ライフサイエンスコーパス: biliary

1 , and arterial (4% versus 12%; P = 0.19) and biliary (16% versus 17%; P = 0.94) complications were si

2 w patients post-cholecystectomy, whereas non-biliary abdominal pain persists in >40%, particularly in

3 n studies and biochemical analyses show that biliary abnormalities in Anks6-deficient livers result f

4 Both TPS and NKF have good biliary access rate in patient with difficult cannulatio

5 patients underwent TPS and NKF for difficult biliary access, respectively.

6 graft biliary duct (=1 versus >1), number of biliary anastomosis (=1 versus >1), AVG thrombosis, AVG

7 cystic catheter usage, bile leakage, type of biliary anastomosis (duct-to-duct, telescopic duct-to-du

8 and safe at resolving post liver transplant biliary anastomotic strictures.

9 and plasma cholesterol levels, and increased biliary and fecal cholesterol levels.

10 h Ghr improved plasma transaminases, reduced biliary and fibrosis markers.

11 We investigated the biliary and gallstone phenotypes in ovariectomized femal

12 ivery of incompletely digested nutrients and biliary and pancreatic secretions to the distal intestin

13 erning and dynamic morphogenesis of hepatic, biliary and pancreatic structures, invaginating from a t

14 ess of the European African-Hepato-Pancreato-Biliary Association (Mainz, Germany, May 23-26, 2017) an

15 doscopic Surgeons, Americas Hepato-Pancreato-Biliary Association, International Hepato-Pancreato-Bili

16 Association, International Hepato-Pancreato-Biliary Association, Society for Surgery of the Alimenta

17 Biliary atresia (BA) is a devastating neonatal cholangio

18 Biliary atresia (BA) is a neonatal cholestatic liver dis

19 Extrahepatic biliary atresia (BA) is a pediatric liver disease with n

20 Biliary atresia (BA) is a severe pediatric liver disease

21 (2DE) criteria to define CCM associated with biliary atresia (BA), or BA-CCM, and correlate presence

22 n = 1,562], oesophageal atresia [n = 6,303], biliary atresia [n = 3,877], diaphragmatic hernia [n = 6

23 actors that affect outcomes of patients with biliary atresia and there are no medical therapies that

24 the Kasai portoenterostomy as treatment for biliary atresia at the region's largest pediatric hepato

25 Biopsies of patients with biliary atresia demonstrated increased RhoU/Wrch1 and He

26 The reference standard was biliary atresia diagnosed at the region's pediatric hepa

27 Among mice with biliary atresia given injections of antioxidants, only N

28 were highest in group A and those <5 kg; and biliary atresia in group C (72.8%).

29 a plant toxin, biliatresone, responsible for biliary atresia in naturally-occurring animal models, th

30 Treating biliary atresia in newborns earlier can delay or prevent

31 measurements detected all known infants with biliary atresia in the study population, although the 95

32 Biliary atresia is a neonatal liver disease with extrahe

33 er, treatment typically occurs later because biliary atresia is difficult to detect during its early

34 5% CI 0.95-1.01, p = 0.19) and children with biliary atresia surviving with native liver (OR = 0.96,

35 creening identified the 7 known infants with biliary atresia with a sensitivity of 100% (95% CI, 56.1

36 duced liver injury and fibrosis in mice with biliary atresia, and increased survival times.

37 th relevance to multiple diseases, including biliary atresia, choledochal cysts and gallbladder agene

38 dren with spina bifida, oesophageal atresia, biliary atresia, diaphragmatic hernia, gastroschisis, an

39 athway of cholangiocyte injury in a model of biliary atresia, which is relevant to human BA and may s

40 the Kasai portoenterostomy for treatment of biliary atresia.

41 tabolism might be developed for treatment of biliary atresia.

42 geal varices (EV) in infants with congenital biliary atresia.

43 cutoff values were associated with low BDI: biliary bicarbonate greater than 18 mmol/L (P = 0.002),

44 ependent of alterations in bile salt output, biliary bile salt hydrophobicity, or increased activity

45 olesterol and phospholipid excretion whereas biliary bile salt output and bile salt composition remai

46 ons in company with hepatic hyposecretion of biliary bile salts, thereby inducing cholesterol-supersa

47 patobiliary function (total bile production, biliary bilirubin, and bicarbonate), and significantly l

48 ly, 281 patients, who suffered from residual biliary calculi after hepatectomy and underwnet POC from

49 to be a conventional technique for residual biliary calculi, its efficacy still needs to be improved

50 tive patients along with refractory residual biliary calculi.

