ライフサイエンスコーパス: alcoholics

1 pe-specific genes with altered expression in alcoholics.

2 the increased frequency of HBV markers among alcoholics.

3 evelopment of hepatocellular carcinoma among alcoholics.

4 cholesterol transport in heavy drinkers and alcoholics.

5 is associated with attempts at suicide among alcoholics.

6 could be a potential therapeutic target for alcoholics.

7 may positively affect treatment outcomes in alcoholics.

8 ure therapy and reduce high relapse rates in alcoholics.

9 etamine hydrochloride in recently detoxified alcoholics.

10 ssion, which increase the risk of relapse in alcoholics.

11 duced and independent depressive episodes in alcoholics.

12 for alcohol, particularly among early onset alcoholics.

13 response of these circuits is blunted among alcoholics.

14 reatment of less depressed and less suicidal alcoholics.

15 oleacetic acid concentration than late-onset alcoholics.

16 nversion of FAs to FAEE may ameliorate AP in alcoholics.

17 We studied 131 recently abstinent alcoholics.

18 ncentrations in abstinent, treatment-seeking alcoholics.

19 alcohol responses in animal models and human alcoholics.

20 es of opportunistic infections and sepsis in alcoholics.

21 n about splicing changes in this receptor in alcoholics.

22 ereby decrease normal signal transduction in alcoholics.

23 documented reductions in the brain tissue of alcoholics.

24 m induced by methylphenidate in controls and alcoholics.

25 ntial therapeutic target for hyperalgesia in alcoholics.

26 -induced metabolic decreases were greater in alcoholics.

27 pivotal for reducing the risk of relapse in alcoholics.

28 ted with increased motivation for alcohol in alcoholics.

29 he impact that these cues have on relapse in alcoholics.

30 at severe drinking and improve abstinence in alcoholics.

31 ociated cognitive tasks that are observed in alcoholics.

32 ) use/abuse and may contribute to relapse in alcoholics.

33 ntoxication and alcohol consumption by human alcoholics.

34 alcohol responses in animal models and human alcoholics.

35 has been described in other large studies of alcoholics.

36 sessed individuals in families with multiple alcoholics.

37 arance (CL) of MDZ was not different between alcoholics (36.9 +/- 12 L/hr) and nonalcoholics (36.6 +/

38 Participants were 342 men and women: 110 alcoholics, 59 with HIV infection, 65 with HIV infection

39 om the frontal cortex (Broadman area 9) of 9 alcoholics (6 males, 3 females, mean age 48 years) and 9

40 and high) and were profoundly attenuated in alcoholics (70 and 50% lower than controls, respectively

41 Most participants were children of alcoholics (79%) and thus at heightened risk for AUD.

42 the oxidized form was higher in the chronic alcoholics (9.8% [2.2 to 14.8%] versus 2.8% [0.4 to 4.0%

43 In human alcoholics, abstinence is often self-imposed, despite al

44 In many human alcoholics, abstinence is self-imposed because of the ne

45 In many human alcoholics, abstinence is self-imposed because of the ne

46 side effects, including reduced efficacy in alcoholics, addiction, and sedation.

47 CSF 5-HIAA concentrations only in late-onset alcoholics after age was controlled for, but the relatio

48 ile the rate of anorexia was not elevated in alcoholics after controlling for other disorders, bulimi

49 history of alcohol dependence (daughters of alcoholics) after challenge does of alprazolam and place

50 to alcohol-related word stimuli, 26 chronic alcoholics (ALC) and 26 healthy controls (CTL) performed

51 Alcoholics also exhibit similar deficits in cognitive fl

52 noprecipitated from the frontal cortex of 10 alcoholics and 10 age and gender-matched controls then l

53 e were administered to 12 adult daughters of alcoholics and 11 comparison subjects after alprazolam c

54 of regional cerebral blood flow (CBF) in 12 alcoholics and 12 control subjects under three condition

55 in glucose utilization in a group of 18 male alcoholics and 12 healthy male control subjects.

56 rotonin and dopamine transporters in 22 male alcoholics and 13 healthy male volunteers was measured w

57 At baseline, 31 (86%) patients were alcoholics and 33 (92%) presented with hyponatremia.

58 lity (ASP), we sequenced genomic DNA from 50 alcoholics and 50 normal controls.

