ライフサイエンスコーパス: MPH

1 MPH + FLX enhanced sensitivity to drug (i.e., cocaine) a

2 MPH + FLX exposure also increased mRNA of ERK2 and its d

3 MPH administration improved behavioral performance and i

4 MPH also improved reaction times to make correct respons

5 MPH enhanced activity within individual neurons, ensembl

6 MPH enhances catecholamine transmission via blockade of

7 MPH is also used, without license, by healthy adults, bu

8 MPH led to an overall suppression of alpha activity acro

9 MPH led to increased rates of target detection, and elec

10 MPH produced a broad inverted-U-shaped facilitation of s

11 MPH resulted in a statistically significant improvement

12 MPH serves to reduce maladaptive electrophysiological pr

13 MPH treatment increased impulsivity in LI rats, and modu

14 MPH-related enhancements occurred without significant ch

15 <0.001; cumulative PH: MD -0.287, P <0.001; MPH: MD -0.288, P <0.001; DPH: MD -0.310, P <0.001).

16 o the enzyme ([Fe(2+)]PAH(R)[L-Phe,5-deaza-6-MPH(4)]), the active site converts to a five-coordinate

17 ence+placebo and (c) 24 h smoking abstinence+MPH.

18 treatment combinations: MAAT/MPH (N=17), ABT/MPH (N=19), MAAT/placebo (N=17), and ABT/placebo (N=18).

19 ning (MAAT/MPH>MAAT/placebo and MAAT/MPH>ABT/MPH), and auditory working memory and divided attention

20 g memory and divided attention (MAAT/MPH>ABT/MPH).

21 mposed of patients who were not administered MPH (brain tumor = 31 and acute lymphoblastic leukemia =

22 ed decreased striatal D2R availability after MPH and these decreases were smaller in METH than in con

23 an in controls, and had no D2R changes after MPH challenge.

24 The opposing effects of ATO and MPH in the NAcb core and shell on impulsivity were unlik

25 in DAT1, previously linked to ADHD risk and MPH behavioural responses, influences the neurophysiolog

26 CA and dominance-related effects for SCA and MPH, and additive-by-dominant effect for MPH was partly

27 ant to note that EX was just as effective as MPH or ATMX in reducing orienting behavior and social in

28 Before MPH treatment, we found that D2/3 receptor availability

29 Both MPH and ATX increased SICI in heterozygotes but not in 1

30 ences the neurophysiological effects of both MPH and ATX.

31 gest that elevated catecholamine activity by MPH can disrupt inhibitory influences on persistent risk

32 , we tested for modulation of this effect by MPH in 40 healthy human adults.

33 sive choice was not altered significantly by MPH, AMPH, or ATO into either mPFC or OFC, indicating th

34 [(1)(1)C]MPH and [(1)(1)C]raclopride dynamic PET scans were perfo

35 Chronic MPH did not differentially alter the course of weight ga

36 interaction between environment and chronic MPH treatment at clinically relevant doses, administered

37 ed the effects of discontinuation of chronic MPH treatment on regional cerebral blood flow (rCBF) in

38 erm neurobiological consequences of combined MPH and FLX treatment (MPH + FLX) during juvenile period

39 shed placebo controlled trials that compared MPH and placebo on executive and nonexecutive memory, re

40 In conclusion, MPH and ATX have similar effects on SICI in children wit

41 These results indicate that concurrent MPH + FLX exposure during preadolescence increases sensi

42 treated with either 0, 2, 4, or 8 mg/kg/day MPH for 3 weeks.

43 at 3 months were associated with first-dose MPH-mediated FC reductions restricted to frontal-prefron

44 cross-over trial of placebo (bid), low-dose MPH (0.3 mg/kg; maximum dose, 10 mg bid), and moderate-d

45 maximum dose, 10 mg bid), and moderate-dose MPH (0.6 mg/kg; maximum dose, 20 mg bid).

46 riatum, which is normalized following either MPH or l-dopa administration.

47 connectivity (FC) associated with the first MPH dose in boys newly diagnosed with ADHD predict MPH-a

48 inutes after the administration of the first MPH dose to 40 stimulant drug-naive boys newly diagnosed

49 and MPH, and additive-by-dominant effect for MPH was partly identified as additive effect; 2) the ran

50 No trend was observed for MPH effectiveness in improving learning of a word associ

51 patients who are more likely to benefit from MPH.

52 No significant side effects from MPH were observed.

53 Recovery from MPH treatment was also examined at 1, 5, and 10 weeks fo

54 rom trait phenotype, and fewer QTL were from MPH than from other dependent variables.

