ライフサイエンスコーパス: cirrhotic

1 ced), and cirrhosis status (noncirrhotic vs. cirrhotic).

2 Of the 72% with GT3, 76% were also cirrhotic.

3 invasion; 68% of HBV versus 89% of HCV were cirrhotic.

4 OL and systemic inflammation compared to non-cirrhotics.

5 al muscle from hyperammonemic rats and human cirrhotics.

6 emale, with a mean age of 50 years; 39% were cirrhotic; 22% were treatment-experienced; 47% were geno

7 fibrosis (noncirrhotic, 63.3% versus 41.9%; cirrhotic, 38.1% versus 21.7%).

8 278 cirrhotics [39% hepatic encephalopathy (HE), 31%DM] unde

9 A total of 111 patients (61 cirrhotic; 50 postliver transplants) with HCV genotype 4

10 187 subjects (40 controls, 147 cirrhotic; 87 with HE) underwent systemic inflammatory a

11 84 patients [90.5% males, 89.2% cirrhotics, 89.2% nodular HCC, median age 63 (34-84) yea

12 At baseline, 49.4% were cirrhotic, 91% were genotype 3 and 91.9% attained SVR.

13 xaminations performed on 42 males, including cirrhotic alcoholics (n = 13), non-cirrhotic alcoholics

14 including cirrhotic alcoholics (n = 13), non-cirrhotic alcoholics (n = 15), non-alcoholic controls (n

15 c FGF19 mRNA expression was increased in non-cirrhotic and cirrhotic tissues (9-fold,p = 0.01; 69-fol

16 estigated the differences of angiogenesis in cirrhotic and non-cirrhotic PHT with special emphasis on

17 summary, statins caused contrary effects in cirrhotic and non-cirrhotic portal hypertension.

18 Cirrhotic and noncirrhotic liver tissues were obtained f

19 ce daily for 12 weeks in genotype 1-infected cirrhotic and noncirrhotic patients who had failed treat

20 achieved high SVR12 rates in treatment-naive cirrhotic and noncirrhotic patients with genotype 1, 4,

21 Cirrhotic and noncirrhotic subjects were matched 1:5 on

22 are up-regulated, in mesentery and liver, in cirrhotic and precirrhotic portal hypertensive rats and

23 e review differences and similarities in the cirrhotic and precirrhotic stages of NAFLD and alcoholic

24 s with chronic hepatitis C: On the one side, cirrhotic and tumor fragments were moderately and highly

25 (80%) were HCV treatment-naive, 14 (6%) were cirrhotic, and 108 (46%) were African American.

26 H3K27me3), and transcription across normal, cirrhotic, and HCC liver tissue.

27 gible articles were stratified into general, cirrhotic, and populations coinfected with human immunod

28 atory and systemic inflammatory responses in cirrhotic animals.

29 hway, a less differentiated phenotype, and a cirrhotic background.

30 In this study, cirrhotic bile duct ligated (BDL) rats with PH were trea

31 Cirrhotic (bile duct ligation/BDL; CCl4 intoxication) an

32 Cirrhotic BM showed an inverse correlation between clust

33 s.c. or intrahepatic injection in normal and cirrhotic (carbon tetrachloride-induced) mice.

34 Cirrhotic cardiomyopathy (CCM) is cardiac dysfunction in

35 Cirrhotic cardiomyopathy (CCM), a comorbidity of end-sta

36 This cardiomyopathy, similar to cirrhotic cardiomyopathy in humans, is characterized by

37 Cirrhotic cardiomyopathy, a condition characterized by i

38 ardiomyopathy in mice as a model for hepatic/cirrhotic cardiomyopathy.

39 ence of underlying cardiac disease is termed cirrhotic cardiomyopathy.

