ライフサイエンスコーパス: steatohepatitis

1 tify liver damage (fibrosis and nonalcoholic steatohepatitis).

2 re collected and analyzed histologically for steatohepatitis.

3 development of fatty liver and nonalcoholic steatohepatitis.

4 ith hepatocellular carcinoma or nonalcoholic steatohepatitis.

5 and show clinical evidence of non-alcoholic steatohepatitis.

6 be a novel treatment approach for alcoholic steatohepatitis.

7 ctional target in the treatment of alcoholic steatohepatitis.

8 ) mice, remained protected from experimental steatohepatitis.

9 s: hepatitis B/C, alcohol, and non-alcoholic steatohepatitis.

10 iral hepatitis and alcoholic or nonalcoholic steatohepatitis.

11 tion, and protects mice from alcohol-induced steatohepatitis.

12 against hepatic steatosis and non-alcoholic steatohepatitis.

13 liraglutide, in patients with non-alcoholic steatohepatitis.

14 tulated the cutaneous pathology of mice with steatohepatitis.

15 markedly reduced in patients with alcoholic steatohepatitis.

16 of hepatic CES1 exacerbated ethanol-induced steatohepatitis.

17 f ethanol-induced fatty liver disease toward steatohepatitis.

18 lthy controls and patients with nonalcoholic steatohepatitis.

19 , was associated with histological NAFLD and steatohepatitis.

20 tory response in the liver and contribute to steatohepatitis.

21 ntribute to the pathogenesis of nonalcoholic steatohepatitis.

22 ed mice demonstrated a marked improvement of steatohepatitis.

23 that CX3CR1 may influence the development of steatohepatitis.

24 epatic leukocyte accumulation in the form of steatohepatitis.

25 al role in the pathogenesis of non-alcoholic steatohepatitis.

26 ic acid in adult patients with non-alcoholic steatohepatitis.

27 ontext of cancer, fibrosis, and nonalcoholic steatohepatitis.

28 alcoholic steatohepatitis vs no nonalcoholic steatohepatitis.

29 se actions of ethanol on hepatosteatosis and steatohepatitis.

30 tty acids and betaine on hepatosteatosis and steatohepatitis.

31 sinusoidal pattern of fibrosis attributed to steatohepatitis.

32 factor 1) knockout mice develop nonalcoholic steatohepatitis.

33 ritical role in the etiology of nonalcoholic steatohepatitis.

34 le of ketogenesis in preventing diet-induced steatohepatitis.

35 mation and fibrosis and lead to nonalcoholic steatohepatitis.

36 o stages of hepatosteatosis and nonalcoholic steatohepatitis.

37 Male WD-fed FXR KO mice had the most severe steatohepatitis.

38 pNaKtide, might attenuate the development of steatohepatitis.

39 B virus, hepatitis C virus, and nonalcoholic steatohepatitis.

40 atty acid metabolism, including nonalcoholic steatohepatitis.

41 titis C virus and alcoholic and nonalcoholic steatohepatitis.

42 nd fibrosis in animal models of nonalcoholic steatohepatitis.

43 he treatment of cholestasis and nonalcoholic steatohepatitis.

44 r cohort of patients at risk of nonalcoholic steatohepatitis.

45 erate activity to improve NAFLD/nonalcoholic steatohepatitis.

46 or 52 weeks, 72 (25%) achieved resolution of steatohepatitis, 138 (47%) had reductions in nonalcoholi

47 granulomatous inflammation (29%), steatosis/steatohepatitis (19.3%), hepatitis B (19%), and hepatiti

48 is C 2.6 versus 3.7, P = 0.002; nonalcoholic steatohepatitis 3.0 versus 4.0, P < 0.001; liver transpl

49 We conclude that alcoholic steatohepatitis accelerates hepatobiliary tumors with ch

50 y liver disease and its subtype nonalcoholic steatohepatitis affect approximately 30% and 5%, respect

51 The results show that high-fat diet-induced steatohepatitis aggravates the inflammation in psoriasif

52 tribute to nonalcoholic fatty liver disease, steatohepatitis, alcoholic liver disease, and cirrhosis.

