ライフサイエンスコーパス: chronic active

1 0.001, Mantel-Cox log-rank test), concurrent chronic active AMR (P=0.03), and time to biopsy (P=0.04)

2 Banff schema, these were acute AMR [23.5%], chronic active AMR [14.7%], suspicious for acute AMR [41

3 icious for acute AMR [41.1%], suspicious for chronic active AMR [2.9%], and only microvascular injury

4 Concurrent chronic active AMR or time to biopsy was not associated

5 classification schema, 29 had acute AMR and chronic active AMR, 18 had acute AMR and acute T-cell me

6 ated rejection (TCMR), and 14 had acute AMR, chronic active AMR, and acute TCMR.

7 multiple sclerosis lesions comprised of both chronic active and chronic silent lesions.

8 e precursor cells after onset of EAE, and in chronic active and inactive lesions from MS brain.

9 emistry and histochemistry, respectively, in chronic active and inactive lesions in progressive multi

10 Chronic active and moderate to severe course of CD is as

11 The aim of this study was to investigate in chronic active and silent MS lesions and control white m

12 TUNEL-positive cells in three active, nine chronic active, and four chronic inactive lesions, howev

13 -center pilot trial enrolled 5 patients with chronic active anterior uveitis.

14 rulopathy (TG) is a diagnostic criterion for chronic active antibody-mediated rejection (CAABMR), wit

15 The Vaa antigen is expressed in vivo during chronic, active arthritis associated with M. hominis inf

16 Chronic active B cell receptor (BCR) signaling, a hallma

17 hetic lethal combinations with inhibitors of chronic active B cell receptor signaling.

18 In this study, we used chronic active B-cell receptor (BCR) signaling in diffus

19 fuse large B-cell lymphoma (DLBCL) relies on chronic active B-cell receptor (BCR) signaling.

20 inase inhibitor ibrutinib, which targets the chronic active B-cell receptor signaling that characteri

21 CRs to self-antigens initiates and maintains chronic active BCR signaling in ABC DLBCL.

22 target the B cell receptor (BCR), fostering chronic active BCR signaling.

23 These findings establish chronic active BCR signalling as a new pathogenetic mech

24 Here we describe a form of 'chronic active' BCR signalling that is required for cell

25 ity were apparent: relapsing-remitting (RR), chronic active (CA), and long quiescent (LQ).

26 The current study aimed to determine whether chronic active cannabis use in humans may alter psychomo

27 Chronic active cannabis use is associated with slower an

28 patients with the cord colitis syndrome had chronic active colitis, with granulomatous inflammation

29 mm3 in active cortical lesions, 1,107/mm3 in chronic active cortical lesions, 25/mm3 in chronic inact

30 In active and chronic active cortical lesions, activated microglia clo

31 lesions of varying ages, including acute and chronic, active demyelinating lesions with macrophages a

32 s associated with a higher PCDAI (p=0.0092), chronic active disease (p=0.0148), underweight at diagno

33 lymphoproliferative disease trait, and as a chronic active disease leading to life-threatening hemop

34 only in cases of corticosteroid dependency, chronic active disease with frequent flares, poor respon

35 nonucleosis requiring hospitalization, 1 had chronic active EBV disease (B-cell type), 1 had EBV-asso

36 Chronic active EBV disease (CAEBV) is a lymphoproliferat

37 red in serum or plasma from 34 patients with chronic active EBV infection (CAEBV) and from 15 healthy

38 ith acute infectious mononucleosis (AIM) and chronic active EBV infection (CAEBV) that were also comp

39 genetic role of T-cell infection with EBV in chronic active EBV infection and in the EBV-positive T-c

40 r virus (EBV) in the pathogenesis of severe, chronic active EBV infection and its complications is un

41 k to 2 months), and 1 patient had documented chronic active EBV infection for 7 years.

42 Treatment of chronic active EBV infection has proven difficult, but n

43 ance with the host as a latent infection, in chronic active EBV infection the host-virus balance is d

44 two Japanese patients diagnosed with severe, chronic active EBV infection who subsequently developed

45 lar disorder in the setting of long-standing chronic active EBV infection.

46 n 1 case serology was consistent with severe chronic active EBV infection.

47 defects have been reported in patients with chronic active EBV infection.

48 family history of XLP) or in 9 patients with chronic active EBV syndrome.

