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1 ll of diverse pathologic processes (i.e. the cholangiopathies).
2 eveloped clinical evidence of posttransplant cholangiopathy.
3 s and is associated with development of AIDS cholangiopathy.
4 in one of the girls demonstrated a low grade cholangiopathy.
5 ostoperative complications, such as ischemic cholangiopathy.
6 iP) has been suggested to be an indicator of cholangiopathy.
7  and fibrogenesis characteristic of COVID-19 cholangiopathy.
8 langitis (PSC) is an idiopathic, progressive cholangiopathy.
9 re relisted for transplantation for ischemic cholangiopathy.
10  primary nonfunction and minimizing ischemic cholangiopathy.
11 tion and decrease the risk of posttransplant cholangiopathy.
12 disposed to primary nonfunction and ischemic cholangiopathy.
13 schemia, and may reduce the rate of ischemic cholangiopathy.
14  of nonfunction, poor function, and ischemic cholangiopathy.
15 chanistic aspects of a virus induced biliary cholangiopathy.
16 determining the likelihood of posttransplant cholangiopathy.
17 ose rotavirus strains that cause obstructive cholangiopathy.
18 tular proliferation that are associated with cholangiopathy.
19  is a chronic, idiopathic, fibroinflammatory cholangiopathy.
20 hs posttransplantation showed no evidence of cholangiopathy.
21  disease and cystic fibrosis (CF)-associated cholangiopathy.
22 ry end point was the development of ischemic cholangiopathy.
23 s developed liver disease with features of a cholangiopathy.
24  used to develop therapies for CF-associated cholangiopathy.
25 y tract destruction found in immune-mediated cholangiopathies.
26  and thus jointly contribute to AIDS-related cholangiopathies.
27 ht open new approaches for the management of cholangiopathies.
28  in the vicinity of the bile ducts in immune cholangiopathies.
29 ss that leads to these infantile obstructive cholangiopathies.
30 tributes to the disease pathogenesis of most cholangiopathies.
31  duct ligation, and in patients with chronic cholangiopathies.
32 ver may play a pathogenic role in subsets of cholangiopathies.
33  as a potential therapeutic option for human cholangiopathies.
34  represent potential therapeutic targets for cholangiopathies.
35 nonuclear cells from patients with fibrosing cholangiopathies.
36  hepatic cell cultures as in vitro models of cholangiopathies.
37  on its role in hepatocellular carcinoma and cholangiopathies.
38 ary sclerosing cholangitis and hepatobiliary cholangiopathies.
39 ed and diseased cholangiocytes, and in human cholangiopathies.
40 d applications for regenerative medicine and cholangiopathies.
41 elevant to the pathogenesis of several human cholangiopathies.
42  be important in developing therapeutics for cholangiopathies.
43 ions on the pathophysiology and treatment of cholangiopathies.
44 itor cell niche activation between these two cholangiopathies.
45 related liver disease and other inflammatory cholangiopathies.
46  inhibits these processes and contributes to cholangiopathies.
47 iary proliferation/damage that is typical of cholangiopathies.
48 rella may lead to the development of chronic cholangiopathies.
49 y HCO3- umbrella might predispose to chronic cholangiopathies.
50 ating cholangiocytes and how this relates to cholangiopathies.
51 e (1239 vs 2065 U/L, P = 0.02), intrahepatic cholangiopathy (0% vs 22%, P = 0.015), biliary complicat
52 RP livers, P = .0559), freedom from ischemic cholangiopathy (0% vs. 27% for non-NRP livers, P < .0001
53 1; P: < 0.0001 and P: < 0.04) or obstructive cholangiopathy (7 +/- 7% and 0.7 +/- 0.6; P: < 0.006 and
54 epresent an important target of study in the cholangiopathies, a group of genetic developmental and a
55 vide the framework for new therapies for the cholangiopathies, a group of important hepatobiliary dis
56 ystic liver disease (PLD) is a member of the cholangiopathies, a group of liver diseases in which cho
57 ysfunction, surgical complications, ischemic cholangiopathy, acute kidney injury, acute cellular reje
58 help to understand the tissue specificity of cholangiopathies and also to identify targets for therap
59 vel therapeutic targets for the treatment of cholangiopathies and cholangiocarcinoma.
60 des a model for studying the pathogenesis of cholangiopathies and for developing therapies to treat t
61  may represent a novel approach for treating cholangiopathy and comorbidities.
62 ., acquired immunodeficiency syndrome (AIDS) cholangiopathy and graft-versus-host disease (GVHD).
63 t study demonstrates lower rates of ischemic cholangiopathy and improved graft survival with NRP alon
64 th acquired immunodeficiency syndrome (AIDS) cholangiopathy and occurs almost exclusively in adult pa
65 associated with a high incidence of ischemic cholangiopathy and other perioperative complications.
66 g theater, although higher rates of ischemic cholangiopathy and worse graft survival were still obser
67 d in most instances were preceded by chronic cholangiopathy and/or cirrhosis.
