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1 radation toward the production of neurotoxic quinolinic acid.
2 tivity promotes the production of neurotoxic quinolinic acid.
3 otic destruction produced in rat striatum by quinolinic acid.
4 destined to die following administration of quinolinic acid.
5 administration of the NMDA receptor agonist quinolinic acid.
6 n, probably as a consequence of formation of quinolinic acid.
7 way that ultimately degrades kynurenine into quinolinic acid.
8 DO and generates the neuroactive metabolite, quinolinic acid.
9 hanced ability to modify the accumulation of quinolinic acid.
10 eiving striatal injections of the neurotoxin quinolinic acid.
11 tive cells in cultures after incubation with quinolinic acid.
12 ytes, occurred during longer incubation with quinolinic acid.
13 by TNFalpha, gp120, and necrosis induced by quinolinic acid.
15 te and dihydroxyacetone phosphate, affording quinolinic acid, a central intermediate in the biosynthe
16 ing inorganic phosphate, 2 mol of water, and quinolinic acid, a central intermediate in the biosynthe
18 r an intrastriatal injection of low doses of quinolinic acid, a N-methyl-D-aspartate receptor agonist
20 brain macrophages and microglia can release quinolinic acid, a neurotoxin and NMDA (N-methyl-D-aspar
22 ults are consistent with the hypothesis that quinolinic acid accumulation in brain tissue contributes
23 used to examine the mechanisms of increased quinolinic acid accumulations and determine the relation
26 AP-1, whose binding peaked about 6 hr after quinolinic acid administration, and E2F-1, which was onl
27 death induced by intrastriatal injection of quinolinic acid, an N-methyl-D-aspartate glutamate recep
28 on resulting from intrastriatal injection of quinolinic acid, an NMDA receptor agonist, and kainic ac
32 d to neurotoxicity through the generation of quinolinic acid and immunosuppression and can alter brai
33 OD-1 activity significantly protects against quinolinic acid and kainic acid neurotoxicity in the mou
34 m is activated, leading to the production of quinolinic acid and kynurenic acid which can modulate N-
36 ) to Cu(I) and Fe(II), respectively, whereas quinolinic acid and the nonphenolic kynurenine catabolit
37 f tryptophan metabolism includes an agonist (quinolinic acid) and an antagonist (kynurenic acid) at t
38 of neurotoxins (tumor necrosis factor-alpha, quinolinic acid, and nitric oxide) in plasma and CSF wer
40 ) metabolism by exploiting microglia-derived quinolinic acid as an alternative source of replenishing
41 Small excitotoxin lesions were made using quinolinic acid at bilateral sites within the dorsolater
42 brains of 2-day-old rats were incubated with quinolinic acid at concentrations known to kill neurons.
50 infant syndrome had increased admission CSF quinolinic acid concentrations compared with children wi
51 of 94 HIV-1-infected patients, elevated CSF quinolinic acid concentrations correlated with worsening
53 bsamples with lower or no immune activation (quinolinic acid: F = 21.027, p < 0.001 [ANOVA]; BTP: F =
54 etabolites in both pathways are converted to quinolinic acid for NAD biosynthesis or to acetyl-CoA fo
55 acid phosphoribosyltransferase (QPRT) to use quinolinic acid for NAD(+) synthesis and prevent apoptos
56 hat significant predictors of BTP levels are quinolinic acid, glomerular filtration rate and age.
