ライフサイエンスコーパス: nonalcoholic steatohepatitis

1 jects to identify liver damage (fibrosis and nonalcoholic steatohepatitis).

2 mpared to healthy controls and patients with nonalcoholic steatohepatitis.

3 tivity may contribute to the pathogenesis of nonalcoholic steatohepatitis.

4 arly in the context of cancer, fibrosis, and nonalcoholic steatohepatitis.

5 -p45-related factor 1) knockout mice develop nonalcoholic steatohepatitis.

6 d to play a critical role in the etiology of nonalcoholic steatohepatitis.

7 romote inflammation and fibrosis and lead to nonalcoholic steatohepatitis.

8 rosis and nonalcoholic steatohepatitis vs no nonalcoholic steatohepatitis.

9 V-infected livers but not in normal liver or nonalcoholic steatohepatitis.

10 sting that Notch activity is associated with nonalcoholic steatohepatitis.

11 uctose in the development of fatty liver and nonalcoholic steatohepatitis.

12 ibrosis are features of the progressive form nonalcoholic steatohepatitis.

13 methylation to stages of hepatosteatosis and nonalcoholic steatohepatitis.

14 cantly improved the histological features of nonalcoholic steatohepatitis.

15 esis of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

16 H, hepatitis B virus, hepatitis C virus, and nonalcoholic steatohepatitis.

17 development of steatosis and progression to nonalcoholic steatohepatitis.

18 insulin resistance, glucose intolerance, and nonalcoholic steatohepatitis.

19 logy of metabolic diseases such as NAFLD and nonalcoholic steatohepatitis.

20 accurately describes the pathophysiology of nonalcoholic steatohepatitis.

21 clinical implications for the management of nonalcoholic steatohepatitis.

22 ctivity for treatment of type 2 diabetes and nonalcoholic steatohepatitis.

23 be differentially expressed in patients with nonalcoholic steatohepatitis.

24 ysregulated fatty acid metabolism, including nonalcoholic steatohepatitis.

25 CLD with hepatitis C virus and alcoholic and nonalcoholic steatohepatitis.

26 nflammation and fibrosis in animal models of nonalcoholic steatohepatitis.

27 target for the treatment of cholestasis and nonalcoholic steatohepatitis.

28 ge multicenter cohort of patients at risk of nonalcoholic steatohepatitis.

29 cial than moderate activity to improve NAFLD/nonalcoholic steatohepatitis.

30 ffects on the development of fatty liver and nonalcoholic steatohepatitis.

31 of patients with hepatocellular carcinoma or nonalcoholic steatohepatitis.

32 n caused by viral hepatitis and alcoholic or nonalcoholic steatohepatitis.

33 .001; hepatitis C 2.6 versus 3.7, P = 0.002; nonalcoholic steatohepatitis 3.0 versus 4.0, P < 0.001;

34 significantly higher rate of improvement in nonalcoholic steatohepatitis (43% vs. 19%, P=0.001), but

35 ain, diminished abdominal fat, and increased nonalcoholic steatohepatitis activities under the AHF di

36 lcoholic fatty liver disease and its subtype nonalcoholic steatohepatitis affect approximately 30% an

37 role, for ER stress response is seen in the nonalcoholic steatohepatitis, alcoholic liver disease, i

38 Specifically, the diverse roles of EVs in nonalcoholic steatohepatitis, alcoholic liver disease, v

39 The association between nonalcoholic steatohepatitis and cardiovascular disease

40 from bland steatosis without inflammation to nonalcoholic steatohepatitis and cirrhosis.

41 he microcirculatory changes in patients with nonalcoholic steatohepatitis and fatty liver disease, Jo

42 ative MR imaging parameters as biomarkers of nonalcoholic steatohepatitis and fatty liver disease.

43 -positive cohort and increased prevalence of nonalcoholic steatohepatitis and hepatocellular carcinom

44 atric and adolescent NAFLD differ from adult nonalcoholic steatohepatitis and should be recognized as

45 ombination with simtuzumab, in patients with nonalcoholic steatohepatitis and stage 2 or 3 liver fibr

46 b may reduce liver fibrosis in patients with nonalcoholic steatohepatitis and stage 2-3 fibrosis.

