ライフサイエンスコーパス: bile duct

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

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

3 arcinoma and other malignant diseases of the bile duct.

4 and the drainage catheter was placed in the bile duct.

5 to palliation of malignant strictures of the bile duct.

6 and posterior (n = 1) branches of the right bile duct.

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

8 extrahepatic biliary tract and intrahepatic bile ducts.

9 s within extrahepatic and large intrahepatic bile ducts.

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

11 amatic and rapid enlargement of extrahepatic bile ducts.

12 ers of patients with PSC and localize around bile ducts.

13 y exhibit phenotypes of both hepatocytes and bile ducts.

14 nfiltration of liver and localization around bile ducts.

15 flox) mice initially developed no peripheral bile ducts.

16 general, efforts should be made to clear the bile ducts.

17 inflammatory destruction of the intrahepatic bile ducts.

18 are found in the mesenchyme surrounding the bile ducts.

19 ignant neoplasm of the liver or extrahepatic bile ducts.

20 followed by an autoimmune response targeting bile ducts.

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

22 shunting may allow improved targeting to the bile ducts.

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

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

25 inistration = 1 x dilatation of intrahepatic bile ducts + 2 x dysmorphy + 1 x portal hypertension; sc

26 ts and results in prolonged patency of hilar bile ducts, a trend for longer survival time, and simila

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

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

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

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

31 ved increased proliferation and expansion of bile duct and liver progenitor cells in cP(f/f)78(f/f) l

32 rvives in the hostile environment within the bile duct and show that metabolic pathways in the parasi

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

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

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

36 istic phenotype of high-density intrahepatic bile ducts and enlarged liver in Rosa(NICD/-)::AlbCre mi

37 l model for biliary atresia, as it loses its bile ducts and gallbladder during metamorphosis.

38 rpretation standard model to score precisely bile ducts and liver parenchyma features.

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

40 Cystic dysplasia of the intrahepatic bile ducts and progressive portal fibrosis characterize

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

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

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

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

45 The targets in this disease are small bile ducts, and the prototypic serologic response includ

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

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

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

49 ct with target cells, such as hepatocytes or bile ducts (BDs).

50 sults showed abundant hybrid cells in portal bile duct BEC, canals of Hering, and immediate periporta

51 Ligation of the bile duct, blocking CCK receptors with proglumide or inh

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

53 Accurate puncture of targeted bile ducts can be achieved using this method.

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

55 oporfin-PDT can safely be delivered to hilar bile duct cancer patients and results in prolonged paten

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

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

58 for gallbladder cancer, 97% of extrahepatic bile duct cancer, 91% of ampula of Vater cancer, 96% of

59 ampula of Vater cancer, 96% of intrahepatic bile duct cancer, and 94% of hepatocellular carcinoma.

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

61 lliation and survival in nonresectable hilar bile duct cancer.

62 olism of fenclozic acid which included a rat bile duct cannulated (BDC) study characterizing the bili

63 DTX formulation, Taxotere, was conducted in bile duct cannulated rats.

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

65 mbines with hepatic ducts to form the common bile duct (CBD) and continues along the CBD.

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

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

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

69 f patients with intermediate risk for common bile duct (CBD) stones require therapeutic intervention.

70 on findings suggesting a stone in the common bile duct (CBD), but these factors are not highly sensit

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

72 Strikingly, bile duct cells in cP(f/f)78(f/f) livers maintained wild

73 ay structural and functional similarities to bile duct cells in normal liver.

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

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

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

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

78 verticulum, namely Todani type II congenital bile duct cyst (BDC).

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

80 5(-/-) mice developed liver inflammation and bile duct damage with similar severity but delayed onset

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

82 uction, intrahepatic T-cell infiltrates, and bile duct damage.

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

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

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

86 cholangiocyte markers or resembling ectopic bile ducts developed in the Prox1-deficient liver parenc

87 n vitro study of the molecular mechanisms of bile duct development and have important potential for t

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

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

90 plantation in risky anastomosis and when the bile duct diameter is less than 7 mm.

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

92 The mean targeted bile duct diameter was 4.9 mm (1.9 to 8.2 mm).

93 patients with tumors exhibiting intrahepatic bile duct differentiation remains controversial.

94 Bile duct differentiation, morphogenesis, and function w

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

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

97 strate that tubule formation of intrahepatic bile ducts during embryonic development as well as N2IC-

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

99 n the submucosal compartment of extrahepatic bile ducts (EHBDs).

