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 logy of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

3 tients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.

4 effective, but less invasive, treatment for nonalcoholic steatohepatitis.

5 herapies for primary biliary cholangitis and nonalcoholic steatohepatitis.

6 rosis and nonalcoholic steatohepatitis vs no nonalcoholic steatohepatitis.

7 methylation to stages of hepatosteatosis and nonalcoholic steatohepatitis.

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

9 ysregulated fatty acid metabolism, including nonalcoholic steatohepatitis.

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

11 nflammation and fibrosis in animal models of nonalcoholic steatohepatitis.

12 target for the treatment of cholestasis and nonalcoholic steatohepatitis.

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

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

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

16 of patients with hepatocellular carcinoma or nonalcoholic steatohepatitis.

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

18 mpared to healthy controls and patients with nonalcoholic steatohepatitis.

19 tivity may contribute to the pathogenesis of nonalcoholic steatohepatitis.

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

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

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

23 romote inflammation and fibrosis and lead to nonalcoholic steatohepatitis.

24 ange of conditions, from simple steatosis to nonalcoholic steatohepatitis.

25 40 in particular, in patients with NAFLD and nonalcoholic steatohepatitis.

26 lammatory and pro-fibrotic shift observed in nonalcoholic steatohepatitis.

27 of NGM282 in patients with biopsy-confirmed nonalcoholic steatohepatitis.

28 new class of molecules for the treatment of nonalcoholic steatohepatitis.

29 in liver tissues of patients with high-grade nonalcoholic steatohepatitis.

30 nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis.

31 tion and treatment of obesity, diabetes, and nonalcoholic steatohepatitis.

32 .001; hepatitis C 2.6 versus 3.7, P = 0.002; nonalcoholic steatohepatitis 3.0 versus 4.0, P < 0.001;

33 hepatic steatosis and its progressive form, nonalcoholic steatohepatitis, a known risk factor for mo

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

35 In the United States, NAFLD and its subtype, nonalcoholic steatohepatitis, affect 30% and 5% of the p

36 Nonalcoholic steatohepatitis affects 3% to 6% of the US

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

38 NAFLD patients with evidence of nonalcoholic steatohepatitis and advanced fibrosis are a

39 Importantly, the presence of nonalcoholic steatohepatitis and advanced hepatic fibros

40 The association between nonalcoholic steatohepatitis and cardiovascular disease

41 ol levels, is a major factor contributing to nonalcoholic steatohepatitis and cardiovascular risk in

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

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

44 Cirrhosis etiologies were nonalcoholic steatohepatitis and hepatitis C virus.

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

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

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

48 ated insulin resistance and biopsy-confirmed nonalcoholic steatohepatitis and stage of liver fibrosis

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

50 Nondiabetic patients with nonalcoholic steatohepatitis and without advanced fibros

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

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

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

54 athophysiology of autoimmune liver diseases, nonalcoholic steatohepatitis, and liver transplantation.

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

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

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

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

59 tion and targeted treatment of patients with nonalcoholic steatohepatitis are needed to improve patie

60 Nonalcoholic steatohepatitis arising from Western diet a

61 nd etiologies of liver disease, particularly nonalcoholic steatohepatitis as additional risk factors

62 enesis of nonalcoholic fatty liver and early nonalcoholic steatohepatitis at the population level, un

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

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

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

66 y 2 blinded expert pathologists according to nonalcoholic steatohepatitis clinical research network c

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

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

69 sion by one or more stage as assessed by the Nonalcoholic Steatohepatitis Clinical Research Network h

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

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

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

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

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

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

76 rovement in liver histology in patients with nonalcoholic steatohepatitis, faithfully replicating ano

77 oblem owing to its propensity to progress to nonalcoholic steatohepatitis, fibrosis, and liver failur

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

79 Patients with nonalcoholic steatohepatitis had significantly higher PA

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

81 sease score, and the increased prevalence of nonalcoholic steatohepatitis has led to an increased num

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

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

84 REP levels and the presence of steatosis and nonalcoholic steatohepatitis highlight the clinical tran

85 C (HR for NHW 1.21; 95% CI, 1.06-1.38), and nonalcoholic steatohepatitis (HR for NHW 1.14; 95% CI, 0

86 1), and alcoholic liver disease, autoimmune, nonalcoholic steatohepatitis (HR, 1.35; P < 0.001), and

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

88 he need for liver transplantation, for which nonalcoholic steatohepatitis is already close to becomin

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

90 tage (Ishak stage 3 of 6) liver fibrosis and nonalcoholic steatohepatitis (Ishak stage 1 of 6 or 1 A

91 chronic inflammation, histologic features of nonalcoholic steatohepatitis, keratin and ubiquitin aggr

92 xposure at different doses induced NAFLD and nonalcoholic steatohepatitis-like phenotypes in mice, re

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

94 ry syndrome with necrotic hepatitis and in a nonalcoholic steatohepatitis model, representing 2 macro

95 ease (LD) was hepatitis C virus (N = 48) and nonalcoholic steatohepatitis (N = 23).

