ライフサイエンスコーパス: cholestasis

1 n Fut2(-/-)(high) mice were not explained by cholestasis.

2 tional regulation of SHP in estrogen-induced cholestasis.

3 much smaller than that shown in EE2-induced cholestasis.

4 de production, hepatic steatosis and biliary cholestasis.

5 tial for neutrophil-mediated liver injury in cholestasis.

6 t soluble vitamin malabsorption with minimal cholestasis.

7 ches for patients suffering from pruritus in cholestasis.

8 hepatic bile ducts that presents as neonatal cholestasis.

9 ruritus and discuss pruritogen candidates in cholestasis.

10 ld be discussed in MVID patients with severe cholestasis.

11 itate liver injury under conditions favoring cholestasis.

12 te formation, and hemorrhage than those with cholestasis.

13 and its downstream effectors in E17G-induced cholestasis.

14 aping of bile acid pool in a rodent model of cholestasis.

15 to treat bile acid-related diseases such as cholestasis.

16 genes in normal liver and during obstructive cholestasis.

17 ung disease, intraventricular hemorrhage, or cholestasis.

18 iver of p38alpha-deficient mice upon chronic cholestasis.

19 r IL-17A in neutrophilic inflammation during cholestasis.

20 te in the promotion of liver fibrosis during cholestasis.

21 nd are more susceptible to acute TDC-induced cholestasis.

22 ansplant surgical approaches to intrahepatic cholestasis.

23 oxins should be beneficial for patients with cholestasis.

24 c bile acid-responsive genes consistent with cholestasis.

25 Neither treatment impaired liver function or cholestasis.

26 bile flow and BS output, suggesting onset of cholestasis.

27 e contribution of TRPC5 in a murine model of cholestasis.

28 s a novel therapeutic target for pruritus of cholestasis.

29 that of Bsep, was not affected by short-term cholestasis.

30 uman liver tissue from patients with chronic cholestasis.

31 er disease progressive familial intrahepatic cholestasis.

32 malies in cholangiocytes, and this may cause cholestasis.

33 ous carriers of the [C] allele for obstetric cholestasis.

34 uld be considered in infants with idiopathic cholestasis.

35 through adaptation of renal transporters in cholestasis.

36 R in mice with intrahepatic and extrahepatic cholestasis.

37 ibute to the pathophysiology of intrahepatic cholestasis.

38 fibrin deposition in livers of patients with cholestasis.

39 ormly, result in improvement of pruritus and cholestasis.

40 al models of estrogen- and endotoxin-induced cholestasis.

41 which coincided with increased fibrosis and cholestasis.

42 le in subepithelial fibrosis observed during cholestasis.

43 in nonraft (low cholesterol) microdomains in cholestasis.

44 activity decline in 17alpha-ethinylestradiol cholestasis.

45 that inhibit the LKB1/AMPK pathway result in cholestasis.

46 hospholipid "toxic" bile causing progressive cholestasis.

47 ut promoting biliary cell paucity and lethal cholestasis.

48 lated by proliferating cholangiocytes during cholestasis.

49 ans, which is characterized by a canalicular cholestasis.

50 normalities of liver tests, including severe cholestasis.

51 accelerated liver fibrosis was attributed to cholestasis.

52 thereby regulating hepatocarcinogenesis and cholestasis.

53 is, particularly as a consequence of chronic cholestasis.

54 p2) from the canalicular membrane leading to cholestasis.

55 e, acceleration of hepatocarcinogenesis, and cholestasis.

56 ndrome (ALGS), 16 with familial intrahepatic cholestasis-1 (FIC1), 18 with bile salt export pump (BSE

57 Only 3 patients (2.1%) developed cholestasis: 1 in the MS, 1 in the MSF, and 1 in the MOS

58 onic hepatitis (14%), acute (9%) and chronic cholestasis (10%), and cholestatic hepatitis (29%).

59 t to portal veins developed mild to moderate cholestasis 2-6 weeks after IRE.

