ライフサイエンスコーパス: urate

1 respect to smoking (nicotine), caffeine, and urate.

2 high-affinity interaction with the substrate urate.

3 , respectively, per 1 SD increment in plasma urate.

4 umin-creatinine ratio (UACR), BUN, and serum urate.

5 ces were explained by higher levels of serum urate.

6 g of Pseudomonas aeruginosa was inhibited by urate.

7 lds of hydroperoxides were formed by LPO and urate.

8 e (XOR), blocks the oxidation of xanthine to urate.

9 3) for a 0.5mg/dl decrease in measured serum urate.

10 gene have increased concentrations of brain urate.

11 after exposure of S. coelicolor cultures to urate.

12 siological concentrations of thiocyanate and urate.

13 C), beta-carotene, retinol (vitamin A), and urate.

14 the genetic variants used as instruments for urate.

15 ta suggest that both crystalline and soluble urate activate various pro-inflammatory pathways.

16 ical consequences of crystallized monosodium urate acutely causing liver/kidney damage or chronically

17 placebo and nifedipine did not affect plasma urate, ADMA, or urine ET-1/creatinine, which reflects re

18 However, urate also possesses antioxidant and neuroprotective pro

19 of monosodium urate (MSU) crystals, soluble urate also primes for inflammatory signals in cells resp

20 The present study investigates whether urate, an antioxidant, Nrf2 activator, and inverse risk

21 manifestations of these in clinical practice-urate and bone marrow edema detection, metal artifact re

22 m underlying the observed pleiotropy between urate and cardiometabolic traits.

23 es our understanding of how hSLC2A9 mediates urate and fructose transport, providing further informat

24 studies confirm that hSLC2A9 transports both urate and fructose, but it interacts with them in differ

25 ogy Collaboration creatinine-cystatin C, and urate and high-sensitivity C-reactive protein using stan

26 t pleiotropic effects of genetic variants on urate and metabolic traits contribute to the observation

27 tream pathological elements influencing both urate and metabolic traits, and this may suggest new opp

28 sociated with urate that do not affect serum urate and PD progression.

29 ecS, indicating a direct interaction between urate and PecS.

30 s of the observational association of plasma urate and risk of coronary heart disease.

31 though a positive association between plasma urate and SSB consumption was found, there was no associ

32 ratory and radiographic tests, such as serum urate and synovial fluid crystal analysis and radiograph

33 to intraperitoneal challenge with monosodium urate and the development of experimental autoimmune enc

34 cohol consumption leads to overproduction of urates and renal function plays a critical role in serum

35 e) and mice (P=0.0003 for eGFR; P=0.0002 for urate) and confirmed as the primary cell type in microdi

36 d in kidney (P=9.1E-8 for eGFR; P=1.2E-5 for urate) and liver (P=6.8.10(-5) for eGFR).

37 d in humans (P=8.5E-5 for eGFR; P=7.8E-6 for urate) and mice (P=0.0003 for eGFR; P=0.0002 for urate)

38 g/dl genetically conferred decrease in serum urate, and 1.05 (95% CI = 1.01-1.10, p = 0.0133) for a 0

39 artery reactivity-glycerol trinitrate, serum urate, and C-reactive protein levels (all P<0.03).

40 ar ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase w

41 ulsive-compulsive disorders, blood pressure, urate, and rapid eye movement (REM) behaviour disorder s

42 uded negative associations with raised serum urate, and single studies or studies with conflicting re

43 ences in circulating ascorbate, retinol, and urate are not associated with differences in AD risk.

44 Since xanthine and urate are produced as part of the oxidative burst during

45 These findings identify and substantiate urate as a biomarker of resistance to PD among LRRK2 mut

46 Our findings establish urate as a likely physiological substrate for LPO that w

47 emiological and clinical data has identified urate as a predictor of both reduced risk and favorable

48 As an example, we identified urate as one of these key players mediating the comorbid

49 e reduction (tolerability), and elevation of urate assessed serially in serum and once (at 3 months)

50 Enrichment analysis, fine-mapping of urate-associated loci and colocalization with gene expre

51 likelihood that it is shared with the serum urate-associated locus.

52 vance using a genetic instrument based on 31 urate-associated single nucleotide polymorphisms (SNPs).

53 e is not the causal agent underlying the SSB-urate association.

54 nificant reductions in body weight and serum urate at week 6.

