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1 ty under high submicellar conditions (10-25% 1-butanol).
2 y and the inhibition of the Shaw2 channel by 1-butanol.
3 S4-S5 linkers conferred weak potentiation by 1-butanol.
4 ed by genistein, PD98059, and PLD-inhibitor, 1-butanol.
5 butane oxidation capability and accumulated 1-butanol.
6 inactivated was unable to grow on butane or 1-butanol.
7 y be more important in the detoxification of 1-butanol.
8 d the excess hydrogen-bond acceptor sites of 1-butanol.
9 well as leucine analogues, such as 3-methyl-1-butanol.
10 and elution with a 2:1 mixture of 1-propanol:1-butanol.
11 ediated signaling, 2,3-diphosphoglycerate or 1-butanol.
12 ethyl-2-buten-1-ol, and 300 mg/L of 3-methyl-1-butanol.
13 uction to 3-methyl-2-buten-1-ol and 3-methyl-1-butanol.
14 tectable 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol.
15 13)C,(1)H] correlations in the test molecule 1-butanol.
16 timulated ERK activity was also inhibited by 1-butanol.
17 However, they show increased resistance to 1-butanol.
18 atment of neutrophils with ethanol (0.8%) or 1-butanol (0.3%), which results in the accumulation of p
20 4-nonadienal, (E,E)-2,4-decadienal, 3-methyl-1-butanol, 1-hexanol, and 2-pentyl-furan, were employed
21 ic compounds identified in this study, e.g., 1-butanol, 1-octen-3-ol, 2-and 3-methyl butanoic acid, h
24 asure concentration gradients in evaporating 1-butanol/1-hexanol droplets on a hydrophobic surface.
25 s and higher alcohol esters, namely 3-methyl-1-butanol, 2,3-butanediol, ethyl lactate, 3-methyl-1-but
27 roduce higher alcohols including isobutanol, 1-butanol, 2-methyl-1-butanol, 3-methyl-1-butanol and 2-
28 of yeast promoted the formation of 3-methyl-1-butanol, 2-methyl-1-propanol and 3-(methylsulfanyl)-pr
29 d acetic acid, followed by hexanol, 3-methyl-1-butanol, 2-phenylethanol, 3-methylbutanal, hexanal, be
30 etate, isoamyl acetate, isobutanol, 2-methyl-1-butanol, 2-phenylethanol, E-2-hexenol, octanal, nonana
31 en the PLS analysis were evaluated, 3-methyl-1-butanol, 2-phenylethyl alcohol, nonanal, and benzaldeh
32 oline/1-octen-3-ol, for Venere, and 3-methyl-1-butanol/2-methyl-1-butanol, for Apollo, were also foun
33 variations during smoking, of which 3-methyl-1-butanol, 3,7-dimethyl-1,3,6-octatriene, hydroxy butano
34 ls including isobutanol, 1-butanol, 2-methyl-1-butanol, 3-methyl-1-butanol and 2-phenylethanol from g
35 aining emulsions had high levels of 2-methyl-1-butanol, 3-methyl-1-butanol, and 2-butanone after stor
37 ed urine 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanol (a biomarker of cigarette smoke exposure) on
38 ry vesicles from the TGN was sensitive to 1% 1-butanol, a concentration that inhibited PLD-catalyzed
39 of BOH and BDH at three different levels of 1-butanol, a nontoxic level (0.1 mM), a growth-supportin
42 known negative regulators of ABA signaling: 1-butanol, an inhibitor of phospholipase D, and abi1-1,
44 -azioctanol, the photoactivatable analogs of 1-butanol and 1-octanol, to photolabel the purified Ig1-
45 o our results, dimethyl disulphide, 3-methyl-1-butanol and 1-octen-3-one odorants showed the highest
48 ethyl acetate, 2-methyl-1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol and furan derivatives l
49 ethyl acetate, 2-methyl-1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol was determined by means
50 nol, 1-butanol, 2-methyl-1-butanol, 3-methyl-1-butanol and 2-phenylethanol from glucose, a renewable
51 e exception of 2-methyl-1-propanol, 3-methyl-1-butanol and 2-phenylethyl alcohol, which decreased 68%
54 d higher levels of 2-phenylethanol, 3-methyl-1-butanol and diethyl succinate, and lower concentration
55 1-propanol, 2-methyl-1-propanol, 3/2-methyl-1-butanol and ethyl octanoate were evaporated whereas th
57 -1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol and furan derivatives like 5-(hydroxymethyl)-2
59 uptake; 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), a biomarker
60 well as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), and cotinin
62 tions, we used a mixture of Triton X-100 and 1-butanol and observed that water-soluble natural and sy
63 y 56% and 44% conversions were achieved when 1-butanol and octadecanol were employed, respectively.
64 exanal concentration was higher and 2-methyl-1-butanol and toluene lower for C and GSC than for GSPC.
