ライフサイエンスコーパス: nonalcoholic

1 g-term abstinent alcoholic (25 women) and 46 nonalcoholic (24 women) participants.

2 d out regarding the chemical compositions of nonalcoholic and alcoholic beverages.

3 as been implicated in the pathophysiology of nonalcoholic and alcoholic steatohepatitis.

4 del for future investigations of nonviral or nonalcoholic causes of HCC development.

5 tis, patients with alcohol use disorder, and nonalcoholic controls using fungal-specific internal tra

6 to patients with alcohol use disorder and to nonalcoholic controls.

7 genus Penicillium dominated the mycobiome of nonalcoholic controls.

8 nique risk factors for recurrent and de novo nonalcoholic fatty liver (NAFLD) and nonalcoholic steato

9 ividual variabilities in the pathogenesis of nonalcoholic fatty liver and early nonalcoholic steatohe

10 Those with concurrent nonalcoholic fatty liver disease (AOR 1.39; 95% CI, 1.05

11 t in liver histology, defined as decrease in nonalcoholic fatty liver disease (NAFLD) Activity Score

12 Nonalcoholic fatty liver disease (NAFLD) affects 25% of

13 Nonalcoholic fatty liver disease (NAFLD) affects a quart

14 tudies have examined the association between nonalcoholic fatty liver disease (NAFLD) and bone minera

15 Nonalcoholic fatty liver disease (NAFLD) and cardiovascu

16 aimed to investigate the association between nonalcoholic fatty liver disease (NAFLD) and cerebral sm

17 signatures associated with human and rodent nonalcoholic fatty liver disease (NAFLD) and hepatocellu

18 In patients with nonalcoholic fatty liver disease (NAFLD) and in obese mi

19 on is a key component in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and insulin res

20 atitis (NASH) is the inflammatory subtype of nonalcoholic fatty liver disease (NAFLD) and is associat

21 iglyceride (IHTG) is the hallmark feature of nonalcoholic fatty liver disease (NAFLD) and is decrease

22 The development of nonalcoholic fatty liver disease (NAFLD) and its progres

23 L) is a key distinguishing characteristic of nonalcoholic fatty liver disease (NAFLD) and nonalcoholi

24 of insulin resistance), and the presence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholi

25 The prevalence of nonalcoholic fatty liver disease (NAFLD) and nonalcoholi

26 ese-NL; n = 24), and (c) obese subjects with nonalcoholic fatty liver disease (NAFLD) and prediabetes

27 ent heterogeneity captured under the acronym nonalcoholic fatty liver disease (NAFLD) and provide sug

28 Patients with nonalcoholic fatty liver disease (NAFLD) are at risk of

29 Abnormal glucose metabolism and nonalcoholic fatty liver disease (NAFLD) are common in p

30 The mechanisms of HCC development in nonalcoholic fatty liver disease (NAFLD) are incompletel

31 and sexual dimorphisms in the development of nonalcoholic fatty liver disease (NAFLD) are still poorl

32 biological processes driving the severity of nonalcoholic fatty liver disease (NAFLD) as reflected in

33 c steatohepatitis (NASH) is a severe form of nonalcoholic fatty liver disease (NAFLD) characterized b

34 y, we assessed the contribution of ChREBP to nonalcoholic fatty liver disease (NAFLD) development in

35 Nonalcoholic fatty liver disease (NAFLD) encompasses a r

36 (n = 126,941), Forns (n = 122,419), and the nonalcoholic fatty liver disease (NAFLD) fibrosis scores

37 emiological data on dietary risk factors for nonalcoholic fatty liver disease (NAFLD) from population

38 Nonalcoholic fatty liver disease (NAFLD) has now become

39 Worldwide, nonalcoholic fatty liver disease (NAFLD) has reached epi

40 In general, physical activity (PA) and nonalcoholic fatty liver disease (NAFLD) have an inverse

41 tools are needed to monitor key features of nonalcoholic fatty liver disease (NAFLD) in children tha

42 A care pathway for nonalcoholic fatty liver disease (NAFLD) in Kaiser Perma

43 long-term risk of disease for patients with nonalcoholic fatty liver disease (NAFLD) in the absence

44 h-fat/high-carbohydrate (HF/HC) diet-induced nonalcoholic fatty liver disease (NAFLD) in wild-type (W

