ライフサイエンスコーパス: bile duct

1 uld be used for prompt identification of the bile duct.

2 al (25 of 28 [89%] vs 24 of 28 [86%]) common bile duct.

3 ned, with its distal end being placed in the bile duct.

4 e characteristics of precancerous lesions of bile duct.

5 om tumors arising in the pancreas and distal bile duct.

6 malign lesions in intraluminal extrahepatic bile ducts.

7 nized in a cellular network encircling large bile ducts.

8 DHOPE is associated with reduced IRI of the bile ducts.

9 extrahepatic biliary tract and intrahepatic bile ducts.

10 first and early lesions are in "downstream" bile ducts.

11 shunting may allow improved targeting to the bile ducts.

12 d fibrosis of the intra- and/or extrahepatic bile ducts.

13 nd monocytes were found to be located around bile ducts.

14 od, hepatocytes, and intra- and extrahepatic bile ducts.

15 nd monocytes were found to be located around bile ducts.

16 s within extrahepatic and large intrahepatic bile ducts.

17 oneum and through the liver to mature in the bile ducts.

18 ed the immunopathological characteristics of bile ducts.

19 tion of the intrahepatic and/or extrahepatic bile ducts.

20 mitive myxoid stroma with cystically dilated bile ducts.

21 reatments for repairing or replacing damaged bile ducts.

22 rogated tumors), liver (73%), kidney (>70%), bile duct (57%), cervix (50%), and, to a lesser extent,

23 l Pkhd1 on the NOD background produces early bile duct abnormalities, initiating a break in tolerance

24 y mesenchymal cells (PMCs) that surround the bile duct after cholestatic and hepatocellular injury.

25 Intrahepatic bile duct anatomy is complex with many common and uncomm

26 ed dilated lymphatic vessels obstructing the bile duct and compound heterozygosity for collagen and c

27 Hepatic artery is the main blood supply to bile duct and lack of adequate HA flow is thought to be

28 The number of connections between the bile duct and the lobular bile canalicular network by th

29 COL15A1-immunoreactive cells adjacent to the bile ducts and canals of Hering in the portal area.

30 Liver-infiltrating Treg reside close to bile ducts and coculture with cholangiocytes or their su

31 obiliary system, it can be visualized in the bile ducts and may help to reveal disorders undetected b

32 by the absence of primary cilia compared to bile ducts and PBG cells in controls and patients with P

33 stem-like properties, and 2) availability of bile ducts and/or venous drainage are limiting factors f

34 ed with an inadequate arterial supply to the bile duct, and multiple arterial anastomoses may protect

35 the azygos vein, right hepatic vein, common bile duct, and superior mesenteric artery.

36 The bile duct wall enhancement, intrahepatic bile ducts, and gallbladder were also evaluated.

37 ions are present in the canalicular network, bile ducts, and gallbladder.

38 PR3 is required for bicarbonate secretion by bile ducts, and its expression is reduced in intrahepati

39 Our results demonstrate that syngeneic bile duct antigens efficiently break immune tolerance of

40 Because curvature and tortuosity of the bile duct are unaltered, this enlargement of the biliary

41 Portal vein and bile duct area index were significantly smaller in the u

42 stem developmental disorder characterized by bile duct (BD) paucity, caused primarily by haploinsuffi

43 fluid (n = 5, collected before surgery) and bile duct brushings (n = 2) were analyzed for translocat

44 well as in matched pancreatic cyst fluid and bile duct brushings.

45 parameters in the pancreatic duct and common bile duct by using a five-point scale.

46 gene loci and their ligands in patients with bile duct cancer (BDC).

47 tionship to the pathogenesis of human distal bile duct cancer (DBDC).

48 ectal, lung, ovarian, pancreatic, gastric or bile duct cancer and 245 healthy individuals.

49 Cholangiocarcinoma (CCA) is a bile duct cancer that originates in the bile duct epithe

50 range 47-88] years) with nonresectable hilar bile duct cancer were treated with T-PDT (median 1 [rang

51 hepatic cholangiocarcinoma (iCCA) is a fatal bile duct cancer with dismal prognosis and limited thera

52 g a risk factor for developing an aggressive bile duct cancer, cholangiocarcinoma, in chronically inf

53 lliation and survival in nonresectable hilar bile duct cancer.