51 MIR1249 expression was increased in CD133+ biliary cancer cells freshly isolated from the stem cell

52 t and whose dysregulation may play a role in biliary cancer.

53 ld be a risk factor for failure of selective biliary cannulation (SBC) and post endoscopic retrograde

54 Selective deep biliary cannulation is the first and the most important

55 Their baseline demographics, success rate of biliary cannulation, and the rate of adverse events were

56 ng roles for Hippo signaling in extrahepatic biliary carcinomas.

57 ansion of both intrahepatic and extrahepatic biliary cells, and ultimately larval lethality.

58 es show that Sox9, a marker of precursor and biliary cells, is a direct transcriptional target of TFE

59 degree of plasticity between hepatocytes and biliary cells.

60 with rapid proliferation of hepatocytes and biliary cells.

61 lid tumour (eligible tumour types were anal, biliary, cervical, endometrial, mesothelioma, neuroendoc

62 cholestatic liver diseases, such as primary biliary cholangitis (PBC) and primary sclerosing cholang

63 levels in livers from patients with primary biliary cholangitis (PBC) and primary sclerosing cholang

64 Primary biliary cholangitis (PBC) frequently recurs after liver

65 Primary biliary cholangitis (PBC) is a chronic cholestatic liver

66 Primary biliary cholangitis (PBC) is a disease of small bile duc

67 Primary biliary cholangitis (PBC) is a rare autoimmune liver dis

68 Primary biliary cholangitis (PBC) is an autoimmune cholestatic l

69 Primary biliary cholangitis (PBC) primarily targets cholangiocyt

70 The relationship between primary biliary cholangitis (PBC), a chronic cholestatic autoimm

71 clerosing cholangitis (PSC, SSC) and primary biliary cholangitis (PBC).

72 s pool are a target of therapies for primary biliary cholangitis and nonalcoholic steatohepatitis.

73 the pathogenesis and progression of primary biliary cholangitis are further clarified, specific targ

74 Up to 40% of patients with primary biliary cholangitis have an incomplete response to first

75 Primary biliary cholangitis is an autoimmune liver disease that

76 er disease and 13 patients with mild primary biliary cholangitis were included in the analysis.

77 is with IgG4-associated cholangitis, primary biliary cholangitis, and secondary cholangitides, becaus

78 ge and liver fibrosis in early-stage primary biliary cholangitis.

79 In patients with primary biliary cholangitis/cirrhosis (PBC), hepatic levels of m

80 CP inhibition actually causes an increase in biliary cholesterol and phospholipid excretion whereas b

81 lar lumen drives bile formation and promotes biliary cholesterol and phospholipid output.

82 s provides an additional level of control to biliary cholesterol and phospholipid secretion.

83 etabolic abnormalities led to an increase in biliary cholesterol concentrations in company with hepat

84 requirement in dietary lipid absorption and biliary cholesterol secretion, due to their micelle-form

85 membrane to bile salts linking to increased biliary cholesterol secretion.

86 g = 0.11 +/- 0.04, P = 4.05 x 10-3), primary biliary cirrhosis (rg = 0.13 +/- 0.05, P = 3.98 x 10-3),

87 d-stage liver disease 15-34, without primary biliary cirrhosis, and not on life support before transp

88 hepatitis, autoimmune hepatitis, and primary biliary cirrhosis.

89 64.1% fulfilled criteria for biliary colic and 74.9% underwent cholecystectomy, with

90 BS, and the difference between resolution of biliary colic and pain-free state in patients with and w

91 FD/IBS was defined by the Rome IV criteria, biliary colic by the Rome III criteria, and pain-free by

92 Biliary colic is reported by only a few patients post-ch

93 omy, 6.1% of patients fulfilled criteria for biliary colic, with no significant difference between th

94 upper quadrant pain that was interpreted as biliary colic.

95 copy of Sox9 in Jag1(+/-) livers impairs the biliary commitment of cholangiocytes and enhances the in

96 of hepatic artery thrombosis (P = 0.043) and biliary complication (P = 0.041) compared with the other

97 The biliary complications (leak and stricture) were higher i

98 urvival outcomes, without increased rates of biliary complications and early graft dysfunction compar

99 ue and to investigate their association with biliary complications and retransplantation (re-LT) free

100 a significant change in the incident-rate of biliary complications between Pre-Share 35 (n = 3018) an

101 there was no change in the incident-rate of biliary complications between the two time periods.

