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1 sodium azide and sodium arsenate but not by sodium cyanide.
2 purifying brain endothelial cells with 10 mM sodium cyanide.
3 moreceptors by a close arterial injection of sodium cyanide.
4 ardiovascular responses to i.v. injection of sodium cyanide.
6 in the presence of the complex IV inhibitor sodium cyanide (3 mM) was significantly greater when it
7 roup with C-nucleophiles (Grignard reagents, sodium cyanide), an S-nucleophile (benzenethiol), and a
8 f a range of aryl-aldehydes to a solution of sodium cyanide and (S)-1-(4-methoxyphenyl)ethylamine aff
10 ole group in 2 and 6 with Grignard reagents, sodium cyanide, and sodium borohydride gave 1,2,3,4-tetr
11 hione peroxidase activity in the presence of sodium cyanide but had no effect on catalase or glutathi
13 of the supernatant with phosphate buffer and sodium cyanide for derivatization in alkaline conditions
14 n amino acids or buffers were incubated with sodium cyanide in aqueous solution at pH 7.4, hydrogen c
15 poptosis, we exposed human Jurkat T cells to sodium cyanide in the presence or absence of iNOS inhibi
18 cantly protected hippocampal neurons against sodium cyanide insult and the subsequent lipid peroxidat
19 on ROS accumulation after exposure to either sodium cyanide, kainic acid or oxygen glucose deprivatio
21 Y5Y human neuroblastoma cells, we found that sodium cyanide (NaCN) up to a concentration of 10 mM had
22 episodes of either the metabolic inhibitor, sodium cyanide (NaCN), or the mitoK(ATP) channel opener,
24 ry responses to hypoxia (P <0.05) and venous sodium cyanide (NaCN; P<0.05), while sham CBD had no eff
27 ntional inhibitors of the respiratory chain, sodium cyanide or sodium azide, neither induced ROS nor
29 with intracarotid administration of 100 nmol sodium cyanide rapidly excited the spinal cord-projectin
31 lysis of the products of their reaction with sodium cyanide, sodium borohydride, and methoxylamine an
32 current dependent and could be stimulated by sodium cyanide to activate this persistent sodium curren
34 Vitamin B12 was extracted in the presence of sodium cyanide, to transform all forms of cobalamin into
35 pparent cyanide resistance revealed that the sodium cyanide was being rapidly depleted from the cell
36 sponse to stimulation of chemoreceptors with sodium cyanide was markedly enhanced in the still normot
37 mulation of the carotid and aortic bodies by sodium cyanide were studied in the anaesthetized cat.
38 he carotid and aortic body chemoreceptors by sodium cyanide, were studied in the cat anaesthetized wi
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