ライフサイエンスコーパス: nonalcoholic

1 ents with ambulatory mild ALD as compared to nonalcoholics.

2 tudies have assessed the effects of food and nonalcoholic beverage (hereafter collectively referred t

3 an in the ENNS, while intakes of alcohol and nonalcoholic beverages were lower in the e-cohort.

4 It can be subdivided into nonalcoholic fatty liver (NAFL) and nonalcoholic steatoh

5 NASH is a potential outcome of nonalcoholic fatty liver (NAFL), a condition that occurs

6 from 61 consecutive patients diagnosed with nonalcoholic fatty liver (NAFL), nonalcoholic steatohepa

7 D) can progress from simple steatosis (i.e., nonalcoholic fatty liver [NAFL]) to nonalcoholic steatoh

8 R = 0.89, 95% CI 0.83-0.97; P = 0.01), and a nonalcoholic fatty liver activity score >/=5 (OR = 0.08,

9 e aminotransferase normalization, age, and a nonalcoholic fatty liver activity score >/=5 may be usef

10 ing and feeding contributes to steatosis and nonalcoholic fatty liver and obesity.

11 42926 C/T) variant on blood lipid traits and nonalcoholic fatty liver disease (NAFLD) across differen

12 Nonalcoholic fatty liver disease (NAFLD) alters drug res

13 essment of disease activity in patients with nonalcoholic fatty liver disease (NAFLD) and alcoholic l

14 Nonalcoholic fatty liver disease (NAFLD) and alcoholic l

15 ves many obesity-related diseases, including nonalcoholic fatty liver disease (NAFLD) and diabetes, a

16 of saturated fat is a likely contributor to nonalcoholic fatty liver disease (NAFLD) and insulin res

17 plore the role of liver aminotransferases in nonalcoholic fatty liver disease (NAFLD) and MetS.

18 L27RA), resembling the phenotype observed in nonalcoholic fatty liver disease (NAFLD) and nonalcoholi

19 Nonalcoholic fatty liver disease (NAFLD) and resulting n

20 The early stages of nonalcoholic fatty liver disease (NAFLD) are characteriz

21 Alcoholic fatty liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are common caus

22 rowing because obesity, type 2 diabetes, and nonalcoholic fatty liver disease (NAFLD) are replacing v

23 Inadvertent inclusion of subjects with nonalcoholic fatty liver disease (NAFLD) as controls can

24 epatic triglyceride (IHTG) content to define nonalcoholic fatty liver disease (NAFLD) by proton magne

25 Nonalcoholic fatty liver disease (NAFLD) can progress fr

26 Nonalcoholic fatty liver disease (NAFLD) comprises a spe

27 Nonalcoholic fatty liver disease (NAFLD) contributes to

28 Nonalcoholic fatty liver disease (NAFLD) encompasses a r

29 Nonalcoholic fatty liver disease (NAFLD) encompasses a s

30 aging technique, are accurate for diagnosing nonalcoholic fatty liver disease (NAFLD) fibrosis.

31 Nonalcoholic fatty liver disease (NAFLD) has become a ma

32 Nonalcoholic fatty liver disease (NAFLD) has become high

33 No treatment for nonalcoholic fatty liver disease (NAFLD) has been approv

34 An association between periodontitis and nonalcoholic fatty liver disease (NAFLD) has been report

35 Pediatric nonalcoholic fatty liver disease (NAFLD) histology demon

36 ients with type 2 diabetes (T2D) and reduces nonalcoholic fatty liver disease (NAFLD) in animal model

