ライフサイエンスコーパス: liver disease

1 , diabetes mellitus, ischemic heart disease, liver disease).

2 the metabolic perturbations preceding fatty liver disease.

3 nd might promote tumorigenesis, in mice with liver disease.

4 and young adult patients suspected of having liver disease.

5 may be a promising therapy for AATD-related liver disease.

6 al in obese patients with nonalcoholic fatty liver disease.

7 rease in the incidence of nonalcoholic fatty liver disease.

8 mic changes in hepatic FFA flux in models of liver disease.

9 s to using these cells in treating end-stage liver disease.

10 ce status of 1 or less, and had Child-Pugh A liver disease.

11 ccumulation, a hallmark feature of alcoholic liver disease.

12 epatic diseases, such as non-alcoholic fatty liver disease.

13 olic syndrome, including non-alcoholic fatty liver disease.

14 tis B, leading to accelerated progression of liver disease.

15 te to the development of non-alcoholic fatty liver disease.

16 esent an important additive cause of chronic liver disease.

17 little is known about their role in chronic liver disease.

18 he protection against the diet-induced fatty liver disease.

19 ist outcomes relative to others with chronic liver disease.

20 h as type 2 diabetes and non-alcoholic fatty liver disease.

21 lpha-1 antitrypsin deficiency which leads to liver disease.

22 , nonalcoholic steatohepatitis, or end-stage liver disease.

23 histologically confirmed nonalcoholic fatty liver disease.

24 rgence of cirrhosis from non-alcoholic fatty liver disease.

25 t Africa, and from patients with established liver disease.

26 tion, and fibrosis in animal models of fatty liver disease.

27 herapeutic target for the treatment of fatty liver disease.

28 etes can be attributed to nonalcoholic fatty liver disease.

29 Its malfunction is associated with severe liver disease.

30 are available in patients with more advanced liver disease.

31 splant survival due to recurrent HCV-related liver disease.

32 vertaken by patients with nonalcoholic fatty liver disease.

33 ation is impaired-a feature of human chronic liver disease.

34 ng kidney failure in patients with end-stage liver disease.

35 ing the inflammatory response during chronic liver disease.

36 cause of morbidity and mortality in chronic liver disease.

37 tential role for Vpr in HIV-associated fatty liver disease.

38 potential therapeutic approach in polycystic liver disease.

39 n pediatric patients with nonalcoholic fatty liver disease.

40 is (AH) is the most severe form of alcoholic liver disease.

41 ve therapy for this and other forms of human liver disease.

42 liver and kidney transplants, and end-stage liver disease.

43 results were reported in nonalcoholic fatty liver disease.

44 isorders, including obesity and nonalcoholic liver disease.

45 % reduction in the risk for mortality due to liver diseases.

46 and fibrosis in the early stages of chronic liver diseases.

47 tal for effective diagnosis and treatment of liver diseases.

48 eutic strategies for patients with end-stage liver diseases.

49 ment and persistence of chronic inflammatory liver diseases.

50 opment of hepatocellular carcinoma and other liver diseases.

51 cated in the pathogenesis of immune-mediated liver diseases.

52 ke of magnesium and risk of mortality due to liver diseases.

53 such as rheumatoid arthritis, diabetes, and liver diseases.

54 for therapeutic intervention of inflammatory liver diseases.

55 arkers for the progression of HBV-associated liver diseases.

56 epatitis B virus (HBV), NAFLD, and alcoholic liver diseases; (2) performance of specific VCTE-defined

57 rly non-AIDS infections (10.8, 9.8-12.0) and liver disease (3.7, 3.3-4.2).

58 trophy, and present with non-alcoholic fatty liver disease; 3) DKO mice demonstrate HF diet-induced e

59 ses of alcohol-related deaths were alcoholic liver disease (65.1%), fibrosis and cirrhosis of the liv

60 P = 2.35 x 10(-6) ), and nonalcoholic fatty liver disease activity score (r = 0.48, P = 4.69 x 10(-6

61 may promote the earliest stage of alcoholic liver disease, alcoholic steatosis.

