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1 eribiliary fibrosis, in the absence of overt necroinflammation.
2 R-122 and positively correlated with hepatic necroinflammation.
3 yl transferase (GGT), two markers of hepatic necroinflammation.
4 ed markers of insulin resistance and hepatic necroinflammation.
5 ssing hepatocytes predominated in areas with necroinflammation.
6 ytes was increased in patients with advanced necroinflammation.
7 ncordance was only fair for most features of necroinflammation.
8 ccurs in NAFLD, particularly for features of necroinflammation.
9 lating the activation of innate immunity and necroinflammation.
10 by hepatic steatosis and varying degrees of necroinflammation.
11 terval (CI), 1.06-3.20]; P=.03) but not with necroinflammation.
12 autoamplification loop, referred to here as necroinflammation.
13 ioglitazone group had a greater reduction in necroinflammation (85% vs. 38%, P=0.001), but the reduct
14 cur in cirrhotic livers that show pronounced necroinflammation, abnormal angiogenesis and extensive f
15 lerance and glucose clearance, steatosis and necroinflammation (all P<0.01-0.001 versus placebo).
16 We observed fatty liver, increased hepatic necroinflammation and apoptosis, and hyperhomocysteinemi
18 the development of histologically detectable necroinflammation and fibrosis (mean damping ratio at 80
19 manner could ameliorate steatosis, but also necroinflammation and fibrosis by reducing oxidative str
20 olic fatty liver disease activity score, and necroinflammation and fibrosis graded and staged accordi
22 play an important role in the development of necroinflammation and fibrosis in the liver parenchyma i
25 iral clearance, but alternately can increase necroinflammation and hepatic decompensation without enh
29 ndependently with increasing age, periportal necroinflammation, and ALT elevations but not with steat
30 affects histological severity of steatosis, necroinflammation, and fibrosis in a cross-sectional coh
33 notransferase elevation, lipid accumulation, necroinflammation, and focal hepatic cell death in mice
34 als, where association with severe fibrosis, necroinflammation, and nonalcoholic steatohepatitis was
35 severe lymphocytic infiltration, apoptosis, necroinflammation, and serum alanine aminotransferase el
36 moderate contribution to the ALT elevation, necroinflammation, apoptosis, a small contribution to th
39 to identify predictors of significant liver necroinflammation as defined by a Histology Activity Ind
40 riers (P < 0.05), had more-severe steatosis, necroinflammation, ballooning, and fibrosis (P < 0.05),
41 serum aminotransferases, hepatic steatosis, necroinflammation, ballooning, and nonalcoholic fatty li
42 ect on hepatic triglyceride content or liver necroinflammation but reduced HSC activation and liver f
43 eta1 (Tgfb1(-/-) mice) acutely develop liver necroinflammation caused by IFN-gamma-producing clusters
46 ulin resistance, and liver fibrosis (but not necroinflammation) deteriorated as quartiles of adipose
47 -years treatment with Pirfenidone influences necroinflammation, fibrosis and steatosis, serum levels
49 C were studied and liver biopsies scored for necroinflammation (grade 0-18) and fibrosis (stage 0-6).
51 genotype was associated with greater hepatic necroinflammation, higher ALT, and worse clinical outcom
52 , glucose metabolism, hepatic steatosis, and necroinflammation in patients with nonalcoholic steatohe
53 exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accum
54 167K variant was associated with more severe necroinflammation (Ishak grade; adjusted P = 0.037) and
55 = 0.005) and with severe (grade 2-3) lobular necroinflammation (odds ratio, 1.47; 95% confidence inte
57 ession rate), where the odds ratio of having necroinflammation or rapid fibrosis progression for pati
60 avenues are further discussed for abrogating necroinflammation-related kidney injury, and questions a
62 as an independent factor for a total Knodell necroinflammation score of >/= 7 (odds ratio, 0.74; 95%
63 After further conditioning for steatosis and necroinflammation, the E167K variant remained associated
64 m tests and assessment of liver fibrosis and necroinflammation through biopsy or noninvasive means.
69 erized by insulin resistance, steatosis, and necroinflammation with or without centrilobular fibrosis
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