ライフサイエンスコーパス: ondansetron

1 with a two-drug regimen of dexamethasone and ondansetron.

2 lled in the trial received dexamethasone and ondansetron.

3 ydroxytryptamine receptor antagonist such as ondansetron.

4 f blocking the excitatory 5HT3 receptor with ondansetron.

5 iness and abnormal vision were reported with ondansetron.

6 anges were recorded with both dolasetron and ondansetron.

7 g/kg dolasetron base, respectively) or 32 mg ondansetron.

8 ea with either dolasetron dose compared with ondansetron.

9 local coherence only in participants taking ondansetron.

10 modulated by the 5-HT(3) receptor antagonist ondansetron.

11 ered intravenous fluids did not receive oral ondansetron.

12 ng alcoholics receiving the 5-HT3 antagonist ondansetron.

13 e function and binding of 5-HT3 receptors to ondansetron.

14 come of treatment of alcohol dependence with ondansetron.

15 s blocked with the 5-HT3-receptor antagonist ondansetron.

16 charge, but this effect was not inhibited by ondansetron.

17 competitive 'setron' antagonists typified by ondansetron.

18 response to the 5-HT(3) receptor antagonist, ondansetron.

19 l injection of the 5-HT3 receptor antagonist ondansetron.

20 ed by capsaicin pretreatment, and blunted by ondansetron.

21 ganglia with the 5-HT(3) receptor antagonist ondansetron (0.4 microm) alone completely and irreversib

22 ean log CDT ratio between those who received ondansetron (1 and 4 microg/kg twice per day) compared w

23 hypothesis, we counted Fos-LI in the DVC of ondansetron (1 mg/kg; 5-HT3 receptor antagonist) and veh

24 Intrathecal ondansetron (1, 3, 10, 30, and 100microg) produced no ef

25 nts with early-onset alcoholism who received ondansetron (1, 4, and 16 microg/kg twice per day) compa

26 Ondansetron (1.0 and 2.0 microg/100 nl) delivered into t

27 signed to receive 11 weeks of treatment with ondansetron, 1 microg/kg (n = 67), 4 microg/kg (n = 77),

28 tigated the effects of spinally administered ondansetron (10, 50 and 100 microg) on the responses of

29 ourth ventricular (i.c.v.) administration of ondansetron (10.0 microg/3.0 microl) significantly atten

30 66 patients were included: 37 had parenteral ondansetron, 14 were treated with traditional therapy, a

31 83); however, the proportion was higher with ondansetron (16/111) than with placebo (6/111; 3.30, 1.0

32 , patients were randomly assigned placebo or ondansetron (24 mg daily) for a further 4 weeks.

33 n, of whom 534 of 1846 (28.9%) received oral ondansetron, 240 of 1846 (13.0%) received intravenous re

34 1 hour before chemotherapy (n = 534) or i.v. ondansetron (32 mg) 30 minutes before chemotherapy (n =

35 l antiemetic control when compared with i.v. ondansetron (32 mg) in patients who received highly emet

36 Single-dose oral granisetron (2 mg) and I.V. ondansetron (32 mg) resulted in equivalent levels of tot

37 lent levels of antiemetic protection as I.V. ondansetron (32 mg).

38 ere 283 European Americans who received oral ondansetron (4 mg/kg of body weight twice daily) or plac

39 Participants received either ondansetron (4 mug/kg twice daily) or placebo for 11 wee

40 Ondansetron, 4 microg/kg twice per day, was superior to

41 dramine (10 mg/kg), hyoscine (21 mg/kg), and ondansetron (5 mg/kg) were administered orally as positi

42 served in hexamethonium, but were blocked by ondansetron (5-HT(3) antagonist), suggesting Dogiel Type

43 ingle-dose oral granisetron (54.7%) and i.v. ondansetron (58.3%) (95% confidence interval [CI], -9.6

44 th recent clinical trials demonstrating that ondansetron, a 5-HT(3) receptor (5-HT(3)R) antagonist, a

45 M 5-HT and this response is blocked by 1 muM ondansetron, a 5-HT3 antagonist, and mimicked by applica

46 disease modeling by exploring the effects of ondansetron, a drug administered to pregnant women and a

47 One exception was found, ondansetron, a drug without previously identified life-s

48 iously shown that systemic administration of ondansetron, a selective serotonin type-3 (5-HT3) recept

49 sk of adverse fetal outcomes associated with ondansetron administered during pregnancy.

50 nal 5-HT(3) serotonin receptors, intrathecal ondansetron administration after TBI dose-dependently at

51 Acute ondansetron administration at the lowest dose (0.1 mg/kg

52 Ondansetron administration attenuated DVC Fos-LI by CCK

53 Furthermore, ondansetron administration attenuated the overall DVC en

54 Strategies focusing on oral ondansetron administration followed by oral rehydration

55 In the GMH cohort (N = 363), ondansetron administration was associated with increased

56 The presence or absence of oral ondansetron administration was identified for each patie

57 eritis-associated vomiting, the provision of ondansetron after an emergency department visit led to l

58 d of acute-phase complete CIV control versus ondansetron alone (RR, 1.28; 95% CI, 1.09 to 1.50).