55 edial prefrontal cortex (mPFC) of rats given MPH showed 55% greater immunoreactivity (-ir) for the ca

56 In hippocampal dentate gyrus, MPH-receiving rats showed a 51% decrease in NET-ir densi

57 Here, MPH was evaluated for its potential to alter stimulus-dr

58 ng ability (SCA) and mid-parental heterosis (MPH).

59 We examined how MPH influenced known electrophysiological precursors of

60 treated with methylphenidate hydrochloride (MPH) to evaluate genetic and behavioral toxicity were ob

61 Although academic gains were not identified, MPH may offer benefits in academic areas not assessed.

62 alamus neuropeptide Y-ir increased by 10% in MPH-exposed rats.

63 ological markers in 16 regions implicated in MPH effects and/or ADHD etiology.

64 he commonly occurring brief interruptions in MPH treatment.

65 possible role of the default mode network in MPH-mediated improvements in inattention and hyperactivi

66 neither in striatal D2R availability nor in MPH-induced striatal DA changes.

67 During transient inhibition, MPH increased prefrontal activation for both groups and

68 core improvement was associated with initial MPH-mediated FC reductions restricted to occipitoparieta

69 A dose of 1 mg/kg intraperitoneal MPH, either single dose or chronic treatment (well withi

70 le-dose, crossover study comparing 0.5 mg/kg MPH with 1.0 mg/kg ATX in 16 children with ADHD, aged 8-

71 and [(18)F]fallypride, rats received 6 mg/kg MPH, orally, twice each day for 28 d.

72 bal learning (MAAT/MPH>MAAT/placebo and MAAT/MPH>ABT/MPH), and auditory working memory and divided at

73 y working memory and divided attention (MAAT/MPH>ABT/MPH).

74 , yielding four treatment combinations: MAAT/MPH (N=17), ABT/MPH (N=19), MAAT/placebo (N=17), and ABT

75 acebo>ABT/placebo), nonverbal learning (MAAT/MPH>MAAT/placebo and MAAT/MPH>ABT/MPH), and auditory wor

76 lls (DCs, 440 +110/-90 Pa), and macrophages (MPHs, 900 +110/-100 Pa).

77 George W. Comstock (1915-2007), MD, MPH, DrPH, was lecturer and then professor of epidemiolo

78 Methylphenidate (MPH) ameliorates attention problems experienced by some

79 Methylphenidate (MPH) has long been used to treat attention-deficit/hyper

80 Methylphenidate (MPH) is a stimulant that increases extracellular levels

81 Methylphenidate (MPH) is an effective symptomatic treatment of attention

82 Methylphenidate (MPH) is an effective treatment for ADHD symptoms, but it

83 Methylphenidate (MPH) is commonly diverted for recreational use, but the

84 Methylphenidate (MPH) is commonly prescribed for children who have been d

85 Methylphenidate (MPH) is used clinically to treat attention-deficit/hyper

86 Methylphenidate (MPH) normalizes cortical function, enhancing task salien

87 Methylphenidate (MPH), a commonly used dopaminergic agent, may affect ani

88 ects of orally administered methylphenidate (MPH), a first-line treatment for attention deficit hyper

89 ation of stimulants such as methylphenidate (MPH) in children with attention deficit hyperactivity di

90 timulant medication such as methylphenidate (MPH); however, approximately 25% of patients show little

91 ined the effects of chronic methylphenidate (MPH) treatment on brain dopamine (DA) systems, developme

92 psychostimulants, including methylphenidate (MPH), are highly effective in the treatment of attention

93 d DA/NE re-uptake inhibitor methylphenidate (MPH), both with proven clinical efficacy in ADHD, on the

94 ts of two ADHD medications, methylphenidate (MPH), a psychostimulant, and atomoxetine (ATX), a select

95 mining the effects of 40 mg methylphenidate (MPH) administration.

96 se in the concurrent use of methylphenidate (MPH) and fluoxetine (FLX) in pediatric populations.

97 The effects of methylphenidate (MPH), atomoxetine (ATMX), and/or physical exercise (EX)

98 eceived direct infusions of methylphenidate (MPH; 6.25, 25.0, or 100mug), amphetamine (AMPH; 0.25, 1.

