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1 surround the bile duct after cholestatic and hepatocellular injury.
2 as been no evidence of rosiglitazone-induced hepatocellular injury.
3         Rosiglitazone may be associated with hepatocellular injury.
4 ttern for HCV genomic RNA and any indices of hepatocellular injury.
5         Liver function tests revealed severe hepatocellular injury.
6 r tissue may be a significant determinant of hepatocellular injury.
7 itical role of invasive ductular reaction in hepatocellular injury.
8  hepatic neutrophil accumulation, edema, and hepatocellular injury.
9 , hypertriglyceridemia, liver steatosis, and hepatocellular injury.
10 etal hepatic collagen deposition, indicating hepatocellular injury.
11 ficiency mitigated coagulation activation or hepatocellular injury.
12 atic accumulation of bile acids (BAs) causes hepatocellular injury.
13 led in health, increasing to 34% after acute hepatocellular injury.
14 ages of fibrosis caused by either biliary or hepatocellular injury.
15 ounted for by biomarkers of inflammation and hepatocellular injury.
16 ne of three treated animals without apparent hepatocellular injury.
17 at mediates activation of coagulation during hepatocellular injury.
18 ependent inflammatory phenotype and leads to hepatocellular injury.
19  the progression of hepatic inflammation and hepatocellular injury.
20 calyx damage correlates with the severity of hepatocellular injury.
21 f HO-1 overexpression on HCV replication and hepatocellular injury.
22 en-induced liver toxicity, causing fulminant hepatocellular injury.
23 itical for IR-induced liver inflammation and hepatocellular injury.
24 to its previously documented central role in hepatocellular injury.
25 flammatory response and significantly reduce hepatocellular injury.
26 bute to operating hepatobiliary junctions on hepatocellular injury.
27 lpha), liver accumulation of neutrophils, or hepatocellular injury.
28 patic intra cellular oxygenation and reduced hepatocellular injury.
29 and reduced tissue oxygenation and increased hepatocellular injury.
30 n accumulation of leukocytes and significant hepatocellular injury.
31 liver regeneration in the setting of ongoing hepatocellular injury.
32  route toward suppressing fibrosis caused by hepatocellular injuries.
33       Absence of Smad3 significantly blunted hepatocellular injury 9 hours post ConA injection, which
34  between HCV replication in liver tissue and hepatocellular injury, a strand-specific in situ hybridi
35 ceptor antagonists convey protection against hepatocellular injury accompanied by a decrease in nitri
36 nt potentiated ischemia-reperfusion-mediated hepatocellular injury, accompanied by increased serum al
37 t HMGB1-HC-KO mice had significantly greater hepatocellular injury after I/R, compared to control mic
38  (FAS) and catabolism (PPARalpha and CPT1)), hepatocellular injury (ALT), hepatic inflammation (mRNA
39 erfusion there was a significant increase in hepatocellular injury and a delay in recovery compared t
40 crosis factor (TNF)-alpha causes much of the hepatocellular injury and cell death that follows toxin-
41           In conclusion, JNK2 contributes to hepatocellular injury and death after I/R in association
42  similarly sensitized to cathepsin-dependent hepatocellular injury and death from IL-1beta/TNF in com
43  found that IL-6-/- mice developed increased hepatocellular injury and defective regeneration with si
44 ced activation of the coagulation system and hepatocellular injury and diminished hepatic fibrin depo
45 atocellular proliferation and an increase of hepatocellular injury and endoplasmic reticulum stress.
46 eatosis, to steatohepatitis with evidence of hepatocellular injury and fibrosis, to cirrhosis.
47 indromatosis (CYLD), confers protection from hepatocellular injury and fibrosis.
48               Immediately after reperfusion, hepatocellular injury and function were improved in HMP
49 icient ethionine-supplemented mouse model of hepatocellular injury and human liver samples were used
50 statin pretreatment significantly attenuated hepatocellular injury and increased survival of male mic
51                                              Hepatocellular injury and inflammation are believed to b
52  of hepatic steatosis but leads to increased hepatocellular injury and inflammation that may be due i
53 onic ethanol consumption can cause sustained hepatocellular injury and inhibit the subsequent regener
54 ated by oxidants and cytokines and regulates hepatocellular injury and insulin resistance, suggesting
55 t toxin-induced hepatic fibrosis, associated hepatocellular injury and intra-hepatic inflammation, an
56 iver neutrophil recruitment by up to 72% and hepatocellular injury and liver edema were each reduced
57                  IL-33 significantly reduced hepatocellular injury and liver neutrophil accumulation
58 of a transgenic line of sickle cell mice for hepatocellular injury and localization of two isoforms o
59                                 The basis of hepatocellular injury and progressive fibrosis in a subs
60                   Cholestasis contributes to hepatocellular injury and promotes liver carcinogenesis.
61 polysaccharide and peptidoglycan resulted in hepatocellular injury and renal dysfunction.