40 GF cirrhotic mice developed similar cirrhotic changes to conventional mice after 4 extra wee

41 can last for one year after treatment in non-cirrhotic CHB patients without a virological breakthroug

42 participants were aged 18-70 years with non-cirrhotic, chronic HCV genotype 4 infection (documented

43 define gut-brain axis alterations in elderly cirrhotics compared to non-cirrhotic individuals based o

44 Liver cancer and cirrhotic complications are rare.

45 s induced in the liver under cholestatic and cirrhotic conditions.

46 mean FIB-4 score >5.88-and time to onset of cirrhotic decompensation in electronic medical records.

47 Cirrhotics demonstrated significant changes on MR spectr

48 ved in 22 patients including 2 fatalities in cirrhotic diabetes patients.

49 Cirrhotic explant livers showed robust HLA-G expression

50 acteristic curve, 0.753) for differentiating cirrhotic from noncirrhotic livers (P = .038 and .003, r

51 routine CT images accurately differentiated cirrhotic from noncirrhotic livers and was highly reprod

52 Accuracy for differentiating cirrhotic from noncirrhotic livers was assessed by area

53 al population, 0.26 (95% CI, .18-.74) in the cirrhotic group, and 0.21 (.10-.45) in the coinfected gr

54 study was carried out on treatment-naive non-cirrhotic (Group A, n = 50) and treatment-naive cirrhoti

55 rhotic (Group A, n = 50) and treatment-naive cirrhotic (Group B, n = 22) patients with genotype 4 HCV

56 Cirrhotics had a prolonged QTc interval, a Q wave, abnor

57 Cirrhotics had in median 27 times more bacterial DNA of

58 Cytokine profiles did not distinguish cirrhotic HBV patients with and without HCC (AUC 0.503)

59 In cirrhotic HCV GT1- or GT3-infected patients, ABT-493 plu

60 a large cohort of DAA-treated patients with cirrhotic HCV, GRS was associated with de novo HCC indep

61 From observational studies among compensated cirrhotic hepatitis C patients treated with interferon-c

62 Cirrhotic HIV/HCV-coinfected patients enrolled in the Fr

63 associated with a high virologic efficacy in cirrhotic HIV/HCV-coinfected patients.

64 Of 137 cirrhotic hospitalized patients, 121 cirrhotic patients

65 ied in difficult-to-treat null responder and cirrhotic human immunodeficiency virus (HIV)-coinfected

66 vels and beta-catenin activation in fibrotic/cirrhotic human liver tissues.

67 mal cell types that are found in healthy and cirrhotic human liver.

68 s critical cell subset may contribute to the cirrhotic immunodeficiency state and heightened risk of

69 ations in elderly cirrhotics compared to non-cirrhotic individuals based on presence of cirrhosis and

70 ocellular carcinoma (HCC), especially in non-cirrhotic individuals.

71 e strategy for well-compensated HCV-infected cirrhotics listed for liver transplantation with hepatoc

72 ed was restricted to well-compensated HCV(+) cirrhotics listed for liver transplantation with hepatoc

73 of patients with HCC is diagnosed in the non-cirrhotic liver (NCL).

74 liver disease and 13.3% in patients with non-cirrhotic liver disease (adjusted RR of 1.49 95% confide

75 ts underwent CRC surgery: 369 (0.9%) had non-cirrhotic liver disease and 158 (0.4%) had liver cirrhos

76 zed them into two cohorts: patients with non-cirrhotic liver disease and patients with liver cirrhosi

77 f a 6-week exercise program in patients with cirrhotic liver disease awaiting LT.

78 iomyopathy (CCM), a comorbidity of end-stage cirrhotic liver disease, remains uncharacterized in chil

79 In a cirrhotic liver environment, cells could differentiate i

80 hate phosphatase 1 in normal human liver and cirrhotic liver from patients with alcohol-related liver

81 normal and 9 cirrhotic livers, we show that cirrhotic liver has a higher mutational burden than norm

82 r in controls between different areas of the cirrhotic liver or between liver and serum.

