ライフサイエンスコーパス: alcoholic liver disease

1 hol-related liver disease (previously termed alcoholic liver disease).

2 nce as an early protective mechanism against alcoholic liver disease.

3 guing for an early protective effect against alcoholic liver disease.

4 to the pathogenesis of early stages of human alcoholic liver disease.

5 olymorphisms were evaluated in patients with alcoholic liver disease.

6 well as in liver biopsies from patients with alcoholic liver disease.

7 potential implication in the pathogenesis of alcoholic liver disease.

8 ent compared to counterparts with HCV and/or alcoholic liver disease.

9 dition developed in patients with underlying alcoholic liver disease.

10 162 (53.5%) patients had NASH and HCV and/or alcoholic liver disease.

11 serve as a potential therapeutic option for alcoholic liver disease.

12 effective therapeutics for the treatment of alcoholic liver disease.

13 terial overgrowth is common in patients with alcoholic liver disease.

14 products into the circulation contributes to alcoholic liver disease.

15 etween inflammation and hepatic steatosis in alcoholic liver disease.

16 to be an important factor in the etiology of alcoholic liver disease.

17 ulation by mucosal antimicrobial proteins in alcoholic liver disease.

18 and attenuate the steatosis associated with alcoholic liver disease.

19 HO-1 may be a useful therapeutic strategy in alcoholic liver disease.

20 developed as therapeutics for patients with alcoholic liver disease.

21 on has a central role in the pathogenesis of alcoholic liver disease.

22 tal metabolic disorder in the progression of alcoholic liver disease.

23 for the development of therapeutics to treat alcoholic liver disease.

24 m has been implicated in the pathogenesis of alcoholic liver disease.

25 ed biochemical/nutritional manifestations of alcoholic liver disease.

26 pplementation may have beneficial effects in alcoholic liver disease.

27 c cellular proliferation in a mouse model of alcoholic liver disease.

28 onships will guide hepatologists in managing alcoholic liver disease.

29 cs, detection, pathogenesis and treatment of alcoholic liver disease.

30 implicated in several pathologies, including alcoholic liver disease.

31 diseases including chronic HCV infection and alcoholic liver disease.

32 gy, pathogenesis, prognosis and treatment of alcoholic liver disease.

33 ons may be implicated in the pathogenesis of alcoholic liver disease.

34 ular SAH as potential therapeutic options in alcoholic liver disease.

35 tabolism and abnormal TNFalpha metabolism in alcoholic liver disease.

36 characteristic damage to hepatocytes seen in alcoholic liver disease.

37 or other approaches may be useful to prevent alcoholic liver disease.

38 alpha) is associated with the development of alcoholic liver disease.

39 for many of the dysfunctions associated with alcoholic liver disease.

40 ndotoxin plays a role in the pathogenesis of alcoholic liver disease.

41 nsaturated fat and iron, plays a key role in alcoholic liver disease.

42 l has been implicated in the pathogenesis of alcoholic liver disease.

43 in patients with type I hyperlipidemias and alcoholic liver disease.

44 ho were more likely to have the diagnosis of alcoholic liver disease.

45 r proteins may contribute to liver injury in alcoholic liver disease.

46 on, and pathological changes in experimental alcoholic liver disease.

47 tors on pathological changes in experimental alcoholic liver disease.

48 otein modification in rats with experimental alcoholic liver disease.

49 dothelial cell proliferation in experimental alcoholic liver disease.

50 provements in chronic outcomes, particularly alcoholic liver disease.

51 of hepatic steatosis markers in experimental alcoholic liver disease.

52 tic steatosis is an initial manifestation of alcoholic liver disease.

53 ) of deaths from suicide, drug overdose, and alcoholic liver disease.

54 cial in the prevention or treatment of human alcoholic liver disease.

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

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

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

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

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

60 r each model, not shared with advanced human alcoholic liver disease.

61 e mucosal barrier facilitates progression of alcoholic liver disease.

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

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

64 novel therapeutic options for patients with alcoholic liver disease.

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

66 driving immune impairments in patients with alcoholic liver disease.

67 th much smaller contributions from NAFLD and alcoholic liver disease.

68 model for end-stage liver disease score, and alcoholic liver disease.

69 thanol-induced liver injury in patients with alcoholic liver disease.

70 of patients had been transplanted because of alcoholic liver disease.

71 the microbiome contribute to pathogenesis of alcoholic liver disease.

