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1  galactose (1.2%), ascorbic acid (1.0%), and uric acid (3.3%).
2  natriuretic peptide (482 +/- 337 pg/mL) and uric acid (8.2 +/- 2.6 mg/dL), decreased left ventricula
3  correlated to BMI, whereas higher levels of uric acid (beta=0.164; P<0.001), proadrenomedullin (beta
4 2A9 on chromosome 4p16.1 are associated with uric acid (chi2df2=3545, p=3.19x10-23).
5                                We found that uric acid (monosodium urate [MSU]) crystals induce a pro
6 rotein (OR, 0.99; 95% CI, 0.98-0.99); higher uric acid (OR, 1.13; 95% CI, 1.04-1.22); working in inst
7              In multivariate analysis, serum uric acid (P = 0.001), estimated glomerular filtration r
8                                Higher plasma uric acid (PUA) levels are associated with lower glomeru
9                                      Soluble uric acid (sUA) is found in high concentrations in the s
10 apable of non-invasively monitoring salivary uric acid (SUA) levels.
11 MP, S100A4 is sensitive to oxidation whereas uric acid (UA) acts primarily as an antioxidant.
12  electrochemical detection of dopamine (DA), uric acid (UA) and ascorbic acid (AA) on three dimension
13 ice was verified by sequential injections of uric acid (UA) and ascorbic acid (AA).
14 ve interferences such as ascorbic acid (AA), uric acid (UA) and dopamine (DA).
15               The relationship between serum uric acid (UA) and outcomes after acute ischemic stroke
16                                              Uric acid (UA) can scavenge the peroxynitrite to avoid t
17  was proposed for the rapid determination of uric acid (UA) using a carbon nano tube paste electrode
18     Importantly, upon exposure to proteases, uric acid (UA) was rapidly released into the airway lume
19                           Elevated levels of uric acid (UA) were detected in mice undergoing sensitiz
20 whether alterations in levels of circulating uric acid (UA), a systemic antioxidant, affects the foll
21 trochemical detection of ascorbic acid (AA), uric acid (UA), and dopamine (DA).
22 i-interference properties in the presence of uric acid (UA), ascorbic acid (AA) and glucose.
23 , Ascorbic Acid (AA), Acetaminophen (Ac) and Uric Acid (UA).
24 e common interferents ascorbic acid (AA) and uric acid (UA).
25                                        While uric acid alone was unable to trigger a chloride secreto
26                                              Uric acid also proved superior to placebo in reducing in
27  Improvement Amendments (CLIA) criterion for uric acid analysis (+/-17%).
28 it is free from common interferences such as uric acid and ascorbic acid.
29 l for electrochemical detection of dopamine, uric acid and ascorbic acid.
30  positive genetic correlations between serum uric acid and BMI z score (rhoG = 0.45, P = 0.002), perc
31 laboratory analysis for the readily detected uric acid and for the clozapine which is present at 100-
32 erence observed in the presence of dopamine, uric acid and fructose.
33 blood was taken for the measurement of serum uric acid and glycosylated haemoglobin (HbA1C).
34 h is modulated by the redox reaction between uric acid and hexacyanoferrate ions.
35 exclusion of the main interfering substances uric acid and hydrogen peroxide.
36 inflammation, where there is large amount of uric acid and inflammatory peroxidases.
37 he device shows a near Nernstian response to uric acid and is highly specific.
38 sted whether there is an association between uric acid and normal variation in trait impulsivity meas
39                          Any interference of uric acid and other electroactive AAs was noticed.
40 the uox mutant, drawing a novel link between uric acid and peroxisome function, which may be relevant
41 d other nonhemodynamic factors, such as high uric acid and renal dysfunction, on changes in the left
42 rinol inhibited the increase in fetal plasma uric acid and suppressed the fetal femoral vasoconstrict
43                                              Uric acid and the GRS were both associated with cardiova
44 e evaluated the association between baseline uric acid and the primary composite outcome of doubling
45 ed agents to increase the renal clearance of uric acid and thereby control hyperuricemia.
46  potential interference by ascorbic acid and uric acid appeared to be negligible.
