ライフサイエンスコーパス: hepatic fibrosis

1 mproved liver enzymes, hepatic steatosis and hepatic fibrosis.

2 apy may be a promising approach for treating hepatic fibrosis.

3 ein had significant shared gene effects with hepatic fibrosis.

4 No patients had evidence of advanced hepatic fibrosis.

5 biliary contribution to cholestasis-induced hepatic fibrosis.

6 /interleukin-9 (IL-9) in the pathogenesis of hepatic fibrosis.

7 nses and may provide important insights into hepatic fibrosis.

8 acute liver injury overlapping pre-existing hepatic fibrosis.

9 chanistically link congestive hepatopathy to hepatic fibrosis.

10 ation of glucocorticoids, and predisposes to hepatic fibrosis.

11 thrombosis and strain, which in turn promote hepatic fibrosis.

12 s reduces DR-cell and B-cell populations and hepatic fibrosis.

13 s, and this result is an indirect measure of hepatic fibrosis.

14 s erythematosus, ankylosing spondylitis, and hepatic fibrosis.

15 hromatosis and this correlates strongly with hepatic fibrosis.

16 and are considered a key factor in promoting hepatic fibrosis.

17 al chemokine signaling pathways also promote hepatic fibrosis.

18 FibroTest is an indirect serum marker of hepatic fibrosis.

19 olic fatty liver disease (NAFLD) may lead to hepatic fibrosis.

20 reas Vdr knockout mice spontaneously develop hepatic fibrosis.

21 n a rat model of thioacetamide (TAA)-induced hepatic fibrosis.

22 TGF-beta antagonism can improve pre-existing hepatic fibrosis.

23 e aimed to investigate the role of SEMA7A in hepatic fibrosis.

24 to aberrant IgG autoantibody production and hepatic fibrosis.

25 n D on initiation rather than progression of hepatic fibrosis.

26 is C virus (HCV) infection is complicated by hepatic fibrosis.

27 se, results in biliary tract obstruction and hepatic fibrosis.

28 Myofibroblasts produce the fibrous scar in hepatic fibrosis.

29 microbes and their metabolites contribute to hepatic fibrosis.

30 thelial cells (LSECs), precedes the onset of hepatic fibrosis.

31 gesting a potential therapeutic approach for hepatic fibrosis.

32 ding nonalcoholic steatohepatitis (NASH) and hepatic fibrosis.

33 ed the contributory role of NOX1 and NOX2 in hepatic fibrosis.

34 cytes do not undergo EMT in murine models of hepatic fibrosis.

35 matory cytokine production, cholestasis, and hepatic fibrosis.

36 ased in the two experimental mouse models of hepatic fibrosis.

37 ed LivKO mice as an animal model of NASH and hepatic fibrosis.

38 hat Egr-1 is required for the development of hepatic fibrosis.

39 llagen deposition and histologically visible hepatic fibrosis.

40 mia, which is associated with progression of hepatic fibrosis.

41 the proinflammatory milieu characteristic of hepatic fibrosis.

42 to play critical roles in the development of hepatic fibrosis.

43 s, and finally a focus on matrix biology and hepatic fibrosis.

44 actant protein (MCP)-1, MCP-2, and MCP-3, in hepatic fibrosis.

45 epresent an effective therapeutic target for hepatic fibrosis.

46 nts per day, was associated with less severe hepatic fibrosis.

47 association between caffeine consumption and hepatic fibrosis.

48 omotes HSC chemotaxis and the development of hepatic fibrosis.

49 ways could reduce HSC activation and improve hepatic fibrosis.

50 pathways and complementary model systems of hepatic fibrosis.

51 rocess will provide targets for treatment of hepatic fibrosis.

52 en recently associated with various forms of hepatic fibrosis.

53 rosamine (DEN) orally for 12 weeks to induce hepatic fibrosis.

54 ple steatosis and identification of advanced hepatic fibrosis.