62  livers harvested to determine the degree of hepatocellular injury and the induction of TNF-, IL-1bet
63 cterized by hepatic steatosis, inflammation, hepatocellular injury, and different degrees of fibrosis
64 ipotoxicity and the underlying inflammation, hepatocellular injury, and fibrosis in metabolic dysfunc
65           Altered hepatic lipid homeostasis, hepatocellular injury, and inflammation are features of
66 t increases in liver neutrophil recruitment, hepatocellular injury, and liver edema, as defined by li
67 , leading to hepatic neutrophil recruitment, hepatocellular injury, and liver edema.
68 hrs in hypotension, acute renal dysfunction, hepatocellular injury, and lung injury.
69  mice would increase cholestasis, steatosis, hepatocellular injury, and mortality and impair hepatocy
70 cterised by hepatic steatosis, inflammation, hepatocellular injury, and progressive liver fibrosis.
71 ing in these models and results in increased hepatocellular injury, apoptosis, and death.
72 howed improved survival, there was extensive hepatocellular injury as indicated by large LDH release
73 ted liver glycogen and significantly reduced hepatocellular injury as measured by LDH release and AST
74 ion, Ad-based IL-13 significantly diminished hepatocellular injury, assessed by serum glutamic oxaloa
75  postnatal week and increased DNA damage and hepatocellular injury at 1-2 weeks of age.
76 urs, followed by predominantly centrolobular hepatocellular injury at 24 hours.
77 ely on the histologic findings of steatosis, hepatocellular injury (ballooning, Mallory bodies), and
78 lly susceptible K8tg mice, HF diet triggered hepatocellular injury, ballooning, apoptosis, inflammati
79 owed no significant changes in steatosis and hepatocellular injury, but a approximately 50% reduction
80  IL-10 KO and IL-10/IL-4 KO mice experienced hepatocellular injury, but only IL-10 KO mice advanced t
81 liferation have the disadvantage of inducing hepatocellular injury by delivery of toxins or by surgic
82 e at reperfusion, stimulated by PAF, mediate hepatocellular injury by triggering leukocyte accumulati
83                       CD8+ T cells can cause hepatocellular injury by two distinct mechanisms.
84 irst time the construction of a hypothetical hepatocellular injury cascade for this disease involving
85 ated the renal dysfunction, lung injury, and hepatocellular injury caused by lipoteichoic acid/peptid
86 start of nefazodone therapy suggested severe hepatocellular injury caused by the drug.
87  identified phenotypes with no liver injury, hepatocellular injury, cholestatic injury, and combined
88 CD8 and L-selectin, but not CD4, ameliorated hepatocellular injury, confirming that CD8(+) cells are
89 se-dependently reduced acetaminophen-induced hepatocellular injury, dampened colitis-associated infla
90 ukin-6 null (IL-6-/-) mice develop increased hepatocellular injury, defective regeneration, delayed w
91    Histological analysis correlated with the hepatocellular injury determined with transaminases and
92 OVID-19 liver, providing the underpinning of hepatocellular injury, ductular reaction, pathologic vas
93 s intrinsic cLT production may contribute to hepatocellular injury during inflammation.
94 following ischemia/reperfusion is a cause of hepatocellular injury during transplantation.
95 but attenuated the renal dysfunction and the hepatocellular injury/dysfunction caused by LTA/PepG.
96                                              Hepatocellular injury, female sex, high levels of TBL, a
97 atic liver diseases are often accompanied by hepatocellular injury, fibrosis, and cirrhosis due to th
98 tial proportion of HCC arises as a result of hepatocellular injury from NASH.
99 ory biomarker IL-6 and for the biomarkers of hepatocellular injury glutamate dehydrogenase, alanine a
100  histology from 128 patients presenting with hepatocellular injury had more severe inflammation, necr
101     The central role of T cell activation in hepatocellular injury has been well documented.
102 ell-characterized DILI [n = 35, including 19 hepatocellular injury (HC) and 16 cholestatic/mixed inju
103 te kidney injury, gastrointestinal symptoms, hepatocellular injury, hyperglycemia and ketosis, neurol
104  is characterized by cholestasis, steatosis, hepatocellular injury, impaired regeneration, a decrease
105 ypothesized that Btk inhibition would reduce hepatocellular injury in a murine model of liver warm he
106                    Neutrophils contribute to hepatocellular injury in a number of acute inflammatory
107                 BTKB66 treatment ameliorated hepatocellular injury in a well-established model of liv
108 otential target to mitigate inflammation and hepatocellular injury in AH.
