ライフサイエンスコーパス: nicotine

1 ns in synaptic plasticity induced by chronic nicotine.

2 enhancing KYNA can counteract the effects of nicotine.

3 ues that had previously been associated with nicotine.

4 terconnections in the behavioral response to nicotine.

5 ignificant relationship was found for plasma nicotine.

6 se sections: diethyl phthalate, caffeine and nicotine.

7 tinction of conditioned aversive response to nicotine.

8 players in mediating the aversive effects of nicotine.

9 ptimized parameters for in-situ detection of nicotine.

10 type with the same caloric value but without nicotine.

11 and alterations in neurochemical effects of nicotine.

12 mediate the positive reinforcing effects of nicotine.

13 f mood disorders and behavioral responses to nicotine.

14 ion for dose by normalizing the exposures to nicotine.

15 may contribute to the behavioral effects of nicotine.

16 regulatory T cells and by compounds such as nicotine.

17 We found that the intake of nicotine (15 and 30 mug/kg/inf) varied among these strai

18 thesis O7460 abolished cognitive deficits of nicotine abstinence, whereas the inhibitor of 2-AG enzym

19 ictures as significantly more pleasant while nicotine abstinent than while nicotine sated.

20 te pictures when they were nicotine sated or nicotine abstinent.

21 hair follicle disorder, and had a history of nicotine abuse and/or obesity, which are known trigger f

22 ished associations with sequence variants in nicotine acetylcholine receptor genes and at other loci.

23 We propose that nicotine activation of this pathway may contribute to ni

24 together, results of this study suggest that nicotine acts through alpha7-nAChR and plays a novel rol

25 the nicotine content of cigarettes to lower nicotine addiction potential in the United States.

26 ed ion channel in the brain and a target for nicotine addiction therapy, and the 19-residue conotoxin

27 ing several types of addiction (most notably nicotine addiction) and other compulsive behaviors.

28 uccessfully used for treatment of opiate and nicotine addiction, but not for cocaine addiction.

29 cal role of mGluR2/3 in different aspects of nicotine addiction, including acquisition and maintenanc

30 activation of this pathway may contribute to nicotine addiction, particularly in individuals with gen

31 ne presented to the brain over the course of nicotine addiction-shapes brain circuits that, among oth

32 to manage several neurological disorders and nicotine addiction.

33 It is also the likely receptor that mediates nicotine addiction.

34 tors are critical for smoking initiation and nicotine addiction.

35 gulin 3 (NRG3) and ErbB4 have been linked to nicotine addiction; however, the neuronal mechanisms and

36 The estimated radiation dose from (11)C-nicotine administration is relatively modest and would a

37 Chronic nicotine administration reversed this hypofrontality, su

38 rs (and increased in nonsmokers) after acute nicotine administration.

39 This clinically relevant nicotine aerosol inhalation (NAI) induced transient redu

40 hat constituents of tobacco smoke other than nicotine affect inflammatory processes.

41 Nicotine alone </=0.5 mM had little to no effect in any

42 roduces greater reward-related behavior than nicotine alone.

43 ed to various concentrations of CSE, STE, or nicotine alone.

44 nd function on midbrain DA neurons more than nicotine alone.

45 e endogenous neurotransmitter acetylcholine, nicotine also binds and activates nAChRs and influences

46 Nicotine also stimulated the proliferation of cholangioc

47 Moreover, nicotine altered nAChR assembly in the ER, resulting in

48 is of novel analogues of natural product (-)-nicotine and antidepressant sertraline by late-stage ami

49 The role of nicotine and e-cigarette derived nicotine on cellular fu

50 We found that both nicotine and e-cigarette inhibit myofibroblast different

51 Nicotine and e-cigarette inhibited OXPHOS complex III ac

52 We hypothesized that nicotine and e-cigarettes affect myofibroblast different

53 n and eliminated the serenic effects of both nicotine and GTS-21 on attack latency.

