ライフサイエンスコーパス: urate crystal

1 al mechanism for the removal of inflammatory urate crystals.

2 ss of the innate immune system to monosodium urate crystals.

3 crystals but not in response to LPS or other urate crystals.

4 rbated the inflammatory response elicited by urate crystals and abrogated the anti-inflammatory effec

5 abbit knee joints with 10 mg of pyrogen-free urate crystals and analyzed IL-8 levels, leukocyte influ

6 ent understanding of the interaction between urate crystals and key cellular components of the gouty

7 ytidylic acid or a combination of monosodium urate crystals and Mycobacterium smegmatis was effective

8 ent-activating structures such as monosodium urate crystals and zymosan was not affected by BCD.

9 phorbol 12-myristate 13-acetate, monosodium urate crystals, and Candida albicans.

10 in the response of mononuclear phagocytes to urate crystals, and these events can be distinguished at

11 f imaging studies suggesting that monosodium urate crystals are deposited in coronary plaques in pati

12 and the inflammatory response to monosodium urate crystals are translating into potential new treatm

13 Using monosodium urate crystals as a model, we demonstrated that this lys

14 ion of the NLRP3 inflammasome in response to urate crystals, ATP and lipotoxic fatty acids.

15 The noninflammatory removal of urate crystals by mature macrophages defines a new pathw

16 estigated macrophage responses to monosodium urate crystals, calcium pyrophosphate crystals, aluminum

17 ith hyperuricemia, which leads to monosodium urate crystal deposition in joints and surrounding tissu

18 Intrarenal urate crystal deposition was absent in all groups.

19 rol disease manifestations related to tissue urate crystal deposition.

20 Although urate crystal diagnosis remains the gold standard for di

21 ia, followed by the deposition of monosodium urate crystal in articular structures and culminating in

22 o the formation and deposition of monosodium urate crystals in and around the joints.

23 itis, caused by the deposition of monosodium urate crystals in and around the joints.

24 sease caused by the deposition of monosodium urate crystals in articular and non-articular structures

25 ization studies, and potentially discovering urate crystals in coronary arteries using advanced imagi

26 Gout is caused by deposition of monosodium urate crystals in joints when plasma uric acid levels ar

27 The role of formalin in dissolving urate crystals in pathologic specimens was further clari

28 s that results from deposition of monosodium urate crystals in the joint.

29 ymorphonuclear cell accumulation elicited by urate crystals in the murine peritoneal cavity.

30 eta release and PMN accumulation elicited by urate crystals in the murine peritoneal cavity.

31 nate immune response to deposited monosodium urate crystals in the setting of hyperuricemia.

32 ute neutrophilic inflammation in response to urate crystals in the subcutaneous air pouch model.

33 Urate crystals induce different classes of neutrophil ch

34 In normal mice, urate crystals induced a 10-fold increase (P < 0.01) in

35 In mIL-8RH(-/-) mice, urate crystals induced a proteinaceous leukocyte-poor ex

36 AC component C6 to determine if MAC mediated urate crystal-induced arthritis.

37 In a model of monosodium urate crystal-induced gout, Traf1 knockout mice exhibite

38 wing stimulation with ATP, while oxalate and urate crystal-induced IL-1B release was unaffected.

39 y abrogated ATP-induced, but not oxalate and urate crystal-induced IL-1B release.

40 tential role for interleukin-1 inhibition in urate crystal-induced inflammation.

41 Analogously, monosodium urate crystal-induced neutrophil migration to the tibiof

42 familial cold autoinflammatory syndrome and urate crystal-induced peritonitis.

43 s was also observed in a model of monosodium urate crystals-induced inflammation.

44 nistically substantiated in acute monosodium-urate-crystal-induced inflammation, where the pro-resolu

45 ndent neutrophil recruitment in a monosodium urate crystal inflammatory murine peritonitis model.

46 odel of gouty arthritis, direct injection of urate crystals into the rat joint provoked a marked infl

47 k in patients with gout; removing monosodium urate crystals or blocking the inflammatory pathway coul

48 ed with calcium-oxalate crystals, monosodium urate crystals, or ATP lead to the robust release of int

49 In contrast, LPS, monosodium urate crystals, or M. smegmatis alone had no activity.

50 cause of inflammatory response to monosodium urate crystals; prevention of gout flares should be the

51 wever, tophi and tissue stores of monosodium urate crystals resolve slowly, particularly in patients

52 i.p. injection of monosodium urate crystals resulted in increased inflammatory cell i

53 inflammation, NLRP3 activation by monosodium urate crystals similarly increased IL-6.

54 Monosodium urate crystals stimulate IL-1beta secretion via cryopyri

55 s was evaluated following LPS and monosodium urate crystal stimulation.

56 peritonitis model of gout, using monosodium urate crystals to activate NLRP3, 15d-PGJ2 caused a sign

57 The potential for antibodies against urate crystals to potentiate further crystallization may

58 inol) leads to the dissolution of monosodium urate crystals, ultimately resulting in the prevention o

59 Likewise, release of the chemokine KC by urate crystals was attenuated by [d-Trp(8)]-gamma-MSH, a

60 Urate crystals were injected into subcutaneous air pouch

61 tion of the NLRP3 inflammasome by monosodium urate crystals with release of IL-1B plays a major role