55 We demonstrate that OAT7 is a very weak urate-butyrate exchanger.

56 at S. coelicolor PecS responds to the ligand urate by attenuated DNA binding in vitro and upregulatio

57 that crystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cystine trigg

58 Elevated urate can cause gout and urolithiasis and is associated

59 n of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger th

60 lar patterns as well as biological crystals (urate, cholesterol, etc.), resulting in expression of IL

61 At physiologically relevant concentrations, urate competed effectively with thiocyanate, the main su

62 o investigate the association between plasma urate concentration and: a) food items: dairy, sugar-swe

63 A 2 mg/dL increment in urate concentration decreased the odds of having PD by a

64 Fetal plasma urate concentration increased significantly during chron

65 Increased circulating plasma urate concentration is associated with an increased risk

66 requiring symptomatic treatment and a serum urate concentration less than 6 mg/dL (the approximate p

67 dose was optimised towards achieving a serum urate concentration of less than 0.357 mmol/L (<6 mg/dL)

68 Mean urate concentration was 283.8+/-72.1 mmol/dL (females: 2

69 coronary heart disease events) a 1 SD higher urate concentration was associated with an odds ratio (O

70 Urate concentration was measured in plasma.

71 nutrients and food products influence plasma urate concentration, to inform the development of eviden

72 day if necessary to achieve the target serum urate concentration.

73 Higher serum urate concentrations predict more favorable prognosis in

74 Serum urate concentrations were 0.69mg/dl lower among individu

75 hat identify an allele associated with lower urate concentrations, and for selected SNPs in other gen

76 smoking, caffeine consumption, higher serum urate concentrations, physical activity, and use of ibup

77 ny genetic loci associated with raised serum urate concentrations.

78 overexpressing the enzyme have reduced brain urate concentrations.

79 were higher among persons with greater serum urate concentrations.

80 her illuminating the molecular mechanisms of urate control.

81 eported dozens of loci associated with serum urate control; however, there has been little progress i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 ure to ascorbate, beta-carotene, retinol, or urate does not lower the risk of AD.

100 ucial site that could directly interact with urate during transport.

101 A urate-elevating agent is currently under investigation a

102 and strengthen the rationale for developing urate-elevating strategies as potential disease-modifyin

103 pidemiological, and clinical data identified urate elevation as a candidate strategy for slowing disa

104 The Safety of Urate Elevation in PD (SURE-PD) study, a randomized, dou

105 7.0 mg/dL) or moderate (7.1-8.0 mg/dL) serum urate elevation using 500-mg capsules taken orally up to

106 Monosodium urate enhanced CD86 and OX40L expression on DCs, indepen

107 at is attenuated by the ligands xanthine and urate, except when promoter DNA is saturated with PecS.

108 ations, but only subtle alterations of renal urate excretion and ABCG2 abundance.

109 de insight into the importance of intestinal urate excretion for serum urate homeostasis.

110 iant, support an important role for ABCG2 in urate excretion in both the human kidney and intestinal

111 significant evidence of reduced extra-renal urate excretion.

112 needed to identify threshold values of serum urate for treatment initiation and to confirm optimal ta

113 e hSLC2A9; however, Ile-335 is necessary for urate/fructose trans-acceleration exchange to occur.

114 This systematic analysis of serum urate GWAS loci identified candidate causal genes at 24

115 Although urate has been classically viewed as an antioxidant with

116 s an essential protein that mainly regulates urate/hexose homeostasis in human kidney and liver.

117 ance of intestinal urate excretion for serum urate homeostasis.

118 e than Prx1 to hyperoxidation caused by both urate hydroperoxide and hydrogen peroxide.

119 erefore, Prx1 and Prx2 are likely targets of urate hydroperoxide in cells.

120 Urate hydroperoxide is a product of the oxidation of uri

121 Oxidation of Prxs by urate hydroperoxide might affect cell function and be pa

122 The formation of urate hydroperoxide might be a key event in vascular inf

123 n data suggest that the oxidation of Prx2 by urate hydroperoxide occurs by a three-step mechanism, wh

124 Urate hydroperoxide oxidized Prx2 from intact erythrocyt

125 Urate hydroperoxide oxidizes glutathione and sulfur-cont

126 cytosolic 2-Cys Prx1 and Prx2 revealed that urate hydroperoxide oxidizes these enzymes at rates comp

127 estry genome-wide association study of serum urate in 457,690 individuals, identifying 183 loci (147

128 ns such as bicarbonate, lactate, citrate and urate in a variety of bio-fluids.

129 The role of urate in cardiovascular diseases (CVDs) has been extensi

130 support a neuroprotective role of endogenous urate in dopaminergic neurons and strengthen the rationa

131 of a causal role for triglyceride in raising urate in men (P(Corrected)=0.018).

