ライフサイエンスコーパス: haloperidol

1 and tri-), and illicit drugs (MA, MDEA, and haloperidol).

2 hat could be attenuated by pretreatment with haloperidol.

3 replicated in rats treated chronically with haloperidol.

4 timuli including antipsychotic drugs such as haloperidol.

5 sponse to single or repeated injections with haloperidol.

6 whether mid- or low-potency FGAs differ from haloperidol.

7 o clinically used drugs such as ketamine and haloperidol.

8 by the dopamine D2-like receptor antagonist haloperidol.

9 mimicked by valproate and clozapine but not haloperidol.

10 nce and presence of the D(2)/D(3)R inhibitor haloperidol.

11 ataleptic response to the antipsychotic drug haloperidol.

12 antagonist, SCH-23390, or the D2 antagonist, haloperidol.

13 arm and blunted the effects of SCH-23390 or haloperidol.

14 nonakinesia dose of the dopamine antagonist haloperidol.

15 e the need for benzodiazepines, opioids, and haloperidol.

16 peridol alone or the combination of METH and haloperidol.

17 anticancer doxorubicin and the antipsychotic haloperidol.

18 -blind study of risperidone, olanzapine, and haloperidol.

19 tic drug and dopamine D2 receptor antagonist haloperidol.

20 ing action relative to subjects treated with haloperidol.

21 cal ventilation and those who never received haloperidol.

22 e expedient synthesis of the medicinal agent haloperidol.

23 , safety, and cost-benefit profile than does haloperidol.

24 is of brain regions activated in response to haloperidol.

25 idal symptoms (RR=0.31, NNH=7) compared with haloperidol.

26 ve like the known sigma1 receptor antagonist haloperidol.

27 elicit a much lower level of catalepsy than haloperidol.

28 regard to efficacy and safety compared with haloperidol.

29 t produced very little catalepsy relative to haloperidol.

30 o HIT by altering the brain concentration of haloperidol.

31 lowing initiation of treatment with low-dose haloperidol.

32 69L 1.0 mg/kg failed to alter the effects of haloperidol (0.1 mg/kg) on DA or ACh efflux in either re

33 While LiCl(2) 3.0mEq/kg IP also augmented haloperidol (0.19mg/kg SC)-induced catalepsy, this lithi

34 countered by the benchmark anti-tic therapy haloperidol (0.3 mg/kg, IP).

35 VPA (50 mg/kg) also potentiated haloperidol (0.5 mg/kg)-induced DA release in the mPFC;

36 ions of either saline or one of two doses of haloperidol (0.5 mg/kg, 1.0 mg/kg), clozapine (7.5 mg/kg

37 ancy, were resistant to catalepsy induced by haloperidol (0.5-5 mg/kg i.p.) or raclopride (2 mg/kg s.

38 to -0.06); clozapine was more effective than haloperidol (-0.22; -0.38 to -0.07) and sertindole (-0.4

39 ive than quetiapine (-0.29; -0.56 to -0.02), haloperidol (-0.29; -0.44 to -0.13), and sertindole (-0.

40 nes with the excitatory actions of a first- (haloperidol; 0.6 mg/kg, i.p.) and a second- (sertindole;

41 atients were randomly assigned to receive IV haloperidol 1 mg or placebo every 6 hours until delirium

42 Twenty rats were pretreated with saline or haloperidol (1 mg/kg of body weight) and then injected w

43 administration of the typical antipsychotic haloperidol (1 mg/kg) and the atypical antipsychotic clo

44 pirone (5 mg/kg), pimavanserin (3 mg/kg), or haloperidol (1 mg/kg) b.i.d. 30 min before PCP (2 mg/kg,

45 A similar number of patients given haloperidol (12/34 [35%]) and placebo (8/34 [23%]) devel

46 web-based randomisation service) to receive haloperidol 2.5 mg or 0.9% saline placebo intravenously

47 (n = 47) or placebo (n = 43) in addition to haloperidol (2 mg) intravenously upon the onset of an ag

