ライフサイエンスコーパス: procainamide

1 T by up to 400% (P<0.001 versus baseline and procainamide).

2 provocative drug testing with epinephrine or procainamide.

3 shortening of cycle length were enhanced by procainamide.

4 similar to that caused by cells treated with procainamide.

5 nd in T cells treated with 5-azacytidine and procainamide.

6 ngth (CL) less (16% versus 26%, P<.001) than procainamide.

7 nsion was the major adverse effect seen with procainamide.

8 soproterenol infusion, and after intravenous procainamide.

9 VF were 345 ms at baseline and 380 ms after procainamide.

10 he effect of intravenous ajmaline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the

11 d administration of verapamil (17 patients), procainamide (10 patients), or saline (20 patients).

12 ody weight per min) shortened (p < 0.05) and procainamide (15 mg/kg, then 2 mg/min) prolonged (p < 0.

13 to 200 Hz at baseline and after addition of procainamide (20 micromol/L) or propafenone (1 micromol/

14 had a significantly higher success rate than procainamide (51% [22 of 43] vs. 21% [8 of 38], p=0.005)

15 had a significantly higher success rate than procainamide (76% [13 of 17] vs. 14% [3 of 22], p=0.001)

16 We report here that the drug procainamide, a nonnucleoside inhibitor of DNA methyltra

17 seline and 4.45+/-1.80 s(-1) x cm(-2) during procainamide administration (P<.001).

18 e up more frequently at baseline than during procainamide administration.

19 ar tachyarrhythmias refractory to lidocaine, procainamide and bretylium were randomized to receive on

20 with a 70% decrease in VF inducibility with procainamide and elimination of VF with propafenone.

21 Procainamide and hydralazine are drugs that cause lupus

22 pigenetic DNA modification, is implicated in procainamide and hydralazine induced lupus, as well as i

23 expressed on CD4(+) lupus T cells as well as procainamide and hydralazine treated T cells, and contri

24 th Dnmt and ERK pathway inhibitors including procainamide and hydralazine.

25 tages, only correction of fever and combined procainamide and hypothermia appeared to be efficacious.

26 procainamide or hypothermia; and 7) combined procainamide and hypothermia.

27 A side effect of therapy with procainamide and numerous other medications is a lupus-l

28 Long-term treatment with procainamide and numerous other medications is occasiona

29 During steady-state pacing, procainamide and propafenone prolonged APD90 by 12% and

30 hyltransferase inhibitors (5-azacytidine and procainamide) and 3 ERK pathway inhibitors known to decr

31 h as chloroquine, haloperidol, erythromycin, procainamide, and ofloxacin known to activate T2Rs.

32 The conversion rates in AFL with ibutilide, procainamide, and placebo were 64% (29 of 45 patients),

33 Seven patients who received procainamide became hypotensive.

34 In TG(N488I) mice with pre-excitation, procainamide blocked bypass tract conduction, whereas ad

35 Wavelength was not changed significantly by procainamide but was shortened fourfold by propafenone a

36 Procainamide decreases the number of wavelets during VF

37 procainamide-hydroxylamine, a metabolite of procainamide, develop autoimmune features resembling dru

38 trial flutter has a fully excitable gap, and procainamide does not convert the gap from full to parti

39 educe the slope of the restitution relation (procainamide) does not prevent the induction of VF, nor

40 n (APD) during VF and that its prevention by procainamide eliminates spontaneous wave break.

41 f the specificity of procainamide for DNMT1, procainamide failed to lower genomic 5-methyl-2'-deoxycy

42 the efficacy and safety of ibutilide versus procainamide for conversion of recent-onset atrial flutt

43 As further evidence of the specificity of procainamide for DNMT1, procainamide failed to lower gen

44 All animals in the procainamide group developed either second-degree or com

45 group compared with 11 (18.3%) of 60 in the procainamide group had successful termination within 1.5

46 t shortening of the first post-AF ERP in the procainamide group.

47 tic peak corresponding to [GlcNAc + Fucose + Procainamide + H](+) in the tandem MS data of fucosylate

48 Procainamide has been shown to inhibit DNA methyltransfe

49 ally when other agents such as lidocaine and procainamide have not been effective.

50 Specifically, procainamide HCl is loaded into the pores of bio-MOF-1 u

51 T cells treated with procainamide, hydralazine, and other Dnmt and ERK pathwa

52 Some of these agents, such as procainamide, hydralazine, and UV-light inhibit T cell D

53 ore the influence of labeling N-glycans with procainamide hydrochloride to inhibit fucose migration d

54 successive 10-min IV infusions of 400 mg of procainamide hydrochloride.

