ライフサイエンスコーパス: alcoholism

1 se, chronic lung disease, diabetes mellitus, alcoholism).

2 me 4q has been linked to alcohol dependence (alcoholism).

3 lnerable populations (e.g., individuals with alcoholism).

4 sure intended to mimic old age, obesity, and alcoholism.

5 in BNST is implicated in the neurobiology of alcoholism.

6 dentify novel pharmacologic targets to treat alcoholism.

7 eased dopamine transmission in the cortex in alcoholism.

8 ence, with implications for vulnerability to alcoholism.

9 are impaired in addictive disorders such as alcoholism.

10 investigated as a promising target to treat alcoholism.

11 executive function, relapse, and outcome in alcoholism.

12 st to mitigate the pulmonary consequences of alcoholism.

13 used for several decades in the treatment of alcoholism.

14 e may represent an important risk factor for alcoholism.

15 ediated epigenetic mechanisms in anxiety and alcoholism.

16 ues may thus be an inherited risk factor for alcoholism.

17 everal neuropsychiatric disorders, including alcoholism.

18 in the human brain and how it is affected in alcoholism.

19 relief and its role in determining risk for alcoholism.

20 in subjects with a greater genetic risk for alcoholism.

21 to important interactions between stress and alcoholism.

22 e RMTg as a potential therapeutic target for alcoholism.

23 ation of the NPSR as a therapeutic target in alcoholism.

24 thanol is inversely correlated with risk for alcoholism.

25 may be a critical step in the progression of alcoholism.

26 logy of many psychiatric disorders including alcoholism.

27 pression, anxiety disorders, drug abuse, and alcoholism.

28 receptor as a useful therapeutic target for alcoholism.

29 t stimuli all can affect individual risk for alcoholism.

30 ial response to pharmacological treatment of alcoholism.

31 2) have been shown to play a central role in alcoholism.

32 unique therapeutic effects in narcolepsy and alcoholism.

33 pothesis generation and follow-up studies of alcoholism.

34 ect individuals' vulnerability to developing alcoholism.

35 -naive, all with varying degrees of familial alcoholism.

36 pharmacological target for the treatment of alcoholism.

37 ve a suitable target for reducing relapse in alcoholism.

38 erience are formed during the development of alcoholism.

39 matter atrophy in poor clinical outcomes in alcoholism.

40 US National Institute on Alcohol Abuse and Alcoholism.

41 on of the use of EEG as an endophenotype for alcoholism.

42 could play an important role in the risk for alcoholism.

43 tructured Assessment for Drug Dependence and Alcoholism.

44 ol consumption in a preclinical rat model of alcoholism.

45 ch may play a key role in the development of alcoholism.

46 ed an analysis of genomic studies related to alcoholism.

47 m the Collaborative Study on the Genetics of Alcoholism.

48 play an important role in the development of alcoholism.

49 as hence become a possible strategy to treat alcoholism.

50 pression, is associated with higher risk for alcoholism.

51 new target for therapeutic intervention for alcoholism.

52 e behavior and pharmacological therapies for alcoholism.

53 s well as represent a therapeutic target for alcoholism.

54 otects nearly all carriers of this gene from alcoholism.

55 ents a potential medication for treatment of alcoholism.

56 ants further investigation as a treatment in alcoholism.

57 s a clear need for new therapeutics to treat alcoholism.

58 mi-Structured Assessment for the Genetics of Alcoholism.

59 derlie some of the behaviors associated with alcoholism.

60 odeling, caused by histone modifications, in alcoholism.

61 us, NFKB1 is an excellent candidate gene for alcoholism.

62 association of NFKB1, located at 4q24, with alcoholism.

63 se donors' hearts regardless of a history of alcoholism.

64 ld be further evaluated for the treatment of alcoholism.

65 n the Collaborative Study on the Genetics of Alcoholism.

66 mber of neuropsychiatric diseases, including alcoholism.

67 being tested clinically for the treatment of alcoholism.