62 ssive alcohol consumption leads to alcoholic liver disease (ALD) characterized by steatosis, inflamma

63 -lipoxygenase (ALOX15) in treating alcoholic liver disease (ALD).

64 th acute hepatitis associated with alcoholic liver disease (ALD).

65 been implicated in the development of fatty liver disease, although its role in biliary hyperplasia

66 (Foxp3+) T cells were evident in both human liver disease and a mouse model of chemically induced li

67 On day 28, mice with ethanol-induced liver disease and advanced fibrosis, and controls, were

68 apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF re

69 h and inflammation play an important role in liver disease and cancer.

70 ted health issues such as nonalcoholic fatty liver disease and cardiovascular disorders are known to

71 elatives of patients with nonalcoholic fatty liver disease and cirrhosis (NAFLD-cirrhosis) is unknown

72 deaths (primarily drug poisonings), chronic liver disease and cirrhosis, and suicide.

73 ver disease, particularly nonalcoholic fatty liver disease and cirrhosis, and this was true even amon

74 tent cellular immune responses contribute to liver disease and control of viral replication in HDV in

75 omplete protection from development of fatty liver disease and glucose dysmetabolism.

76 erlap with biomarkers of non-alcoholic fatty liver disease and its progression to steatohepatosis and

77 acity increases risk for non-alcoholic fatty liver disease and liver-related disease mortality, but m

78 long with an aging population, NAFLD-related liver disease and mortality will increase in the United

79 brosis scores were associated with increased liver disease and overall mortality.

80 Both the severity of liver disease and POPH (as assessed by MELD and PVR, res

81 rved in up to 60% of patients with end-stage liver disease and portends a poor prognosis.

82 that aerobic capacity impacts progression of liver disease and suggest that these effects are mediate

83 f the endothelium in protecting from chronic liver disease and TGFbeta-mediated fibrosis remains uncl

84 iffusion parameters in patients with chronic liver disease and to compare the diagnostic accuracy of

85 clinical development for inborn and acquired liver diseases and could represent a curative treatment

86 ers are at high risk of developing end-stage liver diseases and hepatocellular carcinoma.

87 Prevalence of fatty liver diseases and iron overload was calculated (weighte

88 force study in the prevalence and therapy of liver diseases and training may impact workforce needs.

89 virus (HCV) is one of the leading causes of liver diseases and transplantation worldwide.

90 diarrhoea and one to untreated cholelithases/liver disease) and one in the gefitinib group (related t

91 hronic kidney disease, chronic lung disease, liver disease, and cancer) and all-cause mortality.

92 t were any liver disease, nonalcoholic fatty liver disease, and cirrhosis (any etiology).

93 metabolic (i.e. obesity, non-alcoholic fatty liver disease, and diabetes) and neurological diseases.

94 ature to examine the epidemiology, burden of liver disease, and elimination strategies of hepatitis B

95 changes in NAFLD-related cirrhosis, advanced liver disease, and liver-related mortality were quantifi

96 ce and diabetes mellitus, nonalcoholic fatty liver disease, and obesity.

97 nnate suckling activities, and develop fatty liver disease, arrested alveologenesis in the lung, impa

98 the aging population and nonalcoholic fatty liver disease as a leading indication for transplant.

99 setting and report the prevalence of chronic liver disease as defined by these tests.

100 ons in diagnosis, therapy, and prevention of liver diseases as well as precision medicine in hepatolo

101 ated with mortality were older age, smoking, liver disease, ascites, emergency or semiurgent repair,

102 utic potential in the treatment of alcoholic liver diseases associated with inflammation, oxidative s

103 might lead to new therapeutic strategies for liver disease-associated symptoms.

104 wing recurrence included model for end-stage liver disease at LT >23, time to recurrence, >3 recurren

105 us one of 31 (3%) patients with nonmalignant liver disease at risk for developing HCC (P < 0.0001).

106 h of intestinal Enterococcus, which promotes liver disease, based on data from mouse models and human

107 atients with hepatitis C virus (HCV)-related liver disease be treated for HCV before liver transplant

108 , which, in turn, exacerbate ethanol-induced liver disease both in mice and humans.

109 dults in the UK, is leading to an increasing liver disease burden.

