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1 ied as hepatocellular (44%), mixed (28%), or cholestatic (28%).
2 nstream effector, was not implicated in cAMP cholestatic action.
3           Interestingly, both choleretic and cholestatic agents activate the same intracellular signa
4                               Choleretic and cholestatic agents affect bile formation, in part, by al
5 its expression is induced in the liver under cholestatic and cirrhotic conditions.
6 82-96% of myofibroblasts in models of toxic, cholestatic and fatty liver disease.
7                                        Using cholestatic and hepatotoxic models of liver injury, we c
8 patocellular type and less frequently of the cholestatic and mixed types.
9 iver injury (94% vs. 47%), which was usually cholestatic and sometimes severe.
10 uated experimental fibrosis in the course of cholestatic and toxic liver injury.
11 and nPKCdelta may be involved in choleretic, cholestatic, and anticholestatic effects by inserting, r
12 um BS levels, otherwise markedly elevated in cholestatic animals.
13 st that pruritus and hyperalgesia in chronic cholestatic BDL rats are associated with neuroinflammati
14 growth and secretin-stimulated choleresis in cholestatic bile-duct-ligated (BDL) rats by interaction
15 ing supplements typically induce a prolonged cholestatic but ultimately self-limiting liver injury th
16 y is specifically increased in patients with cholestatic, but not other forms of, systemic pruritus a
17                             Moreover, severe cholestatic complications and mortality after prolonged
18                              In inflammatory cholestatic conditions, loss of activity of liver AP (re
19 ROS levels, liver injury, and fibrosis under cholestatic conditions.
20 rrhosis, intrahepatic cholestasis, and other cholestatic conditions.
21 ead to more effective therapies for specific cholestatic conditions.
22 e pathogenesis and treatment of a variety of cholestatic conditions.
23  with Alagille syndrome, two major pediatric cholestatic conditions.
24 is reduced in association with duct loss and cholestatic destruction of nascent buds.
25 steroids is pertinent in the pathogenesis of cholestatic disease and colon cancer.
26 eripheral blood of biliary atresia and other cholestatic disease controls were characterized by fluor
27                                Patients with cholestatic disease exhibit pruritus and analgesia, but
28 ng cholangitis (PSC) is a rare, but serious, cholestatic disease for which, to date, no effective the
29                                Patients with cholestatic disease have increased systemic concentratio
30 ecede cholestasis but may be of relevance to cholestatic disease progression because altered fatty ac
31 tes with, and is the primary determinant of, cholestatic disease severity in these patients.
32 ry sclerosing cholangitis (PSC) is a chronic cholestatic disease that leads to extensive liver fibros
33  Primary sclerosing cholangitis is a chronic cholestatic disease that may have an autoimmune basis.
34 dings were compared to children with genetic cholestatic disease, age-matched deceased donor controls
35 rs: age, African-American race, hepatitis C, cholestatic disease, body mass index >/= 35, pre-LT diab
36 oxicity is a major source of liver injury in cholestatic disease, we explored the role of SHP in live
37 utants, whose symptoms cover the spectrum of cholestatic disease.
38 d medicine for patients with ABCB4-dependent cholestatic disease.
39 n of the once obscure inherited intrahepatic cholestatic diseases of the liver, which, in turn, provi
40                                        Other cholestatic diseases show similar activation, suggesting
41 ies of disease that will be reviewed include cholestatic diseases, tumors, vascular anomalies, and ac
42  about the pathogenic mechanisms of specific cholestatic diseases, which has limited our ability to m
43                                        Liver cholestatic diseases, which stem from diverse etiologies
44 any missense mutations linked to less severe cholestatic diseases.
45 h has led to novel therapies under study for cholestatic diseases.
46  increase our understanding of these complex cholestatic diseases.
47 nsive cells also occurred in other infantile cholestatic diseases.
48 effective supplemental therapy with UDCA for cholestatic diseases.
49 romising for functional PET of patients with cholestatic diseases.
50 autoimmune cholangitis and potentially other cholestatic diseases.
51 e putative role of liver AP in health and in cholestatic diseases.