68 o our understanding of the neural control of alcoholism.

69 a potential target for clinical treatment of alcoholism.

70 increased in those at high familial risk for alcoholism.

71 actures), high body mass index, smoking, and alcoholism.

72 mi-Structured Assessment for the Genetics of Alcoholism.

73 ia opioid receptors, and is also involved in alcoholism.

74 sferases as potential therapeutic targets in alcoholism.

75 a mifepristone as a therapeutic strategy for alcoholism.

76 n has been implicated in the neurobiology of alcoholism.

77 armacotherapeutic target in the treatment of alcoholism.

78 nts associated with early onset drinking and alcoholism.

79 dolescents and young adults at high risk for alcoholism.

80 proportion of alcoholic etiology and active alcoholism (37% versus 10%), higher platelet count, and

81 e affected individuals with earlier onset of alcoholism (55% of the sample with onset < or =21 years)

82 ailure, 30% for self-reported alcohol use or alcoholism, 6% for body mass index, and 20% for unemploy

83 US National Institute on Alcohol Abuse and Alcoholism (AA012388, AA017168, AA005965, AA013521-INIA)

84 the type of ACLF precipitating event (active alcoholism/acute alcoholic hepatitis, bacterial infectio

85 nt and combined effects of HIV infection and alcoholism along with other factors (acquired immune def

86 We also found association of SGIP1 with alcoholism, an effect that may be mediated via the same

87 l-selective therapeutics in the treatment of alcoholism and addiction.

88 nce is associated with an increased risk for alcoholism and addictive disorders.

89 Familial alcoholism and adolescent binge-drinking have both been

90 Having HIV infection with alcoholism and AIDS had an especially poor outcome on br

91 peduncles), the association between familial alcoholism and altered white matter microstructure dissi

92 early-life stress increases vulnerability to alcoholism and anxiety disorders during adulthood.

93 element of the neuroadaptive changes driving alcoholism and as a major target for its treatment.

94 dopamine (DA) release have been observed in alcoholism and cocaine and heroin dependence.

95 Although alcoholism and depression are highly comorbid, treatment

96 tudies have suggested an association between alcoholism and DNA methylation, a mechanism that can med

97 role of metabotropic glutamate receptors in alcoholism and drug addiction.

98 multilevel modeling, the effects of familial alcoholism and future binge-drinking on white matter mic

99 Alcoholism and hepatitis C infection were associated wit

100 ncirrhotic patients, particularly those with alcoholism and hepatitis C infection.

101 or early diagnosis and improved prognosis of alcoholism and identify future pharmacological targets f

102 psychiatric disorders that are comorbid with alcoholism and involve amygdala dysfunction.

103 for our understanding of the neurobiology of alcoholism and its pharmacotherapy.

104 preliminary work on the pharmacogenetics of alcoholism and its treatment has been promising, the ass

105 A link between highly stigmatized views of alcoholism and lack of services suggests that stigma red

106 talloid volumes, more often had a history of alcoholism and liver disease, and had greater ventilator

107 n plays a role in jeopardizing recovery from alcoholism and may serve as a neural marker to identify

108 It has been reported to be associated with alcoholism and multiple drug abuse and dependence.

109 icacy, albeit moderate, for the treatment of alcoholism and opioid dependence.

110 lop novel pharmacological therapies to treat alcoholism and other addiction-related and compulsive be

111 a stress-related neuropeptide implicated in alcoholism and other addictions, further amplifies the P

112 ver greater long-term benefits characterizes alcoholism and other addictive disorders.

113 to stress are both associated with risk for alcoholism and other substance use disorders.

114 ce variation in this gene is associated with alcoholism and Parkinson's disease, among other disorder

115 nging food environment and predisposition to alcoholism and related disorders.

116 c foci that are shared with the diagnosis of alcoholism and related disorders.

117 ously been associated to a decreased risk of alcoholism and shown to be under selection in East Asian

118 onoamine oxidase A (MAOA) is associated with alcoholism and smoking behavior.