72 of methylation-associated miRNA, miR-34a, in alcoholic liver diseases.

73 in HCV patients but not in alcoholic and non-alcoholic liver diseases.

74 with potential therapeutic benefits in human alcoholic liver diseases.

75 sociated with the development/progression of alcoholic liver diseases.

76 s of patients is recognized as a hallmark of alcoholic liver diseases.

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

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

79 of 60 years or older (17% [$32795]; P=.01); alcoholic liver disease (26% [$49596]; P=.002); Child-Pu

80 (PSC), 6 with non-A, non-B hepatitis, 6 with alcoholic liver disease, 4 with cryptogenic cirrhosis, 4

81 Etiologies for liver disease included non-alcoholic liver disease (58.0%), hepatitis C (26.0%), he

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

83 angitis (SMR 11.0-4.2), and deterioration in alcoholic liver disease (8.3-24.0) and acute liver failu

84 hosis (adjusted odds ratio, 27.2; P <.0001), alcoholic liver disease (adjusted odds ratio, 7.4; P <.0

85 Recidivism after liver transplantation for alcoholic liver disease adversely impacts long-term surv

86 , i.e. non-alcoholic steatohepatitis (NASH), alcoholic liver disease (ALC), and hepatitis C virus (HC

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

88 Alcoholic liver disease (ALD) accounts for 15%-30% of tr

89 g components and its inhibitory factors in 9 alcoholic liver disease (ALD) and 8 healthy control live

90 Therefore, we evaluated the effect of alcoholic liver disease (ALD) and hepatitis C virus (HCV

91 ethanol consumption, which also occurred in alcoholic liver disease (ALD) and in cirrhosis patients,

92 d hepcidin expression is a common feature in alcoholic liver disease (ALD) and in mouse models of eth

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

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

95 Alcoholic liver disease (ALD) and nonalcoholic fatty liv

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

97 e model will be very useful for the study of alcoholic liver disease (ALD) and of other organs damage

98 vidence suggests that innate immunity drives alcoholic liver disease (ALD) and that the interferon re

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

100 Alcoholic liver disease (ALD) causes significant morbidi

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

102 Alcoholic liver disease (ALD) develops as a consequence

103 Alcoholic liver disease (ALD) develops in approximately

104 Alcoholic liver disease (ALD) features increased hepatic

105 transplant protocol to select patients with alcoholic liver disease (ALD) for transplantation.

106 s have had limited utility in distinguishing alcoholic liver disease (ALD) from nonalcoholic fatty li

107 Alcoholic liver disease (ALD) has been among the leading

108 In the United States, alcoholic liver disease (ALD) has recently become the le

109 It has been suggested that patients with alcoholic liver disease (ALD) have more impaired cogniti

110 ecords, the underlying CLD was attributed to alcoholic liver disease (ALD) in 44% of deaths, HCV infe

111 erally thought to promote the development of alcoholic liver disease (ALD) in alcoholics by releasing

112 Alcoholic liver disease (ALD) is a common indication for

113 Alcoholic liver disease (ALD) is a major cause of chroni

114 Alcoholic liver disease (ALD) is a major cause of liver-

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

116 Alcoholic liver disease (ALD) is a significant health ha

117 Alcoholic liver disease (ALD) is associated with intesti

118 Alcoholic liver disease (ALD) is characterized by steato

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

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

121 eintegration was administered by phone to 84 alcoholic liver disease (ALD) OLTX recipients (ALDs) and

122 consumption may modulate 5hmC formation and alcoholic liver disease (ALD) progression.

123 tion of ACSS2-mediated epigenetic control in alcoholic liver disease (ALD) remains incompletely under

124 patients, its role in the pathophysiology of alcoholic liver disease (ALD) remains unclear.

125 Alcoholic liver disease (ALD) samples were used to confi

126 absence of transplantation for patients with alcoholic liver disease (ALD) to assess survival benefit

127 s-species comparison was performed using the alcoholic liver disease (ALD) transcriptomic public data

128 observation in 1911 on the histopathology of alcoholic liver disease (ALD) was the first identificati

129 lic hepatitis (AH) is a distinct spectrum of alcoholic liver disease (ALD) with intense neutrophilic

130 izes endotoxin, a trigger of inflammation in alcoholic liver disease (ALD), activates two signaling p

131 trahepatic complications of viral hepatitis, alcoholic liver disease (ALD), and nonalcoholic fatty li

