ライフサイエンスコーパス: monosodium urate

1 e physiological consequences of crystallized monosodium urate acutely causing liver/kidney damage or

2 ion in response to double-stranded RNA, ATP, monosodium urate, adjuvant aluminium, rotenone, live Esc

3 y response to intraperitoneal challenge with monosodium urate and the development of experimental aut

4 e understanding of the cellular responses to monosodium urate, calcium pyrophosphate dihydrate and ba

5 we report that crystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cy

6 e and humans involved in the pathogenesis of monosodium urate, calcium pyrophosphate dihydrate and hy

7 In addition to monosodium urate, calcium pyrophosphate dihydrate, and a

8 accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can

9 ssociated with hyperuricemia, which leads to monosodium urate crystal deposition in joints and surrou

10 yperuricaemia, followed by the deposition of monosodium urate crystal in articular structures and cul

11 NLRP3-dependent neutrophil recruitment in a monosodium urate crystal inflammatory murine peritonitis

12 althy donors was evaluated following LPS and monosodium urate crystal stimulation.

13 In a model of monosodium urate crystal-induced gout, Traf1 knockout mi

14 Analogously, monosodium urate crystal-induced neutrophil migration to

15 t was mechanistically substantiated in acute monosodium-urate-crystal-induced inflammation, where the

16 sinic-polycytidylic acid or a combination of monosodium urate crystals and Mycobacterium smegmatis wa

17 her complement-activating structures such as monosodium urate crystals and zymosan was not affected b

18 If imaging studies suggesting that monosodium urate crystals are deposited in coronary plaq

19 imal tubule and the inflammatory response to monosodium urate crystals are translating into potential

20 Using monosodium urate crystals as a model, we demonstrated th

21 te, leads to the formation and deposition of monosodium urate crystals in and around the joints.

22 atory arthritis, caused by the deposition of monosodium urate crystals in and around the joints.

23 reatable disease caused by the deposition of monosodium urate crystals in articular and non-articular

24 Gout is caused by deposition of monosodium urate crystals in joints when plasma uric aci

25 ry arthritis that results from deposition of monosodium urate crystals in the joint.

26 ed by an innate immune response to deposited monosodium urate crystals in the setting of hyperuricemi

27 ascular risk in patients with gout; removing monosodium urate crystals or blocking the inflammatory p

28 However, tophi and tissue stores of monosodium urate crystals resolve slowly, particularly i

29 i.p. injection of monosodium urate crystals resulted in increased inflamma

30 eta-driven inflammation, NLRP3 activation by monosodium urate crystals similarly increased IL-6.

31 Monosodium urate crystals stimulate IL-1beta secretion v

32 In a mouse peritonitis model of gout, using monosodium urate crystals to activate NLRP3, 15d-PGJ2 ca

33 Activation of the NLRP3 inflammasome by monosodium urate crystals with release of IL-1B plays a

34 i; that is, phorbol 12-myristate 13-acetate, monosodium urate crystals, and Candida albicans.

35 ere, we investigated macrophage responses to monosodium urate crystals, calcium pyrophosphate crystal

36 ls stimulated with calcium-oxalate crystals, monosodium urate crystals, or ATP lead to the robust rel

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

38 eg, allopurinol) leads to the dissolution of monosodium urate crystals, ultimately resulting in the p

39 ntiproteases was also observed in a model of monosodium urate crystals-induced inflammation.

40 esponsiveness of the innate immune system to monosodium urate crystals.

