ライフサイエンスコーパス: alcohol intake

1 ferences and GABA(A)R subunit specificity in alcohol intake.

2 ealth 2000), with available data on baseline alcohol intake.

3 diabetes, smoking, sedentary behaviors, and alcohol intake.

4 rior or current viral hepatitis or excessive alcohol intake.

5 own of CRMP-2 in the NAc decreases excessive alcohol intake.

6 alcohol use disorder or is a consequence of alcohol intake.

7 re to measure lifetime use or the pattern of alcohol intake.

8 ved stress, depression, dietary factors, and alcohol intake.

9 d portal hypertension in patients with heavy alcohol intake.

10 g properties, which could promote subsequent alcohol intake.

11 l relevance of kinase activity for excessive alcohol intake.

12 l appear to be a crucial factor in promoting alcohol intake.

13 restored BDNF levels and decreased excessive alcohol intake.

14 activity of this neuronal population reduces alcohol intake.

15 a causal relationship between D2R levels and alcohol intake.

16 in the transition from moderate to excessive alcohol intake.

17 ic symptoms of withdrawal and for regulating alcohol intake.

18 nd adjusted for sex, education, smoking, and alcohol intake.

19 e important mediators of this stress-induced alcohol intake.

20 d prevented withdrawal-induced escalation of alcohol intake.

21 tral role in mechanisms underlying excessive alcohol intake.

22 ns with diet have been convincing other than alcohol intake.

23 ce observed in sP rats and to their elevated alcohol intake.

24 wo inbred strains of mice known to differ in alcohol intake.

25 sensitivity in patients with sustained heavy alcohol intake.

26 ids, education, race/ethnicity, smoking, and alcohol intake.

27 ignificant for a model using the most recent alcohol intake.

28 sure and withdrawal known to drive excessive alcohol intake.

29 -to-NAcore inputs sustain aversion-resistant alcohol intake.

30 uch that 7.6% of deaths can be attributed to alcohol intake.

31 tral nucleus of the amygdala (CeA) decreased alcohol intake.

32 gs suggest that a GPR39 agonist would reduce alcohol intake.

33 cent to decipher the genetic architecture of alcohol intake.

34 y history of colorectal cancer, smoking, and alcohol intake.

35 , family history of diabetes, and energy and alcohol intakes.

36 , riboflavin, vitamin B-6, vitamin B-12, and alcohol intakes.

37 g years-of-life-lost were 0.5 years for high alcohol intake, 0.7 years for obesity, 3.9 years for dia

38 how that activation of NAc D1-MSNs increased alcohol intake 1-, 4-, and 24-h after the start of drink

39 under the curve=0.90-0.99) for current heavy alcohol intake (42 g per day in men and 28 g per day in

40 s of coffee per day, 13% and 7% for moderate alcohol intake, 8% and 11% for a high Alternate Healthy

41 r cumulative risk of AF for individuals with alcohol intake above an acceptable range and in the high

42 re most effective at achieving reductions in alcohol intake across the 3 trauma centers.

43 alcohol deprivation effect (the increase in alcohol intake after a period of abstinence) while havin

44 he apparently protective effects of moderate alcohol intake against stroke are largely non-causal.

45 Furthermore, we demonstrate that alcohol intake also blocks glycogen synthase kinase-3bet

46 Here, we show that long-term alcohol intake also increases the expression of the FGF2

47 Our analysis of alcohol intake among men at risk of prostate cancer incl

48 We examine (1) whether alcohol intake among men at risk of prostate cancer is a

49 Our analysis of alcohol intake among men with prostate cancer was restri

50 Total alcohol intake among patients with prostate cancer was n

51 30a-5p in the mPFC produced an escalation of alcohol intake and a preference over water.

52 MICs, higher income, being divorced/widowed, alcohol intake and abdominal obesity had higher odds of

53 We observed a J-shaped association between alcohol intake and all-cause death with a maximal risk r

54 oderate the efficacy of prazosin in reducing alcohol intake and associated secondary outcomes.

55 serotonin receptor agonist) robustly reduced alcohol intake and BALs in HDID-1 mice, providing the fi

56 the established association between lifetime alcohol intake and breast cancer and provide evidence fo

57 idence for an association with postdiagnosis alcohol intake and breast cancer survival.

58 al studies assessing the association between alcohol intake and cardiovascular events in the followin

59 hol intake or dose-response relationships of alcohol intake and cardiovascular events.