96 51.9 +/- 10.6 years, 64.6% males, underlying nonalcoholic steatohepatitis (NASH) (9.4%), previous tob

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

98 total of 176 patients with biopsy-confirmed nonalcoholic steatohepatitis (NASH) (nonalcoholic fatty

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

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

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

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

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

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

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

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

107 vels of galectin 3 have been associated with nonalcoholic steatohepatitis (NASH) and contribute to to

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

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

110 Its natural history, the development of nonalcoholic steatohepatitis (NASH) and fibrosis, is hig

111 d X receptor (FXR) is a promising target for nonalcoholic steatohepatitis (NASH) and fibrosis.

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

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

114 et rapidly develop advanced NAFLD, including nonalcoholic steatohepatitis (NASH) and hepatic fibrosis

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

116 ALR was measured in serum of human nonalcoholic steatohepatitis (NASH) and NASH-induced cir

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

118 giogenesis contributes to the development of nonalcoholic steatohepatitis (NASH) and promotes inflamm

119 well as between those with biopsy-confirmed nonalcoholic steatohepatitis (NASH) and those with no-NA

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

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

122 Patients with nonalcoholic steatohepatitis (NASH) are waitlisted at ol

123 Nonalcoholic steatohepatitis (NASH) arises from a variab

124 liver steatosis including the progression to nonalcoholic steatohepatitis (NASH) as characterized by

125 were 46 participants with borderline zone 1 nonalcoholic steatohepatitis (NASH) at baseline, with re

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

127 biopsy is the reference standard to diagnose nonalcoholic steatohepatitis (NASH) but is invasive with

128 in E improves liver histology in adults with nonalcoholic steatohepatitis (NASH) but not diabetes, bu

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

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

131 Patients with nonalcoholic steatohepatitis (NASH) cirrhosis have excel

132 Nonalcoholic steatohepatitis (NASH) cirrhosis is a commo

133 Nonalcoholic steatohepatitis (NASH) cirrhosis is the fas

134 ed into 4 different studies conducted by the Nonalcoholic Steatohepatitis (NASH) Clinical Research Ne

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

136 blind, randomized clinical trials within the nonalcoholic steatohepatitis (NASH) clinical research ne

137 Fecal microbiomes from children with nonalcoholic steatohepatitis (NASH) had the lowest alpha

138 Nonalcoholic steatohepatitis (NASH) has become a major c

139 Nonalcoholic steatohepatitis (NASH) has been predicted t

140 Compounds in clinical development for nonalcoholic steatohepatitis (NASH) improve liver histop

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

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

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

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

145 ed hepatic pathology reminiscent of advanced nonalcoholic steatohepatitis (NASH) in humans characteri

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

147 Nonalcoholic steatohepatitis (NASH) is a leading cause o

148 Nonalcoholic steatohepatitis (NASH) is a leading cause o

149 iable, noninvasive methods to diagnose early nonalcoholic steatohepatitis (NASH) is a major unmet nee

150 Nonalcoholic steatohepatitis (NASH) is a necro-inflammat

151 Nonalcoholic steatohepatitis (NASH) is a severe form of

152 Nonalcoholic steatohepatitis (NASH) is an inflammatory l

153 Because nonalcoholic steatohepatitis (NASH) is associated with i

154 Nonalcoholic steatohepatitis (NASH) is considered as a p

155 Nonalcoholic steatohepatitis (NASH) is considered as sev

156 Progression of nonalcoholic steatohepatitis (NASH) is incompletely char

157 Therapy for nonalcoholic steatohepatitis (NASH) is limited.

158 With increasing US adiposity, nonalcoholic steatohepatitis (NASH) is now a leading liv

159 neral population, and cirrhosis secondary to nonalcoholic steatohepatitis (NASH) is predicted to beco

160 Nonalcoholic steatohepatitis (NASH) is the inflammatory

161 Nonalcoholic steatohepatitis (NASH) is the most common c

162 Nonalcoholic steatohepatitis (NASH) is the most common l

163 Nonalcoholic steatohepatitis (NASH) is the most prevalen

164 Nonalcoholic steatohepatitis (NASH) is the progressive f

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

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

167 nts with NAFLD who are at increased risk for nonalcoholic steatohepatitis (NASH) or advanced fibrosis

168 potential therapeutics for the treatment of nonalcoholic steatohepatitis (NASH) patients, as they ex

169 rotein that is enriched in liver biopsies of nonalcoholic steatohepatitis (NASH) patients.

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

171 embling changes in microbiota composition in nonalcoholic steatohepatitis (NASH) patients.

172 de novo nonalcoholic fatty liver (NAFLD) and nonalcoholic steatohepatitis (NASH) post-liver transplan

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

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

175 her in clinical practice, and development of nonalcoholic steatohepatitis (NASH) represents another l

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

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

178 n 11 (IL11) signaling in the pathogenesis of nonalcoholic steatohepatitis (NASH) using hepatic stella

179 ween liver tissue samples from patients with nonalcoholic steatohepatitis (NASH) versus without.

