ライフサイエンスコーパス: steatohepatitis

1 Thirty percent had FLD (20% steatosis, 10% steatohepatitis).

2 ues of patients with high-grade nonalcoholic steatohepatitis.

3 fatty liver disease (NAFLD) and nonalcoholic steatohepatitis.

4 patients with biopsy-confirmed nonalcoholic steatohepatitis.

5 rongly increased in a dietary mouse model of steatohepatitis.

6 tment of obesity, diabetes, and nonalcoholic steatohepatitis.

7 is warranted in patients with non-alcoholic steatohepatitis.

8 administration improved glycemia and reduced steatohepatitis.

9 and hyperglycemia in mice with diet-induced steatohepatitis.

10 coholic fatty liver disease and nonalcoholic steatohepatitis.

11 ), a multifunctional protein, are reduced in steatohepatitis.

12 fat fraction in patients with non-alcoholic steatohepatitis.

13 onalcoholic fatty liver disease/nonalcoholic steatohepatitis.

14 levels were similarly increased in mice with steatohepatitis.

15 ut less invasive, treatment for nonalcoholic steatohepatitis.

16 pegbelfermin in patients with non-alcoholic steatohepatitis.

17 re collected and analyzed histologically for steatohepatitis.

18 primary biliary cholangitis and nonalcoholic steatohepatitis.

19 V-HBV coinfection had FLD including 10% with steatohepatitis.

20 alcoholic steatohepatitis vs no nonalcoholic steatohepatitis.

21 o stages of hepatosteatosis and nonalcoholic steatohepatitis.

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

23 pNaKtide, might attenuate the development of steatohepatitis.

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

25 atty acid metabolism, including nonalcoholic steatohepatitis.

26 titis C virus and alcoholic and nonalcoholic steatohepatitis.

27 nd fibrosis in animal models of nonalcoholic steatohepatitis.

28 he treatment of cholestasis and nonalcoholic steatohepatitis.

29 severe AH and in a mouse model of alcoholic steatohepatitis.

30 tions, from simple steatosis to nonalcoholic steatohepatitis.

31 lar, in patients with NAFLD and nonalcoholic steatohepatitis.

32 pro-fibrotic shift observed in nonalcoholic steatohepatitis.

33 athophysiology of nonalcoholic and alcoholic steatohepatitis.

34 is by one stage or more without worsening of steatohepatitis.

35 molecules for the treatment of nonalcoholic steatohepatitis.

36 FLD was defined as >=5% steatosis and/or steatohepatitis.

37 tosis and its progressive form, nonalcoholic steatohepatitis, a known risk factor for mortality.

38 States, NAFLD and its subtype, nonalcoholic steatohepatitis, affect 30% and 5% of the population, re

39 Nonalcoholic steatohepatitis affects 3% to 6% of the US population, i

40 glycogen and triglycerides that can lead to steatohepatitis and a risk for hepatocellular adenoma or

41 NAFLD patients with evidence of nonalcoholic steatohepatitis and advanced fibrosis are at markedly in

42 Importantly, the presence of nonalcoholic steatohepatitis and advanced hepatic fibrosis increase t

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

44 a major factor contributing to nonalcoholic steatohepatitis and cardiovascular risk in type 2 diabet

45 fibrosis, as well as to detect non-alcoholic steatohepatitis and cirrhosis in biopsied samples of hum

46 coholic fatty liver disease to non-alcoholic steatohepatitis and fibrosis (NASH-fibrosis), including

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

48 tentiates and accelerates the development of steatohepatitis and fibrosis, accompanied by increased l

49 t and cholesterol drive NAFLD progression to steatohepatitis and hepatic fibrosis by altering the tra

50 Cirrhosis etiologies were nonalcoholic steatohepatitis and hepatitis C virus.

51 man liver TMEM127 expression correlates with steatohepatitis and insulin resistance.

52 range in severity from steatosis to fibrotic steatohepatitis and is a major cause of hepatic morbidit

53 t intervention to ameliorate alcohol-induced steatohepatitis and liver damage.

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

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

56 resistance and biopsy-confirmed nonalcoholic steatohepatitis and stage of liver fibrosis, the presenc

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

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

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

60 in other histologic variables, resolution of steatohepatitis, and improvement in the NAS >=2.

61 y of autoimmune liver diseases, nonalcoholic steatohepatitis, and liver transplantation.

