ライフサイエンスコーパス: alcoholic

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

2 may positively affect treatment outcomes in alcoholics.

3 ure therapy and reduce high relapse rates in alcoholics.

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

5 alcohol responses in animal models and human alcoholics.

6 alcohol responses in animal models and human alcoholics.

7 es of opportunistic infections and sepsis in alcoholics.

8 ted with increased motivation for alcohol in alcoholics.

9 could be a potential therapeutic target for alcoholics.

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

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

12 Non-alcoholic and alcoholic fatty liver disease (NAFLD and A

13 sensor was tested in real time samples like alcoholic and non-alcoholic drinks and found good correl

14 implicated in plasma lipoprotein metabolism, alcoholic and non-alcoholic fatty liver disease and myoc

15 tients with cACLD with hepatitis C virus and alcoholic and nonalcoholic steatohepatitis.

16 negars are liquid products produced from the alcoholic and subsequent acetous fermentation of carbohy

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

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

19 development and progression of fatty liver, alcoholic, and nonalcoholic liver disease (NAFLD) all ap

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

21 Weakened cardiac contractility in vivo in alcoholic animals is also associated with depressed mito

22 the apoprotein by solvolysis in alcohols and alcoholic aqueous solutions.

23 than Groups I (non-alcoholic beers) and II (alcoholic beers with low bitterness).

24 In general, Group V (alcoholic beers with very high bitterness) presented hig

25 ol and phenolics contents than Groups I (non-alcoholic beers) and II (alcoholic beers with low bitter

26 adjustment for sex, age, household density, alcoholic beverage consumption, smoking habit, and cardi

27 ences; but the aetiology of variation in non-alcoholic beverage preferences is unknown.

28 er drinking pruno, an illicit, prison-brewed alcoholic beverage.

29 d commercially available Hungarian distilled alcoholic beverages (called palinka), in order to decide

30 with seawater, tap water, mineral water, and alcoholic beverages and by comparing with those results

31 , individuals addicted to alcohol also crave alcoholic beverages and spend time and put much effort i

32 Innovative methods to detect methanol in alcoholic beverages are being constantly developed.

33 Alcoholic beverages have been consumed for thousands of

34 Although excessive consumption of alcoholic beverages is commonly regarded to be detriment

35 rganic element contaminant concentrations in alcoholic beverages was investigated.

36 ohol: by current drinkers replacing standard alcoholic beverages with similar beverages of lower alco

37 ss during cooking of liquid foods containing alcoholic beverages, ethanol concentration was measured

38 s food product containers, in particular for alcoholic beverages.

39 obacco, natural latex and plant-food-derived alcoholic beverages.

40 s a poison which is frequently discovered in alcoholic beverages.

41 fluence on variation in liking for seven non-alcoholic beverages: SSBs; NNSBs; fruit cordials, orange

42 rations in synaptic plasticity affecting the alcoholic brain.

43 tildrakizumab 100 mg group; the patient had alcoholic cardiomyopathy and steatohepatitis, and adjudi

44 vely followed-up cohort of 230 patients with alcoholic cirrhosis (AC) using competing risk analyses.

45 irrhosis, primary sclerosing cholangitis, or alcoholic cirrhosis (group I), NASH, and cryptogenic cir

46 26 patients with alcoholic cirrhosis and variceal haemorrhage were studie

47 male patient received a liver transplant for alcoholic cirrhosis and, 6 years later, developed biopsy

48 ress were assessed in SAH patients (n = 90), alcoholic cirrhosis patients (n = 60), and healthy contr

49 ve protein product) was higher in SAH versus alcoholic cirrhosis patients and healthy controls (P < 0

50 tis as first liver decompensation (Group 1), alcoholic cirrhosis with >/=6 months abstinence (Group 2

51 as being associated with the development of alcoholic cirrhosis.

52 rations within the splanchnic circulation of alcoholic cirrhotic patients undergoing TIPSS insertion

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

54 dy reported how factors such as temperature, alcoholic degree, and amino acids concentration are able

55 s ratio for high versus low IgE levels per 1 alcoholic drink per week higher consumption was 1.12 (95

56 in real time samples like alcoholic and non-alcoholic drinks and found good correlation (99%).

