ライフサイエンスコーパス: necroinflammation

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

17 rulonephritis is characterized by glomerular necroinflammation and crescent formation.

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

21 cy was correlated with the severity of liver necroinflammation and fibrosis in CHB.

22 play an important role in the development of necroinflammation and fibrosis in the liver parenchyma i

23 in chronic HCV-infected patients with higher necroinflammation and fibrosis.

24 -treatment liver biopsies were evaluated for necroinflammation and fibrosis.

25 iral clearance, but alternately can increase necroinflammation and hepatic decompensation without enh

26 Increased necroinflammation and higher ALT level were associated w

27 CCl4 produced similar fibrosis and necroinflammation and increased the mRNA and protein exp

28 ted with fibrosis progression alongside with necroinflammation and steatosis.

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

31 Hepatic steatosis, necroinflammation, and fibrosis were increased in saline

32 f lipid peroxidation/oxidant stress, lobular necroinflammation, and fibrosis.

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

37 Although necrosis and necroinflammation are central features of many liver dis

38 Efficient suppression of HBV viremia and necroinflammation as a result of nucleos(t)ide analogue

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

44 Centrilobular necroinflammation (CLNI) associated with an elevated asp

45 The degree of necroinflammation correlates with expression levels of P

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

48 Necroinflammation, fibrosis, and portal pressure were ei

49 C were studied and liver biopsies scored for necroinflammation (grade 0-18) and fibrosis (stage 0-6).

50 At the end of treatment, necroinflammation grading was reduced in an average of 3

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

56 id not translate into worse liver steatosis, necroinflammation or fibrosis.

57 ession rate), where the odds ratio of having necroinflammation or rapid fibrosis progression for pati

58 Changes in the degree of steatosis, necroinflammation, or fibrosis that occurred with therap

59 , P=0.009) and with the reduction in hepatic necroinflammation (r=0.47, P=0.0007).

60 avenues are further discussed for abrogating necroinflammation-related kidney injury, and questions a

61 rsistence, low-level viral protein, and mild necroinflammation remained in liver tissue.

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.

65 Here, the contribution of necroinflammation to AKI is discussed in thrombotic micr

66 Biopsies were scored for necroinflammation using a modified histology activity in

67 Although periportal and lobular necroinflammation vanished, portal inflammation persiste

68 High-grade necroinflammation was present in native livers at LT in

69 erized by insulin resistance, steatosis, and necroinflammation with or without centrilobular fibrosis