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

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

64 eted treatment of patients with nonalcoholic steatohepatitis are needed to improve patient outcomes,

65 ic liver failure from fatty liver disease to steatohepatitis are unavailable.

66 e of the growing prevalence of non-alcoholic steatohepatitis as a transplant indication and the agein

67 of liver disease, particularly nonalcoholic steatohepatitis as additional risk factors for cancer af

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

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

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

71 alcoholic fatty liver and early nonalcoholic steatohepatitis at the population level, uncovering of s

72 This data suggests that MCDD induced steatohepatitis barely affects the core clock mechanism

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

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

75 on diseases such as cirrhosis, non-alcoholic steatohepatitis, chronic renal disease, heart failure, d

76 full spectrum of liver diseases (steatosis, steatohepatitis, cirrhosis, and hepatocellular carcinoma

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

78 xpert pathologists according to nonalcoholic steatohepatitis clinical research network criteria.

79 r more stage as assessed by the Nonalcoholic Steatohepatitis Clinical Research Network histologic sco

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

81 s, expression of markers of inflammation and steatohepatitis, compared to and Il11ra1(+/+) mice on th

82 rn diet with liquid fructose (WDF) to induce steatohepatitis; control mice were fed normal chow.

83 of the metabolic syndrome and non-alcoholic steatohepatitis, despite its irrelevant caloric value.

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

85 donor sex, body mass index, or nonalcoholic steatohepatitis etiology (p>0.05 for each).

86 (56 +/- 8 years old; 62% male; nonalcoholic steatohepatitis etiology 24%; BMI 33.3 +/- 3.2 kg/m(2) ;

87 iver histology in patients with nonalcoholic steatohepatitis, faithfully replicating another key bene

88 t 25 kg/m(2), biopsy-confirmed non-alcoholic steatohepatitis (fibrosis stage 1-3), and a hepatic fat

89 o its propensity to progress to nonalcoholic steatohepatitis, fibrosis, and liver failure.

90 chemically induced fibrosis or diet-induced steatohepatitis given nintedanib or aspirin and clopidog

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

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

93 and the increased prevalence of nonalcoholic steatohepatitis has led to an increased number of older

94 findings: nodular regenerative hyperplasia, steatohepatitis, hemosiderosis, cholestasis, and cirrhos

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

96 d the presence of steatosis and nonalcoholic steatohepatitis highlight the clinical translational rel

97 W 1.21; 95% CI, 1.06-1.38), and nonalcoholic steatohepatitis (HR for NHW 1.14; 95% CI, 0.94-1.39).

98 olic liver disease, autoimmune, nonalcoholic steatohepatitis (HR, 1.35; P < 0.001), and primary scler

99 NASH models should be reproducible and show steatohepatitis (ideally with ballooning) and at least f

100 PCE is a typical feature of steatohepatitis in ARLD and includes oxytalan fibres.

101 PCE was associated with steatohepatitis in ARLD patients and with ARLD when comp

102 The Steatohepatitis in HIV Emerging Research Network, a grou

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

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

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

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

107 the BA and microbiota profiles, and improved steatohepatitis in the lean model.

108 tibody alirocumab attenuated alcohol-induced steatohepatitis in the rat model.

109 iver transplantation, for which nonalcoholic steatohepatitis is already close to becoming the most co

110 pathogenic" steatotic state to Non-Alcoholic Steatohepatitis is an important clinical requirement.

111 tage 3 of 6) liver fibrosis and nonalcoholic steatohepatitis (Ishak stage 1 of 6 or 1 A Mild) in anim

112 with HFD, TCS induces hepatic steatosis and steatohepatitis jointly regulated by the transcription f

113 mmation, histologic features of nonalcoholic steatohepatitis, keratin and ubiquitin aggregates within

114 fferent doses induced NAFLD and nonalcoholic steatohepatitis-like phenotypes in mice, respectively.

115 (LAP1), resulted in fatty liver disease and steatohepatitis, likely from a secretion defect of VLDLs

116 ith necrotic hepatitis and in a nonalcoholic steatohepatitis model, representing 2 macrophage-driven

117 in patients, with more severe steatosis and steatohepatitis, more proinflammatory/profibrotic cytoki

118 c diseases such as type 2 diabetes mellitus, steatohepatitis, myocardial infarction, and stroke has i

119 hepatitis C virus (N = 48) and nonalcoholic steatohepatitis (N = 23).

