ライフサイエンスコーパス: KCN

1 KCN had no effect on endothelial cell ATP content or bar

2 KCN titration assays, carried out on intact uncoupled ce

3 me from the reaction mixture of HRP/H(2)O(2)/KCN was unambiguously identified as cyanoheme by the obs

4 ondrial function with rotenone, antimycin A, KCN, carbonylcyanide-m-chlorophenylhydrazone, or oligomy

5 sion injury (pH paradox) was prevented after KCN washout at pH 6.2.

6 E2 was ineffective against KCN and oligomycin-induced cell death.

7 were inhibited by flavone, antimycin A, and KCN but not by rotenone.

8 n added to SMP pretreated with ascorbate and KCN to reduce the high potential components (iron-sulfur

9 Both 3-NPA and KCN (10 microM-1 mM) reduced neuronal viability in a con

10 urbations (confluence, serum starvation, and KCN treatment) are all expected to result in an increase

11 yanide p-trifluoromethoxyphenylhydrazone and KCN.

12 rial inhibitors, rotenone, 3-NPA, antimycin, KCN, and oligomycin, exhibited concentration dependent t

13 There was no association between KCN and allergic rhinitis, mitral valve disorder, aortic

14 nfluence the extent of cell death induced by KCN/2-DG.

15 O(2) uptake that was completely inhibited by KCN and antimycin A.

16 insensitive to piericidin A but inhibited by KCN.

17 Labeling experiments with [(1)(3)C]KCN demonstrated that the altered CN tolerance could be

18 tively from the readily available [(13/14)C]-KCN.

19 Inhibition of mitochondria with CCCP, KCN, or rotenone blocked intracellular ATP production, A

20 ion stoichiometry and the potassium cyanide (KCN) induced cleavage of the protein suggested that all

21 Potassium cyanide (KCN) treatment and serum starvation of cells yielded sim

22 of cytochrome c oxidase, potassium cyanide (KCN), should compete with LED and reduce its beneficial

23 ropionic acid (3-NPA) and potassium cyanide (KCN), with the production of reactive molecular species

24 imycin A, and 1 and 10 mM potassium cyanide (KCN).

25 he effects of gaseous NO, potassium cyanide (KCN, a mitochondrial respiratory chain inhibitor) and io

26 were designed to avoid the rather dangerous KCN treatment step for the removal of conductive minor p

27 ic acid or potassium cyanide/2-deoxyglucose (KCN/2-DG) for varying lengths of time, and cell death wa

28 2 +/- 0.8; fed + KCN, 32.1 +/- 0.9; fasted + KCN, 0.2 +/- 0.2 micromol x g(-1) x h(-1).

29 ed, 15.1 +/- 2.4; fasted, 4.2 +/- 0.8; fed + KCN, 32.1 +/- 0.9; fasted + KCN, 0.2 +/- 0.2 micromol x

30 of a chiral cyanide ion source, derived from KCN and quaternary ammonium bromide derived from cinchon

31 ge 14.4 years), 4 (1.32%) were found to have KCN, and 4 (1.32%) were KC suspects.

32 nd-organ damage had 52% lower odds of having KCN (adjusted OR, 0.48; 95% CI, 0.40-0.58; P < 0.001) co

33 However, KCN had no effect on total pimonidazole adducts detected

34 ty is energy dependent: it did not happen in KCN-treated cells.

35 , sociodemographic factors, and keratoconus (KCN) among a large, diverse group of insured individuals

36 l and topographical evaluation: the manifest KCN group (n = 30), the subclinical KCN group (n = 32),

37 atistically higher in patients with manifest KCN, subclinical KCN, and topographically normal KCN rel

38 tored neuronal ATP content only at 10 microm KCN but not at higher concentrations of KCN tested.

39 y of LED during exposure to 10 or 100 microm KCN but did not restore enzyme activity to control level

40 red enzyme activity blocked by 10-100 microm KCN.

41 ed neuronal cell death induced by 300 microm KCN from 83.6 to 43.5%.

42 ubation with either N2, antimycin A, or 1 mM KCN in comparison with their appearance under oxygenated

43 s impaired (as with N2, antimycin A, or 1 mM KCN) photoreceptor cells are resistant to short-term epi

44 e presence of N2, 0.01 mM antimycin, or 1 mM KCN, lactic acid production was linear throughout the 60

45 bations with either N2, antimycin A, or 1 mM KCN.