83 ver resection, 168 paired non-tumor adjacent cirrhotic liver samples, and 10 non-tumor liver tissues

84 was determined through the analysis of human cirrhotic liver specimens, widely accepted in vivo anima

85 In nodules of human cirrhotic liver tissue, there was no evidence of chromos

86 SDF-1alpha expression with fibrotic septa in cirrhotic liver tissues as well as with desmoplastic reg

87 erved increased levels of CPEB1 and CPEB4 in cirrhotic liver tissues from patients, compared with con

88 th primary mouse HSCs, human LX2 HSCs, human cirrhotic liver tissues, rats and mice with liver fibros

89 o the most common bacteria translocated into cirrhotic liver, although there were no statistically si

90 liver function after transplantation into a cirrhotic liver, and co-localized with the pericyte mark

91 the same mutational signatures as background cirrhotic liver, but with higher burden.

92 In cirrhotic liver, COL15A1-expressing PMFs adopted a periv

93 In the perfused TAA and BDL cirrhotic liver, INT-747 improved endothelial vasorelaxa

94 of carcinogenesis, as 90% of HCCs arise in a cirrhotic liver.

95 e it removes tumor as well as the underlying cirrhotic liver.

96 from nonenhanced thick-section CT images in cirrhotic livers (3.16; 56 livers) were significantly hi

97 short heterodimer partner were increased in cirrhotic livers (9-fold, p < 0.001; 3.5-fold,p = 0.007;

98 RT6 was significantly down-regulated in both cirrhotic livers and cancer.

99 oteins were highly expressed in DRs of human cirrhotic livers and cholangiocarcinoma.

100 n 19-labeled ductular reaction (DR) in human cirrhotic livers and in an experimental cirrhosis induce

101 found that ductular reaction cells in human cirrhotic livers express hepatocyte nuclear factor 1 hom

102 Patients with cirrhotic livers had significantly increased levels of v

103 Repair of cirrhotic livers occurs, in part, by repopulation with h

104 ysiological features of HCCs, which occur in cirrhotic livers that show pronounced necroinflammation,

105 In fibrotic/cirrhotic livers the degree of future liver remnant hype

106 rimary human liver cancers and in normal and cirrhotic livers using microarray analysis.

107 For cirrhotic livers, a significantly lower total perfusion,

108 In cirrhotic livers, activation of the XBP1-Hrd1 arm of ER

109 lar carcinomas (HCCs) develop in fibrotic or cirrhotic livers, suggesting an important role of liver

110 By contrast, in intrahepatic xenografts in cirrhotic livers, tumors were dominated by epithelial tr

111 s of 100-500 hepatocytes from 5 normal and 9 cirrhotic livers, we show that cirrhotic liver has a hig

112 erences in multiple areas of control non-HCC cirrhotic livers.

113 containing HCC compared with control non-HCC cirrhotic livers.

114 investigated the roles of autophagy in human cirrhotic livers.

115 on of lysosomal cathepsin D were observed in cirrhotic livers.

116 e the original human CCAs when injected into cirrhotic livers.

117 ce, is a major mechanism for repopulation of cirrhotic livers.

118 , and aneuploidy is not commonly observed in cirrhotic livers.

119 mily, is accumulated in hepatocytes of human cirrhotic livers.

120 in hepatic stellate cell (HSC) apoptosis in cirrhotic livers.

121 r patients with hepatocellular carcinoma and cirrhotic livers.

122 red post treatment in a single case of a non-cirrhotic male with genotype 3, who was treated with sof

123 c that decreases lipopolysaccharide (LPS) in cirrhotics, may decrease the elevated levels of microbia

124 GF cirrhotic mice developed similar cirrhotic changes to co

125 GF cirrhotic mice exhibited higher ammonia, compared to GF

126 Conventional cirrhotic mice had higher degrees of neuroinflammation,

127 However, conventional cirrhotic mice had intestinal dysbiosis as well as syste

128 d progression are strongly influenced by the cirrhotic microenvironment, and the exact contributions

129 In both cirrhotic models, FXR expression was decreased.

130 n 2 activation were consistently reversed in cirrhotic muscle (P < 0.01).

