ライフサイエンスコーパス: haloperidol

1 drugs (such as aripiprazole, risperidone and haloperidol).

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

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

4 ve like the known sigma1 receptor antagonist haloperidol.

5 elicit a much lower level of catalepsy than haloperidol.

6 regard to efficacy and safety compared with haloperidol.

7 t produced very little catalepsy relative to haloperidol.

8 o HIT by altering the brain concentration of haloperidol.

9 lowing initiation of treatment with low-dose haloperidol.

10 hat could be attenuated by pretreatment with haloperidol.

11 replicated in rats treated chronically with haloperidol.

12 timuli including antipsychotic drugs such as haloperidol.

13 sponse to single or repeated injections with haloperidol.

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

15 o clinically used drugs such as ketamine and haloperidol.

16 mimicked by valproate and clozapine but not haloperidol.

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

18 ataleptic response to the antipsychotic drug haloperidol.

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

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

21 nonakinesia dose of the dopamine antagonist haloperidol.

22 t could be rescued by the tic-relieving drug haloperidol.

23 classical experiments with the D2-antagonist haloperidol.

24 ease 7-DHC levels such as ARI, trazodone and haloperidol.

25 by the dopamine D2-like receptor antagonist haloperidol.

26 s, but this effect was largely unaffected by haloperidol.

27 e expedient synthesis of the medicinal agent haloperidol.

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

29 is of brain regions activated in response to haloperidol.

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

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

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

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

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

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

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

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

38 Haloperidol 1 mg/kg pretreatment prevented ketamine-depe

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

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

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

42 with a loss of potency compared to the free haloperidol (~18-fold at 10 nM).

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

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

45 a single dose of the D2 receptor antagonist haloperidol (2 mg) on temporal discounting in healthy fe

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

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

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

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

50 mg; brexpiprazole, 3.36 mg/day and 0.54 mg; haloperidol, 6.3 mg/day and 1.01 mg; iloperidone, 20.13

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

52 the abovementioned effects are attenuated by haloperidol (70 ug/kg intraperitoneally).

53 141 were included in the final analysis (71 haloperidol, 70 placebo).

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

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

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

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

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

59 Haloperidol, a typical antipsychotic and D2R blocker, re

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

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

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

63 l fMRI study using 2 mg of the D2 antagonist haloperidol administered acutely before a cued associati

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

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

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

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

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

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

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

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

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

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

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

75 Antipsychotic drugs haloperidol and clozapine, which target monoamine recept

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

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

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

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

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

81 th of evidence [SOE]), and mortality between haloperidol and placebo used for delirium prevention.

82 ed a structure-kinetic relationship study of haloperidol and revealed that subtle structural modifica

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

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

85 , 5-HT(2A) KO mice were cataleptic following haloperidol and risperidone, but did not respond to cloz

86 of stay (moderate SOE), or mortality between haloperidol and second-generation antipsychotics versus

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

88 were blocked by the selective D2R antagonist haloperidol and were decreased by low temperature and hi

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

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

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

92 4.8%; 95% CI, 26.0-43.1%) did not respond to haloperidol, and 86 patients (65.2%; 95% CI, 56.3-73.0%)

93 Following administration of D-cycloserine, haloperidol, and bromocriptine, healthy participants dis

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

95 r L-dopa, 2 mg of the D2 receptor antagonist haloperidol, and placebo.

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

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

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

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

100 lorpromazine at 25 mg every 4 h, or combined haloperidol at 1 mg and chlorpromazine at 12.5 mg every

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

102 Rats treated intravenously with free haloperidol became cataleptic, whereas normal behaviour

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

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

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

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

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

108 experiments, which indicated that conjugated haloperidol can still bind to the D(2) receptors, albeit

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

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

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

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

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

114 substantially faster nondecision times under haloperidol compared with placebo.

115 Specifically, the PEG-haloperidol conjugate (at 10 and 100 nM) was able to sig

116 r was observed in rats that received the PEG-haloperidol conjugate, suggesting that conjugation can e

117 of a poly(ethylene glycol)-haloperidol (PEG-haloperidol) conjugate that retained affinity for its ta

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

119 ACEA and haloperidol cotreatments produced a delayed and sustaine

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

121 nverse agonists risperidone (D(2)R(ris)) and haloperidol (D(2)R(hal)).

