounts of an EtOH-containing (Lieber-DeCarli) or control diet for 11

69 R delta subunit-containing extrasynaptic and EtOH-insensitive alpha1betagamma2 subtype synaptic GABAA

70 cceptorless coupling of amines with MeOH and EtOH affording formamides and acetamides.

71 e EtOH-induced potentiation of GABA(A)Rs and EtOH exposure/withdrawal-induced GABA(A)R plasticity, in

72 omplex of the Nic template with ZnPc-S16 and EtOH-S4 was confirmed by both the high negative Gibbs fr

73 s further decreased in Copp-treated sham and EtOH plus burn groups.

74 EtOH-sensitive alpha2betagamma subtypes and EtOH-sensitive alpha4betagamma2 subtypes.

75 pproximately 50% compared with untreated and EtOH-treated cells.

76 ha transcription by EtOH in vitro as well as EtOH-induced steatosis and TNF dysregulation in vivo.

77 tly into the mediodorsal thalamus attenuated EtOH-induced motor impairment.

78 ivation of autophagy by rapamycin attenuates EtOH-LPS-induced liver steatosis and injury.

79 hether these changes can be predicted before EtOH exposure by behavioral measures of anxiety or intox

80 93 cells show that, in the absence of beta4, EtOH potentiation of activity exhibits acute tolerance,

81 p60/HAT inhibitor, NU9056, was able to block EtOH-induced H4K12ac, enhancing the effect of EtOH on IL

82 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL before burn or sha

83 nted by the GABAA antagonist picrotoxin, but EtOH had no effect on evoked or spontaneous GABA IPSCs.

84 ), and by reduced enhancement of I(tonic) by EtOH, but not by diazepam.

85 dysregulation of TNF-alpha transcription by EtOH in vitro as well as EtOH-induced steatosis and TNF

86 EtOH reward was then examined by challenging EtOH-treated rats with bilateral intra-accumbens shell a

87 d) and self-administered (two-bottle choice) EtOH.

88 dehydrogenase (ADH) activity blunted ChREBP EtOH-induced acetylation in mouse hepatocytes.

89 A)Rs) are major targets of acute and chronic EtOH actions on the brain.

90 During withdrawal from chronic EtOH exposure, WSP mice were tolerant to the anticonvuls

91 hway could be a major consequence of chronic EtOH insult leading to fatty liver.

92 re, we first examined the effects of chronic EtOH on DLS neuronal morphology, synaptic plasticity, an

93 examined PXR-mediated regulation of chronic EtOH-induced hepatic lipid accumulation and hepatotoxici

94 to be critical for these effects of chronic EtOH; however, the molecular mechanisms leading to augme

95 Collectively these data suggest that chronic EtOH consumption may lead to altered regulation of ENaC,

96 d biochemical techniques reveal that chronic EtOH consumption resulted in greater protein expression

97 in vivo studies we demonstrate that chronic EtOH results in increased TNF-alpha transcription, which

98 te liver dysfunction associated with chronic EtOH.

99 Recent studies utilizing contingent EtOH administration through prolonged two-bottle choice

100 Compared with controls, EtOH-exposed hepatocytes showed a drastic inhibition in

101 CSE+EtOH, but neither agent alone, slightly decreased adenos

102 In AR42J and primary acini, CSE+EtOH induced cell death (necrosis and apoptosis), but ne

103 50 mmol/L), CSE (20-40 mug/mL), or both (CSE+EtOH), and analyzed by immunoblotting, quantitative reve

104 Adding an oil, i.e., decane, into a CTAB-EtOH-TEOS ammonia solution leads to thin-film formation

105 intermittent EtOH (CIE) results in decreased EtOH-enhanced GABAAR delta subunit-containing extrasynap

106 (CTL) mice to levels attained by dependent (EtOH) mice.

107 nist LY379268 reduced drinking in dependent (EtOH) mice to nondependent (CTL) levels, whereas having

108 n adsorption of DMF (N,N-dimethylformamide), EtOH, or CO(2), etc., while N(2) is hardly adsorbed and

109 n was assessed by prefeeding the rats either EtOH or sucrose before an extinction test after differen

110 uals, rat or human, contributing to elevated EtOH consumption.

111 eptor desensitization, completely eliminated EtOH modulation of these receptors.

