ライフサイエンスコーパス: biliary

1 Mutations of Pkhd1 produce biliary abnormalities in mice but have not been previous

2 cate aberrant androgen receptor stimulation, biliary acid disturbances, and altered responses to gut

3 In P2X4-KO mice, post-PH biliary adaptation was impaired with a smaller increase

4 Functional assays reveal abnormal biliary anatomy and lipid handling.

5 y (NIR-C) provides real-time, radiation-free biliary anatomy enhancement.

6 Three-dimensional virtual reality (VR) biliary anatomy models can be obtained via software mani

7 otocol illustrates the multimodal imaging of biliary anatomy towards precision cholecystectomy.

8 -/-) and ABCG8 (-/-) mice displayed the same biliary and gallstone phenotypes.

9 iliary injury, with subsequent comparison of biliary and hepatocyte gene expression profiles.

10 erse cholesterol transport pathway, to which biliary and transintestinal cholesterol excretion (TICE)

11 ction, Epstein-Barr virus infection, sepsis, biliary and vascular complications, nor graft dysfunctio

12 The hepatic, biliary, and pancreatic network of stem/progenitor cell

13 Rhesus rotavirus (RRV) can also lead to biliary atresia (a neonatal human disease) in mice.

14 Biliary atresia (BA) is a fibroinflammatory obstruction

15 Biliary atresia (BA) is a neonatal obstructive cholangio

16 atal mice, rhesus rotavirus (RRV) can induce biliary atresia (BA), a disease resulting in inflammator

17 linked to naturally occurring outbreaks of a biliary atresia (BA)-like disease in livestock.

18 among the three main human cholangiopathies (biliary atresia [BA], primary biliary cholangitis [PBC],

19 Advances in treatments for biliary atresia and necrotising enterocolitis have been

20 of common bile duct (CBD) disorders, such as biliary atresia or ischemic strictures, is restricted by

21 al disorders such as oesophageal atresia and biliary atresia through clinical trials because of the r

22 e loops and are associated with extrahepatic biliary atresia, lead to a loss of membrane recognition,

23 ease, and chronic biliary disorders, such as biliary atresia, which remains the most common paediatri

24 Sox17 haploinsufficiency causes biliary atresia-like phenotypes and hepatitis in late or

25 tion in the early pathogenesis of congenital biliary atresia.

26 11 years after liver transplantation due to biliary atresia.

27 tal mice, resulting in an attenuated form of biliary atresia.

28 le-canalicular structures, forming the blood-biliary barrier.

29 y branch biliary ducts when placed above the biliary bifurcation.

30 showed normal serum liver tests, bile flow, biliary bile salt secretion, fecal bile salt loss, and e

31 y and gastrointestinal or hepato-pancreatico-biliary bleeds were the most common indications for mass

32 noma (CCA) includes a heterogeneous group of biliary cancers with poor prognosis.

33 Difficult biliary cannulation in endoscopic retrograde cholangiopa

34 CBD stone removal in patients with difficult biliary cannulation was good with an acceptable complica

35 CBD stone removal in patients with difficult biliary cannulation, and the complications associated wi

36 thus impeding HCC development, but promoting biliary cell paucity and lethal cholestasis.

37 ompensatory proliferation of hepatocytes and biliary cells in progressive models of liver disease ind

38 roliferation of hepatocytes and intrahepatic biliary cells, thus impeding HCC development, but promot

39 regeneration of functional hepatocytes from biliary cells.

40 Thirteen French Hepato-Pancreato-Biliary-centers made commitment to include all patients

41 , ECOs form tissue-like structures retaining biliary characteristics.

42 idate mechanistic aspects of a virus induced biliary cholangiopathy.

43 Primary biliary cholangitis (formerly called primary biliary cir

44 ary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) are human primary cholangiopat

45 Primary biliary cholangitis (PBC) is a chronic, progressive auto

46 Primary biliary cholangitis (PBC) is an autoimmune liver disease

47 Primary biliary cholangitis (PBC) is an autoimmune liver disease

48 ctivation is an important feature of primary biliary cholangitis (PBC) pathogenesis and other cholest

49 (AMAs), but no clinical evidence of primary biliary cholangitis (PBC), are largely unknown.

50 ) is critical to the pathogenesis of Primary Biliary Cholangitis (PBC), we have analyzed the role of

51 rongly predicts long-term outcome in primary biliary cholangitis (PBC).

