ライフサイエンスコーパス: cholestatic

1 s and have impaired glucose tolerance whilst cholestatic.

2 nstream effector, was not implicated in cAMP cholestatic action.

3 Interestingly, both choleretic and cholestatic agents activate the same intracellular signa

4 Choleretic and cholestatic agents affect bile formation, in part, by al

5 its expression is induced in the liver under cholestatic and cirrhotic conditions.

6 82-96% of myofibroblasts in models of toxic, cholestatic and fatty liver disease.

7 lls (PMCs) that surround the bile duct after cholestatic and hepatocellular injury.

8 Using cholestatic and hepatotoxic models of liver injury, we c

9 l, or circadian disruption can contribute to cholestatic and inflammatory diseases, diabetes, and obe

10 patocellular type and less frequently of the cholestatic and mixed types.

11 iver injury (94% vs. 47%), which was usually cholestatic and sometimes severe.

12 and nPKCdelta may be involved in choleretic, cholestatic, and anticholestatic effects by inserting, r

13 um BS levels, otherwise markedly elevated in cholestatic animals.

14 primary biliary cholangitis (PBC), a chronic cholestatic autoimmune liver disease, and the peripheral

15 st that pruritus and hyperalgesia in chronic cholestatic BDL rats are associated with neuroinflammati

16 growth and secretin-stimulated choleresis in cholestatic bile-duct-ligated (BDL) rats by interaction

17 ing supplements typically induce a prolonged cholestatic but ultimately self-limiting liver injury th

18 y is specifically increased in patients with cholestatic, but not other forms of, systemic pruritus a

19 Moreover, severe cholestatic complications and mortality after prolonged

20 In inflammatory cholestatic conditions, loss of activity of liver AP (re

21 with Alagille syndrome, two major pediatric cholestatic conditions.

22 ROS levels, liver injury, and fibrosis under cholestatic conditions.

23 rrhosis, intrahepatic cholestasis, and other cholestatic conditions.

24 n in targeting beta-catenin globally for all cholestatic conditions.

25 is reduced in association with duct loss and cholestatic destruction of nascent buds.

26 Cholestatic disease and fulminant failure were highest i

27 understanding on the mechanisms underpinning cholestatic disease and to enable the development of eff

28 Patients with cholestatic disease exhibit pruritus and analgesia, but

29 ng cholangitis (PSC) is a rare, but serious, cholestatic disease for which, to date, no effective the

30 Patients with cholestatic disease have increased systemic concentratio

31 ecede cholestasis but may be of relevance to cholestatic disease progression because altered fatty ac

32 tes with, and is the primary determinant of, cholestatic disease severity in these patients.

33 ry sclerosing cholangitis (PSC) is a chronic cholestatic disease that leads to extensive liver fibros

34 dings were compared to children with genetic cholestatic disease, age-matched deceased donor controls

35 rs: age, African-American race, hepatitis C, cholestatic disease, body mass index >/= 35, pre-LT diab

36 IRT1 expression in livers from patients with cholestatic disease, in two experimental models of chole

37 utants, whose symptoms cover the spectrum of cholestatic disease.

38 d medicine for patients with ABCB4-dependent cholestatic disease.

39 perimental procedure that mimics obstructive cholestatic disease.

40 gut microbial changes observed during human cholestatic disease.

41 ically, recent studies have highlighted that cholestatic diseases associate with a reduction in the m

42 n of the once obscure inherited intrahepatic cholestatic diseases of the liver, which, in turn, provi

43 usly impair quality of life in patients with cholestatic diseases such as primary or secondary sclero

44 was performed in children with intrahepatic cholestatic diseases who were enrolled in the Longitudin

45 ies of disease that will be reviewed include cholestatic diseases, tumors, vascular anomalies, and ac

46 about the pathogenic mechanisms of specific cholestatic diseases, which has limited our ability to m

47 Liver cholestatic diseases, which stem from diverse etiologies

48 romising for functional PET of patients with cholestatic diseases.

49 autoimmune cholangitis and potentially other cholestatic diseases.

50 e putative role of liver AP in health and in cholestatic diseases.

51 any missense mutations linked to less severe cholestatic diseases.

52 h has led to novel therapies under study for cholestatic diseases.

53 increase our understanding of these complex cholestatic diseases.