55 highly associated with accelerated rates of hepatic fibrosis.

56 stration and protecting against perivascular hepatic fibrosis.

57 sound as a non-invasive tool to characterize hepatic fibrosis.

58 e for HSC activation, the proximate event in hepatic fibrosis.

59 e currently no therapies to directly inhibit hepatic fibrosis.

60 ographics, lifestyle, metabolic factors, and hepatic fibrosis.

61 creased intrahepatic biliary mass (IBDM) and hepatic fibrosis.

62 sease spectrum in humans, including bridging hepatic fibrosis.

63 ha signaling could alter the pathogenesis of hepatic fibrosis.

64 mice resulted in reduced bile duct mass and hepatic fibrosis.

65 less (P = .030) than that for patients with hepatic fibrosis (4.16 kPa).

66 flare values than those with no significant hepatic fibrosis (9.62+/-1.99 photon counts/ms vs. 6.97+

67 ted postnatal growth would lead to increased hepatic fibrosis (a pathological marker of liver dysfunc

68 V) infection is characterized by progressive hepatic fibrosis, a process dependent on monocyte recrui

69 In HIV/HCV-coinfected women, hepatic fibrosis accelerates with reproductive aging.

70 Strong associations with advanced hepatic fibrosis (adjusted odds ratio [95% confidence in

71 and is an independent predictor of advanced hepatic fibrosis among patients with NAFLD.

72 votal event in initiation and progression of hepatic fibrosis and a major contributor to collagen dep

73 ated with an increased risk of both advanced hepatic fibrosis and advanced hepatic inflammatory activ

74 agonist can diminish and potentially reverse hepatic fibrosis and also reduce the number and size of

75 njury that were consistent with decreases in hepatic fibrosis and biliary ductal damage relative to t

76 Hepatic fibrosis and cirrhosis are a growing global heal

77 The risk of hepatic fibrosis and cirrhosis in hereditary hemochromat

78 ression was dramatically reduced in advanced hepatic fibrosis and cirrhosis in humans.

79 Nogo-B (reticulon 4B) accentuates hepatic fibrosis and cirrhosis, but the mechanism remain

80 The proteins identified may help to assess hepatic fibrosis and eliminate the need for invasive liv

81 that CCR5 plays a role in the development of hepatic fibrosis and evaluated the longitudinal effect o

82 a deleterious role of Th9/IL-9 in increasing hepatic fibrosis and exacerbating disease endpoints, ind

83 ed their potential as noninvasive markers of hepatic fibrosis and fibrosis progression in African-Ame

84 a robust readout to screen for regulators of hepatic fibrosis and have identified a novel antifibroti

85 indicator associated with the progression to hepatic fibrosis and hepatocellular carcinoma.

86 stablish lifelong chronic infections causing hepatic fibrosis and hepatocellular carcinoma.

87 We hypothesized that improving hepatic fibrosis and inflammation in chronic hepatitis C

88 rus infection is associated with progressive hepatic fibrosis and liver cancer.

89 ficient mice displayed substantially reduced hepatic fibrosis and macrophage infiltration.

90 et for experimental therapeutics in treating hepatic fibrosis and oncogenesis.

91 postulated that targeting SYK would mitigate hepatic fibrosis and oncogenic progression.

92 Increasing evidence suggests that hepatic fibrosis and pathological angiogenesis are inter

93 cultures correlated with protection against hepatic fibrosis and portal hypertension.

94 Hepatic fibrosis and portal pressure were significantly

95 of childhood, is characterized by congenital hepatic fibrosis and progressive cystic degeneration of

96 of childhood, is characterized by congenital hepatic fibrosis and progressive cystic degeneration of

97 nking is a remarkable feature of progressing hepatic fibrosis and represents an important therapeutic

98 Hepatic fibrosis and ROS generation were attenuated in b

99 ion of B cells by anti-CD20 mAb reduced both hepatic fibrosis and serum levels of ANA and immune comp

100 We investigated the heritability of hepatic fibrosis and steatosis in a community-dwelling t

101 (CAP), which are noninvasive assessments of hepatic fibrosis and steatosis, respectively.