52 langiopathies (biliary atresia [BA], primary biliary cholangitis [PBC], and primary sclerosing cholan

53 estatic liver diseases, particularly primary biliary cholangitis and primary sclerosing cholangitis (

54 a new view on the pathophysiology of primary biliary cholangitis and PSC in the hope that these new d

55 Up to 70% of patients with primary biliary cholangitis develop pruritus (itch) during the c

56 Many patients with primary biliary cholangitis have an inadequate response to first

57 Treatment of pruritus in primary biliary cholangitis is challenging and novel therapies a

58 e effective in only about 50%-60% of primary biliary cholangitis patients, with no effective therapy

59 c pathway; down-regulation of AE2 in primary biliary cholangitis sensitizes cholangiocytes to apoptot

60 INTERPRETATION: In patients with primary biliary cholangitis with pruritus, 14 days of ileal bile

61 transporter (IBAT), in patients with primary biliary cholangitis with pruritus.

62 he standard first-line treatment for primary biliary cholangitis, is largely ineffective for pruritus

63 to 10 numerical rating scale (NRS), primary biliary cholangitis-40 (PBC-40) itch domain score and 5-

64 nce for the treatment of pruritus in primary biliary cholangitis.

65 mmune T lymphocytes similar to human primary biliary cholangitis.

66 n biliary tree, is down-regulated in primary biliary cholangitis.

67 izes lipoprotein secretion with no effect on biliary cholesterol excretion, while forced GATA4 expres

68 in Gata4 diminish Abcg5/Abcg8 expression and biliary cholesterol excretion.

69 Bile cannulations were performed and biliary cholesterol secretion rates were assessed.

70 on, increased bile acid synthesis, decreased biliary cholesterol secretion, and the absence of gallst

71 OCA does not increase biliary cholesterol secretion, but inhibits intestinal c

72 the nonviral chronic liver diseases primary biliary cirrhosis (PBC), primary sclerosing cholangitis

73 clerosing cholangitis, and recurrent primary biliary cirrhosis in terms of the clinical entity, the s

74 Secondary biliary cirrhosis was induced in rats by bile duct ligat

75 biliary cholangitis (formerly called primary biliary cirrhosis) can progress to cirrhosis and death d

76 s, nonalcoholic steatohepatitis, and primary biliary cirrhosis.

77 ldren causes progressive fibrosis leading to biliary cirrhosis; however, its cause(s) and early patho

78 eeding reduces plasma uridine levels through biliary clearance.

79 Two serious adverse events (biliary colic and abdominal pain), occurring in the same

80 The biliary complication rate showed no significant differen

81 hepatic arterial (HA) flow (<400 mL/min) on biliary complications and graft survival after deceased

82 Incidence of biliary complications and graft survival were analyzed.

83 dence of wound infections, wound dehiscence, biliary complications and overall infection, and confers

84 ce, there was a significant reduction in the biliary complications for both grafts.

85 luded to eliminate potential contribution to biliary complications from HA thrombosis.

86 There were fewer biliary complications in era II, and there was no increa

87 No rejection, or vascular or biliary complications occurred.

88 Reduction of biliary complications, especially ITBL, is needed to imp

89 toperative days 7 and 14, graft volume, LOS, biliary complications, Model for End-Stage Liver Disease

90 e HA flow is thought to be a risk factor for biliary complications.

91 HCO3 (-) biliary output, as well as altered biliary composition with reduced adenosine triphosphate

92 The results evidenced that the biliary concentrations of the marker residues were alway

93 artite complexes with albumin and increasing biliary copper excretion.

94 d significantly attenuated endotoxin-induced biliary damage and inflammation in vivo (Cftr knockout m

95 b axis may be important in the management of biliary damage and liver fibrosis in cholangiopathies in

96 may be important in managing obesity-induced biliary damage.

97 he future to study mechanisms of hepatic and biliary development and for disease modeling and drug sc

98 BPJ is essential for liver morphogenesis and biliary development, its specific function in the differ

99 protocol closely recapitulates key stages of biliary development, starting with the differentiation o

100 ate is involved in initiating functional LPC biliary differentiation and the development of the DR, w

101 Compared with alternative protocols for biliary differentiation of hPSCs, our system does not re

102 lution were assessed: LPC proliferation, LPC biliary differentiation, and hepatic stellate cell (HSC)

103 Pericholecystic stranding was seen in 19, biliary dilatation in 12, liver infiltration in 13 and f

104 lbladder wall, cholelithiasis, infiltration, biliary dilatation, lymph nodes, complications.

