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1 p96 level positively correlated with hepatic necroinflammation.
2 lating the activation of innate immunity and necroinflammation.
3  autoamplification loop, referred to here as necroinflammation.
4 eribiliary fibrosis, in the absence of overt necroinflammation.
5 R-122 and positively correlated with hepatic necroinflammation.
6 yl transferase (GGT), two markers of hepatic necroinflammation.
7 ssing hepatocytes predominated in areas with necroinflammation.
8 ytes was increased in patients with advanced necroinflammation.
9 ncordance was only fair for most features of necroinflammation.
10 ccurs in NAFLD, particularly for features of necroinflammation.
11  by hepatic steatosis and varying degrees of necroinflammation.
12 terval (CI), 1.06-3.20]; P=.03) but not with necroinflammation.
13 at trigger an immune response referred to as necroinflammation.
14 ed markers of insulin resistance and hepatic necroinflammation.
15 flammatory response, which is referred to as necroinflammation.
16 ioglitazone group had a greater reduction in necroinflammation (85% vs. 38%, P=0.001), but the reduct
17 cur in cirrhotic livers that show pronounced necroinflammation, abnormal angiogenesis and extensive f
18 lerance and glucose clearance, steatosis and necroinflammation (all P<0.01-0.001 versus placebo).
19   We observed fatty liver, increased hepatic necroinflammation and apoptosis, and hyperhomocysteinemi
20 rulonephritis is characterized by glomerular necroinflammation and crescent formation.
21 ohepatitis (NASH), which is characterised by necroinflammation and faster fibrosis progression than n
22 the development of histologically detectable necroinflammation and fibrosis (mean damping ratio at 80
23  manner could ameliorate steatosis, but also necroinflammation and fibrosis by reducing oxidative str
24 olic fatty liver disease activity score, and necroinflammation and fibrosis graded and staged accordi
25 cy was correlated with the severity of liver necroinflammation and fibrosis in CHB.
26 itor the progression and regression of liver necroinflammation and fibrosis in mouse models of non-al
27 es is clinically associated with progressive necroinflammation and fibrosis in nonalcoholic steatohep
28 play an important role in the development of necroinflammation and fibrosis in the liver parenchyma i
29                        Males had significant necroinflammation and fibrosis more than the females.
30 taneous liver biopsy to evaluate significant necroinflammation and fibrosis using the Meta-analysis o
31 in chronic HCV-infected patients with higher necroinflammation and fibrosis.
32 -treatment liver biopsies were evaluated for necroinflammation and fibrosis.
33 roinflammation only, and 13 (14.8%) had both necroinflammation and fibrosis.
34 iral clearance, but alternately can increase necroinflammation and hepatic decompensation without enh
35                                    Increased necroinflammation and higher ALT level were associated w
36           CCl4 produced similar fibrosis and necroinflammation and increased the mRNA and protein exp
37 ted with fibrosis progression alongside with necroinflammation and steatosis.
38          Thirty-nine (44.3%) had significant necroinflammation and/or fibrosis on histology, 19 (21.6
39 ients can develop advanced hepatic fibrosis, necroinflammation, and allograft failure.
40 ndependently with increasing age, periportal necroinflammation, and ALT elevations but not with steat
41  affects histological severity of steatosis, necroinflammation, and fibrosis in a cross-sectional coh
42                           Hepatic steatosis, necroinflammation, and fibrosis were increased in saline
43 f lipid peroxidation/oxidant stress, lobular necroinflammation, and fibrosis.
44 notransferase elevation, lipid accumulation, necroinflammation, and focal hepatic cell death in mice
45 als, where association with severe fibrosis, necroinflammation, and nonalcoholic steatohepatitis was
46  severe lymphocytic infiltration, apoptosis, necroinflammation, and serum alanine aminotransferase el
47  moderate contribution to the ALT elevation, necroinflammation, apoptosis, a small contribution to th
48                        Although necrosis and necroinflammation are central features of many liver dis
49     Efficient suppression of HBV viremia and necroinflammation as a result of nucleos(t)ide analogue
50  to identify predictors of significant liver necroinflammation as defined by a Histology Activity Ind
51 riers (P < 0.05), had more-severe steatosis, necroinflammation, ballooning, and fibrosis (P < 0.05),
52  serum aminotransferases, hepatic steatosis, necroinflammation, ballooning, and nonalcoholic fatty li
53 ect on hepatic triglyceride content or liver necroinflammation but reduced HSC activation and liver f
54 eta1 (Tgfb1(-/-) mice) acutely develop liver necroinflammation caused by IFN-gamma-producing clusters
55                                Centrilobular necroinflammation (CLNI) associated with an elevated asp
56                                The degree of necroinflammation correlates with expression levels of P
57 ulin resistance, and liver fibrosis (but not necroinflammation) deteriorated as quartiles of adipose
58 -years treatment with Pirfenidone influences necroinflammation, fibrosis and steatosis, serum levels
59                                              Necroinflammation, fibrosis, and portal pressure were ei
60 C were studied and liver biopsies scored for necroinflammation (grade 0-18) and fibrosis (stage 0-6).
61 edictions for MASH Clinical Research Network necroinflammation grades and fibrosis stages were reprod
62                     At the end of treatment, necroinflammation grading was reduced in an average of 3
63 genotype was associated with greater hepatic necroinflammation, higher ALT, and worse clinical outcom
64 r regulator of transcription and a driver of necroinflammation in AKI.
65 , glucose metabolism, hepatic steatosis, and necroinflammation in patients with nonalcoholic steatohe
66 exhibits extensive, spontaneously developing necroinflammation in the liver, accompanied by the accum
67 ontributors to oxalate crystal-induced renal necroinflammation include the NACHT, LRR and PYD domains
68 167K variant was associated with more severe necroinflammation (Ishak grade; adjusted P = 0.037) and
69 = 0.005) and with severe (grade 2-3) lobular necroinflammation (odds ratio, 1.47; 95% confidence inte
70 ibrosis on histology, 19 (21.6%) of whom had necroinflammation only, and 13 (14.8%) had both necroinf
71 id not translate into worse liver steatosis, necroinflammation or fibrosis.
72 ession rate), where the odds ratio of having necroinflammation or rapid fibrosis progression for pati
73          Changes in the degree of steatosis, necroinflammation, or fibrosis that occurred with therap
74 , P=0.009) and with the reduction in hepatic necroinflammation (r=0.47, P=0.0007).
75 avenues are further discussed for abrogating necroinflammation-related kidney injury, and questions a
76 rsistence, low-level viral protein, and mild necroinflammation remained in liver tissue.
77 as an independent factor for a total Knodell necroinflammation score of >/= 7 (odds ratio, 0.74; 95%
78 After further conditioning for steatosis and necroinflammation, the E167K variant remained associated
79 m tests and assessment of liver fibrosis and necroinflammation through biopsy or noninvasive means.
80                    Here, the contribution of necroinflammation to AKI is discussed in thrombotic micr
81                     Biopsies were scored for necroinflammation using a modified histology activity in
82              Although periportal and lobular necroinflammation vanished, portal inflammation persiste
83                                   High-grade necroinflammation was present in native livers at LT in
84 erized by insulin resistance, steatosis, and necroinflammation with or without centrilobular fibrosis