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1 e phenotypes, and proliferate in response to bile duct injury.
2 -17A production and ameliorated intrahepatic bile duct injury.
3 tivity, potentially allowing for exaggerated bile duct injury.
4 have been linked to pathogenic mechanisms of bile duct injury.
5 gen(s) responsible for T-cell activation and bile duct injury.
6 ced, subsequent autoreactive T cell-mediated bile duct injury.
7 ntigen-specific animal model of inflammatory bile duct injury.
8 e might be able to decrease the incidence of bile duct injury.
9 the normal biliary proliferative response to bile duct injury.
10 ,411 for all care related to repair of their bile duct injury.
11 ures with a recognized morbidity relating to bile duct injuries.
12 of laparoscopic cholecystectomy (LC)-related bile duct injuries.
13 my was associated with a lower risk of major bile duct injury [0.28% vs 0.53%, relative risk (RR)=0.5
14 orrhage, 0.3%; subhepatic collections, 2.9%; bile duct injury, 0.08%; and retained stones, 3.1%); the
15 gnant biliary obstruction (1.8%), history of bile duct injury (2.2%), or complications of liver trans
17 s treated at a single institution with major bile duct injuries after laparoscopic cholecystectomy ma
20 PTC and PTBD performed for management of bile duct injury and complications of liver transplantat
24 rimental BA, CD25+ cell depletion aggravated bile duct injury at 12 dpi after RRV inoculation, as pla
28 his analysis were to compare the outcomes of bile duct injuries by specialist over time and the role
32 February 1, 2000, and November 23, 2011 for bile duct injury, cholangiocarcinoma, choledochal cysts,
34 e incidence and mechanism of injury of major bile duct injuries during laparoscopic cholecystectomy h
35 iologic management of 89 patients with major bile duct injuries during laparoscopic cholecystectomy.
36 There seems to be an increase in the rate of bile duct injuries during SILC when compared with histor
38 imary endpoint was the occurrence of a major bile duct injury during laparoscopic cholecystectomy (bi
39 lso be critical in the early phases of small bile duct injury found in primary biliary cirrhosis.
41 after successful surgical repair of a major bile duct injury from a LC treated at the Johns Hopkins
45 ly indicated in the management of iatrogenic bile duct injuries (IBDI), but occasionally, it becomes
48 ed in vivo in multiple models of hepatic and bile duct injury, including bile duct ligation and CCl(4
50 murine biliary atresia, and the progressive bile duct injury is due in part to a bile duct epithelia
51 pathogenesis of biliary atresia (BA) is that bile duct injury is initiated by a virus infection, foll
53 intermittent toxin exposure, which provokes bile duct injury/necrosis and proliferation, fibroblast
54 It has been suggested that the majority of bile duct injuries occur as a result of operator disorie
56 ted at the Johns Hopkins Hospital with major bile duct injuries or postoperative bile duct strictures
57 nfidence interval [CI]: 0.31-0.90], of major bile duct injury or death (1.36% vs 1.88%, RR=0.72, 95%
62 as evaluated from a psychological dimension, bile duct injury patients reported QOL scores in the phy
68 postoperative bile duct strictures and major bile duct injuries remains a challenge for even the most
72 ey bias underestimates the true frequency of bile duct injuries, residency training decreases the lik
74 ata show that errors leading to laparoscopic bile duct injuries stem principally from misperception,
75 o determine the optimal timing for repair of bile duct injuries sustained during cholecystectomy.
78 sults concerning complications, particularly bile duct injury, to those reported in open cholecystect
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