54 nsive cells also occurred in other infantile cholestatic diseases.

55 effective supplemental therapy with UDCA for cholestatic diseases.

56 stasis of pregnancy, or hereditary pediatric cholestatic disorders and may accompany, although less f

57 Most cholestatic disorders are caused by defects in cholangio

58 Infantile cholestatic disorders arise in the context of progressiv

59 ts compared to patients with other infantile cholestatic disorders, thereby establishing a possible e

60 might help us to better understand and treat cholestatic disorders.

61 in intrahepatic bile ducts of patients with cholestatic disorders.

62 d Drug Administration-approved treatment for cholestatic disorders.

63 rosetting of hepatocytes, consistent with a cholestatic drug reaction.

64 This first-in-class study evaluated the anti-cholestatic effects and safety of seladelpar in patients

65 plasma membrane, and nPKCepsilon may mediate cholestatic effects by retrieving MRP2 from the plasma m

66 An emerging theme is that choleretic and cholestatic effects may be mediated by different isoform

67 discriminate between IAC and the more common cholestatic entities, primary (PSC) and secondary sclero

68 Elevated cholestatic enzymes on blood tests raise suspicion of th

69 % chronic, 7% acute on chronic, and 6% acute cholestatic failure.

70 sting, as well as in plasma samples from six cholestatic gene knockout mice and six age- and gender-m

71 Similarly, cholestatic granulomatous hepatitis in liver histoplasmo

72 d male with HCV genotype 1b developed severe cholestatic HCV at 6 months posttransplant with ascites,

73 saki Disease presenting with a predominantly cholestatic hepatic picture.

74 cute (9%) and chronic cholestasis (10%), and cholestatic hepatitis (29%).

75 e patients with advanced fibrosis and 9 with cholestatic hepatitis (74% men, 57% genotype 1a, 63% pre

76 hepatitis C, including those with fibrosing cholestatic hepatitis (FCH) and decompensated cirrhosis

77 All five patients with fibrosing cholestatic hepatitis achieved SVR12 (100%, 90% CI 55-10

78 Nine patients presented with cholestatic hepatitis and 12 patients presented with hep

79 (Mdr2-KO) mice spontaneously develop chronic cholestatic hepatitis and fibrosis that is eventually fo

80 inflammation-mediated HCC, develops chronic cholestatic hepatitis at an early age and HCC at an adul

81 Bile duct loss during acute cholestatic hepatitis is an ominous early indicator of p

82 type 1 HCV and advanced fibrosis (F3-4/4) or cholestatic hepatitis treated with telaprevir- or bocepr

83 P-A, CTP-B, or CTP-C cirrhosis; or fibrosing cholestatic hepatitis.

84 d in 51% with advanced fibrosis and 44% with cholestatic hepatitis.

85 d in 22% with advanced fibrosis and 33% with cholestatic hepatitis.

86 irment, and by all 6 patients with fibrosing cholestatic hepatitis.

87 hepatic impairment; and those with fibrosing cholestatic hepatitis.

88 atients with recurrent advanced fibrosis and cholestatic hepatitis.

89 me with growth failure or transient neonatal cholestatic hepatitis.

90 he most common clinical pattern was a severe cholestatic hepatitis.

91 those with advanced fibrosis (F3-F4) and/or cholestatic hepatitis.

92 Twenty-seven percent had fibrosing cholestatic hepatitis/early aggressive HCV in the graft,

93 Emergence of mixed or cholestatic hepatotoxicity caused the data monitoring co

94 t symptoms and functional outcomes; mixed or cholestatic hepatotoxicity is an identified risk.

95 upper limit of normal indicative of mixed or cholestatic hepatotoxicity, one lasting 7 months and con

96 PDH and nitrosylated HDAC2 were increased in cholestatic human and rat livers reflecting increased co

97 ere tested in cholangiocytes from normal and cholestatic human livers.

98 critical illness are divided primarily into cholestatic, hypoxic, or mixed forms.