132 itis C virus (HCV), hepatitis B virus (HBV), alcoholic liver disease (ALD), and other liver disease u

133 an attractive vertebrate model for studying alcoholic liver disease (ALD), because they possess the

134 in-6 (IL-6) levels is always associated with alcoholic liver disease (ALD), but the significance of s

135 lammation in immune cells in mouse models of alcoholic liver disease (ALD), drug (acetaminophen, APAP

136 ith hepatitis C virus (HCV) infection, NASH, alcoholic liver disease (ALD), or a combination of HCV i

137 ological consequences for the development of alcoholic liver disease (ALD), the underlying mechanisms

138 AM), betaine, and folate in the treatment of alcoholic liver disease (ALD), which was organized by th

139 to steatosis, inflammation, and fibrosis in alcoholic liver disease (ALD).

140 n HCC cases in chronic hepatitis C (CHC) and alcoholic liver disease (ALD).

141 sts that sterile inflammation contributes to alcoholic liver disease (ALD).

142 onic inflammatory hepatic diseases including alcoholic liver disease (ALD).

143 aintained through autophagy, is disrupted in alcoholic liver disease (ALD).

144 ays an essential role in the pathogenesis of alcoholic liver disease (ALD).

145 H compared to hepatitis C virus (HCV) and/or alcoholic liver disease (ALD).

146 factor for all liver diseases, particularly alcoholic liver disease (ALD).

147 iscoveries and results of clinical trials in alcoholic liver disease (ALD).

148 rted abnormalities in proteasome function in alcoholic liver disease (ALD).

149 stasis is associated with the development of alcoholic liver disease (ALD).

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

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

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

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

154 1 has been implicated in the pathogenesis of alcoholic liver disease (ALD).

155 orchestrates inflammatory events leading to alcoholic liver disease (ALD).

156 r dysfunction is an important contributor to alcoholic liver disease (ALD).

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

158 promoter in 150 patients with biopsy-proven alcoholic liver disease and 145 healthy volunteers.

159 hemokines in liver tissue from patients with alcoholic liver disease and a range of disease control s

160 ies often utilize samples from patients with alcoholic liver disease and are confounded by variabilit

161 738409 in PNPLA3 is strongly associated with alcoholic liver disease and clinically evident alcoholic

162 risk of HCC in obese patients is confined to alcoholic liver disease and cryptogenic cirrhosis.

163 stically significant association between non-alcoholic liver disease and FLI-based ultrasound (p < 0.

164 mplications for the liver injury observed in alcoholic liver disease and genetic hemochromatosis in c

165 Patients with alcoholic liver disease and hepatitis C initially had lo

166 s were significantly more likely to have had alcoholic liver disease and infection/sepsis.

167 ubstances but also, for instance, in cancer, alcoholic liver disease and liver cirrhosis.

168 at has been implicated in the progression of alcoholic liver disease and liver fibrosis.

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

170 Inroads are being made into the genetics of alcoholic liver disease and new phenomena are being unco

171 eases that include hepatitis B, hepatitis C, alcoholic liver disease and non-alcoholic steatohepatiti

172 d bacterial translocation in liver fibrosis, alcoholic liver disease and non-alcoholic steatohepatiti

173 Performance was excellent for alcoholic liver disease and nonalcoholic fatty liver dis

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

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

176 tary and alternative medicine agents in both alcoholic liver disease and nonalcoholic steatohepatitis

177 in liver tissues from patients with advanced alcoholic liver disease and nonalcoholic steatohepatitis

178 IL-8 levels and were higher in patients with alcoholic liver disease and parenchymal neutrophil infil

179 r dietary fatty acids in the pathogenesis of alcoholic liver disease and provide a promising therapeu

180 ed 55 to 64 years, primarily attributable to alcoholic liver disease and psychiatric disorders due to

181 apidly through drug overdoses, suicides, and alcoholic liver disease and when the decline in mortalit

182 e the candidate to liver transplantation for alcoholic liver diseases and severe acute alcoholic hepa

183 aine have shown efficacy in animal models of alcoholic liver disease, and "knockout" mice that develo

184 ients with cured HCV, 1.32% in patients with alcoholic liver disease, and 1.24% in patients with NAFL

185 d active HCV, 23.3% had cured HCV, 16.1% had alcoholic liver disease, and 30.1% had NAFLD.

186 hosis, 70 for cholestatic etiologies, 40 for alcoholic liver disease, and 56 for HCV.