53 ly, the diverse roles of EVs in nonalcoholic steatohepatitis, alcoholic liver disease, viral hepatiti

54 Mice with steatohepatitis also displayed moderate cutaneous inflam

55 Cellular mechanisms that mediate steatohepatitis, an increasingly prevalent condition in

56 d be an effective strategy for reducing both steatohepatitis and atherosclerosis.

57 cantly to the development and progression of steatohepatitis and atherosclerosis.

58 The association between nonalcoholic steatohepatitis and cardiovascular disease is clear, tho

59 expression, and unexpectedly protection from steatohepatitis and death.

60 latory changes in patients with nonalcoholic steatohepatitis and fatty liver disease, Joo et al have

61 ing parameters as biomarkers of nonalcoholic steatohepatitis and fatty liver disease.

62 tty liver disease (NAFLD) that progresses to steatohepatitis and fibrosis before HCC detection.

63 to investigate the development of steatosis, steatohepatitis and fibrosis in the FFD-CCl4 model when

64 esents a spectrum of conditions that include steatohepatitis and fibrosis that are thought to emanate

65 ses (NAFLD) ranges from hepatic steatosis to steatohepatitis and fibrosis.

66 pathologies such as extensive liver damage, steatohepatitis and fibrosis.

67 arenchymal cells (LPC) spontaneously develop steatohepatitis and hepatocellular carcinoma (HCC) sugge

68 ort and increased prevalence of nonalcoholic steatohepatitis and hepatocellular carcinoma.

69 the development and progression of NAFLD to steatohepatitis and identify the IL-17 pathway as a nove

70 ice are protected from diet-induced obesity, steatohepatitis and insulin resistance.

71 model for investigating the pathogenesis of steatohepatitis and its complications.

72 acroD1, and ADP-ribosylation in AHR-mediated steatohepatitis and lethality in response to dioxin.

73 inflammation in a murine model of alcoholic steatohepatitis and markedly reduced lethality following

74 th simtuzumab, in patients with nonalcoholic steatohepatitis and stage 2 or 3 liver fibrosis.

75 liver fibrosis in patients with nonalcoholic steatohepatitis and stage 2-3 fibrosis.

76 6(R611C) (LRP6(mut/mut)) mice exhibited both steatohepatitis and steatofibrosis.

77 l be older, more likely to have nonalcoholic steatohepatitis and will wait for transplantation longer

78 Nondiabetic patients with nonalcoholic steatohepatitis and without advanced fibrosis are most l

79 f toxic responses, including hepatic damage, steatohepatitis, and a lethal wasting syndrome; however,

80 the patient had alcoholic cardiomyopathy and steatohepatitis, and adjudication was unable to determin

81 2 and EPO in mice with acute pancreatitis or steatohepatitis, and also in patients with acute inflamm

82 as primary biliary cirrhosis or nonalcoholic steatohepatitis, and certain forms of cancer.

83 reverses hypertriglyceridemia, nonalcoholic steatohepatitis, and diabetes in lipodystrophic mice.

84 gh-fat diet-induced ER stress, inflammation, steatohepatitis, and fibrosis, whereas overexpression of

85 disorders such as fatty liver, nonalcoholic steatohepatitis, and hepatocellular carcinoma.

86 ases sensitivity to dioxin-induced toxicity, steatohepatitis, and lethality.

87 , including bile duct ligation, nonalcoholic steatohepatitis, and obese mice, as well as EVs released

88 es such as alcoholic hepatitis, nonalcoholic steatohepatitis, and primary biliary cirrhosis.

89 t of obesity, type 2 diabetes, non-alcoholic steatohepatitis, and related metabolic disorders.