54 We observed that both nicotine and NRG3 facilitated the conversion of long-ter

55 In addition, nicotine and PNU282987 (alpha7-nAChR agonist) accelerate

56 the development of the first SRM for reduced nicotine and reduced tobacco-specific nitrosamines with

57 In the context of the clinical use of nicotine and related agonists for treating cognitive def

58 y assessed the in vivo distribution of (11)C-nicotine and the absorbed radiation dose from whole-body

59 Addiction to nicotine and the inability to quit smoking are influence

60 and lung cancer cell lines was treated with nicotine and the results showed nicotine increased the p

61 of Science, the 2016 Society for Research on Nicotine and Tobacco 22nd Annual Meeting abstracts, the

62 ects of smoking status and administration of nicotine and varenicline on probabilistic reversal learn

63 e behavioral impairments were mitigated with nicotine and varenicline.

64 abstinent rats or monkeys were reexposed to nicotine and/or cues that had previously been associated

65 Alcohol, nicotine, and cannabis are among the most commonly used

66 ffects of single or combined use of alcohol, nicotine, and cannabis.

67 delivering 0.027, 0.110, 0.231, or 0.763 mg nicotine, and conventional cigarettes.

68 on to intravenously self-administered (IVSA) nicotine, and that social learning promoted nicotine IVS

69 Neural effects of smoking status, nicotine, and varenicline were tested for on MRI contras

70 itry changes within this structure following nicotine application.

71 ns of CSC we used contained similar doses of nicotine as human smokers are exposed to, we argue that

72 Nicotine at 10 micromol/L significantly downregulated th

73 critical contributors to the balance between nicotine aversion and reward.

74 ity to tobacco dependence, yet mechanisms of nicotine avoidance are poorly understood.

75 that stimulate habenular systems to promote nicotine avoidance before its aversive effects are encou

76 tial in vitro-in vivo correlation (IVIVC) of nicotine BA from two, matrix-type, nicotine transdermal

77 and phenylpropanoid pathways as well as the nicotine biosynthetic pathway.

78 riven partly by the physiological effects of nicotine, but also by the distinctive sensory and behavi

79 um imaging in awake mouse models showed that nicotine can differentially influence PFC pyramidal cell

80 Thus, our data suggest that nicotine causes dysregulated repair by inhibition of myo

81 udy results have demonstrated that the BA of nicotine characterized by the IVPT studies correlated wi

82 findings have bearing on the use of reduced-nicotine cigarettes to facilitate smoking cessation and

83 cording to investigate the effect of chronic nicotine (cNIC) on synaptic plasticity in dopamine D2 re

84 nly use may obtain roughly similar levels of nicotine compared with smokers of combustible cigarettes

85 Each successive increase in nicotine concentration (none to low, low to medium, and

86 e-cigarettes within the past 30 days and the nicotine concentration level they used at baseline.

87 Self-report of baseline e-cigarette nicotine concentration of none (0 mg/mL), low (1-5 mg/mL

88 hat the rapid rise pattern of arterial blood nicotine concentration stimulates and then desensitizes

89 Use of e-cigarettes with high (vs no) nicotine concentration was associated with a greater num

90 vidence that use of e-cigarettes with higher nicotine concentrations by youths may increase subsequen

91 uate whether use of e-cigarettes with higher nicotine concentrations is associated with subsequent in

92 high (adjusted RR, 2.23; 95% CI, 1.42-3.03) nicotine concentrations.

93 types are deterred only by unnaturally high nicotine concentrations.

94 Nicotine consumers were characterized by an increment of

95 dication development strategies seek to halt nicotine consumption and prevent relapse to tobacco smok

96 Nicotine containing eCig vapor displayed the most profou

97 ted simultaneously with two equally rewarded nicotine-containing and nicotine-free flower types are d

98 igh natural dose, bees learn the colour of a nicotine-containing flower type more swiftly than a flow

99 Preference for higher over lower nicotine content cigarettes could be reversed by increas

100 e these disparities are needed; reducing the nicotine content in cigarettes should be a policy focus.

101 sation and on policy regarding regulation of nicotine content in cigarettes.

102 n [SD] age, 35.6 [11.4] years), reducing the nicotine content of cigarettes decreased the relative re

103 Reducing the nicotine content of cigarettes may decrease their addict

104 policy is under consideration to reduce the nicotine content of cigarettes to lower nicotine addicti

105 f acute response to research cigarettes with nicotine content ranging from levels below a hypothesize

106 Based on relative nicotine content, CSE was significantly more cytotoxic t

107 addiction respond to cigarettes with reduced nicotine content.