52 stasis of pregnancy, or hereditary pediatric cholestatic disorders and may accompany, although less f
53                                         Most cholestatic disorders are caused by defects in cholangio
54                                    Infantile cholestatic disorders arise in the context of progressiv
55 ts compared to patients with other infantile cholestatic disorders, thereby establishing a possible e
56 d Drug Administration-approved treatment for cholestatic disorders.
57 might help us to better understand and treat cholestatic disorders.
58  in intrahepatic bile ducts of patients with cholestatic disorders.
59  rosetting of hepatocytes, consistent with a cholestatic drug reaction.
60 This first-in-class study evaluated the anti-cholestatic effects and safety of seladelpar in patients
61 plasma membrane, and nPKCepsilon may mediate cholestatic effects by retrieving MRP2 from the plasma m
62     An emerging theme is that choleretic and cholestatic effects may be mediated by different isoform
63 discriminate between IAC and the more common cholestatic entities, primary (PSC) and secondary sclero
64 % chronic, 7% acute on chronic, and 6% acute cholestatic failure.
65 sting, as well as in plasma samples from six cholestatic gene knockout mice and six age- and gender-m
66 d male with HCV genotype 1b developed severe cholestatic HCV at 6 months posttransplant with ascites,
67 cute (9%) and chronic cholestasis (10%), and cholestatic hepatitis (29%).
68 e patients with advanced fibrosis and 9 with cholestatic hepatitis (74% men, 57% genotype 1a, 63% pre
69  hepatitis C, including those with fibrosing cholestatic hepatitis (FCH) and decompensated cirrhosis
70             All five patients with fibrosing cholestatic hepatitis achieved SVR12 (100%, 90% CI 55-10
71                 Nine patients presented with cholestatic hepatitis and 12 patients presented with hep
72 (Mdr2-KO) mice spontaneously develop chronic cholestatic hepatitis and fibrosis that is eventually fo
73  inflammation-mediated HCC, develops chronic cholestatic hepatitis at an early age and HCC at an adul
74                  Bile duct loss during acute cholestatic hepatitis is an ominous early indicator of p
75 type 1 HCV and advanced fibrosis (F3-4/4) or cholestatic hepatitis treated with telaprevir- or bocepr
76 me with growth failure or transient neonatal cholestatic hepatitis.
77 he most common clinical pattern was a severe cholestatic hepatitis.
78 P-A, CTP-B, or CTP-C cirrhosis; or fibrosing cholestatic hepatitis.
79 d in 51% with advanced fibrosis and 44% with cholestatic hepatitis.
80 d in 22% with advanced fibrosis and 33% with cholestatic hepatitis.
81 irment, and by all 6 patients with fibrosing cholestatic hepatitis.
82 hepatic impairment; and those with fibrosing cholestatic hepatitis.
83  those with advanced fibrosis (F3-F4) and/or cholestatic hepatitis.
84 atients with recurrent advanced fibrosis and cholestatic hepatitis.
85           Twenty-seven percent had fibrosing cholestatic hepatitis/early aggressive HCV in the graft,
86 PDH and nitrosylated HDAC2 were increased in cholestatic human and rat livers reflecting increased co
87 ere tested in cholangiocytes from normal and cholestatic human livers.
88  obstruction results in a well-characterized cholestatic inflammatory and fibrogenic process; however
89 suggesting that this is a common response to cholestatic injury in infancy.
90 ration and prevents parenchymal damage after cholestatic injury in mice and thus may mediate the resp
91                                     Although cholestatic injury is common to many forms of liver dise
92 of Mrp4 in a protective adaptive response to cholestatic injury is not known.
93 genesis of liver fibrosis development in the cholestatic injury model, for HSC activation, and for th
94 onversely, histology of the 73 patients with cholestatic injury more often demonstrated bile plugs an
95 dergoes adaptive upregulation in response to cholestatic injury or bile acid feeding.
96                                              Cholestatic injury precedes liver fibrosis, and cholangi
97 judged to become chronic, with drugs causing cholestatic injury predominating.
98 mechanisms regulating liver repair following cholestatic injury remain largely unknown.
99                                              Cholestatic injury was associated with female gender and
100 e treated mice suffering from a steatotic or cholestatic injury with anti-TNF-alpha antibodies (Infli
101  or older (n = 149) were more likely to have cholestatic injury, although mortality and rate of liver
102 ticipates in the regenerative response after cholestatic injury.