60 PLX5622 prevented escalations in voluntary alcohol intake and decreased anxiety-like behavior assoc

61 significant interactions between smoking and alcohol intake and each index on HNC risk.

62 administration, increased aversion-resistant alcohol intake and enhanced stress-induced relapse to al

63 studies of ALD have focused on pathological alcohol intake and few mechanistic studies of moderate a

64 serology, age, nutritional status, smoking, alcohol intake and gastric pH were also analysed.

65 t Scale-cognitive subscale, body mass index, alcohol intake and genetic variables are the most common

66 and Signature E4 is unique in ESCC linked to alcohol intake and genetic variants in alcohol-metaboliz

67 tudies have examined the association between alcohol intake and hip fractures, few have considered sp

68 estimate associations between previous day's alcohol intake and hormone concentrations, whereas Poiss

69 re was a U-shaped relationship between total alcohol intake and incident HF (P=0.0004).

70 aimed to investigate the association between alcohol intake and incident HF.

71 Excess alcohol intake and inherited predisposition may increase

72 ssion was used to assess RR of cycle-average alcohol intake and menstrual cycle function.

73 ssociations were shown between cycle-average alcohol intake and menstrual cycle function.

74 idence intervals for the association between alcohol intake and myocardial infarction, ischemic strok

75 f GalphasDREADD in DMS dMSNs or iMSNs alters alcohol intake and observed that CNO-dependent activatio

76 ling pathway, blocked the effects of FGF2 on alcohol intake and preference.

77 est that relaxin-3/RXFP3 signaling regulates alcohol intake and relapse-like behavior, adding to curr

78 ntake might modulate the association between alcohol intake and risk of hormone-dependent cancer.

79 dorsolateral striatum PDE10A in facilitating alcohol intake and support further investigation of PDE1

80 bjectives were to study the relation between alcohol intake and the risk of hormone-dependent cancers

81 rsive effects negatively modulates voluntary alcohol intake and thus may be important in vulnerabilit

82 studied genotypes did not predict high mean alcohol intake and were not positively associated with b

83 ts suggest that repeated cycles of excessive alcohol intake and withdrawal potentiate glutamatergic s

84 -expressing interneurons in modulating binge alcohol intake and withdrawal-induced anxiety.

85 pioid receptor antagonist, on both voluntary alcohol-intake and alcohol-seeking behaviors.

86 level of education, self-reported diabetes, alcohol-intake and smoking," was constructed for subset

87 of abstinence period, and quantification of alcohol intake), and if the patient is an active drinker

88 cise, body weight reduction, low to moderate alcohol intake, and adequate potassium intake are emphas

89 gs (DREADDs) were delivered after 4-weeks of alcohol intake, and clozapine-N-oxide (CNO) was administ

90 use, adjusted for body mass index, smoking, alcohol intake, and concomitant use of medications.

91 f Fyn to GalphasDREADD-dependent increase in alcohol intake, and found that systemic administration o

92 ly attenuated by the adjustment for smoking, alcohol intake, and intelligence measured at conscriptio

93 ass index, diabetes, chronic kidney disease, alcohol intake, and lipid-lowering therapy.

94 the treatment of hypertension, reduction in alcohol intake, and occlusion of the left atrial appenda

95 Smoking, diet quality, alcohol intake, and physical activity did not further ac

96 such as hedonic responses to palatable food, alcohol intake, and reinstatement of cocaine seeking.

97 baseline body mass index, physical activity, alcohol intake, and several aspects of diet.

98 nt of age, sex, Townsend deprivation scores, alcohol intake, and smoking history.

99 position, physical activity, diet, smoking, alcohol intake, and use of oral contraceptives (per 1-un

100 e mineral density, urticaria pigmentosa, and alcohol intake are easy to collect in clinical practice.

101 Alcohol intake associates with overeating in humans.

102 ensity, absence of urticaria pigmentosa, and alcohol intake at the time of ISM diagnosis were indepen

103 the highly conserved human GAL5.1 enhancer, alcohol intake (AUDIT questionnaire scores) and anxiety

104 of association between maternal or paternal alcohol intake before or during pregnancy and offspring

105 Prior alcohol intake blocked the pro-aggressive effects of ket

106 ffered according to baseline smoking status, alcohol intake, BMI, and diabetes status.