110 lves in "MELD purgatory" with nonprogressive liver disease but a poor quality of life.

111 ual cytokine levels in patients with chronic liver disease, but comprehensive cytokine profiling data

112 3 (PNPLA3) is strongly associated with fatty liver disease, but the underlying mechanism remains obsc

113 Patients with compensated advanced chronic liver disease (cACLD) can safely avoid screening endosco

114 s with previous VTE, chronic kidney disease, liver disease, cancer, and thrombophilia were more likel

115 s with previous VTE, chronic kidney disease, liver disease, cancer, and thrombophilia were more likel

116 sis and add new therapeutic entry points for liver disease caused by ATZ.

117 ultiple deprivation quintile, year of death, liver disease causing death, place of death, time from i

118 with ADPKD was larger than that for serious liver disease, cerebral aneurysms, and inguinal hernias

119 Cystic fibrosis (CF) liver disease (CFLD), a leading cause of death in CF, is

120 ary outcomes were improvement in severity of liver disease (change in MELD) at 3 months and the trend

121 G-CBS treatment prevented an otherwise fatal liver disease characterized by steatosis, death of hepat

122 y biliary cholangitis (PBC) is an autoimmune liver disease characterized by the destruction of interl

123 , liver disease including nonalcoholic fatty liver disease, cirrhosis, hepatocellular carcinoma, gall

124 , congestive heart failure (CHF), or chronic liver disease (CLD) with hepatic impairment.

125 kidney injury (AKI) in patients with chronic liver disease (CLD).

126 is and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular car

127 One hundred forty-two patients with liver disease clinically considered for orthotopic liver

128 e higher risk of progression and severity of liver diseases conferred to patients carrying the I148M

129 ss data linking the intestinal microbiome to liver disease development and therapeutic efforts to mod

130 Ascites, liver disease, diabetes, obesity, and primary suture rep

131 lly those with underlying conditions such as liver diseases, diabetes and immune disorders.

132 Clinical research suggests that paediatric liver disease differs in both severity and rate of progr

133 of the most common genetic disorders and the liver disease due to the Z mutant of AAT (ATZ) is a prot

134 ellular communication in the pathogenesis of liver disease during HCV infection.

135 Liver disease elicits alterations in the intrahepatic CD

136 flammatory bowel disease, celiac disease, or liver disease, endoscopy during pregnancy was not linked

137 nts by 0.99 years in the Model for End-stage Liver Disease era and 1.71 years in the pre-Model for En

138 nd 1.71 years in the pre-Model for End-stage Liver Disease era.

139 Patients with end-stage liver disease (ESLD) often have a high symptom burden.

140 spectively) who received Model for End Stage Liver Disease exception listing for HCC from 2002 to 201

141 ilan criteria for whom a Model for End-Stage Liver Disease exception was approved were retrospectivel

142 h CLRT versus LT, stratified by the stage of liver disease, extent of cancer, and whether SLT was off

143 ecognized disease process, Fontan-associated liver disease (FALD), has emerged.

144 c capacity on susceptibility for progressive liver disease following a 16-week 'western diet' (WD) hi

145 In nonalcoholic fatty liver disease, Gal-9 is involved indirectly in the expan

146 pharmaceuticals to treat heritable metabolic liver diseases have been hampered by the lack of models.

147 f liver disease, such as non-alcoholic fatty liver disease, hazardous alcohol use, or type 2 diabetes

148 n-resistant patients with nonalcoholic fatty liver disease, hepatic mIndy expression was increased an

149 ions for liver transplantation are alcoholic liver disease, hepatocellular carcinoma, and viral hepat

150 95% CI: 1.081-3.323) and model for end stage liver disease (HR = 1.054, 95% CI: 1.020-1.090).

151 Because chronic liver diseases impose a major health burden worldwide af

152 y patients at risk of clinically significant liver disease in a general population setting and report

153 ased pathway to stratify the risk of chronic liver disease in a general population setting.

154 e (XL+), in patients with nonalcoholic fatty liver disease in a multicenter setting.

155 is sufficient to exacerbate ethanol-induced liver disease in mice.