48 Pretreatment with 1 mg/kg haloperidol (2), nonradioactive 13, or BD1047 (18) reduc

49 allocation to a conventional antipsychotic, haloperidol (2-20 mg/d), or an atypical antipsychotic, o

50 core at 8 hours (-4.1 points) than placebo + haloperidol (-2.3 points) (mean difference, -1.9 points

51 quetiapine required fewer days of as-needed haloperidol [3 [(IQR, 2-4)] vs. 4 days (IQR, 3-8; p = .0

52 pride=20, aripiprazole=8, chlorpromazine=13, haloperidol=316, intramuscular olanzapine or haloperidol

53 speridone, 58% from baseline; 6.5 [5-14] for haloperidol, 65% from baseline; p=0.06).

54 141 were included in the final analysis (71 haloperidol, 70 placebo).

55 ime in satisfactory sedation levels than did haloperidol (92.7% [95% CI, 84.5-99.8%] vs 59.3% [95% CI

56 ide, quinpirole (a full D2-like agonist), or haloperidol (a D2-like antagonist) to alter striatal DOP

57 We compared flexible doses of haloperidol (a typical, first-generation antipsychotic d

58 irone, a selective 5-HT(1A) partial agonist, haloperidol, a D(2) antagonist, and pimavanserin, a 5-HT

59 reatment of STHdh(Q7/Q7) cells with ACEA and haloperidol, a D2 antagonist, inhibited BRETEff signals

60 Treatment with haloperidol, a D2 dopamine receptor antagonist, reduces

61 the ability of a typical antipsychotic drug haloperidol, a D2 receptor antagonist, at a dose of 0.1

62 viously reported that the antipsychotic drug haloperidol, a multifunctional D2-like dopamine and sigm

63 mitigated by the dopamine (DA) D2 antagonist haloperidol, a proven pharmacotherapy, and by HA infusio

64 e found that cocaine, a psychostimulant, and haloperidol, a sedation-producing antipsychotic, exert d

65 Haloperidol, a typical antipsychotic and D2R blocker, re

66 totypical atypical antipsychotic, but not by haloperidol, a typical antipsychotic.

67 yzed chromosome substitution strains, imaged haloperidol abundance in brain tissue sections and direc

68 In contrast to haloperidol, AC-260584 did not produce catalepsy.

69 , including fluoroquinolones and intravenous haloperidol (adjusted odds ratio, 0.79; 95% confidence i

70 We report here that subchronic haloperidol administration after a high-dose regimen of

71 ty involving Zif268 induction: the effect of haloperidol administration on striatal gene expression.

72 Changes in synaptic dopamine due to acute haloperidol administration were not detectable with (123

73 Furthermore, we found that administration of haloperidol affects the way the animals integrate prior

74 gra pars compacta were unaffected by METH or haloperidol alone or the combination of METH and haloper

75 on of lorazepam to haloperidol compared with haloperidol alone resulted in a significantly greater re

76 Although effects of clozapine and haloperidol alone were relatively minor, their effects o

77 Haloperidol also elevated BDNF levels in the amygdala, w

78 Cumulative dose of haloperidol among intubated patients did not change thei

79 Chronic blockade with haloperidol, an antipsychotic medication used to treat s

80 Interestingly, two known Sig1R ligands, haloperidol and (+)-pentazocine, disrupted the Nav1.5/Si

81 The protective potency of haloperidol and a number of other butyrophenone compound

82 Remarkably, both haloperidol and clozapine attenuated AMP disruption of L

83 In WKY rats, both haloperidol and clozapine attenuated the CRF-induced dec

84 Both haloperidol and clozapine increased the levels of GAD(67

85 The dissociable effects of haloperidol and clozapine on ketamine-induced hyperoxyge

86 e, pretreatment with the antipsychotic drugs haloperidol and clozapine prevented dizocilpine-induced

87 Antipsychotic drugs haloperidol and clozapine, which target monoamine recept

88 lift the matrix effect in a 1:10 mixture of haloperidol and dipalmitoylphosphatidylcholine (DPPC) th

89 r activity following acute administration of haloperidol and high-dose risperidone, which was most li

90 treatment), terguride had similar effects as haloperidol and increased DOPA accumulation.