132 on, findings suggesting that basal levels of urate in mice do not appreciably protect against oxidati

133 sation analysis implicates a causal role for urate in the development of coronary heart disease, but

134 w summarizes what is known about the role of urate in the inflammatory response.

135 e, p-cresol sulfate, kynurenine, creatinine, urate) include two "drug" transporters of the organic an

136 a significant longitudinal genotype x serum urate interaction effect, consistent in direction with t

137 ere conducted to assess gene variant x serum urate interaction effects on magnetic resonance imaging-

138 ation study to identify gene variant x serum urate interaction effects on the striatal (123) I-ioflup

139 We now demonstrate that urate is a good substrate for bovine LPO.

140 High serum urate is a prerequisite for gout and associated with met

141 Since production of urate is associated with generation of reactive oxygen s

142 Serum urate is highly heritable, yet association studies of si

143 The physiological function of urate is poorly understood.

144 Urate is the end product of purine metabolism in humans,

145 ting in supersaturation of body tissues with urate, leads to the formation and deposition of monosodi

146 Elevated serum urate level (hyperuricaemia) is the major risk factor fo

147 Genetic profile combined with serum urate level can be used to predict disease severity and

148 ring the intervention period, the mean serum urate level decreased from 6.1 to 3.9 mg per deciliter w

149 d participants with type 1 diabetes, a serum urate level of at least 4.5 mg per deciliter, an estimat

150 nome-wide significant interaction with serum urate level to predict striatal dopamine transporter den

151 or each) vs placebo, and cerebrospinal fluid urate level was greater in both inosine groups (P = .006

152 Lowering of the serum urate level with allopurinol may slow the decrease in th

153 albumin:creatinine ratio, 716.9; mean serum urate level, 8.2 mg per deciliter) were included in the

154 ported physician diagnosis of gout and serum urate level.

155 reased risk and may be a surrogate for lower urate levels (associated with faster progression in mani

156 High blood urate levels (hyperuricemia) have been found to be a sig

157 oral allopurinol reduced serum and striatal urate levels 4-fold and 1.3-fold, respectively, it did n

158 associated with genetically determined serum urate levels after multiple testing correction (p < 3.35

159 ed positive associations between circulating urate levels and cardiometabolic diseases, causality rem

160 Urate-lowering therapy decreases serum urate levels and reduces risk for acute gout attacks.

161 s a direct causal relationship between serum urate levels and the development of CKD.

162 Higher serum urate levels are associated with an increased risk of di

163 Elevated serum urate levels are associated with progression of chronic

164 mization approach, we assessed whether serum urate levels are causally relevant in type 2 diabetes me

165 Overall, allopurinol lowered urate levels but did not exacerbate dopaminergic neuron

166 Elevated serum urate levels cause gout and correlate with cardiometabol

167 However, a 1 SD increase in serum urate levels due to the genetic score was associated wit

168 Serum urate levels have been associated with risk for and prog

169 omes related to genetically determined serum urate levels in 339,256 unrelated White British individu

170 eotide polymorphisms known to regulate serum urate levels in association with various vascular and no

171 ive in raising serum and cerebrospinal fluid urate levels in early PD.

172 larly in men, to be partly related to higher urate levels in middle-aged blacks.

173 ts to recommend routine measurement of serum urate levels in patients with CKD and consider initiatio

174 t support a causal role of circulating serum urate levels in T2DM, CHD, ischemic stroke, or HF.

175 Decreasing serum urate levels may not translate into risk reductions for

176 Whereas the high serum urate levels observed in patients with gout predispose t

177 Although lower urate levels reduce risk for recurrent acute attacks, tr

178 hyperuricaemia, sustained elevation of serum urate levels resulting in supersaturation of body tissue

179 Sustained reduction in serum urate levels using urate-lowering therapy is vital in th

180 Urate levels were compared by multiple regression betwee

181 In this study, high serum urate levels were found to be associated with increased

182 Banked plasma samples or urate levels were obtained for 3 cohorts of age- and sex

183 ymorphisms exclusively associated with serum urate levels were used in a genetic risk score to assess

184 , recurrence, intermediate outcomes of serum urate levels, and harms.

185 ed genes likely involved in control of serum urate levels, further illuminating the molecular mechani

186 Serum urate levels, increased by 1 SD due to the genetic score

187 Gout is caused by elevated serum urate levels, which can be treated using inhibitors of t

188 es for an equivalent increase in circulating urate levels.

189 rters that have modest or no effect on serum urate levels.

190 idence of a causal protective effect of high urate levels.

191 opulations to identify 10 new loci for serum urate levels.

192 ators to determine the priority of trials of urate lowering for the prevention of coronary heart dise

193 Novel approaches to urate lowering have led to mechanism-based therapies suc

194 e strategies for both gouty inflammation and urate lowering.