99 r challenge with 60 mg oral methylphenidate (MPH) (to measure DA release) to assess whether it predic

100 is that the psychostimulant methylphenidate (MPH) improves cognitive and social functioning among the

101 ousands of children receive methylphenidate (MPH; Ritalin) for attention deficit/hyperactivity disord

102 it is well established that methylphenidate (MPH) enhances sustained attention, the neural mechanisms

103 We also show that methylphenidate (MPH), which competitively inhibits DA uptake but does no

104 n rodents demonstrates that methylphenidate (MPH; Ritalin) elicits a narrow inverted-U-shaped improve

105 xamined the degree to which methylphenidate (MPH) (Ritalin) acts within distinct frontostriatal subfi

106 gical enhancement (ie, with methylphenidate (MPH) or placebo), for treating persistent cognitive prob

107 Pharmacotherapy with methylphenidate (MPH) seems to be the first-line treatment of choice in a

108 reversed by treatment with methylphenidate (MPH), suggesting a defect in brain catecholamine homeost

109 on was correlated with the initial 90-minute MPH-mediated FC changes.

110 In contrast to the SHRs, neither MPH nor ATMX affected orienting or social behavior in Wi

111 However, neither ATO nor MPH significantly altered impulsive behavior when infuse

112 llin-1 is required for AMPH-induced, but not MPH-induced, hyperlocomotion.

113 The differential action of MPH across regions disappeared at higher concentrations.

114 mine transporter (DAT1), a site of action of MPH, could influence the effects of MPH or ATX on SICI.

115 tial mechanisms of the therapeutic action of MPH.

116 ose sensitivity to the beneficial actions of MPH.

117 washout, the D2/D3 receptor availability of MPH-treated animals did not continue to decline at the s

118 Attention and behavioral benefits of MPH for childhood cancer survivors are maintained across

119 es, the effects of varying concentrations of MPH (0.25, 1.0, and 4.0 muM) on NE and DA efflux were ex

120 Low concentrations of MPH elicited significantly larger increases in extracell

121 the long-term neurochemical consequences of MPH treatment are unknown.

122 ese findings are discussed in the context of MPH effects on the default mode network and the possible

123 Brief discontinuation of MPH treatment is associated with increased motor and ant

124 microinfusion of vehicle or varying doses of MPH (.03-8.0 mug/500 nL) directly into the dorsomedial P

125 mental exposure to high therapeutic doses of MPH has short-term effects on select neurotransmitters i

126 The effects of varying doses of MPH were examined on performance of rats in two tests of

127 mental area (VTA) to determine the effect of MPH, FLX, or MPH + FLX on the extracellular signal-regul

128 Finally, there were no effects of MPH administration on any reported measure.

129 found no relationship between the effects of MPH on impulsivity and D2/3 receptor availability in any

130 support the potentially important effects of MPH on various aspects of cognition known to be associat

131 ction of MPH, could influence the effects of MPH or ATX on SICI.

132 th either a sustained release formulation of MPH or placebo (N=8 per group).

133 vation period, suggesting that the impact of MPH on puberty is not permanent.

134 We measured the impact of MPH, compared with placebo, on behavioral and electrocor

135 ed premature responding whereas infusions of MPH in the core, but not the shell, sub-region significa

136 kg (low dose, n = 10), or (iii) 1.5 mg/kg of MPH increased to 12.5 mg/kg (high dose, n = 10) for a to

137 L/kg of vehicle (n = 10), (ii) 0.15 mg/kg of MPH increased to 2.5 mg/kg (low dose, n = 10), or (iii)

138 nd experiment, 20 subjects received 20 mg of MPH, while 20 matched controls received a placebo.

139 eractivity scores over the first 3 months of MPH medication was correlated with the initial 90-minute

140 ter (DAT) levels and enhances the potency of MPH and amphetamine on dopamine responses and drug-seeki

141 double-blinded, placebo-controlled trial of MPH.

142 olunteers were studied with SPECT on and off MPH.

143 e alpha(1)-antagonist prazosin (.5 mg/kg) on MPH-induced improvement in sustained attention was exami

144 VTA) to determine the effect of MPH, FLX, or MPH + FLX on the extracellular signal-regulated protein

145 We administered saline (VEH), MPH, FLX, or MPH + FLX to juvenile Sprague Dawley male rats from post

146 The patients ingested a placebo (lactose) or MPH (0.6 mg/kg; 20 mg maximum) and repeated selected por

147 n 2 d: after ingesting a single dose of oral MPH (20 mg) or placebo (lactose) in a counterbalanced fa

148 Results show that oral MPH increased responses to this salient cognitive task i

149 We hypothesized that oral MPH will attenuate ACC hypoactivations and improve assoc

150 0.010; DPH: MD -0.765, P <0.001; mesial PH [MPH]: MD -0.285, P = 0.256).