107 rtial agonist of alpha4beta2 nAChRs, reduces alcohol intake, but its use can be limited by side effec

108 this study investigated how NAc MSNs mediate alcohol intake by using Drd1a-iCre and Drd2-iCre transge

109 related to mortality in this cohort-smoking, alcohol intake, caffeine consumption, exercise, body mas

110 Damaging levels of alcohol intake can occur in the absence of dependence.

111 sted HRs over increasing cumulative averaged alcohol intake categories were 1.00 (reference) for nond

112 d on deterrent health factors, like smoking, alcohol intake, cheese consumption and average systolic

113 ol consumption, but, by 24 hours, only heavy alcohol intake conferred continued risk.

114 There was a nadir at light-to-moderate alcohol intake: consuming 7 to <14 standard drinks per w

115 ex, physical activity level, smoking status, alcohol intake, depression, self-reported general health

116 Blink reflex recovery cycle before and after alcohol intake did not differ between groups.

117 nicable diseases (NCDs) only listed smoking, alcohol intake, diet and physical activity (PA) as key m

118 nal assessments of body mass index, smoking, alcohol intake, diet quality, physical activity, and ant

119 utions of health-related behaviors (smoking, alcohol intake, diet, physical activity, and sedentary t

120 Although recent moderate alcohol intake does not appear to have adverse short-ter

121 ear, based on self-reported information: any alcohol intake (drinker/non-drinker status) and the regu

122 ate this, we used a mouse model of voluntary alcohol intake (Drinking-in-the-Dark-Multiple Scheduled

123 between education, beverage and non-beverage alcohol intake, drinking patterns, and acute alcohol-rel

124 enetic and behavioral rhythms and influences alcohol intake during chronodisruption.

125 d behavioral circadian timing and influences alcohol intake during chronodisruption.

126 expectation, D2R upregulation did not reduce alcohol intake during continuous or intermittent access

127 Parental age, body mass index, and alcohol intake during pregnancy, child's birth weight, a

128 ificant reductions of relapse-like excessive alcohol intake during the post-abstinence drinking days,

129 In the home cage, increased alcohol intake emerged in 118GG mice with increasing alc

130 ping behaviors in real life, including binge alcohol intake, emotional eating, and frequency of argum

131 en, cirrhosis incidence increases with total alcohol intake, even at moderate levels of consumption.

132 cancer risk was observed for higher lifetime alcohol intake (for >/=230 drinks/year vs. <60 drinks/ye

133 cross all substance use traits, particularly alcohol intake, for which 38% of the phenotypic variance

134 Additionally, maternal alcohol intake frequency >= 1/week was significantly cor

135 increased EA were associated with increased alcohol intake frequency (B(IVW) = 0.331, 95% CI, 0.267-

136 patients in the control group reduced their alcohol intake from 16.4+/-6.9 to 13.2+/-6.5 drinks per

137 tients in the abstinence group reduced their alcohol intake from 16.8+/-7.7 to 2.1+/-3.7 standard dri

138 ceived a motivational intervention to reduce alcohol intake from either the hygienist or dentist.

139 iology) or with genotype-predicted mean male alcohol intake (genetic epidemiology-ie, Mendelian rando

140 rity, socio-occupational status, smoking and alcohol intake, gestational week of blood sampling, and

141 Alcohol intake >30 g/day yielded increased risk estimate

142 For stroke, genotype-predicted mean alcohol intake had a continuously positive log-linear as

143 ional epidemiology showed that self-reported alcohol intake had U-shaped associations with the incide

144 Moderate alcohol intake has been associated with reduced cardiova

145 tribution of acute withdrawal relief to high alcohol intake has been difficult to model in animals.

146 Although habitual low-to-moderate alcohol intake has been linked with reduced all-cause mo

147 l consumption, the immediate risks following alcohol intake have not been well characterized.

148 le factors (e.g. diet, physical activity and alcohol intake) have been suggested as risk factors for

149 , lifestyle (smoking, physical activity, and alcohol intake), health history and medication use, and

150 s later (year 20): not overweight/obese, low alcohol intake, healthy diet, physically active, nonsmok

151 ion scale (SATED): <8); smoking status; and, alcohol intake (high-risk drinker based on standard drin

152 e, field center, physical activity, smoking, alcohol intake, high-density lipoprotein-cholesterol, to

153 Next, we found that neither alcohol intake history nor the motivational strength of

154 ng (HR = 1.00, 95% CI: 0.84, 1.21), or heavy alcohol intake (HR = 1.00, 95% CI: 0.74, 1.35).

