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 consumption led to a marked down-regulation of gene

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 was found to be the best solvent in terms of extrac

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

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

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

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

14 (H(2) O)(5) ]Br(3) .2 (Cy(3) PO).2 H(2) O .2 EtOH.

15 (H(2) O)(5) ]Br(3) .2 (Cy(3) PO).2 H(2) O.2 EtOH is with B(0) =582.3(5) T significantly larger than

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

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

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

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

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

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

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

23 d materials into food simulants (50% and 95% EtOH and Tenax) and foodstuffs (rice, cereals and milk p

24 gration to infant milk powder, for which 95% EtOH resulted a more suitable simulant.

25 ly produced under "green" conditions (in 96% EtOH or pure water).

26 The binary solvent system of ACE: EtOH (1:1) at 60 degrees C was optimized as extraction s

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

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

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

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

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

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

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

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

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

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

37 lation of punished EtOH self-administration (EtOH-SA).

38 After EtOH exposure, cells produce excessive reactive oxygen s

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

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

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

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

43 4 GABA(A)R subunits as early as 20 min after EtOH exposure and reduced alpha5-containing GABA(A)Rs at

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

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

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

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

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

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

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

51 ular weight oligosaccharides contained in an EtOH/water extract of grape seeds.

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

53 n embryonic stem cell (ESC) model to analyze EtOH's effects on differentiation, we show here that EtO

54 labeled variant of alpha-synuclein A91C, and EtOH (20%) to induce aggregation.

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

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

57 mparison to the larvae reared on AD only and EtOH-added diet.

58 r that is considered as a benign oxidant and EtOH as a green solvent, ease of product separation, rea

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

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

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

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

63 ium metabisulfite (Na(2)S(2)O(5)) in aqueous EtOH rapidly enhanced the cascade reaction that led to d

64 that volatile compounds in CB can attenuate EtOH-induced liver damages.

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

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

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

68 Effects of binge EtOH exposure on brain volumes and neurometabolites repl

69 Brain changes in response to binge EtOH treatment were more pronounced in young relative to

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

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

72 n oculomotor and ocular behaviours caused by EtOH administration across a range of ultra-low BACs (<=

73 In stem cells, EtOH may shift cell fate decisions to alter developmenta

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

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

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

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

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

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

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

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

82 We show that chronic EtOH selectively augments cued fear memory generalizatio

83 mucosa transcriptional responses to chronic EtOH exposure for future hypothesis-driven mechanistic s

84 , these data suggest a model whereby chronic EtOH-driven neuroadaptations in the IL promote fear memo

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

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

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

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

89 50 mmol/L), CSE (20-40 mug/mL), or both (CSE+EtOH), and analyzed by immunoblotting, quantitative reve

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

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

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

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

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

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

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

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

98 used were adapted (Free EtOH-A, Encapsulated EtOH-A) and non-adapted to ethanol (Free, Encapsulated).

99 es, sparkling wines produced by Encapsulated EtOH-A showed sensory properties, in terms of aroma, tas

100 OH detection from other solvents, especially EtOH.

101 Ethanol (EtOH) is a teratogen, but its teratogenic mechanisms are

102 9.9, 26.3 and 5.1 g/100 g of CO(2), ethanol (EtOH) and water-soluble extracts, respectively.

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

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

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

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

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

108 s, including dietary components and ethanol (EtOH), which can impact intestinal health.

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

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

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

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

113 cell response in mice that consumed ethanol (EtOH) had a reduced proliferative capacity as well as th

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

115 ain pathology despite chronic, high ethanol (EtOH) exposure protocols.

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

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

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

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

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

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

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

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

124 de positive and negative valence of ethanol (EtOH)-related stimuli.

125 addition to a significant amount of ethanol (EtOH).

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

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

128 ture, addition of organic solvents (ethanol (EtOH), isopropanol (IPA), tert-butanol (TBA) and tetrahy

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

130 uate sensorimotor disruption due to ethanol (EtOH).

131 s of sensorimotor disruption due to ethanol (EtOH); however, previous studies have focused on deficit

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

133 The PHWE system was modified using ethanol (EtOH) as a cosolvent, while a numerical modelling approa

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

135 havioral impact of chronic alcohol (ethanol; EtOH) on the expression of established fear memories in

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

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

138 WT and fat-1 mice were chronically fed EtOH, and ileum RNA-seq and bioinformatic analyses were

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

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

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

142 etinoic acid 6 (Stra6) gene are required for EtOH induction of Hoxa1 and Cyp26a1 We conclude that EtO

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

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

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

146 four types of yeast used were adapted (Free EtOH-A, Encapsulated EtOH-A) and non-adapted to ethanol

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

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

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

150 racted with different solvent mixtures (e.g. EtOH, H(2)O/EtOH 3:7 and H(2)O/EtOH 7:3) and extractions

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

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

153 This increased susceptibility in X31->EtOH mice was associated with reduced IAV-specific killi

154 D8 T cells into the lungs is reduced in X31->EtOH mice.

155 that then chronically consumed alcohol (X31->EtOH) exhibited increased morbidity and mortality follow

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

157 by deoxygenation and aromatization with HCl/EtOH.