59 Ondansetron alone had no effect on sucrose intake at any

60 e improvement in auditory gating produced by ondansetron alone.

61 Ondansetron also conferred no significantly increased ri

62 , methylphenidate, sertraline hydrochloride, ondansetron, amitriptyline, and melatonin were the only

63 Ondansetron, an antiemetic with known QT-prolonging pote

64 GR113808A) or 5-HT(3)-selective antagonists (ondansetron and 0.3 microM tropisetron).

65 dy, 27 were assigned to receive 24 mg/day of ondansetron and 24 to receive placebo.

66 9,254 study patients, 64,978 (55%) initiated ondansetron and 54,276 (45%) initiated a comparator anti

67 4) or an aprepitant regimen (aprepitant plus ondansetron and dexamethasone on day 1; aprepitant and d

68 rst time were given either standard therapy (ondansetron and dexamethasone on day 1; dexamethasone on

69 rokinin-1 receptor antagonist (NK1RA), to an ondansetron and dexamethasone regimen improves preventio

70 n >/= 70 mg/m(2) for the first time received ondansetron and dexamethasone with a standard aprepitant

71 Given with ondansetron and dexamethasone, single-dose intravenous f

72 as compared in cases who received parenteral ondansetron and in cases who received traditional therap

73 t blocked by the 5-HT(3) receptor antagonist ondansetron and mimicked by the 5-HT(3) receptor agonist

74 mulation of vagal afferent fibres, and since ondansetron and other 5-HT3 antagonists decrease afferen

75 human studies that evaluated the effects of ondansetron and other 5HT3 receptor antagonists on senso

76 ), 16-mg (n = 17), or 24-mg (n = 18) dose of ondansetron and placebo before MRI scanning on separate

77 significant overall mean difference between ondansetron and placebo in drinks per drinking day (22.5

78 here were no significant differences between ondansetron and placebo in the reduction of SP or overal

79 e role of adjunctive therapies, particularly ondansetron and probiotics in improving AGE outcomes.

80 Ondansetron and probiotics may improve patient outcomes

81 s between first-trimester use of intravenous ondansetron and risk of cardiac malformations and oral c

82 ancies in Denmark, women who were exposed to ondansetron and those who were not exposed were included

83 t and robust finding (five studies) was that ondansetron and tropisetron (5HT3 antagonist and alpha7-

84 907 (7.9%) of 163 810 pregnancies exposed to ondansetron, and 17 476 (5.7%) of 306 766 pregnancies ex

85 ngth 5-HT(3A)R in complex with palonosetron, ondansetron, and alosetron.

86 All participants received aprepitant, ondansetron, and dexamethasone during and 2 days after c

87 against postoperative vomiting compared with ondansetron, and the same appears to be true for other d

88 Other agents such as ramosetron and ondansetron are still in use and have not been associate

89 The 5-HT(3) antagonists, granisetron and ondansetron, are useful in combating the nausea associat

90 Likewise, ondansetron attenuated Fos-LI by gastric distension in t

91 ctivation of vagal afferents inhibited using ondansetron, before repeating experiments using water or

92 ta-erythroidine, with the 0.33 mg/kg dose of ondansetron blocked the improvement in auditory gating p

93 Ondansetron by itself was similar to naltrexone and the

94 tation with the aid of an antiemetic such as ondansetron can be as effective and efficient as intrave

95 tion of nicotinic acetylcholine receptors by ondansetron can improve auditory gating parameters in DB

96 iven by a robust reduction in activation for ondansetron compared to placebo for the 24-mg group, wit

97 to test the effects of 4 weeks of high-dose ondansetron compared to placebo on SP severity and brain

98 001), and in 45 of 109 patients who received ondansetron compared with 65 of 108 allocated placebo (0

99 Nineteen percentage of children treated with ondansetron continued vomiting after the administration

100 trexone with (P = .02) or without (P = .049) ondansetron decreased alcohol cue-induced activation of

101 s whether a three-drug antiemetic regimen of ondansetron, dexamethasone, and the neurokinin-1-recepto

102 However, in the presence of CO, ondansetron did not block LTP.

103 uding dexamethasone, digoxin, cyclosporin A, ondansetron, domperidone, and loperamide.

104 Exposure to ondansetron during pregnancy was compared with exposure

105 e, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) either in combination with selective seroto

106 hort study, there was no association between ondansetron exposure during pregnancy and increased risk

107 67-1.23) for fetal death with time-dependent ondansetron exposure during pregnancy, 0.82 (95% CI, 0.6

108 ever, Clinical Dehydration Scale score, oral ondansetron followed by oral rehydration therapy, and in

109 world evidence to support clinical trials of ondansetron for treatment of AKI.