45 The US prevalence of nonalcoholic fatty liver disease (NAFLD) is 30.6% and in

46 Nonalcoholic fatty liver disease (NAFLD) is a global and

47 Nonalcoholic fatty liver disease (NAFLD) is a global pub

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

49 Nonalcoholic fatty liver disease (NAFLD) is a leading et

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

51 Nonalcoholic fatty liver disease (NAFLD) is an increasin

52 Nonalcoholic fatty liver disease (NAFLD) is associated w

53 In HIV-uninfected patients, nonalcoholic fatty liver disease (NAFLD) is associated w

54 Nonalcoholic fatty liver disease (NAFLD) is becoming a m

55 Nonalcoholic fatty liver disease (NAFLD) is considered t

56 Nonalcoholic fatty liver disease (NAFLD) is estimated to

57 The burden of nonalcoholic fatty liver disease (NAFLD) is growing in p

58 Nonalcoholic fatty liver disease (NAFLD) is increasing i

59 The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing w

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

61 Nonalcoholic fatty liver disease (NAFLD) is on the verge

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

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

64 adults who fasted at least 4 hours using the nonalcoholic fatty liver disease (NAFLD) liver fat score

65 sociation between serum vitamin D levels and nonalcoholic fatty liver disease (NAFLD) parameters, suc

66 A crucial component of nonalcoholic fatty liver disease (NAFLD) pathogenesis is

67 s (NASH) is considered as a pivotal stage in nonalcoholic fatty liver disease (NAFLD) progression, gi

68 Pediatric guidelines for the management of nonalcoholic fatty liver disease (NAFLD) recommend a hea

69 d its contribution to the pathophysiology of nonalcoholic fatty liver disease (NAFLD) remains unknown

70 Nonalcoholic fatty liver disease (NAFLD) represents a bu

71 Nonalcoholic fatty liver disease (NAFLD) represents a gr

72 Nonalcoholic fatty liver disease (NAFLD) represents a sp

73 existing type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) to receive lira

74 tigated the role of EGFR in a mouse model of nonalcoholic fatty liver disease (NAFLD) using a pharmac

75 Nonalcoholic fatty liver disease (NAFLD), a common diagn

76 itis B virus (HBV), hepatitis C virus (HCV), nonalcoholic fatty liver disease (NAFLD), and alcohol-as

77 ption is associated with reduced severity of nonalcoholic fatty liver disease (NAFLD), based on histo

78 Lipopolysaccharides (LPS) is increased in nonalcoholic fatty liver disease (NAFLD), but its relati

79 ly, for some chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD), etiological tr

80 In nonalcoholic fatty liver disease (NAFLD), fibrosis is th

81 ased risk of development of type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), or cardiovascu

82 Despite tremendous research advancements in nonalcoholic fatty liver disease (NAFLD), our understand

83 In nonalcoholic fatty liver disease (NAFLD), triglycerides

84 Nonalcoholic fatty liver disease (NAFLD), which has an u

85 plays a pivotal role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), which is the t

86 e novo lipogenesis is a major contributor to nonalcoholic fatty liver disease (NAFLD).

87 testinal microbiota has been associated with nonalcoholic fatty liver disease (NAFLD).

88 me have been associated with the severity of nonalcoholic fatty liver disease (NAFLD).

89 scrutiny in a number of diseases, including nonalcoholic fatty liver disease (NAFLD).

90 (KD) has gained popularity in management of nonalcoholic fatty liver disease (NAFLD).

91 parameter for fat fraction quantification in nonalcoholic fatty liver disease (NAFLD).

92 betes, obesity, cardiovascular diseases, and nonalcoholic fatty liver disease (NAFLD).

93 bolic disturbance of lipids is a hallmark of nonalcoholic fatty liver disease (NAFLD).

94 (PRO-C3) is a biomarker of liver fibrosis in nonalcoholic fatty liver disease (NAFLD).

95 a major cause of mortality in patients with nonalcoholic fatty liver disease (NAFLD).

96 strongly associated with the development of nonalcoholic fatty liver disease (NAFLD).

97 might affect the development and severity of nonalcoholic fatty liver disease (NAFLD).

98 ic syndrome, which manifests in the liver as nonalcoholic fatty liver disease (NAFLD).

99 hepatic lipid metabolism and development of nonalcoholic fatty liver disease (NAFLD).

100 , insulin resistance, and the development of nonalcoholic fatty liver disease (NAFLD).

101 ing might exploit such information to assess nonalcoholic fatty liver disease (NAFLD).

102 oninvasive detection of advanced fibrosis in nonalcoholic fatty liver disease (NAFLD).

103 dentification-58 (CGI-58) mutations manifest nonalcoholic fatty liver disease (NAFLD).