120 such as nonalcoholic fatty liver disease and steatohepatitis (NAFLD/NASH) and insulin resistance.

121 years, 64.6% males, underlying nonalcoholic steatohepatitis (NASH) (9.4%), previous tobacco (52%), p

122 patients with biopsy-confirmed nonalcoholic steatohepatitis (NASH) (nonalcoholic fatty liver disease

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

124 eloping type 2 diabetes (T2D), non-alcoholic steatohepatitis (NASH) and a host of other comorbidities

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

126 tin 3 have been associated with nonalcoholic steatohepatitis (NASH) and contribute to toxin-induced l

127 ogress to advanced stages with non-alcoholic steatohepatitis (NASH) and fibrosis, increasing the risk

128 ral history, the development of nonalcoholic steatohepatitis (NASH) and fibrosis, is highly variable,

129 (FXR) is a promising target for nonalcoholic steatohepatitis (NASH) and fibrosis.

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

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

132 velop advanced NAFLD, including nonalcoholic steatohepatitis (NASH) and hepatic fibrosis.

133 ease, where it can progress to non-alcoholic steatohepatitis (NASH) and lead to liver cirrhosis or li

134 y, insulin resistance, adipose inflammation, steatohepatitis (NASH) and liver fibrosis found in WT an

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

136 was measured in serum of human nonalcoholic steatohepatitis (NASH) and NASH-induced cirrhosis (serum

137 ntributes to the development of nonalcoholic steatohepatitis (NASH) and promotes inflammation, fibros

138 creased in human patients with non-alcoholic steatohepatitis (NASH) and significant liver fibrosis.

139 ts and regularly progresses to non-alcoholic steatohepatitis (NASH) and subsequent cirrhosis.

140 een those with biopsy-confirmed nonalcoholic steatohepatitis (NASH) and those with no-NASH (n = 4 stu

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

142 Animal models of non-alcoholic steatohepatitis (NASH) are important tools in preclinica

143 Pharmacological treatments for non-alcoholic steatohepatitis (NASH) are still unsatisfactory.

144 Patients with nonalcoholic steatohepatitis (NASH) are waitlisted at older ages than

145 Nonalcoholic steatohepatitis (NASH) arises from a variable interplay

146 is including the progression to nonalcoholic steatohepatitis (NASH) as characterized by the additiona

147 icipants with borderline zone 1 nonalcoholic steatohepatitis (NASH) at baseline, with resolution in 2

148 reference standard to diagnose nonalcoholic steatohepatitis (NASH) but is invasive with potential co

149 liver histology in adults with nonalcoholic steatohepatitis (NASH) but not diabetes, but its impact

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

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

152 Patients with nonalcoholic steatohepatitis (NASH) cirrhosis have excellent postlive

153 Nonalcoholic steatohepatitis (NASH) cirrhosis is a common indication

154 Nonalcoholic steatohepatitis (NASH) cirrhosis is the fastest growing

155 ized clinical trials within the nonalcoholic steatohepatitis (NASH) clinical research network from 20

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

157 ferent studies conducted by the Nonalcoholic Steatohepatitis (NASH) Clinical Research Network.

158 microbiomes from children with nonalcoholic steatohepatitis (NASH) had the lowest alpha-diversity (c

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

160 nds in clinical development for nonalcoholic steatohepatitis (NASH) improve liver histopathology in d

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

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

163 ed death) or advanced fibrosis/non-alcoholic steatohepatitis (NASH) in adult individuals with metabol

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

165 thology reminiscent of advanced nonalcoholic steatohepatitis (NASH) in humans characterized by signs

166 Non-alcoholic steatohepatitis (NASH) is a common type of chronic liver

167 Nonalcoholic steatohepatitis (NASH) is a leading cause of chronic liv

168 Nonalcoholic steatohepatitis (NASH) is a leading cause of liver trans

169 asive methods to diagnose early nonalcoholic steatohepatitis (NASH) is a major unmet need.