49 rohn's disease for more than one decade with chronic active enterocolitis, fistula disease as well as

50 Chronic active Epstein-Barr virus (CAEBV) infection synd

51 Chronic active Epstein-Barr virus (EBV) infection is an

52 Chronic active Epstein-Barr virus infection (CAEBV) is a

53 Recently, an individual with chronic active Epstein-Barr virus infection was found to

54 ection with Helicobacter pylori and signs of chronic active gastritis and intestinal metaplasia in ga

55 infection and associated disorders, such as chronic active gastritis and intestinal metaplasia, are

56 Gastric biopsies revealed chronic active gastritis with associated Helicobacter py

57 H pylori infection, chronic active gastritis, and intestinal metaplasia had

58 of the human population worldwide and causes chronic active gastritis, which can lead to peptic ulcer

59 sy-proved Helicobacter pylori infection with chronic active gastritis.

60 ls in the underlying lamina propria, causing chronic, active gastritis.

61 1992 a helical microorganism associated with chronic active hepatitis and a high incidence of hepatoc

62 er hepaticus infection develop a progressive chronic active hepatitis and liver tumors, despite the p

63 e findings suggest that helicobacter-induced chronic active hepatitis arises through the process of l

64 of T cell-mediated diseases such as AIDS and chronic active hepatitis between humans and chimpanzees.

65 s with PBC and 35 disease controls including chronic active hepatitis C, extrahepatic biliary obstruc

66 hepaticus infection in A/JCr mice results in chronic active hepatitis characterized by perivascular,

67 Infection with Helicobacter hepaticus causes chronic active hepatitis in certain strains of mice and

68 etermined in liver samples from HBV-infected chronic active hepatitis patients when compared with nor

69 central pathology review shows 28 (80%) have chronic active hepatitis, 25 (71%) have fibrosis, and 3

70 a newly recognized bacterium associated with chronic active hepatitis, hepatic carcinoma, and inflamm

71 H. hepaticus causes chronic active hepatitis, with progression to hepatocell

72 sions that have previously been described as chronic active hepatitis.

73 tocytes from HBV-positive liver samples with chronic active hepatitis.

74 ion with this ubiquitous bacterium incites a chronic active immune response that persists for the lif

75 particulate nickel subsulfide (Ni3S2) causes chronic active inflammation and fibrosis of the lungs.

76 Chronic active inflammation was observed in 53(56%) (p =

77 e lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in the hypocellular centers

78 In chronic active lesions, a few inflammatory cells display

79 lesions, 875 in the hypocellular centers of chronic active lesions, and less than 1 in normal-appear

80 urteen active multiple-sclerosis lesions, 33 chronic active lesions, and samples of normal-appearing

81 lls in acute lesions, 73% in active areas of chronic active lesions, but in only 17% of those in inac

82 predominantly located at the active edge of chronic active lesions.

83 ng the evaluation of potential therapies for chronic active lesions.

84 In chronic active MS lesions, apart from a general loss of

85 Intriguingly, Del-1 expression decreased in chronic-active MS lesions and in the inflamed CNS in the

86 n important source of IL-23p19 in active and chronic active multiple sclerosis lesions.

87 trophils, and macrophages, indicative of its chronic-active nature in these aged hamsters infected wi

88 In chronic, active, neovascular AMD, EMB is associated with

89 se results do not support the use of EMB for chronic, active, neovascular AMD.

90 IU/ml, and the liver biopsy specimen showed chronic active or chronic persistent hepatitis in 11 chi

91 uced distribution in controls and those with chronic active or inactive MS plaques.

92 ree major types of MS lesions: acute plaque, chronic active plaque and chronic plaque.

93 tissue factor and protein C inhibitor within chronic active plaque samples, suggesting dysregulation

94 The livers also exhibited a range of chronic active portal/interface and lobular inflammation

95 ontrast, there was overexpression of CD1d in chronic, active psoriatic plaques.

96 Two monkeys were sacrificed because of chronic active rejection (days 154 and 221).

97 The monkeys with chronic active rejection showed relatively strong alloan

98 ulating mKatG-reactive T cells were found in chronic active sarcoidosis but not in patients with inac

99 en nearly as large (averaging 80% to 90%) as chronic active smoking.

100 nt arteriolopathy within the descriptions of chronic active T cell-mediated rejection (TCMR) or chron

101 myositis, mixed inflammatory cell arthritis, chronic active tenosynovitis, and multifocal vasculitis.

102 nt ulcers if diagnosed during this period or chronic active ulcers if diagnosed more than 12 months b

103 These were similar to risk factors for chronic active ulcers, except smoking was an additional

104 was an additional important risk factor for chronic active ulcers.

105 Ten children with chronic active uveitis (7 girls and 3 boys, mean age 7.5

106 olarized microglia/macrophages at the rim of chronic active white matter demyelinating lesions.