195 tioxidant benefit offsetting its detrimental urate-lowering effect.

196 ient education, self-management training and urate-lowering medication titration.

197 Among other factors, age and urate-lowering medication were associated with alpha- an

198 ifestyle advice, monitoring and titration of urate-lowering medications have been implemented to impr

199 In addition, new urate-lowering medications to be used alone or in combin

200 oms, targeting interleukin-1beta, as well as urate-lowering therapies including uricase and inhibitor

201 Febuxostat and allopurinol are urate-lowering therapies used to treat patients with gou

202 Moderate-strength evidence suggests that urate-lowering therapy (allopurinol or febuxostat) reduc

203 cal trials that have evaluated the effect of urate-lowering therapy (ULT) on the rate of CKD progress

204 Allopurinol is the first-line urate-lowering therapy and should be started at a low do

205 Urate-lowering therapy decreases serum urate levels and

206 ACP recommends against initiating long-term urate-lowering therapy in most patients after a first go

207 tained reduction in serum urate levels using urate-lowering therapy is vital in the long-term managem

208 ttacks by at least half in patients starting urate-lowering therapy, and moderate-strength evidence i

209 preferences with patients before initiating urate-lowering therapy, including concomitant prophylaxi

210 third to half of patients with gout receive urate-lowering therapy, which is a definitive, curative

211 can reduce gout flares during initiation of urate-lowering therapy.

212 For those with moderate to severe gout, urate-lowering treatment can eliminate acute attacks of

213 5 urate-lowering treatment strategies were evaluated: no t

214 Whether urate-lowering treatment with allopurinol can attenuate

215 dney disease and a high risk of progression, urate-lowering treatment with allopurinol did not slow t

216 opurinol or febuxostat is a suitable initial urate-lowering treatment.

217 n allopurinol (300 mg/day, titrated to serum urate <6 mg/dl).

218 vascular disease, and that lowering of serum urate may assist in control of hypertension.

219 e-rich vegetables intake for lowering plasma urate may be ineffectual, despite current recommendation

220 dual inhibitor PF-562271 reduced monosodium urate-mediated peritonitis, a disease model used for stu

221 e whole-body metabolism, and that enterocyte urate metabolism could potentially be targeted to modula

222 the deposition of poorly soluble monosodium urate monohydrate (MSU) crystals in peripheral joints.

223 ut is a chronic disease caused by monosodium urate (MSU) crystal deposition.

224 g as a model, we demonstrate that monosodium urate (MSU) crystal sensing by Clec12A enhances cytosoli

225 rosulfonamide (NSA) contribute to monosodium urate (MSU) crystal-induced cell death, IL-1beta release

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

227 Phagocytosis of monosodium urate (MSU) crystals and caspase-1 activation were deter

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

229 how the endogenous danger signal monosodium urate (MSU) crystals can alter macrophage functions.

230 form of crystal arthropathy where monosodium urate (MSU) crystals deposit and elicit inflammation in

231 tory disease caused by buildup of monosodium urate (MSU) crystals in the joints.

232 edispose them to the formation of monosodium urate (MSU) crystals, soluble urate also primes for infl

233 f gout patients upon encountering monosodium urate (MSU) crystals.

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

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

236 stigated the contributing role of monosodium urate (MSU) to the pathological processes associated wit

237 ML by arsenic trioxide suppressed monosodium urate (MSU)-induced IL-1beta production, suggesting that

238 We found that uric acid (monosodium urate [MSU]) crystals induce a proinflammatory profile i

239 xogenous delivery of UA crystals (monosodium urate, MSU) restored the allergic phenotype.

240 mia in the absence of a diagnosis of gout or urate nephrolithiasis, an emerging body of evidence supp

241 Less frequent types include urate nephropathy, cystinosis, dihydroxyadeninuria, and

242 tudy, we aimed to clarify any causal role of urate on coronary heart disease risk using Mendelian ran

243 e, but the extent of any causative effect of urate on risk of coronary heart disease is still unclear

244 Crystals of calcium oxalate, monosodium urate, or calcium pyrophosphate dihydrate, as well as si

245 scavenger Tiron, the peroxynitrite scavenger Urate, or the eNOS inhibitor L-NAME and these effects as

246 ase kinase kinase in Magnaporthe oryzae, and urate oxidase (designated ClUrase) were functionally cha

247 We have isolated a urate oxidase (uox) mutant of Arabidopsis thaliana that

248 jugation assay, two sites (W160 and D112) of urate oxidase (Uox), a model therapeutic protein, were s

249 Urate oxidase (Uox), a therapeutic enzyme for treatment

250 Exemplified with urate oxidase (UOx), the enzyme used for hyperuricemia t

251 evolutionary disruption of the gene encoding urate oxidase (UOx).