91 his contrasts with typical APDs, for example haloperidol and perphenazine, which are mainly DA D(2/)D

92 cals inhibiting feeding rate (pharmaceutical haloperidol and pesticide lindane).

93 However, the response to haloperidol and phencyclidine indicates that normal D2R

94 In sum, we confirm that haloperidol and risperidone caused catalepsy in rodents,

95 Olanzapine was superior to haloperidol and risperidone for reduction of negative sy

96 , 5-HT(2A) KO mice were cataleptic following haloperidol and risperidone, but did not respond to cloz

97 iors, in a fashion akin to the antipsychotic haloperidol and the mood stabilizer lithium carbonate.

98 brain tissue sections and directly measured haloperidol (and its metabolite) levels in brain, and ch

99 Finally, therapeutic actions of typical (haloperidol) and atypical (clozapine) antipsychotics in

100 ive measurements revealed Kd of dopamineHCl, haloperidol, and (+)-SCH23390 at 0.874, 25.6, and 0.004n

101 4.8%; 95% CI, 26.0-43.1%) did not respond to haloperidol, and 86 patients (65.2%; 95% CI, 56.3-73.0%)

102 Molindone was superior to risperidone, haloperidol, and olanzapine in terms of weight gain, and

103 lecules, including cocaine, (+)-pentazocine, haloperidol, and small endogenous molecules such as N,N-

104 eptors may contribute to the potentiation of haloperidol- and risperidone-induced DA efflux in the mP

105 We found that the effect of haloperidol antagonism on D2R metabolic signaling events

106 toms and quetiapine with less akathisia than haloperidol, aripiprazole, risperidone, and olanzapine,

107 chewing movements (VCMs) induced by chronic haloperidol as a model of tardive dyskinesia (TD) in rat

108 effects on brain morphology could be due to haloperidol-associated toxicity or greater therapeutic e

109 he presence of the known S1R ligands such as haloperidol, BD-1047, and sphingosine.

110 PD female rats also showed increased (3)H-haloperidol binding and decreased dopamine transporter b

111 distribution of eight nonproprietary drugs (haloperidol, bufuralol, midazolam, clozapine, terfenadin

112 of dexmedetomidine was 17 times greater than haloperidol, but it achieved a mean savings of $4,370 pe

113 01) were significantly more efficacious than haloperidol, but the evidence was very low to moderate q

114 Although haloperidol can be used safely in this population of pat

115 d abnormal T wave morphology, the effects of haloperidol, clotiapine, phenothiazines, and citalopram

116 and 5-HT(2A) knockout (KO) mice treated with haloperidol, clozapine, and risperidone were assessed fo

117 te that a series of antipsychotics including haloperidol, clozapine, aripiprazole, chlorpromazine, qu

118 as blocked by dopamine receptor antagonists (haloperidol, clozapine, eticlopride, and SCH23390).

119 dvanced cancer, the addition of lorazepam to haloperidol compared with haloperidol alone resulted in

120 Group comparison: patient responders to haloperidol (control group) were compared with nonrespon

121 ACEA and haloperidol cotreatments produced a delayed and sustaine

122 otic clozapine and the typical antipsychotic haloperidol could modulate the effects of S-(+)-ketamine

123 .25-3.09) and was decreased for those taking haloperidol decanoate (-0.96 kg; 95% CI, -1.88 to -0.04)

124 ure for paliperidone palmitate compared with haloperidol decanoate (adjusted hazard ratio, 0.98; 95%

125 Intramuscular injections of haloperidol decanoate 25 to 200 mg or paliperidone palmi

126 e disorder, use of paliperidone palmitate vs haloperidol decanoate did not result in a statistically

127 lmitate group gained weight and those in the haloperidol decanoate group lost weight; after 6 months,

128 ridone palmitate group and 47 (32.4%) in the haloperidol decanoate group.