47             Elevated concentrations of serum uric acid are associated with increased risk of gout and
48       To discuss the evolving data regarding uric acid as a potential cause of hypertension and progr
49                 Future studies investigating uric acid as a risk factor for cardiovascular disease sh
50        Current evidence supports the role of uric acid as marker and mediator of risk for both hypert
51 eptor 4 (TLR-4), interleukin-18 (IL-18), and uric acid as markers of the inflammatory host response i
52 dehydrogenase, resulting in the formation of uric acid as well as ROS.
53  (SERS) approach for the routine analysis of uric acid at clinically relevant levels in urine patient
54  been utilized in the nanomolar detection of uric acid at physiological pH in water.
55 d increase in 3-nitrotyrosine formation, and uric acid attenuates Ang II-induced decrease in NO bioav
56 st to pure ZnO, ZnO:N (8% N) thin film based uric acid biosensor gives a high sensitivity of about 1.
57                           A third generation uric acid biosensor has been developed by exploiting the
58                     The genetic score raised uric acid by 17 micromol/L (95% CI 15, 18) per SD increa
59 droperoxide is a product of the oxidation of uric acid by inflammatory heme peroxidases.
60 ower autophagic activity in cells exposed to uric acid compared with control conditions.
61                                  Human serum uric acid concentration (SUA) is a complex trait.
62 vel with incident diabetes and the change in uric acid concentration after a diabetes diagnosis.
63 ing response in the range from 0 to 1.0mM of uric acid concentration and the apparent Michaelis-Mente
64 servational studies have identified elevated uric acid concentration as a risk factor for diabetes, w
65 ated a weighted genetic risk score (GRS) for uric acid concentration based on eight uric acid-regulat
66 ect, we found that a 59.48 micromol/L higher uric acid concentration did not have a causal effect on
67 lectrode is demonstrated for determining the uric acid concentration in human serum and urine.
68  or the lack of UOX per se, but the elevated uric acid concentration in the embryo.
69                             We conclude that uric acid concentration rises prior to diagnosis of diab
70 ch 1-mg/dl increase in genetically predicted uric acid concentration were significant for cardiovascu
71 between the EC-SERS signal intensity and the uric acid concentration.
72  QDs fluorescence, which was proportional to uric acid concentration.
73 .9 +/- 3.1 mg/dL, P < 0.0001), and 24-h mean uric acid concentrations (0%: -0.13 +/- 0.07; 10%: 0.15
74                 In both men and women, serum uric acid concentrations differed significantly by diet
75 investigate the causal effect of circulating uric acid concentrations on type 2 diabetes risk.
76                              In women, serum uric acid concentrations were slightly higher in vegans
77 variation in SLC2A9 is associated with serum uric acid concentrations, an important biomarker of rena
78 eking, were associated with higher levels of uric acid concurrently and when uric acid was measured 3
79 rain samples was determined by measuring the uric acid content of their aqueous extracts.
80  and the damage-associated molecular pattern uric acid contribute to Nlrp3 inflammasome-mediated IL-1
81            The potential mechanisms by which uric acid could cause vasoconstriction and a progressive
82 , the authors believe that TLR-4, IL-18, and uric acid could have a role in the inflammatory patholog
83 ng EPEC and STEC infections, we noticed that uric acid crystals became enmeshed in the neutrophilic e
84                    While trying to visualize uric acid crystals formed during EPEC and STEC infection
85                                              Uric acid crystals were formed in vivo in the lumen of t
86  well as other sterile particulates, such as uric acid crystals, induces DCs to produce IL-2 followin
87  mutation in uricase, the enzyme involved in uric acid degradation in most mammals, that developed du
88 archetypical cofactor-free uricase catalyzes uric acid degradation via a C5(S)-(hydro)peroxide interm
89 nd that gastrointestinal decontamination and uric acid depletion reduced GvHD severity.
90 al selection would allow the accumulation of uric acid despite the physiological consequences of crys
91 sitivity, selectivity, and stability towards uric acid detection in human saliva, covering the concen
92 ient samples have been used for quantitative uric acid detection using a simple, rapid colloidal SERS
93                      Peroxynitrite scavenger uric acid did not affect the first phase but ameliorated
94 ), allows for the absolute quantification of uric acid directly in a complex matrix such as that from
95                                 We find that uric acid directly inhibits uridine monophosphate syntha
96 ve dietary sodium intake and increased serum uric acid during follow-up despite pharmacological contr
97 on, the relationship between change in serum uric acid during follow-up, final left ventricular mass
98 lic blood pressure, sodium intake, and serum uric acid emerged as independent and significant determi
99  identified parameters, including fractional uric acid excretion and plasma copeptin concentration, m
100 glycosuria, increased urinary phosphate, and uric acid excretion.
