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1 ng 0.02% Tween 80 (all media contained 0.02% sodium azide).
2 : 40 mM D-mannitol, 40 mM imidazole or 40 mM sodium azide.
3 2 mM adenosine triphosphate and inhibited by sodium azide.
4 factor, Fzo1p, or by treatment of cells with sodium azide.
5 tion, biomineralization was not inhibited by sodium azide.
6 bolic inhibitors 2,4-dinitrophenol (DNP) and sodium azide.
7 purines with a selected sodium sulfinate and sodium azide.
8  saline (pH 8.4) with 0.1 mM CaCl2 and 0.08% sodium azide.
9 vatives with 61-83% yields when treated with sodium azide.
10 ons and the addition of phenethyl alcohol or sodium azide.
11 ut"; (3) energy starvation by treatment with sodium azide.
12 fects of superoxide dismutase, catalase, and sodium azide.
13 pyrroline N-oxide, but could be protected by sodium azide.
14  zinc acetate and by the metabolic inhibitor sodium azide.
15  (HB-PTC) to enantioselective azidation with sodium azide.
16 ides in the presence of catalytic amounts of sodium azide.
17 tion that was impaired by the SECA inhibitor sodium azide.
18  by aquaporin inhibitors, silver nitrate and sodium azide.
19 vely induced by brief exposure of animals to sodium azide.
20 -we tested the effects of trypsin, serum and sodium azide.
21 he presence of sorbic acid, isopropanol, and sodium azide.
22 nding primary aryl amines with copper(I) and sodium azide.
23 one, 3-nitropropionic acid, antimycin A, and sodium azide.
24 localization is prevented in the presence of sodium azide.
25 c esters via a copper-mediated reaction with sodium azide.
26 sm(s) that can be blocked by the presence of sodium azide.
27 ration and was reduced by preincubation with sodium azide.
28  cells were lysed only after the addition of sodium azide.
29      To test the role of cytochrome oxidase, sodium azide (0.75-2 microM) was added during normoxia t
30 lation was reversed by the energy inhibitors sodium azide/2-deoxyglucose and by the vinca alkaloid, v
31 razone, 44%, and 2,4-dinitrophenol, 26%), by sodium azide (25%), and hydroxyl amine (33%).
32 cles was evaluated both in vitro (PBST+0.02% sodium azide, 37 degrees C) and in vivo (male Sprague-Da
33 trate for class IV ADH isoenzyme) but not by sodium azide (a catalase inhibitor).
34                                              Sodium azide, a collision quencher of singlet oxygen, re
35 dinium ion (MPP+), a complex I inhibitor, or sodium azide, a complex IV inhibitor.
36 also is inhibited by treatment of cells with sodium azide, a potent inhibitor of SecA.
37  minicolumn tests were conducted to identify sodium azide addition as the most broadly effective ster
38 ffectiveness of three sterilization methods: sodium azide addition, autoclaving, and gamma irradiatio
39                                              Sodium azide, an inhibitor of catalase, reduced the incr
40   We have further investigated the effect of sodium azide, an inhibitor of the F-ATPases that has bee
41 nd 95% inhibited by the combination of 20 mm sodium azide and 1 mm salicylhydroxamic acid; thus trans
42                  For example, in our system, sodium azide and 2-deoxy-D-glucose increased the ratio o
43 ibly blocked by treating infected cells with sodium azide and 2-deoxy-D-glucose, which we show rapidl
44  depleted of cellular ATP by the addition of sodium azide and 2-deoxy-D-glucose.
45 ls were depleted of energy by treatment with sodium azide and 2-deoxyglucose or by permeabilization.
46 cells are depleted of ATP by the addition of sodium azide and 2-deoxyglucose to block ATP production
47 halasin B, trifluoperazine, a combination of sodium azide and 2-deoxyglucose, EDTA, incubation at 4 d
48 e peptides was blocked by the energy poisons sodium azide and 2-deoxyglucose, whereas staining of the
49 ido boronic esters has been carried out with sodium azide and a tetrabutylammonium salt as phase-tran
50   NO2- is further reduced to N2O using a 1:1 sodium azide and acetic acid buffer solution using previ
51 er similar to the wild-type signal sequence; sodium azide and carbonyl cyanide 3-chlorophenylhydrazon
52 by treating SH-SY5Y neuroblastoma cells with sodium azide and deoxyglucose.