102 lls as the potential therapeutic targets for hepatic fibrosis and targeting BAFF specifically for att

103 simultaneously, yet independently, directed hepatic fibrosis and the compensatory proliferation of h

104 a negative regulator of both CCl(4)-induced hepatic fibrosis and the oval cell response.

105 rypsin Z (ATZ) variant inside cells, causing hepatic fibrosis and/or carcinogenesis by a gain-of-toxi

106 chemokine inhibitor 35k efficiently reduced hepatic fibrosis, and CCR1- and CCR5-deficient mice disp

107 om nonalcoholic steatohepatitis, for staging hepatic fibrosis, and for identifying NAFLD in patients

108 e, higher initial HCV RNA level, more severe hepatic fibrosis, and higher body weight.

109 mputational approaches to drug discovery for hepatic fibrosis, and identify C1QTNF2 as a potential me

110 HSCs) in response to injury is a key step in hepatic fibrosis, and is characterized by trans-differen

111 Little is known about the heritability of hepatic fibrosis, and the heritability of hepatic steato

112 he relationship between portal inflammation, hepatic fibrosis, and the metabolic syndrome in pediatri

113 ansforming growth factor beta (TGF-beta) and hepatic fibrosis are hallmarks of hepatitis C virus (HCV

114 provides evidence that hepatic steatosis and hepatic fibrosis are heritable traits.

115 atic steatosis, yet the risks for developing hepatic fibrosis are poorly understood.

116 leads to hepatocyte dysfunction, death, and hepatic fibrosis are still unclear.

117 wever, anti-BAFF treatment did not attenuate hepatic fibrosis as measured by collagen deposition, hep

118 f green tea extract prevented CCl(4)-induced hepatic fibrosis, as evidenced by a decreased hydroxypro

119 tors or siRNA can prevent the progression of hepatic fibrosis, as yet no evidence has been provided t

120 607 markedly protected against toxin-induced hepatic fibrosis, associated hepatocellular injury and i

121 l (PZQ) and performed ultrasound to quantify hepatic fibrosis at baseline and 12 months after PZQ tre

122 Neutralization of IL-9 in mice ameliorated hepatic fibrosis, attenuated the activation of hepatic s

123 ; P < 1.1 x 10(-11)) and the heritability of hepatic fibrosis (based on liver stiffness) was 0.5 (95%

124 We investigated changes in hepatic fibrosis, based on transient elastography (TE),

125 CCl4 -cirrhotic rats was linked to decreased hepatic fibrosis, but not in BDL rats, in which the main

126 in (BMP) signaling is known to contribute to hepatic fibrosis, but the role of BMP signaling in the d

127 ive NAFLD progression to steatohepatitis and hepatic fibrosis by altering the transcription and pheno

128 evel in the liver and a reduced incidence of hepatic fibrosis by histological observations.

129 2KO mice and measure biliary hyperplasia and hepatic fibrosis by quantitative PCR and immunostaining

130 between alcohol use categories and advanced hepatic fibrosis, by HIV and chronic HCV status.

131 rophylactic and therapeutic animal models of hepatic fibrosis C9 prevented development of fibrosis or

132 ion cut liver slices, as an ex vivo model of hepatic fibrosis, C9 attenuated the profibrotic response

133 Hepatic fibrosis can also develop from metabolic liver d

134 The presence of hepatic fibrosis can be assessed with good discriminatio

135 for nonalcoholic steatohepatitis (NASH) and hepatic fibrosis, can be used for patients with psoriasi

136 In some contexts (e.g., hepatic fibrosis), changes to the ECM are well recognize

137 s as part of nephronophthisis and congenital hepatic fibrosis (CHF) in the liver.

