ライフサイエンスコーパス: drinking

1 enrollment) compared to those without recent drinking.

2 blood alcohol levels (BALs) after binge-like drinking.

3 f chronic, dependence-driven, and binge-like drinking.

4 cue-elicited activation predicted subsequent drinking.

5 a neuroimmune mechanism of excessive alcohol drinking.

6 genetic risk for high intensity, binge-like drinking.

7 , suggesting pre-systemic feedback gating of drinking.

8 enes on a cross-sectional measure of average drinking.

9 is known about the impact of episodic heavy drinking.

10 An average consumer drinking 1.5 L of water daily that contains between 2 an

11 of 12-month alcohol use, 12-month high-risk drinking, 12-month DSM-IV AUD, 12-month DSM-IV AUD among

12 g/kg, twice/day, for 7 days; or intermittent drinking 20% ethanol in a two-bottle free choice protoco

13 ents with overweight or obesity who reported drinking 4 cups or less of water per day.

14 lowed a low (poly)phenol diet for 2 d before drinking 500 mL of OJ containing 398 mumol of (poly)phen

15 altrexone had an accelerated return to heavy drinking after medication was stopped.

16 en treatment groups on any other measures of drinking, alcohol craving, or alcohol-related consequenc

17 ore anteroventral than those associated with drinking, although there was substantial overlap.

18 no effect on the percentage of days of heavy drinking (AMD -0.4% [-5.7 to 4.9]; p=0.88), the effect o

19 Naltrexone reduces drinking among individuals with alcohol use disorders (A

20 otide polymorphism rs112146896 with lifetime drinking and a negative association with anxiety in heal

21 al trial tested the effects of naltrexone on drinking and alcohol cue-elicited brain activation, eval

22 utamatergic MnPO neurons produces effects on drinking and autonomic thermoregulatory mechanisms, prov

23 as associated with an increased frequency of drinking and binge drinking episodes in adolescents.

24 ffect modification between moderate lifetime drinking and binging (relative excess risk due to intera

25 p between plasma aldosterone levels, alcohol drinking and craving was investigated in alcohol-depende

26 articipates in mechanisms underlying alcohol-drinking and reconsolidation of alcohol-related memories

27 vious findings that naltrexone reduces heavy drinking and reward-related brain activation among treat

28 atus, material deprivation history, smoking, drinking and socioeconomic status, working-age men in fa

29 egative association between lifetime alcohol drinking and superior frontal gyrus volume.

30 dings support a relationship between ethanol drinking and the aldosterone/MR pathway in three differe

31 uroimmune pathways mediate excessive alcohol drinking and these findings will help to prioritize rele

32 e idea that increasing salt intake increases drinking and urine volume is widely accepted.

33 e environments and have potential for use in drinking and wastewater treatment.

34 eptions, increases in alcohol use, high-risk drinking, and DSM-IV AUD between 2001-2002 and 2012-2013

35 Increases in alcohol use, high-risk drinking, and DSM-IV AUD in the US population and among

36 Twelve-month alcohol use, high-risk drinking, and DSM-IV AUD.

37 nner by which STDP responds to binge alcohol drinking, and its sensitivity to dopamine receptor antag

38 nd automatically measures standing, feeding, drinking, and locomotor activities from 3D trajectories.

39 Cognitive impairments, uncontrolled drinking, and neuropathological cortical changes charact

40 We identified far more alcohol-drinking associated bacterial species than traditional m

41 by lay counsellors to patients with harmful drinking attending routine primary health-care settings.

42 ubstantial individual variability in alcohol drinking behaviors in the population, the neural circuit

43 as well as in mechanisms underlying alcohol-drinking behaviors.

44 tend to exhibit heterogeneous postdeployment drinking behaviors.

45 l circuit responsible for individual alcohol drinking behaviors.

46 3beta, that in turn drives excessive alcohol-drinking behaviors.

47 burst activity in HAD mice decreases alcohol drinking behaviors.

48 dence for the involvement of FGF2 in alcohol-drinking behaviors.