103 ular reaction, which are repair responses to cholestatic injury.
104                    The most common causes of cholestatic jaundice are biliary atresia and idiopathic
105 uld be aware that ajmaline may induce severe cholestatic jaundice even after a single dose administra
106 is preceded by hepatic complications such as cholestatic jaundice or hepatomegaly.
107 NICCD and non-NICCD, infants with idiopathic cholestatic jaundice or INH were enrolled.
108 hree weeks later, he presented with painless cholestatic jaundice which peaked in severity at eleven
109   <16.3) but there were no clinical signs of cholestatic jaundice, pruritis, or liver dysfunction.
110 hondrial antibody-positive titer >/=1 in 40, cholestatic liver blood tests, diagnostic or compatible
111 eactive oxygen species that might exacerbate cholestatic liver damage.
112 flammatory response and neutrophil-dependent cholestatic liver damage.
113  in validation cohorts) and in controls with cholestatic liver disease (n = 44).
114 tion, PCN risk was higher in recipients with cholestatic liver disease (SIR 2.78); five of these case
115 ur cohort of 28 MVID patients, 8 developed a cholestatic liver disease akin to progressive familial i
116 -alcoholic steatohepatitis, viral hepatitis, cholestatic liver disease and autoimmune liver diseases.
117 or future pharmacological strategies against cholestatic liver disease and cancer.
118 ulation of bile acid homeostasis can lead to cholestatic liver disease and endoplasmic reticulum (ER)
119 e composition with important applications in cholestatic liver disease and gallstone disease, two ser
120 ry sclerosing cholangitis (PSC) is a chronic cholestatic liver disease and one of the most common ind
121       Primary biliary cirrhosis is a chronic cholestatic liver disease characterised by destruction o
122  Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by strictures of
123  Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by strictures of
124  Primary sclerosing cholangitis is a chronic cholestatic liver disease characterized by strictures of
125 y the ABCB11 gene, causes severe progressive cholestatic liver disease from early infancy.
126  centers with either autoimmune hepatitis or cholestatic liver disease had significantly lower risks
127                           Recent advances in cholestatic liver disease have occurred in several areas
128 r plasminogen activator inhibitor (PAI)-1 in cholestatic liver disease in mice suggested that tissue-
129 sm contribute to the pathogenesis of chronic cholestatic liver disease in mice.
130 ibute to the pathogenesis and progression of cholestatic liver disease in mice.
131 eased awareness of PBC as a cause of chronic cholestatic liver disease is critical in evaluating non-
132 with primary biliary cirrhosis, an important cholestatic liver disease of adults.
133  Primary sclerosing cholangitis is a chronic cholestatic liver disease of unknown etiology.
134 ic bile duct development and their effect on cholestatic liver disease phenotypes.
135 urthermore, nicotine may act as a mitogen in cholestatic liver disease processes, thereby facilitatin
136  1950s as a clinical syndrome of progressive cholestatic liver disease resulting from chronic inflamm
137 , 25% of patients undergoing OLT for chronic cholestatic liver disease still develop de novo fracture
138 liary cirrhosis (PBC) is an uncommon chronic cholestatic liver disease that primarily afflicts young
139 ry sclerosing cholangitis (PSC) is a chronic cholestatic liver disease that progresses to death as a
140                     We used a mouse model of cholestatic liver disease to investigate mechanisms of i
141 malabsorption syndromes (especially owing to cholestatic liver disease), antibiotic therapy, and rena
142  infants transplanted for reasons other than cholestatic liver disease, and patients transplanted bet
143 dents is often studied as an animal model of cholestatic liver disease, characterized by obstruction
144   UDCA, a bile acid used in the treatment of cholestatic liver disease, has anti-inflammatory and cyt
145 alidity of risk stratification in autoimmune cholestatic liver disease, highlighting strengths and we
146                                       During cholestatic liver disease, there is dysregulation in the
147 an age at LTx was 9 months, the majority had cholestatic liver disease, were hospitalized pre-LTx, an
148 neficial use of fenofibrate therapy in human cholestatic liver disease.