252 e and stand in contrast to the mechanisms of urate oxidase and (1H)-3-hydroxy-4-oxoquinaldine 2,4-dio

253 sis involving single and multiple mutants of urate oxidase, xanthine dehydrogenase, nucleoside hydrol

254 rum UA levels to 0 by infusing a recombinant urate oxidase.

255 tration on the second virial coefficient for urate oxidase.

256 In rodents, functional UOx catalyzes urate oxidation to allantoin.

257 During urate oxidation, LPO was diverted from its peroxidase cy

258 rich vegetables was not associated to plasma urate (p = 0.38).

259 from commonly interfering compounds such as urate, paracetamol and l-ascorbate.

260 elevant to therapeutic efforts targeting the urate pathway.

261 d recombinant uricase to directly catabolize urate (pegloticase).

262 cent difference 1.0%, 95% CI 0.0%-2.0%), and urate (percent difference 6%, 95% CI 3%-10%) than those

263 d-type mice, and in both in vivo (monosodium urate peritonitis) and in vitro models of inflammation.

264 ted oxidative damage due to the reduction in urate, protein carbonyl levels, a marker of oxidative da

265 e of clinically meaningful benefits of serum urate reduction with allopurinol on kidney outcomes amon

266 Urate-related compounds are therapeutic candidates in ne

267 kers urinary S-sulphocysteine, xanthine, and urate returned to almost normal concentrations in all ty

268 Serum urate rose by 2.3 and 3.0 mg/dL in the 2 inosine groups

269 Serum urate showed significant genetic correlations with many

270 emonstrates that the I335V mutant transports urate similarly to the wild type hSLC2A9; however, Ile-3

271 s have reported genetic loci affecting serum urate (SU) concentrations, few studies have been conduct

272 n strong positive associations between serum urate (SU) levels and chronic kidney disease (CKD) risk;

273 ies have associated elevated levels of serum urate (SU) with triglycerides and risk of heart disease.

274 hronic disease resulting from elevated serum urate (SU).

275 ave led to mechanism-based therapies such as urate synthesis inhibitors (febuxostat is already FDA ap

276 carriers had significantly higher levels of urate than those who developed PD in each of the 3 indep

277 polymorphisms in other genes associated with urate that do not affect serum urate and PD progression.

278 l data link higher levels of the antioxidant urate to a reduced risk of developing Parkinsons disease

279 , Ser-35 and Phe-365, are also important for urate transport kinetics.

280 e of recent progress in the understanding of urate transport systems.

281 red a disorder of purine metabolism, altered urate transport, both in the gut and the kidneys, has a

282 Furthermore, Trp-110 is a critical site for urate transport.

283 e of sex hormones in the regulation of ABCG2 urate transporter and its potential implications for the

284 olic syndrome in mice lacking the enterocyte urate transporter Glut9 (encoded by the SLC2A9 gene).

285 es including uricase and inhibitors of renal urate transporter proteins.

286 CNPs upstream of the urate transporter SLC2A9 on chromosome 4p16.1 are associ

287 g on the intracellular uptake of sUA via the urate transporter SLC2A9/GLUT9.

288 as recently identified as an important human urate transporter, and a common mutation, a Gln to Lys s

289 ated the promoter of ABCG2, encoding a major urate transporter, in kidney cells, and that HNF4A p.Thr

290 acity hexose transporter and a high capacity urate transporter.

291 nd for selected SNPs in other genes encoding urate transporters that have modest or no effect on seru

292 e Q141K ABCG2 variant display elevated serum urate, unaltered FEUA, and significant evidence of reduc

293 ught to determine whether lowering levels of urate using allopurinol results in exacerbated neurotoxi

294 transcription factor that may regulate serum urate via the pentose-phosphate pathway and MRPS7 and ID

295 n peroxide was added to saliva, oxidation of urate was dependent on its concentration and peroxidase

296 Urate was oxidized by LPO to produce the electrophilic i

297 of certain SNPs with risk factors other than urate, we additionally did both a multivariable Mendelia

298 Further, IS and urate were found to be independent predictors of change

299 by each of ascorbate, N-acetylcysteine, and urate when compared to alpha-TOH.

300 can be efficiently attenuated by the ligand urate, which also quenches the intrinsic fluorescence of

301 etermined rate constants for the reaction of urate with compound I (k1 = 1.1 x 10(7) M(-1) s(-1)) and