109     Because nefazodone seems to cause severe hepatocellular injury in an idiosyncratic manner, routin
110 l therapy and therapeutic protection against hepatocellular injury in HCV infection.
111      CLP induced cholestasis, steatosis, and hepatocellular injury in interleukin-6 -/-, but not inte
112           There was continued alleviation of hepatocellular injury in knockout mice despite ongoing c
113 f c-Jun kinase, a process that may cause the hepatocellular injury in nonalcoholic steatohepatitis.
114 pha); to correlate inversely with markers of hepatocellular injury in patients with liver ischemia; a
115 acterial lipopolysaccharide (LPS) results in hepatocellular injury in rats, the onset of which occurs
116 drial dysfunction may be important causes of hepatocellular injury in the steatotic liver.
117 TNFalpha, liver neutrophil accumulation, and hepatocellular injury in wild-type mice.
118 mmation-mediated STAT3 activation attenuates hepatocellular injury induced by CCl(4) in myeloid-speci
119  observed conditions included renal failure, hepatocellular injury, infections, and hematologic malig
120                         Following sacrifice, hepatocellular injury, inflammation, and biliary and ste
121 ulation of excessive liver lipids leading to hepatocellular injury, inflammation, and fibrosis that g
122                   In contrast, biomarkers of hepatocellular injury, inflammatory gene induction, and
123                                    On severe hepatocellular injury, invasive DR has been proposed to
124                                              Hepatocellular injury is caused by toxicity of the mutan
125                                 Drug-induced hepatocellular injury is identified internationally by a
126        One such protective pathway to reduce hepatocellular injury is the up-regulation of heme oxyge
127 is (FIB-4, APRI, and Forns index scores) and hepatocellular injury (levels of aminotransferases).
128 erase, alanine aminotransferase (markers for hepatocellular injury), lipase (indicator of pancreatic
129 s correlated with effluent concentrations of hepatocellular injury markers, including alkaline phosph
130 patocytes, suggesting that in these settings hepatocellular injury may be altered by the decrease in
131  of infection in humans, including prolonged hepatocellular injury, necrosis, hyperplasia, and an ele
132 om mild necrosis and inflammation to extreme hepatocellular injury, nodular regeneration, and bile du
133 tic hepatitis and 12 patients presented with hepatocellular injury, of which six had an autoimmune ph
134                Histologic features including hepatocellular injury (P = .005), Mallory-Denk bodies (P
135 ted in hypotension, acute renal dysfunction, hepatocellular injury, pancreatic injury, and increased
136         The remaining HDS cases presented as hepatocellular injury, predominantly in middle-aged wome
137 ) progression, influencing processes such as hepatocellular injury, regeneration, inflammation, fibro
138 on of deleted vectors in mice resulted in no hepatocellular injury relative to that seen with first-g
139 isms by which lysosomal iron participates in hepatocellular injury remain uncertain.
140  accumulation at 6 hours correlated with the hepatocellular injury seen at 24 hours.
141 ttenuate further the small level of residual hepatocellular injury seen in leukopenic rats.
142 ent of renal dysfunction (serum creatinine), hepatocellular injury (serum alanine aminotransferase an
143        We hypothesized that hypoxia promotes hepatocellular injury, shifts nutrient metabolism, and a
144 ligation, FAAH(-/-) mice displayed increased hepatocellular injury, suggesting that FAAH protects hep
145 kout-transgenic SCD mice indicated extensive hepatocellular injury that was accompanied by increased
146                        In retrorsine-induced hepatocellular injury the capacity of fully differentiat
147                    Endotoxin (LPS) can cause hepatocellular injury under several circumstances, and l
148                                              Hepatocellular injury was assessed by alanine aminotrans
149 n antibody-treated mice were fed an HFD, and hepatocellular injury was assessed by histology, propidi
150 tic neutrophil recruitment, liver edema, and hepatocellular injury were all significantly reduced by
151 s of T cell immunity, virus replication, and hepatocellular injury were studied in two HAV-infected c
152      Steatotic liver responds with increased hepatocellular injury when exposed to an ischemic-reperf
153                       NO stimulation reduced hepatocellular injury, whereas inhibition of nitric oxid
154            His blood profile showed a severe hepatocellular injury with jaundice (alanine transaminas

 
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