ライフサイエンスコーパス: stimulant

1 raditional medicine as a physical and mental stimulant.

2 -uninfected individuals, irrespective of the stimulant.

3 ption but only gluconasturtiin was a feeding stimulant.

4 ist capsaicin, a clinically relevant tussive stimulant.

5 n mouse lungs after administration with a co-stimulant.

6 ighly addictive central nervous system (CNS) stimulant.

7 in coffee and tea and is a broadly consumed stimulant.

8 istration, as well as inhalation of a beta 2 stimulant.

9 SGA initiators who were concomitantly using stimulants.

10 ependence) in individuals experimenting with stimulants.

11 nsitivity of these cells to various external stimulants.

12 tions without an antipsychotic, and 1.2% for stimulants.

13 ffect on ROS triggered by a variety of other stimulants.

14 pharmacotherapy for ADHD, particularly with stimulants.

15 ithium salts, sedatives and anxiolytics, and stimulants.

16 in three-component vaccines with both these stimulants.

17 other structurally related amphetamine-type stimulants.

18 regions than OSU who preferred prescription stimulants.

19 rom P. gingivalis were used as the bacterial stimulants.

20 g upon the nature and quantities of external stimulants.

21 e transgenic manipulations or treatment with stimulants.

22 incoming/outgoing diversion of prescription stimulants.

23 about the responsiveness of synaptic ERK to stimulants.

24 nd whose main drugs injected were opioids or stimulants.

25 opioids and 33.0% (24.3-42.0) mainly inject stimulants.

26 litate covert use of a range of psychoactive stimulants.

27 Mutant alleles at the LGS1 (LOW GERMINATION STIMULANT 1) locus drastically reduce Striga germination

28 -based adjuvant AS01 incorporates two immune stimulants, 3-O-desacyl-4'-monophosphoryl lipid A and th

29 ceive 3 months of contingency management for stimulant abstinence plus treatment as usual or treatmen

30 e studied gamblers with and without previous stimulant abuse and age- and sex-matched controls.

31 In addition, previous stimulant abuse had a marked effect on the amplitude of

32 t pathological gamblers without a history of stimulant abuse had lower PCC power during the stop-sign

33 Furthermore, gamblers with a history of stimulant abuse had up to four times higher power at the

34 ave an essential role in treatment-resistant stimulant abuse, suggesting new approaches for the devel

35 'stop' or to 'go' are more likely to develop stimulant abuse.

36 g to alternative strategies aimed at abating stimulant abuse.

37 the development of effective medications for stimulant abuse.

38 red with controls and gamblers with previous stimulant abuse.

39 which could not be explained by a history of stimulant abuse.

40 ion could reduce vulnerability to relapse in stimulant abuse.

41 te preclinical indicators of both opioid and stimulant abuse.

42 locus drastically reduce Striga germination stimulant activity.

43 Although stimulant addiction research has largely focused on DA,

44 ocessing deficits in individuals at risk for stimulant addiction.

45 atement of social reward in the treatment of stimulant addiction.

46 ive therapeutic targets for the treatment of stimulant addiction.

47 creased the discounting of future rewards in stimulant addicts without affecting a go/no-go task.

48 nned with [(11)C]raclopride before and after stimulant administration (methylphenidate) to measure st

49 mg oral NTX 60 min before active or placebo stimulant administration during 10 separate laboratory s

50 rimotor gating and altered responsiveness to stimulant agents.

51 angial cell proliferation compared with each stimulant alone.

52 ncrease in IL-6 secretion compared with each stimulant alone.

53 e, codeine, oxycodone, hydrocodone) and five stimulants (amphetamine, methamphetamine, 3,4-methylened

54 Paradoxically, alcohol acts as both a stimulant and a sedative.

55 Human beta defensin DEFB103 acts as both a stimulant and an attenuator of chemokine and cytokine re

56 vity and with absent or blunted responses to stimulant and dopaminergic agonist drugs, in conjunction

57 pressive symptomatology, IBUD attenuated the stimulant and mood-altering effects of alcohol as compar

58 symptomatic] to 54 [most symptomatic]), both stimulant and nonstimulant medications led to clinically

