ライフサイエンスコーパス: sodium azide

1 ng 0.02% Tween 80 (all media contained 0.02% sodium azide).

2 tion that was impaired by the SECA inhibitor sodium azide.

3 saline (pH 8.4) with 0.1 mM CaCl2 and 0.08% sodium azide.

4 ons and the addition of phenethyl alcohol or sodium azide.

5 ut"; (3) energy starvation by treatment with sodium azide.

6 fects of superoxide dismutase, catalase, and sodium azide.

7 pyrroline N-oxide, but could be protected by sodium azide.

8 zinc acetate and by the metabolic inhibitor sodium azide.

9 vely induced by brief exposure of animals to sodium azide.

10 -we tested the effects of trypsin, serum and sodium azide.

11 nding primary aryl amines with copper(I) and sodium azide.

12 one, 3-nitropropionic acid, antimycin A, and sodium azide.

13 localization is prevented in the presence of sodium azide.

14 sm(s) that can be blocked by the presence of sodium azide.

15 ration and was reduced by preincubation with sodium azide.

16 cells were lysed only after the addition of sodium azide.

17 by aquaporin inhibitors, silver nitrate and sodium azide.

18 : 40 mM D-mannitol, 40 mM imidazole or 40 mM sodium azide.

19 2 mM adenosine triphosphate and inhibited by sodium azide.

20 factor, Fzo1p, or by treatment of cells with sodium azide.

21 tion, biomineralization was not inhibited by sodium azide.

22 bolic inhibitors 2,4-dinitrophenol (DNP) and sodium azide.

23 To test the role of cytochrome oxidase, sodium azide (0.75-2 microM) was added during normoxia t

24 lation was reversed by the energy inhibitors sodium azide/2-deoxyglucose and by the vinca alkaloid, v

25 razone, 44%, and 2,4-dinitrophenol, 26%), by sodium azide (25%), and hydroxyl amine (33%).

26 cles was evaluated both in vitro (PBST+0.02% sodium azide, 37 degrees C) and in vivo (male Sprague-Da

27 trate for class IV ADH isoenzyme) but not by sodium azide (a catalase inhibitor).

28 Sodium azide, a collision quencher of singlet oxygen, re

29 dinium ion (MPP+), a complex I inhibitor, or sodium azide, a complex IV inhibitor.

30 also is inhibited by treatment of cells with sodium azide, a potent inhibitor of SecA.

31 Sodium azide, an inhibitor of catalase, reduced the incr

32 We have further investigated the effect of sodium azide, an inhibitor of the F-ATPases that has bee

33 nd 95% inhibited by the combination of 20 mm sodium azide and 1 mm salicylhydroxamic acid; thus trans

34 For example, in our system, sodium azide and 2-deoxy-D-glucose increased the ratio o

35 ibly blocked by treating infected cells with sodium azide and 2-deoxy-D-glucose, which we show rapidl

36 depleted of cellular ATP by the addition of sodium azide and 2-deoxy-D-glucose.

37 ls were depleted of energy by treatment with sodium azide and 2-deoxyglucose or by permeabilization.

38 cells are depleted of ATP by the addition of sodium azide and 2-deoxyglucose to block ATP production

39 halasin B, trifluoperazine, a combination of sodium azide and 2-deoxyglucose, EDTA, incubation at 4 d

40 e peptides was blocked by the energy poisons sodium azide and 2-deoxyglucose, whereas staining of the

41 ido boronic esters has been carried out with sodium azide and a tetrabutylammonium salt as phase-tran

42 NO2- is further reduced to N2O using a 1:1 sodium azide and acetic acid buffer solution using previ

43 er similar to the wild-type signal sequence; sodium azide and carbonyl cyanide 3-chlorophenylhydrazon

44 by treating SH-SY5Y neuroblastoma cells with sodium azide and deoxyglucose.

45 suppressed by the singlet oxygen scavengers sodium azide and dithiothreitol.