60 for transient abnormal LFTs was drug-induced cholestasis (34.1%), whereas fatty liver was the most fr

61 During PN, liver histology weighted with cholestasis (38% of patients on PN versus 0% of patients

62 icacy of nontransplant surgery for pediatric cholestasis, 58 clinically diagnosed children, including

63 modulating BSEP activity in estrogen-induced cholestasis, a novel finding that might help us to bette

64 Before the onset of cholestasis, Abcb11 KO mice have altered hepatic lipid m

65 During cholestasis, accumulation of conjugated bile acids may o

66 Cholestasis activates bile acid receptor farnesoid X rec

67 protected mice from obstructive extrahepatic cholestasis after bile duct ligation or administration o

68 tified, with 76% demonstrating resolution of cholestasis after FO therapy.

69 hosis because of PNALD who had resolution of cholestasis after treatment with FO from 2004 to 2012.

70 Interestingly, estrogen-induced cholestasis also led to increased recruitment of estroge

71 EE2 at a low dose (that does not cause cholestasis) also increased SHP (by approximately 50%) a

72 treated with FO, 86% achieved resolution of cholestasis and 14% failed therapy.

73 cause of renal dysfunction in patients with cholestasis and advanced liver disease, but the underlyi

74 n of TRPC5 contributes to the development of cholestasis and associated dyslipidemia.

75 d be reserved for situations of intercurrent cholestasis and cholangitis, not for cholestasis in end-

76 up-regulated in the livers of patients with cholestasis and correlated with levels of inflammatory m

77 that loss of VDR restricts the adaptation to cholestasis and diminishes bile duct integrity in the se

78 SOLE to a FOLE in PN-dependent children with cholestasis and dyslipidemia was associated with a drama

79 therapy but may be complicated by PN-induced cholestasis and dyslipidemia.

80 A liver biopsy demonstrated centrilobular cholestasis and focal rosetting of hepatocytes, consiste

81 cl3(-/-)Mdr2(-/-) mice developed more severe cholestasis and had increased markers of liver injury an

82 BSEP deficiency leads to severe cholestasis and hepatocellular carcinoma (HCC) in young

83 e was reduced after eHx, and associated with cholestasis and impaired liver function.

84 ritical illness does not necessarily reflect cholestasis and instead may be an adaptive response that

85 e (Mdr2(-/-)), a mouse model of inflammatory cholestasis and liver fibrosis.

86 nt between more benign and potentially fatal cholestasis and makes these patients more acutely sensit

87 ls from two unrelated families with neonatal cholestasis and mutations in NR1H4, which encodes the fa

88 as a therapeutic target for the treatment of cholestasis and nonalcoholic steatohepatitis.

89 e of NHERF-1 in the inflammatory response in cholestasis and other forms of liver injury should lead

90 Bile ducts from rats with cholestasis and patients with cholangiopathic disorders

91 Cholestasis and performance significantly improved when

92 Despite resolution of cholestasis and portal inflammation, significant liver f

93 es such as progressive familial intrahepatic cholestasis and primary sclerosing cholangitis.

94 , most children now experience resolution of cholestasis and rarely progress to end-stage liver disea

95 w that MYO5B deficiency may lead to isolated cholestasis and that MYO5B should be considered as an ad

96 Two patients developed AZA-induced cholestasis and the avMeMPN concentration was higher in

97 between patients who achieved resolution of cholestasis and those who failed therapy.

98 rin IX into heme, leading to protoporphyria, cholestasis, and bridging cirrhosis.

99 s for interleukin-13 in fibrosis, steatosis, cholestasis, and ductular reaction.

100 lier onset of jaundice (<9 months), neonatal cholestasis, and higher ALT levels.

101 D responded to FO therapy with resolution of cholestasis, and liver transplantation was rarely requir

102 reat primary biliary cirrhosis, intrahepatic cholestasis, and other cholestatic conditions.