37 Nonalcoholic fatty liver disease (NAFLD) in non-obese pa

38 V) as an independent biomarker of CT-defined nonalcoholic fatty liver disease (NAFLD) in the offsprin

39 The histologic spectrum of nonalcoholic fatty liver disease (NAFLD) includes fatty

40 Nonalcoholic fatty liver disease (NAFLD) is a burgeoning

41 Nonalcoholic fatty liver disease (NAFLD) is a common liv

42 Nonalcoholic fatty liver disease (NAFLD) is a common pro

43 Nonalcoholic fatty liver disease (NAFLD) is a complex ch

44 BACKGROUND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is a consequenc

45 Nonalcoholic fatty liver disease (NAFLD) is a leading ca

46 Nonalcoholic fatty liver disease (NAFLD) is a major caus

47 Nonalcoholic fatty liver disease (NAFLD) is a major caus

48 Importance: Nonalcoholic fatty liver disease (NAFLD) is a major chro

49 Nonalcoholic fatty liver disease (NAFLD) is a rapidly em

50 Nonalcoholic fatty liver disease (NAFLD) is a risk facto

51 Nonalcoholic fatty liver disease (NAFLD) is a significan

52 There is evidence that nonalcoholic fatty liver disease (NAFLD) is affected by

53 ection of liver fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) is an important

54 Nonalcoholic fatty liver disease (NAFLD) is an increasin

55 BACKGROUND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is associated w

56 Nonalcoholic fatty liver disease (NAFLD) is associated w

57 Nonalcoholic fatty liver disease (NAFLD) is characterize

58 Nonalcoholic fatty liver disease (NAFLD) is characterize

59 Although nonalcoholic fatty liver disease (NAFLD) is closely link

60 oderate alcohol consumption in patients with nonalcoholic fatty liver disease (NAFLD) is common, yet

61 Nonalcoholic fatty liver disease (NAFLD) is highly preva

62 ver, the role of FOXOs in the development of nonalcoholic fatty liver disease (NAFLD) is not well und

63 Nonalcoholic fatty liver disease (NAFLD) is now the most

64 With no approved pharmacological treatment, nonalcoholic fatty liver disease (NAFLD) is now the most

65 Nonalcoholic fatty liver disease (NAFLD) is one of the m

66 Nonalcoholic fatty liver disease (NAFLD) is the most com

67 Nonalcoholic fatty liver disease (NAFLD) is the most com

68 Nonalcoholic fatty liver disease (NAFLD) is the most com

69 Nonalcoholic fatty liver disease (NAFLD) is the most com

70 Nonalcoholic fatty liver disease (NAFLD) is the most com

71 Nonalcoholic fatty liver disease (NAFLD) is the most pre

72 Nonalcoholic fatty liver disease (NAFLD) is widespread i

73 e is ongoing debate on whether screening for nonalcoholic fatty liver disease (NAFLD) is worthwhile i

74 model of the development and progression of nonalcoholic fatty liver disease (NAFLD) over time is la

75 inations and forms (alive or lyophilized) in nonalcoholic fatty liver disease (NAFLD) prevention.

76 c steatosis among HIV-infected patients with nonalcoholic fatty liver disease (NAFLD) receiving EFV p

77 Nonalcoholic fatty liver disease (NAFLD) represents an e

78 Nonalcoholic fatty liver disease (NAFLD) represents the

79 Nonalcoholic fatty liver disease (NAFLD) was the most co

80 Nonalcoholic fatty liver disease (NAFLD), a common prelu

81 e and insulin sensitivity are widely used in nonalcoholic fatty liver disease (NAFLD), although they

82 plays a relevant role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), and both risky

83 Most researchers focused on nonalcoholic fatty liver disease (NAFLD), in which incre

84 s (NASH), a clinically aggressive variant of nonalcoholic fatty liver disease (NAFLD), is becoming an

85 PPARgamma activation may induce obesity and nonalcoholic fatty liver disease (NAFLD), one of the mos

86 Nonalcoholic fatty liver disease (NAFLD), the most commo

87 Despite the high prevalence of nonalcoholic fatty liver disease (NAFLD), therapeutic op

88 Type 1 diabetes has been recently linked to nonalcoholic fatty liver disease (NAFLD), which is known

89 cohort of adult patients suspected of having nonalcoholic fatty liver disease (NAFLD).