129 Patients taking haloperidol decanoate had significantly larger increases

130 reater increases in serum prolactin, whereas haloperidol decanoate was associated with more akathisia

131 On the other hand, haloperidol decreased the time spent dodging while showi

132 anges was topographically distinct: with the haloperidol decreases more prominent rostral, the lithiu

133 all trials (total number of patients = 133), haloperidol did not appear to be effective in treating d

134 rlier SPECT finding, acute administration of haloperidol did not induce a significant change in (123)

135 ydroxy-L-phenylalanine; L-DOPA) or reducing (haloperidol) dopaminergic function.

136 elds from four standard compounds, arginine, haloperidol, DPPC, and angiotensin II, have been measure

137 en treated with an atypical antipsychotic or haloperidol during pregnancy.

138 r estimated relapse rates, and for different haloperidol equivalent comparator doses.

139 There was no association with haloperidol equivalent dosage.

140 bitter, with compounds such as chloroquine, haloperidol, erythromycin, procainamide, and ofloxacin k

141 We also assessed whether N-n-butyl haloperidol (F2), which exerts protective effects during

142 Systemic clozapine and PD149163 but not haloperidol facilitated PPI in BN rats (p < .001).

143 ponses, whereas the D(2) receptor antagonist haloperidol failed to do so.

144 ct of lorazepam vs placebo as an adjuvant to haloperidol for persistent agitation in patients with de

145 d for more studies regarding the efficacy of haloperidol for treatment of delirium among older medica

146 ncer and agitated delirium despite scheduled haloperidol from February 11, 2014, to June 30, 2016, wi

147 cue neuroleptics (2.0 mg) than the placebo + haloperidol group (4.0 mg) (median difference, -1.0 mg [

148 s hypokinesia (3 patients in the lorazepam + haloperidol group [19%] and 4 patients in the placebo +

149 group [19%] and 4 patients in the placebo + haloperidol group [27%]).

150 Ten (29%) patients in the haloperidol group reported symptoms consistent with akat

151 The lorazepam + haloperidol group required less median rescue neurolepti

152 ing the 21-day study period, patients in the haloperidol group spent a similar number days alive with

153 Patients in the haloperidol group spent about the same number of days al

154 ], P = .007; nurses: 77% for the lorazepam + haloperidol group vs 30% for the placebo + haloperidol g

155 nurses (caregivers: 84% for the lorazepam + haloperidol group vs 37% for the placebo + haloperidol g

156 events were oversedation (11 patients in the haloperidol group vs six in the placebo group) and QTc p

157 and QTc prolongation (seven patients in the haloperidol group vs six in the placebo group).

158 + haloperidol group vs 37% for the placebo + haloperidol group; mean difference, 47% [95% CI, 14% to

159 + haloperidol group vs 30% for the placebo + haloperidol group; mean difference, 47% [95% CI, 17% to

160 tive matched nonusers, individuals receiving haloperidol had an increased mortality risk of 3.8% (95%

161 Haloperidol had no effect on the absolute ketamine O2 si

162 ain areas in rats, whereas administration of haloperidol had no effect.

163 Haloperidol (HAL) (1.0 mg/kg s.c.)+/-amfonelic acid (AFA

164 3 days) but not clinically relevant doses of haloperidol (HAL) (1.3 to 4 micromol/kg twice a day s.c.

165 oral and molecular markers of the effects of haloperidol (HAL) in aged mice.

166 l effects of four APs: chlorpromazine (CLP), haloperidol (HAL), risperidone (RIS) and clozapine (CLZ)

167 However, haloperidol (HAL)-induced catalepsy was unchanged in eit

168 thamphetamine (MAP-0.5 and 1.0 mg/kg, i.p.), haloperidol (HAL-0.12 mg/kg, i.p.), and sulfated cholecy

169 ther amphetamine (AMPH; 0.5 or 1.0 mg/kg) or haloperidol (HAL; 0.1 mg/kg) were injected before 1 or a

170 nically relevant dosing of an antipsychotic (haloperidol, HAL) or lithium (Li) on brain volume using

171 to delirium in nonintubated patients in whom haloperidol has failed, and it seems to have a better ef

172 stimulant treatment, while the antipsychotic haloperidol has the opposite effect.

