ライフサイエンスコーパス: flumazenil

1 trazepam), negative (Ro15-4513), or neutral (flumazenil).

2 ta2gamma2 GABAA receptors was not blocked by flumazenil.

3 e, as did the benzodiazepine site antagonist flumazenil.

4 empiric administration of both naloxone and flumazenil.

5 g), and returned to control levels following flumazenil.

6 ; its effects are reversed by the antagonist flumazenil.

7 The sleep-inducing effect was blocked by flumazenil.

8 augmentation by diazepam which is blocked by flumazenil.

9 with the benzodiazepine receptor antagonist, flumazenil.

10 umazenil, and a full antagonism at 10 microM flumazenil.

11 dations, and adverse effects of naloxone and flumazenil.

12 The benzodiazepine antagonist flumazenil (0.1-10 microM) unexpectedly potentiated alph

13 behavior and CNS neurons were antagonized by flumazenil (10 mg/kg in vivo; 10 muM in vitro), the benz

14 Intraseptal infusion of the BDZ antagonist, flumazenil (10 nmol), enhanced the amplitude of the dent

15 itron emission tomography (PET) with [(11) C]flumazenil ([(11) C]FMZ), an antagonist of the central b

16 ancement produced by zolpidem was reduced by flumazenil (-31 +/- 13 %, relative to the AHP HW during

17 different amounts of isotopically unmodified flumazenil (4, 20, 100, or 400 mug) to cover a wide rang

18 The administration of flumazenil, a benzodiazepine (BZ) antagonist, is effecti

19 which functions upstream of Abp1, plus (iii) flumazenil, a benzodiazepine antagonist that binds to GA

20 Flumazenil, a benzodiazepine antagonist, blocked the dia

21 n at 10 pM was fully antagonised by 1 microM flumazenil, a benzodiazepine receptor antagonist.

22 The binding of [(11)C]flumazenil, a benzodiazepine-specific PET radiotracer, w

23 The transport of flumazenil across the blood-brain barrier and the bindin

24 -constant infusion method was used for (11)C-flumazenil administration.

25 This concentration of flumazenil also antagonised the decrease in firing rate

26 Intraseptal flumazenil also significantly enhanced the magnitude of

27 Although the density and affinity of [3H]flumazenil and [3H]imidazenil binding failed to change i

28 ant alpha4beta3delta receptors is blocked by flumazenil and beta-carboline-ethyl ester (beta-CCE).

29 ptors bind the imidazo-benzodiazepines (BZs) flumazenil and Ro15-4513 with high affinity (K(d) < 10 n

30 [3H]Ro15-4513 was displaced by Ro15-4513, flumazenil and Ro19-4603, but not by RU34347.

31 The relative potencies of flumazenil and zolpidem in blocking convulsions induced

32 sm of the peak effect was seen with 1 microM flumazenil, and a full antagonism at 10 microM flumazeni

33 hough the benzodiazepine ligands flurazepam, flumazenil, and methyl-6,7-dimethoxy-4 ethyl-beta-carbol

34 acid A-benzodiazepine receptor ligand, (11)C-flumazenil, and the reconstructed images were compared w

35 serious adverse events including the use of flumazenil, assisted ventilation, permanent injury or de

36 in P-glycoprotein (P-gp)-mediated efflux of flumazenil at the blood-brain barrier may confound inter

37 ioral alcohol antagonism of Ro15-4513 (i.e., flumazenil, beta-carbolinecarboxylate ethyl ester (beta-

38 sociation between decreases in cortical [11C]flumazenil binding and revised ALS functional rating sca

39 al association between reduced cortical [11C]flumazenil binding and the ALSFRS-R, rather than the UMN

40 D90A subjects, a small focus of reduced [11C]flumazenil binding at the left fronto-temporal junction

41 ons of cerebral cortex with disproportionate flumazenil binding compared with local grey matter volum

42 in the distribution of reduced cortical [11C]flumazenil binding in homD90A compared with sALS patient

43 included regions not found to have abnormal flumazenil binding on analysis of the PET data alone.

44 We hypothesized that (11)C-flumazenil binding potential (BPND) would be higher in i

45 Flumazenil binding was decreased in some MCDs with incre

46 m of the present study was to investigate if flumazenil blood-brain barrier transport and binding to

47 There was close agreement in (11)C-flumazenil BPND values between awake and anesthetized co

48 EtOH effect, and that Ro15-4513 differs from flumazenil by only a single group in the molecule (an az

49 Naloxone and flumazenil can be used as diagnostic as well as therapeu

50 The fact that only Ro15-4513, but not flumazenil, can inhibit the EtOH effect, and that Ro15-4

51 Flumazenil caused a modest increase in total sleep, and

52 In this subgroup, [(11)C]flumazenil DeltaVT in the medial temporal lobe was corre

53 roup but not the schizophrenia group, [(11)C]flumazenil DeltaVT was positively associated with gamma-

54 ocedure: after injection of 20 mCi of [(11)C]flumazenil, dynamic emission images of the brain were ac