66 he homologous series of 1-alkanols (ethanol, 1-butanol, and 1-hexanol) with Shaw2 K(+) channels in Xe
67 ation of four alcohols (ethanol, 1-propanol, 1-butanol, and 1-pentanol) to the corresponding carboxyl
69 ella, Lachnospiraceae, 4-methyl-2-pentanone, 1-butanol, and 2-butanone could discriminate NAFLD patie
71 aPKCs were inhibited by genistein, PD98059, 1-butanol, and expression of dominant-negative forms of
72 e, urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol, and hair and nail nicotine levels were measur
73 enyl)-7H-pyrrolo[2,3-d]pyrimidin-4-y l]amino-1-butanol, and NBI-27914 at doses (30 mg/kg, i.p.) that
75 The substrate activation with ethanol and 1-butanol are explained by an ordered mechanism with an
76 that several biological processes blocked by 1-butanol are not affected by FIPI, suggesting the need
77 for oxidation of ethanol, cyclohexanol, and 1-butanol are quantitatively explained with the abortive
81 nickel to generate a catalyst that generates 1-butanol at unprecedented faradaic efficiencies (xi = 4
83 ol (MeOH), ethanol (EtOH), 2-propanol (IPA), 1-butanol (BuOH), acetonitrile (ACN) and the solvent mix
84 that increasing concentrations of ethanol or 1-butanol but not 2-butanol (0.05-0.5%) inhibited fMLP-i
85 e mutant of PLD1 or by the presence of 50 mM 1-butanol but not tert-butanol, an indication that these
86 O(2) and 5% CO(2)) in the presence of 0.05% 1-butanol, but not tertiary-butanol, stimulated PLD as e
88 ersion of the product of the PLD reaction by 1-butanol caused a partial loss of the [3H]thymidine res
89 were inhibited by genistein, PD98059, UO126, 1-butanol, cell-permeable myristoylated PKC-zeta pseudos
90 l, trans-2-hexenal) and alcohols (1-hexanol, 1-butanol, cis-3-hexenol) and had significant discrimina
92 reover, the pretreatment of neutrophils with 1-butanol decreased Fgr activity in cells stimulated wit
93 Conversely, inhibition of PLD1 activity by 1-butanol decreases betaAPP trafficking in both wt and P
94 alkanols, the step that limits 2-butanol and 1-butanol dehydration rates; the latter two reactions sh
95 a grown on butane or 1-butanol expresses two 1-butanol dehydrogenases, a quinoprotein (BOH) and a qui
96 ol/vol) O(2), CuSO(4) (0.5 microM) repressed 1-butanol-dependent induction of beta-galactosidase acti
97 the mineral salts of standard growth medium, 1-butanol-dependent induction was significantly represse
98 kers showed that the potentiation induced by 1-butanol depends on the combination of a single mutatio
99 A structural analog of choline, 3,3-dimethyl-1-butanol (DMB), is shown to non-lethally inhibit TMA fo
104 e solvent environment most closely resembles 1-butanol (epsilon = 17), although the energetic contrib
106 typic responses of E. coli to 1.2% (vol/vol) 1-butanol exposure included the following: (i) decreased
107 Pseudomonas butanovora grown on butane or 1-butanol expresses two 1-butanol dehydrogenases, a quin
109 y in organic solvents, ImmE1 was purified by 1-butanol extraction of isolated membranes, followed by
110 for Venere, and 3-methyl-1-butanol/2-methyl-1-butanol, for Apollo, were also found to act as ageing
111 time the direct photosynthetic production of 1-butanol from cyanobacteria Synechococcus elongatus PCC
113 d methyl heptenone) and four minor (3-methyl-1-butanol, gamma-hexalactone, 2-nonanone, and dodecanoic
115 okers by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol had similar severity of lung injury as patient
116 nd urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol identified 27 of the 28 nonsmokers by history
117 nd urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol identified considerably more active smokers th
118 sing 100 mM sodium dodecyl sulfate (SDS) and 1-butanol in 10 mM sodium-phosphate (pH 7.2) at a flow r
119 opha H16, to produce isobutanol and 3-methyl-1-butanol in an electro-bioreactor using CO(2) as the so
122 l compound using an alcohol (e.g., methanol, 1-butanol) in the presence of a relatively strong Lewis
124 ications to the 2- and 3-carbon positions of 1-butanol increased potency, whereas modifications that
126 le, brefeldin A (BFA), and primary alcohols (1-butanol) induce reversible fragmentation of the Golgi
127 alactosidase activity, was used to show that 1-butanol induced the BMO promoter in the presence or ab
131 butol [Emb; dextro-2,2'-(ethylenediimino)-di-1-butanol] is used to treat tuberculosis as well as diss
133 tyrate and ethyl 2-methylbutyrate), 3-methyl-1-butanol, isopropyl acetate, and finally the two sulfid
134 on PKC translocation and degranulation, and 1-butanol itself had no effect on PKC translocation when
136 nts with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels consistent with active smoking and was
137 nts with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels in the active smoking range were younge
138 Urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels were consistent with active smoking in
140 otonated monomers and proton-bound dimers of 1-butanol, limits of detection of 1.9 ppt(v) and 110 ppt
143 ng catalyst system toward chemically similar 1-butanol makes it possible to synthesize the competent
144 r under micellar conditions using 1-2% (v/v) 1-butanol mobile phase to remove plasma proteins and con