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

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

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

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

104 Donor common bile duct excised at implantation showed preservation of

105 es, including splenectomy (0.7% MIS), common bile duct exploration (24.9% MIS), gastrostomy (25.9% MI

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

107 e women and 95% had a cholecystectomy and/or bile duct exploration.

108 infections: cancer of liver and intrahepatic bile duct; fibrosis, cirrhosis, and other liver diseases

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

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

111 number of hepatic arteries without affecting bile duct formation.

112 Bile ducts from rats with cholestasis and patients with

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

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

115 At 3-4 weeks, albNS(cko) livers develop bile duct hyperplasia and show increased apoptotic cells

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

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

118 hepatocellular carcinoma (HCC), intrahepatic bile duct (IBD), and gallbladder and biliary tract cance

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

120 The potential for intrahepatic bile duct (IHBD) regeneration in patients with bile duct

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

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

123 ly localized around the damaged interlobular bile ducts in PBC.

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

125 th constitutive activation of AKT and YAP in bile ducts induced cholangiocarcinoma with liver metasta

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

127 having bile leaks (type A, n = 239, 45%) or bile duct injuries (types B-E, n = 289, 55%).

128 Outcomes of bile duct injuries are best with surgical management and

129 his analysis were to compare the outcomes of bile duct injuries by specialist over time and the role

130 Almost all bile leaks and many bile duct injuries can be managed successfully by endosc

131 Postoperative bile duct injuries require multidisciplinary management.

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

133 Patients with bile duct injuries were managed most often by endoscopis

134 my was associated with a lower risk of major bile duct injury [0.28% vs 0.53%, relative risk (RR)=0.5

135 ency of serious rare complications including bile duct injury and death.

136 Bile duct injury during cholecystectomy is a serious com

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

138 pathogenesis of biliary atresia (BA) is that bile duct injury is initiated by a virus infection, foll

139 nfidence interval [CI]: 0.31-0.90], of major bile duct injury or death (1.36% vs 1.88%, RR=0.72, 95%

140 No bile duct injury or death occurred.

141 Secondary outcomes included major bile duct injury or death, 30-day postcholecystectomy mo

142 The primary outcome was major bile duct injury requiring operative repair within 6 mon

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

144 February 1, 2000, and November 23, 2011 for bile duct injury, cholangiocarcinoma, choledochal cysts,

145 e phenotypes, and proliferate in response to bile duct injury.

146 -17A production and ameliorated intrahepatic bile duct injury.

147 le duct (IHBD) regeneration in patients with bile duct insufficiency diseases is poorly understood.

148 We studied a mouse model of bile duct insufficiency with liver epithelial cell-speci

149 tigate the role of VDR in the maintenance of bile duct integrity in mice challenged with biliary-type

150 the adaptation to cholestasis and diminishes bile duct integrity in the setting of biliary-type liver

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

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

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

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

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

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

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

158 m)Tc-mebrofenin was severely impaired in the bile duct-ligated animal, as evidenced by elevated hepat

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

160 Friend virus B wild-type mice (untreated, bile duct-ligated, vehicle- or rifampicin-treated) and s

161 ecretin-stimulated choleresis in cholestatic bile-duct-ligated (BDL) rats by interaction with melaton

162 or this, thioacetamide (TAA)-intoxicated and bile-duct-ligated (BDL) rats were used as models.

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

164 ditionally disrupting Hh signaling in MFs of bile-duct-ligated mice inhibited Notch signaling and blo

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

166 study, we aimed to first validate rats with bile duct ligation (BDL) as a model for hepatic pruritus

167 unctions) and (2) proliferate in response to bile duct ligation (BDL) by activation of cyclic adenosi

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

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

170 ol (AA) (periportal injury), as well as in a bile duct ligation (BDL) model.

171 high-fat diet (HFD) were subjected to either bile duct ligation (BDL) or CCl4 treatment.

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

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

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

175 Experimental fibrosis was induced by bile duct ligation (BDL), CCl4 intoxication, thioacetami

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

177 After bile duct ligation (BDL), the hepatic expression of Th17

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

179 nduced liver injury and fibrosis, a model of bile duct ligation (BDL)-induced hepatic fibrosis in viv

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

181 eding (a model of sclerosing cholangitis) or bile duct ligation (BDL).

182 chloride (CCl4 ), and a rat model induced by bile duct ligation (BDL).

183 ioration of cholestasis in a murine model of bile duct ligation (BDL).

184 hosis due to carbon tetrachloride (CCl4 ) or bile duct ligation (BDL).

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

186 hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL).