102 The majority of biliary complications resolved with endoscopic managemen

103 A higher incidence of biliary complications was observed in the DCD SLK group,

104 The overall rate of biliary complications was significantly higher (P = 0.00

105 , primary nonfunction, serum creatinine, and biliary complications.

106 ed by progressive development of symptomatic biliary cysts.

107 ecretin/secretin receptor signaling mediates biliary damage and liver fibrosis in early-stage primary

108 lution can prolong graft survival and reduce biliary damage.

109 d pruritus (VAS, P = .01) suggesting reduced biliary damage.

110 )/neurokinin 1 receptor (NK1R) axis triggers biliary damage/senescence and liver fibrosis in bile duc

111 Biliary decompression can reduce symptoms and improve qu

112 ) liver phenotypes with a permissive role in biliary development.

113 ne 17), a transcription factor that promotes biliary differentiation and phenotype maintenance, has b

114 0.0001), as was the presence of extrahepatic biliary disease (HR = 1.45; P = 0.01).

115 g and regeneration can be uncoupled in adult biliary disease and regeneration.

116 involving the surgical management of benign biliary disease given the emotional, physical, and finan

117 ll be essential in developing treatments for biliary disease.

118 erformed in the management of pancreatic and biliary disease.

119 tation is often required as a consequence of biliary disorders because of the lack of alternative tre

120 duct hyperplasia and is commonly observed in biliary disorders.

121 developing incisional SSI were preoperative biliary drainage (odds ratio, 3.04; 95% confidence inter

122 Preoperative biliary drainage should be performed in selected patient

123 stents have become the standard of care for biliary drainage with the aim of improving hepatic funct

124 Portoenterostomy may reestablish biliary drainage, but, despite drainage, virtually all a

125 there are no medical therapies that increase biliary drainage.

126 t, telescopic duct-to-duct), number of graft biliary duct (=1 versus >1), number of biliary anastomos

127 Hepatocellular carcinoma with biliary ductal invasion is rare and associated with a si

128 maintenance of both intra- and extrahepatic biliary ducts.

129 Biliary dysgenesis, but not larval lethality, is driven

130 an interaction of chronic immune damage with biliary epithelial cell responses and encompass complex,

131 The biliary epithelial cells (BEC), expressing TLR-4, are co

132 Here, we describe how regenerating biliary epithelial cells express Wnt-Planar Cell Polarit

133 Overexpression of PRH in primary human biliary epithelial cells is sufficient to increase cell

134 tor cells differentiate into hepatocytes and biliary epithelial cells to ensure a functional liver re

135 al deletion of Yap/Taz in hepatocytes and/or biliary epithelial cells, and measured the behavior of d

136 Hepatocytes, biliary epithelial cells, Kupffer cells, stellate cells,

137 ote the proliferation and differentiation of biliary epithelial cells.

138 antly, E2-stimulated Esr2b activity promoted biliary epithelial differentiation at the expense of hep

139 More importantly, we observed biliary epithelial hyperplasia, which is an indicator of

140 ent of PBG cells in regenerating the injured biliary epithelium and identified the signaling pathways

141 lial proliferation, micropapillary growth of biliary epithelium, focal bile duct stricture formation

142 d with damage to the barrier function of the biliary epithelium.

143 -sensitive distal nephron, distal colon, and biliary epithelium.

144 ired hepatic manganese uptake for subsequent biliary excretion has been proposed as the underlying di

145 sk of C difficile infection because of their biliary excretion into the gastrointestinal tract and di

146 Unfortunately, liver accumulation, biliary excretion, and no tumor uptake were observed on

147 n an ordinal 0-2 scale: hepatic enhancement, biliary excretion, and the signal intensity in the porta

148 egulated cholesterol transport genes for its biliary excretion, including scavenger receptor class B

149 Conclusion: Prom1 plays an important role in biliary fibrogenesis, in part through integrin-mediated

150 rom1)-expressing hepatic progenitor cells to biliary fibrogenesis.

151 GL(-/-) mice were protected from DDC-induced biliary fibrosis and inflammation with reduced serum liv

152 th improved liver enzymes, inflammation, and biliary fibrosis.