138 Congenital hepatic fibrosis (CHF) is a disease of the biliary epith

139 ss of fibrocystin function causes congenital hepatic fibrosis (CHF), Caroli disease (CD), and autosom

140 bolic syndrome, that can lead to progressive hepatic fibrosis, cirrhosis and hepatic failure.

141 s, which progressively leads to cholestasis, hepatic fibrosis, cirrhosis, and eventually liver failur

142 and PNPLA3 rs738409 genotype), with advanced hepatic fibrosis/cirrhosis.

143 a NASH phenotype in OLETFs characterized by hepatic fibrosis (collagen 1alpha1 mRNA and hydroxyproli

144 Hepatic fibrosis, collagen content, inflammatory cytokin

145 splay a more extensive ductular reaction and hepatic fibrosis compared to Mdr2(-/-) mice.

146 Finally, TANGO1(+/-) mice displayed less hepatic fibrosis compared to WT mice in two separate mur

147 17A were significantly elevated in mice with hepatic fibrosis compared with controls.

148 steatohepatitis are at an increased risk of hepatic fibrosis compared with premenopausal women.

149 ate that HIV-infected macrophages accelerate hepatic fibrosis during HCV/HIV co-infection by amplifyi

150 R-200b axis may be key for the management of hepatic fibrosis during the progression of PSC.

151 reates an environment that is permissive for hepatic fibrosis; elucidation of these early events in t

152 ant towards developing strategies to prevent hepatic fibrosis especially following HCV recurrence in

153 ing of therapeutic PDGFR-alpha inhibition in hepatic fibrosis, especially in combination with other t

154 ween total testosterone and risk of advanced hepatic fibrosis (F3 and F3/F4) and inflammatory activit

155 Baseline advanced hepatic fibrosis (FIB-4 score >3.25) (HR, 5.45 [CI, 3.79

156 th high intake of alcohol against markers of hepatic fibrosis (FIB-4, APRI, and Forns index scores) a

157 tuberculosis and in granuloma formation and hepatic fibrosis following chronic percutaneous infectio

158 (IL)-10, IL-12p40, and IL-13Ralpha2 regulate hepatic fibrosis following infection with the helminth p

159 Stellate cell activation leads to hepatic fibrosis; furthermore, their activation is suppr

160 ferase to platelet ratio index score >/=1.5, hepatic fibrosis >/=F3, and hepatic steatosis >/=S2 were

161 d in chronic hepatitis B (CHB) patients with hepatic fibrosis, HBV-associated liver cirrhosis (LC) pa

162 ng-term HBV DNA suppression and reduction in hepatic fibrosis, hepatic decompensation, and liver-rela

163 tiple lines of evidence demonstrate that the hepatic fibrosis/hepatic stellate cell activation may be

164 congestion (congestive hepatopathy) leads to hepatic fibrosis; however, the mechanisms involved in th

165 R-200b is associated with the progression of hepatic fibrosis; however, the role of the GnRH/GnRHR1/m

166 sistent liver mononuclear cell infiltration, hepatic fibrosis, hypergammaglobulinemia, anti-nuclear a

167 (CBZ) decreased the hepatic load of ATZ and hepatic fibrosis in a mouse model of AT deficiency-assoc

168 y may have promise as noninvasive markers of hepatic fibrosis in a predominantly white HCV genotype 1

169 f being used to estimate the degree of early hepatic fibrosis in a rat model.

170 imaging techniques to more accurately stage hepatic fibrosis in a rat model.

171 erated postnatal catch-up growth caused more hepatic fibrosis in adulthood, which was associated with

172 siglitazone altered liver enzymes and caused hepatic fibrosis in APOE4 mice.

173 antagonist reduced biliary proliferation and hepatic fibrosis in BDL WT and Mdr2(-/-) mice.

174 s was independently associated with advanced hepatic fibrosis in both groups.