49 Stimulation also produced drinking behaviour that was inhibited as water was inges

50 ter adjustment for weekly consumption, binge drinking, BMI, and smoking.

51 We found that repeated drinking bouts modulate differently synaptic plasticity

52 in the VTA did not alter binge-like ethanol drinking, but inhibition of VTA-projecting CRF neurons f

53 a distributed thirst circuit that motivates drinking by the common mechanism of drive reduction.

54 tion of these neurons is sufficient to drive drinking, cardiovascular responses, and negative reinfor

55 h as those generated by other people eating, drinking, chewing, and breathing [1-8].

56 einated coffee and for coffee with additives.Drinking coffee, either caffeinated or decaffeinated, ma

57 Sixty-eight AH patients, 65 heavy drinking controls without liver disease (HDC), and 20 he

58 ars of heavy drinking, in which cessation in drinking could prevent the disease.

59 ugh the primary outcome, percentage of heavy drinking days, was lower in participants receiving ABT-4

60 Binge drinking, defined as reaching a blood alcohol level of 8

61 Secondary outcomes were the effect of drinking, disability score, days unable to work, suicide

62 pendent rats and the correlates with ethanol drinking during acute withdrawal.

63 dex, pregnancy complications, and smoking or drinking during pregnancy.

64 but not placebo, experienced the least heavy drinking during the following 14 weeks.

65 est, interventions enacted in and around the drinking environment lead to small reductions in acute a

66 availability, information and education, the drinking environment, drink-driving, and brief intervent

67 an increased frequency of drinking and binge drinking episodes in adolescents.

68 mesostriatal neuroadaptations, resulting in drinking escalation and addiction phenotypes.

69 ncreased risk associated with heavy episodic drinking, especially among moderate lifetime drinkers.

70 ositivity were similar across smoking and/or drinking exposure groups: HRfor low exposure, 0.52; 95%

71 Unlike this excessive drinking, for which treatments exist, compulsive alcohol

72 ssociation of rs11720469 with heavy episodic drinking (frequency of consuming 5+ drinks within 24 h).

73 lcohol consumption (units per week and binge drinking) from Scottish Health Surveys done in 1995, 199

74 unique neuroadaptations between the alcohol drinking groups.

75 = 0.52; 95% CI: 0.30 to 0.89), whereas those drinking >1 glass/day had significantly higher risk (RR

76 k of clinical AL progression for individuals drinking >1 glass/day was 34% higher than non-drinkers (

77 th accelerated fibrosis progression, whereas drinking >14 drinks per week showed increased rates of f

78 VTA dopamine neuron activity in high alcohol drinking (HAD) mice does not differ from alcohol naive m

79 The results reveal how drinking history alters the association between brain FC

80 s anatomic sites, independent of smoking and drinking history.

81 hazard ratios were increased for ever binge drinking (HR = 1.29, 95% CI: 1.15, 1.45) or blacking out

82 ong male primary care attendees with harmful drinking in a setting in India.

83 synaptic proteins with novel links to heavy drinking in BXD mice.

84 ed anxiety-like behavior and compulsive-like drinking in dependent rats.

85 For long-term studies of alcohol drinking in mice we used IntelliCages.

86 We used drinking in the dark (DID) as a model of binge alcohol d

87 High Drinking in the Dark (HDID-1) mice are a genetic model o

88 Tlr4 knockdown in mouse NAc did not decrease drinking in the two-bottle choice continuous or intermit

89 The prevalence of binge drinking in the United States is rising.

90 in the past 14 days among those who reported drinking in this period (37.0 g [SD 44.2] vs 31.0 g [27.

91 s is usually preceded by many years of heavy drinking, in which cessation in drinking could prevent t

92 In mice, (+)-naloxone did not decrease drinking-in-the-dark and only modestly inhibited depende

93 n the VTA CRF system were assessed following drinking-in-the-dark procedures.

94 on-treatment-seeking alcohol-dependent heavy-drinking individuals.