57 capita (0.54% of expenditure on food and non-alcoholic drinks) in the lowest SEIFA quintile, a differ

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

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

60 omatic cocktail bitters are derived from the alcoholic extraction of a variety of plant materials and

61 Herein, alcoholic extracts of Agaricus bisporus were studied for

62 Alcoholic fatty liver disease (ALD) and nonalcoholic fat

63 Non-alcoholic and alcoholic fatty liver disease (NAFLD and AFLD, respectiv

64 models (n = 3-5) and in human samples of non-alcoholic fatty liver disease (NAFLD) (n = 72-135).

65 Non-alcoholic fatty liver disease (NAFLD) affects a large pr

66 ne fetuin-A may impair renal function in non alcoholic fatty liver disease (NAFLD) by altering inflam

67 and more effective hepatitis C therapy, non-alcoholic fatty liver disease (NAFLD) could soon emerge

68 The approach was developed on a non-alcoholic fatty liver disease (NAFLD) data set.

69 Non-alcoholic fatty liver disease (NAFLD) has been recently

70 iver function in bariatric patients with non-alcoholic fatty liver disease (NAFLD) in a randomized cl

71 ent studies have raised the concept that non-alcoholic fatty liver disease (NAFLD) in adults is disti

72 The incidence of non-alcoholic fatty liver disease (NAFLD) increases with age

73 Non-alcoholic fatty liver disease (NAFLD) is a common metabo

74 Non-alcoholic fatty liver disease (NAFLD) is a major risk fa

75 Non-alcoholic fatty liver disease (NAFLD) is one of the most

76 Non-alcoholic fatty liver disease (NAFLD) is the most common

77 Non-alcoholic fatty liver disease (NAFLD) represents a spect

78 The process initiates with non-alcoholic fatty liver disease (NAFLD) that progresses to

79 FXR and CAR in disease progression from non-alcoholic fatty liver disease (NAFLD) to HCC.

80 ome (PCOS) is frequently associated with non-alcoholic fatty liver disease (NAFLD), but the mechanism

81 tophagy is associated with steatosis and non-alcoholic fatty liver disease (NAFLD), however the mecha

82 In non-alcoholic fatty liver disease (NAFLD), lipid build-up an

83 od spot testing-is often misdiagnosed as non-alcoholic fatty liver disease (NAFLD), non-alcoholic ste

84 ein F (APO-F), a potential biomarker for non-alcoholic fatty liver disease (NAFLD).

85 isms differ in drug induced (DIS) and/or non-alcoholic fatty liver disease (NAFLD).

86 creased oxidative damage are features of non-alcoholic fatty liver disease (NAFLD).

87 as a potential plasma marker to diagnose non-alcoholic fatty liver disease (NAFLD).

88 BR) is beneficial for obesity-associated non-alcoholic fatty liver disease (NAFLD).

89 icacy of sevelamer in treating mice with non-alcoholic fatty liver disease (NAFLD).

90 ic control in pre-diabetic patients with non-alcoholic fatty liver disease (NAFLD).

91 creased oxidative damage are features of non-alcoholic fatty liver disease (NAFLD).

92 t), as well as elevated inflammation and non-alcoholic fatty liver disease activity scores, and hepat

93 Non-alcoholic fatty liver disease and early fibrosis were in

94 a substantial overlap with biomarkers of non-alcoholic fatty liver disease and its progression to ste

95 Low aerobic capacity increases risk for non-alcoholic fatty liver disease and liver-related disease

96 ma lipoprotein metabolism, alcoholic and non-alcoholic fatty liver disease and myocardial infarction

97 to various metabolic diseases, including non-alcoholic fatty liver disease and type 2 diabetes.

98 Ninety four eligible patients who have non-alcoholic fatty liver disease and who are insulin resist

99 lications such as insulin resistance and non-alcoholic fatty liver disease are reaching epidemic prop

100 y, and prevents metabolic stress-induced non-alcoholic fatty liver disease in mice.