149 itochondrial morphology has been observed in cholestatic liver disease.
150  tight-junction structure, leading to severe cholestatic liver disease.
151 ochondrial morphology to the pathogenesis of cholestatic liver disease.
152 , MDR3 is a potential therapeutic target for cholestatic liver disease.
153 d (TUDC), is a mainstay for the treatment of cholestatic liver disease.
154 ndings from genetic studies of patients with cholestatic liver disease.
155  the formation of bile and the prevention of cholestatic liver disease.
156  were increased in livers from patients with cholestatic liver disease.
157 n the liver and prevent hepatocyte injury in cholestatic liver disease.
158 g colon cancer formation and progression and cholestatic liver disease.
159 fusion (IR) injury is frequently followed by cholestatic liver disease.
160 rine when hepatic elimination is impaired by cholestatic liver disease.
161 ted here suggest that PHB1 is also linked to cholestatic liver disease.
162 which is frequently used in the treatment of cholestatic liver disease.
163 ocrine phenotypes of cholangiocytes in human cholestatic liver diseases (ie, cholangiopathies) that a
164 langiocytes occurs during the progression of cholestatic liver diseases and is critical for the maint
165 igands may ameliorate human diseases such as cholestatic liver diseases and the associating acute ren
166  epidemiology, and treatment of a variety of cholestatic liver diseases and their associated complica
167                                              Cholestatic liver diseases are caused by a range of hepa
168                                Human chronic cholestatic liver diseases are characterized by cholangi
169  target of cholangiopathies that are chronic cholestatic liver diseases characterized by loss of prol
170  a modifier gene in patients with concurrent cholestatic liver diseases such as cystic fibrosis.
171 ymptom commonly experienced by patients with cholestatic liver diseases such as primary biliary chola
172 ruritus is a common symptom in patients with cholestatic liver diseases such as primary biliary cirrh
173 but is believed to play an important role in cholestatic liver diseases such as primary familial intr
174 peutic indications in constipation, dry eye, cholestatic liver diseases, and inflammatory lung disord
175 ression of many of these genes is altered in cholestatic liver diseases, but few have been extensivel
176  advances have been made in the treatment of cholestatic liver diseases, including primary biliary ci
177                         During the course of cholestatic liver diseases, mitotically dormant cholangi
178  In this review we develop the argument that cholestatic liver diseases, particularly primary biliary
179  cholangitis (PSC) are infrequent autoimmune cholestatic liver diseases, that disproportionate to the
180 e for the maintenance of biliary mass during cholestatic liver diseases.
181 itus and painless jaundice that occur during cholestatic liver diseases.
182 ial targets for pharmacological therapies of cholestatic liver diseases.
183 r (FXR) and its potential therapeutic use in cholestatic liver diseases.
184 beticholic acid for the treatment of chronic cholestatic liver diseases.
185 gies targeting BA transport and signaling in cholestatic liver diseases.
186  DHEA-S levels was not seen in patients with cholestatic liver diseases.
187 et to modulate bile flow in the treatment of cholestatic liver diseases.
188 his review focuses on the recent advances in cholestatic liver diseases.
189  frequently the most debilitating symptom of cholestatic liver diseases.
190 dvance our understanding of the treatment of cholestatic liver diseases.
191  better understanding of the pathogenesis of cholestatic liver diseases.
192  better understanding of the pathogenesis of cholestatic liver diseases.
193 biting PAI-1 might attenuate liver injury in cholestatic liver diseases.
194 ary cholangitis (PBC) pathogenesis and other cholestatic liver diseases.
195 aling may be important for the management of cholestatic liver diseases.
196 rters and are natural targets for therapy of cholestatic liver diseases.
197 ry sclerosing cholangitis (PSC) is a chronic cholestatic liver disorder characterized by inflammation
198 Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disorder that can progress to cirrhosi
199 eriously disabling symptom accompanying many cholestatic liver disorders.
200  modulate bile formation in the treatment of cholestatic liver disorders.
201 and therapy, such as fenofibrate, in various cholestatic liver disorders.
202 y gastrointestinal diseases, including human cholestatic liver disorders.