46 Inhibition of SecA with sodium azide and mutations in SecB, SecD, and SecF, all

47 Use of sodium azide and NIR radiate on at 4 degrees C revealed

48 exposed to highly cytotoxic model compounds (sodium azide and paracetamol) or subjected to freeze-tha

49 ficantly decreased by high concentrations of sodium azide and sodium arsenate but not by sodium cyani

50 eto-hexofuranoses followed by treatment with sodium azide and sodium borohydride reduction gave 5-azi

51 s completely abolished by the SecA inhibitor sodium azide and therefore still required the participat

52 egrees C, at 4 degrees C, in the presence of sodium azide and tyrosine kinase inhibitors herbimycin A

53 ut 250 microm, and both showed resistance to sodium azide and vanadate and sensitivity to nanomolar c

54 Sodium azide and vanadate inhibited sterol uptake, consi

55 bited at 4 degrees C, 24% inhibited by 20 mm sodium azide, and 95% inhibited by the combination of 20

56 as suppressed by the singlet oxygen quencher sodium azide, and as mRNA expression of LMNA was not ind

57 was inhibited by vanadate, N-ethylmaleimide, sodium azide, and calcium; and was unidirectional (i.e.,

58 nd metabolic inhibitors, such as ouabain and sodium azide, and in the absence of sodium to delineate

59 P plus UVA-induced 8-OHdG, whereas catalase, sodium azide, and mannitol exhibited no effect.

60 o model chemotoxins: sodium hypochlorite and sodium azide, and one model biotoxin, concanavalin A.

61 d, we first identified nonimpairing doses of sodium azide (approximately 0.75 mg/kg per hr) and corti

62 ly reduced when metabolic inhibitors such as sodium azide are added.

63 using N-methyl-2-pyrrolidone as solvent and sodium azide as azide source demonstrate that all evalua

64 Continuous systemic infusion of sodium azide at approximately 1 mg/kg per hr inhibited c

65 NAr reaction between halodinitrobenzenes and sodium azide at rt in aqueous media is reported.

66 friendly protocol that converts alkenes and sodium azide-both readily available feedstocks-to 1,2-di

67 Linear detection of sodium azide by entrapped hepatocytes was 0-10 microM, w

68 Metabolic inhibition by sodium azide can also inhibit both TREK and TASK channel

69 sure to staurosporine and hypoxia induced by sodium azide) caused significant increase in ATF3 expres

70 flowing over bulk beta-sodium azide or beta-sodium azide dispersed on 100 nm long multiwall carbon n

71 ns did not increase sensitivity to paraquat, sodium azide, divalent metal ions (Fe(II) or Cu(II)), or

72 he uranium(III) complex [U(Tren(TIPS))] with sodium azide followed by abstraction and encapsulation o

73 n of alpha-O-nosyl-beta-hydroxyester 18 with sodium azide, followed by LiAlH(4) reduction of the azid

74 A sodium azide-generated Bdpmt-1 missense mutant had no (<

75 yeast with the electron transport inhibitor sodium azide has similar effects on the YRO as visible l

76 Gaseous ClN3 generated from sodium azide, hypochlorite, and acetic acid can be explo

77 ith further reduction to nitrous oxide using sodium azide in an acetic acid buffer.

78 and 1,3-diketones) with molecular iodine and sodium azide in aqueous DMSO providing a general access

79 be generated in situ from aluminum chloride, sodium azide in N-methyl-2-pyrrolidone.

80 The inhibition of SecA ATPase activity by sodium azide in the presence of IMVs and a functional si

81 culture may be explained by the presence of sodium azide in this preparation.

82 eatment with 4-toluene sulfonyl chloride and sodium azide in toluene at elevated temperature is descr

83 ant scavengers (i.e. reduced glutathione and sodium azide) indicating a possible oxidation reaction w

84 r perturbants (i.e., 0.45 M sucrose and 5 mM sodium azide), indicating that cell surface proteins or

85 ole, staurosporine, protease inhibitors, and sodium azide, indicating that cytoskeletal rearrangement

86 ompounds exhibited strong protection against sodium azide induced mutagenicity of Salmonella typhimur

87 The three sodium azide induced mutants ant30-245, ant30-272 and an

88 cocorticoid in the rat, would potentiate the sodium azide-induced learning deficit.

89 n of CHOP expression significantly decreased sodium azide-induced neuronal death.

90 ole-4-carboxamide riboside, antimycin A, and sodium azide inhibited cell growth and lowered the expre

91 pling of anilines, primary alkyl amines, and sodium azide is described in the presence of TBHP at mod

92 present evidence that inhibition of SecA by sodium azide is incomplete even at high concentrations o

93 ide from iodine monochloride vapor and solid sodium azide is safe and convenient.

94 Sodium azide-killed cells were used as a control.

95 nucleophile can be identified via classical sodium azide-mediated rescue of mutants thereof.