101 le nucleotide polymorphisms (SNPs) and serum uric acid explain a small fraction of the heritability.
102 om healthy volunteers were first primed with uric acid for 24 h and then subjected to stimulation wit
103                      The mean level of serum uric acid for both the groups was within normal range an
104                    Quantitative detection of uric acid for rapid and routine diagnosis of early preec
105                            Although blocking uric acid formation by allopurinol did not affect outcom
106                     We wondered, however, if uric acid generated by XO also had biological effects in
107 gical and experimental evidence suggest that uric acid has a role in the etiology of type 2 diabetes
108                                      Because uric acid has been implicated as a mediator of adjuvant
109                                              Uric acid has been linked to the progression of native k
110 ng of epithelial absorption and secretion of uric acid has recently emerged, aided in particular by t
111 etic and regulatory networks with effects on uric acid homeostasis have also emerged.
112 scopy and used for quantitative detection of uric acid in 0.1 M NaF and synthetic urine at clinically
113 g lipid/lipoprotein risk factors for CVD and uric acid in adults [age: 18-40 y; body mass index (in k
114 ant of Arabidopsis thaliana that accumulates uric acid in all tissues, especially in the developing e
115 tocol is then employed for the estimation of uric acid in blood serum samples of healthy individuals.
116 ation of surprisingly high concentrations of uric acid in both cultured cell and animal models of inf
117 etween RNFL and macular thickness with serum uric acid in both the groups.
118 438 was associated with an increase in serum uric acid in European American males.
119     Our results show that variation in serum uric acid in Hispanic children is under considerable gen
120 s that impulsivity is associated with higher uric acid in humans and mice.
121 ited the expected pharmacodynamics to remove uric acid in hyperuricemic blood in vitro and multiple f
122 ricemic blood in vitro and multiple forms of uric acid in hyperuricemic geese.
123   These studies identify a key role AMPD and uric acid in mediating hepatic gluconeogenesis in the di
124 wed significantly higher level of mean serum uric acid in no diabetic retinopathy group (p = 0.004 re
125 n blood digestion, a massive accumulation of uric acid in the midgut posterior region, and a signific
126 es a reliable and sensitive determination of uric acid in the serum.
127 ayer (RNFL) and macular thickness with serum uric acid in type 2 diabetic patients.
128                               High levels of uric acid in urine and serum can be indicative of hypert
129  quantum dots (QDs) for the determination of uric acid in urine sample is described.
130 filtering out signals from ascorbic acid and uric acid interferents.
131 pite its role in converting highly insoluble uric acid into 5-hydroxyisourate.
132 ce of data support the hypothesis that serum uric acid is a cause or exacerbating factor of hypertens
133                                              Uric acid is a damage-associated molecular pattern (DAMP
134                                              Uric acid is a final breakdown product of purine catabol
135                                              Uric acid is a potential important biomarker in urine an
136 d Mendelian randomization to examine whether uric acid is an independent and causal cardiovascular ri
137                      These data suggest that uric acid is associated with IF/TA and thus may be a via
138              These results suggest that high uric acid is causally related to adverse cardiovascular
139                             In addition, how uric acid is cleared from the circulation is incompletel
140                                        Serum uric acid is determined by production and the net balanc
141 om disparate lines of research suggests that uric acid is elevated in psychiatric disorders character
142  reanalysis of the URICO-ICTUS trial whether uric acid is superior to placebo in improving the functi
143 as to investigate whether variation in serum uric acid is under genetic influence and whether the ass
144 e (35.2 [33.0-38.0] vs 33.0 [30.0-35.5] cm), uric acid level (4.9 [4.0-5.8] vs 4.5 [3.7-5.5] mg/dL),
145  (95% confidence interval: 0.04, 0.15) lower uric acid level after adjustment.
146  evidence shows a strong correlation between uric acid level and essential hypertension, supporting i
147 antified the independent association between uric acid level and incident diabetes via Cox proportion
148       Current evidence supports use of serum uric acid level as a biomarker for diagnosis of essentia
149 ildren, presenting the possibility for serum uric acid level to serve as a biomarker for diagnosis an
150                                              Uric acid level was associated with diabetes even after
151 n between duration of diabetes and change in uric acid level was examined via linear regression.
