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1 phate (NADPH)-oxidase enzyme expression, and hepatocellular damage.
2 -17A production, exacerbated obesity-induced hepatocellular damage.
3 SFB depletion protected from obesity-induced hepatocellular damage.
4 centrations and serum ALT level, a marker of hepatocellular damage.
5  the induction of inflammatory pathology and hepatocellular damage.
6 ile acids may occur in the liver and lead to hepatocellular damage.
7 ssociation between PFOA and ALT, a marker of hepatocellular damage.
8 unction, rather than as a direct effector of hepatocellular damage.
9 ion of IL-10 restored local inflammation and hepatocellular damage.
10 ow, increased bile production, and decreased hepatocellular damage.
11 activation leading to liver inflammation and hepatocellular damage.
12 ow, increased bile production, and decreased hepatocellular damage.
13 demonstrated great promise in reducing acute hepatocellular damage.
14 NFalpha), liver neutrophil accumulation, and hepatocellular damage.
15 reperfusion, and coinciding with the maximal hepatocellular damage.
16 3 (STAT3) activation, but less steatosis and hepatocellular damage after alcohol or HFD feeding.
17  how these distinct NKT cell subsets mediate hepatocellular damage after IRI.
18 d greater glucose use), and less evidence of hepatocellular damage (alanine aminotransferase, asparta
19 on and hepatic resection is characterized by hepatocellular damage and a deleterious inflammatory res
20 like in controls, Sivelestat ameliorated the hepatocellular damage and decreased local neutrophil act
21  only the hepatic porphyria but also general hepatocellular damage and elevation of plasma hepatic en
22 IKK2-mediated NF-kappaB activation prevented hepatocellular damage and HCC in NEMO(LPC-KO) mice.
23 lizing anti-CXCR3 Ab treatment to ameliorate hepatocellular damage and improve 14-day survival of 30-
24    Anti-TIM-1 Ab monotherapy ameliorated the hepatocellular damage and improved liver function due to
25 VSOP-NO for steatotic partial livers reduces hepatocellular damage and improves graft viability and m
26 may provide a useful approach for preventing hepatocellular damage and improving outcomes in liver tr
27 gh regulation of HGF level, CYLD ameliorates hepatocellular damage and liver fibrogenesis.
28 l studies revealed that anti-TIM-3 increased hepatocellular damage and local neutrophil infiltration,
29  not used because of biochemical evidence of hepatocellular damage and one because of cirrhosis.
30  IL-17 neutralization prevented the enhanced hepatocellular damages and liver inflammation in these a
31 iver pathologies, including hypoproteinemia, hepatocellular damage, and in severe cases, frank whole-
32 d Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hep
33 ter resuscitation were attributed to hypoxic hepatocellular damage associated with the severity of th
34 Expression of this transgene induced diffuse hepatocellular damage beginning at 3 weeks of age, and h
35 IL-6 or hepatic STAT3 restored steatosis and hepatocellular damage but further enhanced liver inflamm
36 , neutralization of IL-1beta ameliorated the hepatocellular damage by inhibiting nuclear factor kappa
37  levels and reduced histological evidence of hepatocellular damage compared with controls.
38 TLR4(-/-) ) mice had significantly increased hepatocellular damage, compared to WT mice.
39 fects in acute-phase response, and increased hepatocellular damage, compared with control mice.
40 nce that allows viral expansion with limited hepatocellular damage during early stages of infection-a
41 the induction of inflammation leading to the hepatocellular damage during liver ischemia/reperfusion
42 tion of beta-catenin signaling increased the hepatocellular damage, enhanced hepatic DC maturation/fu
43 pecific inhibitor, SB216763, ameliorated the hepatocellular damage, evidenced by reduced serum alanin
44           A20 expression in the liver limits hepatocellular damage hence maintains bilirubin clearanc
45 acerbates liver inflammation, steatosis, and hepatocellular damage in alcoholic and nonalcoholic fatt
46 ion of hepatic STAT3 increased steatosis and hepatocellular damage in ALDH2(-/-) mice.
47 is a widely used index of liver integrity or hepatocellular damage in clinics as well as a key enzyme
48             This corresponded with increased hepatocellular damage in HO-1(+/-) mice, compared with W
49 ion of intrahepatic inflammation, leading to hepatocellular damage in liver ischemia/reperfusion inju
50 atic STAT3 may reduce rather than accelerate hepatocellular damage in patients with chronic liver dis
51 velopment of severe hepatic inflammation and hepatocellular damage in steatotic livers, presenting he
52 eadily recreated local inflammation response/hepatocellular damage in the CD11b-DTR mouse system.
53 fenin is a good predictor of the severity of hepatocellular damage in toxic-induced liver disease.
54  IL-17A significantly reduced obesity-driven hepatocellular damage in wild-type mice.
55  response but are resistant to steatosis and hepatocellular damage induced by ethanol or HFD feeding.
56 ng CYLD (CYLD-/-) were highly susceptible to hepatocellular damage, inflammation, and fibrosis and re
57                                              Hepatocellular damage, inflammation, and metabolic effec
58 7-H1 monoclonal antibody treatment augmented hepatocellular damage, its stimulation following B7-H1 i
59 sured by myeloperoxidase (MPO) content], and hepatocellular damage [measured by serum alanine aminotr
60  with no eosinophil-dependent differences in hepatocellular damage observed.
61                                              Hepatocellular damage, oxidative and nitrosative stress,
62 TIM-3 Ab were characterized by: (1) enhanced hepatocellular damage (sALT levels, liver Suzuki's histo
63 lure in WT and Stat6 KO mice, as assessed by hepatocellular damage (serum alanine aminotransferase [s
64 followed by OLT, as assessed by 1) decreased hepatocellular damage (serum glutamic oxaloacetic transa
65 ta by macrophage pacification attenuates the hepatocellular damage, suggesting that these mediators p
66                              Despite similar hepatocellular damage, TG2(-/-) mice had more gallstones
67 fect on liver blood flow and protect against hepatocellular damage under pathophysiological condition
68 ne protects rat livers from IRI and prevents hepatocellular damage upon transplantation into syngenei
69 trinsic PACAP and its receptors, whereas the hepatocellular damage was exacerbated in PACAP-deficient
70 /-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(
71 a containing only EHCV, and evidence of mild hepatocellular damage was observed.
72 e prevalent among Egyptians, and evidence of hepatocellular damage was significantly greater among Eg

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