112 Ethanol (EtOH) is the most widely abused substance in the United

113 Ethanol (EtOH), isopropyl alcohol (IPA), and propylene glycol (PG

114 posing 4 dpf zebrafish larvae to 2% ethanol (EtOH) for 32 hours achieves approximately 80 mM intracel

115 Exposure to 70% ethanol (EtOH) either before or after mechanical disruption was e

116 oratory has demonstrated that acute ethanol (EtOH) exposure before burn injury results in intestinal

117 se model of binge drinking as acute ethanol (EtOH) intoxication has become an alarming health problem

118 roperties of centrally administered ethanol (EtOH) were examined using a conditioned place preference

119 cking, and mouse models of alcohol (ethanol (EtOH)) intake-induced depressive-like behavior have not

120 atory have shown that acute alcohol/ethanol (EtOH) intoxication combined with burn injury suppresses

121 Nicotine and ethanol (EtOH) are among the most widely co-abused substances, an

122 , was used in rats exposed to binge ethanol (EtOH) to provide insight into a mechanism of reversible

123 er, GABA co-release is modulated by ethanol (EtOH) at concentrations seen in blood alcohol after bing

124 d is one of the regions affected by ethanol (EtOH), including exposure during the third trimester-equ

125 Chronic ethanol (EtOH) abuse results in the development of steatosis, alc

126 ed in response to acute and chronic ethanol (EtOH) exposure.

127 eptor (DOR) agonist DPDPE decreases ethanol (EtOH) consumption when injected into the ventral tegment

128 spase-2 upstream of mitochondria in ethanol (EtOH)-treated corneal fibroblasts.

129 orted that Golgi disorganization in ethanol (EtOH)-treated hepatocytes is caused by impaired dimeriza

130 Hepatocytes metabolize ethanol (EtOH) primarily through two steps of oxidative catabolis

131 atory beta subunits, are targets of ethanol (EtOH) action.

132 We studied the combined effects of ethanol (EtOH) and cigarette smoke extract (CSE) on ER stress and

133 e supplemented with either 90 mL of ethanol (EtOH) daily (50%/V, EtOH) or 80 g of sucrose of equal ca

134 ss adaptation and the regulation of ethanol (EtOH) intake.

135 used to characterize the effects of ethanol (EtOH) on neuronal function.

136 anism of PXR-mediated activation of ethanol (EtOH)-induced steatosis is unclear.

137 with a single intoxicating dose of ethanol (EtOH).

138 M cells with dexamethasone (DEX) or ethanol (EtOH) and by generating stable cell lines that overexpre

139 Remarkably, ethanol (EtOH) addition can be used to controllably tune DNA bond

140 l genetically susceptible to severe ethanol (EtOH) withdrawal, Withdrawal Seizure-Prone (WSP) mice.

141 tion and tested the hypothesis that ethanol (EtOH) would affect lung fluid clearance by up-regulating

142 the development of sensitization to ethanol (EtOH), implicating the HPA axis in this process.

143 to lever-press to earn unsweetened ethanol (EtOH) (10%).

144 g is achieved photochemically using ethanol (EtOH) as a sacrificial reductant.

145 Over repeated cycles of CIE exposure, EtOH mice exhibited significant escalation in drinking (

146 Naive alpha4 subunit knockout mice express EtOH-sensitive mIPSCs in hippocampal slices, correlating

147 Ethanol-fed (EtOH) KO mice exhibited systemic toxicity and early mort

148 onstrated depression-like behavior following EtOH abstinence in singly housed female C57BL/6J mice.

149 protect the intestine from damage following EtOH and burn injury.

150 disturbances measured in the NSFT following EtOH abstinence utilizing the N-methyl D-aspartate recep

151 intestinal edema and permeability following EtOH and burn injury.

152 O(2)(-), p47(phox), and p67(phox) following EtOH and burn injury.

153 1 in neutrophil O(2)(-) production following EtOH and burn injury.

154 that CRF1 signaling pathways are crucial for EtOH-induced sensitization.

155 n-1 (Ucn1), we tested Ucn1 knockout mice for EtOH sensitization and found normal sensitization in thi

156 , rats form reliable learned preferences for EtOH-paired locations (CPPs) that are potentiated by iv

157 We find that operant responding for EtOH early in training is goal-directed and reduced by d

158 Thus, the actomyosin complex forces EtOH-induced Golgi disorganization, and the targeting of

159 ive species and releasing a proton (formally EtOH(2)(+)) and a chloride ion to the medium.

160 cumbens core (NAcore) during abstinence from EtOH self-administration.

161 tion of autophagy by rapamycin protects from EtOH-LPS-induced liver injury, probably through reduced

162 Furthermore, EtOH and DMSO can disrupt the main driving forces of the

163 and Fermentation was able to achieve 191.5 g EtOH/kg untreated CS, at an ethanol concentration of 40.