153 ated, H3K9ac, and can be targeted to prevent biliary fibrosis.

154 of progressive ductopenia, cholestasis, and biliary fibrosis.

155 n of Kat2a was protective in mouse models of biliary fibrosis.

156 ee-dimensional (3D) organoids that express a biliary genetic phenotype.

157 ), biliary pH greater than 7.48 (P = 0.019), biliary glucose less than 16 mmol/L (P = 0.013), and bil

158 Liver damage, mast cell (MC) activation, biliary H2HR, and histamine serum levels were studied.

159 rding drain management from hepato-pancreato-biliary (HPB) surgeons in the ACS-NSQIP HPB Collaborativ

160 VB/N (wild-type) and Mdr2KO mice and measure biliary hyperplasia and hepatic fibrosis by quantitative

161 We investigated Ghr's effects on biliary hyperplasia and hepatic fibrosis in Mdr2-knockou

162 ceptor (5HTR)1A/1B receptor agonists inhibit biliary hyperplasia in bile-duct ligated (BDL) rats, whe

163 ions were made for (1) use of intraoperative biliary imaging for uncertainty of anatomy or suspicion

164 ion, liver fibrosis, biliary senescence, and biliary inflammation were observed in NK1R(-/-)/Mdr2(-/-

165 of vanishing bile duct syndrome(3), subacute biliary injury and immune cholangitis.(4).

166 treatment induces a mild protection against biliary injury in the early stages of treatment, it come

167 yperplasia in vivo in the DDC-mediated mouse biliary injury model.

168 ked down (KD) in KO for 2 weeks, hepatic and biliary injury were exacerbated in comparison to KO give

169 tion and migration of PBG cells after severe biliary injury.

170 g for uncertainty of anatomy or suspicion of biliary injury; and (2) referral of patients with confir

171 a patient with hepatocellular carcinoma and biliary invasion, who had his diagnosis confirmed by his

172 20 resected pancreatic IOPNs and 3 resected biliary IOPNs using a broad RNA-based targeted sequencin

173 in PRKACA and PRKACB genes in pancreatic and biliary IOPNs, as well as in PDACs and pancreatic cyst f

174 with high output cardiac failure, and 1 with biliary ischemia.

175 c liver transplant; however, she developed a biliary leak delaying the HSCT.

176 atocyte fate, whereas loss of esr2b impaired biliary lineage commitment.

177 se gene expression signatures of hepatic and biliary lineage potential.

178 ux through the liver and thereby to decrease biliary lipid excretion.

179 Conclusion: NTCP inhibition increases biliary lipid secretion, which is independent of alterat

180 uded as a potential contributor to increased biliary lipid secretion.

181 inating the possibility that the increase in biliary lipids was derived from enhanced uptake of high-

182 CH pathway reactivation has been reported in biliary malignancies to conflicting degrees, hindering p

183 cholangiocyte organoids (COs) expressing key biliary markers and retaining functions of primary extra

184 rmation of dysplastic cell masses expressing biliary markers, suggesting roles for Hippo signaling in

185 Intrahepatic biliary mass was detected by cytokeratin-19 and F4/80 to

186 were collected, and liver damage, changes in biliary mass/senescence, and inflammation as well as liv

187 volve ~3% of cases, most frequently in liver biliary, melanoma, sarcoma, stomach, and kidney cancers.

188 d severe Mn excess and impaired systemic and biliary Mn excretion.

189 ctomy, and pathology surprisingly revealed a biliary mucinous cystadenoma.

190 Thus, a pan-genomic biliary network interaction between hosts and their bact

191 wever, the effect of this host-microorganism biliary network on the adaptive immune system remains po

192 n outcome measure was freedom from recurrent biliary obstruction (within the stent) requiring re-inte

193 system appears to be effective at relieving biliary obstruction and preventing re-intervention withi

194 et, prospective study included patients with biliary obstruction due to a malignant neoplasm treated

195 al analysis yielded the absence of recurrent biliary obstruction in 99.0% of patients at 1 month (n =

196 Freedom from symptomatic recurrent biliary obstruction requiring re-intervention was achiev

197 Of the 16 patients with symptoms of biliary obstruction, 13 had resolution of their symptoms

198 iliary stent for the palliation of malignant biliary obstruction.

199 particularly in subjects without evidence of biliary obstruction.