59 Cocaine is a strong central nervous system stimulant and one of the most commonly abused drugs.

60 idence for efficacy has been established for stimulant and osmotic laxatives, new intestinal secretog

61 l suited for this task, with a wide range of stimulants and a number of impressive examples, demonstr

62 an islet chamber with the ability to perfuse stimulants and an amino acid measurement system with der

63 iated with multiple-drug regimens, including stimulants and antidepressants, as well as individual SG

64 wn significant improvements in symptoms with stimulants and atomoxetine; however, data on long-term b

65 sing the medical and nonmedical use (NMU) of stimulants and diversion is a challenge, especially amon

66 eport that SMCs synergize with innate immune stimulants and immune checkpoint inhibitor biologics to

67 in and aliphatic glucosinolates were feeding stimulants and indole glucosinolates were feeding deterr

68 isotopes and amended with specific microbial stimulants and inhibitors, and subsampled over 12 days.

69 ntrol subjects, suggesting shared effects of stimulants and nonstimulants on a key prefrontal dysfunc

70 properties of ketamine, and comparisons with stimulants and other NMDA antagonists.

71 c medications (from 5.5% to 8.9%), including stimulants and related medications (from 4.0% to 6.6%),

72 ing IFN-alpha and IL-10 responses to certain stimulants and responses to phytohemagglutinin.

73 s and anxiolytics, 2.9 (95% CI, 2.3-3.5) for stimulants, and 2.4 (95% CI, 2.1-2.7) for antidepressant

74 inhaled steroids, long-acting inhaled beta2-stimulants, and leukotriene receptor antagonists, increa

75 s several pharmacological properties: energy stimulant, antimicrobial, chemoprophylactic, antigenotox

76 Moreover, the DCs expressing the super stimulant are more potent to provoke both cellular and h

77 atory gene expression, indicating that blood stimulants are accessible to the macrophages and that th

78 Concerns about in utero exposure to stimulants are based primarily on the impact these medic

79 incorporate inhaled exposure to psychomotor stimulants are not commonly available.

80 psychostimulant methylphenidate and the non-stimulant atomoxetine are used in the pharmacotherapy of

81 g MIPs-based sensors toward amphetamine-type stimulants (ATS).

82 The well-known stimulant caffeine, and its xanthine alkaloid precursors

83 hbouring PACs, whereas the physiological PAC stimulant cholecystokinin failed to evoke Ca(2+) signals

84 that mediate the reinforcing action of this stimulant class.

85 enhanced by an injection of the psychomotor stimulant cocaine (10 mg/kg, i.p.).

86 after the administration of two dopaminergic stimulants, cocaine and GBR-12909.

87 e consistent with a model in which breathing stimulant compounds PKTHPP, A1899, and doxapram inhibit

88 of NF-kappaB in single cells under different stimulant concentrations by real-time imaging.

89 e highly caffeinated energy drinks and other stimulants, creating further disruptions in sleep.

90 V between male control subjects and men with stimulant dependence (P = .625).

91 ects [28 women, 40 men] and 59 patients with stimulant dependence [28 women, 31 men]) underwent T1-we

92 t changes in GMV were observed in women with stimulant dependence after prolonged abstinence, but wer

93 rove this balance may enhance treatments for stimulant dependence and other disorders that involve ma

94 ontal and temporal GMV changes in women with stimulant dependence but not in the other groups.

95 red with female control subjects, women with stimulant dependence had significantly lower GMV in wide

96 Human research on action inhibition in stimulant dependence has highlighted impaired performanc

97 ognitive endophenotype has been proposed for stimulant dependence, based on behavioral measures of in

98 g cocaine recreationally with 50 adults with stimulant dependence, their nondependent siblings (n = 5

99 outpatients with serious mental illness and stimulant dependence.

100 stimulant users (OSU) at risk for developing stimulant dependence.

101 her this inefficiency predicts transition to stimulant dependence.

102 er evaluation as an adjunctive treatment for stimulant dependence.