110 r mild symptoms), pyridoxine-doxylamine, and ondansetron (for moderate symptoms) were associated with

111 Combined with Ondansetron, GRASP led to an even greater attenuation of

112 ree in the granisetron group (55.4%) and the ondansetron group (59%) (95% CI, -9.6 to 2.4).

113 2% in the granisetron group and 67.1% in the ondansetron group (95% CI, -11.7 to -0.1).

114 cebo group, versus 6.5 per week (3.9) in the ondansetron group (estimated difference 6.8 [95% CI 4.0-

115 , trend in vomiting scores was better in the ondansetron group (P = .042).

116 LL individuals in the ondansetron group also had a lower number of drinks per

117 The ondansetron group also showed significant improvement, c

118 cipants for whom data were available) in the ondansetron group and 12.5% (55 of 441) in the placebo g

119 cebo, and 14 ondansetron; one patient in the ondansetron group dropped out owing to accidental injury

120 LL/TT individuals in the ondansetron group had a lower number of drinks per drink

121 ng episodes without vomiting per week in the ondansetron group, compared with 0.2 in the placebo grou

122 ecreased on average by 7.6 h per week in the ondansetron group, compared with 2.3 h in the placebo gr

123 ndividuals with the LL genotype who received ondansetron had a lower mean number of drinks per drinki

124 Ondansetron has been suggested as an adjunctive treatmen

125 a pronociceptive role in the spinal cord and ondansetron has previously been shown to produce antinoc

126 e located abundantly on sensory pathways and ondansetron has shown some clinical utility in disorders

127 The 5-HT(3) receptor antagonist, ondansetron, has been shown to correct the auditory gati

128 iemetics, such as serotonin antagonists like ondansetron, have demonstrated efficacy in relief of vom

129 ith 50 mg of naltrexone (n = 23), 0.50 mg of ondansetron hydrochloride (n = 23), the combination of t

130 Ondansetron hydrochloride use in children with gastroent

131 ere blocked by the 5-HT3 receptor antagonist ondansetron (IC50 = 103 pM) and by the non-selective age

132 Ondansetron improves outcomes when administered in emerg

133 setron were compared with intravenous (I.V.) ondansetron in chemotherapy-naive patients who received

134 ty and efficacy to a single 32-mg IV dose of ondansetron in patients receiving cisplatin chemotherapy

135 o test this, we acutely injected intrathecal ondansetron in rats between 14 and 30 days after SNL and

136 The cardiac safety of ondansetron in the hemodialysis population is unknown.

137 In hemodialysis, ondansetron initiation versus initiation of lesser QT-pr

138 egies are needed to optimally integrate oral ondansetron into clinical practice to maximize its poten

139 Administration of ondansetron into the medial NTS completely reversed supp

140 e intake in response to direct injections of ondansetron into various sites of the dorsal hindbrain.

141 The 5-HT3 receptor antagonist ondansetron is a good candidate for the modulation of in

142 Ondansetron is a peripherally active antagonist of the s

143 Ondansetron is a selective serotonin (5HT3) receptor ant

144 Ondansetron is commonly used to treat HG, but studies ar

145 Single-dose oral ondansetron is effective and safe in reducing hospital a

146 Ondansetron is frequently used to treat nausea and vomit

147 Ondansetron is frequently used to treat nausea and vomit

148 Parenteral ondansetron is significantly more effective than traditi

149 gnatures, the presumed therapeutic effect of ondansetron may be elicited through the NF-KB pathway an

150 ional ondansetron use: low (<5% administered ondansetron), medium (5%-25%), or high (>25%).

151 xylamine, hydration, and adequate nutrition; ondansetron, metoclopramide, promethazine, and intraveno

152 ve either oral granisetron (n = 542) or I.V. ondansetron (n = 543).

153 Ondansetron, naltrexone, topiramate, and baclofen are ex

154 The combination of pergolide and ondansetron normalized not only behavioral sensitization

155 attenuation of distension-induced Fos-LI by ondansetron occurred in the NTS, particularly in the med

156 s of both acute and chronically administered ondansetron on auditory gating in DBA/2 mice.