90 e 2 diabetes, dyslipidemia, and nonalcoholic steatohepatitis, and their potential therapeutic applica

91 Postmenopausal women with nonalcoholic steatohepatitis are at an increased risk of hepatic fibr

92 Alcohol-induced and non-alcoholic steatohepatitis are two rising hepatic problems.

93 Nonalcoholic steatohepatitis arising from Western diet and lifestyle

94 form dermatitis was exacerbated in mice with steatohepatitis as compared to animals fed with a standa

95 olesterol uptake function; and iii) moderate steatohepatitis, as evidenced by histopathological chara

96 lmethionine (SAMe) and spontaneously develop steatohepatitis, as well as C57Bl/6 mice (controls); the

97 d the hypothesis that during early alcoholic steatohepatitis (ASH) development, hepatocytes (HCs) rel

98 y low levels of PGC1A in liver, exacerbating steatohepatitis associated with diets high in fructose a

99 actions synergize to correct hyperlipidemia, steatohepatitis, atherosclerosis, glucose intolerance, a

100 ucose clearance, beta-cell survival, reduced steatohepatitis, browning of white adipose tissue, and i

101 d standard for the diagnosis of nonalcoholic steatohepatitis but the definition may vary among pathol

102 d the histological features of non-alcoholic steatohepatitis, but its long-term benefits and safety n

103 increases liver fat and risk of progressive steatohepatitis by interfering with lipoprotein secretio

104 er inflammation and fibrosis in nonalcoholic steatohepatitis can lead to cirrhosis and liver failure

105 In the MCD model of steatohepatitis, carbohydrate-derived palmitate in the l

106 There was a significant difference between steatohepatitis categories at both low and high frequenc

107 elastography provided better distinction of steatohepatitis categories at high frequencies than at l

108 ion, and fibrosis) and modified nonalcoholic steatohepatitis categories were used as reference standa

109 The latter leads to steatohepatitis, cirrhosis, and the formation of hepatic

110 liver biopsies scored using the Nonalcoholic Steatohepatitis Clinical Research Network histological s

111 er biopsy assessment (using the nonalcoholic steatohepatitis Clinical Research Network histological s

112 , 1, 2, and 3, according to the Nonalcoholic Steatohepatitis Clinical Research Network scoring system

113 oring system for NAFLD from the Nonalcoholic Steatohepatitis Clinical Research Network Scoring System

114 Kleiner fibrosis stage and the Nonalcoholic Steatohepatitis Clinical Research Network system for por

115 psy had resolution of definite non-alcoholic steatohepatitis compared with two (9%) of 22 such patien

116 ighly induced in patients with non-alcoholic steatohepatitis, diabetic mice and mice fed a high-fat d

117 onalcoholic fatty liver disease/nonalcoholic steatohepatitis, drug-associated toxicities, and other m

118 In these mice, pNaKtide not only improved steatohepatitis, dyslipidemia, and insulin sensitivity,

119 ZDs), has been shown to reduce steatosis and steatohepatitis effectively and to improve liver functio

120 (56 +/- 8 years old; 62% male; nonalcoholic steatohepatitis etiology 24%; BMI 33.3 +/- 3.2 kg/m(2) ;

121 haracterized cohorts encompassing steatosis, steatohepatitis, fibrosis and cirrhosis (combined n=1,07

122 ith hepatic steatosis and its progression to steatohepatitis, fibrosis, and cancer.

123 entiating steatosis (NAFL) from nonalcoholic steatohepatitis, for staging hepatic fibrosis, and for i

124 and 20-week feeding, 0.044 +/- 0.012 in the steatohepatitis group vs 0.014 +/- 0.008 in the control

125 nd 48-week feeding, 0.51 kPa +/- 0.12 in the steatohepatitis group vs 0.29 kPa +/- 0.01 in the contro

126 Patients with nonalcoholic steatohepatitis had significantly higher PAI-1 values th

127 In patients with nonalcoholic steatohepatitis, half of deaths are due to cardiovascula

128 chronic hepatitis B or C viral infection and steatohepatitis, have been shown to predispose to the de

129 fficient for the development of nonalcoholic steatohepatitis, hepatic stem cell activation, and hepat

130 high fat diet (STZ-HFD) induced nonalcoholic steatohepatitis-hepatocellular carcinoma (NASH-HCC) muri

131 In two independent models of diet-induced steatohepatitis (high-fat diet and methionine/choline-de

132 Nonalcoholic steatohepatitis, i.e., fatty liver accompanied by necroi

133 Administration of SAMe reduced features of steatohepatitis in MAT1A-KO mice.

134 holic fatty liver disease, and non-alcoholic steatohepatitis in mice by increasing numbers of intesti