99 Liver enzyme elevation was cholestatic in pattern; 8 (21%) had drug-related enzyme

100 Circulating Ghr is reduced in cholestatic injuries, however Ghr's role in cholestasis

101 onclusion: AREG-EGFR signaling protects from cholestatic injury and participates in the physiological

102 gical (JZL184) inhibition of MGL ameliorated cholestatic injury in DDC-fed WT mice and protected Mdr2

103 ration and prevents parenchymal damage after cholestatic injury in mice and thus may mediate the resp

104 genesis of liver fibrosis development in the cholestatic injury model, for HSC activation, and for th

105 onversely, histology of the 73 patients with cholestatic injury more often demonstrated bile plugs an

106 thoxycarbonyl-1,4-dihydrocollidine to induce cholestatic injury or were given carbon tetrachloride to

107 Cholestatic injury precedes liver fibrosis, and cholangi

108 mechanisms regulating liver repair following cholestatic injury remain largely unknown.

109 Cholestatic injury was associated with female gender and

110 e treated mice suffering from a steatotic or cholestatic injury with anti-TNF-alpha antibodies (Infli

111 or older (n = 149) were more likely to have cholestatic injury, although mortality and rate of liver

112 ular reaction, which are repair responses to cholestatic injury.

113 ticipates in the regenerative response after cholestatic injury.

114 to fibrosis in models of hepatocellular and cholestatic injury.

115 after most types of liver damage, including cholestatic injury.

116 and surround the biliary tree in response to cholestatic injury.

117 and acquired a myofibroblast phenotype after cholestatic injury; Gli1(+) PMCs were found only surroun

118 stigator-initiated FITCH trial (Fibrates for cholestatic ITCH) was to assess effects of bezafibrate o

119 PRX4 is a promising strategy for alleviating cholestatic itch.

120 pon acute injection of BAs and in a model of cholestatic itch.

121 The most common causes of cholestatic jaundice are biliary atresia and idiopathic

122 uld be aware that ajmaline may induce severe cholestatic jaundice even after a single dose administra

123 is preceded by hepatic complications such as cholestatic jaundice or hepatomegaly.

124 NICCD and non-NICCD, infants with idiopathic cholestatic jaundice or INH were enrolled.

125 opsy-proven disseminated histoplasmosis with cholestatic jaundice to highlight histoplasmosis involve

126 hree weeks later, he presented with painless cholestatic jaundice which peaked in severity at eleven

127 r unresponsive to antibiotics and related to cholestatic jaundice, oedema or erythema of the extremit

128 <16.3) but there were no clinical signs of cholestatic jaundice, pruritis, or liver dysfunction.

129 xplore the role of MGL in the development of cholestatic liver and bile duct injury in mouse models o

130 hondrial antibody-positive titer >/=1 in 40, cholestatic liver blood tests, diagnostic or compatible

131 eactive oxygen species that might exacerbate cholestatic liver damage.

132 SIRT1 is essential to protect the liver from cholestatic liver damage.

133 tion, PCN risk was higher in recipients with cholestatic liver disease (SIR 2.78); five of these case

134 ur cohort of 28 MVID patients, 8 developed a cholestatic liver disease akin to progressive familial i

135 -alcoholic steatohepatitis, viral hepatitis, cholestatic liver disease and autoimmune liver diseases.

136 or future pharmacological strategies against cholestatic liver disease and cancer.

137 ing evidence supports an association between cholestatic liver disease and changes in the composition

138 e composition with important applications in cholestatic liver disease and gallstone disease, two ser

139 ry sclerosing cholangitis (PSC) is a chronic cholestatic liver disease and one of the most common ind

140 type 3 (PFIC3), an inherited juvenile-onset, cholestatic liver disease caused by homozygous mutation

141 Primary sclerosing cholangitis (PSC) is a cholestatic liver disease characterised by chronic infla

142 Primary biliary cirrhosis is a chronic cholestatic liver disease characterised by destruction o

143 y the ABCB11 gene, causes severe progressive cholestatic liver disease from early infancy.

144 centers with either autoimmune hepatitis or cholestatic liver disease had significantly lower risks

145 arbonyl-1,4-dihydrocollidine diet, to induce cholestatic liver disease in germ-free mice and germ-fre

146 sm contribute to the pathogenesis of chronic cholestatic liver disease in mice.

147 ibute to the pathogenesis and progression of cholestatic liver disease in mice.

148 totic receptor whose contribution to chronic cholestatic liver disease is unclear.