119 gic state contributes to the pathogenesis of alcoholism and that acamprosate may exert its actions by

120 o further characterize genetic influences in alcoholism and the effects of alcohol consumption on pre

121 higher and predicted from family history of alcoholism and/or problem drinking.

122 tion of disulfiram, an FDA approved drug for alcoholism, and (64)CuCl2 (termed (64)Cu-Dis).

123 ith HIV infection, 65 with HIV infection and alcoholism, and 108 healthy control subjects.

124 ffect of naltrexone as a pharmacotherapy for alcoholism, and a recent study has suggested that the ef

125 es, inflammatory bowel disease, hepatitis B, alcoholism, and alcoholic liver disease did not reduce t

126 ure due to diabetes, aging, stress, obesity, alcoholism, and chronic disease affects millions of peop

127 rly a low-protein diet, thiamine deficiency, alcoholism, and hypothyroidism.

128 r multiple mood disorders including anxiety, alcoholism, and major depression.

129 with positive family history, early onset of alcoholism, and maximum number of drinks in adults as we

130 hromboembolic events, subsequent depression, alcoholism, and self-harm (p < 0.01 for each).

131 brain functions, including pain perception, alcoholism, and substance addiction.

132 the National Institute on Alcohol Abuse and Alcoholism, and the National Institute on Drug Abuse.

133 The high prevalence of renal failure, alcoholism, and unemployment among Navajo adults compare

134 occurrence, by age 50, of major depression, alcoholism, and use of mood-altering drugs (tranquilizer

135 get to treat multiple indications, including alcoholism, anxiety, and nonmalignant pain.

136 Drug addictions including alcoholism are characterized by degradation of executive

137 l behavioral plasticity that are relevant to alcoholism are initiated by a shared mechanism.

138 The factors underlying vulnerability to alcoholism are largely unknown.

139 Alcohol abuse and alcoholism are major health problems and one of the lead

140 that therapeutic responses to naltrexone in alcoholism are moderated by variation at the mu-opioid r

141 individual differences in alcohol abuse and alcoholism, as well as represent a therapeutic target fo

142 , the Collaborative Study on the Genetics of Alcoholism (ascertained for alcohol use disorder; n = 64

143 hat subtle white matter fiber degradation in alcoholism attenuated the normal pattern of hemispheric

144 hol (National Institute on Alcohol Abuse and Alcoholism binge model) or chow diets along with water c

145 rative disorder, personality traits, type II alcoholism, borderline personality disorders, aggressive

146 Asian populations and reduces their risk for alcoholism, but because of very low allele frequencies t

147 riety of neuropsychiatric diseases including alcoholism, but development of NMDAR antagonists for the

148 Acamprosate is approved for the treatment of alcoholism, but its mechanism of action remains unclear.

149 luntary alcohol consumption is a hallmark of alcoholism, but its neural substrates remain unknown.

150 rawal is included in diagnostic criteria for alcoholism, but the contribution of acute withdrawal rel

151 herapeutic value of the DOR for treatment of alcoholism by showing that its relevant synaptic action

152 bjects (n = 57) as well as in a rat model of alcoholism by state-of-the-art (1)H-magnetic magnetic re

153 Alcoholism can disrupt neural synchrony between nodes of

154 ompromise of microstructural connectivity in alcoholism can influence modulation of functional connec

155 Alcoholism can result in fatty liver that can progress t

156 of control over drinking is a key deficit in alcoholism causally associated with malfunction of the m

157 To determine if ethanol consumption and alcoholism cause global DNA methylation disturbances, we

158 m the Collaborative Study of the Genetics of Alcoholism (COGA) who were recruited as early as age 12

159 d the Collaborative Study on the Genetics of Alcoholism (COGA), we identified a subnetwork of 39 gene

160 m the Collaborative Study on the Genetics of Alcoholism (COGA), we performed a genome-wide associatio

161 m the Collaborative Study on the Genetics of Alcoholism (COGA), we performed a Multi-Trait Analyses o

162 : the Collaborative Study on the Genetics of Alcoholism (COGA); the Study of Addiction, Genetics, and

163 Despite considerable prevalence of HIV-alcoholism comorbidity, few studies examined the potenti

164 iseases such as obesity, mood disorders, and alcoholism could be better resolved by the use of small-

165 the National Institute on Alcohol Abuse and Alcoholism criteria.