59 response, compared with 36% of nonabstinent alcoholics and 50% of patients with viral cirrhosis.

60 hepatic 4-HNE contents present in both human alcoholics and alcohol-fed animals.

61 l transcripts occur in postmortem brain from alcoholics and animals exposed to alcohol, and null muta

62 rietal network have been observed in chronic alcoholics and associated with alcohol-related cognitive

63 ce can remain stable in some placebo-treated alcoholics and can respond to desipramine.

64 With practice, alcoholics and control subjects achieved similar task ac

65 gh Vmax) are significantly different between alcoholics and controls (P<10-5).

66 al DNA methylation disturbances, we examined alcoholics and controls using methylation specific micro

67 rats as well as post-mortem brains of human alcoholics and controls were analyzed for the expression

68 the functional polymorphism at ADH3, between alcoholics and controls, can be accounted for by the dis

69 H3*2 are not significantly different between alcoholics and controls, on a constant ADH2 background (

70 e 2 locus, ALDH2, in populations of Japanese alcoholics and controls.

71 ns because allele frequencies differ between alcoholics and controls.

72 ntify genes whose expression differs between alcoholics and controls.

73 , occurs in approximately 5% of hospitalized alcoholics and has a mortality rate approaching 15%.

74 ntral serotonergic functions in subgroups of alcoholics and in healthy comparison subjects.

75 ve to female comparison subjects, while male alcoholics and male comparison subjects had similar leve

76 Hepatitis B virus (HBV) is common in alcoholics and may result in chronic infection.

77 Here we address this question in sober alcoholics and non-substance-abusing control subjects an

78 Additional samples of alcoholics and normal controls were also screened for th

79 In samples both of alcoholics and of controls from three Taiwanese populati

80 Previously, pancreata of dying alcoholics and pancreatic necrosis in severe AP, respect

81 differences for the SSR markers in the case (alcoholics) and control populations would have detected

82 ent comparison groups, early- and late-onset alcoholics, and healthy comparison subjects were studied

83 been previously reported in cocaine abusers, alcoholics, and heroine abusers.

84 evelop CP; the risk is higher among smokers, alcoholics, and men.

85 ousing rate, residing in an area far from an Alcoholics Anonymous meeting location, having the chief

86 olics in treatment - multi-family community/ alcoholics anonymous) regularly versus those who did not

87 rosis, intestinal bypass procedures, chronic alcoholics, anorexia nervosa, and restrictive diets.

88 Therefore, alcoholics are at increased risk of acquiring serious ba

89 rison subjects, which could mean that female alcoholics are more susceptible to gray matter injury th

90 Particularly, alcoholics are more susceptible to pulmonary infections.

91 inical and epidemiological observations that alcoholics are often dependent smokers.

92 an alcohol challenge in 19 year-old sons of alcoholics as well as in sons of nonalcoholic control su

93 interact in both sexes, which puts all older alcoholics at particular risk for the negative sequelae

94 ha is associated with increased mortality in alcoholics, but its role in early alcohol-induced liver

95 markers of ondansetron treatment response in alcoholics by examining polymorphisms in the HTR3A and H

96 The authors randomized 283 alcoholics by genotype in the 5'-regulatory region of th

97 that naltrexone reduces relapse rates among alcoholics by modifying the reinforcing effects of initi

98 elopment of alcoholic liver disease (ALD) in alcoholics by releasing free fatty acids and inflammator

99 y to diazepam was assessed in 51 children of alcoholics by using two eye movement measures: peak sacc

100 Untested, however, are whether the DMN in alcoholics can rebound normally from the relatively depr

101 nt with alterations in executive function in alcoholics, CIE-exposed rats exhibited deficits in behav

102 Children of alcoholics (COAs) are at elevated risk to develop alcoho

103 Children of alcoholics (COAs) are two to ten times more likely to de

104 0.06 variance) showed expression changes in alcoholics/cocaine addicts; these factors included genes

105 alcium wave propagation rates were faster in alcoholics compared to controls.

106 s B virus (HBV) serologic markers in chronic alcoholics compared with the general population.