135 dation, a high-fat diet challenge aggravated steatohepatitis in mice with hepatocyte-specific deletio

136 lay a role in progression of liver injury to steatohepatitis in NASH produced by high-fat feeding dur

137 nographic (US) elastography for detection of steatohepatitis in rats by using histopathologic finding

138 ped varying degrees of hepatic steatosis and steatohepatitis, in the order starch-oleate < starch-pal

139 Alcohol feeding results in steatohepatitis indicated by increased pro-inflammatory

140 In experimental steatohepatitis induced by feeding mice a methionine-cho

141 plays a role in the etiology of nonalcoholic steatohepatitis is unclear.

142 heir efficacy in patients with non-alcoholic steatohepatitis is unknown.

143 identification of patients with nonalcoholic steatohepatitis may help improve patient outcomes throug

144 With progression to steatohepatitis, metabolic pathway activation persisted

145 ptogenic cirrhosis (CC, n=289), nonalcoholic steatohepatitis (NASH) (n=221), hepatitis B virus (HBV)

146 Nonalcoholic steatohepatitis (NASH) affects 2%-3% of the US populatio

147 Nonalcoholic steatohepatitis (NASH) affects 3%-5% of the U.S. populat

148 hology, including 34 (55%) with nonalcoholic steatohepatitis (NASH) and 11 (18%) with bridging fibros

149 y-proven NAFLD, 26 had definite nonalcoholic steatohepatitis (NASH) and 15 were not-NASH.

150 y process in the progression of nonalcoholic steatohepatitis (NASH) and a promising target for treatm

151 strongly up-regulated in human nonalcoholic steatohepatitis (NASH) and alcohol cirrhosis; the latter

152 key role in the pathogenesis of nonalcoholic steatohepatitis (NASH) and associated cardiovascular ris

153 frequencies were reduced during nonalcoholic steatohepatitis (NASH) and chronic hepatitis C virus (HC

154 In fact, those patients with nonalcoholic steatohepatitis (NASH) and fibrosis are at the greatest

155 severe NAFLD lesions, that is, nonalcoholic steatohepatitis (NASH) and fibrosis, in a well-character

156 igh hepatic cholesterol causes non-alcoholic steatohepatitis (NASH) and fibrosis.

157 eath is an important feature of nonalcoholic steatohepatitis (NASH) and has been associated with disr

158 broSure, a noninvasive test for nonalcoholic steatohepatitis (NASH) and hepatic fibrosis, can be used

159 abolic dysregulation, including nonalcoholic steatohepatitis (NASH) and insulin resistance.

160 be more likely to progress to non-alcoholic steatohepatitis (NASH) and NAFLD-related fibrosis or cir

161 The metabolic defects of nonalcoholic steatohepatitis (NASH) and prediabetes or type 2 diabete

162 r disease (NAFLD) and resulting nonalcoholic steatohepatitis (NASH) are highly prevalent in the Unite

163 ent into hepatic lipid rafts in nonalcoholic steatohepatitis (NASH) are unclear.

164 vide treatment to patients with nonalcoholic steatohepatitis (NASH) because one third of patients wit

165 a mouse model of developmental nonalcoholic steatohepatitis (NASH) by feeding a high polyunsaturated

166 Hepatocyte apoptosis in nonalcoholic steatohepatitis (NASH) can lead to fibrosis and cirrhosi

167 Nonalcoholic steatohepatitis (NASH) cirrhosis is the fastest growing

168 in participants enrolled in the Nonalcoholic Steatohepatitis (NASH) Clinical Research Network.