203                                              Cholestatic liver dysfunction (CLD) and biliary sludge o
204 s acute, chronic, acute-on-chronic, or acute cholestatic liver failure.
205           Liver specimens from patients with cholestatic liver fibrosis had increased numbers of MSLN
206                                 In addition, cholestatic liver fibrosis induced by BDL, as determined
207           RA treatment in mice with existing cholestatic liver fibrosis inhibits HSC activation and p
208                                              Cholestatic liver fibrosis is caused by obstruction of t
209 ike inhibitor of differentiation 1 (EID1) in cholestatic liver fibrosis.
210 e, enteric TNFRI is an important mediator of cholestatic liver fibrosis.
211 been identified as an important mechanism of cholestatic liver injury and bile duct loss.
212 enteral nutrition (PN)-dependent may develop cholestatic liver injury and cirrhosis (PN-associated li
213 intestinal FXR dysfunction in a rat model of cholestatic liver injury and evaluated effects of obetic
214 stigate the relevance of Fra-1 expression in cholestatic liver injury and fibrosis.
215 le of the RBP, human antigen R (HuR), during cholestatic liver injury and hepatic stellate cell (HSC)
216 indings indicate that Kupffer cells abrogate cholestatic liver injury by cytokine-dependent mechanism
217 ponents of the fibrinolytic pathway modulate cholestatic liver injury by regulating activation of hep
218 sed by cells of the innate immune system, to cholestatic liver injury has not been explored.
219            SRT1720 administration alleviates cholestatic liver injury in mice by increasing hydrophil
220                                      Chronic cholestatic liver injury induced by cholestasis in roden
221 esses the hepatoprotective potential against cholestatic liver injury induced by hepatotoxin such as
222                   The effect of serotonin on cholestatic liver injury is not known.
223             This transcriptional response to cholestatic liver injury likely promotes partial de-diff
224 rvations support a pivotal role for TRAIL in cholestatic liver injury mediated by NK 1.1-positive NK/
225 iethoxycarbonyl-1,4-dihydrocollidine-feeding cholestatic liver injury model.
226             PHB1 is an important mediator of cholestatic liver injury that regulates the activity of
227      Moreover, murine models of fibrotic and cholestatic liver injury were used to demonstrate that t
228 (-/-) mice), a model of inflammation-induced cholestatic liver injury, fibrosis, and cancer.
229      We have combined a mouse model of acute cholestatic liver injury, partial bile duct ligation (pB
230 g the fibroproliferative response to chronic cholestatic liver injury, suggesting a role for Hh signa
231  the key role of Gal3 in the pathogenesis of cholestatic liver injury, we generated dnTGF-betaRII/gal
232 nd promoting sickness behaviors in mice with cholestatic liver injury.
233 s and partial deficiencies in MDR3 result in cholestatic liver injury.
234 on is an effective strategy for ameliorating cholestatic liver injury.
235 otein 2 (MIP-2), which, in turn, exacerbates cholestatic liver injury.
236 ed whether serotonin affects the severity of cholestatic liver injury.
237  of canalicular bile acid secretion leads to cholestatic liver injury.
238 ine bile duct ligation (BDL) model to induce cholestatic liver injury.
239 cal activation of Nrf2 may be beneficial for cholestatic liver injury.
240  bile secretion, and its deficiency leads to cholestatic liver injury.
241 ant NKT (iNKT) cells have been implicated in cholestatic liver injury.
242 role in the adaptive response to obstructive cholestatic liver injury.
243 fects on HGF activation critically influence cholestatic liver injury.
244 1 could be potentially targeted to alleviate cholestatic liver injury.
245 L SR(-/-) mice, or Mdr2(-/-) mouse models of cholestatic liver injury.
246 irt1 presents a novel therapeutic target for cholestatic liver injury.
247 romised Sirt1 expression in rodent models of cholestatic liver injury.
248 ectin-3 regulates inflammasome activation in cholestatic liver injury.
249 w summarizes present Kupffer cell studies in cholestatic liver injury.
250 potentially serve as an indicator of chronic cholestatic liver injury.
251 that lipid metabolism contributed to chronic cholestatic liver injury; crossing peroxisome proliferat
252 range of potentially valuable actions on the cholestatic liver, has not yet been proved to make a sub
253 d to effectively extrude bile acids from the cholestatic liver.