103 Stimulant-dependent individuals (SDIs), their unaffected

104 e function was significantly impaired in the stimulant-dependent individuals across a range of domain

105 d limbic-striatal enlargement were shared by stimulant-dependent individuals and their unaffected sib

106 We found that neuroimaging studies in stimulant-dependent individuals consistently report a gr

107 While stimulant-dependent individuals continue to make risky d

108 metry meta-analysis of published MRI data in stimulant-dependent individuals to clarify the most robu

109 Since the first study in stimulant-dependent individuals using structural MRI was

110 Conversely, stimulant-dependent individuals were significantly more

111 Stroop to 27 recreational cocaine users, 50 stimulant-dependent individuals, and 52 healthy control

112 which inhibitory control deficits emerge in stimulant-dependent individuals.

113 reased abstinence from stimulant drug use in stimulant-dependent patients with serious mental illness

114 cAMP was confirmed by treatment with the AC6 stimulant desmopressin.

115 While stimulants do not appear to be associated with major con

116 Lower, behavioral-stimulant doses enhance the cAMP response element-bindin

117 thwest and Mexican Northwest likely consumed stimulant drinks in communal, ritual gatherings.

118 theobromine, and theophylline) indicative of stimulant drinks, probably concocted using either cacao

119 lated on brain abnormalities associated with stimulant drug dependence.

120 protected vaginal intercourse (p = 0.026) or stimulant drug use (p = 0.026), and more likely to repor

121 ey also reported significantly fewer days of stimulant drug use during the 3-month follow-up.

122 as associated with increased abstinence from stimulant drug use in stimulant-dependent patients with

123 vulnerability for dependence or with regular stimulant drug use.

124 e administration of the first MPH dose to 40 stimulant drug-naive boys newly diagnosed with ADHD whil

125 l FH of substance use disorders (n = 16); 2) stimulant drug-naive healthy control subjects with no kn

126 (17 male, 7 female; age 23.0 +/- 6.2 years) stimulant drug-naive subjects who underwent PET [(11)C]r

127 Clandestine chemists synthesize novel stimulant drugs by exploiting structural templates known

128 The research began with the finding that stimulant drugs enhanced memory in rats when administere

129 m may account for the therapeutic effects of stimulant drugs in clinical disorders such as ADHD.

130 ility in the left ventral striatum, and that stimulant drugs modulate impulsivity and striatal D2/3 r

131 shared by individuals who were dependent on stimulant drugs or used cocaine recreationally.

132 Stimulant drugs such as cocaine and amphetamine have a h

133 seen in only a fraction of those exposed to stimulant drugs such as cocaine.

134 Ephedrine and pseudoephedrine are stimulant drugs whose use is prohibited in athletic comp

135 Ds), and acute stress augments the locomotor stimulant effect of cocaine in animal models.

136 Cocaine exerts its behavioral stimulant effects by facilitating synaptic actions of ne

137 Cocaine's behavioral-stimulant effects derive from potentiation of synaptic s

138 SNs is required and permissive for the motor stimulant effects of cocaine and the activation of signa

139 egimen caused sensitization to the locomotor stimulant effects of cocaine, and these effects were aga

140 assessed for sensitization to the locomotor stimulant effects of cocaine.

141 In contrast, locomotor stimulant effects of SNC80 (DOR agonist) and SKF81297 (D

142 meta-analysis of the fMRI findings of acute stimulant effects on ADHD brain function.

143 l is completed by young adulthood, assessing stimulant effects on bone density in growing children is

144 drugs of abuse (e.g., hallucinogens, central stimulants, empathogens), the latter of which are the pr

145 relationship between dopamine receptors and stimulant-enhanced flexibility was partially mediated by

146 fication and the lack of cocaine-cues during stimulant exposure.

147 ize by ages 3 to 4 months after cessation of stimulant exposure.

148 ethanol-related behavioral changes, such as stimulant followed by depressant effects, and (2) chroni

149 Light is a powerful stimulant for human alertness and cognition, presumably

150 duction of cis-3-hexenal acting as a feeding stimulant for M. sexta larvae in OPR3-RNAi plants.

151 e has been used for decades as a respiratory stimulant for patients with chronic obstructive pulmonar

152 aicin (10 microg/ml, 50 microl), a selective stimulant for TRPV1 receptors, in anesthetized preparati

153 Participants treated with stimulants for 3 months or longer had significantly lowe

154 on and increased beta-cell workload are both stimulants for beta-cell proliferation but are TGFbeta r

155 development, neurotransmitters are important stimulants for the development of the central nervous sy

156 ironmental Ag could be the initial antigenic stimulants for the IgG4 autoimmune responses in FS.