105 NOD.c3c4 mice develop spontaneous autoimmune biliary disease (ABD) with anti-mitochondrial Abs, histo

106 In this study, we eliminate clinical biliary disease by backcrossing this Pkhd1 mutation onto

107 ing system-incorporating features of chronic biliary disease-again showed the strongest predictive va

108 ristic and potential mediator of progressive biliary disease.

109 n the ABCB4 gene are responsible for several biliary diseases, including progressive familial intrahe

110 ocytes is a major limitation in the study of biliary disorders and the testing of novel therapeutic a

111 sease, autoimmune liver disease, and chronic biliary disorders, such as biliary atresia, which remain

112 als who collectively had 39 partial external biliary diversions (PEBDs), 11 ileal exclusions (IEs), a

113 nage (640 events) and 12.3% for percutaneous biliary drainage (208 events) (P < .001).

114 The routine use of preoperative biliary drainage before pancreaticoduodenectomy (PD) rem

115 results support the finding that endoscopic biliary drainage for malignant biliary obstruction is a

116 cute cholangitis prior to ERC and incomplete biliary drainage, the beneficial effect of intraductal a

117 Biliary ductal cells proliferate from the portal areas o

118 stent with decreases in hepatic fibrosis and biliary ductal damage relative to the control animals, a

119 ic stent(s) inserted to the secondary branch biliary ducts for the treatment of anastomosis stricture

120 T) because they can occlude secondary branch biliary ducts when placed above the biliary bifurcation.

121 o occlusion of unrecognized secondary branch biliary ducts.

122 acterized by the destruction of interlobular biliary ductules, which progressively leads to cholestas

123 e renal insufficiency, and in the liver with biliary dysgenesis, portal tract fibrosis, and portal hy

124 lic clearance, minimize transporter-mediated biliary elimination while maintaining acceptable aqueous

125 sly injected fluorescent dyes DY-780 (hepato-biliary elimination) and DY-654(renal elimination) were

126 diated endocytosis, cellular trafficking and biliary elimination.

127 e model in which p53 deletion is targeted to biliary epithelia and CC induced using the hepatocarcino

128 rected to differentiate into hepatocytes and biliary epithelia.

129 velopment to repress YAP and TAZ in both the biliary epithelial and hepatocyte lineages.

130 hepatoblasts or hepatocytes to commit to the biliary epithelial cell (BEC) lineage.

131 Based on the thesis that apoptosis of biliary epithelial cells (BECs) is critical to the patho

132 nd other functions at the apical membrane of biliary epithelial cells (i.e., cholangiocytes).

133 s, hepatic sinusoidal endothelial cells, and biliary epithelial cells from healthy or diseased liver

134 not hepatic sinusoidal endothelial cells and biliary epithelial cells from patients with ALF, secrete

135 CLiPs can differentiate into both MHs and biliary epithelial cells that can form functional ductal

136 branched three-dimensional network lined by biliary epithelial cells, but how its branching patterns

137 ription regulator 1 (TAZ) in hepatocytes and biliary epithelial cells, thereby regulating liver cell

138 show that higher levels of YAP are found in biliary epithelial cells, while in hepatocytes YAP level

139 ly in CCA cells compared with non-neoplastic biliary epithelial cells.

140 ary network and influenced actin dynamics in biliary epithelial cells.

141 that lead to the inflammatory destruction of biliary epithelial cells.

142 is required for viral binding and entry into biliary epithelial cells.

143 xpressing the Notch agonist JAG1 resulted in biliary epithelial differentiation.

144 synthesized by hypothalamic neurons and the biliary epithelium and exerts its biological effects on

145 tological study revealed minimal hepatocyte, biliary epithelium and vascular endothelium injury durin

146 onstruct the gallbladder wall and repair the biliary epithelium following transplantation into a mous

147 iocytes during liver regeneration to restore biliary epithelium integrity.

148 liary tract, knowledge of these receptors in biliary epithelium physiology and in non-malignant chola

149 ors in physiology and physiopathology of the biliary epithelium.