41 d occurs because of inflammatory response to monosodium urate crystals; prevention of gout flares sho

42 Monosodium urate enhanced CD86 and OX40L expression on D

43 peruricemia can lead to crystal formation of monosodium urate in the joints, causing a painful inflam

44 ted IL-1beta normally in response to ATP and monosodium urate, indicating that caspase-11 is engaged

45 ed Pyk2/FAK dual inhibitor PF-562271 reduced monosodium urate-mediated peritonitis, a disease model u

46 Monosodium urate monohydrate (MSU) and calcium pyrophosp

47 recognition of dormant articular and bursal monosodium urate monohydrate (MSU) crystal deposits, the

48 ruitment of polymorphonuclear cells (PMN) in monosodium urate monohydrate (MSU) crystal-induced infla

49 Although monosodium urate monohydrate (MSU) crystals have been re

50 Monosodium urate monohydrate (MSU) crystals have remarka

51 s caused by the deposition of poorly soluble monosodium urate monohydrate (MSU) crystals in periphera

52 The mechanism by which monosodium urate monohydrate (MSU) crystals intracellula

53 Articular deposition of monosodium urate monohydrate (MSU) crystals may promote

54 Monosodium urate monohydrate (MSU) crystals promote gout

55 Monosodium urate monohydrate (MSU) crystals were adminis

56 ete proinflammatory cytokines in response to monosodium urate monohydrate (MSU) crystals.

57 e of mononuclear phagocytes to the uptake of monosodium urate monohydrate (MSU) crystals.

58 Gout is a chronic disease caused by monosodium urate (MSU) crystal deposition.

59 I) signaling as a model, we demonstrate that monosodium urate (MSU) crystal sensing by Clec12A enhanc

60 hibitor necrosulfonamide (NSA) contribute to monosodium urate (MSU) crystal-induced cell death, IL-1b

61 600-IL-1Ra and PAS800-IL-1Ra for efficacy in monosodium urate (MSU) crystal-induced peritonitis.

62 ck-/-Fgr-/-Lyn-/- mutation abrogated various monosodium urate (MSU) crystal-induced pro-inflammatory

63 Phagocytosis of monosodium urate (MSU) crystals and caspase-1 activation

64 , calcium pyrophosphate dihydrate (CPPD), or monosodium urate (MSU) crystals and placed on a microsco

65 Although monosodium urate (MSU) crystals are known to trigger inf

66 ls and damaged tissues release uric acid and monosodium urate (MSU) crystals as important endogenous

67 nvestigated how the endogenous danger signal monosodium urate (MSU) crystals can alter macrophage fun

68 Phagocyte ingestion of monosodium urate (MSU) crystals can induce proinflammato

69 While it is known that monosodium urate (MSU) crystals cause the disease gout,

70 Gout is a form of crystal arthropathy where monosodium urate (MSU) crystals deposit and elicit infla

71 mmatory arthritis caused by precipitation of monosodium urate (MSU) crystals in individuals with hype

72 atory disorder associated with deposition of monosodium urate (MSU) crystals in joints and periarticu

73 ic inflammatory disease caused by buildup of monosodium urate (MSU) crystals in the joints.

74 oint diseases characterized by deposition of monosodium urate (MSU) crystals which trigger an innate

75 ith gout predispose them to the formation of monosodium urate (MSU) crystals, soluble urate also prim

76 he joints of gout patients upon encountering monosodium urate (MSU) crystals.

77 t do not rely solely on the documentation of monosodium urate (MSU) crystals.

78 t do not rely solely on the documentation of monosodium urate (MSU) crystals.

79 f calcium pyrophosphate dihydrate (CPPD) and monosodium urate (MSU) deposited in synovium and articul

80 Here, it is reported that monosodium urate (MSU) results in exocytosis of Weibel-P

81 e have investigated the contributing role of monosodium urate (MSU) to the pathological processes ass

82 dothelial cells treated with uric acid (UA), monosodium urate (MSU), or serum from gout patients show

83 nduced sepsis, alum-induced peritonitis, and monosodium urate (MSU)-induced arthritis.

84 lation of PML by arsenic trioxide suppressed monosodium urate (MSU)-induced IL-1beta production, sugg

85 We found that uric acid (monosodium urate [MSU]) crystals induce a proinflammator

86 xis while exogenous delivery of UA crystals (monosodium urate, MSU) restored the allergic phenotype.

87 Crystals of calcium oxalate, monosodium urate, or calcium pyrophosphate dihydrate, as

88 pTG and wild-type mice, and in both in vivo (monosodium urate peritonitis) and in vitro models of inf