169 Nonalcoholic steatohepatitis (NASH) has become a major cause of cirrh

170 Nonalcoholic steatohepatitis (NASH) has been predicted to become the

171 e correlated with biopsy-proven nonalcoholic steatohepatitis (NASH) in a hospital cohort of individua

172 epatic steatosis in adults with nonalcoholic steatohepatitis (NASH) in a multi-center study, using ce

173 n signaling, and development of nonalcoholic steatohepatitis (NASH) in an obese, diabetic mouse model

174 NAFLD and nonalcoholic steatohepatitis (NASH) in AYAs often go unrecognized and

175 esis, lipid accumulation drives nonalcoholic steatohepatitis (NASH) initiation by triggering oxidativ

176 Nonalcoholic steatohepatitis (NASH) is a necro-inflammatory response

177 Nonalcoholic steatohepatitis (NASH) is an inflammatory lipotoxic diso

178 Non-alcoholic steatohepatitis (NASH) is associated with hepatic fibrog

179 As non-alcoholic steatohepatitis (NASH) is associated with hyperinsulinem

180 Because nonalcoholic steatohepatitis (NASH) is associated with impaired liver

181 Non-alcoholic steatohepatitis (NASH) is characterized by liver lipid a

182 Therapy for nonalcoholic steatohepatitis (NASH) is limited.

183 Non-alcoholic steatohepatitis (NASH) is often seen together with compo

184 The incidence of non-alcoholic steatohepatitis (NASH) is rising but the efficacy of lif

185 Nonalcoholic steatohepatitis (NASH) is the most common liver disease

186 Nonalcoholic steatohepatitis (NASH) is the most prevalent cause of ch

187 e showed mild steatosis but no non-alcoholic steatohepatitis (NASH) lesions were found.

188 bariatric surgery in patients with NAFLD or steatohepatitis (NASH) may impair liver function.

189 AFLD) and its more severe form non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hep

190 sidered a benign condition, but nonalcoholic steatohepatitis (NASH) may progress to fibrosis and prom

191 y, could detect MPO activity in nonalcoholic steatohepatitis (NASH) mouse models and human liver biop

192 fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) patients.

193 by ballooned hepatocytes drives nonalcoholic steatohepatitis (NASH) progression in mice.

194 ociated with reduced liver fat, nonalcoholic steatohepatitis (NASH) remission, and also reduction of

195 gold standard method to assess nonalcoholic steatohepatitis (NASH) resolution after therapeutic inte

196 Biopsies from patients with nonalcoholic steatohepatitis (NASH) revealed the presence of alterati

197 ally relevant rodent models of non-alcoholic steatohepatitis (NASH) that resemble the human condition

198 Non-alcoholic steatohepatitis (NASH) was associated with a higher prev

199 lic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) was found in CHIP(-/-)-mice over

200 V, hepatitis B virus (HBV), and nonalcoholic steatohepatitis (NASH) were identified.

201 eloped NAFLD and early signs of nonalcoholic steatohepatitis (NASH) when challenged with a lipogenic,

202 ease and of its aggressive form nonalcoholic steatohepatitis (NASH) will require novel therapeutic ap

203 lantation (LT) is increasing in nonalcoholic steatohepatitis (NASH) with good post-transplant outcome

204 istology in patients with NAFLD/nonalcoholic steatohepatitis (NASH) with normal or elevated ALT level

205 pathology similar to NAFLD and nonalcoholic steatohepatitis (NASH) without changes to body weight or

206 r tissues from 25 patients with nonalcoholic steatohepatitis (NASH), 27 patients with NAFLD, 15 healt

207 Nonalcoholic steatohepatitis (NASH), a clinically aggressive variant

208 or AnxA1 in the pathogenesis of nonalcoholic steatohepatitis (NASH), a disease commonly associated wi

209 simple steatosis (SS), 19 with nonalcoholic steatohepatitis (NASH), and 24 healthy controls.

210 cent of children with NAFLD had nonalcoholic steatohepatitis (NASH), and 34% had significant (stage F

211 aining to current therapies for nonalcoholic steatohepatitis (NASH), as there are currently no Food a

212 have shown efficacy in treating nonalcoholic steatohepatitis (NASH), but their widespread use is cons

213 lcoholic fatty liver [NAFL]) to nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer.