101 ion and fibrosis in humans and mice with non-alcoholic fatty liver disease is accompanied by accumula

102 Non-alcoholic fatty liver disease is associated with hepatoc

103 Non-alcoholic fatty liver disease is the most rapidly growin

104 The progressive non-alcoholic fatty liver disease observed in the LCR rats f

105 l syndrome, and metabolic (i.e. obesity, non-alcoholic fatty liver disease, and diabetes) and neurolo

106 progression of alcoholic liver disease, non-alcoholic fatty liver disease, and non-alcoholic steatoh

107 h risk factors of liver disease, such as non-alcoholic fatty liver disease, hazardous alcohol use, or

108 d progression of liver diseases, such as non-alcoholic fatty liver disease, non-alcoholic steatohepat

109 Non-alcoholic fatty liver disease, the most prevalent liver

110 e 2 diabetes mellitus has been linked to non-alcoholic fatty liver disease, which can progress to inf

111 atherosclerosis, increased obesity, and non-alcoholic fatty liver disease.

112 might be a novel therapeutic target for non-alcoholic fatty liver disease.

113 MKK2 function confers protection against non-alcoholic fatty liver disease.

114 n implicated in fatty liver formation in non-alcoholic fatty liver disease.

115 egulated de novo lipogenesis involved in non-alcoholic fatty liver disease.

116 vide unique targets for the treatment of non-alcoholic fatty liver disease.

117 therapeutic role of PHLPP2 activators in non-alcoholic fatty liver disease.

118 metabolic outcomes in participants with non-alcoholic fatty liver disease.

119 e liver fibrosis, mostly associated with non-alcoholic fatty liver disease.

120 ction in other hepatic diseases, such as non-alcoholic fatty liver disease.

121 res of the metabolic syndrome, including non-alcoholic fatty liver disease.

122 s (ROS) contribute to the development of non-alcoholic fatty liver disease.

123 lic diseases such as type 2 diabetes and non-alcoholic fatty liver disease.

124 atitis C and emergence of cirrhosis from non-alcoholic fatty liver disease.

125 tabolic conditions including obesity and non-alcoholic fatty liver disease.

126 adipocyte hypertrophy, and present with non-alcoholic fatty liver disease; 3) DKO mice demonstrate H

127 lipolysis pathway was altered in a model of alcoholic fatty liver, primary hepatocytes from rats fed

128 ngths (E=0.8kV/cm & 5kV/cm) prior and during alcoholic fermentation (AF) of red grapes on improving d

129 discuss about the role of proline during the alcoholic fermentation and the generation of certain vol

130 by the traditional method requires a second alcoholic fermentation of a base wine in sealed bottles,

131 should be optimized in order to control the alcoholic fermentation of the concentrated grape must (C

132 as been detected both at the half and end of alcoholic fermentation, and at the end of malolactic fer

133 At the end of the alcoholic fermentation, the contents of anthocyanins for

134 of matrix composition or the yeasts used for alcoholic fermentation.

135 ip with the volatile compounds formed during alcoholic fermentation.

136 ile fructose residues remained at the end of alcoholic fermentation.

137 e is reduced to (R)-delta-decalactone during alcoholic fermentation.

138 d 2 elastography techniques for diagnosis of alcoholic fibrosis and cirrhosis; liver biopsy with Isha

139 eak acid ion exchanger capable of exchanging alcoholic group protons for cations (Ca(+2)).

140 Alcoholic hepatitis (AH) develops in only a small propor

141 BACKGROUND & AIMS: Patients with severe alcoholic hepatitis (AH) have a high risk of death withi

142 Severe alcoholic hepatitis (AH) is a life-threatening disease f

143 Alcoholic hepatitis (AH) is a syndrome of jaundice and l

144 Alcoholic Hepatitis (AH) is major source of alcohol-rela

145 Alcoholic hepatitis (AH) is the most severe form of alco

146 Alcoholic hepatitis (AH) is the most severe form of alco

147 The diagnosis of alcoholic hepatitis (AH) often requires a transjugular l

148 s on effective therapeutic interventions for alcoholic hepatitis (AH), the most severe form of alcoho

149 alterations in circulating albumin in severe alcoholic hepatitis (SAH) patients and their contributio

150 nfections are common in patients with severe alcoholic hepatitis (SAH), but little information is ava

151 nfections are common in patients with severe alcoholic hepatitis (SAH), but little information is ava

152 ents were stratified into two groups: severe alcoholic hepatitis as first liver decompensation (Group

153 short-term and long-term survival in severe alcoholic hepatitis based on baseline disease severity,

154 ted in increasing mortality in patients with alcoholic hepatitis but the underlying mechanisms are no

155 blood mononuclear cells of patients with ALD/alcoholic hepatitis compared to controls.

