ライフサイエンスコーパス: crystal-induced

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

2 Medium-sized crystals induced a particular reparative process that we

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

4 s leukocyte-poor exudate at 4 hours, despite crystal-induced activation of resident cells (documented

5 deficiency of RIPK3 or MLKL prevents oxalate crystal-induced acute kidney injury.

6 ital microscopy in models of IRI and oxalate crystal-induced acute kidney injury.

7 d calcium entry/IL-8 axis is involved in MSU crystal-induced aggregated NET formation, but MRS2578 co

8 hogenesis of both osteoarthritis and calcium crystal-induced arthritis and our limited ability to acc

9 ill hasten understanding of the pathology of crystal-induced arthritis and provide new therapies.

10 ons, such as ischemia reperfusion injury and crystal-induced arthritis, as well as with chronic disea

11 m pyrophosphate dihydrate and hydroxyapatite crystal-induced arthritis.

12 ve unveiled mechanisms in the development of crystal-induced arthritis.

13 ponent C6 to determine if MAC mediated urate crystal-induced arthritis.

14 a more effective management of other common crystal-induced arthritis.

15 The crystal-induced arthropathies are characterized by self-

16 ons that have stimulated renewed interest in crystal-induced arthropathies.

17 ations presage advances in the management of crystal-induced arthropathies.

18 al therapeutic targets for management of the crystal-induced arthropathies.

19 tion of gout is described as an inflammatory crystal-induced arthropathy that afflicts peripheral joi

20 ralization agent and a specific inhibitor of crystal-induced biologic effects.

21 trum of a 5-MHz fundamental frequency quartz crystal induced by a water-miscible room-temperature ion

22 e we further elucidate the mechanisms of BCP crystal-induced cell activation as BCP crystals activate

23 stals and the signal transduction pathway of crystal-induced cell activation offer a unique opportuni

24 Previous work suggested that BCP crystal-induced cell activation required intracellular c

25 ineating the mechanism of calcium-containing crystal-induced cell activation: (1) the identification

26 namide, an inhibitor for human MLKL suppress crystal-induced cell death in human renal progenitor cel

27 chondrial permeability transition suppressed crystal-induced cell death in primary human tubular epit

28 e (NSA) contribute to monosodium urate (MSU) crystal-induced cell death, IL-1beta release, and autoin

29 nase domain-like (MLKL), did not prevent MSU crystal-induced cell death.

30 activator of MAPKs, significantly inhibited crystal-induced cell proliferation, suggesting that the

31 esent study, we found that calcium phosphate crystals induced cell death in human aortic vascular smo

32 ic hollow structures and constructing an ice-crystal-induced cellular microstructure, BHGMs can achie

33 stream of PKC and p44/42 MAPK to mediate BCP crystal-induced cellular responses.

34 tly of, a JNK-AP-1-dependent network driving crystal-induced chemokine and cytokine expression.

35 ith TLR2-blocking Ab suppressed CPPD and MSU crystal-induced chondrocyte release of NO, an inflammato

36 icate that P2X7 receptor is not required for crystal-induced CKD and it is unlikely to be a suitable

37 oma-related M1-like macrophages may drive UA crystal-induced CKD progression.

38 the role of the P2X7 receptor in response to crystal-induced cytokine release, inflammation, and kidn

39 IPK3 and MLKL are molecular targets to limit crystal-induced cytotoxicity, tissue injury and organ fa

40 vation, and a second stimulus such as ATP or crystal-induced damage is required for NLRP3 activation.

41 In a model of monosodium urate crystal-induced gout, Traf1 knockout mice exhibited more

42 timulation with ATP, while oxalate and urate crystal-induced IL-1B release was unaffected.

43 gated ATP-induced, but not oxalate and urate crystal-induced IL-1B release.

44 Attenuated MSU crystal-induced IL-1beta release in CD14(-/-) BMDMs was

45 crystalline inflammasome activators, cystine crystal-induced IL-1beta secretion required activation o

46 pecies, and potassium efflux reduced cystine crystal-induced IL-1beta secretion.

47 activation and microbial ligand-, DAMP-, and crystal-induced IL-1beta secretion.

48 ERK-2 pathway was essential for MSU and CPPD crystal-induced IL-8 mRNA expression, whereas the p38 pa

49 Finally, crystal-induced IL-8 promoter activation was mediated by

50 rgic P2X7 receptor signaling is critical for crystal-induced inflammasome activation and renal injury

51 uses crystal precipitation in renal tubules, crystal-induced inflammasome activation, and renal fibro

52 Interventional studies probed the role of crystal-induced inflammation and macrophages in the path

53 n of cryopyrin plays a role in mediating MSU crystal-induced inflammation in this model.