131 acellular concentrations similar to those in cirrhotic muscle.

132 s in tissues from non-cirrhotic (n = 24) and cirrhotic (n = 21) patients along with control tissues (

133 response to cholestasis in tissues from non-cirrhotic (n = 24) and cirrhotic (n = 21) patients along

134 ed out this phenomenon of HCC arising in non-cirrhotic NASH (1), and a recent meta-analysis of 19 stu

135 has shown that the prevalence of HCC in non-cirrhotic NASH was up to 38.0% (2).

136 Accurate characterization of cirrhotic nodules and early diagnosis of hepatocellular

137 promoter mutations in the transformation of cirrhotic nodules into hepatocellular carcinoma (HCC).

138 ity of exogenous signatures between adjacent cirrhotic nodules varied by up to tenfold within each pa

139 d to profile miRNA expression in 55 samples (cirrhotic nodules; CNs), LGDNs, HGDNs, early HCCs, and s

140 Livers from cirrhotic Nogo-B KO mice showed significantly reduced fi

141 ical centres in the USA in patients with non-cirrhotic, non-alcoholic steatohepatitis to assess treat

142 chemistry in 91% of HH-HCC, 0% of HH-related cirrhotic or dysplastic nodules and 79% of mixed-aetiolo

143 Cirrhotic outpatients with/without DM underwent stool an

144 uct ligation/BDL; CCl4 intoxication) and non-cirrhotic (partial portal vein ligation/PPVL) rats recei

145 Of the cirrhotic participants, 96% were Child-Turcotte-Pugh cla

146 Of 137 cirrhotic hospitalized patients, 121 cirrhotic patients (88.3 %) with AKI-prone conditions we

147 treatment was less than $100,000 per QALY in cirrhotic patients (genotype 2 or 3 and treatment-naive

148 tis C virus (HCV) patients (n = 20), group 3 cirrhotic patients (LC) (n = 20), and HCC group (n = 20)

149 K NAFLD cohort, in the overall cohort of non-cirrhotic patients (n = 913, 41 with HCC) the T allele r

150 NT-proBNP changes at the end of drainage in cirrhotic patients (P < 0.01).

151 ICU admissions for variceal bleeding in cirrhotic patients accounted for 4,003 (0.6%) of all 720

152 We prospectively enrolled cirrhotic patients admitted at the King Chulalongkorn Me

153 ay, discharge destinations, and mortality of cirrhotic patients admitted to the ICU for variceal blee

154 During the period, 207 cirrhotic patients among 525 LT were studied.

155 ith an MRR of 0.64 (95% CI, 0.40-1.01) among cirrhotic patients and 2.33 (1.47-3.67) compared with th

156 The study included 41,076 cirrhotic patients and 204,244 noncirrhotic controls fro

157 icant difference between the total cohort of cirrhotic patients and controls.

158 of ascitic fluid; it has a high incidence in cirrhotic patients and it is associated with high mortal

159 sR were increased in splanchnic vessels from cirrhotic patients and rats compared with healthy contro

160 Perioperative management is challenging in cirrhotic patients and the ability to recognize and trea

161 sma OPN in the diagnosis of HCC in alcoholic cirrhotic patients and to investigate whether increased

162 Lactulose therapy was effective for cirrhotic patients as primary prophylaxis to prevent ove

163 y, plasma FA lipidome was investigated in 51 cirrhotic patients before liver transplantation and in 9

164 tly higher active TB rate was maintained for cirrhotic patients compared with their noncirrhotic coun

165 A total of 957 of 41,076 (2.32%) cirrhotic patients developed TB, yielding a rate that wa

166 Nearly 80% of cirrhotic patients diagnosed with hepatocellular carcino

167 However, the risk of TB in cirrhotic patients has rarely been investigated.

168 Cirrhotic patients have a greater risk of TB than noncir

169 We enrolled cirrhotic patients hospitalized with the first presentat

170 in predicting the presence of varices among cirrhotic patients in northwestern Tanzania.