95 The ability to inhibit drinking is a significant challenge for recovering alcoh

96 Alcohol drinking is an established risk factor for several malig

97 Underage drinking is widely recognized as a leading public health

98 was not a critical determinant of excessive drinking, it was important in the acute sedative effects

99 pulsively seeking alcohol, before eventually drinking large amounts.

100 r deployment that regressed to predeployment drinking levels 2 years after deployment.

101 Never-smoker males drinking </=1 glass/week had significantly lower risk fo

102 parental social class, maternal smoking and drinking, maternal mental health, offspring stressful li

103 d NASH and fibrosis; however, heavy episodic drinking may accelerate fibrosis progression and moderat

104 Binge drinking may be an early indicator of vulnerability to a

105 c strength in DMS D1- and D2-MSNs of alcohol-drinking mice and control mice.

106 vivo microdialysis procedures in MA high/low drinking mice, as well as in isogenic C57BL/6J mice that

107 In drinking monkeys, evoked firing of OFC pyramidal neurons

108 ntrol glutamatergic signaling in chronically drinking monkeys.

109 2) that discriminated between low- and heavy-drinking monkeys.

110 onfirmed the increase in GluA1 expression in drinking monkeys.

111 Compared with drinking no coffee, coffee consumption was associated wi

112 In addition, the role of alcohol drinking on outcomes in patients with cancer is in its f

113 dees aged 18-65 years screening with harmful drinking on the Alcohol Use Disorders Identification Tes

114 o placebo, reduced VS activation and bar-lab drinking only among carriers of the DAT1 9-repeat allele

115 nded as first-line interventions for harmful drinking, only a small fraction of people globally recei

116 etween baseline and week 2 and reduced heavy drinking over 16 weeks.

117 s extensive epidemiological support for this drinking pattern, a consensus has not been reached.

118 umption, even after accounting for different drinking patterns, obesity, and smoking status at the in

119 were used to test the hypothesis that heavy drinking produces neuroadaptations in the macaque OFC.

120 oped symptoms compatible with botulism after drinking pruno, an illicit, prison-brewed alcoholic beve

121 refore, if supported by evidence of benefit, drinking reduction goals could broaden the appeal of tre

122 n the aim of treatment, many drinkers prefer drinking reduction goals.

123 atment goals and clinical recommendations on drinking reduction.

124 nsing TRCs in thirsty animals induced robust drinking responses toward light even without water.

125 Reduction in WHO drinking risk level predicted significantly lower odds o

126 results support the use of reductions in WHO drinking risk levels as an efficacy outcome in clinical

127 test the relationship between change in WHO drinking risk levels between Waves 1 and 2, and alcohol

128 clinical trials, including reduction in WHO drinking risk levels-very high, high, moderate, and low-

129 -0.4% [-5.7 to 4.9]; p=0.88), the effect of drinking (Short Inventory of Problems score AMD-0.03 [-1

130 cidal behaviour, percentage of days of heavy drinking, Short Inventory of Problems score, WHO Disabil

131 n the DMS is a positive regulator of alcohol drinking.SIGNIFICANCE STATEMENT Long-term alcohol intake

132 gative emotional state that drives excessive drinking.SIGNIFICANCE STATEMENT The central amygdala (Ce

133 ypes could be derived using the Inventory of Drinking Situations, a 30-item self-report questionnaire

134 , and biochemical variables at admission and drinking status during follow-up were obtained.

135 , smokers (SMK), drinkers (DRN), smoking-and-drinking subjects (SAD), marijuana users (MAR), smoking-

136 ted with medication in predicting subsequent drinking, such that individuals with greater reduction i

137 oking moderated the effects of medication on drinking, such that naltrexone was superior to placebo o

138 than comparison groups and less problematic drinking than classic psychedelic users.

139 discovered several proteins related to heavy drinking that have potential as novel targets for treati

140 oup drank equal volumes of water and avoided drinking the juices.