104 ic variant associated with susceptibility to nonalcoholic fatty liver disease [NAFLD]) is associated

105 nfirmed nonalcoholic steatohepatitis (NASH) (nonalcoholic fatty liver disease activity score >= 4), f

106 lusion criteria were biopsy-proven NASH with Nonalcoholic Fatty Liver Disease Activity Score >=4, sta

107 ctive models of NASH and disease activity by nonalcoholic fatty liver disease activity score (NAS) us

108 At week 12, NGM282 significantly reduced nonalcoholic fatty liver disease activity score (NAS; -1

109 onse was defined as a 2-point improvement in nonalcoholic fatty liver disease activity score without

110 tin had no significant effect on fibrosis or nonalcoholic fatty liver disease activity score, and liv

111 ltrasound data are accurate for diagnosis of nonalcoholic fatty liver disease and hepatic fat fractio

112 In nonalcoholic fatty liver disease and in patients with ty

113 Defects in hepatic lipid metabolism cause nonalcoholic fatty liver disease and insulin resistance,

114 The rapidly increasing prevalence of nonalcoholic fatty liver disease and its aggressive form

115 Background Nonalcoholic fatty liver disease and its consequences ar

116 ons for understanding the pathophysiology of nonalcoholic fatty liver disease and nonalcoholic steato

117 ng non-bile duct medical conditions, such as nonalcoholic fatty liver disease and nonspecific cirrhos

118 function was more prevalent in patients with nonalcoholic fatty liver disease and predicted major adv

119 en implicated in metabolic disorders such as nonalcoholic fatty liver disease and steatohepatitis (NA

120 roles of the ECS in metabolism, obesity, and nonalcoholic fatty liver disease and the anti-inflammato

121 t a target for therapies that aim to reverse nonalcoholic fatty liver disease and type-2 diabetes.

122 r fat accumulation across the full range and nonalcoholic fatty liver disease are associated with car

123 Chronic hepatitis B (CHB) and nonalcoholic fatty liver disease are increasingly observ

124 The effects of alcohol use in nonalcoholic fatty liver disease are unclear.

125 etabolic inflammation in type 2 diabetes and nonalcoholic fatty liver disease by reestablishing a con

126 Nonalcoholic fatty liver disease encompasses a spectrum

127 Nonalcoholic fatty liver disease encompasses a spectrum

128 iated with impairment in PROs: ELF, >=10.43; Nonalcoholic Fatty Liver Disease Fibrosis Score, >=1.80;

129 Patients with hepatitis C or nonalcoholic fatty liver disease had among the lowest AC

130 coholic steatohepatitis (NASH), a subtype of nonalcoholic fatty liver disease has also augmented cons

131 c of obesity and diabetes, the prevalence of nonalcoholic fatty liver disease has progressively incre

132 ated using data from the TONIC (Treatment of Nonalcoholic Fatty Liver Disease in Children) trial.

133 epatitis, alcoholic liver disease (ALD), and nonalcoholic fatty liver disease in the United States.

134 Nonalcoholic fatty liver disease is a major risk factor

135 Nonalcoholic fatty liver disease is a rapidly rising pro

136 Nonalcoholic fatty liver disease is closely associated w

137 Nonalcoholic fatty liver disease is the most prevalent l

138 icient (MCD) and streptozotocin-western diet nonalcoholic fatty liver disease mouse models, and in vi

139 a methionine-choline-deficient diet causing nonalcoholic fatty liver disease or to Lieber DeCarli di

140 to modify gut microbiota signatures; improve nonalcoholic fatty liver disease outcomes; and detail, w

141 Nonalcoholic fatty liver disease prevalences were 1.0%,

142 In 25% of patients, nonalcoholic fatty liver disease progresses to nonalcoho

143 Long noncoding RNA FLRL2 alleviated nonalcoholic fatty liver disease through Arntl-Sirt1 pat

144 measured by magnetic resonance imaging, and nonalcoholic fatty liver disease was defined as liver fa

145 ithin the normal range (<5.0% liver fat) and nonalcoholic fatty liver disease were associated with hi

146 tis (NASH), which is the progressive form of nonalcoholic fatty liver disease, a disorder underlying

147 how this impacts diseases such as diabetes, nonalcoholic fatty liver disease, and anorexia-cachexia

148 from excess adiposity, such as hypertension, nonalcoholic fatty liver disease, and depression.