54 Hepatocyte, fibrotic lesion, and bile duct (cancer) were classified and HCA mapping showe

55 Bile duct cannulation was successful in 23 patients (74.

56 tion for 0, 30, 60, 180, or 300 s after deep bile duct cannulation.

57 d functional assays (including ileectomy and bile duct catheterization), we identify KLF15 as the fir

58 In contrast, Yap/Taz deletion in adult bile ducts caused severe defects and delay in liver rege

59 The treatment of common bile duct (CBD) disorders, such as biliary atresia or is

60 Algorithms for diagnosis of malignant common bile duct (CBD) stenoses are complex and lack accuracy.

61 The role of common bile duct (CBD) stenting in the establishment of bile st

62 raphy (ERCP) can result in failure of common bile duct (CBD) stone removal and pancreatitis.

63 namely, the duodenum, ampulla, distal common bile duct (CBD), or head of the pancreas.

64 Bile duct cells expressed the LPS receptor, Toll-like re

65 ll as in PDACs and pancreatic cyst fluid and bile duct cells from the same patients.

66 copy to characterize periductal fibrosis and bile duct cells progressing to CCA induced by inoculatin

67 expression and also decreased sensitivity of bile duct cells to calcium agonist stimuli.

68 e of the biliary epithelium characterized by bile duct changes resembling ductal plate malformations

69 f LTB in cholangiocytes that formed reactive bile ducts compared with control liver tissues.

70 h rare, obstructive jaundice due to external bile duct compression or rupture of the HAA into the bil

71 Small and large intrahepatic bile ducts consist of small and large cholangiocytes, re

72 illary neoplasms (IOPNs) of the pancreas and bile duct contain epithelial cells with numerous, large

73 tes, that line intrahepatic and extrahepatic bile ducts, contribute substantially to biliary secretor

74 bility rates were determined in 423 positive bile duct cultures and 197 corresponding blood cultures

75 IL) and direct bilirubin (DBIL) with minimal bile duct damage in the ANIT treated rats.

76 ested by increased periportal infiltrations, bile duct damage, granulomas and fibrosis.

77 fficient to partially suppress the Jag1(+/-) bile duct defects.

78 chanistically, we showed that Yap/Taz mutant bile ducts degenerated, causing cholestasis, which stall

79 itions allowing long-term expansion of adult bile duct-derived bipotent progenitor cells from human l

80 C) is a rare progressive disorder leading to bile duct destruction; approximately 75% of patients hav

81 missense mutant of Jag1 (Jag1(Ndr)) disrupts bile duct development and recapitulates Alagille syndrom

82 agonizes Hippo signaling in the liver during bile duct development by binding to Hippo pathway effect

83 by which mutations in ciliary genes lead to bile duct developmental abnormalities is not understood.

84 atients with benign biliary strictures and a bile duct diameter 6 mm or more in whom the covered meta

85 Patients with a bile duct diameter less than 6 mm and those with an inta

86 ghts into the regulatory network controlling bile duct differentiation and morphogenesis during liver

87 Bile duct differentiation, morphogenesis, and function w

88 he number of patients diagnosed with chronic bile duct disease is increasing and in most cases these

89 Although bile duct disorders are well-recognized causes of liver

90 sional (3D) architecture of the interlobular bile duct during cholestasis, we used 3D confocal imagin

91 RNA sequencing of NOD.Abd3 common bile duct early in disease demonstrates upregulation of

92 and expressing low amounts of Sox9 and other bile-duct-enriched genes, undergo extensive proliferatio

93 gated miRNA regulation of InsP3R3 in primary bile duct epithelia (cholangiocytes) and in the H69 chol

94 er parenchyma is composed of hepatocytes and bile duct epithelial cells (BECs).

95 It is mainly found in bile duct epithelial cells, the intestinal tract, and th

96 our arising from malignant transformation of bile duct epithelial cells.

97 progenitor cells and are able to respond to bile duct epithelial loss with proliferation, differenti

98 able revealed decreased PKD1L1 expression in bile duct epithelium when compared to normal livers and

99 is a bile duct cancer that originates in the bile duct epithelium.