141 n the dark (DID) as a model of binge alcohol drinking to assess its effects on spike timing-dependent

142 Excessive drinking to intoxication is the major behavioral charact

143 rial are the susceptibility of self-reported drinking to social desirability bias, the modest partici

144 agement was associated with changes in heavy drinking, treatment attendance, drug use, cigarette smok

145 ing-and-marijuana users (SAM), marijuana-and-drinking users (MAD), and users of all three substances

146 othesis that TLR4 mediates excessive ethanol drinking using the following models: (1) Tlr4 knock-out

147 Moderate drinking (vs abstinence) is associated with lower risk o

148 Coffee drinking was associated with reduced risk for death from

149 nse to naltrexone, whereas individuals whose drinking was driven by negative reinforcement (ie, relie

150 PREDICT proposed individuals whose drinking was driven by positive reinforcement (ie, rewar

151 mental Protection Agency limit for Cu(2+) in drinking water (20 muM).

152 e fed a high fat diet with 5% sucrose in the drinking water (HFS) for 7 months and then were fed for

153 fat diet supplemented with 30% d-fructose in drinking water (obesogenic diet) for 25-33 weeks.

154 ed PI-IBS following exposure to contaminated drinking water 7 years ago.

155 The 1974 Safe Drinking Water Act (SDWA) regulates >170,000 public wate

156 fs that are not presently considered in Safe Drinking Water Act regulatory analyses.

157 ronmental Protection Agency (EPA)'s National Drinking Water Advisory Council (NDWAC) recommended esta

158 is dramatically exceeded recommendations for drinking water after one treatment cycle ( approximately

159 presence of other complex species in natural drinking water and an affordable water-purification devi

160 relationship between lead concentrations in drinking water and BLLs in children.

161 ng nonoccupationally exposed U.S. residents, drinking water and diet are considered primary exposure

162 to two groups: controls provided with normal drinking water and DOCA provided with DOCA pellets and s

163 EDS) model estimated mean iAs exposures from drinking water and rice were 4.2 mug/day and 1.4 mug/day

164 EDS) model estimated mean iAs exposures from drinking water and rice were [Formula: see text] and [Fo

165 uvial flood-risk management and forecasting, drinking water and sewer network operation and managemen

166 n potential cumulative endocrine activity in drinking water and to inform prioritization of future mo

167 , especially among those with relatively low drinking water arsenic exposure.

168 most commonly identified causative agent in drinking water associated with disease outbreaks, can be

169 h-based, household action level" for lead in drinking water based on children's exposure.

170 breaks, can be harbored by and released from drinking water biofilms.

171 bsequent accumulation of cadmium in food and drinking water can result in accidental consumption of d

172 GenX was also detected in drinking water collected from 3 out of 4 municipalities

173 Ongoing exposures to even relatively low drinking water concentrations of long-chain PFAAs substa

174 uation was conducted based on representative drinking water conditions to determine a minimal model (

175 el (3 reactions, 8 constants) applicable for drinking water conditions.

176 and therefore they may pose greater risks to drinking water consumers given their widespread occurren

177 Drinking water containing the highest level of GenX also

178 Among the different classes of drinking water contaminants, toxic trace elements (e.g.,

179 n, however, whether consumption of sodium in drinking water could have similar effects on health.

180 s by bloom-forming cyanobacteria can lead to drinking water crises, such as the one experienced by th

181 nogenic N-nitrosodimethylamine (NDMA) during drinking water disinfection is a major challenge.

182 In conventional drinking water disinfection, N-chloroisobutyraldimine ca

183 m climates and has the potential to colonize drinking water distribution systems (DWDSs).

184 bacterial and fungal taxa commonly found in drinking water distribution systems through the treatmen

185 rently installed treatment processes at U.S. drinking water facilities to be on the order of $500 mil

186 s) since the U.S. EPA analysis suggested few drinking water facilities would be affected by bromide d

187 n credits by distributing almost one million drinking water filters in rural Kenya to avert the use o

188 lm-associated L. pneumophila under simulated drinking water flow containing a disinfectant residual w

189 of 2014, when the city was rendered without drinking water for >2 days.

190 Some mice were given antibiotics via their drinking water for 4 weeks to deplete their microbiota.

191 y addition of 2.5% dextran sodium sulfate to drinking water for 5-9 consecutive days.