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

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

189 and liver-specific p38alpha knockout mice by bile duct ligation and animals were sacrificed at 12 and

190 Two mouse models of liver injury (bile duct ligation and carbon tetrachloride) also exhibi

191 either carbon tetrachloride intoxication or bile duct ligation and promote fibrosis regression.

192 O mice treated with carbon tetrachloride and bile duct ligation developed reduced fibrosis versus wil

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

194 procedure to reconstruct biliary flow after bile duct ligation in C57BL/6 mice to generate a model o

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

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

197 vo by carbon tetrachloride i.p. injection or bile duct ligation in wild-type and SEMA7A knockout (KO)

198 After bile duct ligation or upon a cholic acid-enriched diet,

199 Upon carbon tetrachloride injection or bile duct ligation surgery-mediated liver injury, mesode

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

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

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

203 carbon tetrachloride intoxication, following bile duct ligation, and in tissue culture models.

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

205 totoxin (carbon tetrachloride) injection and bile duct ligation, constitutive FGFR1 signalling in liv

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

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

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

209 duced cholestasis in mouse livers via common bile duct ligation.

210 ntibody or control IgG and subjected them to bile duct ligation.

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

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

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

214 onyl-1, 4-dihydrocollidine (DDC) feeding and bile-duct ligation (BDL) in mice.

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

216 sed mesenteric vascular beds from rats after bile-duct ligation.

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

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

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

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

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

222 Bile duct loss during acute cholestatic hepatitis is an

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

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

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

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

227 uced liver injury with histologically proven bile duct loss.

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

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

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

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

232 nic inflammatory insults in the intrahepatic bile ducts might shed light on the cystadenocarcinogenes

233 into cholangiocytes, premature intrahepatic bile duct morphogenesis, and biliary hyperplasia occurre

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

235 to restore the integrity and function of the bile duct mucosa in diseased states.

236 ommunicate between different segments of the bile duct mucosa.

237 iced patients with periampullary or proximal bile duct neoplasms who are candidates for PD or major l

238 hepatectomy due to periampullary or proximal bile duct neoplasms.

239 st, pancreatic, prostate, liver/intrahepatic bile duct, non-Hodgkin lymphoma, head/neck, ovarian, or

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

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

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

243 n of cholestasis, decreased the incidence of bile duct obstruction, and improved survival above wild-

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

245 ts are placed for palliation of extrahepatic bile duct obstruction.

246 -/-) mice did not have hyperbilirubinemia or bile duct obstruction.

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

248 atresia patient serum and in the livers and bile ducts of mice with experimental biliary atresia.

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

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

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

252 sed with increasing distance from the common bile duct (P-trend < 0.001).

253 Normal bile duct, pancreatic duct, and tumor-associated metapla

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

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

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

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

258 Furthermore, the liver and bile duct phenotypes could be recapitulated with constit

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

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

261 Rather, bile duct proliferation underpinned the increased fibros

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

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

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

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

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

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

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

269 enectomy (67%) and sometimes by extrahepatic bile duct resection (23%).

270 Extrahepatic bile duct resection with hepaticoenterostomy was the mos

271 e by limited adaptive response and increased bile duct rupture.

272 -cadherin staining associated with increased bile duct rupture.

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

274 es, leading to reduced calcium signaling and bile duct secretion.

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

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

277 The optimal strategy for common bile duct stones (CBDSs) encountered during cholecystect

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

279 operative bacteremia and an 18% incidence of bile duct stricture within 6 months.

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

281 biliary epithelium, resulting in multifocal bile duct strictures that can affect the entire biliary

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

283 essively more differentiated hepatocytes and bile duct structures.

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

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

286 ibroinflammatory obstruction of extrahepatic bile ducts that presents as neonatal cholestasis.

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

288 athogenesis of hepatocellular carcinoma with bile duct tumor thrombus (HCC-BDTT).

289 Hepatocellular carcinoma with bile duct tumor thrombus is a challenging condition beca

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

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

292 holangiocyte cells and secretion in isolated bile duct units.

293 sibility of an in vivo biopsy of the porcine bile duct using untethered microgrippers is demonstrated

294 Chemotherapy deposit doses in the bile duct walls were quantified by means of high-pressur

295 The targeted bile duct was determined using the RVS system before the

296 onsidered to be successful when the targeted bile duct was punctured and the drainage catheter was pl

297 Adjacent intrahepatic bile ducts were dilated.

298 hed in all patients because the non-targeted bile ducts were successfully punctured alternatively.

299 The targeted bile ducts were: B3 (n = 24), B5 (n = 7), B8 (n = 3), B6

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

301 owing to creation of an RYHJ to intrahepatic bile ducts with concomitant liver resection.