152          We examined both the association of uric acid level with incident diabetes and the change in
153 height, family history of ESRD, higher serum uric acid level, and lower measured GFR.
154 sma AST, salivary AST, and salivary ALT with uric acid level.
155 interest was hyperuricemia, defined as serum uric acid levels >/=6 mg/dL.
156 tricular ejection fraction </=40%, and serum uric acid levels >/=9.5 mg/dL to receive allopurinol (ta
157 difference = 1.7, 95% CI: -0.1, 3.4), plasma uric acid levels (for those born early preterm, differen
158 nd the allopurinol groups had baseline serum uric acid levels (SDs) of 8.7 (1.6) mg/dl and 8.3 (1.4)
159 ) has been shown to be associated with serum uric acid levels and gout in Asians, Europeans, and Euro
160        These results indicate that, although uric acid levels are elevated in the airways of NO2-expo
161                             A modest rise in uric acid levels beginning early after donation, and a s
162 purinol effectively and safely lowered serum uric acid levels in adults with stage 3 CKD and asymptom
163 etween maternal serum fructose and placental uric acid levels in humans.
164                             Moreover, plasma uric acid levels in mice fed the WD were decreased after
165 ed cell systems and in the intestine in vivo Uric acid levels in the gut lumen increased in response
166  and non-human primates and normalized serum uric acid levels in uricase-deficient mice.
167 py number polymorphisms (CNPs) contribute to uric acid levels is unknown.
168           In this regard, humans have higher uric acid levels than most mammals due to a mutation in
169                                              Uric acid levels were significantly reduced with allopur
170          We evaluated whether lowering serum uric acid levels with allopurinol improves endothelial d
171 d hemoglobin, albuminuria, triglycerides and uric acid levels, and worse measured glomerular filtrati
172 dase inhibitor allopurinol reduced placental uric acid levels, prevented placental inefficiency, and
173                  Upon further adjustment for uric acid levels, there was modest attenuation of the as
174  with reduced ejection fraction and elevated uric acid levels, xanthine oxidase inhibition with allop
175 vels significantly correlated with placental uric acid levels.
176 , more data will be required to determine if uric acid lowering therapy will become a mainstay of man
177 om episodic, longitudinal sequences of serum uric acid measurements in 4368 individuals we produced c
178 intestinal electrolyte transporters, hepatic uric acid metabolism, as well as renal and cardiomyocyte
179                      Next, we tested whether uric acid might mediate inflammasome activation in cells
180               We also examined the effect of uric acid on behavior by comparing wild-type mice, which
181 s not support a causal effect of circulating uric acid on diabetes risk.
182 sociated molecular patterns (DAMPs), such as uric acid or ATP, via NLRP3, which leads to caspase-1-de
183 sizes, expressed as the percentage change in uric acid per deleted copy, are most pronounced among wo
184 ctivated protein kinase phosphorylation, but uric acid priming induced phosphorylation of AKT and pro
185  broad inflammatory pathways associated with uric acid priming, with NF-kappaB and mammalian target o
186  oxygen species production was diminished by uric acid priming.
187 etion/export with a concomitant reduction of uric acid production.
188 acologic and nonpharmacologic means of serum uric acid reduction prior to clinical use as a therapy f
189                 In addition, ORMDL3 mediated uric acid release, another marker of cellular stress.
190 we investigated the mechanisms through which uric acid selectively lowers human blood monocyte produc
191                                        Serum uric acid showed a poor correlation with RNFL and macula
192 ared with placebo, allopurinol lowered serum uric acid significantly but did not improve endothelial
193 terovesicular junction stone on imaging, and uric acid stone composition.
194 were higher with potassium citrate; however, uric acid supersaturation was lower.
195    In the placenta, fructose induced de novo uric acid synthesis by activating the activities of the
196  used for ammonia detoxification and [(13)C] uric acid synthesis through multiple metabolic pathways,
197 rmediate of the electrochemical oxidation of uric acid that has a lifetime in solution of 23 ms as we
198                                              Uric acid therapy was associated with reduced infarct gr
199                                              Uric acid therapy was more effective than placebo in lim
200 sporter and sterically hinder the transit of uric acid through the substrate channel, albeit with vas
201  peroxidase), which is involved in oxidizing uric acid to allaintoin and hydrogen peroxide.
