ライフサイエンスコーパス: MSU

1 MSU and CPPD crystal-induced mitogen-activated protein k

2 MSU and CPPD crystals (0.5 mg/ml) induced activation of

3 MSU crystal-induced inflammatory responses were comparab

4 MSU crystal-induced production of interleukin-1beta (IL-

5 MSU crystals also were injected into mouse synovial-like

6 MSU crystals also were injected into mouse synovium-like

7 MSU crystals induced TNFalpha, IL-1beta, and IL-6 (but n

8 MSU crystals produced a knee joint inflammation that was

9 MSU crystals were a potent stimulus for IL-1 and TNF alp

10 MSU crystals were incubated with freshly isolated mononu

11 MSU crystals, but not latex beads, directly bound recomb

12 MSU induced MMP-3 and iNOS expression and NO release in

13 MSU induced rapid tyrosine phosphorylation of Pyk-2 and

14 MSU-induced functional signaling by specific protein kin

15 The role of TNF alpha was then studied in an MSU crystal-induced monarthritis model, in the presence

16 owing to earlier treatment, the costs of an MSU program may be offset by a reduction in the costs of

17 nophils migrate toward soluble uric acid and MSU crystals in a gradient-dependent manner.

18 and alternative pathways of complement, and MSU crystals directly cleave C5 on the crystal surface.

19 nt with TLR2-blocking Ab suppressed CPPD and MSU crystal-induced chondrocyte release of NO, an inflam

20 ction was associated with increased CPPD and MSU crystal-induced NO release.

21 We conclude that CPPD and MSU crystals critically use TLR2-mediated signaling in c

22 diate chondrocyte responsiveness to CPPD and MSU crystals in vitro.

23 nonuclear phagocytes in response to CPPD and MSU crystals.

24 in chondrocytes stimulated by both CPPD and MSU crystals.

25 Quiescent MCF10A and MSU cells expressing p300-specific antisense sequences s

26 Previous laboratory research conducted at MSU has indicated that low-field nuclear magnetic resona

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

28 ominant-negative mutant both failed to block MSU-induced NO release or MMP-3 expression in parallel e

29 The boehmitic MSU-S/B intermediates formed from the chloride salts of

30 But MSU crystals also activate the classical and alternative

31 viously reported renoprotection conferred by MSU likely results from exocytosis of Weibel-Palade bodi

32 not due to apoptosis or steric hindrance by MSU crystals.

33 ration in mediating NET formation induced by MSU crystals.

34 lished from tumors formed in athymic mice by MSU-1.1 cells transformed in culture by various methods

35 lished from tumors formed in athymic mice by MSU-1.1-derived cell strains independently transformed i

36 tion during pregnancy, which is triggered by MSU crystals and leads to reduced fetal growth.

37 receptor, blocked NET formation triggered by MSU crystals.

38 In chondrocytes, MSU crystals activate a signaling kinase cascade typical

39 Finally, at higher concentrations, MSU crystals promoted P2R-dependent release of a granule

40 to a surfactant-boehmite mesophase, denoted MSU-S/B, with a lathlike framework made of boehmite nano

41 mily of mesoporous molecular sieves (denoted MSU-G) with vesiclelike hierarchical structures and unpr

42 stalline gamma-Al(2)O(3) pore walls, denoted MSU-gamma, with retention of the lathlike framework morp

43 ed clearance of apoptotic neutrophils during MSU crystal-induced peritonitis.

44 etic cell populations showed that effective, MSU-mediated antitumor activity required coadministratio

45 Macrophage activation by extracellular MSU crystals involves apparent recognition and ingestion

46 t epithelial cells (MCF10A) and fibroblasts (MSU) by using adenovirus vectors expressing p300-specifi

47 the slit-shaped framework pores in the final MSU-gamma phases and to the introduction of intra- and i

48 actor beta1 (TGFbeta1) was induced following MSU crystal stimulation (mean +/- SEM 1.50 +/- 0.24 ng/m

49 tro, and these cytokines fully accounted for MSU crystal-stimulated, monocyte-mediated endothelial ac

50 nate immune receptors, TLRs, are central for MSU-induced inflammation (see the related article beginn

51 of the ERK-1/ERK-2 pathway was essential for MSU and CPPD crystal-induced IL-8 mRNA expression, where

52 L-18 receptor (IL-18R) are not essential for MSU-induced inflammation.

53 at (LRR) domain of cryopyrin is required for MSU crystal-induced inflammation.