68 s, alcoholic liver disease, viral hepatitis, cholangiopathies, and hepatobiliary malignancies are emp
69 hages are involved in the pathophysiology of cholangiopathies, and these hepatic cells orchestrate th
70 ed allograft dysfunction, need for dialysis, cholangiopathy, and retransplantation).
71         Three DCD liver recipients developed cholangiopathy, and this was associated with an inabilit
72                                              Cholangiopathies are a diverse group of progressive dise
73                                          The cholangiopathies are a group of hepatobiliary diseases i
74                                              Cholangiopathies are characterized by impaired cholangio
75                                              Cholangiopathies are poorly understood disorders with no
76 ltifactorial, with obliterative extrahepatic cholangiopathy as the common endpoint.
77 successful surgical bypass of the congenital cholangiopathy as well as subsequent transplant-free sur
78 rease commonly seen with chronic obstructive cholangiopathy, because of less hepatocyte proliferation
79 observed in the DCD SLK group, with ischemic cholangiopathy being the most common (10.0% vs 0.0%, P =
80 ular connectivity among the three main human cholangiopathies (biliary atresia [BA], primary biliary
81 t to investigate the role of HAI-1 and -2 in cholangiopathies by exploring their functions in fetal l
82 sults demonstrate the potential for treating cholangiopathy by safely harnessing FGF19 biology to sup
83 tis can be challenging because other chronic cholangiopathies can present similarly; however, the dis
84                                              Cholangiopathies caused by biliary epithelial cell (BEC)
85  biliary cholangitis (PBC) are human primary cholangiopathies characterized by the damage of mature c
86   Biliary atresia (BA) is a chronic neonatal cholangiopathy characterized by fibroinflammatory bile d
87 Congenital hepatic fibrosis (CHF), a genetic cholangiopathy characterized by fibropolycystic changes
88 erosing cholangitis (PSC) is a heterogeneous cholangiopathy characterized by progressive biliary fibr
89 uct epithelia are the target of a number of "cholangiopathies" characterized by disordered bile ductu
90 is an inflammatory, fibrosclerosing neonatal cholangiopathy, characterized by a periductal infiltrate
91                                              Cholangiopathies comprise a spectrum of chronic intrahep
92               In livers that did not develop cholangiopathy, concentrations of sodium, potassium, and
93  21%; P < 0.001) and, specifically, ischemic cholangiopathy (DCD 44% vs. DBD 1.6%; P < 0.001) occurre
94 ngitis (PSC) is a chronic, fibroinflammatory cholangiopathy (disease of the bile ducts) of unknown pa
95                           In other selective cholangiopathies, ductular cells positive for HAI-1 or H
96 h biliary atresia, the most common childhood cholangiopathy, exhibit increased levels of Th2-promotin
97  cholangitis (PSC) is a chronic inflammatory cholangiopathy frequently complicated by cholangiocarcin
98 olangitis (IRSC), to the spectrum of chronic cholangiopathies has created the clinical need for relia
99                       DR is observed in many cholangiopathies, highlighting overlapping similarities
100 ry atresia are thought to be immune-mediated cholangiopathies, however, gaps in knowledge remain with
101 DCD: 47% vs DBD: 26%; P < 0.01) and ischemic cholangiopathy (IC) (DCD: 34% vs DBD: 1%; P < 0.01) were
102 safety net for patients who develop ischemic cholangiopathy (IC) following DCD LT.
103                        Concerns for ischemic cholangiopathy (IC), a disease of diffuse intrahepatic s
104 ociated with a greater incidence of ischemic cholangiopathy (IC), leading to several programs to aban
105                    No difference in ischemic cholangiopathy (IC), vascular thrombosis/stenosis or gra
106 the time of procurement to minimize ischemic cholangiopathy (IC).
107 1l1 in developing hepatoblasts would lead to cholangiopathy in mice.
108 ug VX809 rescues the disease phenotype of CF cholangiopathy in vitro.
109 langiocytes will have broad applications for cholangiopathies, in disease modeling and for screening
110  are thought to influence the progression of cholangiopathies, in particular primary sclerosing chola
111  group of chronic liver diseases termed the "cholangiopathies," in which cholangiocytes react to exog
112 ment of biliary damage and liver fibrosis in cholangiopathies including PSC.
113             In extrahepatic bile duct (EHBD) cholangiopathies, including primary sclerosing cholangit
114 ay be a potential approach in treating human cholangiopathies, including primary sclerosing cholangit
115 ent a therapeutic approach for management of cholangiopathies, including PSC.
116  3D organoids; these BDOs retain features of cholangiopathies, including the ability to react to infl
117 y epithelium physiology and in non-malignant cholangiopathies is far from complete.
118 s of the inflammatory processes in fibrosing cholangiopathies is highlighted.
119 ies in the susceptibility to immune-mediated cholangiopathies is reviewed.
120 y of intrahepatic bile ducts and progressive cholangiopathy lead to end-stage cirrhosis.