156 ugar, mimicking a Western diet, causes fatty liver disease in mice.

157 metabolic stress-induced non-alcoholic fatty liver disease in mice.

158 are the key factors associated with advanced liver disease in nonobese patients.

159 f moderate alcohol use on cardiovascular and liver disease in patients with NAFLD.

160 little is known about the risk for incident liver disease in psoriasis (PsO), psoriatic arthritis (P

161 miR-200a are promising novel biomarkers for liver disease in the ART-treated, HIV-1-infected populat

162 in patients with higher model for end-stage liver disease in the same disease group; and lysoPC a C2

163 dations of the Lancet Standing Commission on Liver Disease in the UK, which aim to reduce the unaccep

164 itlists to evaluate changes in the burden of liver disease in the United States.

165 (NAFLD) could soon emerge as the most common liver disease in this population.

166 disease is becoming the most common chronic liver disease in Western countries, and limited therapeu

167 The manifestation of liver disease in young infants may be different than in

168 total magnesium intake and mortality due to liver diseases in the Third National Health and Nutritio

169 olonic diverticular disease, polyps, cancer, liver disease including nonalcoholic fatty liver disease

170 e were no differences in Model for End-Stage Liver Disease including serum sodium and Child Pugh Scor

171 ity was 28.0% from all causes and 0.82% with liver disease, including primary liver cancer.

172 -free DAA regimens in patients with advanced liver disease, including those with decompensated cirrho

173 replication.IMPORTANCE HCV can cause severe liver diseases, including cirrhosis and hepatocellular c

174 SG-index is a possible marker of severity of liver disease independent of body mass index.

175 inoma patients compared to healthy and other liver disease individuals.

176 Histological severity of liver disease (inflammation, ballooning, and fibrosis) w

177 Chronic liver disease is a growing problem that has substantial

178 Liver disease is a leading cause of morbidity and mortal

179 Liver disease is a major cause of non-AIDS-related death

180 Hepatitis C virus (HCV)-mediated chronic liver disease is a serious health problem around the wor

181 Polycystic liver disease is a well described manifestation of autos

182 Neonatal liver disease is an important source of morbidity in the

183 liver failure or from decompensated chronic liver disease is an increasing problem worldwide and res

184 Nonalcoholic fatty liver disease is becoming the most common chronic liver

185 Fatty liver disease is common in the United States and worldwi

186 cardiovascular disease risk is elevated and liver disease is common.

187 Liver disease is one of the main contributors to the inc

188 Nonalcoholic fatty liver disease is one of the most prevalent metabolic dis

189 of HBc in the occurrence and development of liver disease is still unclear.

190 A comprehensive set of outcome measures for liver diseases is not currently available.

191 Toxin-induced liver diseases lack effective therapies despite increase

192 ent was associated with a lower incidence of liver disease, liver-related death, and diabetes mellitu

193 ute kidney injury (AKI), model for end stage liver disease (MELD) and septic shock are the independen

194 was defined as DC if the Model for End-Stage Liver Disease (MELD) at WL was >/=15 or hepatocellular c

195 cinoma (HCC) can receive Model for End-Stage Liver Disease (MELD) exception points to increase waitli

196 whom 4,599 (27.9%) had a Model for End-Stage Liver Disease (MELD) score >/=35.

197 ents frequently attain a Model for End-Stage Liver Disease (MELD) score of 40 or higher before transp

198 The Model for End-Stage Liver Disease (MELD) score predicts higher transplant he

199 Model for End-Stage Liver Disease (MELD) score transiently worsened postanti

200 ients with cirrhosis and Model for End-Stage Liver Disease (MELD) score within 3 months of initial li

201 rns of 123 genes and the model for end-stage liver disease (MELD) scores to assign patients to groups

202 -Turcotte-Pugh (CTP) and Model for End-stage Liver Disease (MELD) scores were calculated.

203 of therapy on changes in model for end-stage liver disease (MELD) scores were derived from the SOLAR-

204 higher risk recipients (Model for End-Stage Liver Disease [MELD] score >/=35, inpatient or ventilate

205 Liver disease mortality increased by 400% in the UK betw

206 tic liver from patients with alcohol-related liver disease (n = 6).