96 mutagens, namely 4-nitro-o-phenylenediamine, sodium azide, mitomycin C, benzo[a]pyrene, aflatoxin B1

97 K(ir)2.3 was inhibited by 3 mm sodium azide (NaN(3)), whereas K(ir)2.1 and K(ir)2.2 wer

98 Vehicle or sodium azide (NaN3) (25-100 mM) was added to these QCMs

99 d commercial CRP (dCRP) to remove azide, and sodium azide (NaN3) alone at equivalent concentrations t

100 cose deprivation or metabolic poisoning with sodium azide (NaN3).

101 of the respiratory chain, sodium cyanide or sodium azide, neither induced ROS nor killed yeast cells

102 diphenylsulfoxide, tetramethylethylene, and sodium azide) on the photosensitized oxidation was inves

103 atic substitution (S(N)Ar) with alcohols and sodium azide onto the pentafluorophenyl moiety of a tran

104 ma cells could be depleted by treatment with sodium azide or 2,4-dinitrophenol; restoration of the or

105 of nitrogen and argon flowing over bulk beta-sodium azide or beta-sodium azide dispersed on 100 nm lo

106 If SecA is inhibited by sodium azide or if the SecE in the cell is depleted, the

107 Low temperature or metabolic inhibitors, sodium azide or iodoacetamide, have little influence on

108 Biochemical activity was unaffected by sodium azide or other inhibitors of ATPases.

109 ted to occur when cells were pretreated with sodium azide or Triacsin C.

110 Aminotriazole, L-buthionine sulfoximine, and sodium azide partly abrogated the RGC resistance to oxid

111 Sodium azide prevents HemA turnover in vivo, suggesting

112 ellular glucose or metabolic inhibition with sodium azide reduced the firing rate of a subpopulation

113 or energy depletion using 2-deoxy-D-glucose/sodium azide restored flutamide accumulation to that of

114 Treatment with sodium azide resulted in cell death in a dose-responsive

115 etitive inhibition, whereas, citric acid and sodium azide showed mixed inhibition of PPO activity.

116 modification reagents N-bromosuccinimide and sodium azide significantly inhibited POD-A activity.

117 ide is easily substituted by silver acetate, sodium azide, sodium iodide, and silver nitrate.

118 The method utilizes aqueous sodium azide solution as the azide source and can be per

119 duct studies for the reaction of 2 in dilute sodium azide solutions suggest that the tetrol-forming r

120 carbonyl cyanide m-chlorophenylhydrazone or sodium azide, suggesting that this initial translocation

121 by ascorbic acid and a peroxidase inhibitor, sodium azide, suggesting the potential role of phenoxyl

122 olled and regiocontrolled epoxide opening by sodium azide to form the 2-azido-3,4-dihydroxy alkanoate

123 m corticosterone, acted synergistically with sodium azide to inhibit cytochrome oxidase activity.

124 The addition of sodium azide to nitriles to give 1H-tetrazoles is shown

125 Addition of sodium azide to the medium to inhibit MPO prevented neut

126 raacetic acid (EGTA), or inhibitors, such as sodium azide, to compare the relative permeability of HD

127 To achieve this objective, a sodium azide-treated M(2)/M(3) population of barley cult

128 ion of o-alkynylaldehydes in the presence of sodium azide under mild reaction conditions is described

129 and boron-directed double ring-opening with sodium azide under Miyashita conditions.

130 yclopropane hemimalonates, when treated with sodium azide, undergo a tandem ring-opening decarboxylat

131 localized SYP121 and VAMP722 in response to sodium azide was detected in real-time.

132 The singlet oxygen quencher, sodium azide, was tested for its ability to reduce DNA d

133 d staurosporine and induction of necrosis by sodium azide were accompanied by an increase in the leve

134 ells depleted of ATP with 2-deoxyglucose and sodium azide were unable to properly regulate pH.

135 different injection intervals of a biocide (sodium azide) which allowed monitoring biofilm destabili

136 Sodium azide, which is an inhibitor of MPO, completely i

137 A depletion conditions or in the presence of sodium azide, which is known to inhibit SecA.

138 -pot three-component reaction of alkynes and sodium azide with organic halides or alpha-bromo ketones

139 UN3)4, have been synthesized by reduction of sodium azide with organometallic metallocene derivatives

140 exposure to the cytochrome oxidase inhibitor sodium azide, with near complete protection at 30 microM