90 t may re-program liver for increased risk of nonalcoholic fatty liver disease (NAFLD).

91 of type 2 diabetes (T2D), and improvement of nonalcoholic fatty liver disease (NAFLD).

92 ls in the serum, is strongly associated with nonalcoholic fatty liver disease (NAFLD).

93 restimates the severity of liver fibrosis in nonalcoholic fatty liver disease (NAFLD).

94 s of fibrosis and steatosis in patients with nonalcoholic fatty liver disease (NAFLD).

95 2 p.E167K, and GCKR p.P446L) associated with nonalcoholic fatty liver disease (NAFLD).

96 ave emphasized the role of gut microbiota in nonalcoholic fatty liver disease (NAFLD).

97 atic steatosis in different murine models of nonalcoholic fatty liver disease (NAFLD).

98 decreased in obesity, a key risk factor for nonalcoholic fatty liver disease (NAFLD).

99 n of LRH-1 SUMOylation to the development of nonalcoholic fatty liver disease (NAFLD).

100 oses to the full spectrum of liver damage in nonalcoholic fatty liver disease (NAFLD).

101 s of fibrosis and steatosis in patients with nonalcoholic fatty liver disease (NAFLD).

102 fibrosis, a major determinant of outcome in nonalcoholic fatty liver disease (NAFLD).

103 er plays a causal role in the progression of nonalcoholic fatty liver disease (NAFLD).

104 e leading cause of death among patients with nonalcoholic fatty liver disease (NAFLD).

105 the most important predictor of mortality in nonalcoholic fatty liver disease (NAFLD).

106 Despite this, little evidence of nonalcoholic fatty liver disease (NAFLD)/nonalcoholic st

107 in AAs (BCAAs), are often found increased in nonalcoholic fatty liver disease (NAFLD); however, if th

108 fructose and other sugars has been linked to nonalcoholic fatty liver disease (NAFLD); however, the s

109 Nonalcoholic fatty liver disease (steatosis) is the most

110 In post-hoc analyses of patients with nonalcoholic fatty liver disease activity score >/=4 (n

111 evalence of fibrosis (P = 0.04) and a higher nonalcoholic fatty liver disease activity score (P = 0.0

112 ammation (r = 0.49, P = 2.35 x 10(-6) ), and nonalcoholic fatty liver disease activity score (r = 0.4

113 Although a decrease in the nonalcoholic fatty liver disease activity score could se

114 was a reduction of at least 2 points in the nonalcoholic fatty liver disease activity score in 2 his

115 logistic regression, adjusting for baseline nonalcoholic fatty liver disease activity score.

116 ausal women with (1) histologic diagnosis of nonalcoholic fatty liver disease and (2) self-reported i

117 Diet-related health issues such as nonalcoholic fatty liver disease and cardiovascular diso

118 s in first-degree relatives of patients with nonalcoholic fatty liver disease and cirrhosis (NAFLD-ci

119 associated with liver disease, particularly nonalcoholic fatty liver disease and cirrhosis, and this

120 -fat diet, the KO mice developed features of nonalcoholic fatty liver disease and had increased level

121 iant rs58542926 is a genetic risk factor for nonalcoholic fatty liver disease and progression to fibr

122 Both alcoholic liver disease (ALD) and nonalcoholic fatty liver disease are characterized by ma

123 kely increase given the aging population and nonalcoholic fatty liver disease as a leading indication

124 the TM6SF2 gene is associated with pediatric nonalcoholic fatty liver disease but may confer protecti

125 expression was observed in a subset of human nonalcoholic fatty liver disease cases.

126 atio index (APRI), fibrosis-4 (FIB-4) score, nonalcoholic fatty liver disease fibrosis score (NFS), a

127 (M+) and extra large (XL+), in patients with nonalcoholic fatty liver disease in a multicenter settin

128 cerides (IHTGs), and is the primary cause of nonalcoholic fatty liver disease in obese individuals.

