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 failed to trigger neutrophil and monocyte recruitmen

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

14 MSU induced rapid tyrosine phosphorylation of Pyk-2 and

15 MSU use was not associated with an increased risk of all

16 MSU-42011 markedly decreased the tumor number, size, and

17 MSU-induced functional signaling by specific protein kin

18 The Src-family inhibitor dasatinib abrogated MSU crystal-induced responses of human neutrophils and r

19 stroke, both a conventional ambulance and an MSU, when available, were dispatched.

20 reviously unrecognized connection between an MSU crystal-sensing receptor and the IFN-I response, and

21 Prehospital management in an MSU (vs standard EMS management).

22 s thrombolysis, prehospital management in an MSU compared with standard EMS management was associated

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

24 received either prehospital management in an MSU or standard EMS management between August 1, 2018, a

25 Prehospital management in an MSU was associated with a better score on the UW-mRS at

26 (6.4%) received prehospital management in an MSU.

27 Simultaneous dispatch of an MSU (computed tomographic scanning with or without angio

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

29 Similarly, patients with an MSU dispatched had lower 3-month coprimary disability sc

30 Patients with an MSU dispatched had lower median mRS scores at month 3 (1

31 nge [IQR], 0-3) than did patients without an MSU dispatched (2; IQR, 0-3; common OR for worse mRS, 0.

32 nd 52 (7.1%) had died vs patients without an MSU dispatched: 605 (78.0%) had none to moderate disabil

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

34 opherol alleviated acute gouty arthritis and MSU-induced peritonitis.

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

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

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

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

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

40 in chondrocytes stimulated by both CPPD and MSU crystals.

41 nonuclear phagocytes in response to CPPD and MSU crystals.

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

43 cognizes a variety of danger signals such as MSU, ATP, or Abeta.

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

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

46 h equimolar anakinra or PAS800-IL-1Ra before MSU challenge similarly reduced inflammatory markers.

47 equimolar anakinra administered 24 h before MSU challenge was ineffective.

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

49 In vivo, colchicine blocked MSU-induced recruitment of neutrophils to the peritoneum

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

51 compared based on the initial dispatch (both MSU and conventional ambulance or conventional ambulance

52 But MSU crystals also activate the classical and alternative

53 igible to receive t-PA; 617 received care by MSU and 430 by EMS.

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

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

56 ration in mediating NET formation induced by MSU crystals.

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

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

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

60 receptor, blocked NET formation triggered by MSU crystals.

61 Compared with usual care, MSU use was associated with an approximately 65% increas

62 Compared with usual care, MSU use was associated with excellent outcome (adjusted

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

64 Studies comparing MSU deployment and usual care for patients with suspecte

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

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

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

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

69 Moreover, the diagnostic MSU culture was unable to discriminate between patients

70 m management of gout, which aims to dissolve MSU crystals, suppress gout flares and resolve tophi.

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

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

73 estingly, addition of PTX3 in vitro enhanced MSU crystal phagocytosis by monocytes and resulted in hi

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

75 rn recognition molecule in gout facilitating MSU crystal phagocytosis and contributing to the pathoge

76 econdary clinical outcomes generally favored MSUs.

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

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

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

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

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

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

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

84 hyperuricaemia) is the major risk factor for MSU crystal deposition and development of gout.

85 rexinoids and demonstrate the potential for MSU-42011 to be developed for the treatment of KRAS-driv

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

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

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

89 nating-week trial, we assessed outcomes from MSU or EMS management within 4.5 hours after onset of ac

90 monolayers stimulated with supernatants from MSU-treated monocytes.

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

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

93 sequently, GSDMD or MLKL loss did not hinder MSU crystal-mediated release of bioactive IL-1beta.

