ライフサイエンスコーパス: joint destruction

1 re unrecognized role in rheumatoid arthritis joint destruction.

2 ion, antirheumatic treatment, or severity of joint destruction.

3 sting a role for this cytokine in rheumatoid joint destruction.

4 , may amplify local inflammation, leading to joint destruction.

5 thways play a significant role in rheumatoid joint destruction.

6 ncreased Th1 T cell responses, and increased joint destruction.

7 blematic site, eventually protecting against joint destruction.

8 r of studies to identify novel correlates of joint destruction.

9 immune response contributes substantially to joint destruction.

10 s (OA) is a pathology that ultimately causes joint destruction.

11 ance-2 important issues in S. aureus-induced joint destruction.

12 ase Activity Score (DAS), is associated with joint destruction.

13 , exacerbate clinical arthritis, and augment joint destruction.

14 quality of life, functional impairment, and joint destruction.

15 e infiltration, angiogenesis, and ultimately joint destruction.

16 d arthritis suppresses both inflammation and joint destruction.

17 for histologic evidence of inflammation and joint destruction.

18 isease, as well as retard the progression of joint destruction.

19 herapeutic interventions designed to prevent joint destruction.

20 s) that function to promote inflammation and joint destruction.

21 omote local T cell activation and consequent joint destruction.

22 both cartilage and synovium, thus promoting joint destruction.

23 s and its response to steroid therapy before joint destruction.

24 lpha (TNF-alpha), which may lead to bone and joint destruction.

25 s in the periarticular soft tissues, without joint destruction.

26 mprove the efficacy of treatments to prevent joint destruction.

27 products important in joint inflammation and joint destruction.

28 arthritis (RA) and are directly involved in joint destruction.

29 eposition, formation of bony outgrowths, and joint destruction.

30 c degradation of the joint matrices leads to joint destruction.(4,5) The early phase of RA is charact

31 featuring multiple exostoses, enchondromas, joint destruction and bony deformities.

32 ate treatment of SA can lead to irreversible joint destruction and disability.

33 a novel susceptibility gene underlying both joint destruction and growth retardation of the KBD.

34 st that the movement strategy may perpetuate joint destruction and impede the long-term success of re

35 e affected joints of Nfat5+/- mice increased joint destruction and macrophage infiltration, demonstra

36 Joint destruction and osteoclast differentiation were lo

37 (JRA) have persistently active disease with joint destruction and profound growth delay despite maxi

38 , inflammatory polyarthritis that results in joint destruction and significant disability.

39 by chronic inflammatory synovitis leading to joint destruction and systemic bone loss.

40 inical symptoms, retarded the progression of joint destruction, and delayed disability.

41 significantly increased joint inflammation, joint destruction, and expression of interleukin-6 (IL-6

42 However, clinical arthritis, joint destruction, and synovial gene expression in the p

43 igher joint compression and could exacerbate joint destruction, and therefore needs to be altered to

44 ncy and severity of arthritis and subsequent joint destruction as compared with Deltafmt mutant strai

45 antibody significantly inhibited SCW-induced joint destruction, as measured by its ability to block i

46 tors on human synoviocytes may contribute to joint destruction by increasing IL-6 expression.

47 arthritis model, including the inflammation, joint destruction, cartilage prostaglandin depletion, os

48 synovial hyperplasia, osteoclast formation, joint destruction, cathepsin activity, and inflammatory

49 edema correlates with inflammation severity, joint destruction, clinical signs and symptoms of rheuma

50 cted gene transfer may ameliorate hemophilic joint destruction, even in the absence of circulating FI

51 hibited joint inflammation and periarticular joint destruction in a dose-dependent manner.

52 lts in potent inhibition of inflammation and joint destruction in a model of autoimmune arthritis in

53 L-1)-induced collagenase gene expression and joint destruction in arthritis.

54 MKK-6 is a crucial regulator of inflammatory joint destruction in CIA.

55 isease, can also be an important mediator of joint destruction in inflammatory bone disorders, such a

56 r selective loss of JNK-2 function decreases joint destruction in JNK-2 knockout mice, in order to de

57 elineate the contribution of aggrecanases to joint destruction in Lyme arthritis.

58 contribute to synovial lining expansion and joint destruction in RA.