171 Bariatric surgery in obese cirrhotic patients is not associated with excessive mort

172 post-liver transplantation (LT) mortality in cirrhotic patients is unanswered.

173 Single-center study that included all cirrhotic patients listed for LT between 2014 and 2017.

174 Two cirrhotic patients relapsed and 2 discontinued treatment

175 ression of CD95(Fas) in CD27(+) B-cells from cirrhotic patients that was inversely correlated with pe

176 ce of esophageal varices varies widely among cirrhotic patients this has not been assessed in Tanzani

177 In cirrhotic patients transplanted with large splenorenal s

178 Information on the outcome of cirrhotic patients undergoing a transplant for HCC and w

179 Adult cirrhotic patients undergoing first-time liver transplan

180 Cirrhotic patients undergoing first-time liver transplan

181 Among 336 cirrhotic patients undergoing LT between 2000 and 2011,

182 thin the splanchnic circulation of alcoholic cirrhotic patients undergoing TIPSS insertion for varice

183 Forty-six cirrhotic patients were included with hepatitis C (87%)

184 While memory B-cells from cirrhotic patients were resistant to Fas-mediated apopto

185 The outcomes and optimal management of cirrhotic patients who develop cryptococcosis before tra

186 Among cirrhotic patients who underwent evaluation for HCC with

187 Conclusion ELF is not uncommon in cirrhotic patients with a MELD score of 12 or less who u

188 sed to provide prognostic information in HBV cirrhotic patients with ACLF.

189 This prospective study included 113 cirrhotic patients with actively bleeding esophageal var

190 890 HBV associated cirrhotic patients with acute decompensation (AD) were e

191 ed corticosteroid insufficiency is common in cirrhotic patients with acute gastroesophageal variceal

192 rospective cohort study was conducted on 235 cirrhotic patients with acute peptic ulcer hemorrhage wh

193 r the early detection of AKI in hospitalized cirrhotic patients with AKI-prone conditions; however, i

194 invasive early detection of HCC from at-risk cirrhotic patients with an area under receiver operator

195 data obtained from 16S rDNA sequencing of 90 cirrhotic patients with and without long-term PPI use an

196 Cirrhotic patients with ascites are prone to develop var

197 diseases for 30-day and 90-day mortality of cirrhotic patients with ascites were 1.81 (1.54-2.11) an

198 Of the total 4,576 cirrhotic patients with ascites, 1,294 (28.2%) were diag

199 al Health Insurance Program, to enroll 4,576 cirrhotic patients with ascites, who were discharged fro

200 ses increased 30-day and 90-day mortality of cirrhotic patients with ascites.

201 y from 12 to 8 weeks in treatment naive, non-cirrhotic patients with baseline HCV RNA levels <6 milli

202 C/EI of beta-lactams in cirrhotic patients with BSI may improve outcomes and fac

203 pective, multicenter study that enrolled 312 cirrhotic patients with BSI.

204 Finally, in a combined cohort of non-cirrhotic patients with chronic hepatitis C or alcoholic

205 coexisting DM and CKD increase mortality in cirrhotic patients with EVB remains unclear.

206 Among the cirrhotic patients with EVB, all-cause mortality at 42-d

207 Records from 861 cirrhotic patients with HCC consecutively listed for eit

208 Cirrhotic patients with HCV who achieve SVR should there

209 eat analysis of overall survival (ITT-OS) of cirrhotic patients with hepatocellular carcinoma (HCC) l

210 e safety profile was acceptable, even though cirrhotic patients with low albuminemia and platelets sh

211 Resting-state fMRI was administered to 33 cirrhotic patients with MHE and 43 cirrhotic patients wi

212 However, cirrhotic patients with null-responses to EBV peptides h

213 Peripheral blood was obtained from 22 cirrhotic patients with systemic inflammation, 13 cirrho

214 er transplantation (LT) in the management of cirrhotic patients with tumors exhibiting intrahepatic b

215 Infections in cirrhotic patients with upper gastrointestinal bleeding

216 Admission rate to ICU and mortality of cirrhotic patients with variceal bleeding has declined s

217 red to 33 cirrhotic patients with MHE and 43 cirrhotic patients without MHE (NMHE).