149 ential as a therapeutic target for diabetes, nonalcoholic fatty liver disease, and inflammatory bowel

150 volved in pathological conditions, including nonalcoholic fatty liver disease, atherosclerosis, viral

151 c viral infections, alcoholic cirrhosis, and nonalcoholic fatty liver disease, genetic factors that c

152 sulted in structural changes associated with nonalcoholic fatty liver disease, such as decay of bile

153 isk factor for HCC is the growing problem of nonalcoholic fatty liver disease, which is usually assoc

154 on-based assessment of hepatic steatosis and nonalcoholic fatty liver disease, with objective data th

155 strongly associated with the development of nonalcoholic fatty liver disease.

156 fraction for hepatic steatosis assessment in nonalcoholic fatty liver disease.

157 (TM6SF2) is a genetic factor predisposing to nonalcoholic fatty liver disease.

158 ed fibrosis have only examined patients with nonalcoholic fatty liver disease.

159 munodeficiency virus (PWH) may be at risk of nonalcoholic fatty liver disease.

160 s to reduce insulin resistance, obesity, and nonalcoholic fatty liver disease.

161 se with implications for the pathogenesis of nonalcoholic fatty liver disease.

162 lipid metabolism in HH and susceptibility to nonalcoholic fatty liver disease.

163 and nine have previously been implicated in nonalcoholic fatty liver disease.

164 ajor adverse cardiac events independently of nonalcoholic fatty liver disease.

165 etabolic defects such as type 2 diabetes and nonalcoholic fatty liver disease.

166 B virus during treatment, and alcoholic and nonalcoholic fatty liver disease.

167 ma in both men and women, which is linked to nonalcoholic fatty liver disease.

168 ohepatitis (NASH) is the progressive form of nonalcoholic fatty liver disease.

169 ompared with profiles found in patients with nonalcoholic fatty liver disease/nonalcoholic steatohepa

170 ugar, can cause significant dyslipidemia and nonalcoholic fatty liver disease; the diet has an especi

171 Nonalcoholic fatty liver diseases (NAFLDs), especially n

172 siology of metabolic diseases, which include nonalcoholic fatty liver diseases, through the gut-liver

173 t loss goal of 7%-10% to improve features of nonalcoholic fatty liver diseases.

174 th biopsy-proven NAFLD, 25 simple steatosis (nonalcoholic fatty liver) and 25 nonalcoholic steatohepa

175 The presence of cirrhosis in nonalcoholic-fatty-liver-disease (NAFLD) is the most imp

176 brain responsivity in alcoholic compared to nonalcoholic groups, as well as gender differences in th

177 The prevalence of nonalcoholic liver disease (NAFLD) is increasing worldwi

178 osis and fibrosis in patients with suspected nonalcoholic liver disease (NAFLD).

179 s with the increasing prevalence of obesity, nonalcoholic liver disease, and alcohol overuse worldwid

180 men (ALC(M)) was significantly lower than in nonalcoholic men (NC(M)) in regions including rostral mi

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

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

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

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

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

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

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

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

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

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

191 Nonalcoholic steatohepatitis (NASH) arises from a variab

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

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

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

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

196 Patients with nonalcoholic steatohepatitis (NASH) cirrhosis have excel

197 Nonalcoholic steatohepatitis (NASH) cirrhosis is the fas

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

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

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

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

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

203 Nonalcoholic steatohepatitis (NASH) is a leading cause o

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

205 Nonalcoholic steatohepatitis (NASH) is a severe form of

206 Nonalcoholic steatohepatitis (NASH) is considered as a p

207 Nonalcoholic steatohepatitis (NASH) is considered as sev

208 Progression of nonalcoholic steatohepatitis (NASH) is incompletely char

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

210 Nonalcoholic steatohepatitis (NASH) is the inflammatory

211 Nonalcoholic steatohepatitis (NASH) is the most common c

212 Nonalcoholic steatohepatitis (NASH) is the progressive f

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

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

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

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

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

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

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

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

221 Nonalcoholic steatohepatitis (NASH), a subtype of nonalc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 Nonalcoholic steatohepatitis (NASH)-related cirrhosis ha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 Cirrhosis etiologies were nonalcoholic steatohepatitis and hepatitis C virus.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 logy of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis.

296 tients with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.

297 herapies for primary biliary cholangitis and nonalcoholic steatohepatitis.

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

299 40 in particular, in patients with NAFLD and nonalcoholic steatohepatitis.

300 s higher in alcoholic women (ALC(W)) than in nonalcoholic women (NC(W)) in superior frontal and supra