187 y cirrhosis, primary sclerosing cholangitis, alcoholic liver disease, and chronic hepatitis C), and h

188 oholic fatty liver disease, steatohepatitis, alcoholic liver disease, and cirrhosis.

189 Chief among these is alcoholic liver disease, and heavy use is detrimental ir

190 ng human liver after submassive necrosis, in alcoholic liver disease, and in focal nodular hyperplasi

191 sative stress are key to the pathogenesis of alcoholic liver disease, and there is now greater emphas

192 ty liver disease, liver fibrosis, cirrhosis, alcoholic liver diseases, and chronic hepatitis.

193 Genetic mechanisms for alcoholic liver disease are being discovered in addition

194 ne system and the mechanisms of apoptosis in alcoholic liver disease are better appreciated, especial

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

196 ontaining liquid diet for 6 months developed alcoholic liver disease as measured by serum alanine tra

197 The importance of K8/K18 in alcoholic liver disease as well as in established cirrho

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

199 The other group contained mainly alcoholic liver disease, autoimmune hepatitis, and prima

200 evious malignancy (HR, 1.34; P < 0.001), and alcoholic liver disease, autoimmune, nonalcoholic steato

201 ghts are being made into the pathogenesis of alcoholic liver disease but safe and effective therapies

202 There have been no treatment advances for alcoholic liver disease but, on balance, steroids are st

203 sidered independent risk factors involved in alcoholic liver disease, but mutual relationships or int

204 n to occur in both experimental and clinical alcoholic liver disease, but the signaling pathway remai

205 thionine cycle, its deficiency could promote alcoholic liver disease by enhancing ethanol-induced per

206 n diseases, such as AIDS, Alzheimer disease, alcoholic liver disease, cardiovascular disease, diabete

207 hs and diseases including alcohol addiction, alcoholic liver disease, cardiovascular disease, diabete

208 important role in non-HHC diseases, such as alcoholic liver disease, chronic viral hepatitis, and po

209 mellitus, atherosclerosis, alcoholic and non-alcoholic liver disease, cirrhosis, hepatocellular carci

210 cysts, hepatitis B virus, hepatitis C virus, alcoholic liver disease, cirrhosis, inflammatory bowel d

211 Alcoholic liver diseases comprise a spectrum of clinical

212 The pathologic features of alcoholic liver disease develop over prolonged periods,

213 d beige fat through cold exposure suppressed alcoholic liver disease development.

214 bowel disease, hepatitis B, alcoholism, and alcoholic liver disease did not reduce the risk for ICC

215 a potential therapeutic option to ameliorate alcoholic liver disease, due to its antioxidant, antiapo

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

217 Patients with alcoholic liver disease frequently exhibit iron overload

218 Because alcoholic liver disease has been linked to oxidative str

219 rated fatty acids against the development of alcoholic liver disease has long been known, but the und

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

221 Treatment of alcoholic liver disease has stagnated, but transplantati

222 group (uninsured Hispanic men with viral or alcoholic liver disease) has not been reached through ed

223 from fully alcohol-attributable causes (eg, alcoholic liver disease) have increased in the past deca

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

225 including nonalcoholic fatty liver disease, alcoholic liver disease, HIV/HCV co-infection and primar

226 4; 95% confidence interval [CI], 1.01-1.08), alcoholic liver disease (HR, 1.66; 95% CI, 1.02-2.71), a

227 Early discoveries in alcoholic liver disease identified increased levels of b

228 s characteristic of early stages of clinical alcoholic liver disease in humans.

229 Complement is involved in the development of alcoholic liver disease in mice; however, the mechanisms

230 e disrupts SIRT1 activity and contributes to alcoholic liver disease in rodents, but the exact pathog

231 untries, but the opposite is true elsewhere; alcoholic liver disease is a considerable burden worldwi

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

233 Alcoholic liver disease is a leading cause of mortality.

234 Alcoholic liver disease is a pathological condition caus

235 Alcoholic liver disease is a predominant cause of liver-

236 Alcoholic liver disease is an attractive target for gene

237 Alcoholic liver disease is associated with abnormal hepa

238 Alcoholic liver disease is associated with abnormal hepa

239 Alcoholic liver disease is associated with sustained liv

240 Alcoholic liver disease is associated with zinc decrease

241 Alcoholic liver disease is becoming more common in many

242 ity, frequency, and patterns of drinking and alcoholic liver disease is limited.