156 tocol showed that early transplant in severe alcoholic hepatitis could improve survival with low inci

157 tion of lipin-1 ameliorated inflammation and alcoholic hepatitis in mice via activation of endocrine

158 that new therapeutic development for severe alcoholic hepatitis must target liver injury in the shor

159 ion, such as those observed in patients with alcoholic hepatitis or cirrhosis.

160 PBMs isolated from alcoholic hepatitis patients had high expression of SIRT

161 , analysis of circulating EVs from plasma of alcoholic hepatitis patients revealed increased numbers

162 rly linked to key clinical symptoms of acute alcoholic hepatitis such as fever, neutrophilia, and was

163 PTX3 levels were increased in patients with alcoholic hepatitis, a prototypic acute-on-chronic condi

164 precipitating event (active alcoholism/acute alcoholic hepatitis, bacterial infection, and others); (

165 blood monocytes isolated from patients with alcoholic hepatitis, expression of TNFalpha mRNA was rob

166 t to transplant selected patients with acute alcoholic hepatitis, initiated in October 2012.

167 e treatment of inflammatory diseases such as alcoholic hepatitis, nonalcoholic steatohepatitis, and p

168 addition to being a potential biomarker for alcoholic hepatitis, PTX3 participates in the wound-heal

169 ssue and serum samples from 54 patients with alcoholic hepatitis.

170 timize the therapeutic development in severe alcoholic hepatitis.

171 17 could be a viable approach in attenuating alcoholic hepatitis.

172 al research identified cognitive deficits in alcoholic individuals as a risk factor for relapse, and

173 ndividuals as a risk factor for relapse, and alcoholic individuals display deficits on cognitive task

174 to executive cognitive function deficits in alcoholic individuals.

175 If alcoholic ketoacidosis is suspected, dextrose-containing

176 in patients with alcohol use disorders, and alcoholic ketoacidosis were selected.

177 alcohol problems had a much greater risk for alcoholic liver cirrhosis compared to the general popula

178 ful use, or dependence) during 1998-2002 for alcoholic liver cirrhosis development (n = 36,044).

179 The IRR for alcoholic liver cirrhosis in the cohort relative to the

180 RRs) were estimated as the incidence rate of alcoholic liver cirrhosis in these patients relative to

181 Alcoholic liver cirrhosis is usually preceded by many ye

182 hol diagnosis were significant predictors of alcoholic liver cirrhosis risk in men and women, whereas

183 entified predictors of the absolute risk for alcoholic liver cirrhosis.

184 ll ethnic groups combined (52%), followed by alcoholic liver disease (21%).

185 minant causes of alcohol-related deaths were alcoholic liver disease (65.1%), fibrosis and cirrhosis

186 her CES1 played a role in the development of alcoholic liver disease (ALD) and methionine and choline

187 s significant overlap in the pathogenesis of alcoholic liver disease (ALD) and NAFLD, although studie

188 Both alcoholic liver disease (ALD) and nonalcoholic fatty liv

189 Nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are common causes of chron

190 onic, excessive alcohol consumption leads to alcoholic liver disease (ALD) characterized by steatosis

191 Alcoholic liver disease (ALD) develops in approximately

192 The spectrum of alcoholic liver disease (ALD) is a major cause of mortal

193 Alcoholic liver disease (ALD) is associated with intesti

194 The pathogenesis of alcoholic liver disease (ALD) is not well established.

195 nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) is still unsettled, but es

196 patient with acute hepatitis associated with alcoholic liver disease (ALD).

197 ry signaling by Kupffer cells contributes to alcoholic liver disease (ALD).

198 ), primary sclerosing cholangitis (PSC), and alcoholic liver disease (ALD).

199 1 has been implicated in the pathogenesis of alcoholic liver disease (ALD).

200 idonate 15-lipoxygenase (ALOX15) in treating alcoholic liver disease (ALD).