170 Non-alcoholic steatohepatitis (NASH) is a progressive form of Non-alco

171 Nonalcoholic steatohepatitis (NASH) is a severe form of nonalcoholic

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

173 Non-alcoholic steatohepatitis (NASH) is characterised by hepatic steat

174 Nonalcoholic steatohepatitis (NASH) is considered as a pivotal stage

175 Nonalcoholic steatohepatitis (NASH) is considered as severe hepatic m

176 Progression of nonalcoholic steatohepatitis (NASH) is incompletely characterized.

177 Therapy for nonalcoholic steatohepatitis (NASH) is limited.

178 Non-alcoholic steatohepatitis (NASH) is major health burden lacking ef

179 With increasing US adiposity, nonalcoholic steatohepatitis (NASH) is now a leading liver transplant

180 ion, and cirrhosis secondary to nonalcoholic steatohepatitis (NASH) is predicted to become the leadin

181 Nonalcoholic steatohepatitis (NASH) is the inflammatory subtype of no

182 Nonalcoholic steatohepatitis (NASH) is the most common cause of chron

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

184 Nonalcoholic steatohepatitis (NASH) is the progressive form of nonalc

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

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

187 D who are at increased risk for nonalcoholic steatohepatitis (NASH) or advanced fibrosis.

188 erapeutics for the treatment of nonalcoholic steatohepatitis (NASH) patients, as they exert positive

189 es in microbiota composition in nonalcoholic steatohepatitis (NASH) patients.

190 s enriched in liver biopsies of nonalcoholic steatohepatitis (NASH) patients.

191 coholic fatty liver (NAFLD) and nonalcoholic steatohepatitis (NASH) post-liver transplant (LT) remain

192 al practice, and development of nonalcoholic steatohepatitis (NASH) represents another leading cause

193 ignaling in the pathogenesis of nonalcoholic steatohepatitis (NASH) using hepatic stellate cells (HSC

194 ssue samples from patients with nonalcoholic steatohepatitis (NASH) versus without.

195 ts of NAFLD including NAFL and non-alcoholic steatohepatitis (NASH) were analyzed.

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

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

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

199 tifying effective therapies for nonalcoholic steatohepatitis (NASH) with fibrosis is a pressing chall

200 Nonalcoholic steatohepatitis (NASH), a clinically aggressive variant

201 ntributes to the development of nonalcoholic steatohepatitis (NASH), a disorder characterized by lipo

202 Nonalcoholic steatohepatitis (NASH), a subtype of nonalcoholic fatty

203 c fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), alcohol-related cirrhosis, and l

204 in different etiologies, i.e. non-alcoholic steatohepatitis (NASH), alcoholic liver disease (ALC), a

205 led J protein) as a target for non-alcoholic steatohepatitis (NASH), an advanced phase of NAFLD.

206 nimal models with steatosis and nonalcoholic steatohepatitis (NASH), and (2) the effects of LPI and g

207 onalcoholic fatty liver) and 25 nonalcoholic steatohepatitis (NASH), and in mice with diet-induced NA

208 l infiltration is a hallmark of nonalcoholic steatohepatitis (NASH), but how this occurs during the p

209 eability in the pathogenesis of nonalcoholic steatohepatitis (NASH), but the underlying mechanisms re

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

211 is (pure NAFLD) can progress to nonalcoholic steatohepatitis (NASH), cirrhosis and hepatocellular car

212 anging from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and liver cancer.

213 forms of liver injury including nonalcoholic steatohepatitis (NASH), fibrosis, and hepatocellular car

214 r diseases (NAFLDs), especially nonalcoholic steatohepatitis (NASH), have become a major cause of liv

215 fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH), have steadily increased and now

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 rogressive form of NAFLD termed nonalcoholic steatohepatitis (NASH), it can progress to advanced fibr

219 c fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), or cirrhosis that was associated

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

221 sease ranges from steatosis to non-alcoholic steatohepatitis (NASH), potentially progressing to cirrh

222 isease and its aggressive form, nonalcoholic steatohepatitis (NASH), requires novel therapeutic appro

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

224 tty liver disease progresses to nonalcoholic steatohepatitis (NASH), which increases the risk for the

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

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

227 file of patients diagnosed with nonalcoholic steatohepatitis (NASH), which is the progressive form of

228 is a well-established model of nonalcoholic steatohepatitis (NASH), yet brain metabolism has not bee

229 Nonalcoholic steatohepatitis (NASH)-related cirrhosis has become one

230 hose with alcohol-associated or nonalcoholic steatohepatitis (NASH)-related cirrhosis.

231 ism, leading to improvements in nonalcoholic steatohepatitis (NASH).