200 e quality of life in patients with malignant biliary obstruction.

201 luding gastrointestinal luminal obstruction; biliary obstruction; recurrent acute pancreatitis; fistu

202 nd PAO (defined as gastric, hepatic, complex biliary, or pancreatic operations other than PD) and dic

203 northern GoM had significantly higher total biliary PAH concentrations than the West Florida Shelf,

204 Conversely, biliary PAH concentrations were relatively low for most

205 The highest concentrations of biliary PAH metabolites occurred in Yellowfin Tuna (Thun

206 es, long-term-cultured microdissected hepato-biliary-pancreatic organoids develop into segregated mul

207 two consecutive days, in patients with acute biliary pancreatitis (ABP).

208 al refeeding is safe in predicted mild acute biliary pancreatitis patients, does not cause adverse ga

209 nts with a diagnosis of predicted mild acute biliary pancreatitis were divided into Group A (early or

210 uent injury during cholestasis, such as from biliary pancreatitis.

211 nzymes in patients with predicted mild acute biliary pancreatitis.

212 arbonate greater than 18 mmol/L (P = 0.002), biliary pH greater than 7.48 (P = 0.019), biliary glucos

213 sampled from 359 locations and evaluated for biliary polycyclic aromatic hydrocarbon (PAH) concentrat

214 The extraction of the intra-biliary portion of HCC resulted in complete resolution o

215 SP/NK1R/TGF-beta1/miR-31 axis in regulating biliary proliferation and liver fibrosis during cholesta

216 s and is characterized by liver fibrosis and biliary proliferation.

217 with community-acquired cholangitis without biliary prosthesis who do not need intensive care, piper

218 tes were 15% with only one patient requiring biliary reconstruction.

219 hat B cells infiltrate diseased iBA and BASM biliary remnant tissue.

220 e Ig chain DNA was performed on iBA and BASM biliary remnants and lymph nodes obtained from the Child

221 transforming growth factor-beta1 (TGF-beta1) biliary secretion.

222 This newly designed and marketed biliary SEMS system appears to be effective at relieving

223 Biliary senescence was determined by immunofluorescence

224 Decreased ductular reaction, liver fibrosis, biliary senescence, and biliary inflammation were observ

225 er motility and promoting the development of biliary sludge in the early stage of gallstone formation

226 by a genetic mutation in HES1 abolishes the biliary specification potential in culture, as seen in v

227 specifically for patients with preoperative biliary stent and/or jaundice.

228 ing of open PD patients with jaundice and/or biliary stent confirmed a decrease in all-type SSI (19%

229 ristics of a newly-designed, uncovered metal biliary stent for the palliation of malignant biliary ob

230 ad-abx amongst patients with jaundice and/or biliary stent only, regardless of wound protector use (o

231 osis, whereas other liver disease, including biliary stone disease (OR, 4.06; CI, 2.24-7.36; P < 0.00

232 define the incidence and natural history of biliary stricture caused by NP.

233 Biliary stricture developed in 108 (16%) patients.

234 Median time from NP onset to biliary stricture diagnosis was 4.2 months (IQR, 1.8-10.

235 Biliary stricture in necrotizing pancreatitis (NP) has n

236 Biliary stricture occurs frequently after necrotizing pa

237 SUMMARY/BACKGROUND DATA: Benign biliary stricture occurs secondary to bile duct injury,

238 Biliary stricture risk factors and outcomes were evaluat

239 Biliary stricture was identified on cholangiography as n

240 Operative treatment of biliary stricture was more likely in patients with infec

241 al study in patients with symptomatic benign biliary strictures (N = 187) due to various etiologies r

242 emains the high incidence of non-anastomotic biliary strictures (NAS).

243 its use in the evaluation and management of biliary strictures and stones.

244 it does not seem to prevent non-anastomotic biliary strictures in livers donated after circulatory d

245 The evaluation of biliary strictures in patients with PSC is especially ch

246 osis of cholangiocarcinoma, and treatment of biliary strictures poses a similarly significant clinica

247 w up of 542 days, 4 (18%) patients developed biliary strictures requiring re-transplantation.

248 ospital stays, rejection, and nonanastomotic biliary strictures were highest in group A with lowest s

249 No differences in non-anastomotic biliary strictures, primary nonfunction and hepatic arte

250 lammatory response of NP creates challenging biliary strictures.