166 In 2001-2002, women with a family history of alcoholism (defined as having a biological parent or sib

167 pse risk.SIGNIFICANCE STATEMENT Persons with alcoholism demonstrate increased motor impulsivity durin

168 from humans for the glutamate hypothesis of alcoholism, demonstrate the comparability of human and a

169 neurobehavioral disorders including anxiety, alcoholism, depression, autism, and obsessive-compulsive

170 has protective activity in animal models of alcoholism, depression, traumatic brain injury, schizoph

171 hy associated with vincristine chemotherapy, alcoholism, diabetes, and human immunodeficiency virus/a

172 trics which are normally impacted in chronic alcoholism (e.g., reaction time and threshold detection)

173 n immunodeficiency virus (HIV) infection and alcoholism each carries liability for disruption of brai

174 As alcoholism evolves, stress systems in the brain play an

175 In alcoholism, excessive glutamatergic neurotransmission ha

176 week and were balanced in family history of alcoholism (FH, 26 positive).

177 (the Collaborative Study on the Genetics of Alcoholism) genome-wide association study (GWAS) data se

178 ndividuals family-history positive (FHP) for alcoholism have increased risk for the disorder, which m

179 A greater percentage of relatives with alcoholism (hazard ratio: 1.04, 95% CI=1.02-1.07), male

180 ce status significantly correlated with age, alcoholism, hypoalbuminemia, hyperbilirubinemia, renal i

181 the National Institute on Alcohol Abuse and Alcoholism in a large representative sample of US adults

182 type consisting of compulsivity, anxiety and alcoholism in addition to the characteristic motor pheno

183 effects of this allele on the development of alcoholism in adolescents and young adults, and demonstr

184 white matter integrity and increased risk of alcoholism in adulthood.

185 Subtyping alcoholism in adults into an early-onset type, with chro

186 the National Institute on Alcohol Abuse and Alcoholism in collaboration with the Office of Dietary S

187 l relevance to adolescent binge drinking and alcoholism in humans to test whether alcohol damages mye

188 1, and gamma1 subunits genetically linked to alcoholism in humans, our findings indicate that these n

189 ts, while TACR1 variation is associated with alcoholism in humans.

190 The importance of alcoholism in local suicides was unanticipated and not a

191 rphism has been convincingly associated with alcoholism in numerous studies of several populations in

192 e germline and may be critically involved in alcoholism-inherited diseases.

193 sex-dependent difference in genetic risk of alcoholism-inherited diseases.

194 mal atRA shares pathological conditions with alcoholism, inhibition of retinol (vitamin A) activation

195 hat disulfiram, a drug used to treat chronic alcoholism, inhibits G. lamblia CK and kills G. lamblia

196 f the Integrative Neuroscience Initiative on Alcoholism (INIA-Neuroimmune) consortium participated in

197 f the Integrative Neuroscience Initiative on Alcoholism (INIA-Neuroimmune) consortium tested the hypo

198 tructured Assessment for Drug Dependence and Alcoholism interview.

199 mi-Structured Assessment for the Genetics of Alcoholism interview.

