ライフサイエンスコーパス: alcoholics

1 ted with increased motivation for alcohol in alcoholics.

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

3 the increased frequency of HBV markers among alcoholics.

4 evelopment of hepatocellular carcinoma among alcoholics.

5 cholesterol transport in heavy drinkers and alcoholics.

6 is associated with attempts at suicide among alcoholics.

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

8 etamine hydrochloride in recently detoxified alcoholics.

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

10 duced and independent depressive episodes in alcoholics.

11 for alcohol, particularly among early onset alcoholics.

12 alcohol responses in animal models and human 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 es of opportunistic infections and sepsis in alcoholics.

17 We studied 131 recently abstinent alcoholics.

18 ncentrations in abstinent, treatment-seeking alcoholics.

19 n about splicing changes in this receptor in alcoholics.

20 ereby decrease normal signal transduction in alcoholics.

21 documented reductions in the brain tissue of alcoholics.

22 alcohol responses in animal models and human alcoholics.

23 m induced by methylphenidate in controls and alcoholics.

24 -induced metabolic decreases were greater in alcoholics.

25 pivotal for reducing the risk of relapse in alcoholics.

26 at severe drinking and improve abstinence in alcoholics.

27 ociated cognitive tasks that are observed in alcoholics.

28 could be a potential therapeutic target for alcoholics.

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

30 ntoxication and alcohol consumption by human alcoholics.

31 may positively affect treatment outcomes in alcoholics.

32 has been described in other large studies of alcoholics.

33 sessed individuals in families with multiple alcoholics.

34 ure therapy and reduce high relapse rates in alcoholics.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 Alcoholics also exhibit similar deficits in cognitive fl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 ns because allele frequencies differ between alcoholics and controls.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Particularly, alcoholics are more susceptible to pulmonary infections.

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

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

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

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

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

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

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

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

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

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

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

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

99 0.06 variance) showed expression changes in alcoholics/cocaine addicts; these factors included genes

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

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

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

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

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

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

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

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

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

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

110 Human alcoholics exhibit similar cognitive deficits suggesting

111 However, female alcoholics exhibited significantly less N-acetylaspartat

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

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

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

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

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

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

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

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

120 Alcoholics had larger volumes of cortical sulci and late

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 In alcoholics, Pearson correlation showed a positive associ

149 Alcoholics performed poorly in tests of memory and motor

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

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

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

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

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

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

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

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

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

159 Alcoholics show blunted neuroendocrine responses to mCPP

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

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

162 Alcoholics showed selective differences from control sub

163 Alcoholics showed the opposite pattern: activation durin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 Compared with alcoholics who had never attempted suicide, significantl

185 In contrast, alcoholics who have compromised callosal integrity showe

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

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

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

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

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

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

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

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

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

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