57 que with encephalitis showed that almost all quinolinic acid (>98%) was synthesized locally within th
59 necrosis factor-alpha (TNFalpha), gp120 and quinolinic acid have been implicated as agents for the c
61 in the interferon-gamma-induced synthesis of quinolinic acid in primary cultures of cultured human pe
62 kynurenine pathway, based on high levels of quinolinic acid, in patients with IBD compared with cont
63 vels of tryptophan metabolites-especially of quinolinic acid-indicated a high activity of tryptophan
64 be a new non-invasive biomarker to indicate quinolinic acid-induced impaired blood-brain barrier int
65 te whether BTP might non-invasively indicate quinolinic acid-induced impaired blood-brain barrier int
67 pared with sham-operated controls, rats with quinolinic acid-induced medial striatal lesions showed a
69 areas of encephalitis, rather than entry of quinolinic acid into the brain from the meninges or bloo
70 r, monkeys received unilateral injections of quinolinic acid into the previously implanted striatum t
72 catabolize tryptophan, it is unclear whether quinolinic acid is produced in gliomas and whether it is
73 ncrease in the macrophage-derived neurotoxin quinolinic acid is seen following severe TBI in children
76 n of IDO1 pathway metabolites kynurenine and quinolinic acid led to activation of beta-catenin and pr
78 ed CPP, rats received bilateral infusions of quinolinic acid (lesion group) or vehicle (sham group) i
80 The present study examined the effects of quinolinic acid lesions of the dorsal anterior cingulate
83 nificant correlations between elevated serum quinolinic acid levels with those in CSF and brain paren
85 These findings raise the possibility that quinolinic acid may play a role in secondary injury afte
86 table isotope-labeled precursors tryptophan, quinolinic acid, nicotinic acid, and nicotinamide were a
87 tory behavior were recorded before and after quinolinic acid or radiofrequency (RF) lesions were made
90 but not nonneoplastic astrocytes, expressed quinolinic acid phosphoribosyltransferase (QPRT) to use
93 ed by microglial cells, as expression of the quinolinic acid-producing enzyme 3-hydroxyanthranilate o
96 forms nicotinate mononucleotide (NAMN) from quinolinic acid (QA) and 5-phosphoribosyl 1-pyrophosphat
97 tide, carbon dioxide, and pyrophosphate from quinolinic acid (QA) and 5-phosphoribosyl 1-pyrophosphat
98 o, rats were given the NMDA receptor agonist quinolinic acid (QA) by intrastriatal infusion, and the
99 sic striatal neurons by a local injection of quinolinic acid (QA) dramatically enhances the magnitude
100 tum with either 6-hydroxydopamine (6OHDA) or quinolinic acid (QA) exaggerated their dystonic attacks.
103 cal lesions, by using either the excitotoxin quinolinic acid (QA) or the complex II mitochondria inhi
104 mon architecture for both nicotinic acid and quinolinic acid (QA) phosphoribosyltransferases (PRTase)
105 genes of the kynurenine pathway required for quinolinic acid (QA) production from tryptophan are pres
107 selective detection of endogenous neurotoxin quinolinic acid (QA) whose elevated level in serum is ma
108 nd neurotoxic (3-hydroxykynurenine (3HK) and quinolinic acid (QA)) kynurenine pathway metabolites wer
111 inic acid (NAc) and its metabolic precursor, quinolinic acid (QA), are produced in yields as high as
112 The enzyme NadA catalyzes the synthesis of quinolinic acid (QA), the precursor of the universal nic
113 ydrating enzyme involved in the synthesis of quinolinic acid (QA), the universal precursor of the ess
114 s, kynurenine (KYN), kynurenic acid (KA) and quinolinic acid (QA), were examined in terms of their ef
119 e metabolites were measured: the excitotoxin quinolinic acid (QA); the protective receptor antagonist
120 eived unilateral injection (1 microliter) of quinolinic acid (QA, 40 micrograms in 0.1 M phosphate bu
121 events triggered by intrastriatally injected quinolinic acid (QA, 60 nmol) and kainic acid (KA, 2.5 n
122 5-phosphoribosyl 1-pyrophosphate (PRPP) and quinolinic acid (QA, pyridine 2,3-dicarboxylic acid).
123 me animals received unilateral injections of quinolinic acid (QA; 225 nmol) into the ipsilateral stri
124 thletes had significantly elevated levels of quinolinic acid (QUIN) and significantly lower ratios of
129 d chronic intrastriatal dialytic exposure to quinolinic acid (QUIN), malonate, or a combination of QU
131 ted by the neurotoxin and related metabolite quinolinic acid (QUIN), the mitochondrial toxin 3-nitrop
132 ctive metabolites, including the neurotoxin, quinolinic acid (QUIN), the neuroprotective agent, picol
134 ween neurotoxic [3-hydroxykynurenine (3-HK); quinolinic acid (QUIN)] and neuroprotective [kynurenic a
136 mage in the mouse brain by (i) administering quinolinic acid to conditional mutant animals lacking CB
138 mulations and determine the relationships of quinolinic acid to encephalitits and systemic responses.
141 als, the levels of the downstream metabolite quinolinic acid were also greatly decreased in liver and
143 bolites kynurenine, 3-hydroxykynurenine, and quinolinic acid were unchanged in the brain and liver of
144 icity of these associations, blood levels of quinolinic acid were unrelated to striatal and limbic vo
145 3-HK, 3-hydroxyanthranilic acid (3-HAA), and quinolinic acid, which are considered neurotoxic owing t
147 enase in accelerating the local formation of quinolinic acid within the brain tissue, particularly in
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