54 ine expression in response to endotoxin-free MSU crystals under serum-free conditions.

55 WT) mice were challenged with endotoxin-free MSU crystals under serum-free conditions.

56 monolayers stimulated with supernatants from MSU-treated monocytes.

57 o previous definitive gout diagnosis who had MSU analysis of joint aspirate.

58 o previous definitive gout diagnosis who had MSU analysis of joint aspirate.

59 udy was undertaken to define and compare how MSU and CPPD crystals stimulate IL-8 messenger RNA (mRNA

60 , the aim of this study was to determine how MSU crystals stimulate chondrocytes.

61 arization microscope is validated by imaging MSU crystals made from a gout patient's tophus and stero

62 pecific role of macrophage TG2 expression in MSU crystal-induced inflammation.

63 firmed depletion of von Willebrand factor in MSU-treated aortic endothelial cells.

64 rated calcium entry/IL-8 axis is involved in MSU crystal-induced aggregated NET formation, but MRS257

65 neutrophils (P < 0.05) but not monocytes in MSU crystal-induced knee synovial fluid from C6-deficien

66 An attenuated rise in MSU crystal-induced joint effusion levels of IL-8 also w

67 and IL-1R activation play essential roles in MSU-triggered inflammation.

68 a significant decrease (>60%) in swelling in MSU crystal-injected knees of C6-deficient animals as co

69 Here we show that trends in MSU channel 2 temperatures are weak because the instrume

70 tion and the capacity of the cells to ingest MSU crystals.

71 25118925XX (P2Y2 antagonist) did not inhibit MSU crystal-stimulated NET release.

72 Last, MSU crystal-induced leukocyte influx at 6 h was reduced

73 a novel BPH resistance gene, LOC_Os06g03240 (MSU LOCUS ID), from the rice variety Ptb33 in the interv

74 To make MSU deployment more practical, the vascular neurologist

75 omain of cryopyrin plays a role in mediating MSU crystal-induced inflammation in this model.

76 Monosodium urate monohydrate (MSU) and calcium pyrophosphate dihydrate (CPPD) crystals

77 lar and bursal monosodium urate monohydrate (MSU) crystal deposits, thereby inducing self-limiting bo

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

79 Although monosodium urate monohydrate (MSU) crystals have been recognized since the 18th centur

80 Monosodium urate monohydrate (MSU) crystals have remarkable inflammatory potential.

81 anism by which monosodium urate monohydrate (MSU) crystals intracellularly activate the cryopyrin inf

82 deposition of monosodium urate monohydrate (MSU) crystals may promote cartilage and bone erosion.

83 Monosodium urate monohydrate (MSU) crystals promote gouty inflammation that is critica

84 Monosodium urate monohydrate (MSU) crystals were administered into rat knee joints eit

85 in response to monosodium urate monohydrate (MSU) crystals.

86 the uptake of monosodium urate monohydrate (MSU) crystals.

87 Moreover, MSU does not stimulate HEK cells expressing TLR1-11 to a

88 innate immune cellular recognition of naked MSU crystals by specific TLRs as a major factor in deter

89 ccharide (LPS) in the presence or absence of MSU.

90 cells, partially reproducing the actions of MSU.

91 Correspondingly, administration of MSU crystals to rats during late gestation induced place

92 Coating of MSU crystals with sCD14, but not sTLR2 or sTLR4, restore

93 The detection of MSU crystals by optical microscopy is enhanced by their

94 The proinflammatory effect of MSU crystals was accompanied by trophoblast apoptosis an

95 The proinflammatory effects of MSU crystals were shown to be IL-1-dependent using a cas

96 tion and blocked characteristic formation of MSU crystal-NET aggregates called aggregated NETs.