157 We investigated the effects of ondansetron on bulimic behaviours in patients with sever

158 <12 years) on days 2 and 3, or placebo plus ondansetron on day 1 followed by placebo on days 2 and 3

159 125 mg for ages 6 months to <12 years) plus ondansetron on day 1, followed by aprepitant (80 mg for

160 There was no effect of high-dose ondansetron on SP.

161 equired to observe the inhibitory effects of ondansetron on spinal neuronal excitability and behavior

162 stration of the 5-HT(3) receptor antagonist, ondansetron (OND), to the posterior IC impaired the esta

163 12 patients were assigned placebo, and 14 ondansetron; one patient in the ondansetron group droppe

164 Children who received ondansetron or no therapy were less likely to require an

165 egivers were provided with six doses of oral ondansetron or placebo to administer in response to ongo

166 NTS by either the chronic administration of ondansetron or the genetic inactivation of Tph2 in cauda

167 Dolasetron, granisetron, ondansetron, palonosetron, and tropisetron have similar

168 Our results suggest that ondansetron (particularly the 4 microg/kg twice per day

169 In contrast, ondansetron, pentazocine, and dimenhydrinate may be usef

170 th 59,450 of 334,264 (17.8%) during the high ondansetron period (adjusted percentage change = -0.33%;

171 3 of 232,706 children (18.7%) during the low ondansetron period compared with 59,450 of 334,264 (17.8

172 Receipt of ondansetron plus aprepitant or fosaprepitant was associa

173 dified protocol, with or without intravenous ondansetron pretreatment (4 mg).

174 Ondansetron prevented these changes.

175 Ondansetron produced less marked effects on thermal resp

176 Ondansetron produced little effect on the electrically e

177 Among ondansetron recipients, the number of drinks per drinkin

178 l data that suggest that both naltrexone and ondansetron reduce alcohol-stimulated dopamine output in

179 wever, when used as an augmentation to SRIs, ondansetron reduced overall OCD severity, which may be r

180 (5-hydroxytryptamine-3) receptor antagonist ondansetron reduced the amplitude of the CMMC, the propu

181 In conclusion, high-dose ondansetron reduces activation of several areas importan

182 olasetron mesylate 1.8 mg/kg, 2.4 mg/kg, and ondansetron, respectively, were 49.2%, 45.6%, and 50.4%

183 Ondansetron reverses sensory gating deficits and improve

184 Ondansetron's ability to modulate brainstem connectivity

185 The intrathecal injection of ondansetron showed that loss of DNIC was not due to exce

186 f casopitant mesylate plus dexamethasone and ondansetron significantly reduced CINV events in patient

187 evidence of dehydration and lack of an oral ondansetron-supported oral rehydration period.

188 Ondansetron taken during pregnancy was not associated wi

189 hin 48 hours after enrollment was lower with ondansetron than with placebo (adjusted rate ratio, 0.76

190 Administration of IV ondansetron, the most predominant antiemetic used at GMH

191 athecal injection of the 5-HT(3)R antagonist ondansetron; the 5-HT(2A)R antagonist MDL-11 939 had no

192 ight the need to focus efforts to administer ondansetron to children at greatest risk for oral rehydr

193 sted the ability of three different doses of ondansetron to engage neural regions involved in interoc

194 propose a new pharmacogenetic approach using ondansetron to treat severe drinking and improve abstine

195 s study, they explored additional markers of ondansetron treatment response in alcoholics by examinin

196 decrease in binge-eating and vomiting under ondansetron treatment was not achieved by compensatory c

197 l-level analyses of the associations between ondansetron use and 3 outcomes: intravenous rehydration

198 outcomes varied widely between low and high ondansetron use categories at an institutional level.

199 Ondansetron use has increased significantly; however, 'r

200 Although ondansetron use increased during the study period, intra

201 Oral ondansetron use increased from a median institutional ra

202 During the transition from low to high ondansetron use, we observed no change in the hospitaliz

203 sits were categorized based on institutional ondansetron use: low (<5% administered ondansetron), med

204 Initiation of ondansetron versus a comparator antiemetic was associate

205 e association between the initiation of oral ondansetron versus antiemetics with lesser QT-prolonging

206 analog scale [VAS] score, 4.1 [SD, 2.9] for ondansetron vs 5.7 [SD, 2.3] for metoclopramide [P = .02

207 he parenteral (intravenous or intramuscular) ondansetron vs traditional therapy to resolve the sympto

208 justment for site, weight, and missing data, ondansetron was associated with a lower risk of moderate

209 mitant serotonin reuptake inhibitors (SRIs), ondansetron was associated with a significant decrease i

210 esser QT-prolonging potential, initiation of ondansetron was associated with higher short-term cardia

211 Ondansetron was associated with improvement for a range

212 One RCT (n = 83) found that ondansetron was associated with lower nausea scores on d

213 Oral ondansetron was associated with reduced odds of intraven

214 Ondansetron was dosed per the product label for paediatr

215 Receipt of ondansetron was not associated with a significantly incr

216 Oral ondansetron was provided to 13.5% (95% CI, 13.3% to 13.7

217 colon; and (9) the 5-HT3 receptor antagonist ondansetron, which reduced CMMCs and blocked their propa

218 Addition of aprepitant to ondansetron with or without dexamethasone is effective f