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

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

182 89R mice) developed NAFLD and early signs of nonalcoholic steatohepatitis (NASH) when challenged with

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

184 Identifying effective therapies for nonalcoholic steatohepatitis (NASH) with fibrosis is a p

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

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

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

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

189 Nonalcoholic steatohepatitis (NASH), a clinically aggres

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

191 flammation contributes to the development of nonalcoholic steatohepatitis (NASH), a disorder characte

192 Nonalcoholic steatohepatitis (NASH), a subtype of nonalc

193 as well as animal models with steatosis and nonalcoholic steatohepatitis (NASH), and (2) the effects

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

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

196 steatosis (nonalcoholic fatty liver) and 25 nonalcoholic steatohepatitis (NASH), and in mice with di

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

198 Neutrophil infiltration is a hallmark of nonalcoholic steatohepatitis (NASH), but how this occurs

199 testinal permeability in the pathogenesis of nonalcoholic steatohepatitis (NASH), but the underlying

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

201 imple steatosis (pure NAFLD) can progress to nonalcoholic steatohepatitis (NASH), cirrhosis and hepat

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

203 of diseases ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and live

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

205 more severe forms of liver injury including nonalcoholic steatohepatitis (NASH), fibrosis, and hepat

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

207 ic fatty liver diseases (NAFLDs), especially nonalcoholic steatohepatitis (NASH), have become a major

208 nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH), have steadily incre

209 ho have the progressive form of NAFLD termed nonalcoholic steatohepatitis (NASH), it can progress to

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

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

212 fatty liver disease and its aggressive form, nonalcoholic steatohepatitis (NASH), requires novel ther

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

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

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

216 nalcoholic fatty liver disease progresses to nonalcoholic steatohepatitis (NASH), which increases the

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

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

219 mic serum profile of patients diagnosed with nonalcoholic steatohepatitis (NASH), which is the progre

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

221 t (MCD) diet] is a well-established model of nonalcoholic steatohepatitis (NASH), yet brain metabolis

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

223 Nonalcoholic steatohepatitis (NASH)-related cirrhosis ha

224 ceipt among those with alcohol-associated or nonalcoholic steatohepatitis (NASH)-related cirrhosis.

225 lipid metabolism, leading to improvements in nonalcoholic steatohepatitis (NASH).

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

227 ltimately lead to cirrhosis in patients with nonalcoholic steatohepatitis (NASH).

228 ed for practical approaches to patients with nonalcoholic steatohepatitis (NASH).

229 fects of bariatric surgery for patients with nonalcoholic steatohepatitis (NASH).

230 eps of liver injury ranges from steatosis to nonalcoholic steatohepatitis (NASH).

231 gents have demonstrated clinical efficacy in nonalcoholic steatohepatitis (NASH).

232 be associated with histologic improvement in nonalcoholic steatohepatitis (NASH).

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

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

235 he primary recommendations for patients with nonalcoholic steatohepatitis (NASH).

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

237 eat interest for their potential in treating nonalcoholic steatohepatitis (NASH).

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

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

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

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

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

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

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

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

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

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

248 osis is an independent predictor of death in nonalcoholic steatohepatitis (NASH).

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

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

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

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

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

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

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

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

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

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

259 ion constitute the metabolic underpinning of nonalcoholic steatohepatitis (NASH).

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

261 Liver cell death has an essential role in nonalcoholic steatohepatitis (NASH).

262 ry cytokines and promotes the development of nonalcoholic steatohepatitis (NASH).

263 n and cirrhosis development in patients with nonalcoholic steatohepatitis (NASH).

264 st of farnesoid X receptor, in patients with nonalcoholic steatohepatitis (NASH).

265 lled study in patients with biopsy-confirmed nonalcoholic steatohepatitis (NASH).

266 is a need for continued drug development for nonalcoholic steatohepatitis (NASH).

267 rogressive necroinflammation and fibrosis in nonalcoholic steatohepatitis (NASH).

268 Up to 1 in 4 NAFLD patients may have nonalcoholic steatohepatitis (NASH).

269 ption is a known independent risk factor for nonalcoholic steatohepatitis (NASH).

270 ffect in the liver of mice with experimental nonalcoholic steatohepatitis (NASH).

271 ictive of advanced fibrosis in patients with nonalcoholic steatohepatitis (NASH).

272 are a key element of the pathophysiology of nonalcoholic steatohepatitis (NASH).

273 mber of clinical trials for the treatment of nonalcoholic steatohepatitis (NASH).

274 ity largely because of the growing burden of nonalcoholic steatohepatitis (NASH).

275 be screened for NAFLD and, more importantly, nonalcoholic steatohepatitis (NASH); (4) we recommend th

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

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

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

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

280 ing cholangitis, alcoholic liver disease, or nonalcoholic steatohepatitis or individuals without dise

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

282 hepatocellular carcinoma, hepatitis C virus, nonalcoholic steatohepatitis, or Medicare insurance.

283 Ncoa5(+/-) mice are similar to the livers of nonalcoholic steatohepatitis patients as well as the adj

284 Nonalcoholic steatohepatitis patients had increased HDC/

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

286 in the development of a rapidly progressive nonalcoholic steatohepatitis phenotype in the offspring

287 ic oxide synthase (iNOS) are associated with nonalcoholic steatohepatitis progression.

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

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

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

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

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

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

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

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