150 ents are at 10-fold higher risk of recurrent biliary event while waiting for a delayed CCY compared w

151 CCY (no CCY), calculating rate of recurrent biliary events (defined as an emergency department visit

152 RCP) with stone extraction reduces recurrent biliary events compared to expectant management.

153 ry outcome measure was the rate of recurrent biliary events in the 365 days after discharge from inde

154 early CCY had an 87% lower risk of recurrent biliary events than patients with no CCY (P < .001) and

155 layed CCY had an 88% lower risk of recurrent biliary events than patients with no CCY (P < .001).

156 Early CCY reduced relative risk of recurrent biliary events within 60 days by 92%, compared with dela

157 ally reduce the risk of subsequent recurrent biliary events, patients are at 10-fold higher risk of r

158 nterventions that targeted the synthesis and biliary excretion of bile acids prevented the rise in fe

159 these findings establish a new paradigm for biliary fibrosis and represent a model to understand the

160 en)-integrin-alphaMbeta2 interaction reduces biliary fibrosis and suggests a novel putative therapeut

161 esents an attractive therapeutic strategy in biliary fibrosis.

162 duced significantly increased pancreatic and biliary fluid rich in bicarbonate.

163 ctal, lung, esophageal, and hepato-pancreato-biliary/gastric cancer.

164 To compare the diagnostic accuracy of hepato-biliary (HB) phase with gadolinium-ethoxybenzyl-diethyle

165 atocellular carcinomas (HCCs) expressing the biliary/hepatic progenitor cell marker keratin 19 (K19)

166 , P2X4 contributes to the complex control of biliary homeostasis through mechanisms involving perican

167 longed exposure to complete darkness reduces biliary hyperplasia and liver fibrosis in bile-duct-liga

168 of fatty liver disease, although its role in biliary hyperplasia is unknown.

169 Biliary hyperplasia was induced in rats via bile duct li

170 re protected against Gram-negative bacterial biliary infection (TT: 0% vs. CC/CT: 22.5%; P = 0.02).

171 te immune response by CD14 is crucial during biliary infection and stricture formation.

172 okines during bacterial infection leading to biliary inflammation and hyperplasia.

173 ed Mdr2(-/-) mice, which develop spontaneous biliary inflammation, as well as Bcl3(-/-)Mdr2(-/-) mice

174 could complement to reduce the likelihood of biliary injuries (NCT01881399).

175 dequate sepsis control and delayed repair of biliary injuries should be considered for patients prese

176 ion, inflammatory leukocyte recruitment, and biliary injury in rhesus rotavirus-induced BA.

177 nses orchestrate progression of intrahepatic biliary injury in this disease.

178 the earliest stage of biliatresone-mediated biliary injury, with subsequent comparison of biliary an

179 iver BA levels, and upon BA- or drug-induced biliary insults, these mice exhibit exacerbated cholesta

180 particular are associated with ischemic-type biliary lesions (ITBL) with subsequent impaired graft su

181 cell markers), or to transdifferentiate into biliary-like cells (which give rise to iCCA).

182 well as the nonmalignant human intrahepatic biliary line, H69.

183 R and/or ErbB2 were recently demonstrated in biliary lithiasis and primary sclerosing cholangitis, tw

184 ined in the Mdr2 -/- mouse model of advanced biliary liver fibrosis how the subcutaneously injected m

185 ptide mimetics, which cause hypoalbuminemia, biliary loss of albumin, and increased intracellular acc

186 angiocyte progenitors (CPs) expressing early biliary markers and mature CLCs displaying cholangiocyte

187 rganize into bile duct-like tubes expressing biliary markers following transplantation under the kidn

188 identify commonly dysregulated pathways and biliary markers.

189 f GnRH to normal rats increased intrahepatic biliary mass (IBDM) and hepatic fibrosis.

190 Biliary mass and cholangiocyte proliferation were evalua

191 ling may be effective for the maintenance of biliary mass during cholestatic liver diseases.

192 ted serum melatonin levels and inhibition of biliary mass, along with reduction of liver fibrosis and

193 WT HFD mice had increased biliary mass, biliary proliferation, senescence, fibrosi

194 cholangiocyte proliferation and intrahepatic biliary mass, liver damage, and inflammation, whereas bl

195 -200b inhibitor or control before evaluating biliary mass, liver fibrosis, and angiogenesis.

196 Melatonin levels, biliary mass, liver fibrosis, angiogenesis and miR-200b

197 crowded branching defect in the intrahepatic biliary network and influenced actin dynamics in biliary

198 led to reduced branching in the intrahepatic biliary network in zebrafish.

199 The intrahepatic biliary network is a highly branched three-dimensional n

200 branching morphogenesis of the intrahepatic biliary network.