175 The gradual accumulation of hepatic fibrosis in chronic liver disease results in cli

176 lls, isolated from wild type livers restored hepatic fibrosis in Cxcr6(-/-) mice upon experimental st

177 Both NOX1 and NOX2 have an important role in hepatic fibrosis in endogenous liver cells, including HS

178 These findings suggest that hepatic fibrosis in HIV-1 infected patients can be modul

179 ories were strongly associated with advanced hepatic fibrosis in HIV/HCV-coinfected patients.

180 ing the mechanisms of schistosome-associated hepatic fibrosis in humans, and few biomarkers for risk

181 loride (CCl(4))-induced oxidative stress and hepatic fibrosis in male ICR mice.

182 ted Ghr's effects on biliary hyperplasia and hepatic fibrosis in Mdr2-knockout (Mdr2KO) mice, a recog

183 Ghr treatment reduced ductular reaction and hepatic fibrosis in Mdr2KO mice, regulating cholangiocyt

184 on to augment TGFbeta production and promote hepatic fibrosis in mice and to induce a profibrogenic p

185 against CCl(4)-induced oxidative stress and hepatic fibrosis in mice by inhibiting oxidative damage

186 ediators interact to slow the progression of hepatic fibrosis in mice with schistosomiasis.

187 so attenuated the development of BDL-induced hepatic fibrosis in mice.

188 d by genetic labeling does not contribute to hepatic fibrosis in mice.

189 d by gross pathology and histopathology, and hepatic fibrosis in patients was examined with ultrasoun

190 We aimed to describe congenital hepatic fibrosis in patients with ARPKD, confirmed by de

191 consumption (CC) is associated with reduced hepatic fibrosis in patients with chronic liver diseases

192 toring of the development and progression of hepatic fibrosis in patients with psoriasis receiving lo

193 uggesting the development and progression of hepatic fibrosis in patients with psoriasis receiving lo

194 ient elastography (VCTE) in the detection of hepatic fibrosis in patients with severe to morbid obesi

195 rotein 10 [IP-10]) have been associated with hepatic fibrosis in predominantly white hepatitis C viru

196 H/GnRHR1/miR-200b axis in the development of hepatic fibrosis in PSC is unknown.

197 tial pharmaceutical intervention to decrease hepatic fibrosis in response to ethanol.

198 1(Cre)/Dyn2K44A(fl/fl) mice showed increased hepatic fibrosis in response to liver injury.

199 a promising biomarker for assessing risk of hepatic fibrosis in schistosomiasis and, potentially, ot

200 The presence and severity of hepatic fibrosis in subjects with NAFLD was determined b

201 ell population, macrophage accumulation, and hepatic fibrosis in the Mdr2(-/-) model of cholestasis.

202 dark therapy or melatonin administration on hepatic fibrosis in the multidrug resistance gene 2-knoc

203 Fructose consumption predicts increased hepatic fibrosis in those with nonalcoholic fatty liver

204 n individuals annually and cause significant hepatic fibrosis in up to 20%.

205 a model of bile duct ligation (BDL)-induced hepatic fibrosis in vivo, and isolated liver-derived cel

206 brotic genes in vitro and decreased IBDM and hepatic fibrosis in vivo.

207 of nonalcoholic steatohepatitis and advanced hepatic fibrosis increase the risk for systemic comorbid

208 ch HIV/HCV group, the prevalence of advanced hepatic fibrosis increased as alcohol use category incre

209 of diabetes was associated with more severe hepatic fibrosis independent of iron loading, male gende

210 At 12 mo, hepatic fibrosis, indexes of inflammation, oxidative str

211 onstrates that 1D11 can reverse pre-existing hepatic fibrosis induced by extended dosing of TAA.