149 y biliary cholangitis (PBC) is an autoimmune cholestatic liver disease linked to symptoms including f

150 ta support the hypothesis that patients with cholestatic liver disease might benefit from UDCA with r

151 with primary biliary cirrhosis, an important cholestatic liver disease of adults.

152 ic bile duct development and their effect on cholestatic liver disease phenotypes.

153 urthermore, nicotine may act as a mitogen in cholestatic liver disease processes, thereby facilitatin

154 1950s as a clinical syndrome of progressive cholestatic liver disease resulting from chronic inflamm

155 Biliary atresia (BA) is a neonatal cholestatic liver disease that is the leading cause of p

156 We used a mouse model of cholestatic liver disease to investigate mechanisms of i

157 dents is often studied as an animal model of cholestatic liver disease, characterized by obstruction

158 diseases, including end-stage renal disease, cholestatic liver disease, endocrine/metabolic diseases,

159 UDCA, a bile acid used in the treatment of cholestatic liver disease, has anti-inflammatory and cyt

160 alidity of risk stratification in autoimmune cholestatic liver disease, highlighting strengths and we

161 ineural hearing loss, nystagmus, progressive cholestatic liver disease, pancreatic insufficiency, hyp

162 During cholestatic liver disease, there is dysregulation in the

163 eficiency of Mdr2 that progressively develop cholestatic liver disease, we investigated the contribut

164 ted here suggest that PHB1 is also linked to cholestatic liver disease.

165 which is frequently used in the treatment of cholestatic liver disease.

166 neficial use of fenofibrate therapy in human cholestatic liver disease.

167 therapeutic medications used in treatment of cholestatic liver disease.

168 the autoantibody production associated with cholestatic liver disease.

169 itochondrial morphology has been observed in cholestatic liver disease.

170 tight-junction structure, leading to severe cholestatic liver disease.

171 ochondrial morphology to the pathogenesis of cholestatic liver disease.

172 , MDR3 is a potential therapeutic target for cholestatic liver disease.

173 d (TUDC), is a mainstay for the treatment of cholestatic liver disease.

174 ndings from genetic studies of patients with cholestatic liver disease.

175 ave limited therapeutic benefits in treating cholestatic liver disease.

176 to be studied as potential therapeutics for cholestatic liver disease.

177 Primary sclerosing cholangitis is a chronic cholestatic liver disease.

178 NHW in cases of hepatocellular carcinoma or cholestatic liver disease.

179 imary biliary cholangitis (PBC) is a chronic cholestatic liver disease.

180 ificant causes of morbidity in children with cholestatic liver disease.

181 eptor (FXR); we here investigate its role in cholestatic liver disease.

182 ocrine phenotypes of cholangiocytes in human cholestatic liver diseases (ie, cholangiopathies) that a

183 langiocytes occurs during the progression of cholestatic liver diseases and is critical for the maint

184 Cholestatic liver diseases are caused by a range of hepa

185 Human chronic cholestatic liver diseases are characterized by cholangi

186 ymptom commonly experienced by patients with cholestatic liver diseases such as primary biliary chola

187 ruritus is a common symptom in patients with cholestatic liver diseases such as primary biliary cirrh

188 but is believed to play an important role in cholestatic liver diseases such as primary familial intr

189 peutic indications in constipation, dry eye, cholestatic liver diseases, and inflammatory lung disord

190 ression of many of these genes is altered in cholestatic liver diseases, but few have been extensivel

191 In cholestatic liver diseases, ductular reactive (DR) cells

192 During the course of cholestatic liver diseases, mitotically dormant cholangi

193 In this review we develop the argument that cholestatic liver diseases, particularly primary biliary

194 Chronic cholestatic liver diseases, such as primary biliary chol

195 cholangitis (PSC) are infrequent autoimmune cholestatic liver diseases, that disproportionate to the

196 e the leading extrahepatic manifestations of cholestatic liver diseases, the mechanism underlying thi

197 ial targets for pharmacological therapies of cholestatic liver diseases.

198 gies targeting BA transport and signaling in cholestatic liver diseases.

199 ary cholangitis (PBC) pathogenesis and other cholestatic liver diseases.

200 aling may be important for the management of cholestatic liver diseases.

201 rters and are natural targets for therapy of cholestatic liver diseases.

202 itus and painless jaundice that occur during cholestatic liver diseases.