47 andidates will be older, more likely to have nonalcoholic steatohepatitis and will wait for transplan

48 Nondiabetic patients with nonalcoholic steatohepatitis and without advanced fibros

49 We randomly assigned 247 adults with nonalcoholic steatohepatitis and without diabetes to rec

50 , 53.1% of patients had steatosis, 20.4% had nonalcoholic steatohepatitis, and 73.5% had fibrosis on

51 a key process in drug-induced liver injury, nonalcoholic steatohepatitis, and alcoholic steatohepati

52 Reliable biomarkers for steatosis, nonalcoholic steatohepatitis, and assessment of fibrosis

53 sorders such as primary biliary cirrhosis or nonalcoholic steatohepatitis, and certain forms of cance

54 protonophore reverses hypertriglyceridemia, nonalcoholic steatohepatitis, and diabetes in lipodystro

55 apoptosis, oxidative stress, development of nonalcoholic steatohepatitis, and hepatocarcinogenesis.

56 iver-specific disorders such as fatty liver, nonalcoholic steatohepatitis, and hepatocellular carcino

57 liver injury, including bile duct ligation, nonalcoholic steatohepatitis, and obese mice, as well as

58 matory diseases such as alcoholic hepatitis, nonalcoholic steatohepatitis, and primary biliary cirrho

59 ) is significantly elevated in patients with nonalcoholic steatohepatitis, and steatotic hepatocytes

60 obesity, type 2 diabetes, dyslipidemia, and nonalcoholic steatohepatitis, and their potential therap

61 Postmenopausal women with nonalcoholic steatohepatitis are at an increased risk of

62 Alcoholic and nonalcoholic steatohepatitis are characterized by fatty

63 ance our understanding of why diabetics with nonalcoholic steatohepatitis are prone to develop more s

64 Nonalcoholic steatohepatitis arising from Western diet a

65 was an improvement in histologic features of nonalcoholic steatohepatitis, as assessed with the use o

66 y score = 2.4) and features of more advanced nonalcoholic steatohepatitis at 12 months, including liv

67 me (ALIOS) model developed features of early nonalcoholic steatohepatitis at 6 months (mean NAFLD act

68 still the gold standard for the diagnosis of nonalcoholic steatohepatitis but the definition may vary

69 Chronic liver inflammation and fibrosis in nonalcoholic steatohepatitis can lead to cirrhosis and l

70 is, inflammation, and fibrosis) and modified nonalcoholic steatohepatitis categories were used as ref

71 During development of nonalcoholic steatohepatitis, CCL2 and its receptor are

72 lyzed from 1,026 adults (>/=18 years) in the Nonalcoholic Steatohepatitis Clinical Research Network (

73 t of NAFLD patients (n = 90) enrolled in the Nonalcoholic Steatohepatitis Clinical Research Network (

74 The Nonalcoholic Steatohepatitis Clinical Research Network (

75 i in 592 cases of European ancestry from the Nonalcoholic Steatohepatitis Clinical Research Network a

76 ry, exam, liver biopsy assessment (using the nonalcoholic steatohepatitis Clinical Research Network h

77 temporaneous liver biopsies scored using the Nonalcoholic Steatohepatitis Clinical Research Network h

78 lly (grades 0, 1, 2, and 3, according to the Nonalcoholic Steatohepatitis Clinical Research Network s

79 histologic scoring system for NAFLD from the Nonalcoholic Steatohepatitis Clinical Research Network S

80 ssessed using Kleiner fibrosis stage and the Nonalcoholic Steatohepatitis Clinical Research Network s

81 ected from adults with NAFLD enrolled in the Nonalcoholic Steatohepatitis Clinical Research Network u

82 er histology in 849 patients enrolled in the Nonalcoholic Steatohepatitis Clinical Research Network.