107 sion scores of desipramine-treated depressed alcoholics decreased significantly, controlling for base

108 cing actions, and its dysregulation in human alcoholics drives their negative emotional state and mot

109 alcoholics (late onset) (N = 16) or type II alcoholics (early onset with antisocial traits) (N = 24)

110 Among treatment-seeking alcoholics, early age at onset is generally associated w

111 eq data from postmortem hippocampus of eight alcoholics, eight cocaine addicts and eight controls.

112 Forty verified alcoholics, either exclusively (n = 10) or with cocaine

113 Hyperalgesia often occurs in alcoholics, especially during abstinence, yet the underl

114 ng is a significant challenge for recovering alcoholics, especially in the presence of alcohol-associ

115 n (a concentration reported to be present in alcoholics), ethanol induced an eight-fold increase in T

116 Human alcoholics exhibit similar cognitive deficits suggesting

117 However, female alcoholics exhibited significantly less N-acetylaspartat

118 r first- or second-degree relatives who were alcoholics (family-positive group) and 16 nonalcoholic c

119 trexone's effects on drinking outcomes among alcoholics following discontinuation of treatment and to

120 genetic association findings differentiating alcoholics from non-alcoholics is with variants in the i

121 und between Mission Indian men and women and alcoholics from the Collaborative Study on the Genetics

122 In male and female alcoholics, frontal lobe white matter concentrations of

123 the treatment-seeking, primarily white male alcoholics had a lifetime history of psychiatric disorde

124 ciation analysis, the 183 Finnish antisocial alcoholics had a significantly higher HTR1B-861C allele

125 The daughters of alcoholics had greater pleasant mood responses after a s

126 Alcoholics had larger volumes of cortical sulci and late

127 Patients who reported both parents to be alcoholics had particularly low mean cerebrospinal fluid

128 We determined that otherwise healthy chronic alcoholics had significantly decreased ELF concentration

129 and follow-up analyses revealed that female alcoholics had significantly lower N-acetylaspartate con

130 This local perfusion deficit in alcoholics has the potential to impair ability to switch

131 Previous research has found that alcoholics have a greater preference for sweet solutions

132 , recent studies have highlighted that human alcoholics have an increased susceptibility to IAV infec

133 c liver disease, to test the hypothesis that alcoholics have greater complexity than matched nonalcoh

134 is study were significantly more likely than alcoholics in the COGA to experience binge drinking, phy

135 ly attended self-help groups (SHGs) (club of alcoholics in treatment - multi-family community/ alcoho

136 ipation in self-help groups for AUD (club of alcoholics in treatment, anonymous family members, other

137 ality characteristic associated with Type II alcoholics, in a pleiotropic manner.

138 een suggested that liver disease is worse in alcoholics infected with HCV.

139 risk factor for acquiring hepatitis C among alcoholics is injection drug use.

140 esipramine to reduce relapse in nondepressed alcoholics is not supported.

141 Alcohol use by alcoholics is uncommon in the first 5 years after liver

142 findings differentiating alcoholics from non-alcoholics is with variants in the inhibitory gamma-amin

143 he criteria of von Knorring et al. as type I alcoholics (late onset) (N = 16) or type II alcoholics (

144 iodontal and demographic factors showed that alcoholics manifest AL by greater increases in GM than n

145 e sweet preference observed previously among alcoholics may be a consequence of chronic alcohol consu

146 oncentrations observed in heavy drinkers and alcoholics may directly act on HDL and apolipoproteins a

147 Furthermore, alcoholics may have reduced sensitivity of 5-HT2C recept

148 : 1) the increased plasma mAspAT observed in alcoholics may reflect pharmacologic upregulation of mAs

149 In controls, but not in alcoholics, metabolism in orbitofrontal cortex (region i

150 ylphenidate in 20 controls and 20 detoxified alcoholics, most of whom smoked.

151 s performed on 42 males, including cirrhotic alcoholics (n = 13), non-cirrhotic alcoholics (n = 15),

152 cirrhotic alcoholics (n = 13), non-cirrhotic alcoholics (n = 15), non-alcoholic controls (n = 14) and

153 We recruited otherwise healthy alcoholics (n = 17) and matched control subjects (n = 17

154 Early-onset alcoholics (onset of excessive consumption before 25 yea

155 pe 1 (HIV-1)-infected individuals are either alcoholics or prone to alcoholism.