207 lated diseases, including nonalcoholic fatty liver disease (NAFLD) and diabetes, and has received gre

208 s a likely contributor to nonalcoholic fatty liver disease (NAFLD) and insulin resistance, but the me

209 Nonalcoholic fatty liver disease (NAFLD) and resulting nonalcoholic steatoh

210 The early stages of nonalcoholic fatty liver disease (NAFLD) are characterized by the accumulat

211 nclusion of subjects with nonalcoholic fatty liver disease (NAFLD) as controls can compromise study v

212 impair renal function in non alcoholic fatty liver disease (NAFLD) by altering inflammatory signallin

213 (IHTG) content to define nonalcoholic fatty liver disease (NAFLD) by proton magnetic resonance spect

214 ive hepatitis C therapy, non-alcoholic fatty liver disease (NAFLD) could soon emerge as the most comm

215 Non-alcoholic fatty liver disease (NAFLD) has been recently identified as a

216 between periodontitis and nonalcoholic fatty liver disease (NAFLD) has been reported by experimental

217 t biomarker of CT-defined nonalcoholic fatty liver disease (NAFLD) in the offspring cohort of the Fra

218 he histologic spectrum of nonalcoholic fatty liver disease (NAFLD) includes fatty liver (NAFL) and st

219 The incidence of non-alcoholic fatty liver disease (NAFLD) increases with age.

220 Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem wor

221 BACKGROUND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is a consequence of defects in div

222 There is evidence that nonalcoholic fatty liver disease (NAFLD) is affected by gut microbiota.

223 Although nonalcoholic fatty liver disease (NAFLD) is closely linked to obesity, arou

224 XOs in the development of nonalcoholic fatty liver disease (NAFLD) is not well understood.

225 Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chroni

226 Nonalcoholic fatty liver disease (NAFLD) is widespread in adults and childr

227 opment and progression of nonalcoholic fatty liver disease (NAFLD) over time is lacking.

228 IV-infected patients with nonalcoholic fatty liver disease (NAFLD) receiving EFV plus 2 nucleoside an

229 Nonalcoholic fatty liver disease (NAFLD), a common prelude to cirrhosis and

230 is often misdiagnosed as non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NA

231 te the high prevalence of nonalcoholic fatty liver disease (NAFLD), therapeutic options and noninvasi

232 determinant of outcome in nonalcoholic fatty liver disease (NAFLD).

233 ole in the progression of nonalcoholic fatty liver disease (NAFLD).

234 e-diabetic patients with non-alcoholic fatty liver disease (NAFLD).

235 death among patients with nonalcoholic fatty liver disease (NAFLD).

236 e damage are features of non-alcoholic fatty liver disease (NAFLD).

237 ver for increased risk of nonalcoholic fatty liver disease (NAFLD).

238 p.P446L) associated with nonalcoholic fatty liver disease (NAFLD).

239 ion to the development of nonalcoholic fatty liver disease (NAFLD).

240 teatosis in patients with nonalcoholic fatty liver disease (NAFLD).

241 often found increased in nonalcoholic fatty liver disease (NAFLD); however, if this is due to increa

242 with a wide range of noncirrhotic metabolic liver diseases (NCMLD).

243 pertension, pulmonary hypertension, renal or liver disease, New York Heart Association III/IV symptom

244 Outcomes of interest were any liver disease, nonalcoholic fatty liver disease, and cir

245 valuated in patients with nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, or end-stag

246 rocedure type, age, race, smoking, diabetes, liver disease, obesity, renal failure, and malnutrition

247 n light of dampened CD8(+) T-cell responses, liver disease often manifests systemically as immunoglob

248 centages of patients with nonalcoholic fatty liver disease or ALD.

