ライフサイエンスコーパス: necroinflammatory

1 In those HCV cases showing evidence of necroinflammatory activity (grade) and individual featur

2 as blinded histological evaluation, based on necroinflammatory activity (grading score:0-18) and fibr

3 ypes before any antiviral treatment included necroinflammatory activity (n = 1,098), fibrosis (n = 1,

4 hepatitis C virus (HCV) infection, including necroinflammatory activity (N = 970), fibrosis (N = 980)

5 , fibrosis stage (stage 1 versus stage 2/3), necroinflammatory activity (NAFLD Activity Score; <or=4

6 rized by lymphoplasmacytic inflammation with necroinflammatory activity (NIA), comparable with findin

7 OR = 2.29, 95% CI = 1.35-3.91), but not with necroinflammatory activity (P = 0.3).

8 Mean T1rho values did not correlate with necroinflammatory activity (r = 0.31; P = .23), degree o

9 evaluate determinants of liver fibrosis and necroinflammatory activity among HIV/HCV coinfected pati

10 Improvements or worsening of METAVIR necroinflammatory activity and fibrosis were defined as

11 )Tc-mebrofenin transport was associated with necroinflammatory activity and not hepatic fibrosis.

12 Three years of lamivudine therapy reduces necroinflammatory activity and reverses fibrosis (includ

13 e (r = -0.65, P < .0001) and moderately with necroinflammatory activity grades (r = -0.41, P = .002)

14 ecruited to hepatic lobules during bursts of necroinflammatory activity in chronic hepatitis C infect

15 a suggest that in spite of mild histological necroinflammatory activity in general, the stage of fibr

16 In the last liver biopsy, high necroinflammatory activity indicating chronic hepatitis

17 s associated with significant improvement in necroinflammatory activity noted on liver biopsy.

18 r biopsy specimens show no more than grade 1 necroinflammatory activity or stage 1 fibrosis.

19 of necroinflammatory score >/= 4 or Metavir necroinflammatory activity score >/= 2 and significant l

20 The median necroinflammatory activity score was 3 (range, 0-9 of 18

21 High necroinflammatory activity was associated significantly

22 Necroinflammatory activity was generally mild.

23 ibrosis; however, significantly less hepatic necroinflammatory activity was observed among persons wh

24 aminotransferase (ALT) levels, histological necroinflammatory activity, and fibrosis.

25 int improvement and 24/63 (38%) no change in necroinflammatory activity; after 2 additional years of

26 All dialysis patients had mild or moderate necroinflammatory activity; fibrosis was frequent with 1

27 patients on dialysis showed mild or moderate necroinflammatory activity; the majority (22/28 = 79%) o

28 antiviral therapy, and the finding of severe necroinflammatory and fibrotic changes is helpful in det

29 We suggest that targeting ZBP1-initiated necroinflammatory cell lysis, either alone or in combina

30 By 5 weeks, necroinflammatory change was noteworthy, and by 8 weeks

31 in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE).

32 Under these conditions, necroinflammatory changes caused by ethanol were also si

33 ments are often associated with decreases in necroinflammatory changes in the liver.

34 The prevention of necroinflammatory changes in thromboxane-treated groups

35 Improvements in necroinflammatory changes were noted in liver biopsy spe

36 ohepatitis, i.e., fatty liver accompanied by necroinflammatory changes, is mostly defined by the NAFL

37 ethanol-induced oxidative damage as well as necroinflammatory changes.

38 A was detected in the livers of rats showing necroinflammatory changes.

39 tography to potentially enable assessment of necroinflammatory, congestive, and fibrotic processes of

40 o naive OVA-BIL mice led to biliary-centered necroinflammatory damage in a dose-dependent manner.

41 -associated steatohepatitis, the progressive necroinflammatory disease form that can progress to fibr

42 who received ribavirin, serum ALT levels and necroinflammatory features of liver histology were impro

43 These findings were associated with necroinflammatory, fibrogenic, and pro-oxidant activity

44 Necroinflammatory foci were increased significantly in e

45 st, sinusoidal inflammation with perivenular necroinflammatory foci, and many acidophilic bodies scat

46 s were significantly associated with lobular necroinflammatory grade and HCV genotype 1.

47 characterized by spontaneous development of necroinflammatory hepatitis that is restricted by geneti

48 ALB/c-TGF-beta1(-/-) mice developed a lethal necroinflammatory hepatitis that was not observed in TGF

49 generated by cross-breeding, did not develop necroinflammatory hepatitis, demonstrating that IFN-gamm

50 C chemokines was seen in the rats exhibiting necroinflammatory injury (fish oil-ethanol [FE] and corn

51 tage fat-dependent increase in steatosis and necroinflammatory injury (P < 0.05).

52 ld increase the risk of liver steatosis with necroinflammatory lesions and fibrosis.

53 se cells was associated with more pronounced necroinflammatory lesions in the liver.

54 ical consequences or trigger immune-mediated necroinflammatory liver damage.

55 All forms of chronic necroinflammatory liver disease examined correlate with

56 ly establish an immune-mediated etiology for necroinflammatory liver disease in BALB/c-TGF-beta1(-/-)

57 mal cells, cytokine release, and a transient necroinflammatory liver disease in both lineages.

58 cific cytotoxic T lymphocytes (CTL) induce a necroinflammatory liver disease in HBV-transgenic mice.

59 genic mouse model of chronic immune-mediated necroinflammatory liver disease that progresses to HCC.

60 required for the spontaneous development of necroinflammatory liver disease, BALB/c-TGF-beta1(-/-) m

61 ory cytokine TGF-beta1 spontaneously develop necroinflammatory liver disease, but the immune basis fo

62 mice prevented the subsequent development of necroinflammatory liver disease, indicating that CD4(+)

63 7-H1 and B7-DC, are modulated during chronic necroinflammatory liver disease, we investigated express

64 of age, accompanied by CD4+T cell-dependent necroinflammatory liver disease.

65 showed extended survival and did not develop necroinflammatory liver disease.

66 ndividuals, those from patients with chronic necroinflammatory liver diseases (hepatitis B virus, hep

67 Based on their histologic fibrosis (F) and necroinflammatory (NI) scores, patients were divided int

68 severe pediatric liver disease resulting in necroinflammatory obliteration of the extrahepatic bilia

69 in a CCR2- and M-CSF-mediated pathway at the necroinflammatory phase and differentiated into ephemera

70 ection from the liver but sustains a chronic necroinflammatory process that contributes to the develo

71 and supports the notion that immune-mediated necroinflammatory reactions are an important cause of he

72 sed on bile duct epithelium induced an acute necroinflammatory response specific to the liver, with a

73 Importantly, the necroinflammatory response to cells that die by necropto

74 greatest increase in ALT (200-300 U/L), and necroinflammatory responses characterized by portal infi

75 mice was accompanied by decreased placental necroinflammatory responses in both C57BL/6 TLR4(-/-) an

76 as defined by a Histology Activity Index of necroinflammatory score >/= 4 or Metavir necroinflammato

77 hin this initial NASH group, the mean global necroinflammatory score significantly improved with trea

78 serum hepatitis C virus RNA, and histologic necroinflammatory scores all decreased significantly (P<