53  suppressed by the singlet oxygen scavengers sodium azide and dithiothreitol.
54                      Inhibition of SecA with sodium azide and mutations in SecB, SecD, and SecF, all
55                                       Use of sodium azide and NIR radiate on at 4 degrees C revealed
56 exposed to highly cytotoxic model compounds (sodium azide and paracetamol) or subjected to freeze-tha
57 erentiate between the pure laccase inhibitor sodium azide and radical scavengers such as gallic and k
58 ficantly decreased by high concentrations of sodium azide and sodium arsenate but not by sodium cyani
59 eto-hexofuranoses followed by treatment with sodium azide and sodium borohydride reduction gave 5-azi
60  temperature, which could further react with sodium azide and subsequently cyclizes intermolecularly
61 s completely abolished by the SecA inhibitor sodium azide and therefore still required the participat
62 egrees C, at 4 degrees C, in the presence of sodium azide and tyrosine kinase inhibitors herbimycin A
63 ut 250 microm, and both showed resistance to sodium azide and vanadate and sensitivity to nanomolar c
64                                              Sodium azide and vanadate inhibited sterol uptake, consi
65 oxyl radicals (mannitol) and singlet oxygen (sodium azide) and carbon-centered radicals (DMPO) were t
66 bited at 4 degrees C, 24% inhibited by 20 mm sodium azide, and 95% inhibited by the combination of 20
67 as suppressed by the singlet oxygen quencher sodium azide, and as mRNA expression of LMNA was not ind
68 was inhibited by vanadate, N-ethylmaleimide, sodium azide, and calcium; and was unidirectional (i.e.,
69 nto a one-pot protocol with terminal alkyne, sodium azide, and diaryliodonium salt as starting compou
70 nd metabolic inhibitors, such as ouabain and sodium azide, and in the absence of sodium to delineate
71 P plus UVA-induced 8-OHdG, whereas catalase, sodium azide, and mannitol exhibited no effect.
72 o model chemotoxins: sodium hypochlorite and sodium azide, and one model biotoxin, concanavalin A.
73  quenching agents (sorbic acid, isopropanol, sodium azide, and tert-butanol) that are commonly employ
74 d, we first identified nonimpairing doses of sodium azide (approximately 0.75 mg/kg per hr) and corti
75 ly reduced when metabolic inhibitors such as sodium azide are added.
76  using N-methyl-2-pyrrolidone as solvent and sodium azide as azide source demonstrate that all evalua
77 condary propargyl alcohol as C-3 synthon and sodium azide as cycloaddition counterpart.
78              Continuous systemic infusion of sodium azide at approximately 1 mg/kg per hr inhibited c
79 lthio)-4-(het)arylidene-but-1-en-3-ones with sodium azide at higher temperatures.
80 NAr reaction between halodinitrobenzenes and sodium azide at rt in aqueous media is reported.
81 ing the CTT make E. coli less susceptible to sodium azide at subinhibitory concentrations.
82  friendly protocol that converts alkenes and sodium azide-both readily available feedstocks-to 1,2-di
83                          Linear detection of sodium azide by entrapped hepatocytes was 0-10 microM, w
84                      Metabolic inhibition by sodium azide can also inhibit both TREK and TASK channel
85 sure to staurosporine and hypoxia induced by sodium azide) caused significant increase in ATF3 expres
86  flowing over bulk beta-sodium azide or beta-sodium azide dispersed on 100 nm long multiwall carbon n
87 ns did not increase sensitivity to paraquat, sodium azide, divalent metal ions (Fe(II) or Cu(II)), or
88 he uranium(III) complex [U(Tren(TIPS))] with sodium azide followed by abstraction and encapsulation o
89 n of alpha-O-nosyl-beta-hydroxyester 18 with sodium azide, followed by LiAlH(4) reduction of the azid
90                                            A sodium azide-generated Bdpmt-1 missense mutant had no (<
91 the reaction of aldehydes, nitroalkanes, and sodium azides/glycosyl azides in the presence of 1,1,1,3
92  yeast with the electron transport inhibitor sodium azide has similar effects on the YRO as visible l
93                  Gaseous ClN3 generated from sodium azide, hypochlorite, and acetic acid can be explo
94  scale from 1,2-dibromotetrafluoroethane and sodium azide in a novel process initiated by organomagne
95 ith further reduction to nitrous oxide using sodium azide in an acetic acid buffer.