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

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

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

97 , IL-1beta induction and autoinflammation in MSU crystal-induced peritonitis was not reduced in GSDMD

98 The same elevation in MSU levels was also detected in serum and vitreous of st

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

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

101 MD or the other lytic effector implicated in MSU crystal killing, mixed lineage kinase domain-like (M

102 DR, we have found a significant increase in MSU levels that correlated with the presence of inflamma

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

104 leukocyte influx and inflammatory markers in MSU-induced peritonitis, whereas equimolar anakinra admi

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

106 ression, pro-IL-1beta and IL-8 production in MSU stimulated THP-1 macrophages (p < 0.01).

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

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

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

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

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

112 25118925XX (P2Y2 antagonist) did not inhibit MSU crystal-stimulated NET release.

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

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

115 ce of solubilized urate, stimulated with LPS/MSU crystals.

116 To make MSU deployment more practical, the vascular neurologist

117 Compared with standard management, MSU care was associated with more tissue-defined averted

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

119 tudied the significance of CD44 in mediating MSU inflammation in-vivo.

120 CD44, a transmembrane receptor, in mediating MSU phagocytosis by macrophages.

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

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

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

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

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

126 poorly soluble monosodium urate monohydrate (MSU) crystals in peripheral joints.

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

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

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

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

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

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

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

134 Whether and how much MSUs alter outcomes has not been extensively studied.

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

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

137 cells, partially reproducing the actions of MSU.

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

139 cretion and paw edema upon administration of MSU crystals.

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

141 The combination of MSU-42011 and carboplatin and paclitaxel reduced macroph

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

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

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

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

146 is not only a substrate for the formation of MSU crystals but also an intrinsic inhibitor of MSU crys

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

148 crystals but also an intrinsic inhibitor of MSU crystal-induced tissue inflammation.

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

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

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

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

153 ignificant role in mediating phagocytosis of MSU and downstream inflammation and is a novel target in

154 contribution of PTX3 to the phagocytosis of MSU crystals and consequent production of IL-1beta occur

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

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

157 eriarticular tissue of mice postinjection of MSU crystals.

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

159 determinant of the inflammatory potential of MSU crystals.

160 olocalized with alpha-tubulin as a result of MSU exposure and ECD-shedding reduced MSU phagocytosis i

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

162 these studies support a contributing role of MSU in diabetes-induced retinal inflammation and suggest

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

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

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

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

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

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

169 mptoms (LUTS) below the diagnostic cutoff on MSU culture may still harbor bacterial infection and tha

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

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

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

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

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

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

176 ocrystal-free preparation suppressed LPS- or MSU crystal-induced monocyte activation, a process depen

177 Collectively, UA or MSU causes endothelial dysfunction via SREBP2 transactiv

178 Mechanistically, UA- or MSU-induced SREBP2 expression and its transcriptional ac

179 nockdown by siRNA partially abolished UA- or MSU-induced YAP activity, pro-inflammatory gene expressi

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

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

182 licy efforts to expand access to prehospital MSU management.

183 e kinase domain-like (MLKL), did not prevent MSU crystal-induced cell death.

184 d macrophage killing, also failed to prevent MSU crystal-mediated cell death.

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

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

187 ult of MSU exposure and ECD-shedding reduced MSU phagocytosis in murine and human macrophages.

188 Cd44(-/-) BMDMs showed reduced MSU phagocytosis, LDH release, IL-1beta expression and p

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

190 We showed that the routine MSU culture, adopting the UK interpretation criteria tai

191 low SREBP induction, and activation of RXR, MSU-42011 was selected as our lead compound.

192 valuated the results of the United Kingdom's MSU culture in symptomatic patients and controls.

193 In conclusion, the United Kingdom's MSU protocol misses a significant proportion of bacteria

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

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

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

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

198 an increased risk of gout in humans and that MSU crystals lead to elevated IL-1beta levels in Tet2 kn

199 We demonstrate that MSU crystals, the etiological agent of gout, rapidly act

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

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

202 The MSU may be particularly valuable for treatment of patien

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

204 The MSU strategy could dramatically transform the way acute

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

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

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

208 ed Rankin scale at discharge was 0.57 in the MSU group and 0.51 in the EMS group (adjusted odds ratio

209 n patients eligible for t-PA was 0.72 in the MSU group and 0.66 in the EMS group (adjusted odds ratio

210 administration of t-PA was 72 minutes in the MSU group and 108 minutes in the EMS group.