254  contributes to accelerating fibrogenesis in cholestatic livers by mediating the initial inflammation
255 not produce FGF19, nonparenchymal cells from cholestatic livers produce FGF19.
256 n was tested in cholangiocytes of normal and cholestatic livers.
257 kout mice, as well as in myrcludex B-treated cholestatic mice, whereas plasma FGF19 was not induced i
258 -regulation of ATP11C protein in livers from cholestatic mice, which coincided with reduced OATP1B2 l
259 cluding 19 hepatocellular injury (HC) and 16 cholestatic/mixed injury (CS)] and AIH (n = 28) were eva
260 er disease, ischemia/reperfusion injury, and cholestatic models of liver disease.
261                                 Females from cholestatic mothers developed a severe obese, diabetic p
262 b treatment, at least in these steatotic and cholestatic mouse models, is the safer approach since it
263 nalysis, cotrimoxazole was associated with a cholestatic or ductopenic injury (OR = 7.05 [2.50-19.89]
264                           After UDCA removal cholestatic parameters, taurine species of cholic acid a
265 iary insults, these mice exhibit exacerbated cholestatic pathologies.
266 ong-sought pruritogenic signaling cascade in cholestatic patients suffering from itch.
267                                          Ten cholestatic patients were identified as vitamin A-defici
268 provide evidence for renal tubular injury in cholestatic patients with cholemic nephropathy.
269 ption lower the BS load and are best used in cholestatic patients.
270  is more common in younger patients, whereas cholestatic pattern increases with older age.
271                                            A cholestatic pattern was found in 60.0% of patients and w
272              In this study, we show that the cholestatic phenotype induced by common bile duct ligati
273                Our data demonstrate that the cholestatic potential of certain drugs may be aggravated
274 elieve this is the first report showing that cholestatic pregnancy in the absence of altered maternal
275 ased transplacental cholesterol transport in cholestatic pregnancy.
276 ocesses, including vasculogenesis, fibrosis, cholestatic pruritus and tumour progression.
277 s, including cancer, fibrosis, inflammation, cholestatic pruritus, and pain.
278 enesis, neuropathic pain, fibrotic diseases, cholestatic pruritus, lymphocyte homing, and thrombotic
279 s TRPA1, might be developed for treatment of cholestatic pruritus.
280 rvating the skin is thought to contribute to cholestatic pruritus.
281 atidic acid (LPA), as potential mediators of cholestatic pruritus.
282  sertraline and to evaluate its efficacy for cholestatic pruritus.
283 ve and mechanistic research in patients with cholestatic pruritus.
284 PDH nitrosylation was assessed in normal and cholestatic rat and human livers.
285 he liver of 17alpha-ethinylestradiol-induced cholestatic rats improves bile flow, in part by enhancin
286                           AdhAQP1-transduced cholestatic rats increased the biliary output of major e
287                        In AdhAQP1-transduced cholestatic rats, BSEP showed a canalicular microdomain
288 a, 30% METAVIR F3-F4, 4% decompensation, 11% cholestatic recurrence, 7% had kidney transplant, and 82
289 alpha and beta isoforms exhibited heightened cholestatic sensitivity.
290 e regulation of bile formation in normal and cholestatic states and greater insight into the pathogen
291            Testing the chip on subjects with cholestatic syndromes identified disease-causing mutatio
292 ns of transporter genes can cause hereditary cholestatic syndromes in both infants and adults as well
293 w insights into the pathogenesis of specific cholestatic syndromes including primary biliary cirrhosi
294 iver samples from individuals with different cholestatic syndromes, suggesting that reduced FOXA2 abu
295 ns of transporter genes can cause hereditary cholestatic syndromes, the study of which has shed much
296 rthered our understanding of cholestasis and cholestatic syndromes.
297 e molecular basis of hereditary and acquired cholestatic syndromes.
298             Recent studies have identified a cholestatic variant of nonalcoholic fatty liver disease
299                   Adult livers were severely cholestatic, with levels of bile salts >1 mM, but no evi
300 iver enzymes were significantly increased in cholestatic WT mice and significantly blunted in TRPC5 K

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