100 Donor common bile duct excised at implantation showed preservation of

101 Although laparoscopic common bile duct exploration (LCBDE) deals with gallstones and

102 ecystectomy (ERCP+LC) vs laparoscopic common bile duct exploration with laparoscopic cholecystectomy

103 A left hepatectomy was done and dilated bile ducts filled with caseous necrotic material were se

104 enitor cells underlies liver development and bile duct formation as well as liver regeneration and di

105 number of hepatic arteries without affecting bile duct formation.

106 Bile ducts from rats with cholestasis and patients with

107 cterised by a chronic and destructive, small bile duct, granulomatous lymphocytic cholangitis, with t

108 .019), distal (non-hilar) obstruction of the bile ducts (HR 3.711, P=0.008), Bismuth-Corlette type IV

109 DR is pathologically recognized as bile duct hyperplasia and is commonly observed in biliar

110 tric oxide synthase (iNOS), a gene linked to bile duct hyperplasia and liver fibrosis.

111 induced iNOS expression, liver fibrosis, and bile duct hyperplasia were significantly reduced in WT m

112 a-deficient mice had reduced iNOS induction, bile duct hyperplasia, and liver fibrosis.

113 e (Jag1(+/-) ) exhibit impaired intrahepatic bile duct (IHBD) development, decreased SOX9 expression,

114 Preoperative knowledge of intrahepatic bile duct (IHD) anatomy is critical for planning liver r

115 captured essential features of a simplified bile duct in structure and organ-level functions and rep

116 ies not only the tubular architecture of the bile duct in three dimensions, but also its barrier func

117 and IRE induces sufficient local heating to bile ducts in 24% of ablations.

118 Reactive bile ducts in patients with chronic liver diseases have

119 Biliary epithelial cells (BECs) form bile ducts in the liver and are facultative liver stem c

120 oderate to severe (<50% of portal areas with bile ducts) in 14 and mild (50%-75%) in 12.

121 , morphological changes were observed in the bile duct, including ductal epithelial proliferation, mi

122 aracterized by the proliferation of reactive bile ducts induced by liver injuries.

123 ly indicated in the management of iatrogenic bile duct injuries (IBDI), but occasionally, it becomes

124 on of CVS contributes to the stable rates of bile duct injuries in LC.

125 o determine the optimal timing for repair of bile duct injuries sustained during cholecystectomy.

126 Bile duct injuries were recognized intraoperatively only

127 y of bile biochemistry for the assessment of bile duct injury (BDI).

128 ost common associated complications included bile duct injury (n = 397), bowel perforation (n = 96),

129 ell Polarity signalling components following bile duct injury and promote the formation of ductular s

130 Bile duct injury during cholecystectomy is a serious com

131 in the development of cholestatic liver and bile duct injury in mouse models of sclerosing cholangit

132 ategies to block progression of intrahepatic bile duct injury in patients with BA.

133 Bile duct injury was induced by the administration of 3,

134 orrhage, 0.3%; subhepatic collections, 2.9%; bile duct injury, 0.08%; and retained stones, 3.1%); the

135 Benign biliary stricture occurs secondary to bile duct injury, anastomotic narrowing, or chronic infl

136 On multivariable analysis, bile duct injury, bowel perforation, and high clinical s

137 -17A production and ameliorated intrahepatic bile duct injury.

138 on in the portal region, without evidence of bile duct injury.

139 ect role in liver regeneration by preserving bile duct integrity and securing immune cell recruitment

140 Furthermore, dilated bile duct is the only risk factor for bile duct stone re

141 The cystic-common bile duct junction was visualized before Calot triangle

142 terised by destruction of small intrahepatic bile ducts, leading to fibrosis and potential cirrhosis

143 Whether reduced IRI of the bile ducts leads to lower incidence of NAS after DCD liv

144 decreases proportionally to the increase in bile duct length, suggesting that no novel connections a

145 In this study, cirrhotic bile duct ligated (BDL) rats with PH were treated with I

146 iary damage/senescence and liver fibrosis in bile duct ligated and Mdr2(-/-) (alias Abcb4(-/-)) mice

147 ptor agonists inhibit biliary hyperplasia in bile-duct ligated (BDL) rats, whereas 5HTR2B receptor an

148 Bile duct-ligated (BDL) and sham-treated rats were image

149 e balance between biliary growth and loss in bile duct-ligated (BDL) rats modulated by neuroendocrine

150 ts of KCa3.1 inhibition were investigated in bile duct-ligated and carbon tetrachloride intoxicated r