55 Two intrathymic injections of procainamide-hydroxylamine (PAHA), a reactive metabolite

56 Two intrathymic injections of procainamide-hydroxylamine (PAHA), a reactive metabolite

57 ggest that prevention of anergy induction by procainamide-hydroxylamine may also take place in vivo d

58 Mice injected in the thymus with procainamide-hydroxylamine, a metabolite of procainamide

59 anergy induction required 2 h of exposure to procainamide-hydroxylamine, and this state remained for

60 Addition of procainamide-hydroxylamine, but not procainamide or its

61 ndergo positive selection in the presence of procainamide-hydroxylamine, they fail to establish unres

62 1 Brugada pattern was induced by intravenous procainamide in 3 of 4.

63 nversion efficacy of ibutilide compared with procainamide in AFL is correlated with a relatively grea

64 y, with emphasis on combined hypothermia and procainamide in difficult cases, appears to be an effect

65 effects of ibutilide with the class IA agent procainamide in humans during AFL and AF.

66 In AF, ibutilide and procainamide induced similar increases in atrial CL (48%

67 ation were registered at baseline and during procainamide infusion (serum concentration, 9.3+/-1.9 mi

68 In an additional 6 RVs, procainamide infusion converted VF to VT.

69 ms, and 51+/-16 mm, respectively, and during procainamide infusion, values became 125+/-11 ms (P<.001

70 seline and in 6 of the 100 runs of VF during procainamide infusion.

71 Procainamide infusions did not identify additional affec

72 droxylamine (PAHA), a reactive metabolite of procainamide, into (C57BL/6 x DBA/2)F1 mice resulted in

73 Procainamide is a competitive DNA methyltransferase (Dnm

74 Procainamide is commonly used for conversion of recent-o

75 Therapeutic treatment with procainamide is occasionally associated with the develop

76 pamil, but not the sodium channel antagonist procainamide, markedly attenuates acute, AF-induced chan

77 th epigenetic alterations in carcinogenesis, procainamide may be a useful drug in the prevention of c

78 s studied after the administration of either procainamide (n = 3) or quinidine (n = 3).

79 e-blinded comparative studies or intravenous procainamide (n=53) in a concurrent open-label study.

80 However, the effects of procainamide on the characteristics of activation waves

81 was to determine the effect of verapamil and procainamide on these manifestations of AF-induced elect

82 The effects of propafenone and procainamide on these parameters, and their antiarrhythm

83 5) phenytoin or propranolol or verapamil; 6) procainamide or hypothermia; and 7) combined procainamid

84 ition of procainamide-hydroxylamine, but not procainamide or its further oxidation products during an

85 T cell clones was used to determine whether procainamide or one of its metabolites could prevent dev

86 e length and refractory periods prolonged on procainamide or quinidine, but no tachyarrhythmias could

87 Ajmaline, procainamide, or flecainide administration resulted in S

88 Procainamide (PA) at 10 microgram/mL decreased the numbe

89 ents compared with 90% and 80% of saline and procainamide patients (P<.01 versus verapamil).

90 This study compared the effects of procainamide (Pca) and hydralazine (Hyd) with those of s

91 n with mass spectrometry (HILIC-UHPLC-MS) of procainamide (PROC) labeled N-glycans were the analytica

92 Ibutilide shortened and procainamide prolonged action potential diastolic interv

93 on of Dnmt catalytic activity with RG108 and procainamide protected cultured neurons from excessive D

94 The use of prophylactic beta-blockers and procainamide reduces the incidence of AF whereas digoxin

95 droxylamine (PAHA), a reactive metabolite of procainamide, resulted in prompt production of IgM antid

96 ide such that their effects are enhanced and procainamide's effects are diminished.

97 Procainamide's prolongation of action potential duration

98 Procainamide's prolongation of action potential duration

99 This includes procainamide-sensitive, adenosine-resistant accessory pa

100 By doing so, procainamide significantly decreased the processivity of

101 Procainamide slowed mean CT by 40% during S2-S5 pacing,

102 We report here that procainamide specifically inhibits the hemimethylase act

103 Adenosine and isoproterenol interact with procainamide such that their effects are enhanced and pr

104 Ibutilide increased MAPD/CL ratio, whereas procainamide tended to decrease this ratio (13% versus -

105 ive conduction disease, a low sensitivity to procainamide testing, and a relatively good prognosis in

106 nel blockers such as flecainide, ajmaline or procainamide, thus identifying patients at risk.

107 duced by injecting male and female mice with procainamide-treated T cell clones.

108 At micromolar concentrations, procainamide was found to be a partial competitive inhib

109 Procainamide was not a potent inhibitor of the de novo m

110 shes the superior efficacy of ibutilide over procainamide when administered to patients to convert ei

111 s at baseline and >380 ms in the presence of procainamide would have been required to avoid VF.