201 mice, serum leptin levels increased, whereas biliary Ob-R expression decreased.

202 s short- and long-term outcomes of malignant biliary obstruction (MBO) treatment by percutaneous tran

203 sfunction in patients with some evidence for biliary obstruction (previously SOD type II, now called

204 accounted for benign and malignant causes of biliary obstruction and procedural complications.

205 Patients with biliary obstruction are at high risk to develop septic c

206 uction, Bismuth- Corlette type IV stricture, biliary obstruction caused by gallbladder cancer and whe

207 at endoscopic biliary drainage for malignant biliary obstruction is a first-line intervention.

208 , younger patients suspected of having acute biliary obstruction likely benefit from MR cholangiopanc

209 holedocholithiasis and alternative causes of biliary obstruction.

210 2015, including 823 patients with malignant biliary obstruction.

211 isk patients, including those with malignant biliary obstruction.

212 post-ERC infectious events in patients with biliary obstruction.

213 diol cholestasis improvement, we studied the biliary output of bile salts (BS) and the functional exp

214 a smaller increase in bile flow and HCO3 (-) biliary output, as well as altered biliary composition w

215 distinguish from sclerosing cholangitis and biliary/pancreatic malignancies (CA).

216 ch; colon and rectum; liver; gallbladder and biliary; pancreatic; larynx; tracheal, bronchus, and lun

217 Acute biliary pancreatitis is a sudden and severe condition in

218 stitis, choledocholithiasis, cholangitis, or biliary pancreatitis), mortality, and cost by CCY cohort

219 Acute biliary pancreatitis, caused by bile reflux into the pan

220 sease revealed positive correlations between biliary periductal fibrosis during opisthorchiasis and C

221 sion syndrome and vasoplegia, and monitoring biliary pH, rather than absolute bile production, may be

222 ocellular adenomas (HCAs) also often express biliary/progenitor markers and frequently act as precurs

223 The expression of biliary/progenitor markers by hepatocellular carcinoma (

224 on molecule; and enriched for transcripts of biliary/progenitor markers such as prominin 1, Cd44, and

225 Histamine induces biliary proliferation and fibrosis and regulates leptin

226 inhibition of MC-derived histamine decreases biliary proliferation and fibrosis.

227 SR antagonist reduced biliary proliferation and hepatic fibrosis in BDL WT and

228 Secretin stimulates biliary proliferation by down-regulation of let-7a and s

229 Inhibition of miR-200b in Mdr2(-/-) ablates biliary proliferation, liver fibrosis, and angiogenesis.

230 WT HFD mice had increased biliary mass, biliary proliferation, senescence, fibrosis, and hepatic

231 ver injury and release histamine, increasing biliary proliferation.

232 sections, liver transplantations and complex biliary reconstructive surgery.

233 Prolonged biliary reflux might be the most important risk factor o

234 ors that mediate progression of chronic acid biliary reflux to Barrett's esophagus and cancer.

235 Cumulative bile production and biliary secretion of bilirubin and bicarbonate were sign

236 the liver, but this is not due to changes in biliary secretion.

237 atic bile ducts, contribute substantially to biliary secretory functions and bile transport.

238 tamine receptor axis, ductular reaction, and biliary senescence were evaluated in patients with nonal

239 this study, hepatomegaly, cholelithiasis and biliary sludge were the most common hepatobiliary ultras

240 one (2%) person had cholelithiasis, one (2%) biliary sludge, one (2%) fatty liver and none hepatomega

241 tomegaly, 15 (30%) cholelithiasis and 3 (6%) biliary sludge.

242 eviously SOD type II, now called "Functional Biliary Sphincter Disorder - FBSD") and with idiopathic

243 iological findings of a case of extraluminal biliary stent migration into the pelvic region that caus

244 n 115 mumol/L serum bilirubin 2-5 days after biliary stenting (HR 3.274, P=0.019), distal (non-hilar)

245 actors for superficial SSI were preoperative biliary stenting (odds ratio [OR], 4.81; 95% CI, 1.25-18

246 (MBO) treatment by percutaneous transhepatic biliary stenting (PTBS) with uncovered selfexpandable me

247 Preoperative biliary stenting and coriticosteroid use increase superf

248 d risk of deep incisional SSIs, preoperative biliary stenting in patients underging PD should be used

249 Biliary stenting provides temporary relief for patients

250 In multivariate analysis, biliary stenting was confirmed as a risk factor for deep

251 Preoperative biliary stenting was confirmed as an independent risk fa

252 pic retrograde cholangiopancreatography with biliary stenting was performed.