145 ordination environment upon interaction with 1-butanol molecules, which after a thermal treatment abo
146 ributions suggests that the formation of the 1-butanol monolayer is driven by an excellent match betw
148 g/L) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) (0.2 ng/L) along with the reduction of
150 smoking: 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its O-glucuronide, 4-[(methylnitros
151 NNK) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) as the targets, we first developed a so
152 tabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine is frequently used as a biomar
153 rosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) is present in the urine of tobacco user
154 ine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a metabolite of the powerful lung carc
156 abolite, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), is an important mechanism for 4-(methy
157 ry total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), N'-nitrosonornicotine (NNN), and cotin
158 NK), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), NNAL-N-beta-glucuronide, and NNAL-O-be
160 product 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), which, in turn, can be glucuronidated,
163 omarker [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL)], an established biomarker (cotinine),
164 tabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol [NNAL]) and VOCs (including metabolites of the
166 ncluding 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol [NNAL]), metals, polycyclic aromatic hydrocarb
169 cal content of ImmE1 is approximately 80% in 1-butanol or 2,2,2-trifluoroethanol, consistent with a p
171 NZVI (RL-Pd-NZVI) when reacted with TCE in a 1-butanol organic phase with limited amounts of water re
173 odel is proposed in which the electrons from 1-butanol oxidation follow a branched electron transport
174 ion of 1-hexanol production by extending the 1-butanol pathway provides the possibility to produce ot
175 holipase D (PLD) activity, the PLD inhibitor 1-butanol prevented the unsaturated fatty acid-induced r
177 fficiency occurs at -1.48 V vs Ag/AgCl, with 1-butanol production commencing at an overpotential of 3
179 ed upon exposure of the calcined material to 1-butanol, providing stability against water and, most i
180 alyst for the Guerbet reaction of ethanol to 1-butanol, providing turnover numbers up to 725 000 Ru(-
181 ation of Maillard reaction products 3-methyl-1-butanol, pyrazine, 2-ethylpyrazine, 2-ethyl-3-methylpy
183 regulation of phosphoinositide production by 1-butanol resulted in diminished PIP(2) in the plasma me
184 D-mediated PA synthesis, by incubation with 1-butanol, resulted in the complete fragmentation of the
185 wth hormone and prolactin, were treated with 1-butanol resulting in the synthesis of phosphatidylbuta
186 h 0.4M perchloric acid and purification with 1-butanol significantly shortened sample preparation (30
187 iquid interfaces of mutually saturated water/1-butanol solutions at a temperature of 298.15 K were in
188 everal alcohols, notably isoamyl alcohol and 1-butanol, stimulate filamentous growth in haploid cells
189 by extending the coenzyme A (CoA)-dependent 1-butanol synthesis reaction sequence catalyzed by exoge
190 . butanovora could tolerate higher levels of 1-butanol than the P. butanovora boh::tet strain and the
192 en-1-ol, 3-methyl-2-buten-1-ol, and 3-methyl-1-butanol, three C5 alcohols that serve as potential bio
194 expressing wild-type Arf6 by treatment with 1-butanol to inhibit the formation of phosphatidic acid
195 ce of nucleophilic and biomimetic substrates 1-butanol, tosylhydrazine, or tetrahydrofurfuryl alcohol
196 nalytical methodologies were applied to both 1-butanol-treated and control cells to draw correlations
199 -1-propanol, 3-methyl-1-butanol and 2-methyl-1-butanol was determined by means of head space solid ph
200 story or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol was not associated with acute respiratory dist
201 by urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol was significantly associated with acute respir
205 the TSNA 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol were identified and quantified in authentic dr
206 anone, 2-pentanone, 2-heptanone and 3-methyl-1-butanol were identified as relevant VOCs for Lactobaci
207 anone, 2-pentanone, 2-heptanone and 3-methyl-1-butanol were identified as relevant VOCs for Lactobaci
210 L [urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol] were measured to categorize smoking status.
213 on of PA is inhibited by the primary alcohol 1-butanol, which has thus been widely employed to identi
214 broblasts deficient in PLD activity and also 1-butanol, which inhibits phosphatidic acid production b
215 resistant membrane fractions is inhibited by 1-butanol, which subverts production of phosphatidic aci
216 sporulation, because treatment of cells with 1-butanol, which supports Spo14p-catalyzed PtdCho breakd
217 edium in the presence of different levels of 1-butanol, wild-type P. butanovora could tolerate higher
221 ten from flour defatted with water-saturated 1-butanol (WSB; extracted at 20 degrees C) and 2-propano
222 ith adenoviruses overnight or the inhibitors 1-butanol, Y-27632, or C3 exotoxin before stimulation wi