121                  The etiopathogenesis of the cholangiopathies likely includes disease-specific mediat
122  these common responses contribute to DR and cholangiopathies may identify novel therapeutic targets
123 gitis and acquired immunodeficiency syndrome cholangiopathy, MRCP depicted the biliary tract as clear
124                             Neither ischemic cholangiopathy nor vascular complications occurred in th
125        Biliary atresia (BA) is a destructive cholangiopathy of childhood in which Th1 immunity has be
126           Biliary atresia is the most common cholangiopathy of childhood.
127 ft survival and higher incidence of ischemic cholangiopathy of DCD compared with DBD recipients were
128           Biliary atresia is an obliterative cholangiopathy of infancy that is fatal if untreated.
129        Biliary atresia (BA) is a devastating cholangiopathy of infancy.
130  susceptibility to biliary atresia, a severe cholangiopathy of neonates.
131           Biliary atresia (BA) is a neonatal cholangiopathy of unknown etiology.
132 sclerosing cholangitis (PSC) is an incurable cholangiopathy of unknown etiopathogenesis.
133 rome, which is characterized by a congenital cholangiopathy of variable severity.
134 s should be considered at increased risk for cholangiopathy or malignancy.
135         No graft failure due to intrahepatic cholangiopathy or nonfunction occurred in HOPE-treated l
136  were increased for recipients with ischemic cholangiopathy or retransplantation by 53% (P = 0.01) an
137 cantly associated with freedom from ischemic cholangiopathy (P < .0001).
138 llograft dysfunction (P < .001) and ischemic cholangiopathy (P < .001) was significantly greater in t
139 (RRV) infection of newborn pups results in a cholangiopathy paralleling human BA and has been used to
140 (RRV) infection of newborn pups results in a cholangiopathy paralleling that of human BA.
141 the study of the pathogenesis and therapy of cholangiopathies, particularly PSC.
142 spholipid flippase, cause a wide spectrum of cholangiopathy phenotypes in humans.
143 asis and primary sclerosing cholangitis, two cholangiopathies regarded as risk factors for CCA.
144 ver, the mechanisms of pathogen-induced AIDS cholangiopathy remain unclear.
145                                     Ischemic cholangiopathy remained low (2-y proportion free: 97% ve
146 ity from chronic biliary diseases (i.e., the cholangiopathies) remains substantial.
147 nd acquired diseases of the biliary tree, or cholangiopathies, represent a significant source of morb
148                                        Human cholangiopathies share pathways enriched by immunity gen
149 acids drive disease progression in fibrosing cholangiopathies such as biliary atresia or primary scle
150 histological, and clinical features of human cholangiopathies such as progressive familial intrahepat
151                                              Cholangiopathies, such as primary sclerosing cholangitis
152            The biliary tree is the target of cholangiopathies that are chronic cholestatic liver dise
153  atresia (BA) is a progressive, inflammatory cholangiopathy that culminates in fibrosis of extrahepat
154 rosing cholangitis is a chronic, progressive cholangiopathy that frequently affects men and is associ
155 brosis-associated liver disease is a chronic cholangiopathy that negatively affects the quality of li
156      Biliary atresia is a fibro-inflammatory cholangiopathy that obstructs the extrahepatic bile duct
157    Biliary atresia is a neonatal obstructive cholangiopathy that progresses to end-stage liver diseas
158 liary atresia (BA) is a neonatal obstructive cholangiopathy that progresses to end-stage liver diseas
159 liary atresia (BA) is a devastating neonatal cholangiopathy that progresses to fibrosis and end-stage
160 tes in human cholestatic liver diseases (ie, cholangiopathies) that are characterized by ductular rea
161  graft loss in patients who develop ischemic cholangiopathy, the significant reduction seen in DCD do
162 sodeoxycholic acid (UDCA) is widely used for cholangiopathy treatment, but its effects on cholangiocy
163                    The incidence of ischemic cholangiopathy was 11%, which was lower than in the stan
164    In the same groups, incidence of ischemic cholangiopathy was 3.3%, 4.9%, and 3.3%.
165                                     Ischemic cholangiopathy was lower in the NRP alone group (0%) and
166                                           No cholangiopathy was observed despite the use of extended
167 ased odds of IC (95% CI = 4.8-24.2).Ischemic cholangiopathy was present in 16% of DCD compared with 3
168 ility to biliary atresia, a severe pediatric cholangiopathy, we engineered multi-compartment biliary
169                         No cases of ischemic cholangiopathy were diagnosed, and no graft loss was obs
170 cidences of acute kidney injury and ischemic cholangiopathy were greater in DCD recipients (32.6% vs.
171  8 mo, no vascular complications or ischemic cholangiopathy were reported.
172 tion; 8 of the 9 treated livers were free of cholangiopathy, whereas the ninth had a proximal duct st
173 ad and heterogenous class of diseases termed cholangiopathies, which can present with phenotypes rang
174 ng cholangiocyte organoids in the context of cholangiopathies, which represent a key reason for liver
175 ement causes injuries including intrahepatic cholangiopathy, which may lead to graft loss.
176 I-1 and -2 are overexpressed in the liver in cholangiopathies with ductular reactions and are possibl
177 e studies have shown lower rates of ischemic cholangiopathy with advanced perfusion.
178                                       Severe cholangiopathy with loss of luminal biliary epithelium h
179 erogeneous and progressive fibroinflammatory cholangiopathy with no known etiology or effective treat

 
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