108 While a large body of research on nicotine continues to inform us about mechanisms related

109 oking, driven by the addictive properties of nicotine, continues to be a worldwide health problem.

110 We report that nicotine controls synaptic plasticity in the OFC through

111 the second study, intranasal insulin reduced nicotine cravings over time (b=0.065, P0.05) and the eff

112 utions were tested for equivalent and higher nicotine delivery compared to 3R4F.

113 Based on equivalent or higher nicotine delivery, an acute exposure to e-cigarette aero

114 datasets: the Collaborative Genetic Study of Nicotine Dependence (ascertained for tobacco use disorde

115 he primary eligibility criteria were current nicotine dependence (DSM criteria), smoking 10 or more c

116 acetylcholine receptors (nAChR) subunits and nicotine dependence (ND), only few studies were performe

117 l data showed the genetic pleiotropy between nicotine dependence and COPD or lung function.

118 To independently assess the effects of nicotine dependence and stimulation of the nicotinic ace

119 In this largest-ever GWAS meta-analysis for nicotine dependence and the largest-ever cross-ancestry

120 4-77%) was associated with increased risk of nicotine dependence at P=3.7 x 10(-8) (odds ratio (OR)=1

121 h was negatively associated with severity of nicotine dependence in slow metabolizers.

122 s, (1) whether the genetic predisposition of nicotine dependence influence COPD risk and lung functio

123 with ND measured by the Fagerstrom Test for Nicotine Dependence score; of these, 11 SNPs remained si

124 We found the genetic predisposition of nicotine dependence was associated with COPD risk, even

125 y smoking, number of cigarettes per day, and nicotine dependence was greater in females than in males

126 ence syndrome they were 1.72 (1.57-1.87) for nicotine dependence, 2.67 (2.38-2.99) for cannabis depen

127 fluenced regulation in brain on the risks of nicotine dependence, heavy smoking and consequent lung c

128 de association study (GWAS) meta-analysis of nicotine dependence, totaling 38,602 smokers (28,677 Eur

129 Nicotine dependence, which reduces the likelihood of qui

130 an hormones on the etiology and treatment of nicotine dependence.

131 Two known nicotine dependent loci (15q25.1 and 19q13.2) were assoc

132 The study included 24 nicotine-dependent smokers (12 women and 12 men; mean [S

133 Nicotine-dependent smokers and nonsmokers completed a pr

134 effects in slow metabolizers, but depends on nicotine dose in normal metabolizers.

135 were exposed to the cigarettes with varying nicotine doses across fourteen 2- to 4-hour outpatient s

136 The use of cigarettes delivering different nicotine doses allows evaluation of the contribution of

137 ke (R(2) = 0.85, p < 0.0001) between the two nicotine doses.

138 While exposure to nicotine during developmental periods can significantly

139 raving and withdrawal reflects primarily non-nicotine effects in slow metabolizers, but depends on ni

140 Fluids containing nicotine exerted cytotoxicity as demonstrated by increas

141 ed a phenome-wide association study in 3,401 nicotine-exposed elderly subjects considering 358 phenot

142 otype of the F1 mice resulting from paternal nicotine exposure could be attenuated by viral manipulat

143 e establish a paternal effect model based on nicotine exposure in mice, enabling pharmacological inte

144 Nicotine exposure increased epibatidine trapping by incr

145 In the present study, nicotine exposure induced depression in the paternal gen

146 gs reflect the role of paternal or postnatal nicotine exposure, as opposed to maternal or in utero ni

147 We demonstrate that nicotine exposure, independent of drug withdrawal effect

148 exposure, as opposed to maternal or in utero nicotine exposure, this study underlines the importance

149 egulation of nAChRs on the cell surface upon nicotine exposure.

150 ns of varenicline (Chantix) during long-term nicotine exposure.

151 two equally rewarded nicotine-containing and nicotine-free flower types are deterred only by unnatura

152 t in the cytoplasm of fibroblasts exposed to nicotine-free fluids.

153 te the relative effects of heat on the BA of nicotine from TDS with different formulations.