103 This eventually leads to cholestasis, and this causes bile salt (BS)-mediated tox

104 The liver has a great capacity to adapt to cholestasis, and this may contribute to a variable sympt

105 re," "DILI," "hepatitis," "hepatotoxicity," "cholestasis," and "aminotransferase," cross-referenced w

106 with arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome containing mutations in C14or

107 Arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome is a fatal recessive disorder

108 Arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome is caused by deficiencies in

109 Arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome-associated mutations in VPS33

110 The endocrine signals that cause cholestasis are not known but 3alpha-sulfated progestero

111 , outcomes for cirrhosis after resolution of cholestasis are unknown and patients continue to be cons

112 sion of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflamma

113 4 age-appropriate subjects with intrahepatic cholestasis as diseased controls and seven normal contro

114 Adaptation to cholestasis, ascertained by expression of genes involved

115 th features of benign recurrent intrahepatic cholestasis associated with a heterozygous mutation in t

116 PSC is characterized by chronic cholestasis associated with chronic inflammation of the

117 nts still exhibited mild gradually improving cholestasis at the end of follow-up).

118 To induce chronic cholestasis, Balb/c mice were given 2 weekly intraperito

119 intermittent (benign recurrent intrahepatic cholestasis; BRIC) to progressive familial intrahepatic

120 e phosphatase (AP) is not only a signpost of cholestasis but also a surrogate marker of the severity

121 These metabolic changes precede cholestasis but may be of relevance to cholestatic disea

122 MRP3, MRP4 was also observed in ANIT-induced cholestasis but were attenuated or normalized by YCHT.

123 r disease, progressive familial intrahepatic cholestasis, but cause and effect is less clear, with ma

124 can cause progressive familial intrahepatic cholestasis, but known genes cannot account for all fami

125 quently present with asymptomatic, anicteric cholestasis, but many develop progressive biliary strict

126 erum ATX levels are specific for pruritus of cholestasis, but not pruritus of uremia, Hodgkin's disea

127 Phytosterols are elevated in neonatal cholestasis, but the relation remains controversial.

128 iver of p38alpha-deficient mice upon chronic cholestasis, but unexpectedly proliferating cell nuclear

129 ndings indicate that adult lampreys tolerate cholestasis by altering hepatic bile salt composition, w

130 Drugs induce cholestasis by diverse and still poorly understood mecha

131 We induced cholestasis by ligation of the bile duct (BDL) in either

132 IL-17A promotes hepatic inflammation during cholestasis by synergistically enhancing bile acid-induc

133 evated in the circulation and tissues during cholestasis, cause itch and analgesia by activating the

134 olic causes, including neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) especial

135 0.05); we interpreted this result to be mild cholestasis caused by the catheter.

136 e to myosin 5B (MYO5B) mutations may develop cholestasis characterized by a progressive familial intr

137 riety of complications, including steatosis, cholestasis, cirrhosis, and liver failure.

138 displayed greater numbers of HCC and severe cholestasis compared with NEMO(Deltahepa) animals.

139 Severe cholestasis decreased VRC elimination by 52%.

140 isruption of Cxcr2 shortened the duration of cholestasis, decreased the incidence of bile duct obstru

141 erwent liver transplantation for progressive cholestasis despite treatment with corticosteroids and u

142 Patients whose cholestasis does not resolve with FO may progress to end

143 er hepatic impairment of expected in chronic cholestasis downregulation of CYP7A1 and upregulation of

144 While drug-induced cholestasis due to the inhibition of the bile salt expor

145 Here we show that maternal cholestasis (due to Abcb11 deficiency) produces neonatal

146 rations parallel the portal inflammation and cholestasis during PN, thereby reinforcing their contrib

147 As chronic cholestasis evolved the binucleation rate decreased in w

148 er PH, severe hepatocyte necrosis, prolonged cholestasis, exacerbated inflammatory response, and dela

149 rum markers associated with liver damage and cholestasis, extensive bile duct proliferation, and incr

150 Necrosis, cholestasis, fatty degeneration, fibrosis, infiltrate, a

151 esults suggest that in this model of chronic cholestasis, fibrin constrains the release of bile const

152 In experimental cholestasis, FXR agonism improved ileal barrier function

153 additional progressive familial intrahepatic cholestasis gene.