164 anxious animals and those with the greatest EtOH-induced motor impairment have the most robust DPDPE

165 One group (EtOH mice) received repeated weekly cycles of chronic in

166 s in the one framework lattice (one- (1.(H2O,EtOH)), two- (1.3H2O) and three-stepped (1.

167 by deoxygenation and aromatization with HCl/EtOH.

168 enotype was associated with impaired hepatic EtOH metabolism as a consequence of reduced ADH activity

169 could be correlated with upregulated highly EtOH-sensitive alpha2betagamma subtypes and EtOH-sensiti

170 ls in a novel rat model of compulsive, human EtOH seeking.

171 uate the development of CPPs produced by icv EtOH administration.

172 Importantly, EtOH withdrawal rendered WSP mice less sensitive to ALLO

173 eating glucose and lysine at 70 degrees C in EtOH/HEPES buffer at pH 7.0 and pH 8.0.

174 ntified caspase-2 as an initiator caspase in EtOH-treated corneal fibroblasts.

175 atments produced temporal plastic changes in EtOH-induced anxiolysis or withdrawal anxiety, and the p

176 r study describes a novel role for ChREBP in EtOH metabolism and unravels its protective effect again

177 utylryl-(+)-camphorato) Eu(III) complexes in EtOH and CHCl3 solutions substantiating the stereospecif

178 ompound was shown to be stable for 7 days in EtOH and for longer than three months as a solid.

179 TBOA also further increased drinking in EtOH mice.

180 In contrast, CR amplitude was impaired in EtOH rats at the highest US intensity only.

181 oned eyeblink response (CR) were impaired in EtOH rats relative to UC rats.

182 data show that these reactions using KOH in EtOH/H(2)O under non-ion-pairing conditions produce a mi

183 ly mixing three common starting materials in EtOH in the presence of 20 mol % NaOH under microwave ir

184 yrimidine/pyridine group) using 20% NaOEt in EtOH affording a novel class of 3-(pyrimidin-2(1H)-ylide

185 idazoles with carbon monoxide carried out in EtOH at 100 degrees C under a 5/2 mixture of CO-CO2 at 7

186 s cell death and features of pancreatitis in EtOH-sensitized acinar cells by suppressing the adaptive

187 y was rescued by resveratrol pretreatment in EtOH-treated hepatocytes, a significant decrease in ADH

188 P450 2E1 protein levels were up-regulated in EtOH WT mice, but were nearly undetectable in KO mice.

189 tion and function, playing a crucial role in EtOH withdrawal symptoms and dependence.

190 ate, thiobutanoate, and ketone substrates in EtOH/H(2)O, with beta-tosyloxy, acetoxy, and 3-trifluoro

191 NAc were increased approximately twofold in EtOH mice compared with CTL mice, and this difference wa

192 ptic alpha4betagamma2 subtype, and increased EtOH sensitivity of GABAAR miniature postsynaptic curren

193 physical dependence significantly increased EtOH withdrawal severity, measured by handling-induced c

194 Loss of caspase-2 inhibited EtOH-induced apoptosis.

195 he loss of caspase-2 significantly inhibited EtOH-induced mitochondrial dysfunction, Bax translocatio

196 wal from acute EtOH and chronic intermittent EtOH (CIE) results in decreased EtOH-enhanced GABAAR del

197 s achieves approximately 80 mM intracellular EtOH and up-regulation of hepatic cyp2e1, sod, and bip,

198 has been investigated using isotope-labeled EtOH and H2 O.

199 diastereomers was assigned by (S)-Binol/LAH/EtOH reduction of the corresponding enone.

200 digm may favor the development of habit-like EtOH consumption.

201 g-term exposure of neonatal male rats to low EtOH concentrations abolishes LTP-GABAA by inhibiting L-

202 meter a*) following topical challenge to 5 M EtOH, IPA, PG, and butanol (ButOH).

203 droalcoholic saline solutions (NaOH: 0.54 M, EtOH: 1.17 v, NaCl: 2.5%) to end the protein hydrolysis

204 A mixed MeCN/EtOH solvent system was found to enable effective C-N bo

205 e-2 acts upstream of mitochondria to mediate EtOH-induced apoptosis.

206 r 2-hydroxybenzaldeyhyde oxime and L = MeOH, EtOH) via the use of derivatized oxime ligands and bulky

207 deltaH68A receptors by 1 muM diazepam, 30 mM EtOH, and 1 muM beta-carboline-3-carboxy ethyl ester (bu

208 s of the motor impairing effects of moderate EtOH consumption.