251 The development of the biliary system is a complex yet poorly understood proces

252 ates with the intestine via the portal vein, biliary system, and mediators in the circulation.

253 n the normal development of the intrahepatic biliary system.

254 t and the most important step before further biliary therapy.

255 ione metabolism underlies sensitivity to the biliary toxin biliatresone and may account for the repor

256 g proof-of-concept toxicity studies with the biliary toxin, biliatresone, and the bile acid, glycoche

257 Intraductal papillary neoplasm of the biliary tract (B-IPN) is a scarcely known entity in our

258 tients and revealed findings from the liver, biliary tract and pancreas in 55% of examined patients (

259 Lifetime risk of biliary tract cancer (BTC) in primary sclerosing cholang

260 Patients were eligible for the biliary tract cancer cohort if they were aged 18 years o

261 multidisciplinary management, patients with biliary tract cancer have a poor outcome.

262 d-line systemic therapy options for advanced biliary tract cancer on the basis of advancements of our

263 47 patients were enrolled; 223 patients with biliary tract cancer resected with curative intent were

264 tumorigenesis and genetic landscape of each biliary tract cancer subtype, which facilitates precisio

265 Common genes implicated in biliary tract cancer tumorigenesis include IDH1, IDH2, F

266 , 2018, 43 patients with BRAF(V600E)-mutated biliary tract cancer were enrolled to the study and were

267 , metastatic, locally advanced, or recurrent biliary tract cancer, an Eastern Cooperative Oncology Gr

268 he advancements in molecular pathogenesis of biliary tract cancer, especially in an era of personalis

269 ctivity in patients with BRAF(V600E)-mutated biliary tract cancer, with a manageable safety profile.

270 ations should be considered in patients with biliary tract cancer.

271 pared with observation following surgery for biliary tract cancer.

272 therapy in patients with BRAF(V600E)-mutated biliary tract cancer.

273 ave been associated with chemo-resistance in biliary tract cancers (BTCs).

274 h include hepatocellular carcinoma (HCC) and biliary tract cancers (i.e., cholangiocarcinoma and gall

275 Biliary tract cancers constitute approximately 3% of gas

276 section is also the definitive treatment for biliary tract cancers, and liver transplantation can be

277 lion), esophageal disorders ($18.1 billion), biliary tract disease ($10.3 billion), abdominal pain ($

278 sclerosing cholangitis (PSC), a progressive biliary tract disease without approved medical therapy,

279 allow leakage of bile from the BS-overloaded biliary tract into blood, thereby protecting the liver f

280 ancy (in particular, cholangiocarcinoma) and biliary tract stone formation.

281 ns in the BRAF gene have been found in 5% of biliary tract tumours.

282 o evaluate the intrahepatic and extrahepatic biliary tract, and MRI also provides information about t

283 d facilitate therapeutic manipulation of the biliary tract.

284 s which begins in the liver tissue or in the biliary tracts.

285 Defects in biliary transport proteins, MDR3 in humans and Mdr2 in m

286 anisms underlying the repair of extrahepatic biliary tree (EHBT) after injury have been scarcely expl

287 arker of mesenchymal cells that surround the biliary tree but not epithelial cells of the canals of H

288 Ink injection experiments reveal impaired biliary tree formation in the periphery of P30 Jag1(+/-)

289 a myofibroblast phenotype, and surround the biliary tree in response to cholestatic injury.

290 langiocytes, the epithelial cells lining the biliary tree in the liver, express primary cilia that ca

291 Sox9 heterozygosity worsens the P30 biliary tree phenotype and impairs the partial recovery

292 Human biliary tree stem/progenitor cells (BTSC) within PBGs we

293 angiography as narrowing of the extrahepatic biliary tree to < 75% of the diameter of the unaffected

294 minal CT demonstrated a dilated intrahepatic biliary tree with left proximal intrahepatic hyperdensit

295 s a highly malignant epithelial tumor of the biliary tree with poor prognosis.

296 gressive and heterogeneous malignancy of the biliary tree.

297 mmune-mediated damage of hepatocytes and the biliary tree.

298 nflammatory obliteration of the extrahepatic biliary tree.

299 ve growth pattern with a tendency to involve biliary, vascular, and extra hepatic structures can be e

300 ly, a vitamin K transintestinal efflux and a biliary vitamin K efflux were observed, but the specific