214 esistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH), disorders that increase risk of

215 tients, can lead to progressive nonalcoholic steatohepatitis (NASH), fibrosis, and ultimately hepatoc

216 c fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), hereditary dyslipidaemia, or cry

217 of patients with NASH develop non-alchoholic steatohepatitis (NASH), histologically defined by lobula

218 following groups: obese, NAFLD, nonalcoholic steatohepatitis (NASH), or NASH with fibrosis.

219 onalcoholic fatty liver (NAFL), nonalcoholic steatohepatitis (NASH), or obesity and 54 healthy contro

220 lated steatosis and advances to nonalcoholic steatohepatitis (NASH), steatofibrosis, and cirrhosis.

221 e of cirrhosis in subjects with nonalcoholic steatohepatitis (NASH), the histological form of NAFLD a

222 ting feature of an asymptomatic nonalcoholic steatohepatitis (NASH), the progressive form of NAFLD.

223 ease (NAFLD) includes fatty liver (NAFL) and steatohepatitis (NASH), which can progress to cirrhosis

224 of the advanced pathologies is nonalcoholic steatohepatitis (NASH), which is associated with inducti

225 viduals with NAFLD will develop nonalcoholic steatohepatitis (NASH), which is associated with progres

226 or 2 (Nrf2) develop more severe nonalcoholic steatohepatitis (NASH), with cirrhosis, than wild-type (

227 y recapitulated key features of nonalcoholic steatohepatitis (NASH)-driven hepatocellular carcinoma (

228 prediabetes as risk factors for nonalcoholic steatohepatitis (NASH).

229 ine whether NAFLD progresses to nonalcoholic steatohepatitis (NASH).

230 flammation in a murine model of nonalcoholic steatohepatitis (NASH).

231 ntrolled trial of patients with nonalcoholic steatohepatitis (NASH).

232 sion, and outcomes of NAFLD and nonalcoholic steatohepatitis (NASH).

233 lcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH).

234 ammation are characteristics of nonalcoholic steatohepatitis (NASH).

235 ranges from simple steatosis to nonalcoholic steatohepatitis (NASH).

236 in fibrosis score in mice with nonalcoholic steatohepatitis (NASH).

237 t as estimated by ultrasound in nonalcoholic steatohepatitis (NASH).

238 cal agents for the treatment of nonalcoholic steatohepatitis (NASH).

239 fat diet (HFD) animal model of non-alcoholic steatohepatitis (NASH).

240 is of type 2 diabetes (T2D) and nonalcoholic steatohepatitis (NASH).

241 vestigated for the treatment of nonalcoholic steatohepatitis (NASH).

242 ing nonalcoholic fatty liver or nonalcoholic steatohepatitis (NASH).

243 teatosis to the more aggressive nonalcoholic steatohepatitis (NASH).

244 O4) gene to be associated with non-alcoholic steatohepatitis (NASH).

245 borderline and 10% had definite nonalcoholic steatohepatitis (NASH).

246 tures of liver in patients with nonalcoholic steatohepatitis (NASH).

247 ciated progression of NAFLD to non-alcoholic steatohepatitis (NASH).

248 es from patients with NAFLD and nonalcoholic steatohepatitis (NASH).

249 esistance, type 2 diabetes, and nonalcoholic steatohepatitis (NASH).

250 ammation, which are features of nonalcoholic steatohepatitis (NASH).

251 y and inflammation resulting in nonalcoholic steatohepatitis (NASH).

252 ients with simple steatosis and nonalcoholic steatohepatitis (NASH).

253 e children and adolescents with nonalcoholic steatohepatitis (NASH).

254 atory stage of steatohepatitis [nonalcoholic steatohepatitis (NASH)].

255 of patients with cirrhosis from nonalcoholic steatohepatitis [NASH]), CLF (decreases in percentages o

256 ates (nonalcoholic fatty liver, nonalcoholic steatohepatitis [NASH], NASH-fibrosis, NASH-compensated

257 IL-17RA(-/-) mice, which exhibited decreased steatohepatitis, nicotinamide adenine dinucleotide phosp

258 arly in those with the inflammatory stage of steatohepatitis [nonalcoholic steatohepatitis (NASH)].

