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1 ith LV-Co, and correlated with biomarkers of hepatocellular damage.
2 erized by liver steatosis, inflammation, and hepatocellular damage.
3 reperfusion, and coinciding with the maximal hepatocellular damage.
4 phate (NADPH)-oxidase enzyme expression, and hepatocellular damage.
5 -17A production, exacerbated obesity-induced hepatocellular damage.
6 an infiltration of T-lymphocytes in areas of hepatocellular damage.
7 SFB depletion protected from obesity-induced hepatocellular damage.
8 centrations and serum ALT level, a marker of hepatocellular damage.
9  the induction of inflammatory pathology and hepatocellular damage.
10 unction, rather than as a direct effector of hepatocellular damage.
11 ion of IL-10 restored local inflammation and hepatocellular damage.
12 ow, increased bile production, and decreased hepatocellular damage.
13 activation leading to liver inflammation and hepatocellular damage.
14 ile acids may occur in the liver and lead to hepatocellular damage.
15 ow, increased bile production, and decreased hepatocellular damage.
16 demonstrated great promise in reducing acute hepatocellular damage.
17 ssociation between PFOA and ALT, a marker of hepatocellular damage.
18 NFalpha), liver neutrophil accumulation, and hepatocellular damage.
19 liver steatosis, inflammation, fibrosis, and hepatocellular damage.
20 3 (STAT3) activation, but less steatosis and hepatocellular damage after alcohol or HFD feeding.
21  how these distinct NKT cell subsets mediate hepatocellular damage after IRI.
22 d greater glucose use), and less evidence of hepatocellular damage (alanine aminotransferase, asparta
23 on and hepatic resection is characterized by hepatocellular damage and a deleterious inflammatory res
24 ve hepatic nutrient signaling does not cause hepatocellular damage and carcinomas, unlike genetic act
25 like in controls, Sivelestat ameliorated the hepatocellular damage and decreased local neutrophil act
26  only the hepatic porphyria but also general hepatocellular damage and elevation of plasma hepatic en
27 IKK2-mediated NF-kappaB activation prevented hepatocellular damage and HCC in NEMO(LPC-KO) mice.
28 on and visceral damage to the liver, causing hepatocellular damage and hemosiderosis.
29 lizing anti-CXCR3 Ab treatment to ameliorate hepatocellular damage and improve 14-day survival of 30-
30    Anti-TIM-1 Ab monotherapy ameliorated the hepatocellular damage and improved liver function due to
31 VSOP-NO for steatotic partial livers reduces hepatocellular damage and improves graft viability and m
32 may provide a useful approach for preventing hepatocellular damage and improving outcomes in liver tr
33 gh regulation of HGF level, CYLD ameliorates hepatocellular damage and liver fibrogenesis.
34 l studies revealed that anti-TIM-3 increased hepatocellular damage and local neutrophil infiltration,
35  not used because of biochemical evidence of hepatocellular damage and one because of cirrhosis.
36  IL-17 neutralization prevented the enhanced hepatocellular damages and liver inflammation in these a
37  liver to NASH, which involves inflammation, hepatocellular damage, and fibrosis.
38 iver pathologies, including hypoproteinemia, hepatocellular damage, and in severe cases, frank whole-
39 d Ptpn6(f/f) littermates, along with reduced hepatocellular damage as revealed by serum levels of hep
40 ter resuscitation were attributed to hypoxic hepatocellular damage associated with the severity of th
41 Expression of this transgene induced diffuse hepatocellular damage beginning at 3 weeks of age, and h
42 IL-6 or hepatic STAT3 restored steatosis and hepatocellular damage but further enhanced liver inflamm
43 , neutralization of IL-1beta ameliorated the hepatocellular damage by inhibiting nuclear factor kappa
44 otected mouse livers from warm IR stress and hepatocellular damage by inhibiting prolyl hydroxylase d
45  levels and reduced histological evidence of hepatocellular damage compared with controls.