157 n the design of small molecule adjuvants and stimulants for use in immunotherapies.

158 ce that was intermediate between that of the stimulant group and the healthy CT group.

159 as the first-line intervention, noting that stimulants have a much broader evidence base and larger

160 yed antrum formation [indicative of follicle stimulant hormone (FSH) dependence] and increased sensit

161 Nicotine is the major stimulant in tobacco products including e-cigarettes.

162 C-MS/MS) analysis allowing detection of five stimulants in finger prick blood.

163 2) induction of IFN-I by Toll-like receptor stimulants in peripheral blood mononuclear cells of 60 h

164 romise in altering the behavioral effects of stimulants in rodents, nonhuman primates, and humans.

165 ) subtype (alpha1, alpha2, and beta) to five stimulant-induced behaviors relevant to addiction: locom

166 icable pathological phenomena such as psycho stimulant-induced contraversive rotations in animal mode

167 ement is associated with large reductions in stimulant,injection drug, and alcohol use.Reductions in

168 nethylamine core with other amphetamine-type stimulants, it also incorporates a covalently linked xan

169 PIMs included: long-term use of stimulant laxatives and high-dosages of ferrous sulfate,

170 When used appropriately, available stimulant laxatives such as senna and bisacodyl are both

171 Here, we show that stimulants like cocaine and methamphetamine greatly incr

172 us studies have shown that the innate immune stimulant LPS augments mechanical ventilation-induced pu

173 We found that proinflammatory stimulants LPS, IL-6 and IL-1beta up-regulated the expre

174 ontrolled trials show short-term benefits of stimulant medication and atomoxetine.

175 Previous use of stimulant medication does not seem to modify subsequent

176 most women can successfully avoid the use of stimulant medication during pregnancy, there are cases i

177 rder (ADHD) often present to clinics seeking stimulant medication for late-onset ADHD symptoms.

178 nown whether prolonged childhood exposure to stimulant medication for the treatment of attention defi

179 cohort of adult patients and if a history of stimulant medication has an effect on brain structure, m

180 Stimulant medication has long been effective in treating

181 ttention-deficit/hyperactivity disorder with stimulant medication neither protects nor increases the

182 months in which patients received prescribed stimulant medication or atomoxetine relative to the risk

183 inates of clusters of significant effects of stimulant medication relative to placebo or off medicati

184 DHD) symptoms are most commonly treated with stimulant medication such as methylphenidate (MPH); howe

185 egression methods explored age and long-term stimulant medication use effects.

186 attention tasks, exploring age and long-term stimulant medication use effects.

187 preliminary evidence suggests that long-term stimulant medication use may be associated with more nor

188 r the attention domain showed that long-term stimulant medication use was associated with more simila

189 ey may be influenced by age and by long-term stimulant medication use.

190 Stimulant medication was associated with larger regional

191 hen co-occurring externalizing behaviors and stimulant medication were considered.

192 ns regarding potential iatrogenic effects of stimulant medication, particularly with respect to incre

193 nned twice at 12 months interval but without stimulant medication.

194 elease methylphenidate and amphetamine class stimulant medications (level 1B based on Oxford Centre f

195 e the acute increases in dopamine induced by stimulant medications have been associated with symptom

196 itiation of treatment and against the use of stimulant medications or empiric continuous positive air

197 risk groups: school-aged children initiating stimulant medications to treat attention-deficit/hyperac

198 Stimulant medications used to treat attention-deficit/hy

199 eractivity disorder (ADHD) could explain why stimulant medications, which increase dopamine signaling

200 d physician diagnosis of ADHD or were taking stimulant medications.

201 reported that adolescent treatment with the stimulant methylphenidate, a dopamine (DAT) and norepine

202 y must also be vigilant to the potential for stimulant misuse and diversion.