154 Elucidating genetic causes of cholestasis has proved to be important in understanding

155 liary ductules, which progressively leads to cholestasis, hepatic fibrosis, cirrhosis, and eventually

156 d with RBP-J loss, a phenotype consisting of cholestasis, hepatic necrosis, and fibrosis is observed

157 unable to improve BSEP protein expression in cholestasis; however, its transport activity, assessed b

158 o the mechanisms of 17alpha-ethinylestradiol cholestasis improvement, we studied the biliary output o

159 DAM17 activity, resulting in amelioration of cholestasis in a murine model of bile duct ligation (BDL

160 that inflammation might be the cause for the cholestasis in Cic-L(-/-) mice.

161 current cholestasis and cholangitis, not for cholestasis in end-stage disease.

162 factor in the early CPZ-induced intrahepatic cholestasis in human hepatocytes.

163 alpha-naphthylisothiocyanate (ANIT)-induced cholestasis in male Wistar rats.

164 ion in the intestine protects the liver from cholestasis in mice by inducing FGF15 expression and red

165 levels of BAs and protecting the liver from cholestasis in mice.

166 We also induced cholestasis in mouse livers via common bile duct ligatio

167 Our results suggest that cholestasis in MVID patients results from (1) impairment

168 affect hepatic biliary function and lead to cholestasis in MVID patients.

169 ion and the mitotic index was very high upon cholestasis in p38alpha-deficient mice.

170 this approach might be developed to reverse cholestasis in patients.

171 Compared with wild-type mice, obstructive cholestasis in pregnant Abcg2(-/-) knockout mice induced

172 d maternal cholanemia induced by obstructive cholestasis in pregnant rats.

173 In conclusion, chronic cholestasis in PSC induces adaptive changes in expressio

174 estrogen receptor alpha) that lead to acute cholestasis in rat liver with retrieval of the canalicul

175 Chronic cholestatic liver injury induced by cholestasis in rodents is associated with hepatic fibrin

176 ligation (BDL) is a frequently used model of cholestasis in rodents.

177 r genes relevant to the adaptive response to cholestasis in tissues from non-cirrhotic (n = 24) and c

178 rn diet, whereas matched mice not exposed to cholestasis in utero did not.

179 AC inhibitor parthenolide during obstructive cholestasis in vivo promote genomic reprogramming, leadi

180 features of severe, persistent NR1H4-related cholestasis include neonatal onset with rapid progressio

181 Adaptive control of cholestasis, including bile salt homeostasis, is necessa

182 Cholestasis, including primary biliary cirrhosis (PBC) a

183 During obstructive cholestasis, increased concentrations of bile acids acti

184 together, our data indicate that EE2-induced cholestasis increases SHP and represses CYP2D6 expressio

185 ere measured in liver tissues from rats with cholestasis (induced by administration of alpha-napthyli

186 le in regulating the biliary contribution to cholestasis-induced hepatic fibrosis.

187 in mice and thus may mediate the response to cholestasis-induced human liver disease.

188 effect of KD3010 was confirmed in a model of cholestasis-induced liver injury and fibrosis using bile

189 Cholestasis induces adaptive mechanisms protecting the l

190 Obstructive cholestasis induces liver injury, postoperative complica

191 antigen was down-regulated at 12 days after cholestasis induction and the mitotic index was very hig

192 bited a 50% decrease in mean life-span after cholestasis induction.

193 Cholestasis is a clinical disorder defined as an impairm

194 Cholestasis is a common complication in liver diseases t

195 Cholestasis is a liver disorder characterized by impaire

196 Neonatal cholestasis is a potentially life-threatening condition

197 In this syndrome, it is speculated that cholestasis is caused by Claudin-1 absence, leading to i

198 Cholestasis is characterized by impairment of excretion

199 Early FO initiation once biochemical cholestasis is detected in parenteral nutrition-dependen

200 r, the role of mitochondrial shape change in cholestasis is not defined.

201 its role in the pathogenesis of drug-induced cholestasis is poorly understood.