96 and 1,3-diketones) with molecular iodine and sodium azide in aqueous DMSO providing a general access
97      Treatment of N-chlorodimethylamine with sodium azide in dichloromethane does not lead to N-azido
98 be generated in situ from aluminum chloride, sodium azide in N-methyl-2-pyrrolidone.
99 rophiles derived from beta-chloroamines with sodium azide in the presence of a chiral bisurea catalys
100  1,3-bis(het)arylmonothio-1,3-diketones with sodium azide in the presence of IBX catalyst, has been r
101    The inhibition of SecA ATPase activity by sodium azide in the presence of IMVs and a functional si
102  culture may be explained by the presence of sodium azide in this preparation.
103 eatment with 4-toluene sulfonyl chloride and sodium azide in toluene at elevated temperature is descr
104 sonitriles, N,N-dibromoarylsulfonamides, and sodium azides in the presence of K(2)CO(3).
105 ant scavengers (i.e. reduced glutathione and sodium azide) indicating a possible oxidation reaction w
106 r perturbants (i.e., 0.45 M sucrose and 5 mM sodium azide), indicating that cell surface proteins or
107 ole, staurosporine, protease inhibitors, and sodium azide, indicating that cytoskeletal rearrangement
108 ompounds exhibited strong protection against sodium azide induced mutagenicity of Salmonella typhimur
109                                    The three sodium azide induced mutants ant30-245, ant30-272 and an
110 cocorticoid in the rat, would potentiate the sodium azide-induced learning deficit.
111 n of CHOP expression significantly decreased sodium azide-induced neuronal death.
112 ole-4-carboxamide riboside, antimycin A, and sodium azide inhibited cell growth and lowered the expre
113 pling of anilines, primary alkyl amines, and sodium azide is described in the presence of TBHP at mod
114  present evidence that inhibition of SecA by sodium azide is incomplete even at high concentrations o
115 ide from iodine monochloride vapor and solid sodium azide is safe and convenient.
116   The reaction of beta-ketodithioesters with sodium azide is shown to furnish beta-ketonitriles in go
117                                              Sodium azide-killed cells were used as a control.
118 l chlorides and 6-chloropyrimidines 2'o with sodium azide, leading to final products in higher yields
119  nucleophile can be identified via classical sodium azide-mediated rescue of mutants thereof.
120 mutagens, namely 4-nitro-o-phenylenediamine, sodium azide, mitomycin C, benzo[a]pyrene, aflatoxin B1
121                                            A sodium azide mutant population in cv Sudan was generated
122 erivatives via [3 + 2] cycloaddition between sodium azide (NaN(3)) and organic nitrile derivatives.
123               K(ir)2.3 was inhibited by 3 mm sodium azide (NaN(3)), whereas K(ir)2.1 and K(ir)2.2 wer
124                                   Vehicle or sodium azide (NaN3) (25-100 mM) was added to these QCMs
125 d commercial CRP (dCRP) to remove azide, and sodium azide (NaN3) alone at equivalent concentrations t
126 cose deprivation or metabolic poisoning with sodium azide (NaN3).
127  of the respiratory chain, sodium cyanide or sodium azide, neither induced ROS nor killed yeast cells
128  diphenylsulfoxide, tetramethylethylene, and sodium azide) on the photosensitized oxidation was inves
129 atic substitution (S(N)Ar) with alcohols and sodium azide onto the pentafluorophenyl moiety of a tran
130 ma cells could be depleted by treatment with sodium azide or 2,4-dinitrophenol; restoration of the or
131 of nitrogen and argon flowing over bulk beta-sodium azide or beta-sodium azide dispersed on 100 nm lo
132                      If SecA is inhibited by sodium azide or if the SecE in the cell is depleted, the
133     Low temperature or metabolic inhibitors, sodium azide or iodoacetamide, have little influence on
134       Biochemical activity was unaffected by sodium azide or other inhibitors of ATPases.
135 ted to occur when cells were pretreated with sodium azide or Triacsin C.