154 with and was predictive of the in vivo BA of nicotine from the respective TDS, evaluated under the ma

155 Nicotine has strong addictive as well as procognitive pr

156 o suggest that a combination of cannabis and nicotine have more contrasting effects on the brain than

157 Nicotine-impaired stimulus discrimination in this task w

158 AUCs and post-treatment residual content of nicotine in TDS from the in vitro and in vivo data sets

159 (40-160 microg/ml) of CSC and confirmed that nicotine in the CSC was metabolized to cotinine.

160 endent behavior, we evaluated the effects of nicotine in the go/no-go task.

161 sin acids, polycyclic aromatic hydrocarbons, nicotine) in the mass spectra were used to assign PMF fa

162 treated with nicotine and the results showed nicotine increased the proliferation of these cells.

163 (capsaicin) or insignificantly (gossypol and nicotine) induced L-ACY-1 expression in H. armigera, but

164 Interestingly, FSTL1 attenuated nicotine-induced BEAS2B and lung cancer cell line prolif

165 Menthol also enhances nicotine-induced changes in DA neuron excitability.

166 mouse models, we show that menthol enhances nicotine-induced changes in nicotinic acetylcholine rece

167 FSTL1 may prevent nicotine-induced lung cancer cell proliferation.

168 Altogether, our data indicate that nicotine-induced synaptic plasticity in the OFC and cogn

169 f smokers who participated in an intravenous nicotine infusion study that followed overnight smoking

170 After nicotine infusion, abstinent smokers with the withdrawal

171 e hypothesis that cigarette smoking-relevant nicotine inhalation during pregnancy impairs cardiovascu

172 Maternal smoking with obligatory nicotine inhalation is associated with preterm delivery,

173 These findings challenge the safety of pure nicotine inhalation, i.e., E-cigarettes.

174 ing the highest absorbed dose from the (11)C-nicotine injection were the urinary bladder wall (14.68

175 Recently, perinatal nicotine injections in rats were reported to induce pero

176 Further, there was a strong correlation in nicotine intake (R(2) = 0.85, p < 0.0001) between the tw

177 ate GLP-1 receptors, respectively, decreased nicotine intake in mice.

178 These data showed that nicotine intake in the socially acquired nicotine self-a

179 Tobacco smokers titrate their nicotine intake to avoid its noxious effects, sensitivit

180 The heritability of nicotine intake was estimated to be 0.54-0.65.

181 Nicotine intake was highly correlated with the extinctio

182 erences in salivary or urinary biomarkers of nicotine intake were found.

183 cuit abolished nicotine reward and decreased nicotine intake, whereas their knockdown or pharmacologi

184 of GLP-1 neurons in NTS similarly decreased nicotine intake.

185 nal problems than their co-twins had greater nicotine involvement, consistent with possible causal in

186 Withdrawal from nicotine is an important contributor to smoking relapse.

187 In mice, nAChR activation by nicotine is anti-aggressive, or 'serenic,' an effect whi

188 healing and gel contraction suggesting that nicotine is responsible for dysregulated repair during i

189 Nicotine is the major stimulant in tobacco products incl

190 mplicated in cognitive functions improved by nicotine is the prefrontal cortex (PFC).

191 hibited (capsaicin and gossypol) or induced (nicotine) it in H. assulta.

192 tested the hypothesis that socially acquired nicotine IVSA is a heritable trait by using female rats

193 nicotine, and that social learning promoted nicotine IVSA with flavor cues.

194 determine TSPO affinity genotype and plasma nicotine levels.

195 Furthermore, nicotine may act as a mitogen in cholestatic liver disea

196 se data suggest that procognitive effects of nicotine may involve development of enhanced gamma oscil

197 rontality, suggesting that administration of nicotine may represent a therapeutic strategy for the tr

198 The predominant subunit responsible for nicotine-mediated proliferation in normal and cancer cel

199 identifying the neurons that are altered by nicotine, menthol, and acetylcholine.

200 iation in the CYP2A6 gene alters the rate of nicotine metabolic inactivation and is associated with s

201 smokers, these data suggest that the rate of nicotine metabolism-and thus the concentration of nicoti

202 finding is related to CYP2A6 involvement in nicotine metabolism.