212 Hepatic fibrosis is a global health problem currently wi

213 Severe hepatic fibrosis is associated with a high risk of early

214 Hepatic fibrosis is associated with an overproduction of

215 Hepatic fibrosis is characterized by both intense intrah

216 Hepatic fibrosis is considered as a physiological wound-

217 Severity of hepatic fibrosis is greater in postmenopausal than in pr

218 Hepatic fibrosis is marked by activation of hepatic stel

219 Hepatic fibrosis is the net accumulation of matrix tissu

220 ons, although the significance of persisting hepatic fibrosis is unknown.

221 er this variant promotes clinically relevant hepatic fibrosis is unknown.

222 Although it may not be measuring hepatic fibrosis, its components suggest that increases

223 effects of supplementation with synbiotic on hepatic fibrosis, liver enzymes, and inflammatory marker

224 Plasma cholesterol (P < 0.001), histological hepatic fibrosis, liver hydroxyproline content (P = 0.00

225 in the generation of T regulatory cells, in hepatic fibrosis LSECs induce an immunogenic T cell phen

226 y fat fraction >/=5%), and 8.2% (10/122) had hepatic fibrosis (magnetic resonance elastography >/=3 k

227 cellent diagnostic performance for assessing hepatic fibrosis; MR elastography was more technically r

228 ersus 56.0%; non-CC, 44.1% versus 16.2%) and hepatic fibrosis (noncirrhotic, 63.3% versus 41.9%; cirr

229 Advanced hepatic fibrosis, obesity, and steatosis are factors ass

230 Hepatic fibrosis occurs during most chronic liver diseas

231 Hepatic fibrosis occurs during the progression of primar

232 N was independently associated with advanced hepatic fibrosis (odds ratio [OR], 1.66; 95% confidence

233 rphometry can provide precise measurement of hepatic fibrosis on a continuous scale.

234 ) was independently associated with advanced hepatic fibrosis on multiple regression analysis after a

235 We found that hepatic fibrosis onset can be partially attributed to th

236 03, following histological proof of advanced hepatic fibrosis or cirrhosis (Ishak score 4-6).

237 al [CI]: 1.014-1.082, P = 0.005), and severe hepatic fibrosis (OR 2.177, 95% CI: 1.043-4.542, P = 0.0

238 was associated with significant decrease in hepatic fibrosis (p < 0.001), and nuclear factor-kappa B

239 ce have unprecedented degree and rapidity of hepatic fibrosis progression and clinically relevant cir

240 versible cross-linking is thought to promote hepatic fibrosis progression and limit its reversibility

241 to support the hypothesis that HCV enhances hepatic fibrosis progression through the generation of R

242 ence that HIV and HCV independently regulate hepatic fibrosis progression through the generation of R

243 TG2 and TG activity are up-regulated during hepatic fibrosis progression, but do not contribute to f

244 HIV/HCV coinfection leads to accelerated hepatic fibrosis progression, with higher rates of cirrh

245 man immunodeficiency virus (HIV) accelerates hepatic fibrosis progression.

246 oxidase (LOX) to collagen stabilization and hepatic fibrosis progression/reversalin vivousing chroni

247 negative relationship between coffee CC and hepatic fibrosis (r = -0.215; P = 0.035).

248 Hepatic fibrosis reduced the correlation between biopsy

249 bilobar disease and/or associated congenital hepatic fibrosis remains challenging.

250 ent during and after DAA therapy can improve hepatic fibrosis remains unclear.

251 Early diagnosis and staging of hepatic fibrosis represent a major challenge.

252 Induction of substantial hepatic fibrosis requires 12 weeks of CCl4 administratio

253 ese data suggest that schistosome-associated hepatic fibrosis results, in part, from excessive inhibi

254 the first family, the proband presents with hepatic fibrosis, retinitis pigmentosa, and postaxial po

255 icant association of a higher NASH FibroSure hepatic fibrosis score in women (Spearman rho = 0.21; P

256 The rate of hepatic fibrosis score progression (RFSP) in predicting

257 rferon-stimulated gene levels in T cells and hepatic fibrosis score.

258 otoxic effects, and monitor for worsening of hepatic fibrosis scores during MTX therapy.