151 Vehicle-treated bile duct-ligated rats exhibited decreased FXR pathway e

152 es biliary hyperplasia and liver fibrosis in bile-duct-ligated (BDL) rats; however, no information ex

153 o murine models of cholestatic liver injury, bile duct ligation (BDL) and alpha-naphthyl-isothiocyana

154 In livers of mice subjected to bile duct ligation (BDL) and in cultured activated hepat

155 e 1 (ICAM-1) is induced in mouse liver after bile duct ligation (BDL) and plays a key role in neutrop

156 kout) mice (SIRT(hep-/-) ) were subjected to bile duct ligation (BDL) and were fed with a 0.1% DDC (3

157 Our results show that the bile duct ligation (BDL) experimental model of cholestas

158 Here we show that bile duct ligation (BDL) in mice leads to severe anemia

159 Bile duct ligation (BDL) is a frequently used model of c

160 Bile duct ligation (BDL) is an experimental procedure th

161 Here, using the murine bile duct ligation (BDL) model, we showed that the abund

162 Bile duct ligation (BDL) surgery in rodents is often stu

163 Biliary hyperplasia was induced in rats via bile duct ligation (BDL) surgery, and galanin was increa

164 s were performed in wild-type (WT) mice with bile duct ligation (BDL), BDL SR(-/-) mice, or Mdr2(-/-)

165 (HA) and MCs infiltrate the liver following bile duct ligation (BDL), increasing intrahepatic bile d

166 massive hepatic necrosis and mortality after bile duct ligation (BDL), whereas treatment of these mic

167 erize the detailed hemodynamics of mice with bile duct ligation (BDL)-induced liver fibrosis, by moni

168 he pathogenesis of liver fibrosis induced by bile duct ligation (BDL).

169 injected with 600 mg/kg of APAP or underwent bile duct ligation (BDL).

170 cholestatic liver injury and fibrosis after bile duct ligation (BDL).

171 l of acute cholestatic liver injury, partial bile duct ligation (pBDL), with a novel longitudinal bio

172 the cerebral cortex using rat models of HE (bile duct ligation [BDL] and induced hyperammonemia) and

173 s, rats and mice with liver fibrosis (due to bile duct ligation [BDL] or administration of carbon tet

174 s were studied 4-weeks after sham surgery or bile duct ligation and were injected with saline or LPS

175 e established by thioacetamide injection and bile duct ligation in Balb/C mice and treated with soraf

176 n-transposase complex was coupled with lobar bile duct ligation in C57BL/6 mice, followed by administ

177 th portal hypertension was established using bile duct ligation in rats.

178 In conclusion, our results support that bile duct ligation induces changes in the microbiome tha

179 In beta-Arr2-deficient mice, bile duct ligation injury (BDL) led to significantly red

180 A 4-week bile duct ligation model was used to develop cirrhosis w

181 sis and fibrosis or were subjected to either bile duct ligation or CCl(4) injury.

182 Mice underwent bile duct ligation or were fed 3,5-diethoxycarbonyl-1,4-

183 lated in three mouse models of liver injury (bile duct ligation, 1% cholic acid [CA] fed, and the Mdr

184 ers with biliary damage (Mdr2(-/-) knockout, bile duct ligation, 3,5-diethoxycarbonyl-1,4-dihydrocoll

185 jury through carbon tetrachloride treatment, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-di

186 f PDGFRalpha in murine carbon tetrachloride, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-di

187 ly impedes liver fibrosis induced by CCl(4), bile duct ligation, and more importantly NASH.

188 ary biliary cirrhosis was induced in rats by bile duct ligation, and portal hypertension was induced

189 er models of chronic liver injury, including bile duct ligation, nonalcoholic steatohepatitis, and ob

190 In the experimental model of bile duct ligation, silencing of PHB1 induced liver fibr

191 rkedly inhibited the fibrogenic phenotype in bile duct ligation- or thioacetamide-treated mice.

192 Spraque-Dawley rats with common bile duct ligation-induced cirrhosis or sham operation r

193 ocyte-selective knockout of EZH2 exacerbates bile duct ligation-induced fibrosis whereas MDR2(-/-) mi

194 mice in two separate murine models: CCl4 and bile duct ligation.

195 liver fibrosis induced by CCl4 treatment or bile duct ligation.