201 rrhotic patients with chronic hepatitis C or alcoholic liver disease (n = 1121), the T allele was ind

202 hibitor use increases the risk of developing alcoholic liver disease among alcohol-dependent patients

203 lular carcinoma (HCC) develops with advanced alcoholic liver disease and liver fibrosis.

204 variation in the progression and outcomes of alcoholic liver disease and nonalcoholic fatty liver dis

205 ctors that contribute to the pathogenesis of alcoholic liver disease and nonalcoholic fatty liver dis

206 ic hepatitis (AH) is the most severe form of alcoholic liver disease for which there are no effective

207 proinflammatory cytokine production in early alcoholic liver disease has not been addressed.

208 Alcoholic liver disease is a leading cause of liver-rela

209 Alcoholic liver disease is a pathological condition caus

210 Alcoholic liver disease is becoming more common in many

211 ers that display a ductular response such as alcoholic liver disease or sclerosing cholangitis.

212 of ceramides, bioactive lipids implicated in alcoholic liver disease pathogenesis.

213 rite guidelines on Liver Transplantation for Alcoholic Liver Disease to summarize current knowledge a

214 Alcoholic liver disease was the most common cause of cir

215 es, use of 3.0 T, presence of cirrhosis, and alcoholic liver disease were all significantly associate

216 Alcoholic liver disease will shortly overtake ischaemic

217 ic enzymes may promote the earliest stage of alcoholic liver disease, alcoholic steatosis.

218 nalcoholic fatty liver diseases (NAFLD); and alcoholic liver disease, are a leading cause of morbidit

219 nt indications for liver transplantation are alcoholic liver disease, hepatocellular carcinoma, and v

220 roton pump inhibitors promote progression of alcoholic liver disease, non-alcoholic fatty liver disea

221 ed to influence histological liver damage in alcoholic liver disease, nonalcoholic fatty liver diseas

222 oles of EVs in nonalcoholic steatohepatitis, alcoholic liver disease, viral hepatitis, cholangiopathi

223 ic hepatitis (AH) is the most severe form of alcoholic liver disease.

224 ts common genetic variant is associated with alcoholic liver disease.

225 s are available for noninvasive diagnosis of alcoholic liver disease.

226 P2B10 that may contribute to the etiology of alcoholic liver disease.

227 lyceride accumulation, a hallmark feature of alcoholic liver disease.

228 e mucosal barrier facilitates progression of alcoholic liver disease.

229 olic hepatitis (AH), the most severe form of alcoholic liver disease.

230 rrhotic and precirrhotic stages of NAFLD and alcoholic liver disease.

231 novel therapeutic options for patients with alcoholic liver disease.

232 l on monocytes and macrophages contribute to alcoholic liver disease.

233 ve therapeutic potential in the treatment of alcoholic liver diseases associated with inflammation, o

234 Alcoholic liver diseases comprise a spectrum of clinical

235 s (HCV), hepatitis B virus (HBV), NAFLD, and alcoholic liver diseases; (2) performance of specific VC

236 In conclusion, NOX4 is induced in early alcoholic liver injury and regulates CCR2/CCL2 mRNA stab

237 As the role of this NOX in early alcoholic liver injury has not been addressed, we studie

238 of inflammatory cells is a major feature of alcoholic liver injury however; the signals and cellular

239 ctivation in culture and in a mouse model of alcoholic liver injury in vivo, and its expression corre

240 A was significantly induced in patients with alcoholic liver injury, and was co-localized with alphaS

241 function are important to the development of alcoholic liver injury.

242 The alcoholic medium was then used as a seed broth for aceti

243 r inflammation caused by viral hepatitis and alcoholic or nonalcoholic steatohepatitis.

244 Strong complexation of the alcoholic oxygen with Mg(II)bisporphyrin rigidifies the

245 pancreatitis, accelerates the development of alcoholic pancreatitis.

246 sease (ALD) develops in approximately 20% of alcoholic patients, with a higher prevalence in females.