59 roduction and has important implications for joint destruction in RA.

60 antibodies were associated with more severe joint destruction in RA.

61 of potential therapeutic value in inhibiting joint destruction in RA.

62 culature is important for the development of joint destruction in RA.

63 High expression of galectin 3 at sites of joint destruction in rheumatoid arthritis (RA) suggests

64 joint are key mediators of inflammation and joint destruction in rheumatoid arthritis (RA).

65 atrix metalloproteinase (MMP) expression and joint destruction in rheumatoid arthritis (RA).

66 important elements in the events leading to joint destruction in rheumatoid arthritis (RA).

67 metalloproteinase (MMP) gene expression and joint destruction in rheumatoid arthritis (RA).

68 viocytes (FLS) play a major role in invasive joint destruction in rheumatoid arthritis (RA).

69 signed to suppress synovial inflammation and joint destruction in rheumatoid arthritis.

70 IL-8 as a major mediator of inflammation and joint destruction in rheumatoid arthritis.

71 IL-15 is a mediator of joint destruction in S. aureus-induced arthritis and con

72 n of c-Jun N-terminal kinase (JNK) decreases joint destruction in the rat adjuvant arthritis model.

73 logy reveals 63 and 77% reduction in overall joint destruction in two independent experiments.

74 conclude that the DR3-TL1A pathway regulates joint destruction in two murine models of arthritis and

75 D-JNKi dramatically reduced inflammation and joint destruction in WT mice.

76 ese interactions finally lead to progressive joint destruction, in a way that is different from all o

77 ulated in RA and contribute significantly to joint destruction, in the present study we investigated

78 The pathology of joint destruction is associated with elevated production

79 matory drugs, may have limited efficacy once joint destruction is complete.

80 ion, time-averaged disease activity fits the joint destruction model better than one-time disease act

81 In addition to joint destruction, mutant mice also develop aortic root

82 The chronic inflammation and progressive joint destruction observed in rheumatoid arthritis (RA)

83 ough TLR-2 and TLR-4 in the inflammation and joint destruction of RA.

84 uvette assay, was positively correlated with joint destruction (r = 0.7) and inflammation (r = 0.8).

85 Since joint destruction reflects the history of disease activi

86 Optimal treatment to prevent or reduce joint destruction remains controversial.

87 ll migration and invasion, but their role in joint destruction remains unknown.

88 le it is clear that pigment deposits lead to joint destruction, renal stone formation and cardiac val

89 IL-6 and MMP-1 promote inflammation and joint destruction, respectively.

90 Postmenopausal osteoporosis and rheumatoid joint destruction result from increased osteoclast forma

91 perienced poor long-term outcomes, including joint destruction, severe functional declines, considera

92 ciency suppresses inflammatory arthritis and joint destruction, suggesting it might be a therapeutic

93 arthritis and histological scores measuring joint destruction, synovial lining, macrophage infiltrat

94 disease activity would better correlate with joint destruction than one-time disease activity.

95 to apoptosis and less efficient at promoting joint destruction than were NFAT5-sufficient macrophages

96 (TNF) and interleukin 1 (IL-1), mediate the joint destruction that characterizes rheumatoid arthriti

97 insights into the pathogenesis of autoimmune joint destruction that is reminiscent of JIA.

98 Rheumatoid arthritis culminates in joint destruction that, in mouse models of disease, is s

99 etic markers predicting rapid progression of joint destruction; the role of serology, in particularly

100 nvading cartilage and bone in RA may mediate joint destruction through direct effects on cartilage or

101 Although joint destruction was decreased in Jnk2(-/-) mice with C

102 The severity of synovitis and joint destruction was significantly decreased in IL-15 k

103 the joints showed that both inflammation and joint destruction were blocked by the IKK inhibitor.

104 ted course of RA, structural consequences of joint destruction were more pronounced in women.

105 istent synovial inflammation and progressive joint destruction, which are mediated by innate and adap

106 al disorders characterized by osteolysis and joint destruction, which can mimic severe rheumatoid art

107 Complete inhibition of MMP expression and joint destruction will likely require combined JNK-1 and

108 understanding of the molecular mechanisms of joint destruction will pave the way for new therapeutic

109 owed statistically significant reductions in joint destruction with PB-145 and PPS treatments (P < 0.