259 l 0.61-0.96, P = 0.0233) and of nonalcoholic steatohepatitis (odds ratio = 0.75, 95% confidence inter

260 lt mice, we evaluate the effect of alcoholic steatohepatitis on early hepatobiliary carcinoma after i

261 , we investigated the impact of diet-induced steatohepatitis on the severity of imiquimod-induced pso

262 Patients with fibrosis, regardless of steatohepatitis or NAFLD activity score, had shorter sur

263 nalcoholic fatty liver disease, nonalcoholic steatohepatitis, or end-stage liver disease.

264 Nonalcoholic steatohepatitis patients had increased HDC/histamine/his

265 ough lipoapoptosis in NAFLD and nonalcoholic steatohepatitis patients.

266 alcoholic fatty liver disease, non-alcoholic steatohepatitis, primary sclerosing cholangitis, total p

267 es through CX3CR1 is crucial for controlling steatohepatitis progression, which recognizes CX3CR1 as

268 Mice fed with a high-fat diet developed steatohepatitis reminiscent of human NASH with balloonin

269 ey are noticeable in diabetes, non-alcoholic steatohepatitis, serine deficiencies, and other diseases

270 , 4, 8, or 12 weeks to induce a continuum of steatohepatitis severity.

271 s curves to detect ballooning, steatosis, or steatohepatitis (SH) were slightly better for M30 (P < 0

272 ts with chronic hepatitis C and nonalcoholic steatohepatitis significantly up-regulated hepatocytic H

273 ugh the ability to identify the nonalcoholic steatohepatitis subtype within those with nonalcoholic f

274 ced alcoholic liver disease and nonalcoholic steatohepatitis than in control liver tissues.

275 te fat in the liver and develop nonalcoholic steatohepatitis than those without.

276 diabetes mellitus, obesity, and nonalcoholic steatohepatitis, the delineation of the potential mechan

277 n patients with non-cirrhotic, non-alcoholic steatohepatitis to assess treatment with obeticholic aci

278 pharmacological target for the treatment of steatohepatitis, type 2 diabetes, and obesity.

279 f left untreated can result in non-alcoholic steatohepatitis, ultimately resulting in liver cirrhosis

280 otomized stages of fibrosis and nonalcoholic steatohepatitis vs no nonalcoholic steatohepatitis.

281 to histological resolution of non-alcoholic steatohepatitis, warranting extensive, longer-term studi

282 Moreover, steatohepatitis was associated with an epidermal activat

283 Definite steatohepatitis was divided into steatohepatitis with fi

284 Steatohepatitis was induced with a choline-deficient, hi

285 ibrosis, necroinflammation, and nonalcoholic steatohepatitis was observed (P < 0.05).

286 ciation of lnc18q22.2 to liver steatosis and steatohepatitis was replicated in 44 independent liver b

287 f patients with NAFLD and MAT1A-KO mice with steatohepatitis, we identified 2 major subtypes of NAFLD

288 s stage, but no other histologic features of steatohepatitis, were associated independently with long

289 Ethanol exposure promotes the development of steatohepatitis, which can progress to end stage liver d

290 besity and alcohol consumption contribute to steatohepatitis, which increases the risk for hepatitis

291 iver histology in patients with nonalcoholic steatohepatitis, which is a manifestation of the metabol

292 Nonalcoholic steatohepatitis will increase from 18% of waitlist addit

293 or obesity are thought to have nonalcoholic steatohepatitis with advanced fibrosis.

294 ome of such mice with fatty liver (8 weeks), steatohepatitis with early fibrosis (16-24 weeks) and ad

295 ranging from isolated hepatic steatosis, to steatohepatitis with evidence of hepatocellular injury a

296 Definite steatohepatitis was divided into steatohepatitis with fibrosis stage 1 or lower and stage

297 mice and progresses to advanced nonalcoholic steatohepatitis with highly dysplastic liver nodules.

298 Italian individuals at risk of nonalcoholic steatohepatitis with liver histology evaluated according

299 ure was resolution of definite non-alcoholic steatohepatitis with no worsening in fibrosis from basel

300 ients with simple steatosis and nonalcoholic steatohepatitis without fibrosis in the reference compar