203 Pharmacotherapy provision based on Nicotine Metabolite Ratio (NMR) status (slow/normal meta

204 ticipants also rated each cigarette, and the nicotine metabolite ratio (NMR) was used to identify par

205 Salivary nicotine metabolites were measured and NMR (3-hydroxycot

206 They suggest that normal and slow nicotine metabolizers would respond differently to nicot

207 The uncharged and hydrophilic nicotine molecule showed no direct interactions with Abe

208 ified and reference mass fraction values for nicotine, N-nitrosonornicotine, 4-(methylnitrosamino)-1-

209 tic modifier of sensitivity to l-DOPA and of nicotine neuroprotection in PD.

210 tein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Abeta) accumulat

211 ngs, we examined the effects of the alkaloid nicotine on bumblebee foraging performance.

212 The role of nicotine and e-cigarette derived nicotine on cellular functions including profibrotic res

213 ng several of the pharmacological effects of nicotine on cognition, attention, and affective states.

214 tra-individual ovarian hormone variation and nicotine on suppression of tobacco withdrawal symptoms a

215 Therefore, we studied the effects of nicotine on the growth of cholangiocarcinoma cells in vi

216 Here we assessed the impact of nicotine on unit activity and local field potential osci

217 of the e-cigarette liquids (with and without nicotine) on the same experimental model.

218 e receiving a placebo pill, wearing either a nicotine or a placebo patch.

219 ollowing injection of toxic levels of either nicotine or cocaine, accompanied by hepatic upregulation

220 erior cingulate cortex were not mitigated by nicotine or varenicline.

221 of animals chronically treated with saline, nicotine, or undergoing 24 h withdrawal.

222 occasions, in the presence and absence of a nicotine patch.

223 bsorbed radiation dose from whole-body (11)C-nicotine PET imaging of 11 healthy (5 male and 6 female)

224 olar region-targeted aerosol method produced nicotine pharmacokinetics resembling cigarette smoking i

225 nduced levels of defense metabolites such as nicotine, phenolamides, and diterpenoid glycosides.

226 ine metabolism-and thus the concentration of nicotine presented to the brain over the course of nicot

227 Paternal exposure to nicotine prior to reproduction induced a broad protectiv

228 An acute dose of nicotine produced a predominantly inhibitory influence o

229 e (CPP) assay, we observed that menthol plus nicotine produces greater reward-related behavior than n

230 ne metabolizers would respond differently to nicotine reduction in cigarettes, but that irrespective

231 aining acidic vesicles that is selective and nicotine-regulated.

232 gh relapse rates are attributed to pervasive nicotine-reinforced associative learning of incentive cu

233 ene) previously implicated in behavioral and nicotine-related studies (albeit with inconsistent major

234 Induction of long-term depression by nicotine relied on nicotinic receptor activation and key

235 al consequences of NRG3-ErbB4 sensitivity to nicotine remain elusive.

236 The evidence about nicotine replacement therapies was inconclusive (RR: 1.2

237 ette use only, former smokers with long-term nicotine replacement therapy (NRT) use only, long-term d

238 abstinence and by pharmacotherapies such as nicotine replacement therapy and varenicline tartrate ma

239 alth, smoking and treatment characteristics (nicotine replacement therapy vs. other pharmacotherapy;

240 that stocked cessation medications, 96% had nicotine replacement therapy, 28% had bupropion, and 1%

241 he availability, sales, and affordability of nicotine replacement therapy, bupropion, and varenicline

242 levamisole and pyrantel, but not morantel or nicotine, require the unc-38 and/or unc-29 genes.

243 cigarettes and, to a lesser degree, 0.763-mg nicotine research cigarettes increased sustained attenti

244 detoxification-related genes associated with nicotine resistance.

245 These mitochondrial associated effects by nicotine resulted in inhibition of myofibroblast differe

246 erquantel was a noncompetitive antagonist of nicotine, revealing N-type nAChRs.

247 1 receptors in the MHb-IPN circuit abolished nicotine reward and decreased nicotine intake, whereas t

248 A neurons to menthol-induced enhancements of nicotine reward-related behavior and may help explain ho

249 ens shell, a brain area believed to underlie nicotine reward.

250 However, nicotine's involvement in the pathogenesis of cholangioc

251 antness of cigarette pictures when they were nicotine sated or nicotine abstinent.

252 pleasant while nicotine abstinent than while nicotine sated.

253 taking, nicotine withdrawal, and persistent nicotine seeking even after prolonged abstinence.