83 We also found that patients with nonalcoholic steatohepatitis, compared with other types

84 d by viral hepatitis (n = 136), alcoholic or nonalcoholic steatohepatitis disorders (n = 113), or som

85 hepatitis, nonalcoholic fatty liver disease/nonalcoholic steatohepatitis, drug-associated toxicities

86 ted the study (56 +/- 8 years old; 62% male; nonalcoholic steatohepatitis etiology 24%; BMI 33.3 +/-

87 ce for differentiating steatosis (NAFL) from nonalcoholic steatohepatitis, for staging hepatic fibros

88 Patients with nonalcoholic steatohepatitis had significantly higher PA

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

90 s that individuals with NAFLD (specifically, nonalcoholic steatohepatitis) harbor an increased and in

91 e alone is sufficient for the development of nonalcoholic steatohepatitis, hepatic stem cell activati

92 reptozotocin-high fat diet (STZ-HFD) induced nonalcoholic steatohepatitis-hepatocellular carcinoma (N

93 Hypothyroidism has been associated with nonalcoholic steatohepatitis; however, the association b

94 y increases the risk for type 2 diabetes and nonalcoholic steatohepatitis; however, the pathogenic me

95 Nonalcoholic steatohepatitis, i.e., fatty liver accompan

96 was superior to placebo for the treatment of nonalcoholic steatohepatitis in adults without diabetes.

97 Nonalcoholic steatohepatitis is a common liver disease t

98 Nonalcoholic steatohepatitis is characterized by hepatic

99 GAT activity plays a role in the etiology of nonalcoholic steatohepatitis is unclear.

100 e latter category of syndrome, HAART-related nonalcoholic steatohepatitis, liver fibrosis, portal hyp

101 Early identification of patients with nonalcoholic steatohepatitis may help improve patient ou

102 erred increased risk of severe steatosis and nonalcoholic steatohepatitis; more-severe hepatic, muscl

103 (n=152), cryptogenic cirrhosis (CC, n=289), nonalcoholic steatohepatitis (NASH) (n=221), hepatitis B

104 NAFLD and nonalcoholic steatohepatitis (NASH) affect hepatic cytoc

105 Nonalcoholic steatohepatitis (NASH) affects 2%-3% of the

106 Nonalcoholic steatohepatitis (NASH) affects 3%-5% of the

107 ant liver pathology, including 34 (55%) with nonalcoholic steatohepatitis (NASH) and 11 (18%) with br

108 en with biopsy-proven NAFLD, 26 had definite nonalcoholic steatohepatitis (NASH) and 15 were not-NASH

109 cytes is a key process in the progression of nonalcoholic steatohepatitis (NASH) and a promising targ

110 s with NAFLD and to identify determinants of nonalcoholic steatohepatitis (NASH) and advanced fibrosi

111 xpression was strongly up-regulated in human nonalcoholic steatohepatitis (NASH) and alcohol cirrhosi

112 ed to play a key role in the pathogenesis of nonalcoholic steatohepatitis (NASH) and associated cardi

113 Liver CD34 frequencies were reduced during nonalcoholic steatohepatitis (NASH) and chronic hepatiti

114 MDBs are characteristic of alcoholic and nonalcoholic steatohepatitis (NASH) and discriminate bet

115 In fact, those patients with nonalcoholic steatohepatitis (NASH) and fibrosis are at

116 of diabetes mellitus (DM) is associated with nonalcoholic steatohepatitis (NASH) and fibrosis in pati

117 dysbiosis and severe NAFLD lesions, that is, nonalcoholic steatohepatitis (NASH) and fibrosis, in a w

118 ively benign simple steatosis to progressive nonalcoholic steatohepatitis (NASH) and fibrosis, is an

119 on and cell death is an important feature of nonalcoholic steatohepatitis (NASH) and has been associa

120 te if NASH FibroSure, a noninvasive test for nonalcoholic steatohepatitis (NASH) and hepatic fibrosis

121 The pathogenesis of nonalcoholic steatohepatitis (NASH) and inflammasome act

122 y-related metabolic dysregulation, including nonalcoholic steatohepatitis (NASH) and insulin resistan

123 The metabolic defects of nonalcoholic steatohepatitis (NASH) and prediabetes or t

124 nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) and the effects of h

125 ic fatty liver disease (NAFLD) and resulting nonalcoholic steatohepatitis (NASH) are highly prevalent