192 Mice were given (13)C-acetate in drinking water for measurement of cholesterol synthesis.

193 bent with the potential to improve access to drinking water for millions living in developing countri

194 Groundwater is the major source of drinking water for people living in rural areas of India

195 he 44.5 million U.S. residents drawing their drinking water from private wells face higher risks of w

196 population at risk from elevated arsenic in drinking water from private wells.

197 for direct determination of free cyanide in drinking water has been reported.

198 However, its removal and fate in drinking water has never been reported before.

199 onmental Protection Agency to issue lifetime drinking water health advisories for perfluorooctanoic a

200 Arsenic exposure via drinking water impacts millions of people worldwide.

201 detectable incidence of waterborne AGI from drinking water in the systems and time periods studied.

202 ndicator of microbiological contamination of drinking water in time-series studies attempting to disc

203 reported MCL violations to the national Safe Drinking Water Information System (SDWIS).

204 Daily drinking water intake and rice consumption rate distribu

205 the distribution of iAs exposure rates from drinking water intakes and rice consumption in the U.S.

206 ection Agency (EPA) for inorganic mercury in drinking water is 0.002 mg L(-1) (10 nM).

207 Access to safe drinking water is a human right, crucial to combat inequ

208 etection marker for mercury ions (Hg(2+)) in drinking water is of great interest for toxicology asses

209 approach that can be used to determine what drinking water lead concentrations keep children's blood

210 han the US Environmental Protection Agency's drinking water limit (2 ppb), within 10 min.

211 Drinking water maximum contaminant levels (MCL) are esta

212 Long-term increased lithium exposure in drinking water may be associated with a lower incidence

213 a on municipality of residence and data from drinking water measurements combined with time-specific

214 Drinking water microbial communities impact opportunisti

215 ng water treatment processes shape the final drinking water microbial community via selection of comm

216 idepressant, acetyl-l-carnitine (LAC) in the drinking water opposed the direction of these changes.

217 Comparison of drinking water PFOA concentrations to those study findin

218 N-Cl-DCAM tends to deprotonate under typical drinking water pH conditions, and the anionic form of N-

219 ses in disinfection byproducts at downstream drinking water plants.

220 Complexities associated with drinking water plumbing systems can result in undesirabl

221 ) adsorbed to granular activated carbon in a drinking water production plant, which cannot be labeled

222 ty in surface waters and treatability during drinking water production.

223 he classical disinfection treatments used in drinking water production.

224 ts both carbon cycling in surface waters and drinking water production.

225 Chlorination of drinking water protects humans from water-born pathogens

226 ate for routine environmental monitoring and drinking water quality assessment since the guideline va

227 In the USA, impacts to drinking water quality, biogeochemical cycles, and aquat

228 sehold sanitation access on child health and drinking water quality.

229 Lead exposure via drinking water remains a significant public health risk;

230 ions on the chemical composition of DOC in a drinking water reservoir by Fourier transform ion cyclot

231 water quality is of widespread importance to drinking water safety in many areas where hydraulic frac

232 ate change to hydraulic fracturing, and from drinking water safety to wildfires, environmental challe

233 Additionally, drinking water samples were collected from municipalitie

234 cible results were obtained from analysis of drinking water samples with recoveries of 98.3-101.2% an

235 tform for measurements of fluoride levels in drinking water samples.

236 e higher exposures than adults from the same drinking water source.

237 pical de facto potable reuse scenario, where drinking water sources are located downstream of treated

238 research was key to the nation's first-ever drinking water standard for CrVI adopted by California i

239 nd groundwaters at levels above health-based drinking water standards.

240 rtant role in the removal of impurities from drinking water supplies.

241 ill identify the dangers hidden in America's drinking water supply and redirect attention to ensure s

242 m these regions contribute up to half of the drinking water supply for some European countries.