151 e rehabilitation (MAAT) and pharmacotherapy (MPH) can improve aspects of attention, episodic and work

152 At PND135, MPH-exposed rats exhibited decreased anxiety in the elev

153 se in boys newly diagnosed with ADHD predict MPH-associated changes in ADHD inattentiveness and hyper

154 nitive complaints were randomized to receive MPH or placebo and MAAT or ABT, yielding four treatment

155 with therapeutic doses of sustained release MPH did not have a significant influence on the regulati

156 Funding assistance for AD's MPH from Scottish Intensive Care Society, Scottish Socie

157 In these studies, MPH-induced improvement in sustained attention was aboli

158 The clinical application of such MPH-induced brain-behavior enhancements remains to be te

159 When the subjects were not taking MPH, rCBF was higher in the motor, premotor, and the ant

160 ssary for accurate performance in this task, MPH infusion into this region did not affect working mem

161 n mice mimics these effects, confirming that MPH self-administration-induced increases in DAT levels

162 We found that MPH and ATX had similar effects on SICI.

163 Our findings indicate that MPH administration, beginning before puberty, and which

164 Here we show that MPH self-administration in rats increases dopamine trans

165 Our results showed that MPH at all doses increased Bax in the cortex; the Bcl-2

166 In conclusion, our results suggest that MPH influences plasticity in the brain of young and adul

167 Our findings suggest that MPH treatment modulates motor and anterior cingulate cor

168 system and behavior, and also suggests that MPH administration may not have long-term consequences.

169 This work suggests that MPH, acting via noradrenergic mechanisms, can substantia

170 For the MPH group, repeated measures analysis of variance reveal

171 Eligibility criteria for the MPH trial included an estimated intelligence quotient gr

172 A trend for greater improvement in the MPH group on a measure of verbal memory failed to reach

173 premedication baseline and at the end of the MPH trial while on medication.

174 ERK2 activity within the VTA, we rescued the MPH and FLX-induced behavioral deficits seen in the forc

175 ebo group, the 15 patients randomized to the MPH group had a significantly greater improvement on the

176 neurobiological consequences of exposure to MPH at high, abused doses are not well defined.

177 Here we show in rats that exposure to MPH during pre-adolescence causes behavioral and neurobi

178 lternatively, our findings may be related to MPH withdrawal.

179 s found for the SLC6A3 40 bp and response to MPH with only two studies selected.

180 sequences of combined MPH and FLX treatment (MPH + FLX) during juvenile periods are unknown.

181 be pathologies; however, in clinical trials, MPH did not improve treatment outcome in cocaine addicti

182 We administered saline (VEH), MPH, FLX, or MPH + FLX to juvenile Sprague Dawley male r

183 ons in the core and shell, or increased when MPH was infused into either the core and shell sub-regio

184 It was not possible to resolve whether MPH delayed the initiation of the onset of puberty or re

185 t increase in the parietal P3 amplitude with MPH, indicative of enhanced perceptual evidence accumula

186 cerebellum there was an increase of Bax with MPH at all doses, however, there was a reduction of Bcl-

187 ime, chronic modulation of young brains with MPH may exert effects on brain neurochemistry that modif

188 n of Bcl-2, caspase-3, and cytochrome c with MPH (2 and 10mg/kg); in the striatum the treatment with

189 ats showed major structural differences with MPH exposure.

190 hrome c were reduced in the hippocampus with MPH (10mg/kg).

191 red to placebo, significant improvement with MPH was reported by teachers and parents on the Conners'

192 the Bcl-2 and caspase-3 were increased with MPH (1mg/kg) and were reduced with MPH (2 and 10mg/kg);

193 nt in children, male rats were injected with MPH (5 mg/kg) or vehicle twice daily from postnatal day

194 ased with MPH (1mg/kg) and were reduced with MPH (2 and 10mg/kg); the cytochrome c was reduced in the

195 In contrast, subjects treated with MPH gambled at a consistent rate, well above chance, acr

196 (PD90) Sprague Dawley rats were treated with MPH or saline.

197 Treatment with MPH (0.125 mg/kg), ATMX (0.125 mg/kg), or EX (3 weeks of

198 10mg/kg); in the striatum the treatment with MPH (10mg/kg) decreased caspase-3 and cytochrome c; trea

199 d caspase-3 and cytochrome c; treatment with MPH (2 and 10mg/kg) increased Bax and decreased Bcl-2 in

200 s reduced in the cortex after treatment with MPH at all doses; in the cerebellum there was an increas

201 o, we investigated if chronic treatment with MPH at doses of 1, 2 and 10mg/kg could alter the levels

202 Treatment with MPH can at least temporarily reduce some attentional and

203 Juvenile treatment with MPH may result in long-lasting, potentially permanent, c