126 R)-4 recruitment into hepatic lipid rafts in nonalcoholic steatohepatitis (NASH) are unclear.

127 s for specific liver diseases and listing of nonalcoholic steatohepatitis (NASH) as an etiology for l

128 The relative frequency of nonalcoholic steatohepatitis (NASH) as an indication for

129 ortant to provide treatment to patients with nonalcoholic steatohepatitis (NASH) because one third of

130 e established a mouse model of developmental nonalcoholic steatohepatitis (NASH) by feeding a high po

131 ents with nonalcoholic fatty liver (NAFL) or nonalcoholic steatohepatitis (NASH) can be differentiate

132 Hepatocyte apoptosis in nonalcoholic steatohepatitis (NASH) can lead to fibrosis

133 Nonalcoholic steatohepatitis (NASH) cirrhosis is the fas

134 gic scoring was obtained by consensus of the Nonalcoholic Steatohepatitis (NASH) Clinical Research Ne

135 Liver histology was assessed using the nonalcoholic steatohepatitis (NASH) Clinical Research Ne

136 ts/223 children) individuals enrolled in the Nonalcoholic Steatohepatitis (NASH) Clinical Research Ne

137 ere measured in participants enrolled in the Nonalcoholic Steatohepatitis (NASH) Clinical Research Ne

138 Preclinical models of acute OS and nonalcoholic steatohepatitis (NASH) comprised CCl4 -trea

139 Nonalcoholic steatohepatitis (NASH) has become a major c

140 Nonalcoholic steatohepatitis (NASH) has been predicted t

141 and inflammatory and fibrogenic activity in nonalcoholic steatohepatitis (NASH) has not been explore

142 GV levels were correlated with biopsy-proven nonalcoholic steatohepatitis (NASH) in a hospital cohort

143 d change in hepatic steatosis in adults with nonalcoholic steatohepatitis (NASH) in a multi-center st

144 (PTX) improved the histological features of nonalcoholic steatohepatitis (NASH) in a recent randomiz

145 n, adiponectin signaling, and development of nonalcoholic steatohepatitis (NASH) in an obese, diabeti

146 NAFLD and nonalcoholic steatohepatitis (NASH) in AYAs often go unr

147 implicated in the development of obesity and nonalcoholic steatohepatitis (NASH) in humans.

148 idative stress and subsequent development of nonalcoholic steatohepatitis (NASH) in some individuals.

149 AFLD pathogenesis, lipid accumulation drives nonalcoholic steatohepatitis (NASH) initiation by trigge

150 Development of nonalcoholic steatohepatitis (NASH) involves the innate

151 Nonalcoholic steatohepatitis (NASH) is a common preneopl

152 Nonalcoholic steatohepatitis (NASH) is a leading cause o

153 Nonalcoholic steatohepatitis (NASH) is a liver disorder

154 Nonalcoholic steatohepatitis (NASH) is a necro-inflammat

155 Nonalcoholic steatohepatitis (NASH) is a progressive for

156 Nonalcoholic steatohepatitis (NASH) is a serious liver d

157 Nonalcoholic steatohepatitis (NASH) is a well-recognized

158 Nonalcoholic steatohepatitis (NASH) is an independent pr

159 Nonalcoholic steatohepatitis (NASH) is an inflammatory l

160 Because nonalcoholic steatohepatitis (NASH) is associated with i

161 Nonalcoholic steatohepatitis (NASH) is characterized by

162 Nonalcoholic steatohepatitis (NASH) is characterized by

163 Nonalcoholic steatohepatitis (NASH) is currently the thi

164 The diagnosis of nonalcoholic steatohepatitis (NASH) is defined by the pr

165 Nonalcoholic steatohepatitis (NASH) is increasing in pre

166 Nonalcoholic steatohepatitis (NASH) is increasingly reco

167 Therapy for nonalcoholic steatohepatitis (NASH) is limited.

168 Advanced liver fibrosis in nonalcoholic steatohepatitis (NASH) is often accompanied

169 Previous studies have shown that human nonalcoholic steatohepatitis (NASH) is often associated

170 Nonalcoholic steatohepatitis (NASH) is the commonest liv

171 Nonalcoholic steatohepatitis (NASH) is the most common e

172 Nonalcoholic steatohepatitis (NASH) is the most common l

173 Nonalcoholic steatohepatitis (NASH) is the most prevalen

174 Although nonalcoholic steatohepatitis (NASH) is typically associa

175 erides is considered a benign condition, but nonalcoholic steatohepatitis (NASH) may progress to fibr