155 [CI], 1.16; 3.25; P = 0.012); past excessive alcohol intake (HR, 1.55; 95% CI, 1.02; 2.36; P = 0.041)

156 e combination of a high index score and high alcohol intake (HRs: 2.29 for all-cause and 1.78 for CVD

157 p with low mental health index score and low alcohol intake, HRs (95% CIs) for all-cause mortality we

158 Clinically, low and moderate alcohol intake improves human health with protection aga

159 entration, naltrexone selectively suppressed alcohol intake in 118GG animals to a level virtually ide

160 nine dinucleotide (CpG) sites in relation to alcohol intake in 13 population-based cohorts (ntotal=13

161 We assessed pre- and postdiagnostic alcohol intake in a cohort of 22,890 women with incident

162 udy provides evidence in support of limiting alcohol intake in adherence to the USDGA recommendations

163 eceptor (GR) antagonist mifepristone reduces alcohol intake in alcohol-dependent rats but not in nond

164 e in current drinkers and genotype-predicted alcohol intake in all men had similarly strong positive

165 GSK1521498) reduced both alcohol seeking and alcohol intake in compulsive and non-compulsive rats, in

166 nnel inhibitor apamin into the NAc increased alcohol intake in control C57BL/6J mice, while spontaneo

167 e conditioning response rate decreased under alcohol intake in controls, it increased in patients (an

168 Usual alcohol intake in current drinkers and genotype-predicte

169 naptome found cross-species genetic links to alcohol intake in discrete proteins (e.g., C2CD2L, DIRAS

170 on alcohol intake while inhibition increased alcohol intake in Drd2-iCre rats for 1-h in males and 4-

171 ats, it remains unknown how NAc MSNs control alcohol intake in either sex.

172 dian dysfunction may contribute to increased alcohol intake in ENT1 KO mice.

173 the BNST dose-dependently blocked excessive alcohol intake in ethanol-dependent rats without affecti

174 Even low alcohol intake in fatty liver disease is associated with

175 g concept was demonstrated for monitoring of alcohol intake in human subjects over multiple drinking

176 er and how ghrelin administration may impact alcohol intake in humans is not clear.

177 contraceptive pills in females, smoking and alcohol intake in males did not differ significantly amo

178 14 days dose-dependently decreased voluntary alcohol intake in Marchigian Sardinian rats.

179 diovascular risk and genotype-predicted mean alcohol intake in men, contrasting the findings in men w

180 ol drinking, but CNO injection did not alter alcohol intake in mice that were treated with control vi

181 ing in the dorsolateral striatum (DLS) keeps alcohol intake in moderation.

182 Cs) and that intra-CeA LTCC blockade reduces alcohol intake in nondependent rats.

183 g LTCCs, and intra-CeA LTCC blockade reduces alcohol intake in nondependent rats.

184 tory factor and was recently found to reduce alcohol intake in rats by approximately 50%.

185 g roles for how NAc D1- and D2-MSNs modulate alcohol intake in rats of both sexes.

186 inputs to DA cells and CB1 receptors affect alcohol intake in rodents, we hypothesized that the endo

187 ntake in the instrumental context as well as alcohol intake in the choice procedure.

188 to self-reported mental health problems and alcohol intake in the general population.

189 uced both cue-controlled alcohol seeking and alcohol intake in the instrumental context as well as al

190 cted drinking behaviors, including amount of alcohol intakes (in total and various types), drinking f

191 Mechanistically, alcohol intake increased RA levels in serum and adipose

192 We have reported that alcohol intake increases Pol III gene transcription to p

193 Moderate alcohol intake induces thermogenic brown/beige adipocyte

194 In conclusion, moderate alcohol intake induces thermogenic brown/beige adipocyte

195 Alcohol intake influences plasma lipid levels, and such

196 f a highly prevalent form of drinking, binge alcohol intake, influences enzyme priming or the functio

197 nificantly related to higher total amount of alcohol intake (inverse-variance weighted method (IVW):

198 The lack of reliable measures of alcohol intake is a major obstacle to the diagnosis and

199 Excessive alcohol intake is associated with 5.9% of global deaths.

200 Compared with no alcohol consumption, heavy alcohol intake is associated with a higher rate of heart

201 Alcohol intake is associated with increased circulating

202 derly community-based population, increasing alcohol intake is associated with subtle alterations in

203 It is unknown whether alcohol intake is associated with the risk of lethal (me

204 o measure population-level association where alcohol intake is stratified by sex.