122 .25-3.09) and was decreased for those taking haloperidol decanoate (-0.96 kg; 95% CI, -1.88 to -0.04)

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

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

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

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

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

128 Patients taking haloperidol decanoate had significantly larger increases

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

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

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

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

133 Haloperidol displays fast association/slow dissociation

134 ere randomly assigned to receive intravenous haloperidol dose escalation at 2 mg every 4 h, neurolept

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

136 le of participants, supporting the idea that haloperidol elevated dopamine neurotransmission (e.g., b

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

138 There was no association with haloperidol equivalent dosage.

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

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

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

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

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

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

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

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

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

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

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

150 The lorazepam + haloperidol group required less median rescue neurolepti

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

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

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

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

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

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

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

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

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

160 Haloperidol had no effect on the absolute ketamine O2 si

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

162 3 days) but not clinically relevant doses of haloperidol (HAL) (1.3 to 4 micromol/kg twice a day s.c.

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

164 ine the effects of chronic (9-week) typical (haloperidol (HAL)) and atypical (clozapine (CLZ)) APDs o

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

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

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

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

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

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

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

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

173 132 nonintubated patients were treated with haloperidol in the initial haloperidol titration phase.

174 y reported elevated caudate activation under haloperidol in this sample of participants, supporting t

175 ) and blocking dopamine receptors (1.5 mg of haloperidol) in the context of a novel dynamic effort ta

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

177 Compound 27o was also active in reversing haloperidol induced catalepsy in a rodent preclinical mo

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

179 ) = 10 muM) and dose dependently counteracts haloperidol-induced catalepsy in mice from 30 mg/kg by t

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

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

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

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

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

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

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

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

188 and scopolamine were also able to reverse a haloperidol-induced deficit in PR performance, however o

189 Aripiprazole also removes haloperidol-induced depolarization block in MAM rats, wh

190 These findings are compatible with a haloperidol-induced increase in striatal dopamine (e.g.,

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

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

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

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

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

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

197 Haloperidol is a typical antipsychotic drug (APD) associ

198 Haloperidol is the most commonly used drug for delirium

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

200 ination of model basic drugs (nortriptyline, haloperidol, loperamide, and papaverine) in physiologica

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

202 Conversely, haloperidol markedly decreased the production of dry lic

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

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

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

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

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

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

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

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

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

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

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

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

215 vidence was found to determine the effect of haloperidol on cognitive function, delirium severity (in

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

217 a single dose of the D2 receptor antagonist haloperidol on temporal discounting and choice dynamics

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

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

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

221 eated animals, sub-chronic administration of haloperidol or clozapine counteracted the reduction of s

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

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

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

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

226 ent evidence does not support routine use of haloperidol or second-generation antipsychotics for prev

227 ent evidence does not support routine use of haloperidol or second-generation antipsychotics to treat

228 e chronically treated with the antipsychotic haloperidol or vehicle.

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

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

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

232 receptor agonists/antagonists (bromocriptine/haloperidol), or placebo in a randomized, double-blind,

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

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

235 20 second-generation antipsychotic drugs and haloperidol (oral and long-acting injectable, LAI) in pe

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

237 ted the synthesis of a poly(ethylene glycol)-haloperidol (PEG-haloperidol) conjugate that retained af

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

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

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

241 e drift diffusion model, which revealed that haloperidol reduced the nondecision time and reduced imp

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

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

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

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

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

247 Lorazepam + haloperidol resulted in a significantly greater reductio

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

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

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

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

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

253 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

254 t this polymer-drug conjugate would localise haloperidol's activity either centrally or peripherally,

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

256 allow development of novel APDs based on the haloperidol scaffold with improved side-effect profiles.

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

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

259 Haloperidol, sertindole, clotiapine, phenothiazines, flu

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

261 osphatidylcholine (DPPC) that suppresses the haloperidol signal.

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

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

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

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

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

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

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

269 Initial haloperidol titration: all patients received IV bolus do

270 r BMI from -0.25 kg/m(2) (-0.68 to 0.17) for haloperidol to 1.07 kg/m(2) (0.90 to 1.25) for olanzapin

271 ged from -0.23 kg (95% CI -0.83 to 0.36) for haloperidol to 3.01 kg (1.78 to 4.24) for clozapine; for

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

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

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

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

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

277 Haloperidol-treated rats did not have altered expression

278 arization block of dopamine neurons by acute haloperidol treatment (0.6 mg/kg i.p.), aripiprazole (1

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

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

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

282 s and endophenotypes were rescued by chronic haloperidol treatment.

283 f extrapyramidal symptoms induced by chronic haloperidol treatment.

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

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

286 Haloperidol use reduced the hours per study day spent ag

287 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

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

289 SOE) and cognitive functioning (low SOE) for haloperidol versus second-generation antipsychotics, wit

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

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

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

293 While haloperidol was found to be a potent neuroprotective age

294 00 mg every 12 hrs) if more than one dose of haloperidol was given in the previous 24 hrs.

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

296 Better association memory under haloperidol was linked with higher activity in the left

297 , improved recognition of verbal items under haloperidol was reflected by enhanced novelty detection

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

299 with refractory agitation, despite low-dose haloperidol, were randomly assigned to receive intraveno

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