136 Aminotriazole, L-buthionine sulfoximine, and sodium azide partly abrogated the RGC resistance to oxid
137 over 9 weeks in PBS + 0.02% Tween 80 + 0.02% sodium azide pH 7.4 (PBST) at 37 degrees C.
138 man epidermal keratinocytes at 4(o)C or with sodium azide prevented SNA uptake, suggesting active end
139                                              Sodium azide prevents HemA turnover in vivo, suggesting
140 ion of long-chain alkanoyl halobenzenes with sodium azide, promoted by copper(I) chloride, is reporte
141 ellular glucose or metabolic inhibition with sodium azide reduced the firing rate of a subpopulation
142 lecules, but methods that employ inexpensive sodium azide remain scarce.
143 ation for the method were 54.9 and 166 ng of sodium azide respectively.
144 c-active bacteria using gamma-irradiation or sodium azide, respectively.
145  or energy depletion using 2-deoxy-D-glucose/sodium azide restored flutamide accumulation to that of
146                               Treatment with sodium azide resulted in cell death in a dose-responsive
147 etitive inhibition, whereas, citric acid and sodium azide showed mixed inhibition of PPO activity.
148 modification reagents N-bromosuccinimide and sodium azide significantly inhibited POD-A activity.
149 ide is easily substituted by silver acetate, sodium azide, sodium iodide, and silver nitrate.
150                  The method utilizes aqueous sodium azide solution as the azide source and can be per
151 duct studies for the reaction of 2 in dilute sodium azide solutions suggest that the tetrol-forming r
152  carbonyl cyanide m-chlorophenylhydrazone or sodium azide, suggesting that this initial translocation
153 by ascorbic acid and a peroxidase inhibitor, sodium azide, suggesting the potential role of phenoxyl
154 , including continuously feeding 300 mg/L of sodium azide, three cycles of autoclaving, and 10-12 kGy
155 olled and regiocontrolled epoxide opening by sodium azide to form the 2-azido-3,4-dihydroxy alkanoate
156 m corticosterone, acted synergistically with sodium azide to inhibit cytochrome oxidase activity.
157                              The addition of sodium azide to nitriles to give 1H-tetrazoles is shown
158                                  Addition of sodium azide to the medium to inhibit MPO prevented neut
159 raacetic acid (EGTA), or inhibitors, such as sodium azide, to compare the relative permeability of HD
160                 To achieve this objective, a sodium azide-treated M(2)/M(3) population of barley cult
161                         Lastly, we show that sodium azide treatment, which increases lactate levels u
162       Hydrazoic acid was formed in situ from sodium azide under acidic conditions to react with termi
163 of propiolaldehydes for the first time) with sodium azide under metal- and oxidant-free conditions fo
164 ion of o-alkynylaldehydes in the presence of sodium azide under mild reaction conditions is described
165  and boron-directed double ring-opening with sodium azide under Miyashita conditions.
166 yclopropane hemimalonates, when treated with sodium azide, undergo a tandem ring-opening decarboxylat
167 a wide range of aryl/heteroaryl halides with sodium azide using a photocatalyst powder consisting of
168  localized SYP121 and VAMP722 in response to sodium azide was detected in real-time.
169                 The singlet oxygen quencher, sodium azide, was tested for its ability to reduce DNA d
170 d staurosporine and induction of necrosis by sodium azide were accompanied by an increase in the leve
171 ells depleted of ATP with 2-deoxyglucose and sodium azide were unable to properly regulate pH.
172  different injection intervals of a biocide (sodium azide) which allowed monitoring biofilm destabili
173 that affect the susceptibility of E. coli to sodium azide, which inhibits SecA-mediated translocation
174                                              Sodium azide, which is an inhibitor of MPO, completely i
175 A depletion conditions or in the presence of sodium azide, which is known to inhibit SecA.
176 synthesized in high yield by the reaction of sodium azide with 2H-azirine-2-carbonyl chlorides, gener
177 -pot three-component reaction of alkynes and sodium azide with organic halides or alpha-bromo ketones
178 UN3)4, have been synthesized by reduction of sodium azide with organometallic metallocene derivatives
179 exposure to the cytochrome oxidase inhibitor sodium azide, with near complete protection at 30 microM
180                               Treatment with sodium azide yielded the desired azides, and the deprote

 
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