211 Mortality at 90 days was 8.9% in the MSU group and 11.9% in the EMS group.

212 the patients eligible for t-PA, 55.0% in the MSU group and 44.4% in the EMS group had a score of 0 or

213 Of patients eligible for t-PA, 97.1% in the MSU group received t-PA, as compared with 79.5% in the E

214 the bacterial enrichment capabilities of the MSU culture with those of a 50-ul uncentrifuged culture,

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

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

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

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

219 e showed reduced inflammation in response to MSU crystal injection compared with wild-type mice, incl

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

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

222 showed a suppressed inflammatory response to MSU crystals compared with Glut9 (lox/lox) controls with

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

224 ted higher levels of IL-1beta in response to MSU crystals in vitro, which was ameliorated through gen

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

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

227 eviates the painful inflammatory response to MSU crystals.

228 ophages initiate inflammation in response to MSU mediated by NF-kappaB nuclear translocation and NLRP

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

230 may drive the gouty inflammatory response to MSU.

231 mediated p38 MAPK activation in response to MSU.

232 of NLRP3-dependent inflammatory responses to MSU crystals in patients with gout.

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

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

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

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

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

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

239 armacological inhibitor, attenuated the UA-, MSU-, or gout serum-induced endothelial cell inflammatio

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

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

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

243 hospital management in a mobile stroke unit (MSU) improves functional outcomes in patients with acute

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

245 ared patients treated by mobile stroke unit (MSU) versus standard management.

246 cumulative evidence that mobile stroke unit (MSU; specialized ambulance equipped with computed tomogr

247 Mobile stroke units (MSUs) are ambulances with staff and a computed tomograph

248 dminister thrombolysis (mobile stroke units [MSUs]) before arriving at the hospital have been shown t

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

250 chronic disease caused by monosodium urate (MSU) crystal deposition.

251 model, we demonstrate that monosodium urate (MSU) crystal sensing by Clec12A enhances cytosolic RNA-i

252 namide (NSA) contribute to monosodium urate (MSU) crystal-induced cell death, IL-1beta release, and a

253 800-IL-1Ra for efficacy in monosodium urate (MSU) crystal-induced peritonitis.

254 mutation abrogated various monosodium urate (MSU) crystal-induced pro-inflammatory responses of neutr

255 Phagocytosis of monosodium urate (MSU) crystals and caspase-1 activation were determined b

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

257 Although monosodium urate (MSU) crystals are known to trigger inflammation, publish

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

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

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

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

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

263 caused by precipitation of monosodium urate (MSU) crystals in individuals with hyperuricemia.

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

265 sease caused by buildup of monosodium urate (MSU) crystals in the joints.

266 acterized by deposition of monosodium urate (MSU) crystals which trigger an innate immune response me

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

268 patients upon encountering monosodium urate (MSU) crystals.

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

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

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

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

273 d the contributing role of monosodium urate (MSU) to the pathological processes associated with the i

274 eated with uric acid (UA), monosodium urate (MSU), or serum from gout patients showed increased expre

275 m-induced peritonitis, and monosodium urate (MSU)-induced arthritis.

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

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

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

279 Midstream urine (MSU) culture remains the gold standard diagnostic test f

280 We next used MSU-42011 to treat established tumors in a clinically re

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

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

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

284 but this was abolished by coincubation with MSU crystals.

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

286 response to CPPD crystals in comparison with MSU crystals.

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

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

289 also produced by eosinophils incubated with MSU crystals.

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

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

292 sections of lung tumors in mice treated with MSU-42011 exhibited reduced cell density and fewer activ

293 sessed in cultured chondrocytes treated with MSU.

294 riglycerides and cholesterol, treatment with MSU-42011 did not increase these biomarkers, demonstrati

295 ability outcomes at 90 days were better with MSUs than with EMS.