254 Treatment with Ro 61-8048 decreased nicotine self-administration in rats and monkeys, but di

255 hat nicotine intake in the socially acquired nicotine self-administration model is controlled by gene

256 pha7 nicotinic receptors (nAChRs) can reduce nicotine self-administration, suggesting that a positive

257 ental realization of a SPR based fiber optic nicotine sensor having coatings of silver and graphene d

258 Our work unravels a complex nicotine-stress bidirectional interplay and identifies a

259 on, including acquisition and maintenance of nicotine taking, nicotine withdrawal, and persistent nic

260 knockout mice consumed greater quantities of nicotine than wild-type mice.

261 culating levels of cotinine, a metabolite of nicotine that is proportional to tobacco smoke exposure.

262 may therefore serve as 'satiety sensors' for nicotine that stimulate habenular systems to promote nic

263 Nicotine, the main addictive substance in tobacco, is kn

264 ne as a smoking cessation agent differs from nicotine through trapping in alpha4beta2R-containing aci

265 Female smokers randomized to 21 mg nicotine (TNP; n=37) or placebo (PBO; n=43) transdermal

266 In rats, Ro 61-8048 reduced the ability of nicotine to induce dopamine release in the nucleus accum

267 ses allows evaluation of the contribution of nicotine to the smoking experience.

268 To compare exposure to nicotine, tobacco-related carcinogens, and toxins among

269 samples and were analyzed for biomarkers of nicotine, tobacco-specific N-nitrosamines (TSNAs), and v

270 IVIVC) of nicotine BA from two, matrix-type, nicotine transdermal delivery systems (TDS).

271 ns were suppressed consistently across daily nicotine treatments.

272 E-cigarette fluids (with and without nicotine) trigger molecular and morphologic responses in

273 ssociation was observed in a sample of 3,245 nicotine-unexposed individuals from the same discovery c

274 Menthol plus nicotine upregulates nAChR number and function on midbra

275 Varenicline reduced nicotine upregulation of alpha4beta2-type nicotinic rece

276 ted for covariates, such as early alcohol or nicotine use, early dysphoric or anhedonic mood, conduct

277 , free of any comorbid conditions, including nicotine use.

278 ol and lifestyle choices such as alcohol and nicotine use.

279 eved by predicting in vivo concentrations of nicotine using two approaches: Approach I requiring only

280 Pregnant rats exposed to episodic inhaled nicotine via a novel lung alveolar region-targeted aeros

281 ch is rescued by activating OLM neurons with nicotine-via alpha2beta2-containing nicotinic receptors-

282 The mean effective dose for (11)C-nicotine was 5.44 +/- 0.67 muSv/MBq.

283 After an initial CT attenuation scan, (11)C-nicotine was administered via intravenous injection.

284 The interaction of nicotine with ZnO: graphene nanostructures alters the di

285 er on chromosome 5 that were associated with nicotine withdrawal (P<5 x 10(-8)).

286 ed a genome-wide association study of DSM-IV nicotine withdrawal in a sample of African American (AA)

287 ha, -beta and -gamma genes and their role in nicotine withdrawal may inform the development of novel

288 is crucial because cognitive deficits during nicotine withdrawal may predict relapse in humans.

289 l hippocampus separately in mediating select nicotine withdrawal phenotypes.

290 and synaptic plasticity may underlie certain nicotine withdrawal phenotypes.

291 airment and spine density changes induced by nicotine withdrawal precipitated by the nicotinic antago

292 All doses reduced Minnesota Nicotine Withdrawal Scale total scores (range of mean de

293 of subjective effects, such as the Minnesota Nicotine Withdrawal Scale.

294 Memory impairment during nicotine withdrawal was blocked by the CB1R antagonist r

295 uisition and maintenance of nicotine taking, nicotine withdrawal, and persistent nicotine seeking eve

296 decreased 4 days after the precipitation of nicotine withdrawal, when the cognitive deficits were st

297 sal, hippocampus resulted in amelioration of nicotine withdrawal-induced anxiety-like behavior in the

298 ulatory variation influences the severity of nicotine withdrawal.

299 AG), but not anandamide, was observed during nicotine withdrawal.

300 o improve cognitive performance during early nicotine withdrawal.