200 Alcoholism involves long-term cognitive deficits, includ

201 Alcoholism is a chronic, relapsing illness in which stre

202 Alcoholism is a complex and debilitating syndrome affect

203 Alcoholism is a complex disorder influenced by interacti

204 Alcoholism is a heritable disease that afflicts about 8%

205 Alcoholism is a pervasive disorder perpetuated in part t

206 Alcoholism is a significant public health problem.

207 Although alcoholism is a worldwide problem resulting in millions

208 Alcoholism is associated with changes in brain reward an

209 Chronic alcoholism is associated with decreased plasticity and r

210 Alcoholism is associated with gray matter volume deficit

211 Alcoholism is characterized by a compulsion to seek and

212 Medication for the treatment of alcoholism is currently not particularly robust.

213 Alcoholism is frequently co-morbid with post-traumatic s

214 est, given the fact that early-onset type II alcoholism is more common among men and that, among addi

215 Alcoholism is one of the most prevalent neuropsychiatric

216 Alcoholism is one of the most prevalent psychiatric dise

217 Because a history of alcoholism is prevalent among potential heart donors, we

218 in the genetic predisposition to anxiety and alcoholism is unknown.

219 However, the role of Arc in alcoholism is unknown.

220 Alcohol addiction (alcoholism) is one of the most prevalent substance abuse

221 Before achieving better treatments for alcoholism, it is necessary to understand the critical a

222 Chronic alcoholism leads to the onset and progression of alcohol

223 drug abuse pharmacotherapies, especially for alcoholism, little is known about the role of this syste

224 ol use disorder, including family history of alcoholism, male sex, impulsivity, and low level of resp

225 ave shown that the effects of naltrexone for alcoholism may be moderated by the Asn40Asp single-nucle

226 , some of which are associated with familial alcoholism, may be used to predict which adolescents are

227 ent, and its in vivo activity in preclinical alcoholism models.

228 Although no animal model duplicates alcoholism, models for specific factors, like the withdr

229 ath with significantly raised mortality were alcoholism, motor vehicle accidents with pedestrians, mo

230 as compared to subjects without a history of alcoholism (n = 6) (aged 32-56 years, all males).

231 60% diminished in subjects with a history of alcoholism (n = 6) as compared to subjects without a his

232 g obsessive-compulsive disorder, autism, and alcoholism, occur more frequently in ALS kindreds than i

233 The chronic alcoholism of donors was found to be a protective factor

234 m the Collaborative Study of the Genetics of Alcoholism on alcohol dependence in a sample of moderate

235 this research is to determine the effects of alcoholism on zinc bioavailability and alveolar macropha

236 inor allele of rs1439047 on NTRK2 delays the alcoholism onset age, but the additive minor allele of r

237 nor allele of rs63319 on ALDH1A1 advance the alcoholism onset age; and the dominant minor allele of r

238 Two other cases were attributed to alcoholism or active chronic hepatitis B virus infection

239 ological parent or sibling with a history of alcoholism or alcohol problems) had 49% higher odds of o

240 symptoms of nausea and diarrhea, history of alcoholism or chronic lung disease, and abnormal laborat

241 y gastrointestinal symptoms and a history of alcoholism or chronic lung disease, may be useful in gui

242 Three percent had an alcoholism or substance abuse history, 6.4% had hepatiti

243 CI: 2.2, 14.5), self-reported alcohol use or alcoholism (OR = 2.9, 95% CI: 1.5, 5.4), body mass index

244 Alcoholism, or alcohol use disorder, is a major public h

245 hizophrenia, psychosis, suicide, depression, alcoholism, or autism (relative risk [RR], 1.50; 95% CI,

246 e that a gene(s) on chromosome 9p influences alcoholism, our results can facilitate human research on

247 ere the Child-Pugh score (p = 0.003), active alcoholism (p = 0.035), and no antibiotic prophylaxis (p

248 dence and a positive family history (FHP) of alcoholism, participated in a randomized, double-blind,

249 tions in NFKB1 appear to affect the risk for alcoholism, particularly contributing to an earlier onse

250 Food and Drug Administration (FDA)-approved alcoholism pharmacotherapy, naltrexone, relative to plac

251 Further dissection of the alcoholism phenotype, to disentangle the influence of co

252 ry artery disease, congestive heart failure, alcoholism, proteinuria, reduced kidney function, and hy

253 unction in patients with a family history of alcoholism, raising the possibility that alcohol effects

254 ntrations and reported no history of stroke, alcoholism, recent anemia therapy, or diseases of the li