203 r (FXR) and its potential therapeutic use in cholestatic liver diseases.

204 e for the maintenance of biliary mass during cholestatic liver diseases.

205 ry sclerosing cholangitis (PSC) is a chronic cholestatic liver disorder characterized by inflammation

206 and therapy, such as fenofibrate, in various cholestatic liver disorders.

207 y gastrointestinal diseases, including human cholestatic liver disorders.

208 and Mdr2 in mice, can lead to a spectrum of cholestatic liver disorders.

209 eriously disabling symptom accompanying many cholestatic liver disorders.

210 Cholestatic liver dysfunction (CLD) and biliary sludge o

211 s acute, chronic, acute-on-chronic, or acute cholestatic liver failure.

212 Liver specimens from patients with cholestatic liver fibrosis had increased numbers of MSLN

213 In addition, cholestatic liver fibrosis induced by BDL, as determined

214 RA treatment in mice with existing cholestatic liver fibrosis inhibits HSC activation and p

215 Cholestatic liver fibrosis is caused by obstruction of t

216 ike inhibitor of differentiation 1 (EID1) in cholestatic liver fibrosis.

217 e, enteric TNFRI is an important mediator of cholestatic liver fibrosis.

218 ere given injections of CCl(4) to induce non-cholestatic liver fibrosis.

219 YLD from LPCs protects mice from DDC-induced cholestatic liver fibrosis.

220 enteral nutrition (PN)-dependent may develop cholestatic liver injury and cirrhosis (PN-associated li

221 intestinal FXR dysfunction in a rat model of cholestatic liver injury and evaluated effects of obetic

222 ynthesis, thus preventing the development of cholestatic liver injury and fibrosis after bile duct li

223 Cholestatic liver injury and fibrosis were assessed by s

224 stigate the relevance of Fra-1 expression in cholestatic liver injury and fibrosis.

225 le of the RBP, human antigen R (HuR), during cholestatic liver injury and hepatic stellate cell (HSC)

226 the EGFR ligand, amphiregulin (AREG), during cholestatic liver injury and regulation of AREG expressi

227 ponents of the fibrinolytic pathway modulate cholestatic liver injury by regulating activation of hep

228 3, with juvenile mice developing progressive cholestatic liver injury due to impaired biliary phospha

229 SRT1720 administration alleviates cholestatic liver injury in mice by increasing hydrophil

230 Chronic cholestatic liver injury induced by cholestasis in roden

231 esses the hepatoprotective potential against cholestatic liver injury induced by hepatotoxin such as

232 The effect of serotonin on cholestatic liver injury is not known.

233 This transcriptional response to cholestatic liver injury likely promotes partial de-diff

234 iethoxycarbonyl-1,4-dihydrocollidine-feeding cholestatic liver injury model.

235 PHB1 is an important mediator of cholestatic liver injury that regulates the activity of

236 Moreover, murine models of fibrotic and cholestatic liver injury were used to demonstrate that t

237 In two murine models of cholestatic liver injury, bile duct ligation (BDL) and a

238 (-/-) mice), a model of inflammation-induced cholestatic liver injury, fibrosis, and cancer.

239 We have combined a mouse model of acute cholestatic liver injury, partial bile duct ligation (pB

240 the key role of Gal3 in the pathogenesis of cholestatic liver injury, we generated dnTGF-betaRII/gal

241 ronic intestinal failure (CIF) often develop cholestatic liver injury, which may lead to liver failur

242 1 could be potentially targeted to alleviate cholestatic liver injury.

243 L SR(-/-) mice, or Mdr2(-/-) mouse models of cholestatic liver injury.

244 irt1 presents a novel therapeutic target for cholestatic liver injury.

245 romised Sirt1 expression in rodent models of cholestatic liver injury.

246 ectin-3 regulates inflammasome activation in cholestatic liver injury.

247 w summarizes present Kupffer cell studies in cholestatic liver injury.

248 potentially serve as an indicator of chronic cholestatic liver injury.

249 s and partial deficiencies in MDR3 result in cholestatic liver injury.

250 on is an effective strategy for ameliorating cholestatic liver injury.

251 otein 2 (MIP-2), which, in turn, exacerbates cholestatic liver injury.

252 ed whether serotonin affects the severity of cholestatic liver injury.