55 In contrast, the promnestic BDZ ligand, flumazenil, enhances dentate granule cell responsivity,

56 itron emission tomography was used with [11C]flumazenil (FMZ) and [18F]fluorodeoxyglucose to study GA

57 hy (PET) study using the BZR antagonist [11C]flumazenil (FMZ) found two- to threefold greater cerebra

58 [11C]flumazenil (FMZ) imaged with PET allows the computation

59 [(11)C]Flumazenil (FMZ) PET images most subtypes of GABA(A) rec

60 [(11)C]Flumazenil (FMZ) PET images the majority of GABA(A) rece

61 Studies report that (11)C-flumazenil (FMZ) PET more specifically localizes the epi

62 sing statistical parametric mapping and [11C]flumazenil (FMZ) PET we have previously shown reduction

63 imaging was performed using the tracer [11C]flumazenil (FMZ), a ligand that binds to alpha subunits

64 ) perfusion and follow-up quantitative (11)C-flumazenil (FMZ)-PET to map SNL in the non-infarcted tis

65 10 nM flumazenil fully antagonised the second, declining, phas

66 Flumazenil given by itself had no significant effects on

67 At a dose of 0.76 microg, flumazenil had no effect on sleep when given alone, and

68 The GABA(A) receptor PET ligand [11C]flumazenil has demonstrated motor and extra-motor cortic

69 treatment increased brain concentrations of flumazenil in both groups, but B(max) estimates were not

70 vo positron emission tomography marker (11)C-flumazenil in humans.

71 Although the empiric use of naloxone and flumazenil in the comatose adult patient who presents to

72 Decreases in the binding of [11C]flumazenil in the sALS group were found within premotor

73 with the benzodiazepine receptor antagonist flumazenil, into the MPA.

74 ion with the benzodiazepine receptor blocker flumazenil, into the MPA.

75 raphy and the benzodiazepine receptor ligand flumazenil labeled with carbon 11 to assess the regional

76 The CGS 8216, but neither flumazenil nor ZK 93426, reliably reversed the RO19-4603

77 but not by microinjection of 5 micrograms of flumazenil or 200 ng of PK 11195.

78 barrier may confound interpretation of (11)C-flumazenil PET in epilepsy.

79 sALS) and 10 homD90A patients underwent [11C]flumazenil PET of the brain.

80 total, 29 rats underwent 2 consecutive (11)C-flumazenil PET scans, each one lasting 30 min.

81 Previous MRI and [11C]flumazenil PET studies have demonstrated widespread stru

82 In this study, we used [11C]flumazenil PET to explore differences in the pattern of

83 of neuronal integrity measured with [(18)F] flumazenil PET.

84 Using [11C]flumazenil-PET and statistical parametric mapping (SPM),

85 normal control high-resolution MRI and [11C]flumazenil-PET image using a novel technique.

86 obe the right or left hemisphere), and (11)C-flumazenil positron emission tomography generating bindi

87 Acute/subacute flumazenil positron emission tomography studies are bein

88 By using [11C]flumazenil-positron emission tomography ([11C]FMZ-PET),

89 on of the benzodiazepine receptor antagonist flumazenil, resulted in a dose-dependent recovery of sup

90 Positron emission tomography with [11C]flumazenil revealed normal benzodiazepine receptor distr

91 This anticonflict effect is blocked by flumazenil (Ro 15-1788), indicating that like benzodiaze

92 nce of flurazepam or the BZD-site antagonist flumazenil (Ro15-1788) decreased the rate of modificatio

93 s were not influenced, suggesting that (11)C-flumazenil scanning is not confounded by alterations in

94 e ligands, detected as an increase in [(11)C]flumazenil tissue distribution volume (VT).

95 up-regulated; and (iii) the binding of [(3)H]flumazenil to hippocampal synaptic membranes is decrease

96 ed the benzodiazepine GABA(A) marker [(11)C] flumazenil to study cerebral dysfunction in amyotrophic

97 There was no difference in flumazenil transport across the blood-brain barrier betw

98 Tariquidar treatment also decreased flumazenil transport out of the brain by 73%, increased

99 e A (GABAA)-benzodiazepine radiotracer (11)C-flumazenil under anesthetized and awake conditions.

100 esence of amitriptyline that is increased by flumazenil, unlike augmentation by diazepam which is blo

101 We calculated [(11)C]flumazenil volume of distribution ([(11)C]FMZ-V(d)) afte

102 were derived to localize changes in regional flumazenil volumes of distribution (FMZVD), which correl

103 with positive symptoms, and baseline [(11)C]flumazenil VT in the medial temporal lobe was negatively

104 [(11)C]Flumazenil VT was significantly increased across all cor

105 tion in the blood-brain barrier transport of flumazenil was observed.

106 with the benzodiazepine receptor antagonist flumazenil, which has no effects on membrane fluidity or

107 ombination with the BDZ receptor antagonists flumazenil, ZK 93426, and CGS 8216 (20 mg/kg) in selecti