ライフサイエンスコーパス: alcoholic liver disease

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

2 dition developed in patients with underlying alcoholic liver disease.

3 162 (53.5%) patients had NASH and HCV and/or alcoholic liver disease.

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

5 effective therapeutics for the treatment of alcoholic liver disease.

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

7 products into the circulation contributes to alcoholic liver disease.

8 etween inflammation and hepatic steatosis in alcoholic liver disease.

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

10 ulation by mucosal antimicrobial proteins in alcoholic liver disease.

11 and attenuate the steatosis associated with alcoholic liver disease.

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

13 developed as therapeutics for patients with alcoholic liver disease.

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

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

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

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

18 ed biochemical/nutritional manifestations of alcoholic liver disease.

19 pplementation may have beneficial effects in alcoholic liver disease.

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

21 onships will guide hepatologists in managing alcoholic liver disease.

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

23 implicated in several pathologies, including alcoholic liver disease.

24 diseases including chronic HCV infection and alcoholic liver disease.

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

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

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

28 tabolism and abnormal TNFalpha metabolism in alcoholic liver disease.

29 characteristic damage to hepatocytes seen in alcoholic liver disease.

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

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

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

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

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

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

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

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

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

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

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

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

42 tors on pathological changes in experimental alcoholic liver disease.

43 otein modification in rats with experimental alcoholic liver disease.

44 dothelial cell proliferation in experimental alcoholic liver disease.

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

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

47 e mucosal barrier facilitates progression of alcoholic liver disease.

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

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

50 novel therapeutic options for patients with alcoholic liver disease.

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

52 driving immune impairments in patients with alcoholic liver disease.

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

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

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

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

57 the microbiome contribute to pathogenesis of alcoholic liver disease.

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

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

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

61 olymorphisms were evaluated in patients with alcoholic liver disease.

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

63 potential implication in the pathogenesis of alcoholic liver disease.

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

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

66 with potential therapeutic benefits in human alcoholic liver diseases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 Alcoholic liver disease (ALD) and nonalcoholic fatty liv

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

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

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

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

90 Alcoholic liver disease (ALD) develops as a consequence

91 Alcoholic liver disease (ALD) develops in approximately

92 Alcoholic liver disease (ALD) features increased hepatic

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

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

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

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

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

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

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

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

101 Alcoholic liver disease (ALD) is associated with intesti

102 Alcoholic liver disease (ALD) is characterized by steato

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 1 has been implicated in the pathogenesis of alcoholic liver disease (ALD).

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

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

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

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

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

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

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

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

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

135 738409 in PNPLA3 is strongly associated with alcoholic liver disease and clinically evident alcoholic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Alcoholic liver diseases comprise a spectrum of clinical

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

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

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

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

177 Patients with alcoholic liver disease frequently exhibit iron overload

178 Because alcoholic liver disease has been linked to oxidative str

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

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

181 Treatment of alcoholic liver disease has stagnated, but transplantati

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

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

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

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

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

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

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

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

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

191 Alcoholic liver disease is a leading cause of mortality.

192 Alcoholic liver disease is a pathological condition caus

193 Alcoholic liver disease is a predominant cause of liver-

194 Alcoholic liver disease is an attractive target for gene

195 Alcoholic liver disease is associated with abnormal hepa

196 Alcoholic liver disease is associated with abnormal hepa

197 Alcoholic liver disease is associated with sustained liv

198 Alcoholic liver disease is associated with zinc decrease

199 Alcoholic liver disease is becoming more common in many

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

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

202 Alcoholic liver disease is mediated via activation of TL

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 Alcoholic liver disease patients have increased levels o

223 Alcoholic liver disease purportedly develops more readil

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

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

226 Experimental alcoholic liver disease requires translocation of bacter

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

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

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

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

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

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

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

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

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

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

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

238 Alcoholic liver disease was the most common cause of cir

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

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

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

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

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

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

245 2E1 (CYP2E1) is suggested to play a role in alcoholic liver disease, which includes alcoholic fatty

246 Alcoholic liver disease will shortly overtake ischaemic

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