173 e of olanzapine, risperidone, quetiapine, or haloperidol in 1999-2001 after at least 3 months with no

174 nically important benefit of olanzapine over haloperidol in improving negative symptoms when the PANS

175 nzapine and olanzapine greater efficacy than haloperidol in reducing aggressive behavior.

176 Olanzapine was superior to haloperidol in reducing the number and severity of aggre

177 lozapine was superior to both olanzapine and haloperidol in reducing the number and severity of physi

178 e disruptive effects of the D2/D3 antagonist haloperidol in reversal but show normal sensitivity to i

179 d-generation antipsychotics were superior to haloperidol in terms of all-cause discontinuation.

180 132 nonintubated patients were treated with haloperidol in the initial haloperidol titration phase.

181 ted effects of a typical antipsychotic drug, haloperidol, in inducing catalepsy behavior.

182 , ML182 was shown to be orally active in the haloperidol induced catalepsy model, a well-established

183 nmol of VU0155041 dose-dependently decreased haloperidol-induced catalepsy and reserpine-induced akin

184 ) = 10 muM) and dose dependently counteracts haloperidol-induced catalepsy in mice from 30 mg/kg by t

185 mptoms after intraperitoneal administration: haloperidol-induced catalepsy in mouse and the rat 6-hyd

186 No changes in haloperidol-induced catalepsy or MK-801-induced locomoti

187 examined the impact of early-life stress on haloperidol-induced catalepsy using the rat model of pre

188 's disease including mouse and rat models of haloperidol-induced catalepsy, mouse and rat models of r

189 's disease including mouse and rat models of haloperidol-induced catalepsy, mouse model of reserpine-

190 t-term bi-directional selective breeding for haloperidol-induced catalepsy, starting from three mouse

191 in potentiating endogenous GLP-1R to reverse haloperidol-induced catalepsy.

192 y explains the refractoriness of PRS rats to haloperidol-induced catalepsy.

193 acteristic extrapyramidal symptoms caused by haloperidol-induced toxicity (HIT), which limits its cli

194 t a single 1 mg/kg dose of the antipsychotic haloperidol induces enough dopamine release to compete w

195 f D2R signaling by the typical antipsychotic haloperidol induces parkinsonism in humans and catalepsy

196 Low-dose scheduled haloperidol, initiated early in the ICU stay, does not p

197 haloperidol=316, intramuscular olanzapine or haloperidol injection=62, olanzapine=144, placebo=75, qu

198 For example, haloperidol is a potent dopamine antagonist that is used

199 The antipsychotic drug haloperidol is an antagonist of Sigma-1 receptors and in

200 Haloperidol is the most commonly used drug for delirium

201 abinol, and opiates; the antipsychotic drug, haloperidol; juvenile enrichment; sucrose drinking; calo

202 tipsychotics olanzapine (M1R antagonist) and haloperidol (low M1R affinity), was assessed in rats ex

203 Conversely, haloperidol markedly decreased the production of dry lic

204 inistration of the dopamine receptor blocker haloperidol markedly increased the production of dry lic

205 ic management of METH-induced psychoses with haloperidol may be contraindicated because of a resultan

206 gle or multiple low doses of risperidone and haloperidol may be innocuous to subsequent recovery afte

207 anzapine (mean=72.1%, SD=42.0%), followed by haloperidol (mean=65.5%, SD=40.3%), risperidone (mean=49

208 bute to the ability of lithium to potentiate haloperidol-mediated catalepsy.

209 , we assessed whether DeltaFosB induction by haloperidol mediates the positive or negative consequenc

210 (+/-)-MRJF22 [(+/-)-2], a novel prodrug of haloperidol metabolite II (sigma-1 receptor antagonist/s

211 gest that a low dose of acutely administered haloperidol might have a novel application as a protecti

212 e results do not support the hypothesis that haloperidol modifies duration of delirium in critically

213 e, and erythromycin) to little or no effect (haloperidol, moxifloxacin, and verapamil).

214 ine characteristics were similar between the haloperidol (n = 34) and placebo (n = 34) groups.

215 clozapine (n = 37), olanzapine (n = 37), or haloperidol (n = 36).