176 (MPO) activity, could detect MPO activity in nonalcoholic steatohepatitis (NASH) mouse models and hum

177 teatosis occurs in some individuals, whereas nonalcoholic steatohepatitis (NASH) occurs in others.

178 f vitamin D 25-hydroxylases in patients with nonalcoholic steatohepatitis (NASH) or chronic hepatitis

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

180 d production by ballooned hepatocytes drives nonalcoholic steatohepatitis (NASH) progression in mice.

181 hronic inflammation is the major hallmark of nonalcoholic steatohepatitis (NASH) progression.

182 The mechanisms triggering nonalcoholic steatohepatitis (NASH) remain poorly define

183 ethnicity in determining disease severity in nonalcoholic steatohepatitis (NASH) remains unclear.

184 ght loss, associated with reduced liver fat, nonalcoholic steatohepatitis (NASH) remission, and also

185 biopsy is the gold standard method to assess nonalcoholic steatohepatitis (NASH) resolution after the

186 Biopsies from patients with nonalcoholic steatohepatitis (NASH) revealed the presenc

187 The pathophysiology of nonalcoholic steatohepatitis (NASH) should be approached

188 dences of hepatocellular carcinoma (HCC) and nonalcoholic steatohepatitis (NASH) suggest that a subst

189 Liver inflammation is greater in nonalcoholic steatohepatitis (NASH) than steatosis, sugg

190 egating lesions into normal liver, NAFLD, or nonalcoholic steatohepatitis (NASH) was built based on s

191 of nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) was found in CHIP(-/

192 or LT from HCV, hepatitis B virus (HBV), and nonalcoholic steatohepatitis (NASH) were identified.

193 89R mice) developed NAFLD and early signs of nonalcoholic steatohepatitis (NASH) when challenged with

194 e of this disease and of its aggressive form nonalcoholic steatohepatitis (NASH) will require novel t

195 liver transplantation (LT) is increasing in nonalcoholic steatohepatitis (NASH) with good post-trans

196 relation to histology in patients with NAFLD/nonalcoholic steatohepatitis (NASH) with normal or eleva

197 the reference standard for the detection of nonalcoholic steatohepatitis (NASH) within nonalcoholic

198 loped hepatic pathology similar to NAFLD and nonalcoholic steatohepatitis (NASH) without changes to b

199 those of liver tissues from 25 patients with nonalcoholic steatohepatitis (NASH), 27 patients with NA

200 Nonalcoholic steatohepatitis (NASH), a clinically aggres

201 ssible role for AnxA1 in the pathogenesis of nonalcoholic steatohepatitis (NASH), a disease commonly

202 We review accumulating evidence that nonalcoholic steatohepatitis (NASH), a more advanced for

203 complication of obesity that can progress to nonalcoholic steatohepatitis (NASH), a serious liver pat

204 patients with simple steatosis (SS), 19 with nonalcoholic steatohepatitis (NASH), and 24 healthy cont

205 ifty-five percent of children with NAFLD had nonalcoholic steatohepatitis (NASH), and 34% had signifi

206 terature pertaining to current therapies for nonalcoholic steatohepatitis (NASH), as there are curren

207 lidinediones have shown efficacy in treating nonalcoholic steatohepatitis (NASH), but their widesprea

208 Nonalcoholic steatohepatitis (NASH), characterized by li

209 s (i.e., nonalcoholic fatty liver [NAFL]) to nonalcoholic steatohepatitis (NASH), cirrhosis, and canc

210 is, insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH), disorders that incr

211 iver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrh

212 inority of patients, can lead to progressive nonalcoholic steatohepatitis (NASH), fibrosis, and ultim