156 ifest AL by greater increases in GM than non-alcoholics (P<0.07).

157 In alcoholics, Pearson correlation showed a positive associ

158 Alcoholics performed poorly in tests of memory and motor

159 transmission has been found in a subgroup of alcoholics, possibly those with more aggressive, assault

160 ssues of alcohol-dependent rats and deceased alcoholics, primarily in frontal and striatal areas.

161 All alcoholics received a low-monoamine diet for a minimum o

162 in the severity of alcohol consumption among alcoholics receiving the 5-HT3 antagonist ondansetron.

163 e differences in the test scores observed in alcoholics reflect the greater severity of their liver d

164 ACTH response to the m-CPP infusion than the alcoholics regardless of subtype.

165 Approximately 90% of alcoholics relapse within 4 years, in part because of an

166 rted more anger and anxiety, and the type II alcoholics reported increased euphoria and a greater lik

167 ial effects among the alcoholics; the type I alcoholics reported more anger and anxiety, and the type

168 Alcoholics show blunted neuroendocrine responses to mCPP

169 s, but compared with the healthy volunteers, alcoholics showed a smaller area of mCPP-induced activat

170 ex bands per sample whereas Child's-Pugh B/C alcoholics showed intermediate complexity.

171 Alcoholics showed selective differences from control sub

172 Alcoholics showed the opposite pattern: activation durin

173 Ethanol, at a level attained by alcoholics, significantly suppressed the expression of f

174 Because most alcoholics smoke, the effects of alcohol on MAOB activit

175 gulate and extrastriate cortex activation in alcoholics than controls when processing bilateral compa

176 tensive and robust and the slopes steeper in alcoholics than in controls despite their attenuated dop

177 CHZ CL was significantly higher in alcoholics than in nonalcoholics (31.5 +/- 11.9 vs. 23.4

178 Binding was found to be higher in alcoholics than in nonalcoholics for all of the brain re

179 ts of alprazolam are greater in daughters of alcoholics than in subjects without a history of parenta

180 ailability of MDZ was significantly lower in alcoholics than in the nonalcoholics (0.28 +/- .09 vs. 0

181 btype-related differential effects among the alcoholics; the type I alcoholics reported more anger an

182 the result of an increased susceptibility of alcoholics to infection and/or to an ethanol-mediated st

183 In postmortem brain samples from human alcoholics we found a strong down-regulation of the D1 r

184 artate aminotransferase (mAspAT) observed in alcoholics, we cultured HepG2 hepatoma cells in ethanol.

185 troviruses and genes with high GC content in alcoholics were associated with DNA hypomethylation and

186 A consecutive series of 333 alcoholics were interviewed about whether or not they ha

187 e increases were greater in controls than in alcoholics, whereas methylphenidate-induced metabolic de

188 ate and posterior callosal fibers in chronic alcoholics, which is consistent with functional imaging

189 stem serotonin transporters was found in the alcoholics, which was significantly correlated with life

190 t depressions) were observed in 15.2% of the alcoholics, while 26.4% reported at least one substance-

191 These findings imply that alcoholics who also have a marginal intake of essential

192 attempted suicide, significantly more of the alcoholics who had attempted suicide reported that a fir

193 Compared with alcoholics who had never attempted suicide, significantl

194 In contrast, alcoholics who have compromised callosal integrity showe

195 Among 74 alcoholics who were followed a mean of 5 months after tr

196 CE STATEMENT The vast majority of recovering alcoholics will relapse at least once and understanding

197 The frequency differences between alcoholics with ASP and normal controls for this haploty

198 Comparison of alcoholics with ASP to normal controls for both mutation

199 t outcome in the subset of actively drinking alcoholics with depression, this would be of clinical im

200 CV) infection is a major clinical problem in alcoholics with liver disease and may result from ethano

201 ated in the 15-year follow-up of 453 sons of alcoholics with no history of antisocial personality dis

202 Pancreatic fibrosis is frequently seen in alcoholics without chronic pancreatitis, and this makes

203 h the high pancreatic FAEE concentrations in alcoholics without pancreatitis and high FA concentratio

204 dies have shown increased cerebral spaces in alcoholics, yet, the effect of ethanol on cerebrospinal