46 We found that exposure to 1 mM KCN/2 mM 2-DG for 2 h produced consistent delayed cell d

47 With 10 mM KCN (pH 8.9), retinal lactate production was severely de

48 The deleterious effects of 10 mM KCN on these parameters were lessened to varying degrees

49 In contrast, use of 10 mM KCN produced an entirely different set of results.

50 olated rat retinas to media containing 10 mM KCN results from the inhibition of both respiration and

51 upted after incubation of retinas with 10 mM KCN.

52 However, at 1-100 mm KCN, the protective effects of LED decreased, and neuron

53 ion at 0 degreesC or in the presence of 2 mM KCN abolished high-affinity iron uptake, suggesting that

54 subclinical KCN, and topographically normal KCN relatives compared with controls.

55 Upon addition of KCN to Cu-grown cells, the brownish coloration was bleac

56 scence increase in darkness upon addition of KCN, was much less in DeltandhD1/D2 and M55 than in Delt

57 ne pH (8.9) found when this concentration of KCN was simply added to bicarbonate-buffered media and a

58 and glycolysis by this high concentration of KCN.

59 crom KCN but not at higher concentrations of KCN tested.

60 The large number of KCN genes for potassium channel subunits and the heterog

61 lagen vascular disease had 35% lower odds of KCN (adjusted OR, 0.65; 95% CI, 0.47-0.91; P = 0.01).

62 diabetes mellitus (DM) had 20% lower odds of KCN (adjusted OR, 0.80; 95% CI, 0.71-0.90; P = 0.002), a

63 r conditions found to have increased odds of KCN included sleep apnea (adjusted OR, 1.13; 95% CI, 1.0

64 rtain systemic diseases affected the odds of KCN.

65 oquinone pool in darkness in the presence of KCN was up to fivefold slower in the mutants than in the

66 In the presence of KCN, leaf tissue of either mutant or wild-type AOX overe

67 ealth with a control group with no record of KCN.

68 Patients with DM have lower risk of KCN, potentially because of corneal glycosylation.

69 Herein, stocks of KCN and NaCN were analyzed for trace anions by high perf

70 estored to pH 7.4 with or without washout of KCN (simulated reperfusion).

71 no protective effect at all against 3-NPA or KCN toxicity at concentrations up to 1 mM.

72 Similarly, KCN titration assays on digitonin-permeabilized cells ha

73 , and 200 mg/kg/day) inhibited growth of SMS-KCN-69n tumor xenografts in a dose-dependent fashion, wi

74 The addition of small amounts of solid KCN to solution and solid-phase esters in THF/MeOH/50% a

75 r in patients with manifest KCN, subclinical KCN, and topographically normal KCN relatives compared w

76 manifest KCN group (n = 30), the subclinical KCN group (n = 32), the KCN relatives group (n = 53), an

77 ng alternative sources of cyanide other than KCN/HCN or TMSCN for this important reaction.

78 30), the subclinical KCN group (n = 32), the KCN relatives group (n = 53), and the control group (n =

79 fully consistent with those obtained in the KCN titration experiments.

80 A study of the influence of water on the KCN-catalyzed cross silyl benzoin addition revealed more

81 eta,gamma,delta-unsaturated acylsilanes with KCN under phase-transfer catalyst conditions using n-Bu4

82 ing the mitochondrial respiratory chain with KCN decreased protein-bound pimonidazole adducts.

83 When the receiving arm is charged with KCN, transport is much faster (ca. 100 h) and higher K2M

84 .50-0.75; P < 0.001) of being diagnosed with KCN compared with whites.

85 .26-1.62; P < 0.001) of being diagnosed with KCN compared with whites.

86 anolysis of the DTNB-inactivated enzyme with KCN led to the elimination of 2 equiv of 5-thio-2-nitrob

87 elial cells exposed to chemical hypoxia with KCN (2.5 mmol/L) to simulate the adenosine triphosphate

88 ere obtained when SMP were treated only with KCN or NaN(3), reagents that inhibit cytochrome oxidase,

89 ol (or MOA-stilbene or stigmatellin) or with KCN and ascorbate to reduce the high potential centers o

90 Sixteen thousand fifty-three patients with KCN were matched 1:1 with persons without KCN.

91 Clinicians caring for persons with KCN should inquire about breathing or sleeping and, when

92 Persons with KCN were identified using billing codes and matched by a

93 Imines were reacted with KCN/NH(4)Cl in aqueous ethanol to produce alpha-arylamin

94 ansformed, but not overexpressor, roots with KCN treatment.

95 c oxidase, and wild type cells treated with KCN (a cytochrome c oxidase inhibitor).

96 th KCN were matched 1:1 with persons without KCN.