209 is further increased by IPA and PG, but not EtOH or ButOH.

210 awal anxiety, and the presence or absence of EtOH-sensitive synaptic currents correlated with cell su

211 However, the mechanism of action of EtOH is poorly understood.

212 To determine whether self-administration of EtOH is required to change VTA DOR function, we compared

213 dopamine (DA) pathways in the development of EtOH reward was then examined by challenging EtOH-treate

214 Single doses of EtOH (3 g/kg via i.p. injection in rats) produced decrea

215 pG2 cells impaired the stimulatory effect of EtOH on ChREBP activity.

216 lar mechanisms responsible for the effect of EtOH on fracture healing are still incompletely understo

217 tOH-induced H4K12ac, enhancing the effect of EtOH on IL-15, RANTES, TGF-beta1, and TNF-alpha cytokine

218 nd these studies, we examined the effects of EtOH exposure and burn injury on Th17 responses within i

219 ifepristone does not block the expression of EtOH sensitization.

220 acquisition and prevented the expression of EtOH-induced psychomotor sensitization.

221 Protein levels, but not mRNAs levels, of EtOH-metabolizing enzymes, including alcohol dehydrogena

222 mportantly, ChREBP silencing in the liver of EtOH-fed mice prevented alcohol-induced triglyceride acc

223 et gene promoters were increased in liver of EtOH-fed mice.

224 be accumulated by photochemical oxidation of EtOH.

225 can be formed by photochemical oxidation of EtOH.

226 rative fashion once a critical percentage of EtOH is reached.

227 ood, and this study investigated the role of EtOH in affecting OPN-dependent TGF-beta1 expression in

228 2)), all while in contact with a solution of EtOH and cyclohexene.

229 aAuCl4.2H2O (10 mol %) in a mixed solvent of EtOH/H2O/CH2Cl2 (4:1:1) at room temperature to give the

230 limbic nuclei during abstinence from operant EtOH self-administration.

231 s, photolysis conditions, and nanocrystal or EtOH concentrations.

232 nts/g DW, with the highest activities of PLE-EtOH/H2O extract.

233 R alpha4 and delta subunits at 5-15 min post-EtOH in hippocampus CA1 and dentate gyrus, verifying our

234 As early as 5 min post-EtOH, there is an initial increase in association betwee

235 wed by a decrease in association 15 min post-EtOH.

236 eceptor antagonist strychnine also prevented EtOH's effect on holding current and spike firing, and w

237 The pretreatment of CoQ10 prevented EtOH-induced caspase-2 activation and mitochondria-media

238 ncrease in fluid clearance in mice receiving EtOH diet.

239 seizure susceptibility; DHM greatly reduced EtOH consumption in an intermittent voluntary EtOH intak

240 Furthermore, NAcore AGS3 knockdown reduced EtOH seeking to pre-abstinence levels in a novel rat mod

241 t G i alpha knockdown, significantly reduced EtOH seeking to pre-abstinence levels.

242 ts (GABAAR IPSCs) is associated with reduced EtOH consumption.

243 as reduced, suggesting that ChREBP regulates EtOH metabolism and ADH activity through its direct cont

244 to gate the uncontrolled motivation to seek EtOH during abstinence.

245 Furthermore, WT mice had higher serum EtOH levels and developed hepatic steatosis characterize

246 efect with the use of systemic ALN after SIM-EtOH injections (0.93 +/- 0.12 and 0.78 +/- 0.11 mm with

247 line either during or 3 to 4 weeks after SIM-EtOH injections.

248 plied: 1) 0.5 mg simvastatin in ethanol (SIM-EtOH); 2) 0.5 mg simvastatin in alendronate-cyclodextrin

249 rations (0.32 +/- 0.10 mm) or short-term SIM-EtOH injections (0.35 +/- 0.10 mm).

250 Three SIM-EtOH groups of long-term rats also were subjected to 2 w

251 and fully reversible by 2 weeks after single EtOH dosing, but unexplainably persisted long after with

252 ried out in environmentally benign solvents (EtOH).