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

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

160 Tpy-Zn]-SPP complex (K(ass) 106,000 M(-1) in EtOH-CHCl(3)) with 5.8 muM LOD in HEPES buffer (10 mM, p

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

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

163 synthesized in the presence of a catalyst in EtOH under mild conditions, and all products were obtain

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

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

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

167 TBOA also further increased drinking in EtOH mice.

168 dentify novel genes and pathways involved in EtOH-associated gut pathology and discern the impact of

169 d emission of blue light upon irradiation in EtOH in the region of 404-422 nm.

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

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

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

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

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

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

176 nishment probe test negated the reduction in EtOH lever presses but not in aborts.

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

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

179 luteolin) in ACE (acetone) and RT (rutin) in EtOH (ethanol) solvent at 60 degrees C.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 different types of dietary fats can modulate EtOH-induced changes in the intestine; however, mechanis

195 different solvent mixtures (e.g. EtOH, H(2)O/EtOH 3:7 and H(2)O/EtOH 7:3) and extractions were accomp

196 ixtures (e.g. EtOH, H(2)O/EtOH 3:7 and H(2)O/EtOH 7:3) and extractions were accomplished using a micr

197 , respectively, using NaBH(4)/NiCl(2).6H(2)O/EtOH as a reducing system, is described.

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

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

200 he additional mouse models of low dosages of EtOH and of blending baijiu validated that volatile comp

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

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

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

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

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

206 rent carriers, we found that the increase of EtOH in the diet is negatively correlated with insect de

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

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

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

210 can be formed by photochemical oxidation of EtOH.

211 be accumulated by photochemical oxidation of EtOH.

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

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

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

215 amygdala, partially reversed suppression of EtOH lever presses on probe testing.

216 ute to the beneficial effects of n3 PUFAs on EtOH-induced intestinal pathology.

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

218 PLE-EtOH extract contained 12.2 mg/g of cyanidin-3-glucoside

219 ins (15.9 g/100 g pomace) was present in PLE-EtOH extract.

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

221 rom sixteen participants, both pre- and post-EtOH administration.

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

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

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

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

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

227 in neuronal correlates of footshock-punished EtOH-SA.

228 ated these regions in regulation of punished EtOH self-administration (EtOH-SA).

229 ections to basolateral amygdala, to punished EtOH-SA.

230 used lower degrees of liver injury than pure EtOH by protecting against the decrease of the relative

231 ncrease in fluid clearance in mice receiving EtOH diet.

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

233 Punishment reduced EtOH lever pressing and elicited aborted presses (lever

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

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

236 trate a key role for the vmPFC in regulating EtOH-SA after punishment, with implications for understa

237 histochemistry for Arc/arg3.1 (Arc) revealed EtOH-induced decreases in Arc expression in the infralim

238 stimulation of IL pyramidal neurons reversed EtOH-driven fear memory overgeneralization, identifying

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

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

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

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

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

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

245 ried out in environmentally benign solvents (EtOH).

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

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

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

249 erentiation-associated mRNA levels, and that EtOH decreases pluripotency-related mRNAs.

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

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

252 uction of Hoxa1 and Cyp26a1 We conclude that EtOH stimulates stem cell differentiation by increasing

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

254 omologous recombination, we demonstrate that EtOH signals via RARgamma binding to RA response element

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

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

257 Furthermore, we demonstrated that EtOH-induced alteration of the gut microbiota profoundly

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

259 ffects on differentiation, we show here that EtOH and acetaldehyde, but not acetate, increase differe

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

261 We also report that EtOH-mediated increases in homeobox A1 (Hoxa1) and cytoc

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

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

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

265 family member A2 (Aldh1a2), suggesting that EtOH-mediated induction of Hoxa1 and Cyp26a1 requires RO

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

267 The EtOH exposure also increased mRNAs encoding hepatic cons

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

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

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

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

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

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

274 e vmPFC and dmPFC exhibited phasic firing to EtOH lever presses and aborts, but only in the vmPFC was

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

276 e downregulated in fat-1 mice in response to EtOH, while defense responses and PPAR signaling were up

277 a markedly plastic transcriptome response to EtOH.

278 ined intestinal transcriptional responses to EtOH in WT and transgenic fat-1 mice (which endogenously

279 inetics, charge transfer, and sensitivity to EtOH.

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

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

282 ed quantity were achieved by adopting 12%v/v EtOH/H(2)O solvent and by swelling bentonites for 24 h b

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

284 - 0.107 versus 1.08 +/- 0.138 for SUC versus EtOH; P=0.014), and microvascular reactivity were signif

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

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

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

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

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

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

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

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

293 Compared with EtOH feeding, CB feeding resulted in higher concentratio

294 stsynaptic currents (mIPSCs) correlated with EtOH dependence.

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

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

297 , 4.36 muM), suggesting DHM interaction with EtOH involves the BZ sites on GABA(A)Rs.

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

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

300 a Ni-catalyzed esterification reaction with EtOH to give valuable N-Boc protected amines.