205 ctor for stroke, but the effect of stroke on alcohol intake is unknown.

206 , a behavior characterized by rapid repeated alcohol intake, is most prevalent in young adults and is

207 triatal, and limbic structures that regulate alcohol intake, it has been difficult to disentangle how

208 Excessive alcohol intake leads to mesostriatal neuroadaptations, a

209 Repeated alcohol intake leads to mesostriatal neuroadaptations, r

210 Kcnn3 in the NAc negatively correlated with alcohol intake levels in BXD strains, and alcohol depend

211 om Checklist, and according to self-reported alcohol intake (low, <2; light, 2-11.99; moderate, 12-23

212 Preventive efforts focused on minimizing alcohol intake may be broadly applicable.

213 However, reported alcohol intake may be unreliable, and associations are l

214 ol drinking.SIGNIFICANCE STATEMENT Long-term alcohol intake may lead to neuroadaptations in the mesos

215 Thinner inner retina was associated with alcohol intake (most significant for GCIPL: -0.46 mum fo

216 ied into 4 categories based on self-reported alcohol intake: nondrinkers, drinkers of </=7, >/=7 to 1

217 the transition from moderate to uncontrolled alcohol intake occurs, in part, upon a breakdown of this

218 mass index (weight (kg)/height (m)(2)), and alcohol intake (odds ratio = 0.82, 95% confidence interv

219 of 21% (95% confidence interval, 5%-34%) at alcohol intake of 0-9 g/day compared to lifetime abstain

220 ects on CeA activity and drive the escalated alcohol intake of alcohol-dependent rats.

221 ects on CeA activity and drive the escalated alcohol intake of alcohol-dependent rats.

222 However, more modest levels of alcohol intake on a regular basis may also increase the

223 e regarding the largely adverse influence of alcohol intake on cardiovascular health in an Asian popu

224 ortality and morbidity, the effect of recent alcohol intake on female reproductive function has not b

225 were to investigate the effects of moderate alcohol intake on thermogenic brown/beige adipocyte form

226 d not include women, had data on smoking and alcohol intake only in a subsample, and lacked repeated

227 mic risk stratification, and to test whether alcohol intake or body mass index interacts with polygen

228 and Laird random-effects models to model any alcohol intake or dose-response relationships of alcohol

229 adult socioeconomic status, current smoking, alcohol intake or physical activity.

230 icity, sex, body mass index, smoking status, alcohol intake, or diabetes status.

231 oL, cancer-related fatigue, fruit, fiber, or alcohol intake, or smoking.

232 e of lower mortality risk with low levels of alcohol intake over time but higher mortality risk for t

233 association remained consistent when we used alcohol intakes over different latency periods (0-4, 4-8

234 ors, such severe overweight and a history of alcohol intake (P = 0.005).

235 Myoclonus improved significantly after alcohol intake (p = 0.016).

236 ociations of body mass index (BMI), smoking, alcohol intake, parity and age at menarche with changes

237 otential confounders such as sleep duration, alcohol intake, physical activity, and current smoking.

238 ter, year of screening exam, smoking status, alcohol intake, physical activity, education level, tota

239 cy body mass index (BMI), parity, education, alcohol intake, physical activity, smoking, and breastfe

240 ational position, 25 x 25 risk factors (high alcohol intake, physical inactivity, current smoking, hy

241 social class, education, physical activity, alcohol intake, plasma vitamin C, history of cardiovascu

242 We assessed the association between alcohol intake, polygenic predisposition to AF, and inci

243 Alcohol intake prevented body weight gain, induced the f

244 Here, we show that a history of excessive alcohol intake produces neuroadaptations in the DLS that

245 Together, these data suggest that alcohol intake produces profound functional and structur

246 In a subpopulation with longitudinal data, alcohol intake remained stable over time in >80% of subj

247 a premorbid risk factor or a consequence of alcohol intake remains unclear.

248 core combined with light, moderate, and high alcohol intake, respectively, and 1.11 (0.98, 1.25; p =

249 core combined with light, moderate, and high alcohol intake, respectively.

250 combined with low, light, moderate, and high alcohol intake, respectively.

251 combined with low, light, moderate, and high alcohol intake, respectively.