216 nsland, Australia, were randomly assigned to haloperidol (n=28), risperidone (n=29), or placebo (n=29

217 yl-2,3,4,5-tetrahydro-1H-3-benzazepine) plus haloperidol] nor a calcineurin inhibitor (cyclosporine),

218 ble for antipsychotics other than clozapine, haloperidol, olanzapine, and risperidone.

219 r analyses in monkeys chronically exposed to haloperidol, olanzapine, or placebo were also conducted.

220 specimens from 18 macaque monkeys exposed to haloperidol, olanzapine, or sham long-term.

221 A new prescription for an antipsychotic (haloperidol, olanzapine, quetiapine, and risperidone), v

222 tegy of the animals and reveals an effect of haloperidol on integration of prior information with evi

223 gic agonist (amphetamine) and an antagonist (haloperidol) on food protection behavior initiated to av

224 Here, we report that co-administration of haloperidol, one available treatment for Tourette syndro

225 ceptor (C94A,V190C), both in a sigma-ligand (haloperidol or (+)-pentazocine)-sensitive manner.

226 ed with exposure to a typical antipsychotic, haloperidol or an atypical antipsychotic, olanzapine.

227 We treated BN rats with haloperidol or clozapine to determine if the BN rat is a

228 ivity to the antipsychotic effects of either haloperidol or clozapine, suggesting that these compound

229 re explored in mice treated for 21 days with haloperidol or clozapine.

230 These effects were not mimicked by haloperidol or genetic ablation of dopamine D2 and D3 re

231 t of chronic (8 weeks) treatment with either haloperidol or olanzapine on the rat cortex.

232 e chronically treated with the antipsychotic haloperidol or vehicle.

233 Patients were randomly assigned to receive haloperidol or ziprasidone or placebo every 6 hrs for up

234 ctivity was ameliorated by clozapine but not haloperidol or ziprasidone.

235 tic (risperidone, olanzapine, quetiapine, or haloperidol) or valproic acid and its derivatives (as a

236 ham groups (4.5 mg/kg risperidone, 0.5 mg/kg haloperidol, or 1 mL/kg vehicle).

237 Pretreatment with known S1R compounds, haloperidol, or BD1047, before radioligand administratio

238 Vagotomy, systemic haloperidol, or intracerebroventricular raclopride (a ty

239 5 mg/kg, or 4.5 mg/kg risperidone; 0.5 mg/kg haloperidol; or 1 mL/kg vehicle) or three sham groups (4

240 nce showed a clinically important benefit of haloperidol over olanzapine for improving positive sympt

241 ly treatments of risperidone (4.5 mg/kg) and haloperidol (p < .05).

242 t mice with the dopamine receptor antagonist haloperidol precipitated motor behavior deficits in aged

243 d olanzapine showed superior efficacy versus haloperidol, quetiapine, and ziprasidone.

244 nced the regularity of this pattern, whereas haloperidol reduced its regularity.

245 with pharmacologic antagonists (pimozide and haloperidol) reduced proliferation of pancreatic cancer

246 vivo, an acute low dose (0.05 mg/kg s.c.) of haloperidol reduces by half the ischemic lesion volume i

247 he individual SGAs outperformed FGAs (mainly haloperidol) regarding study-defined relapse, except for

248 We observed significant enrichments of haloperidol-regulated genes in schizophrenia GWAS loci a

249 rast to the other antagonists, spiperone and haloperidol respectively increased the atomic distance b

250 s were successful, with large differences in haloperidol response emerging within three generations.

251 Lorazepam + haloperidol resulted in a significantly greater reductio

252 Addition of the antipsychotics, spiperone or haloperidol, resulted in re-organization of D3R quaterna

253 Quetiapine added to as-needed haloperidol results in faster delirium resolution, less

254 D(2) antagonists, but not typical APDs, eg, haloperidol, reverses the PCP-induced NOR deficit in rat

255 ra-AcbSh AC187 on its own disrupted PPI in a haloperidol-reversible manner (0.1 mg/kg).