218 otic patients with systemic inflammation, 13 cirrhotic patients without systemic inflammation and 14

219 Among cirrhotic patients, 46% never had hepatic imaging.

220 ), 92.6% (95% CI, 75.7%-99.1%; n = 25/27) in cirrhotic patients, 94.6% (95% CI, 81.8%-99.3%; n = 35/3

221 by co-culturing these cells with plasma from cirrhotic patients, a sensitivity partially mediated by

222 are relatively safe and effective in stable cirrhotic patients, but are in need of further study in

223 was associated with a reduction in MR among cirrhotic patients, but the MR remained higher than the

224 ontent was lower in the skeletal muscle from cirrhotic patients, hyperammonaemic portacaval anastomos

225 al spectra of overt EH and the complexity of cirrhotic patients, it is very difficult to perform qual

226 Esophageal varices were prevalent among cirrhotic patients, most of which were at risk of bleedi

227 ul diagnostic biomarker for HCC in alcoholic cirrhotic patients, particularly in the early stages.

228 In cirrhotic patients, pre-LT BNP serum level was an indepe

229 The FA pattern was markedly altered in cirrhotic patients, who showed, compared with healthy co

230 with short-term mortality in critically ill cirrhotic patients.

231 infections and reduced rebleeding events in cirrhotic patients.

232 r diagnosing AKI and its prognostic value in cirrhotic patients.

233 tion may be the optimal treatment for HCC in cirrhotic patients.

234 a mechanism by which sarcopenia develops in cirrhotic patients.

235 loride and its association with mortality in cirrhotic patients.

236 was found to improve its predictive value in cirrhotic patients.

237 nt should be performed systematically in all cirrhotic patients.

238 t of actively bleeding esophageal varices in cirrhotic patients.

239 erichia coli in undiluted ascitic fluid from cirrhotic patients.

240 of uNGAL for diagnosing AKI in hospitalized cirrhotic patients; and (2) to explore the association o

241 known to increase mortality in hospitalized cirrhotic patients; therefore early identification is ut

242 er in abundance in cirrhotic relative to non-cirrhotic PBC patients.

243 noncirrhotic PBC, seven female patients with cirrhotic PBC, and 11 healthy female controls were recru

244 TRbeta1 and miR-181a was also found in human cirrhotic peritumoral tissue, compared to normal liver.

245 Thirty one percent of cirrhotic persons were Child-Pugh C, and 67.9% of HCC pa

246 ther evaluation as a potential treatment for cirrhotic PH.

247 erences of angiogenesis in cirrhotic and non-cirrhotic PHT with special emphasis on the canonical (Sh

248 ignaling pathways in different rat models of cirrhotic portal hypertension (PHT).

249 caused contrary effects in cirrhotic and non-cirrhotic portal hypertension.

250 ts and two other patients (1%) developed non-cirrhotic portal hypertension.

251 intrahepatic portosystemic shunt (TIPS) for cirrhotic portal hypertension.

252 anaemia and treatment discontinuation in non-cirrhotic previously untreated and previously treated pa

253 Among cirrhotic prior null responders, SVR12 was achieved by 9

254 of a substantial degree of regression in the cirrhotic process, with the possible prevention of hepat

255 travenous injection of C/EBPalpha-saRNA in a cirrhotic rat model with multifocal liver tumors increas

256 eviously shown to enhance ammonia removal in cirrhotic rats and holds promise for the treatment of hy

257 change in liver fibrosis was observed in BDL-cirrhotic rats but an increase in the eNOS pathway.