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

248 ntation time and temperature) resulted in an alcoholic product that meets ethanol (79g/kg) and residu

249 main parameters that were monitored included alcoholic proof, l-lactic acid content, glucose+fructose

250 and Pb levels in 8 Brazilian spirits plus an alcoholic simulant were initially measured, and then mea

251 conclusion, crude soapstone in contact with alcoholic solutions acts as an adsorbent of trace elemen

252 Using epitaxial growth in an alcoholic solvent, we show exquisite control over the di

253 The spirit/alcoholic/solvent character generated by higher alcohols

254 cal) and 2D (platelet) micelles in water and alcoholic solvents via crystallization-driven self-assem

255 , we tested the hypothesis that during early alcoholic steatohepatitis (ASH) development, hepatocytes

256 High hepatic cholesterol causes non-alcoholic steatohepatitis (NASH) and fibrosis.

257 and might be more likely to progress to non-alcoholic steatohepatitis (NASH) and NAFLD-related fibro

258 Non-alcoholic steatohepatitis (NASH) is characterized by liv

259 The incidence of non-alcoholic steatohepatitis (NASH) is rising but the effic

260 -)/HFD mice showed mild steatosis but no non-alcoholic steatohepatitis (NASH) lesions were found.

261 hysiologically relevant rodent models of non-alcoholic steatohepatitis (NASH) that resemble the human

262 n-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), hereditary dyslipidaem

263 s on high-fat diet (HFD) animal model of non-alcoholic steatohepatitis (NASH).

264 We conclude that alcoholic steatohepatitis accelerates hepatobiliary tumo

265 vation and inflammation in a murine model of alcoholic steatohepatitis and markedly reduced lethality

266 liver biopsy had resolution of definite non-alcoholic steatohepatitis compared with two (9%) of 22 s

267 , non-alcoholic fatty liver disease, and non-alcoholic steatohepatitis in mice by increasing numbers

268 tes, but their efficacy in patients with non-alcoholic steatohepatitis is unknown.

269 Using adult mice, we evaluate the effect of alcoholic steatohepatitis on early hepatobiliary carcino

270 tcome measure was resolution of definite non-alcoholic steatohepatitis with no worsening in fibrosis

271 e treatment of obesity, type 2 diabetes, non-alcoholic steatohepatitis, and related metabolic disorde

272 ch as non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, primary sclerosing cholangiti

273 ease and if left untreated can result in non-alcoholic steatohepatitis, ultimately resulting in liver

274 d, and led to histological resolution of non-alcoholic steatohepatitis, warranting extensive, longer-

275 overweight and show clinical evidence of non-alcoholic steatohepatitis.

276 ling could be a novel treatment approach for alcoholic steatohepatitis.

277 l multifunctional target in the treatment of alcoholic steatohepatitis.

278 etiologies: hepatitis B/C, alcohol, and non-alcoholic steatohepatitis.

279 c strategy against hepatic steatosis and non-alcoholic steatohepatitis.

280 analogue, liraglutide, in patients with non-alcoholic steatohepatitis.

281 CES1 were markedly reduced in patients with alcoholic steatohepatitis.

282 ipid-droplet protein that is up-regulated in alcoholic steatosis and associated with hepatic accumula

283 d glucose and lipid homeostasis in mice with alcoholic steatosis and in ethanol-incubated human hepat

284 as specifically up-regulated in experimental alcoholic steatosis in vivo and in vitro and was up-regu

285 e earliest stage of alcoholic liver disease, alcoholic steatosis.

286 up-regulated in zone 3 hepatocytes in human alcoholic steatosis.

287 e for ceramide synthase 6 in mouse and human alcoholic steatosis.

288 obtained for methanol (r(2)=99.4; RPD=12.8), alcoholic strength (r(2)=97.2; RPD=6.0), acetaldehyde (r

289 ee potential mechanisms for how reduction of alcoholic strength could affect harmful use of alcohol:

290 Reduction of alcoholic strength of beer has been proposed and initiat

291 The potential of alcoholic strength reduction is independent of initiatio

292 eflectance (ATR) was used for predicting the alcoholic strength, the methanol, acetaldehyde and fusel

293 ic beverages with similar beverages of lower alcoholic strength, without increasing the quantity of l

294 been approved for reducing ethanol intake in alcoholic subjects.

295 e of thorium-catalyzed transformations of an alcoholic substrate and the first example of uranium com

296 with cirrhosis (92% Child class A or B, 70% alcoholic) treated at 10 medical centers in Germany.

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

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

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

300 of Artemisia absinthium were quantified from alcoholic wormwood extracts during four phenological sta