253 rtinent to PD, particularly in patients with biliary stents.

254 Ten patients with CBD obstruction due to biliary stones were included as controls.

255 12 men, aged 51+/-11 years) with anastomotic biliary stricture after LDLT.

256 ng was favored with pretest probabilities of biliary stricture or malignancy 0%-73% for patients aged

257 transplant, 162 (21.8%) patients developed a biliary stricture, of which 88 (11.8%) exhibited intrahe

258 years was associated with increased rate of biliary strictures (hazard ratio [HR], 1.67; 95% confide

259 low less than 400 mL/min was associated with biliary strictures (HR, 1.53; 95% CI, 1.04-2.24; P = 0.0

260 le and safe for the treatment of anastomotic biliary strictures after LDLT.

261 ences in IC among centers, the importance of biliary strictures as a risk factor for graft failure, a

262 mary outcome was development of intrahepatic biliary strictures consistent with IC.

263 crease the intraoperative HA flow to prevent biliary strictures in such patients.

264 L/min were associated with increased rate of biliary strictures in younger donors (<50 years old), an

265 00 mL/min was associated with higher rate of biliary strictures in younger donors with duct-to-duct r

266 is the first-line treatment for most benign biliary strictures; it is possible that fully covered, s

267 nced gastrointestinal and hepato-pancreatico-biliary surgeons.

268 may be helpful in detecting anomalies of the biliary system.

269 y correlated with hepatic fibrosis stage and biliary taurocholate levels.

270 mic strictures, is restricted by the lack of biliary tissue from healthy donors suitable for surgical

271 receptor 6 (P = 0.004) were up-regulated in biliary tissue of PSC patients with the TT versus the CC

272 Biliary tissue, bile, and whole blood of PSC patients an

273 han from mice without AP, and were higher in biliary tissues from Mdr2(-/-) mice than from control mi

274 nts had associated extraintestinal location (biliary tract [n = 3] and lung [n = 1]).

275 inflammatory obstruction of the extrahepatic biliary tract and intrahepatic bile ducts.

276 ver fibrosis is caused by obstruction of the biliary tract and is associated with early activation of

277 represents the most common malignancy of the biliary tract and is highly lethal with less than 5% ove

278 Biliary tract cancers (BTC) comprise a group of uncommon

279 Biliary tract complications are less well recognized.

280 with ADPKD had higher rates of admission for biliary tract disease (rate ratio [RR], 2.24; 95% confid

281 antially, but ADPKD remained associated with biliary tract disease (RR, 1.19; 95% CI, 1.08 to 1.31) a

282 Absolute excess risk of biliary tract disease associated with ADPKD was larger t

283 Overall, biliary tract disease seems to be a distinct and importa

284 The ADPKD versus non-ADPKD RRs for biliary tract disease were larger for men than women (he

285 Hospitalization rates for biliary tract disease, serious liver complications, and

286 d a hypothesis that ADPKD is associated with biliary tract disease.

287 rse events (one acute coronary syndrome, one biliary tract infection, one other neoplasms, and two co

288 holangiocarcinoma (CCA), a malignancy of the biliary tract, knowledge of these receptors in biliary e

289 creased TGF-beta signaling in the kidney and biliary tract, respectively.

290 n G4 (IgG4)-related disease (IgG4-RD) of the biliary tree and pancreas is difficult to distinguish fr

291 inflammatory obstruction of the extrahepatic biliary tree in neonates.

292 f human cholangiocytes from the extrahepatic biliary tree in the form of extrahepatic cholangiocyte o

293 Human biliary tree stem/progenitor cells (hBTSCs) are being us

294 t compression or rupture of the HAA into the biliary tree with occlusion of the lumen from blood clot

295 principal bicarbonate secretor in the human biliary tree, is down-regulated in primary biliary chola

296 usion, ECOs can successfully reconstruct the biliary tree, providing proof of principle for organ reg

297 rtially thrombosed mycotic aneurysm into the biliary tree.

298 dality for the pancreas and the extrahepatic biliary tree.

299 tases from 53% to 77% and a reverse trend in biliary tumors from 24% to 9% were observed.

300 Patients with a metallic biliary Wallstent, epilepsy, or ventricular arrhythmias