253 e other with the 2-hydroxyethyl substituent (EtOH-S4), were synthesized to serve as functional monome

254 tonic) magnitude and tolerance to short-term EtOH enhancement of I(tonic), followed by reduced basal

255 a and significant potentiation by short-term EtOH; in addition, GABA(A)R currents exhibited reduced e

256 We conclude that EtOH acts in a novel mechanism by interfering directly w

257 scein-5-maleimide labeling, we conclude that EtOH exposure modifies cysteines of alpha-ENaC while dat

258 We demonstrate that EtOH concentrations just above the legal limits for into

259 Lastly, our results demonstrated that EtOH attenuates the antiviral function of the ADH-ALDH p

260 We have demonstrated that EtOH inhibits OPN-induced TGF-beta1 protein expression,

261 genase and in rat hepatocytes, we found that EtOH administration reduces the complex between giantin

262 On day 1 after injury, we found that EtOH combined with burn injury significantly increased n

263 ults summarized in this review indicate that EtOH acts by altering the LPS-induced redistribution of

264 epatic cyp2e1, sod, and bip, indicating that EtOH is metabolized and provokes oxidant stress.

265 pathway, which suggests the possibility that EtOH-retinol metabolic competition is one of the molecul

266 Last, we showed that EtOH exposure reduces the TGF-beta1 protein levels in mo

267 Animal models have shown that EtOH decreases fracture callus volume, diameter, and bio

268 These data suggest that EtOH inhibits alpha7 responses through a PKA-dependent e

269 cid ethyl ester (Ro15-4513), suggesting that EtOH/Ro15-4513-sensitive receptors mediate important beh

270 The EtOH exposure also increased mRNAs encoding hepatic cons

271 genation of acetaldehyde, which reverses the EtOH photooxidation reaction.

272 (A)Rs, we showed for the first time that the EtOH-induced loss of I(tonic) and cell-surface delta/alp

273 eduction of these quinones with NaBH4 in THF/EtOH in an oxygen atmosphere gave the respective dihydro

274 This EtOH-induced inhibition is mediated by a decrease in cAM

275 Cells pre-exposed to EtOH (60 mM) for 30 min showed, 1 h after EtOH withdrawa

276 ity to enhancement by short-term exposure to EtOH (60 mM) of GABA(A)R-mediated tonic current (I(tonic

277 ediate the maintained anxiolytic response to EtOH in dependent individuals, rat or human, contributin

278 A blunted endocrine response to EtOH was found only in the genotypes showing no sensitiz

279 adoxically increased mIPSC responsiveness to EtOH (10-100 mm).

280 inetics, charge transfer, and sensitivity to EtOH.

281 ors do not show psychomotor sensitization to EtOH, a phenomenon that was also absent in CRF1 + 2 rece

282 suggested for expression of sensitization to EtOH.

283 d expression of psychomotor sensitization to EtOH.

284 Brain slice recordings showed tolerance to EtOH's effects on spike patterning in KO but not in WT m

285 on, beta4 KO mice develop rapid tolerance to EtOH's locomotor effects, whereas WT mice do not.

286 Taken together, EtOH-induced mitochondria-mediated apoptosis is initiate

287 asis of cation-exchange chromatography using EtOH/HCl medium has been developed.

288 either 90 mL of ethanol (EtOH) daily (50%/V, EtOH) or 80 g of sucrose of equal caloric value (SUC), s

289 - 0.107 versus 1.08 +/- 0.138 for SUC versus EtOH; P=0.014), and microvascular reactivity were signif

290 er low-powered field in sucrose (SUC) versus EtOH; P=0.004), myocardial perfusion (ratio of blood flo

291 alpha4betadelta-GABA(A)-R following in vivo EtOH administration, in which the delta-ICD increases in

292 ampal neurons many of the effects of in vivo EtOH exposure on GABA(A) receptors (GABA(A)Rs).

293 tOH consumption in an intermittent voluntary EtOH intake paradigm in rats.

294 , primary hepatocytes from rats fed a 6-week EtOH-containing Lieber-DeCarli diet were treated with cA

295 orrelated with behavioral measures only when EtOH was self-administered.

296 e C-N bond formation using aryl amines while EtOH is not required for the coupling of alkyl amines.

297 When combined with EtOH intoxication, burn injury significantly decreased I

298 stsynaptic currents (mIPSCs) correlated with EtOH dependence.

299 mice, approximately 25 g, were gavaged with EtOH (2.9 mg/kg) before receiving an approximately 12.5%

300 rats (approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100

301 Cells were incubated with EtOH (50 mmol/L), CSE (20-40 mug/mL), or both (CSE+EtOH)

302 , 4.36 muM), suggesting DHM interaction with EtOH involves the BZ sites on GABA(A)Rs.

303 ad range of literature results obtained with EtOH as the hole quencher.

304 yl-2,4-pentanediolato) silicate reacted with EtOH and catalytic acid to give Si(OEt)4 in 60% yield, t

305 The rate constant for the htADH x NAD+ x EtOH --> htADH x NAD+ x EtO- proton dissociation, which