202                               We found serum uric acid to be significantly heritable [h(2) +/- SD = 0
203         Searching for the molecular cause of uric acid toxicity, we discovered a local defect of pero
204 9-deficient mice develop impaired enterocyte uric acid transport kinetics, hyperuricaemia, hyperurico
205                  High affinity inhibition of uric acid transport requires URAT1 residues Cys-32, Ser-
206 n method was done with SU as the exposure, a uric acid transporter genetic risk score as instrumental
207 which can be treated using inhibitors of the uric acid transporter, URAT1.
208 which can be treated using inhibitors of the uric acid transporter, URAT1.
209                                              Uric acid triggered inflammatory responses in the gut, i
210  15, 18) per SD increase and explained 4% of uric acid variation.
211 nd study that compared the administration of uric acid versus placebo in stroke patients treated with
212                                     Baseline uric acid was 5.57+/-1.48 mg/dL; male sex, higher BMI, d
213                        Continuous sensing of uric acid was also performed using this biosensor which
214 ver time, a 1 mg/dL increase in time-varying uric acid was associated with a 2.39 mL/min lower final
215                                       Higher uric acid was associated with a higher diabetes risk aft
216                                              Uric acid was associated with a range of prevalent disea
217                                              Uric acid was associated with an increased rate of excel
218 variate analysis adjusting for baseline GFR, uric acid was associated with doubling of interstitium o
219                                       Higher uric acid was associated with impulsivity in both humans
220 ant activity, we sought to determine whether uric acid was elevated and participated in a mouse model
221                          The level of plasma uric acid was found to be highly significantly increased
222           The linearity of the system toward uric acid was in the concentration range of 125-1000 mic
223                                We found that uric acid was increased in the airways of mice exposed t
224 er levels of uric acid concurrently and when uric acid was measured 3 to 5 years later.
225                                        Serum uric acid was measured in 3315 patients of the Ludwigsha
226                               The mean serum uric acid was significantly higher in patient with HbA1C
227 rotein (HDL) cholesterol, triglycerides, and uric acid were also measured.
228 cy questionnaire and serum concentrations of uric acid were measured.
229 s not known whether the association of serum uric acid with SLC2A9 polymorphisms manifests in childre
230 g lipid/lipoprotein risk factors for CVD and uric acid within 2 wk.
231 rips were developed for on-site detection of uric acid without involving any sophisticated instrument
232 ed uricase towards the oxidation of analyte (uric acid) and promotes the direct transfer of electrons
233 ), foods (fructose), and metabolic products (uric acid) function as survival signals to help reduce w
234 principle, this biosensor was used to detect uric acid, a biomarker for wound severity and healing, i
235                           Excess circulating uric acid, a product of hepatic glycolysis and purine me
236 lymphocytes, monocytes, glucose, creatinine, uric acid, albumin, bilirubin, total cholesterol, trigly
237 eading to de novo lipogenesis, production of uric acid, and accumulation of visceral and ectopic fat.
238  signals, such as high-mobility group box 1, uric acid, and ATP, that activate the dendritic cell net
239              Fasting glucose, triglycerides, uric acid, and bilirubin levels were decreased in the sa
240 of glomerulonephritis, higher serum level of uric acid, and blood cyclosporine trough level (C0) and
241 of glomerulonephritis, higher serum level of uric acid, and blood cyclosporine trough level (C0) and
242 nism for SLC2A9-mediated modulation of serum uric acid, and detail a bioinformatic approach for asses
243  that apes, including humans, cannot oxidize uric acid, and it appears that multiple, independent evo
244 serum urea nitrogen, serum creatinine, serum uric acid, and serum phosphorus; and faster rate of decl
245 iated with any biochemical marker except for uric acid, arguing against pleiotropy.
246 omavirus, dopamine, glutamic acid, IgG, IgE, uric acid, ascorbic acid, acetlycholine, cortisol, cytos
247 ng compounds in biological fluids, including uric acid, ascorbic acid, glucose and acetaminophen.
248 rofluorescein acellular assay but not by the uric acid, ascorbic acid, glutathione, or dithiothreitol
249                                              Uric acid, C-reactive protein, galectin-3, carboxy-termi
250 ated with higher levels of serum creatinine, uric acid, calcium and lower urine pH level.