256 the metabolic syndrome for olanzapine versus haloperidol (risk differences, 2% and 22%), and higher i

257 ntia (RR 1.19, 95% CI 1.07-1.33), receipt of haloperidol (RR 1.35, 95% CI 1.21-1.50), and severity of

258 duced parkinsonian akinesia (0.03-0.07 mg/kg haloperidol, s.c.) or control (vehicle injection) condit

259 irium prevention effects are associated with haloperidol, second-generation antipsychotics, iliac fas

260 INTERPREATION: Haloperidol seems to be a suboptimum treatment option fo

261 Haloperidol, sertindole, clotiapine, phenothiazines, flu

262 f trials in progress, the use of intravenous haloperidol should be reserved for short-term management

263 osphatidylcholine (DPPC) that suppresses the haloperidol signal.

264 rphine significantly increased and 0.1 mg/kg haloperidol significantly decreased the blink rate.

265 CP, or tandospirone, but not pimavanserin or haloperidol, significantly prevented the PCP-induced NOR

266 es were examined in rats treated with either haloperidol (Sprague-Dawley rats [N=16]) or clozapine (L

267 approximately 4; selectivity was reduced by haloperidol, suggesting that binding was D(2)/D(3)R-spec

268 nger prior on where reversals would occur on haloperidol than on levodopa (l-DOPA) or placebo.

269 e also identified several novel drugs, e.g., haloperidol, that increased the risk of fetal loss.

270 responsible for metabolizing risperidone and haloperidol, the possibility that the augmentation of an

271 were treated with haloperidol in the initial haloperidol titration phase.

272 Initial haloperidol titration: all patients received IV bolus do

273 ng CB1 and D2L treated with ACEA, binding of haloperidol to D2 receptors switched CB1 coupling from G

274 for the distinctive ability of spiperone and haloperidol to disrupt D3R dimerization.

275 ce, and administration of the DRD2 inhibitor haloperidol to mice with orthotopic xenograft tumors red

276 Moreover, a genetic association study in a haloperidol-treated human cohort indicates that human AB

277 measurements were repeated in vagotomized or haloperidol-treated mice, and in animals intracerebroven

278 Haloperidol-treated patients exhibited significant decre

279 Haloperidol-treated rats did not have altered expression

280 However, haloperidol treatment also led to strengthening of a sub

281 ransgenic mice, it was found that 2 weeks of haloperidol treatment induced both intrinsic and synapti

282 oupling from Galphai to Galphas In addition, haloperidol treatment reduced ACEA-induced beta-arrestin

283 f extrapyramidal symptoms induced by chronic haloperidol treatment.

284 s and endophenotypes were rescued by chronic haloperidol treatment.

285 tic treatment (thioridazine, chlorpromazine, haloperidol, trifluoperazine, or risperidone) for 12 mon

286 ion: all patients received IV bolus doses of haloperidol until agitation was controlled (Richmond Agi

287 ential confounders, with patients initiating haloperidol use designated the reference group, diabetes

288 Haloperidol use reduced the hours per study day spent ag

289 P < .01) with an NNH of 8 (95% CI, 6-12) for haloperidol users to 3.2% (95% CI, 1.6%-4.9%; P < .01) w

290 tality for chlorpromazine verus clozapine or haloperidol versus aripiprazole,increased incidence of t

291 Haloperidol was associated with 10 cases (11.6% [95% CI,

292 tes, each additional cumulative milligram of haloperidol was associated with 5% higher odds of next-d

293 Haloperidol was associated with significant reductions i

294 covariate-adjusted intent-to-treat analyses, haloperidol was associated with the highest mortality ra

295 While haloperidol was found to be a potent neuroprotective age

296 00 mg every 12 hrs) if more than one dose of haloperidol was given in the previous 24 hrs.

297 The mortality risk with haloperidol was highest in the first 30 days but decreas

298 ration, normal rats and rats pretreated with haloperidol were imaged in a PET/CT scanner and subseque

299 ital mortality between patients who received haloperidol within 2 days of initiation of mechanical ve

300 as to establish whether early treatment with haloperidol would decrease the time that survivors of cr