202 d granulomatous hepatitis leading to chronic cholestasis is reported along with a review of the hepat

203 Our study demonstrates that intrahepatic cholestasis leading to hepatocyte exposure to bile acids

204 Cholestasis leads to liver cell death, fibrosis, cirrhos

205 If left untreated, cholestasis leads to liver fibrosis and cirrhosis, which

206 rized by a progressive familial intrahepatic cholestasis-like phenotype with normal serum gamma-gluta

207 ients with progressive familial intrahepatic cholestasis-like phenotype with normal serum gamma-gluta

208 In a mouse model of intrahepatic cholestasis, metformin treatment induced FXR phosphoryla

209 Liver histology showed canalicular cholestasis, mild-to-moderate fibrosis, and ultrastructu

210 Progressive familial intrahepatic cholestasis mutations were introduced into the yeast pla

211 omposition of bile have been associated with cholestasis, namely ABCB11, which encodes the bile salt

212 ent to treat enterohepatic disorders such as cholestasis, NASH, and inflammatory bowel disease.

213 Cholestasis occurred before (n = 5) or after (n = 3) ITx

214 Estrogen-induced cholestasis occurs in subjects receiving estrogen for co

215 drome is a genetic disorder characterized by cholestasis, ocular abnormalities, characteristic facial

216 Intrahepatic cholestasis of pregnancy (ICP) affects 1/140 UK pregnanc

217 pregnancy outcome in women with intrahepatic cholestasis of pregnancy (ICP) and treatment with ursode

218 Intrahepatic cholestasis of pregnancy (ICP) is a liver disease of pre

219 Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific d

220 Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific l

221 Intrahepatic cholestasis of pregnancy (ICP) is associated with advers

222 Intrahepatic cholestasis of pregnancy (ICP) is the most common liver

223 Intrahepatic cholestasis of pregnancy (ICP) is the most prevalent dis

224 Intrahepatic cholestasis of pregnancy (ICP) is the most prevalent pre

225 the skin is an early symptom of intrahepatic cholestasis of pregnancy (ICP) or due to benign pruritus

226 Intrahepatic cholestasis of pregnancy (ICP), marked by elevated mater

227 es of babies born to women with intrahepatic cholestasis of pregnancy (ICP).

228 cute and chronic complications, intrahepatic cholestasis of pregnancy [ICP]) were similar in the pati

229 primary sclerosing cholangitis, intrahepatic cholestasis of pregnancy, or hereditary pediatric choles

230 id-associated cholelithiasis or intrahepatic cholestasis of pregnancy.

231 investigated the effects of estrogen-induced cholestasis on CYP2D6 expression.

232 further investigated the effect of maternal cholestasis on the metabolism of adult offspring in the

233 ium when large bile ducts are damaged during cholestasis or by toxins.

234 icate that patients with idiopathic neonatal cholestasis or later onset of unexplained fat-soluble vi

235 replace the native CBD, with no evidence of cholestasis or occlusion of the lumen.

236 rum bilirubin, and no evidence of hepatitis, cholestasis, or haemolysis.

237 -1.2 +/- 4.6, 12 months after resolution of cholestasis (P < 0.001).

238 esterol was 3.9-fold higher in patients with cholestasis (P < 0.05 for both).

239 cadian disruption activates CAR by promoting cholestasis, peripheral clock disruption, and sympatheti

240 r has been described in progressive familial cholestasis (PFIC), and we found that similar to individ

241 ; BRIC) to progressive familial intrahepatic cholestasis (PFIC).

242 se akin to progressive familial intrahepatic cholestasis (PFIC).

243 as not been reported in patients with such a cholestasis phenotype in the absence of intestinal disea

244 imilar with respect to age, BMD, severity of cholestasis, previous fractures, and bone markers.

245 .001) weaning off PN and was correlated with cholestasis (r = 0.428), portal inflammation (r = 0.511)

246 al inflammation (r = 0.549-0.510, P < 0.05), cholestasis (r = 0.501-0.491, P = 0.048-0.053), and seru

247 se at therapy initiation than patients whose cholestasis resolved, as evidenced by lower median (IQR)

248 7.3, 21.4 wk); P = 0.02] than patients whose cholestasis resolved.

249 D may be stable rather than progressive once cholestasis resolves with FO therapy.

250 iral hepatitis, and sickle cell intrahepatic cholestasis (SCIC).

251 erating ductular epithelial cells, and lower cholestasis serum markers within 2 weeks after DDC treat

252 PS levels, evidence of hepatocyte injury and cholestasis (serum aspartate aminotransferase, alanine a

253 he p53 pathway, cAMP-mediated signaling, and cholestasis signaling.

