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

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

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

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

33 The prevention of necroinflammatory changes in thromboxane-treated groups

34 Improvements in necroinflammatory changes were noted in liver biopsy spe

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

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

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

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

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

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

41 Necroinflammatory foci were increased significantly in e

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

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

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

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

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

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

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

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

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

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

52 All forms of chronic necroinflammatory liver disease examined correlate with

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

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

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

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

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

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

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

60 7-H1 and B7-DC, are modulated during chronic necroinflammatory liver disease, we investigated express

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

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

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

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

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

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

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

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

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

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

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

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

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