196 Cirrhotic (bile duct ligation/BDL; CCl4 intoxication) and non-cirrh

197 with INT-747 or vehicle during 10 days after bile-duct ligation and then were assessed for changes in

198 aneous injections of sivelestat or underwent bile-duct ligation.

199 on of mice increased significantly following bile-duct ligation.

200 d development of sickness behavior following bile-duct ligation.

201 n compared with control mice after pIVCL and bile-duct ligation; neutrophil recruitment into sinusoid

202 We performed bile-duct ligations or sham surgeries on C57BL/6 or toll

203 and demonstrate that ECOs self-organize into bile duct-like tubes expressing biliary markers followin

204 ation of YAP transcriptional activity in the bile duct-lining epithelial cells.

205 es (n = 363) were scored for the presence of bile duct loss and assessed for clinical and laboratory

206 Bile duct loss during acute cholestatic hepatitis is an

207 Bile duct loss during the course of drug-induced liver i

208 etary-supplement-associated liver injury had bile duct loss on liver biopsy, which was moderate to se

209 ive factor of poor outcome was the degree of bile duct loss on liver biopsy.

210 Compared to those without, those with bile duct loss were more likely to develop chronic liver

211 uced liver injury with histologically proven bile duct loss.

212 duct ligation (BDL), increasing intrahepatic bile duct mass (IBDM) and fibrosis.

213 receptors in Mdr2KO mice resulted in reduced bile duct mass and hepatic fibrosis.

214 ion was evaluated by changes in intrahepatic bile duct mass and the expression of proliferation and f

215 Treatment with GnRH increased intrahepatic bile duct mass as well as proliferation and function mar

216 C presence or activation; large intrahepatic bile duct mass, inflammation and senescence; and fibrosi

217 tro knockdown of GnRH decreased intrahepatic bile duct mass/cholangiocyte proliferation and fibrosis.

218 Specifically, recent evidence linking non-bile duct medical conditions, such as nonalcoholic fatty

219 and show that ANKS6 function is required for bile duct morphogenesis and cholangiocyte differentiatio

220 invasive imaging method for demonstration of bile duct morphology, which is useful to plan complex su

221 ent typical clinical and radiologic signs of bile duct obstruction and cholangitis, her blood analysi

222 NAC also reduced bile duct obstruction and liver fibrosis and increased s

223 s a neonatal liver disease with extrahepatic bile duct obstruction and progressive liver fibrosis.

224 ally covered) for palliation of extrahepatic bile duct obstruction initially is more expensive than p

225 Malignant bile duct obstruction is a common problem among cancer p

226 Lower survival is also determined by distal bile duct obstruction, Bismuth- Corlette type IV strictu

227 ium, focal bile duct stricture formation and bile duct obstruction.

228 hological signs of inflammation/fibrosis and bile duct obstruction.

229 h Ranson and APACHE II scores and markers of bile duct obstruction.

230 f MRCP obtained with 3T scanners in cases of bile duct obstruction.

231 g precision-cut slices of extrahepatic human bile ducts obtained from discarded donor livers, providi

232 In a separate set of experiments, bile ducts of male Wistar rats were exteriorized, allowi

233 nd its expression is reduced in intrahepatic bile ducts of patients with cholestatic disorders.

234 oinflammatory cholangiopathy (disease of the bile ducts) of unknown pathogenesis.

235 This bile duct-on-a-chip captured essential features of a sim

236 Here, we report on a bile duct-on-a-chip that phenocopies not only the tubula

237 t arise in either the intra- or extrahepatic bile ducts or the gallbladder.

238 ocytes primary cilium and various degrees of bile duct paucity and dysplasia were identified.

239 uct proliferation is universal at diagnosis, bile duct paucity develops later.

240 ckground, Jag1 haploinsufficiency results in bile duct paucity in mice.

241 ng one copy of Rumi suppresses the Jag1(+/-) bile duct phenotype, indicating that Rumi opposes JAG1 f

242 icrog/kg) every 4 days for 28 days exhibited bile duct proliferation and pericholangitis.

243 While intrahepatic bile duct proliferation is universal at diagnosis, bile

244 Rather, bile duct proliferation underpinned the increased fibros

245 with liver damage and cholestasis, extensive bile duct proliferation, and increased collagen depositi

246 receptor 1 (GPBAR1) agonist associated with bile duct proliferation.