249 nisolone, independent of model for end-stage liver disease or Lille score (OR, 2.46; 95% CI, 1.41-4.3

250 is the direct cause (eg, nonalcoholic fatty liver disease) or is a significant risk factor, such as

251 or HIV infection), evidence of decompensated liver disease, or a history of hepatocellular carcinoma

252 those with HCV infection, nonalcoholic fatty liver disease, or ALD did not change between 2003 and 20

253 e Lille (P < 0.0001) and Model for End-Stage Liver Disease (P < 0.0001) scores were independent progn

254 ated with a reduced risk of mortality due to liver disease particularly among alcohol drinkers and th

255 so than RA, PsO and PsA are associated with liver disease, particularly nonalcoholic fatty liver dis

256 iew we develop the argument that cholestatic liver diseases, particularly primary biliary cholangitis

257 es, bioactive lipids implicated in alcoholic liver disease pathogenesis.

258 Dominantly inherited isolated polycystic liver disease (PCLD) consists of liver cysts that are ra

259 Polycystic liver disease (PCLD) is characterized by cystic replacem

260 nicotine may act as a mitogen in cholestatic liver disease processes, thereby facilitating malignant

261 ulcerative colitis had an increased risk of liver disease progression compared with patients with Cr

262 A liver disease progression Markov model, which used a lif

263 er fibrosis is a critical step for end-stage liver disease progression.

264 nodeficiency virus (HIV) are at high risk of liver disease progression.

265 ibute to the increasing incidence of chronic liver disease.Proton pump inhibitors (PPIs) reduce gastr

266 evised American Association for the Study of Liver Diseases recommendations is predicted to reduce ha

267 e risk of hepatocellular carcinoma (HCC) and liver-disease related death, in association with metabol

268 rized in the late 80s, its role in metabolic liver disease remains controversial.

269 nts homozygous for the Z allele, with severe liver disease requiring hepatic transplantation.

270 ensitivity, rarely, it can cause progressive liver disease requiring liver transplantation (LT).

271 00 U/L), were identified across 14 Childhood Liver Disease Research Network (ChiLDReN) centers.

272 Because liver disease results from accumulation of protoporphyri

273 , LT costs, and baseline Model for End-Stage Liver Disease score (DCC analysis only).

274 uisition of CRE post-LT, Model for End-Stage Liver Disease score greater than 32, combined transplant

275 6 +/- 11.7 years with a mean Model End-Stage Liver Disease score of 22.6 +/- 9.8.

276 The mean Model for End-Stage Liver Disease score was 14.5 +/- 4.

277 The baseline Model for End-Stage Liver Disease score was not predictive of long-term outc

278 onor Risk Index with the model for end-stage liver disease score yields an AUC-ROC of 0.764 (95% CI,

279 llected on all patients with alcohol-related liver disease since initiation of the pilot through June

280 ge D ( P < .001), higher Model for End-Stage Liver Disease Sodium scores ( P < .001), higher Child-Tu

281 Because patients with different liver disease stages have been treated with great succes

282 dies targeting patients with risk factors of liver disease, such as non-alcoholic fatty liver disease

283 ion Anxiety Stress Scales (DASS-21), (3) the Liver Disease Symptom Index-2.0 (LDSI-2.0) for testing d

284 he implementation of the model for end-stage liver disease system for liver transplantation (LT).

285 In advanced liver disease, the only option for treatment is liver tr

286 g candidate biomarker for assessing EndMT in liver disease.The transcription factor ERG is key to end

287 he viral load and prevent the progression of liver diseases, they fail to cure the viral infection.

288 lue-based approach for patients with chronic liver diseases to compare results and value of care betw

289 Liver disease was a significant predictor of overall sur

290 Incident nonalcoholic fatty liver disease was highest in patients with PsO prescribe

291 Chronic liver disease was present in 30.6% of study patients.

292 Recipients with immune-mediated liver disease were twice as likely to have no HCC on exp

293 n pneumonitis, and radioembolization-induced liver disease, which may occur despite careful pretreatm

294 y biliary cholangitis (PBC) is an autoimmune liver disease with a strong hereditary component.

295 These animals represented five different liver diseases with a varying combination and extent of

296 , 5, or 6 infection and also had compensated liver disease (with or without cirrhosis) with severe re

297 New pathways to stratify chronic liver disease, with the use of non-invasive markers of l

298 -based, patient-centered approach to chronic liver diseases within a health system.

299 llular carcinoma, is the most common chronic liver disease worldwide.

300 (NAFLD) is the most common cause of chronic liver disease worldwide.