259 Hepatic fibrosis scores were not elevated and did not di

260 dence of clinical outcomes based on baseline hepatic fibrosis stage (classification range, F0-F4): F0

261 Histological specimens were scored for hepatic fibrosis stage according to the METAVIR scoring

262 hat the DR was significantly correlated with hepatic fibrosis stage and biliary taurocholate levels.

263 The hepatic fibrosis stage was assessed histologically by us

264 cohort of patients with HIV/HCV coinfection, hepatic fibrosis stage was independently associated with

265 y in the detection of clinically significant hepatic fibrosis (stage F2-F4) (mean area under the curv

266 ents with chronic HCV infection and advanced hepatic fibrosis, sustained virological response to inte

267 d an inflammatory cell infiltration and mild hepatic fibrosis that was prevented by treatment with ir

268 h factor beta (TGF-beta) plays a key role in hepatic fibrosis, the final common pathway for a variety

269 al adhesion complexes in HSCs is pivotal for hepatic fibrosis therapy, now that small adiponectin-lik

270 HSCs mediate hepatic fibrosis through their activation from a quiesce

271 ratio index (APRI) as a surrogate marker of hepatic fibrosis to characterize liver disease in the Mu

272 tractable CCl(4)-induced model of reversible hepatic fibrosis to identify and characterize the macrop

273 and megakaryocytic precursors, resulting in hepatic fibrosis, transient postnatal thrombocytosis, an

274 Although hepatic fibrosis typically follows chronic inflammation,

275 Moderate ethanol consumption exacerbates hepatic fibrosis upon exposure to CCl4.

276 Moreover, hepatic fibrosis was also evident in these animals in re

277 reactive oxygen species (ROS) generation and hepatic fibrosis was assessed in vitro and in vivo using

278 fter adjusting for covariates, only advanced hepatic fibrosis was associated with greater severity of

279 Advanced hepatic fibrosis was defined by FIB-4 index >3.25.

280 Furthermore, the degree of hepatic fibrosis was enhanced in MCD-fed AnxA1 KO mice,

281 After chronic CCl(4) exposure, hepatic fibrosis was established in both genotypes; howe

282 Hepatic fibrosis was evaluated by staining for desmin, S

283 Histopathologic hepatic fibrosis was graded qualitatively by using the I

284 Hepatic fibrosis was induced by bile duct ligation (BDL)

285 Hepatic fibrosis was induced during 12 weeks of intraper

286 Hepatic fibrosis was induced in wild-type (WT) mice, NOX

287 For each alcohol use category, advanced hepatic fibrosis was more common among HIV-infected than

288 gadoxetate disodium in the setting of active hepatic fibrosis was not associated with increased fibro

289 tosis and a more-robust NAFLD phenotype with hepatic fibrosis was observed at 12 months in OffOb-OD.

290 Advanced hepatic fibrosis was present at low levels of alcohol co

291 Hepatic fibrosis was scored using the Ishak (0-6) scale;

292 Patients with ARPKD and congenital hepatic fibrosis were evaluated at the National Institut

293 Forty four candidate biomarkers for hepatic fibrosis were identified of which 20 were novel

294 ected mice from carbon tetrachloride-induced hepatic fibrosis, whereas global loss of beta(3), beta(5

295 administration for 8 weeks induced extensive hepatic fibrosis, whereupon 1D11 dosing was initiated an

296 Liver stiffness is related to the degree of hepatic fibrosis which ultimately causes portal hyperten

297 ith CCl4 were susceptible to the development hepatic fibrosis with higher levels of ILK, pGSK3b, and

298 ance imaging-proton density fat fraction and hepatic fibrosis with magnetic resonance elastography.

299 Two patients had hepatic fibrosis, with 1 showing a sinusoidal pattern of

300 TFF-fed L-FABP(-/-) mice exhibited decreased hepatic fibrosis, with reduced expression of fibrogenic