97 iagnosis of gout relies on identification of MSU crystals under a compensated polarized light microsc

98 s were suppressed 6 hours after injection of MSU crystals in TLR-2-/- and TLR-4-/- mice and were atte

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

100 In addition, a comparable percentage of MSU crystals taken up by each type of bone marrow-derive

101 DMs) demonstrated unimpaired phagocytosis of MSU crystals but reduced p38 phosphorylation and approxi

102 DeltaLRR Z) mice at 6 hours postinjection of MSU crystals compared with WT mice.

103 in determining the inflammatory potential of MSU crystal deposits and the course of gouty arthritis.

104 determinant of the inflammatory potential of MSU crystals.

105 g case for an active proinflammatory role of MSU crystals at the maternal-fetal interface in patholog

106 ompared with that of a reference standard of MSU crystals in joint aspirate for diagnosing gout.

107 ompared with that of a reference standard of MSU crystals in joint aspirate for diagnosing gout.

108 t sufficient for malignant transformation of MSU-1.1 cells, it may be necessary.

109 Alternatively, the uptake of MSU crystals by mature macrophages can be noninflammator

110 D88-/- BMDMs demonstrated impaired uptake of MSU crystals in vitro.

111 ro and examined with respect to 1) uptake of MSU crystals, 2) expression of macrophage, dendritic cel

112 surface and free-troposphere warming for one MSU record.

113 -derived macrophages in response to not only MSU crystals but also other known stimuli that activate

114 Oxytetracycline did not stain CPPD or MSU crystals or other particulates.

115 e for leading-strand synthesis; with HeLa or MSU-1.2 cell extracts, this value was only 5%, and these

116 h XP variant cell extracts than with HeLa or MSU-1.2 cell extracts.

117 approximately 2.2 photoproducts for HeLa or MSU-1.2 cell extracts.

118 However, the well-ordered MSU-gamma phases made from aluminum nitrate as the prefe

119 ssion in 6A/SB1 cells compared with parental MSU-1.1 cells.

120 ning how the innate immune system recognizes MSU and the identities of the receptors involved.

121 y channel inhibitor (SK&F96365) also reduced MSU crystal-induced NET release.

122 neutralizing antibodies also showed reduced MSU-induced inflammation, demonstrating that IL-1 produc

123 inite life span human fibroblast cell strain MSU-1.1 and an isogenic fibrosarcoma-derived cell line,

124 The nontumorigenic parental cell strain, MSU-1.1, expresses high levels of this mRNA.

125 rom HeLa cells and a fibroblast cell strain, MSU-1.2, for the ability to replicate a UV-irradiated fo

126 We studied MSU crystal-induced peritonitis in TG2-/- and congenic T

127 Further analysis demonstrated that MSU crystal-activated macrophages exhibited NK cell-like

128 Our findings provide evidence that MSU crystal-activated macrophages have the potential to

129 The MSU may be particularly valuable for treatment of patien

130 The MSU may result in an overall shift toward earlier evalua

131 The MSU strategy could dramatically transform the way acute

132 actical, the vascular neurologist aboard the MSU must be replaced by a remote vascular neurologist co

133 ults indicate that IL-1 is essential for the MSU-induced inflammatory response and that the requireme

134 In the MSU crystal-induced monarthritis model, TNF alpha blocka

135 remote vascular neurologist connected to the MSU by telemedicine, reducing manpower requirements and

136 endothelial cell activation, in contrast to MSU-treated cells at an earlier stage of differentiation

137 e quantify the stratospheric contribution to MSU channel 2 temperatures using MSU channel 4, which re

138 Eosinophils exposed to MSU crystals rapidly (i.e., within 1 min of exposure) re

139 uclear leukocyte infiltration in response to MSU crystal injection in all animals, but substantial ne

140 NK cell-surface marker NK1.1 in response to MSU crystals but not in response to LPS or other urate c

141 anced TLR4-mediated signaling in response to MSU crystals in transfected Chinese hamster ovary cells

142 inophils to produce cytokines in response to MSU crystals, and P2 nucleotide receptors, in particular

143 hilic, air pouch inflammation in response to MSU crystals.