203 The CNS stimulants modafinil and methylphenidate are recommended

204 sets and 212 children with ADHD, showed that stimulants most consistently enhanced right IFC/insula a

205 ects consisted of 68 psychotropic (including stimulant)-naive and smoking-naive volunteers between 18

206 Occasional stimulant users (n = 161) and stimulant-naive comparison subjects (CTL) (n = 48) perfo

207 A total of 158 nondependent OSU and 47 stimulant-naive control subjects (CS) were recruited and

208 In 64 RCU, 29 DCU, and 66 stimulant-naive control subjects, PPI of acoustic startl

209 re of anabolics, beta-2 agonists, diuretics, stimulants, narcotics, and beta-blockers) spiked in huma

210 ing episodes, and were more likely to submit stimulant-negative urine and smoking-negative breath sam

211 imes (95% CI=1.9-3.0)more likely to submit a stimulant-negative urine test during treatment.

212 Effects of enzyme stimulants ((NH4)2SO4 and MnCl2.4H2O) concentrations and

213 Activating sGC by its natural stimulant nitric oxide (NO), or by pharmacologic sGC ago

214 LMW HA was a potent stimulant of AA release in a time- and dose-dependent ma

215 Ingested fat is the major stimulant of CCK secretion.

216 Caffeine, generally known as a stimulant of gastric acid secretion (GAS), is a bitter-t

217 glucagon-like peptide 1 (GLP-1), a powerful stimulant of insulin release.

218 evels via the BLT1 receptor and was a potent stimulant of macrophage phagocytosis and NADPH oxidase-d

219 Because thrombin is a potent stimulant of platelet activation, we hypothesized that i

220 Stimulants of acid secretion include histamine, gastrin,

221 Stimulants of acid secretion include histamine, gastrin,

222 4 (TLR4) and the gut microbiome as critical stimulants of CCM formation.

223 Endogenous stimulants of Hepcidin transcription include bone morpho

224 umors and its role in tumor biology, we used stimulants of NOS2 expression in ER(-) and ER(+) breast

225 These results suggest that stimulants of oxidative metabolism could have therapeuti

226 Here we report the effect of such stimulants on signaling pathways of cercariae in relatio

227 e effects of ethanol on neurons, as either a stimulant or a sedative, however remain unclear.

228 d the first to involve mechanisms other than stimulant or dopamine agonist effects.

229 from individuals who are either dependent on stimulants or at risk for dependence.

230 use, or maximal level of cannabis, sedative, stimulant, or cocaine use.

231 icant difference in abstinence from opioids, stimulants, or heavy drinking between the CCM (44%) and

232 e was self-reported abstinence from opioids, stimulants, or heavy drinking.

233 ase in the use of short-acting inhaled beta2-stimulants, parenteral aminophylline, and slow-release t

234 tion and can be highly induced by the T cell-stimulant PHA, suggesting it is a particularly important

235 une activation or in adulthood to the immune stimulant poly(I:C).

236 en shown to be a promising target to prevent stimulant relapse.

237 ion in the frontal cortex may be involved in stimulant-related learning driving appetitive behavior.

238 locomotion and cocaine exerts its canonical stimulant response.

239 ockDelta19) exhibit increased preference for stimulant rewards and sucrose.

240 crete a low-molecular-weight chemoattractive stimulant(s) of macrophages, a phagocyte that they are a

241 ue cells do not secrete this chemoattractive stimulant(s).

242 -type compounds in monkeys with a history of stimulant self-administration, whereas alpha3 subunit-co

243 Methamphetamine (Meth) is a psychomotor stimulant strongly associated with increases in sexual d

244 tional Monitoring of Adolescent Prescription Stimulants Study recruited 11,048 youth 10-18 years of a

245 Despite the prevalent worldwide abuse of stimulants, such as amphetamines and cocaine, no medicat

246 enhancement can be achieved by using psycho-stimulants, such as caffeine or nicotine, but very littl

247 Stimulants, such as methylphenidate hydrochloride, are t

248 In this study, we developed a super DC stimulant that consists of a modified, secretory Toll-li

249 e name Captagon, is a synthetic psychoactive stimulant that has recently been linked to a substance-u

250 Methylphenidate (MPH) is a stimulant that increases extracellular levels of dopamin

251 Nicotine is an important stimulant that is involved in modulating many neuronal p

252 specific components of innate microbiologic stimulants that lead to contrasting effects on wheeze de

253 Liposomal vaccine formulations incorporating stimulants that target innate immune receptors have been

254 rted to differ from those of other synthetic stimulants, the in vivo chemical complexity it manifests

255 s platelet activation by virtually any other stimulant to complete aggregation.