254 eroids can reflect liver pathologies such as cholestasis, steatosis and viral hepatitis.

255 s to hepatic inflammation during obstructive cholestasis, suggesting that bile acids and IL-17A may i

256 holangitis and was diagnosed with lymphedema cholestasis syndrome (LCS).

257 sorder Arthrogryposis, Renal dysfunction and Cholestasis syndrome caused by VIPAR and VPS33B deficien

258 ts with arthrogryposis renal dysfunction and cholestasis syndrome.

259 d histological features with other causes of cholestasis, the diagnosis requires an intraoperative ch

260 er fibrosis in a mouse model of inflammatory cholestasis, therefore suggesting that GH resistance pla

261 n identified here may predispose patients to cholestasis through a delocalization process of BSEP at

262 nt in p38alpha-deficient mice during chronic cholestasis through down-regulation of both AKT and mamm

263 YP2D6-humanized transgenic (Tg-CYP2D6) mice, cholestasis triggered by administration of 17alpha-ethin

264 Progressive familial intrahepatic cholestasis type 2 (PFIC2) is a result of mutations in A

265 seases such as primary familial intrahepatic cholestasis type 2 (PFIC2).

266 olution in progressive familial intrahepatic cholestasis type 2 patients and how they relate to bile

267 ldren with progressive familial intrahepatic cholestasis type 2.

268 orders and progressive familial intrahepatic cholestasis type 2.

269 tient with progressive familial intrahepatic cholestasis type 3 (PFIC-3).

270 including progressive familial intrahepatic cholestasis type 3 (PFIC3), a rare disease that can be l

271 Progressive familial intrahepatic cholestasis type 3 is caused by biallelic variations of

272 c tool for progressive familial intrahepatic cholestasis type 3 patients.

273 ntified in progressive familial intrahepatic cholestasis type 3 patients.

274 model for progressive familial intrahepatic cholestasis type 3.

275 ence cause progressive familial intrahepatic cholestasis type 3.

276 P8B1 cause progressive familial intrahepatic cholestasis type1 in humans, which is characterized by a

277 of jaundice and liver disorders, against the cholestasis using the alpha-naphthylisothiocyanate (ANIT

278 AZA-induced cholestasis was associated with increased MeMPN concentr

279 Resolution of cholestasis was defined as sustained direct bilirubin (D

280 A mouse model of acute cholestasis was induced by common BDL technique, during

281 Cholestasis was induced in wildtype and liver-specific p

282 plasma phytosterol concentrations; however, cholestasis was rare and no difference in liver function

283 Localized dyslipidaemia, secondary to cholestasis, was investigated utilizing a selected lipid

284 ids (BAs) may contribute to kidney injury in cholestasis, we established a mouse model for detailed i

285 tecture of the interlobular bile duct during cholestasis, we used 3D confocal imaging, surface recons

286 layed regeneration, hepatocyte necrosis, and cholestasis were observed in P2X4-KO mice.

287 No cases of cholestasis were observed in the S and OS groups.

288 drug known for years to induce intrahepatic cholestasis, were investigated using the differentiated

289 xamined, including steatosis, apoptosis, and cholestasis, when exposed to nine known hepatotoxins.

290 PKA inhibition prevented E17G-induced cholestasis, whereas exchange protein activated directly

291 ients with biliary atresia or other forms of cholestasis who develop progressive disease, the postmet

292 f ligands in animal models of other forms of cholestasis will be important to set the stage for futur

293 ere significantly altered during obstructive cholestasis with differential Sumo1 recruitment to the p

294 Cholestasis with normal gamma glutamyl transferase chara

295 CV RNA of 12 000 000 IU/mL, and histological cholestasis with pericellular fibrosis.

296 ANIT feeding induced significant cholestasis with substantially increased intrahepatic re

297 Treatment of patients with cholestasis with the bile salt sequestrant, colesevelam,

298 dL (P < 0.001) 12 months after resolution of cholestasis, with a mean time to resolution of 74 days.

299 Because cholestasis worsens after ITx, indication of a combined

300 inophils, rosette formation, and canalicular cholestasis yielded an area under the receiver operating