144 rosis factor alpha (TNFalpha) in response to MSU was measured by enzyme-linked immunosorbent assay.

145 mediated p38 MAPK activation in response to MSU.

146 may drive the gouty inflammatory response to MSU.

147 ition, uptake, and inflammatory responses to MSU crystals, we conducted a study to test the role of T

148 scade, Pyk-2, Src, and p38 kinases transduce MSU-induced NO production and MMP-3 expression.

149 signaling played a major role in transducing MSU-induced NO production and MMP-3 expression.

150 derived from chemical carcinogen transformed MSU-1.1 cells, we identified a novel gene, ST7, showing

151 ollowing injection of carcinogen-transformed MSU-1.1 cells.

152 et al. linearly combine time series from two MSU channels to estimate vertically integrated 850-300-h

153 the satellite-borne Microwave Sounding Unit (MSU channel 2), as well as the inferred temperatures in

154 measured using the Microwave Sounding Unit (MSU) instrument or radiosondes.

155 mperatures from the Microwave Sounding Unit (MSU) since 1979, sea surface temperatures from the Advan

156 There are many ways a mobile stroke unit (MSU) might prove valuable for patients with ischemic and

157 L) located on the Michigan State University (MSU) campus.

158 phate dihydrate (CPPD), or monosodium urate (MSU) crystals and placed on a microscope slide.

159 sues release uric acid and monosodium urate (MSU) crystals as important endogenous danger signals.

160 e endogenous danger signal monosodium urate (MSU) crystals can alter macrophage functions.

161 Phagocyte ingestion of monosodium urate (MSU) crystals can induce proinflammatory responses and t

162 While it is known that monosodium urate (MSU) crystals cause the disease gout, the mechanism by w

163 crystal arthropathy where monosodium urate (MSU) crystals deposit and elicit inflammation in a joint

164 ociated with deposition of monosodium urate (MSU) crystals in joints and periarticular tissues.

165 e them to the formation of monosodium urate (MSU) crystals, soluble urate also primes for inflammator

166 ly on the documentation of monosodium urate (MSU) crystals.

167 ly on the documentation of monosodium urate (MSU) crystals.

168 patients upon encountering monosodium urate (MSU) crystals.

169 phate dihydrate (CPPD) and monosodium urate (MSU) deposited in synovium and articular cartilage initi

170 Here, it is reported that monosodium urate (MSU) results in exocytosis of Weibel-Palade bodies in vi

171 rsenic trioxide suppressed monosodium urate (MSU)-induced IL-1beta production, suggesting that target

172 We found that uric acid (monosodium urate [MSU]) crystals induce a proinflammatory profile in isola

173 s delivery of UA crystals (monosodium urate, MSU) restored the allergic phenotype.

174 ribution to MSU channel 2 temperatures using MSU channel 4, which records only stratospheric temperat

175 ose of this study was to investigate whether MSU crystals induce macrophages to secrete antiinflammat

176 rly elaborated TGFbeta1 when challenged with MSU crystals (0.66 +/- 1.3 ng/ml/10(5) CD14+ cells).

177 but this was abolished by coincubation with MSU crystals.

178 However, coincubation with MSU led to a significant suppression of zymosan-induced

179 response to CPPD crystals in comparison with MSU crystals.

180 macrophage isolates were then incubated with MSU crystals for 24 hours, and culture supernatants were

181 Eosinophils incubated with MSU crystals, but not those incubated with uric acid sol

182 also produced by eosinophils incubated with MSU crystals.

183 eased by monocytes following incubation with MSU crystals, which induce E-selectin expression in vitr

184 Interaction of human neutrophils with MSU crystals was evaluated by high-throughput live imagi

185 sessed in cultured chondrocytes treated with MSU.