46 TLR4(-/-) ) mice had significantly increased hepatocellular damage, compared to WT mice.
47 fects in acute-phase response, and increased hepatocellular damage, compared with control mice.
48 nce that allows viral expansion with limited hepatocellular damage during early stages of infection-a
49 the induction of inflammation leading to the hepatocellular damage during liver ischemia/reperfusion
50 tion of beta-catenin signaling increased the hepatocellular damage, enhanced hepatic DC maturation/fu
51 pecific inhibitor, SB216763, ameliorated the hepatocellular damage, evidenced by reduced serum alanin
52           A20 expression in the liver limits hepatocellular damage hence maintains bilirubin clearanc
53 acerbates liver inflammation, steatosis, and hepatocellular damage in alcoholic and nonalcoholic fatt
54 ion of hepatic STAT3 increased steatosis and hepatocellular damage in ALDH2(-/-) mice.
55 is a widely used index of liver integrity or hepatocellular damage in clinics as well as a key enzyme
56             This corresponded with increased hepatocellular damage in HO-1(+/-) mice, compared with W
57 ion of intrahepatic inflammation, leading to hepatocellular damage in liver ischemia/reperfusion inju
58 atic STAT3 may reduce rather than accelerate hepatocellular damage in patients with chronic liver dis
59 velopment of severe hepatic inflammation and hepatocellular damage in steatotic livers, presenting he
60 eadily recreated local inflammation response/hepatocellular damage in the CD11b-DTR mouse system.
61 fenin is a good predictor of the severity of hepatocellular damage in toxic-induced liver disease.
62 ch to protect the liver against I/R-mediated hepatocellular damage in transplant recipients.
63  IL-17A significantly reduced obesity-driven hepatocellular damage in wild-type mice.
64  response but are resistant to steatosis and hepatocellular damage induced by ethanol or HFD feeding.
65 ng CYLD (CYLD-/-) were highly susceptible to hepatocellular damage, inflammation, and fibrosis and re
66                                              Hepatocellular damage, inflammation, and metabolic effec
67 7-H1 monoclonal antibody treatment augmented hepatocellular damage, its stimulation following B7-H1 i
68                  Understanding mechanisms of hepatocellular damage may lead to new treatments for liv
69 sured by myeloperoxidase (MPO) content], and hepatocellular damage [measured by serum alanine aminotr
70  with no eosinophil-dependent differences in hepatocellular damage observed.
71                                              Hepatocellular damage, oxidative and nitrosative stress,
72  trichostatin-A (TSA) was protective against hepatocellular damage ( P < 0.01 for AST and P < 0.05 fo
73 TIM-3 Ab were characterized by: (1) enhanced hepatocellular damage (sALT levels, liver Suzuki's histo
74 lure in WT and Stat6 KO mice, as assessed by hepatocellular damage (serum alanine aminotransferase [s
75 followed by OLT, as assessed by 1) decreased hepatocellular damage (serum glutamic oxaloacetic transa
76 ta by macrophage pacification attenuates the hepatocellular damage, suggesting that these mediators p
77                              Despite similar hepatocellular damage, TG2(-/-) mice had more gallstones
78 model, we found Nrf2(M-KO) mice showed worse hepatocellular damage than Nrf2-proficient controls base
79  the high CD4 cohort developed a more severe hepatocellular damage than that with low CD4 levels.
80 fect on liver blood flow and protect against hepatocellular damage under pathophysiological condition
81 ne protects rat livers from IRI and prevents hepatocellular damage upon transplantation into syngenei
82 trinsic PACAP and its receptors, whereas the hepatocellular damage was exacerbated in PACAP-deficient
83 /-) CD4(+) T cells overexpressed Fas ligand, hepatocellular damage was observed in Fas(lpr/lpr)Tgfb1(
84 a containing only EHCV, and evidence of mild hepatocellular damage was observed.
85 e prevalent among Egyptians, and evidence of hepatocellular damage was significantly greater among Eg