243 To simulate drinking water system conditions, biofilms were prepared

244 The two municipal drinking water systems of New Orleans, LA, U.S.A. were s

245 Twenty-two (22) public drinking water systems serving 2.5 million people were i

246 tormwater systems differ from wastewater and drinking water systems to which LCA is more frequently a

247 e children chronically exposed to Mn through drinking water to investigate the effect of Mn exposure

248 n potential in Lake Michigan, which provides drinking water to over 10 million people.

249 was observed in samples near the location of drinking water treatment plant (WTP) intakes, eight or m

250 entrations of 2,6-dichlorobenzamide (BAM) in drinking water treatment plants (DWTPs).

251 Study results suggest that centralized drinking water treatment processes shape the final drink

252 amined the effect of lake water chemistry on drinking water treatment processes.

253 water distribution systems, and centralized drinking water treatment represents a potential control

254 ntial operational challenges for distributed drinking water treatment systems.

255 city and chemical consumption for individual drinking water unit processes are used to estimate embed

256 nated dipeptides as chlorination products in drinking water using complementary high-resolution quadr

257 n, weighting the iAs concentrations for each drinking water utility in the Second Six-Year Review dat

258 The distribution of iAs in drinking water was estimated by population, weighting th

259 cation systems are easy ways to obtain clean drinking water when there is no large-scale water treatm

260 illimolar sodium chloride level (freshwater, drinking water, and aquarium water, as well as dechlorid

261 he existence of a variety of heavy metals in drinking water, and the four-electrode sensor can distin

262 lication of our strategy in aqueous samples (drinking water, apple juice, and skim milk).

263 inc in various samples including well water, drinking water, black tea, rice, and milk.

264 d on phenol addition and recovery studies in drinking water, obtaining recoveries rates between 90% a

265 re, for each 100 mg/L reduction in sodium in drinking water, systolic/diastolic BP was lower on avera

266 Given that groundwater is a major source of drinking water, the main objective of this work was to i

267 ore than a billion people lacking accessible drinking water, there is a critical need to convert nonp

268 dipeptides as new disinfection byproducts in drinking water.

269 e resources for recreation and as sources of drinking water.

270 mmunities from the impact of contaminants in drinking water.

271 aking groundwater as their primary source of drinking water.

272 or the removal of E. coli and turbidity from drinking water.

273 can be modulated by providing the inducer in drinking water.

274 he concentration of this chemical present in drinking water.

275 he detection of heavy metal contamination in drinking water.

276 g, indicating persistent nitrate problems in drinking water.

277 g-term exposure to microlevels of lithium in drinking water.

278 d method for the analysis of free cyanide in drinking water.

279 y chlorination products of other peptides in drinking water.

280 for in-field detection of fluoride level in drinking water.

281 ated arsenical, or arsenobetaine exposure in drinking water.

282 ffects in communities where they contaminate drinking water.

283 al and anthropogenic barriers, even reaching drinking water.

284 and analyze fluoride concentration level in drinking water.

285 senite (As(III)) that contaminates crops and drinking water.

286 or microbial community structure in finished drinking water.

287 ovided with DOCA pellets and sodium chloride drinking water.

288 the reaction of BMAA with chlorine, a common drinking-water oxidant/disinfectant, was investigated.

289 wo-day summit to identify options to improve drinking-water quality for N.C. residents served by priv

290 rt study in which we assessed the effects of drinking-water sodium (DWS) on blood pressure (BP) in co

291 cal levels of D-mannose safely achievable by drinking-water supplementation suppressed immunopatholog

292 val of BMAA in the chlorination process of a drinking-water system.

293 dicators to investigate the sources of Mo in drinking-water wells from shallow aquifers in a region o

294 tion byproducts (N-DBPs) whose occurrence in drinking waters has recently been reported in several DB

295 e broadly speaking, N-Cl-HAMs in chlorinated drinking waters is of significance because they are orga

296 tual DCAN degradation product in chlorinated drinking waters.

297 radation are generally atypical for finished drinking waters.

298 he rural area, cigarette smoking and alcohol drinking were associated with insomnia.

299 Predictions of standing, feeding, and drinking were validated, but not locomotor activities.

300 ly significant inverse association of coffee drinking with circulatory disease mortality (HR, 0.78 [C