251  predictors of disease progression including uric acid, creatinine and surprisingly, blood pressure,
252       Elevated brain natriuretic peptide and uric acid, decreased left ventricular ejection fraction,
253 nventional antioxidants, including dopamine, uric acid, epinephrine, serotonin, histamine, and 4-acet
254 ixture of graphene oxide, copper nitrate and uric acid, followed by thermal annealing at 900 degrees
255                                              Uric acid, generated from the metabolism of purines, has
256 selectivity against ascorbic acid, dopamine, uric acid, glucose and bovine serum albumin.
257 ctive to hydrazine without interference from uric acid, glucose, ammonia, caffeine, methylamine, ethy
258 g metabolic and signaling pathways involving uric acid, gut microbiome products, and so-called uremic
259                              Baseline sputum uric acid, high mobility group box-1, CXCL8 mRNA, sputum
260 ion end-products, high-mobility group box 1, uric acid, IL-33, or inflammasome activation.
261 sent study, we sought to investigate whether uric acid, in the soluble form, could also activate the
262 uvant in CD4KO mice might be associated with uric acid, inflammatory cytokines, and the recruitment o
263                           Subjects underwent uric acid, iothalamte GFR, and urine albumin to creatini
264  these damage-associated molecular patterns, uric acid, is increased in the maternal circulation in p
265         We show that XO-derived ROS, but not uric acid, is the trigger for IL1beta release and that X
266 jury associated with ATP depletion, elevated uric acid, oxidative stress and inflammation.
267 tively related to blood urea nitrogen, serum uric acid, proteinuria, and supernatant IL-4; whereas po
268  status, body mass index, haemoglobin, serum uric acid, serum albumin, albuminuria, and C reactive pr
269 waist-to-height ratio, alanine transaminase, uric acid, serum triglycerides, and blood pressure.
270 methyl-4'pyridyl)porphyrin-pentachloride, or uric acid, whereas exogenous ONOO(-) reduced FMD in non-
271 e, and lower GFR were associated with higher uric acid, whereas older age, less than 3 HLA matches an
272 Thus, the Akt-PRAS40 pathway is activated by uric acid, which inhibits autophagy and recapitulates th
273 ovo pyrimidine synthesis-an effect traced to uric acid, which is 10-fold higher in the blood of human
274 ype mice, which naturally have low levels of uric acid, with mice genetically modified to accumulate
275  was performed using a genetic score with 24 uric acid-associated loci.
276 rs placental function via a xanthine oxidase/uric acid-dependent mechanism, and similar effects may o
277 ich inhibits autophagy and recapitulates the uric acid-induced proinflammatory cytokine phenotype.
278                                              Uric acid-lowering therapies may therefore not be benefi
279                    Obesity and diets rich in uric acid-raising components appear to account for the i
280 ) for uric acid concentration based on eight uric acid-regulating single nucleotide polymorphisms.
281  acids in the Escherichia coli xanthine- and uric acid-transporting homologs (XanQ and UacT, respecti
282 I 1.11, 1.30) per 59.48 micromol/L (1 mg/dL) uric acid.
283 , apolipoprotein B, apolipoprotein CIII, and uric acid.
284 endent modulation in optical response toward uric acid.
285 C2A9), polymorphisms with variation in serum uric acid.
286  acid and 100% of glycine, glutamic acid and uric acid.
287 xanthine into xanthine and then further into uric acid.
288 d the first genome-wide analysis of CNPs and uric acid.
289 roactive compounds such as ascorbic acid and uric acid.
290 minophen, 100 muM ascorbic acid, and 100 muM uric acid.
291  and supersaturation for calcium oxalate and uric acid.
292 finity of the prepared bio-electrode towards uric acid.
293 ific AMP downstream metabolite through AMPD, uric acid.
294 ically modified to accumulate high levels of uric acid.
295  pro-oxidant and pro-inflammatory effects of uric acid.
296 thine oxidase of hypoxanthine to xanthine to uric acid.
297                                          The uric acid/xanthine H(+) symporter, UapA, is a high-affin
298 f lipid/lipoprotein risk factors for CVD and uric acid: postprandial triglyceride (0%: 0 +/- 4; 10%:
299 that accurately distinguished (0.97 AUC) the uric-acid signatures of gout vs. acute leukemia despite
300                             Creatinine (Cr), uric (UA) and ascorbic acid (AA) are common constituents

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