213 In human and murine models of nonalcoholic steatohepatitis (NASH), increased hepatocyt

214 ence of NAFLD, including the more aggressive nonalcoholic steatohepatitis (NASH), is increasing with

215 igned to the following groups: obese, NAFLD, nonalcoholic steatohepatitis (NASH), or NASH with fibros

216 gnosed with nonalcoholic fatty liver (NAFL), nonalcoholic steatohepatitis (NASH), or obesity and 54 h

217 fed a choline-deficient diet) that develops nonalcoholic steatohepatitis (NASH), preneoplastic nodul

218 Since the initial description of nonalcoholic steatohepatitis (NASH), several sets of pat

219 gins with isolated steatosis and advances to nonalcoholic steatohepatitis (NASH), steatofibrosis, and

220 Nonalcoholic steatohepatitis (NASH), the aggressive form

221 In nonalcoholic steatohepatitis (NASH), the extent of hepat

222 in the absence of cirrhosis in subjects with nonalcoholic steatohepatitis (NASH), the histological fo

223 be the presenting feature of an asymptomatic nonalcoholic steatohepatitis (NASH), the progressive for

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

225 third of individuals with NAFLD will develop nonalcoholic steatohepatitis (NASH), which is associated

226 of patients with NAFLD progress to fibrosing nonalcoholic steatohepatitis (NASH), which is characteri

227 -related factor 2 (Nrf2) develop more severe nonalcoholic steatohepatitis (NASH), with cirrhosis, tha

228 spontaneously recapitulated key features of nonalcoholic steatohepatitis (NASH)-driven hepatocellula

229 ter reduction in fibrosis score in mice with nonalcoholic steatohepatitis (NASH).

230 uces liver fat as estimated by ultrasound in nonalcoholic steatohepatitis (NASH).

231 pharmacological agents for the treatment of nonalcoholic steatohepatitis (NASH).

232 he pathogenesis of type 2 diabetes (T2D) and nonalcoholic steatohepatitis (NASH).

233 ntly being investigated for the treatment of nonalcoholic steatohepatitis (NASH).

234 from simple steatosis to the more aggressive nonalcoholic steatohepatitis (NASH).

235 FLD, 24% had borderline and 10% had definite nonalcoholic steatohepatitis (NASH).

236 4) and as having nonalcoholic fatty liver or nonalcoholic steatohepatitis (NASH).

237 istologic features of liver in patients with nonalcoholic steatohepatitis (NASH).

238 ning on samples from patients with NAFLD and nonalcoholic steatohepatitis (NASH).

239 sis, and inflammation, which are features of nonalcoholic steatohepatitis (NASH).

240 and increasing in Europe, often occurs with nonalcoholic steatohepatitis (NASH).

241 liver disease (NAFLD) and its progression to nonalcoholic steatohepatitis (NASH).

242 ere insulin resistance, type 2 diabetes, and nonalcoholic steatohepatitis (NASH).

243 ence the degree of fibrosis in patients with nonalcoholic steatohepatitis (NASH).

244 a key pathway involved in the progression of nonalcoholic steatohepatitis (NASH).

245 ent of hepatic inflammation and fibrosis, to nonalcoholic steatohepatitis (NASH).

246 the liver are linked to the pathogenesis of nonalcoholic steatohepatitis (NASH).

247 gesting advanced progression of NAFLD toward nonalcoholic steatohepatitis (NASH).

248 t for up to 11 weeks, which induced advanced nonalcoholic steatohepatitis (NASH).

249 ed the biomarkers for their power to predict nonalcoholic steatohepatitis (NASH).

250 ase liver fat in patients with biopsy-proven nonalcoholic steatohepatitis (NASH).

251 ry signals and may influence iron loading in nonalcoholic steatohepatitis (NASH).

252 differentiation between simple steatosis and nonalcoholic steatohepatitis (NASH).

253 (NAFLD) ranges from simple steatosis (SS) to nonalcoholic steatohepatitis (NASH).

254 ts and can present with advanced fibrosis or nonalcoholic steatohepatitis (NASH).

255 rsus placebo on the histological features of nonalcoholic steatohepatitis (NASH).

256 drial dysfunction is a pathogenic feature of nonalcoholic steatohepatitis (NASH).