129 Nonalcoholic fatty liver disease is associated with hepa

130 Nonalcoholic fatty liver disease is associated with meta

131 Nonalcoholic fatty liver disease is becoming the most co

132 Nonalcoholic fatty liver disease is increasing in preval

133 Nonalcoholic fatty liver disease is one of the most prev

134 The cause of nonalcoholic fatty liver disease is the aberrant accumul

135 nd increases in percentages of patients with nonalcoholic fatty liver disease or ALD.

136 al of 51 NAFL patients, 30 NASH patients, 31 nonalcoholic fatty liver disease patients (without histo

137 e is associated with severity of fibrosis in nonalcoholic fatty liver disease patients of European an

138 ferase expression in a diet-induced model of nonalcoholic fatty liver disease reveals onset of hepati

139 Incident nonalcoholic fatty liver disease was highest in patients

140 s for which obesity is the direct cause (eg, nonalcoholic fatty liver disease) or is a significant ri

141 h poorly controlled type 2 diabetes and with nonalcoholic fatty liver disease, and a common variant o

142 ated with obesity, type 2 diabetes mellitus, nonalcoholic fatty liver disease, and cardiovascular dis

143 Outcomes of interest were any liver disease, nonalcoholic fatty liver disease, and cirrhosis (any eti

144 cal liver damage in alcoholic liver disease, nonalcoholic fatty liver disease, and hepatitis C, but n

145 cyte death is associated with progression of nonalcoholic fatty liver disease, and inhibition of apop

146 s, insulin resistance and diabetes mellitus, nonalcoholic fatty liver disease, and obesity.

147 abetes (T2D) and obesity are associated with nonalcoholic fatty liver disease, cardiomyopathy, and ca

148 ase, polyps, cancer, liver disease including nonalcoholic fatty liver disease, cirrhosis, hepatocellu

149 pe 2 diabetes mellitus, psoriatic arthritis, nonalcoholic fatty liver disease, depression, anxiety, a

150 In nonalcoholic fatty liver disease, Gal-9 is involved indi

151 In obese, insulin-resistant patients with nonalcoholic fatty liver disease, hepatic mIndy expressi

152 hird leading cause of death in patients with nonalcoholic fatty liver disease, is predicted to become

153 y senescence were evaluated in patients with nonalcoholic fatty liver disease, nonalcoholic steatohep

154 CC, proportions of those with HCV infection, nonalcoholic fatty liver disease, or ALD did not change

155 ding cause of fibrosis (viral hepatitis C vs nonalcoholic fatty liver disease, P = .025), inflammatio

156 soriasis may be more severe in patients with nonalcoholic fatty liver disease, particularly in those

157 yte-specific ablation of Tnfaip3 exacerbated nonalcoholic fatty liver disease- and NASH-related pheno

158 reported high failure rates in patients with nonalcoholic fatty liver disease.

159 therapeutic applications in diseases such as nonalcoholic fatty liver disease.

160 ibrosis risk among postmenopausal women with nonalcoholic fatty liver disease.

161 ld liver fibrosis in pediatric patients with nonalcoholic fatty liver disease.

162 s COP1 as a potential therapeutic target for nonalcoholic fatty liver disease.

163 and outcomes of alcoholic liver disease and nonalcoholic fatty liver disease.

164 pathogenesis of alcoholic liver disease and nonalcoholic fatty liver disease.

165 es mediate different aspects of both ALD and nonalcoholic fatty liver disease.

166 brosis severity in postmenopausal women with nonalcoholic fatty liver disease.

167 eing considered as a target for treatment of nonalcoholic fatty liver disease.

168 s also been demonstrated in murine models of nonalcoholic fatty liver disease.

169 , while contrasting results were reported in nonalcoholic fatty liver disease.

170 therapeutic potential in obese patients with nonalcoholic fatty liver disease.

