ライフサイエンスコーパス: sodium cyanide

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.

5 ors were activated with aortic injections of sodium cyanide (0.025 %, 25-75 microl).

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

9 n are completely reversed by the addition of sodium cyanide and can be degraded by proteinase K.

10 olidine ring in the presence of selectfluor, sodium cyanide, and 1,2 aminothiols.

11 ole group in 2 and 6 with Grignard reagents, sodium cyanide, and sodium borohydride gave 1,2,3,4-tetr

12 egically incorporating sodium hydroxide with sodium cyanide as supporting electrolytes, our study dem

13 hione peroxidase activity in the presence of sodium cyanide but had no effect on catalase or glutathi

14 2-ene-1,8-diol formed the THC 7a which, with sodium cyanide/DMSO, gave 1b.

15 of the supernatant with phosphate buffer and sodium cyanide for derivatization in alkaline conditions

16 n amino acids or buffers were incubated with sodium cyanide in aqueous solution at pH 7.4, hydrogen c

17 poptosis, we exposed human Jurkat T cells to sodium cyanide in the presence or absence of iNOS inhibi

18 Sodium cyanide-induced chemical hypoxia triggers a serie

19 However, although sodium cyanide-induced ventilatory responses were virtua

20 cantly protected hippocampal neurons against sodium cyanide insult and the subsequent lipid peroxidat

21 on ROS accumulation after exposure to either sodium cyanide, kainic acid or oxygen glucose deprivatio

22 Removal of this "excess" gold by sodium cyanide leaching leaves the activity intact and t

23 Y5Y human neuroblastoma cells, we found that sodium cyanide (NaCN) up to a concentration of 10 mM had

24 episodes of either the metabolic inhibitor, sodium cyanide (NaCN), or the mitoK(ATP) channel opener,

25 Microinjection of sodium cyanide (NaCN; 150-450 pmol) into the RVL rapidly

26 ry responses to hypoxia (P <0.05) and venous sodium cyanide (NaCN; P<0.05), while sham CBD had no eff

27 emoreceptor stimulation (hypoxia and/or i.v. sodium cyanide, NaCN).

28 Hippocampal slices were challenged with sodium cyanide or kainic acid.

29 ntional inhibitors of the respiratory chain, sodium cyanide or sodium azide, neither induced ROS nor

30 ivity (infiltration with sodium vanadate and sodium cyanide; plant exposure to carbon monoxide) can r

31 Sodium cyanide promoted the facile, intramolecular cycli

32 with intracarotid administration of 100 nmol sodium cyanide rapidly excited the spinal cord-projectin

33 Treatment of the adduct with sodium cyanide regenerates TpT.

34 lysis of the products of their reaction with sodium cyanide, sodium borohydride, and methoxylamine an

35 current dependent and could be stimulated by sodium cyanide to activate this persistent sodium curren

36 Here we employed sodium cyanide to probe the metal-ligand exchange of the

37 Vitamin B12 was extracted in the presence of sodium cyanide, to transform all forms of cobalamin into

38 ers by direct reaction of cyclopropanes with sodium cyanide under typical S(N)2 conditions led to the

39 pparent cyanide resistance revealed that the sodium cyanide was being rapidly depleted from the cell

40 sponse to stimulation of chemoreceptors with sodium cyanide was markedly enhanced in the still normot

41 mulation of the carotid and aortic bodies by sodium cyanide were studied in the anaesthetized cat.

42 he carotid and aortic body chemoreceptors by sodium cyanide, were studied in the cat anaesthetized wi