252 blink reflex recovery cycle before and after alcohol intake resulting in a breath alcohol concentrati

253 bacco smoking (RR, 2.47; 95% CI, 2.12-2.87), alcohol intake (RR, 1.33; 95% CI, 1.17-1.52), body mass

254 odel, adjusted for age; sex; smoking status; alcohol intake; SBP; DBP; cholesterol:high-density lipop

255 extended amygdala are recruited by excessive alcohol intake, sensitized by repeated withdrawal, and c

256 Survival models were adjusted for age, sex, alcohol intake, smoking history, and educational attainm

257 onal hazards regression, after adjusting for alcohol intake, smoking, body mass index, diabetes, and

258 vation, urban or rural residence, education, alcohol intake, smoking, leisure physical activity, recr

259 eg, hypertension, hyperlipidaemia, excessive alcohol intake, smoking, obesity, and sedentary lifestyl

260 r, LM11A-31, significantly reduces excessive alcohol intake suggesting that the drug may be developed

261 in patients who improved significantly with alcohol intake suggests a crucial role of cerebellar net

262 ved regulatory mechanism linking anxiety and alcohol intake that might contribute to increased suscep

263 and D-cycloserine on this aversion-resistant alcohol intake (that persists despite adulteration with

264 cally or intra-PLmPFC, interacted with prior alcohol intake to escalate aggression in ANAs.

265 on adjusted for age, education, smoking, and alcohol intake to estimate the associations between lead

266 We related alcohol intake to measures of cardiac structure and func

267 ight, body mass index (BMI), smoking status, alcohol intake, Townsend deprivation index, education le

268 g, body-mass index (BMI), physical activity, alcohol intake, type 2 diabetes and parity, use of hormo

269 In contrast, alcohol intake up to 49 g/day was associated with a 22%-

270 trast, although genotype-predicted mean male alcohol intake varied widely (from 4 to 256 g per week-i

271 n causes of chronic liver disease are excess alcohol intake, viral hepatitis and non-alcoholic fatty

272 Median alcohol intake was 1013 (range 366-5880) g/week over the

273 Alcohol intake was ascertained every 6 months and use ca

274 In men, increasing alcohol intake was associated with greater left ventricu

275 Increased alcohol intake was associated with increased BCC risk in

276 In both genders, increasing alcohol intake was associated with larger left ventricul

277 In women, increasing alcohol intake was associated with lower left ventricula

278 ex-specific median of dietary fiber intake), alcohol intake was directly associated with hormone-depe

279 Overall, alcohol intake was directly associated with the risk of

280 infarction, however, genotype-predicted mean alcohol intake was not significantly associated with ris

281 Alcohol intake was repeatedly assessed every 2-4 y over

282 Importantly, compulsive alcohol intake was reversed by overexpression of the wil

283 characteristics of patients were comparable; alcohol intake was the most common etiology of cirrhosis

284 In nondependent rats, the decrease in alcohol intake was transient and returned to normal the

285 k factors, overall HRs per 10-g increment in alcohol intake were 0.94 (95% CI: 0.89, 0.98) for CAD an

286 d to saturated fat, vegetables, and moderate alcohol intake were components of the diet quality score

287 HRs and 95% CIs for BCC in association with alcohol intake were computed with the use of Cox proport

288 Body mass index, smoking, and alcohol intake were determined by questionnaire at basel

289 Effects of naltrexone or nalmefene on alcohol intake were examined in continuous access home c

290 with more mental health problems and a high alcohol intake were increased when the risk factors occu

291 , smoking, physical activity, and energy and alcohol intakes were pooled by using a random-effects mo

292 229984), known to be associated with greater alcohol intake, were found to consume less alcohol if th

293 QR 2000-03), the participants reported their alcohol intake, whether consumption was usually with mea

294 A as a neuroadaptation maintaining excessive alcohol intake, which may contribute to the propensity t

295 Postdependent rats showed escalated alcohol intake, which was associated with increased DNA

296 Activation of NAc D2-MSNs had no impact on alcohol intake while inhibition increased alcohol intake

297 To investigate the association of alcohol intake with colorectal cancer risk according to

298 s in the association of obesity, smoking, or alcohol intake with prostate cancer risk and mortality b

299 ith 0.69% (95% CI, 0.58-0.80) for those with alcohol intake within an acceptable range and in the low

300 ensin receptor antagonists), smoking status, alcohol intake, years of education, temperature, and sea