255 These results indicate that different alcoholism-related behaviors are determined independentl

256 The cerebellum is a target of alcoholism-related brain damage in adults, yet no study

257 iation (after Bonferroni correction) with an alcoholism-related phenotype for four different single-n

258 Alcoholism remains a prevalent health concern throughout

259 Alcoholism remains a serious cause of morbidity and mort

260 The treatment of alcoholism requires the proper management of ethanol wit

261 miologic support for a link between familial alcoholism risk and obesity in women and possibly in men

262 We did an extended longitudinal study of alcoholism's trajectory of effect on selective fibre bun

263 ific National Institute on Alcohol Abuse and Alcoholism safe drinking levels.

264 mmon, complex psychiatric diseases including alcoholism, schizophrenia, and anxiety disorders, althou

265 the National Institute on Alcohol Abuse and Alcoholism showed that liver cirrhosis was the 12th lead

266 Psilocybin is being tested for alcoholism, smoking cessation, and in patients with adva

267 nes, stress, diabetes, obesity, medications, alcoholism, smoking, and nutrition.

268 PBIF accurately replicated the alcoholism study, showing a widespread approximately 20%

269 n expression such as psychological distress, alcoholism, substance use, and delirium allow clinicians

270 n the Collaborative Study on the Genetics of Alcoholism, suggest that it is involved in a general ext

271 e, an FDA-approved drug for the treatment of alcoholism, suggesting that their increased glutamatergi

272 sk-free model to simultaneously characterize alcoholism susceptibility and onset age in 65 independen

273 minor allele of rs2134655 on DRD3 increases alcoholism susceptibility; the dominant minor allele of

274 mprehensive understanding of the genetics of alcoholism than previous case-control studies.

275 Immunosuppression is a major complication of alcoholism that contributes to increased rates of opport

276 Based on this and imaging studies of alcoholism that have demonstrated less dopamine in the s

277 conveys a well-confirmed protection against alcoholism, that modern phenotypic manifestation does no

278 rmine whether this allele is associated with alcoholism, the authors conducted a Human Genome Epidemi

279 ession, antisocial personality disorder, and alcoholism, the authors could identify the original crit

280 idence of association of this insertion with alcoholism; the longer allele (with the indel), which ha

281 m the Collaborative Study on the Genetics of Alcoholism to identify novel genes affecting risk for al

282 as useful neural markers of relapse risk and alcoholism treatment outcome.

283 te that MT-7716 is a promising candidate for alcoholism treatment remaining effective with chronic ad

284 GABAB) receptor undergoes splicing and is an alcoholism treatment target, but there is little informa

285 support a personalized medicine approach to alcoholism treatment that takes into account OPRM1 genot

286 l algorithm based on the combination of past alcoholism treatments and age.

287 Age and lack of past alcoholism treatments were independently associated with

288 anagement and remained after controlling for alcoholism typology and baseline demographic differences

289 mean age 25, with a varied family history of alcoholism underwent two [(11)C]RAC PET scans: one while

290 National Institute on Alcohol Abuse and Alcoholism, US National Institutes of Health.

291 s tested whether perceived stigmatization of alcoholism was associated with a lower likelihood of rec

292 Chronic alcoholism was less frequent in patients with a favorabl

293 within that region that are associated with alcoholism, we have tested the association of NFKB1, loc

294 Both future binge-drinking and familial alcoholism were associated with altered frontostriatal w

295 fied where future binge-drinking or familial alcoholism were significantly associated with emergent o

296 op 14 Collaborative Study of the Genetics of Alcoholism, where the MQLS detects genomewide significan

297 Persons with alcoholism who are abstinent exhibit persistent impairme

298 has been to develop a valid animal model of alcoholism with similar imaging phenotypes as those obse

299 Our data support an association of alcoholism with up-regulation of a cluster of miRNAs loc

300 , the Collaborative Study of the Genetics of Alcoholism, yielded replication for DKK2 but not EGF.