54 al models have implicated a general model of crystal-induced inflammation involving innate immunity t

55 occult crystalline disease who, by virtue of crystal-induced inflammation, require more aggressive an

56 ally substantiated in acute monosodium-urate-crystal-induced inflammation, where the pro-resolution f

57 (PMN) in monosodium urate monohydrate (MSU) crystal-induced inflammation.

58 tabolites, and immune cells that account for crystal-induced inflammation.

59 LRR) domain of cryopyrin is required for MSU crystal-induced inflammation.

60 l role for interleukin-1 inhibition in urate crystal-induced inflammation.

61 fic role of macrophage TG2 expression in MSU crystal-induced inflammation.

62 en recently identified as mediators of acute crystal-induced inflammation.

63 also observed in a model of monosodium urate crystals-induced inflammation.

64 MSU crystal-induced inflammatory responses were comparably a

65 of AGDV into closed alphaIIbbeta3 headpiece crystals induced intermediate states similarly to RGDSP.

66 development of specific calcium crystals and crystal-induced intracellular changes.

67 An attenuated rise in MSU crystal-induced joint effusion levels of IL-8 also was o

68 assessed the pathogenic sequelae of 2,8-DHA crystal-induced kidney damage.

69 trophils (P < 0.05) but not monocytes in MSU crystal-induced knee synovial fluid from C6-deficient an

70 Last, MSU crystal-induced leukocyte influx at 6 h was reduced by a

71 Several details of crystal-induced macrophage activation were recently unco

72 GSDMD, 2) document a unique mechanism of MSU crystal-induced macrophage cell death not rescued by pan

73 and potentially therapeutic function against crystal-induced membranolysis is also discussed.

74 rk on calcium pyrophosphate dihydrate (CPPD) crystal-induced membranolysis, we demonstrate, using the

75 le of crystal endocytosis and dissolution in crystal-induced metalloproteinase synthesis and mitogene

76 MSU and CPPD crystal-induced mitogen-activated protein kinase (MAPK)

77 confirm the role of protein kinase C in BCP crystal-induced mitogenesis in human fibroblasts.

78 role of TNF alpha was then studied in an MSU crystal-induced monarthritis model, in the presence or a

79 In the MSU crystal-induced monarthritis model, TNF alpha blockade w

80 stal-free preparation suppressed LPS- or MSU crystal-induced monocyte activation, a process depending

81 volved in the pathogenesis of other types of crystal-induced nephropathies.

82 The detailed mechanism of MSU crystal-induced NET formation remains unknown.

83 annel inhibitor (SK&F96365) also reduced MSU crystal-induced NET release.

84 Analogously, monosodium urate crystal-induced neutrophil migration to the tibiofemural

85 matory effects on LPS, ox-LDL or cholesterol crystal-induced NF-kappaB, c-jun and p38 activation, as

86 n was associated with increased CPPD and MSU crystal-induced NO release.

87 We studied MSU crystal-induced peritonitis in TG2-/- and congenic TG2+/

88 -1beta induction and autoinflammation in MSU crystal-induced peritonitis was not reduced in GSDMD-def

89 in three distinct in vivo models of disease (crystal-induced peritonitis, allergic airway inflammatio

90 influx and cytokine production in a model of crystal-induced peritonitis, and these effects were abse

91 ial cold autoinflammatory syndrome and urate crystal-induced peritonitis.

92 learance of apoptotic neutrophils during MSU crystal-induced peritonitis.

93 L-1Ra for efficacy in monosodium urate (MSU) crystal-induced peritonitis.

94 ion abrogated various monosodium urate (MSU) crystal-induced pro-inflammatory responses of neutrophil

95 MSU crystal-induced production of interleukin-1beta (IL-1bet

96 kely to be a suitable therapeutic target for crystal-induced progressive kidney disease.

97 ddition, T cells and cholesterol monohydrate crystals induced proinflammatory gene expression in the

98 ative mutant of p38 MAP kinase abolishes COM crystal-induced re-initiation of DNA synthesis.

99 ver, we find that stimulation with liposomes/crystals induced reactive oxygen species-dependent calci

100 Oxalate crystal-induced renal inflammation is associated with pr

101 Established contributors to oxalate crystal-induced renal necroinflammation include the NACH

102 Src-family inhibitor dasatinib abrogated MSU crystal-induced responses of human neutrophils and reduc

103 ) crystals are common in osteoarthritis, the crystal-induced signal transduction pathways in human fi

104 he MAPK pathway is a significant mediator of crystal-induced signals.

105 Both crystals induced the binding of nuclear factor kappaB (N

106 stals but also an intrinsic inhibitor of MSU crystal-induced tissue inflammation.

107 MSU crystals induced TNFalpha, IL-1beta, and IL-6 (but not I

108 Both crystals induced transcriptional activation of the IL-8

109 covery of superconductivity in Sb2Se3 single crystal induced via pressure.