232 liver of mice with experimental nonalcoholic steatohepatitis (NASH).

233 anced fibrosis in patients with nonalcoholic steatohepatitis (NASH).

234 ement of the pathophysiology of nonalcoholic steatohepatitis (NASH).

235 er biopsies from patients with non-alcoholic steatohepatitis (NASH).

236 ecause of the growing burden of nonalcoholic steatohepatitis (NASH).

237 ase (NAFLD) and development of Non-alcoholic steatohepatitis (NASH).

238 d to cirrhosis in patients with nonalcoholic steatohepatitis (NASH).

239 cal approaches to patients with nonalcoholic steatohepatitis (NASH).

240 cal trials for the treatment of nonalcoholic steatohepatitis (NASH).

241 injury ranges from steatosis to nonalcoholic steatohepatitis (NASH).

242 fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH).

243 e progression of NAFLD towards non-alcoholic steatohepatitis (NASH).

244 monstrated clinical efficacy in nonalcoholic steatohepatitis (NASH).

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

246 atric surgery for patients with nonalcoholic steatohepatitis (NASH).

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

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

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

250 with histologic improvement in nonalcoholic steatohepatitis (NASH).

251 commendations for patients with nonalcoholic steatohepatitis (NASH).

252 for their potential in treating nonalcoholic steatohepatitis (NASH).

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

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

255 dependent predictor of death in nonalcoholic steatohepatitis (NASH).

256 iver biopsies, of patients with nonalcoholic steatohepatitis (NASH).

257 e the metabolic underpinning of nonalcoholic steatohepatitis (NASH).

258 death has an essential role in nonalcoholic steatohepatitis (NASH).

259 and promotes the development of nonalcoholic steatohepatitis (NASH).

260 acrophages during diet-induced non-alcoholic steatohepatitis (NASH).

261 is development in patients with nonalcoholic steatohepatitis (NASH).

262 id X receptor, in patients with nonalcoholic steatohepatitis (NASH).

263 patients with biopsy-confirmed nonalcoholic steatohepatitis (NASH).

264 continued drug development for nonalcoholic steatohepatitis (NASH).

265 croinflammation and fibrosis in nonalcoholic steatohepatitis (NASH).

266 1 in 4 NAFLD patients may have nonalcoholic steatohepatitis (NASH).

267 own independent risk factor for nonalcoholic steatohepatitis (NASH).

268 or NAFLD and, more importantly, nonalcoholic steatohepatitis (NASH); (4) we recommend that NAFLD pati

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

270 H1B*2 was associated with lower frequency of steatohepatitis (odds ratio [OR], 0.52; P < .01) or fibr

271 s developed hepatic steatosis and subsequent steatohepatitis on a regular chow diet in the absence of

272 is, alcoholic liver disease, or nonalcoholic steatohepatitis or individuals without disease and were

273 Steatohepatitis or steatosis alone (versus none) were as

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

275 r carcinoma, hepatitis C virus, nonalcoholic steatohepatitis, or Medicare insurance.

276 ce are similar to the livers of nonalcoholic steatohepatitis patients as well as the adjacent noncanc

277 opment of a rapidly progressive nonalcoholic steatohepatitis phenotype in the offspring will be discu

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

279 hase (iNOS) are associated with nonalcoholic steatohepatitis progression.

280 osis, alcoholic liver disease, non-alcoholic steatohepatitis, pulmonary fibrosis and cancer(4,11).

281 , 4, 8, or 12 weeks to induce a continuum of steatohepatitis severity.

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

283 tes the transition from hepatic steatosis to steatohepatitis (SH).

284 splay diurnal rhythmicity in mice developing steatohepatitis upon feeding with a methionine and choli

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

286 Steatohepatitis was based on presence of steatosis, ball

287 Definite steatohepatitis was divided into steatohepatitis with fi

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

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

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

291 rweight or obese patients with non-alcoholic steatohepatitis were screened for study inclusion.

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

293 Nonalcoholic steatohepatitis will increase from 18% of waitlist addit

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

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

296 nant, induces steatosis that can progress to steatohepatitis with fibrosis, pathologies that parallel

297 of TCDD-elicited progression of steatosis to steatohepatitis with fibrosis.

298 strong link between histologic resolution of steatohepatitis with improvement in fibrosis in NASH.

299 In accordance, we observed enhanced steatohepatitis with infiltration of inflammatory cells.

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