253 of canalicular bile acid secretion leads to cholestatic liver injury.

254 ine bile duct ligation (BDL) model to induce cholestatic liver injury.

255 ism and energy balance, but excess BAs cause cholestatic liver injury.

256 TRAIL receptor signaling in a mouse model of cholestatic liver injury.

257 nd promoting sickness behaviors in mice with cholestatic liver injury.

258 that lipid metabolism contributed to chronic cholestatic liver injury; crossing peroxisome proliferat

259 d whether elevated microRNA-210 (miR-210) in cholestatic liver promotes BA-induced pathology by inhib

260 leading to increased endotoxin flux into the cholestatic liver.

261 not produce FGF19, nonparenchymal cells from cholestatic livers produce FGF19.

262 n was tested in cholangiocytes of normal and cholestatic livers.

263 iologically regulated by SHP but elevated in cholestatic mice and patients with PBC, promoting BA-ind

264 regulated and BA homeostasis is disrupted in cholestatic mice, but the underlying mechanisms are uncl

265 kout mice, as well as in myrcludex B-treated cholestatic mice, whereas plasma FGF19 was not induced i

266 -regulation of ATP11C protein in livers from cholestatic mice, which coincided with reduced OATP1B2 l

267 cluding 19 hepatocellular injury (HC) and 16 cholestatic/mixed injury (CS)] and AIH (n = 28) were eva

268 er disease, ischemia/reperfusion injury, and cholestatic models of liver disease.

269 role of 5HTR2A/2B/2C agonists/antagonists in cholestatic models.

270 Females from cholestatic mothers developed a severe obese, diabetic p

271 miR-210 levels were elevated in cholestatic mouse models, and in vivo silencing of miR-2

272 b treatment, at least in these steatotic and cholestatic mouse models, is the safer approach since it

273 nalysis, cotrimoxazole was associated with a cholestatic or ductopenic injury (OR = 7.05 [2.50-19.89]

274 er injury can present with a hepatocellular, cholestatic or mixed pattern of disease.

275 After UDCA removal cholestatic parameters, taurine species of cholic acid a

276 iary insults, these mice exhibit exacerbated cholestatic pathologies.

277 Numerous pruritogens are up-regulated in cholestatic patient sera, including bile acids (BAs).

278 ong-sought pruritogenic signaling cascade in cholestatic patients suffering from itch.

279 provide evidence for renal tubular injury in cholestatic patients with cholemic nephropathy.

280 at SIRT1 was highly expressed in livers from cholestatic patients, mice after BDL, and Mdr2 knockout

281 ption lower the BS load and are best used in cholestatic patients.

282 A cholestatic pattern was found in 60.0% of patients and w

283 Our data demonstrate that the cholestatic potential of certain drugs may be aggravated

284 elieve this is the first report showing that cholestatic pregnancy in the absence of altered maternal

285 ased transplacental cholesterol transport in cholestatic pregnancy.

286 ocesses, including vasculogenesis, fibrosis, cholestatic pruritus and tumour progression.

287 s, including cancer, fibrosis, inflammation, cholestatic pruritus, and pain.

288 enesis, neuropathic pain, fibrotic diseases, cholestatic pruritus, lymphocyte homing, and thrombotic

289 ve and mechanistic research in patients with cholestatic pruritus.

290 s TRPA1, might be developed for treatment of cholestatic pruritus.

291 rvating the skin is thought to contribute to cholestatic pruritus.

292 atidic acid (LPA), as potential mediators of cholestatic pruritus.

293 PDH nitrosylation was assessed in normal and cholestatic rat and human livers.

294 he liver of 17alpha-ethinylestradiol-induced cholestatic rats improves bile flow, in part by enhancin

295 AdhAQP1-transduced cholestatic rats increased the biliary output of major e

296 In AdhAQP1-transduced cholestatic rats, BSEP showed a canalicular microdomain

297 a, 30% METAVIR F3-F4, 4% decompensation, 11% cholestatic recurrence, 7% had kidney transplant, and 82

298 Recent studies have identified a cholestatic variant of nonalcoholic fatty liver disease

299 Adult livers were severely cholestatic, with levels of bile salts >1 mM, but no evi

300 iver enzymes were significantly increased in cholestatic WT mice and significantly blunted in TRPC5 K