171 ere has been an increase in the incidence of nonalcoholic fatty liver disease.

172 6.5 kg/m(2) ) with histologically confirmed nonalcoholic fatty liver disease.

173 f fetuin-A and diabetes can be attributed to nonalcoholic fatty liver disease.

174 but is now being overtaken by patients with nonalcoholic fatty liver disease.

175 ng of HIV infection include viral hepatitis, nonalcoholic fatty liver disease/nonalcoholic steatohepa

176 The histological spectrum of nonalcoholic fatty liver diseases (NAFLD) ranges from he

177 s), due to chronic hepatitis C; hepatitis B; nonalcoholic fatty liver diseases (NAFLD); and alcoholic

178 r source of TG in the liver of patients with nonalcoholic fatty liver diseases.

179 Nonalcoholic fatty liver is associated with obesity-rela

180 ogy for fibrosis stage (F0-F4) and as having nonalcoholic fatty liver or nonalcoholic steatohepatitis

181 nts transitioned between nine health states (nonalcoholic fatty liver, nonalcoholic steatohepatitis [

182 ing disease stage (e.g., higher in NASH than nonalcoholic fatty liver, positive correlation with fibr

183 d progression of fatty liver, alcoholic, and nonalcoholic liver disease (NAFLD) all appear to be infl

184 n metabolic disorders, including obesity and nonalcoholic liver disease.

185 al was to estimate trends in added sugars in nonalcoholic packaged beverage products available in the

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

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

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

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

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

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

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

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

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

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

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

197 Nonalcoholic steatohepatitis (NASH) cirrhosis is the fas

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

199 Nonalcoholic steatohepatitis (NASH) has become a major c

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

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

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

203 Nonalcoholic steatohepatitis (NASH) is a necro-inflammat

204 Nonalcoholic steatohepatitis (NASH) is an inflammatory l

205 Because nonalcoholic steatohepatitis (NASH) is associated with i

206 Therapy for nonalcoholic steatohepatitis (NASH) is limited.

207 Nonalcoholic steatohepatitis (NASH) is the most common l

208 Nonalcoholic steatohepatitis (NASH) is the most prevalen

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

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

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

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

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

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

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

216 89R mice) developed NAFLD and early signs of nonalcoholic steatohepatitis (NASH) when challenged with

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

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

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

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

221 Nonalcoholic steatohepatitis (NASH), a clinically aggres

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 .001; hepatitis C 2.6 versus 3.7, P = 0.002; nonalcoholic steatohepatitis 3.0 versus 4.0, P < 0.001;

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

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

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

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

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

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

255 Nondiabetic patients with nonalcoholic steatohepatitis and without advanced fibros

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

257 Nonalcoholic steatohepatitis arising from Western diet a

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

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

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

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

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

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

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

265 Nonalcoholic steatohepatitis patients had increased HDC/

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

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

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

269 Nonalcoholic steatohepatitis will increase from 18% of w

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

271 6 consecutive Italian individuals at risk of nonalcoholic steatohepatitis with liver histology evalua

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

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

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

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

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

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

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

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

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

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

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

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

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

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

286 nflammation and fibrosis in animal models of nonalcoholic steatohepatitis.

287 target for the treatment of cholestasis and nonalcoholic steatohepatitis.

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

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

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

291 of patients with hepatocellular carcinoma or nonalcoholic steatohepatitis.

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

293 mpared to healthy controls and patients with nonalcoholic steatohepatitis.

294 tivity may contribute to the pathogenesis of nonalcoholic steatohepatitis.

295 rosis and nonalcoholic steatohepatitis vs no nonalcoholic steatohepatitis.

296 methylation to stages of hepatosteatosis and nonalcoholic steatohepatitis.

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

298 ysregulated fatty acid metabolism, including nonalcoholic steatohepatitis.

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

300 kidney-, pancreas-, and heart-fibrosis; and nonalcoholic steatohepatosis converge in the activation