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

258 g factors, natural history, and treatment of nonalcoholic steatohepatitis (NASH).

259 vely define the prevalence of both NAFLD and nonalcoholic steatohepatitis (NASH).

260 to cell injury and inflammation resulting in nonalcoholic steatohepatitis (NASH).

261 cimens of patients with simple steatosis and nonalcoholic steatohepatitis (NASH).

262 of consecutive children and adolescents with nonalcoholic steatohepatitis (NASH).

263 diabetes and prediabetes as risk factors for nonalcoholic steatohepatitis (NASH).

264 might determine whether NAFLD progresses to nonalcoholic steatohepatitis (NASH).

265 associated inflammation in a murine model of nonalcoholic steatohepatitis (NASH).

266 nd placebo-controlled trial of patients with nonalcoholic steatohepatitis (NASH).

267 ence, progression, and outcomes of NAFLD and nonalcoholic steatohepatitis (NASH).

268 ded into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH).

269 sociated inflammation are characteristics of nonalcoholic steatohepatitis (NASH).

270 disease that ranges from simple steatosis to nonalcoholic steatohepatitis (NASH).

271 h the inflammatory stage of steatohepatitis [nonalcoholic steatohepatitis (NASH)].

272 nd adolescents with untreated NAFLD (19 with nonalcoholic steatohepatitis [NASH] and 11 without NASH)

273 iopsy-proven NAFLD (simple steatosis [SS] or nonalcoholic steatohepatitis [NASH]) and living liver do

274 r the Treatment of Nondiabetic Patients with Nonalcoholic Steatohepatitis [NASH]) trial demonstrated

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

276 ine health states (nonalcoholic fatty liver, nonalcoholic steatohepatitis [NASH], NASH-fibrosis, NASH

277 psy-proven NAFLD patients, SREBF-2 predicted nonalcoholic steatohepatitis (odds ratio 2.92 [95% CI 2.

278 dence interval 0.61-0.96, P = 0.0233) and of nonalcoholic steatohepatitis (odds ratio = 0.75, 95% con

279 ients with nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, or end-stage liver disease

280 m patients with primary biliary cirrhosis or nonalcoholic steatohepatitis (P < .05).

281 ) cell iron in the liver was associated with nonalcoholic steatohepatitis (P < 0.05) and increased he

282 02), HC ballooning (P = 0.006), and definite nonalcoholic steatohepatitis (P = 0.007) compared to tho

283 Nonalcoholic steatohepatitis patients had increased HDC/

284 may occur through lipoapoptosis in NAFLD and nonalcoholic steatohepatitis patients.

285 dings, patients with chronic hepatitis C and nonalcoholic steatohepatitis significantly up-regulated

286 Even though the ability to identify the nonalcoholic steatohepatitis subtype within those with n

287 ts with advanced alcoholic liver disease and nonalcoholic steatohepatitis than in control liver tissu

288 y to accumulate fat in the liver and develop nonalcoholic steatohepatitis than those without.

289 nt of type 2 diabetes mellitus, obesity, and nonalcoholic steatohepatitis, the delineation of the pot

290 nts with nonalcoholic fatty liver disease or nonalcoholic steatohepatitis; therefore, we assessed the

291 included dichotomized stages of fibrosis and nonalcoholic steatohepatitis vs no nonalcoholic steatohe

292 ression in liver biopsies from patients with nonalcoholic steatohepatitis was increased when steatosi

293 with severe fibrosis, necroinflammation, and nonalcoholic steatohepatitis was observed (P < 0.05).

294 lar injury, and inflammation are features of nonalcoholic steatohepatitis, which contributes signific

295 on improves liver histology in patients with nonalcoholic steatohepatitis, which is a manifestation o

296 Nonalcoholic steatohepatitis will increase from 18% of w

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

298 podystrophic mice and progresses to advanced nonalcoholic steatohepatitis with highly dysplastic live

299 6 consecutive Italian individuals at risk of nonalcoholic steatohepatitis with liver histology evalua

300 lusion of patients with simple steatosis and nonalcoholic steatohepatitis without fibrosis in the ref