247 brosis, reduced animal survival, and induced bile duct proliferation.

248 A significant pathological side effect, bile-duct proliferation, was seen in the liver of AAV2-L

249 cholangitis via immunization with syngeneic bile duct protein (BDP).

250 The diameter of the interlobular bile duct remains constant after BDL, a response that is

251 stratified between those who had a previous bile duct repair or not, including postoperative complic

252 jury to prevent complications, if a previous bile duct repair was attempted.

253 Extrahepatic bile duct resection with hepaticoenterostomy was the mos

254 For reader 1, distal common bile duct scores were significantly higher with BH SPARS

255 c for hydatid disease, cyst rapture into the bile ducts should be included in the differential diagno

256 Postischemic bile duct slices were incubated in oxygenated culture me

257 large balloon dilation (EST-EPLBD) for large bile duct stone extraction with an extent of cutting < 1

258 ilated bile duct is the only risk factor for bile duct stone recurrence in patients undergoing limite

259 lated bile duct was the only risk factor for bile duct stone recurrence in the limited EST-EPLBD grou

260 adial expansion balloons according to common bile duct stone size.

261 The removal of large bile duct stones (> 15 mm) by conventional endoscopic sp

262 (>=18 years) with native papilla and common bile duct stones (<=1.5 cm in size and <2 cm in diameter

263 am; even prior images had evidence of common bile duct stones (CBDS).

264 e conventional surgical management of common bile duct stones (CBDS).

265 ts (HR, 2.52; 95% CI, 1.05-6.04), and common bile duct stones (HR, 11.83; 95% CI, 1.54-91).

266 2017, 3721 consecutive patients with common bile duct stones were recruited, 1718 of whom were exclu

267 We enrolled 185 patients with >=15 mm bile duct stones who received EST, EPLBD and limited EST

268 tomy is the established treatment for common bile duct stones.

269 imum dilation time for the removal of common bile duct stones.

270 d balloon dilation for the removal of common bile duct stones.

271 apillary growth of biliary epithelium, focal bile duct stricture formation and bile duct obstruction.

272 was associated with development of dominant bile duct strictures (P = 0.02).

273 ervals (CIs) were determined for the rate of bile duct strictures, incomplete ablation, and tumor rec

274 essively more differentiated hepatocytes and bile duct structures.

275 ommon, but can be an indication of vanishing bile duct syndrome (VBDS).

276 f patients(2) with case reports of vanishing bile duct syndrome(3), subacute biliary injury and immun

277 duodenum through the cystic duct and common bile duct system.

278 mainly caused by iatrogenic injuries of the bile duct system.

279 rats, we performed bile diversions from the bile duct to the midjejunum or the mid-ileum to match th

280 nes by bile salts during passage through the bile ducts to the gut(4).

281 as well as KIR and KIR-ligand expression in bile duct tumors and control tissues.

282 Bile duct tumors are rare and have poor prognoses.

283 NK cells from bile duct tumors expressed KIRs and were found in tumors

284 Patients with bile duct tumors had multiple alterations at the KIR gen

285 C cells; quercetin also reduced secretion by bile duct units isolated from rats.

286 tion was significantly decreased in isolated bile duct units transfected with miR-506, relative to co

287 holangiocyte cells and secretion in isolated bile duct units.

288 platform to study the pathophysiology of the bile duct using cholangiocytes from a variety of sources

289 suitable for the pretransplant assessment of bile duct viability.

290 The bile duct wall enhancement, intrahepatic bile ducts, and

291 Furthermore, dilated bile duct was the only risk factor for bile duct stone r

292 Adjacent intrahepatic bile ducts were dilated.

293 The density of lesions along extrahepatic bile ducts were measured and compared with pathology and

294 uman cholangiocytes, epithelial cells lining bile ducts, were cultured as polarized epithelia in a Tr

295 The portal tract contains the bile duct, which is surrounded by stromal cells often ca

296 iary cholangitis (PBC) is a disease of small bile ducts, which can lead to morbidity and mortality.

297 is qualitatively distinct from that of large bile ducts, which tend to enlarge their diameters.

298 iver, lymph nodes, pancreas and extrahepatic bile duct with potential for recurrence and persistent l

299 vessels were dissected after division of the bile duct without a porto-caval shunt.

300 reduces the amount of scar formed around the bile duct, without reducing the development of the pro-r