258 nificantly change arterial pressure in CCl4 -cirrhotic rats but decreased it significantly in BDL-cir

259 Cirrhotic rats exposed to CIH exhibited an attenuated va

260 sis were evaluated in CCl4 and thioacetamide-cirrhotic rats treated with RVXB (20 mg/kg/day) or its v

261 naling pathway were measured in CCl4 and BDL cirrhotic rats treated with terutroban (30 mg/kg/day) or

262 decreased hepatic resistance, which in CCl4 -cirrhotic rats was linked to decreased hepatic fibrosis,

263 Normal and cirrhotic rats were exposed for 14 days to repetitive cy

264 Cirrhotic rats with HE showed significantly increased mi

265 In a group of cirrhotic rats, in vivo systemic and hepatic hemodynamic

266 In CCl4 -cirrhotic rats, terutroban reduced liver fibrosis and de

267 ates intrahepatic endothelial dysfunction in cirrhotic rats, which is associated with increased oxida

268 nesis, hepatic angiogenesis, and fibrosis in cirrhotic rats.

269 200mg/kg, thrice-weekly for 8 weeks)-induced cirrhotic rats.

270 c rats but decreased it significantly in BDL-cirrhotic rats.

271 rosis (LF), liver microthrombosis, and PH in cirrhotic rats.

272 of memory B cells were lower in abundance in cirrhotic relative to non-cirrhotic PBC patients.

273 A transcriptome meta-analysis of >500 human cirrhotics revealed global regulatory gene modules drivi

274 icted functions were significantly higher in cirrhotic saliva.

275 odules (LGDNs and HGDNs, respectively), in a cirrhotic setting.

276 a have been shown to affect precirrhotic and cirrhotic stages of liver diseases, which could lead to

277 Cirrhotic stool microbiota demonstrated a significantly

278 he EVR group (n = 76) was younger, had fewer cirrhotic subjects, had a higher proportion with the IL2

279 havioral decline or inflamm-aging in elderly cirrhotic subjects.

280 In livers from CCl4 and BDL-cirrhotic terutroban-treated rats, endothelial dysfuncti

281 36 HCC samples and from matching surrounding cirrhotic tissue and was stained for TK-1 A prospective

282 In vivo, murine and human cirrhotic tissue displayed increased TANGO1 messenger RN

283 T PET can differentiate HCC from surrounding cirrhotic tissue, with PET parameters correlating with T

284 xpression was increased in non-cirrhotic and cirrhotic tissues (9-fold,p = 0.01; 69-fold,p < 0.0001,

285 e measured from both focal liver lesions and cirrhotic tissues (from the 5 HCC patients).

286 ession pattern of 186 genes in corresponding cirrhotic tissues increased its prognostic accuracy.

287 kappaB increased dramatically from normal to cirrhotic to HCC tissues from human patients.

288 r disease and renal impairment are common in cirrhotic transplant candidates.

289 th respect to the survival of non-alcoholic, cirrhotic transplant patients (3 year survival: 66.8% wi

290 alfa-2a (peginterferon) and ribavirin in non-cirrhotic treatment-naive, patients with HCV.

291 tratified by HCV genotype [1a vs 1b]) 60 non-cirrhotic, treatment-naive patients to receive sofosbuvi

292 GF and conventional mice were made cirrhotic using carbon tetrachloride and compared with c

293 GF and conventional C57BL/6 mice were made cirrhotic using CCl4 gavage.

294 CD14 expression percentage in cirrhotics was significantly higher than in the autopsy

295 Cirrhotics were impaired on non-amnestic and selected am

296 nd colonic mucosal microbiome are altered in cirrhotics who get hospitalized with independent predict

297 In compensated cirrhotics with early hepatocellular carcinoma (HCC-cirr

298 ust frailty index scores (<20th percentile), cirrhotics with poor frailty index scores (>80th percent

299 Cirrhotics with very early iCCA or carefully selected pa

300 and hyperammonemia compared to controls and cirrhotics without HE.