243 and clinical research into the mechanisms of alcoholic liver disease is making headway, but has yet t

244 Alcoholic liver disease is mediated via activation of TL

245 protein-1 (MCP-1), elevated in patients with alcoholic liver disease is not yet understood.

246 se (MELD) score in predicting the outcome of alcoholic liver disease is upheld.

247 is seen in the nonalcoholic steatohepatitis, alcoholic liver disease, ischemia/reperfusion injury, an

248 ften insufficient in chronic hepatitis C and alcoholic liver disease, leading to hyperabsorption of i

249 r HCC (hepatitis B virus, hepatitis C virus, alcoholic liver disease, liver cirrhosis, biliary cirrho

250 g M2 polarization during the early stages of alcoholic liver disease may represent an attractive stra

251 teatosis and steatohepatitis associated with alcoholic liver disease, metabolic dysfunction-associate

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

253 tis (n=81), hepatitis C virus (HCV) (n=945), alcoholic liver disease (n=495), alcohol and HCV (n=152)

254 d homeostasis during the pathogenesis of non-alcoholic liver disease (NAFLD).

255 viral hepatitis (n=19) or other chronic non-alcoholic liver diseases (NALD) (n=27).

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

257 llowing chronic liver inflammation including alcoholic liver disease, non-alcoholic steatohepatitis,

258 cated in the pathogenesis of renal fibrosis, alcoholic liver disease, non-alcoholic steatohepatitis,

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

260 , occurring in 11 patients (31 percent), and alcoholic liver disease, occurring in 5 (13 percent).

261 Subjects were composed of 24 patients with alcoholic liver disease of whom 15 had histopathological

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

263 cidin expression, e.g., chronic hepatitis C, alcoholic liver disease, or hereditary hemochromatosis.

264 atients with primary sclerosing cholangitis, alcoholic liver disease, or nonalcoholic steatohepatitis

265 Recipients who were older, had alcoholic liver disease, or were severely ill were the m

266 or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (cont

267 ular disease was significant only in PBC and alcoholic liver disease, owing to high mortality in the

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

269 relapse is common after liver transplant in alcoholic liver disease patients and can lead to worse o

270 Alcoholic liver disease patients have increased levels o

271 ys expressed in DR and genes associated with alcoholic liver disease progression.

272 Alcoholic liver disease purportedly develops more readil

273 Alcoholic liver disease-related WL registrations and liv

274 nts with gram-negative bacterial infections, alcoholic liver disease (relative risk [RR] 4.87, 95% CI

275 by intestinal dysbiosis, and development of alcoholic liver disease requires gut-derived bacterial p

276 Experimental alcoholic liver disease requires translocation of bacter

277 ethyltransferase activity is associated with alcoholic liver disease, resulting in phosphatidylcholin

278 Despite the growing global burden of alcoholic liver diseases, therapeutic options are limite

279 used the intragastric feeding rat model for alcoholic liver disease to investigate the relationship

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

281 patients with compensated and decompensated alcoholic liver disease, to test the hypothesis that alc

282 ucers of oxidative stress and key factors in alcoholic liver disease, to up-regulate alpha 2 collagen

283 Using a murine model of alcoholic liver disease, treatment with high concentrati

284 In alcoholic liver disease, tumor necrosis factor-alpha (TN

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

286 This increase in risk is independent of alcoholic liver disease, viral hepatitis, or demographic

287 In the past, alcoholic liver disease was attributed exclusively to di

288 etabolism is involved in the pathogenesis of alcoholic liver disease was strengthened by our previous

289 Alcoholic liver disease was the main cause of liver dise

290 Alcoholic liver disease was the most common cause of cir

291 To further evaluate CYP2E1 in alcoholic liver disease, we created a transgenic mouse c

292 titis B or C virus, autoimmune hepatitis, or alcoholic liver disease, we detected increased nuclear t

293 In a mouse model of alcoholic liver disease, we found a significant increase

294 play an etiologic role in the initiation of alcoholic liver disease, we had earlier pioneered the de

295 te in promoting pathological liver injury in alcoholic liver disease, we investigated the role of LBP

296 l and polyunsaturated fatty acids (PUFAs) to alcoholic liver disease, we investigated whether chronic

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

298 2E1 (CYP2E1) is suggested to play a role in alcoholic liver disease, which includes alcoholic fatty

299 Alcoholic liver disease will shortly overtake ischaemic

300 a key role in the genesis and progression of alcoholic liver disease with ethanol exposure enhancing