256 Caffeine is the most widely consumed stimulant to counter sleep-loss effects.

257 ive but can be readily activated by upstream stimulants to lead to prolonged strong Ras activity.

258 ystrigol, a highly active Striga germination stimulant, to orobanchol, an SL with opposite stereochem

259 to detect an alarming array of psychoactive stimulants, tranquilizers, and synthetic opioids.

260 cy, there are cases in which the benefits of stimulant treatment outweigh known and putative risks of

261 However, stimulant treatment was previously reported to reduce th

262 x, age 10 to 12 years or 23 to 40 years, and stimulant treatment-naive status.

263 fic to ADHD, dimensions of symptomology, and stimulant treatment.

264 morphological changes support the effects of stimulant treatment.

265 severity of ADHD symptoms and the effects of stimulant treatment.

266 of comorbid mental disorders or a history of stimulant treatment.

267 Because no study has focused on stimulant use among youth as young as 10 and 11, this st

268 ively followed for 3 years and evaluated for stimulant use and abuse/dependence symptoms.

269 jective: To investigate associations between stimulant use and bone mass in children and adolescents.

270 tcomes and Measures: The association between stimulant use and total femur, femoral neck, and lumbar

271 ccasional stimulant users met criteria for a stimulant use disorder (problem stimulant users), while

272 Stimulant use disorders are associated with deficits in

273 elevance: Children and adolescents reporting stimulant use had lower DXA measurements of the lumbar s

274 .S. households, was analyzed for therapeutic stimulant use in children age 18 and younger.

275 rospective studies to examine the effects of stimulant use on bone mass in children.

276 Lifetime prevalence of any stimulant use was 14.8%, with rates highest among rural

277 Stimulant use was associated with lower bone mass after

278 g those with primary mood disorders (14.1%); stimulant use was most common among those with attention

279 Exposures: Stimulant use, determined by questionnaires administered

280 Occasional stimulant users (n = 161) and stimulant-naive comparison

281 ecision-making characteristics of occasional stimulant users (OSU) at risk for developing stimulant d

282 ocessing characteristics in human occasional stimulant users (OSU), a population at risk for dependen

283 ariable linear regression analysis, 159 were stimulant users and 6330 were nonusers.

284 Occasional stimulant users displayed greater anterior insula, infer

285 Occasional stimulant users exhibit inefficient resource allocation

286 At follow-up, 38 occasional stimulant users met criteria for a stimulant use disorde

287 lumbar spine BMC was significantly lower in stimulant users vs nonusers (12.76 g; 95% CI, 12.28-13.2

288 0.98-0.99 g/cm2; P = .05) were also lower in stimulant users vs nonusers.

289 iteria for a stimulant use disorder (problem stimulant users), while 50 had discontinued use (desiste

290 rs), while 50 had discontinued use (desisted stimulant users).

291 red and fifty-seven non-dependent occasional stimulant users, aged 18-24, completed a stop-signal tas

292 phorbol 12,13-dibutyrate (PDBu) or a natural stimulant, UTP, time lapse live cell imaging movies indi

293 The effect of vapor inhalation of the stimulants was found comparable to the locomotor and ICS

294 ressants, antipsychotics, lithium salts, and stimulants were implicated in an estimated 30,707 (95% C

295 Both methcathinone analogs were weak motor stimulants when compared with methamphetamine.

296 eatments for the sleep-disrupting effects of stimulants when used alone and in combination.

297 oproteinase-1 are up-regulated by these NOS2 stimulants, whereas inhibition of NOS2 in MDA-MB-231 bre

298 Cocaine is one of the most commonly misused stimulant which could influence the central nervous syst

299 firing to carbon dioxide (CO2), an odorless stimulant with known trigeminal capacity.

300 participants were defined as those who used stimulants within 30 days following treatment discharge