戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1  by TNFalpha, gp120, and necrosis induced by quinolinic acid.
2 otic destruction produced in rat striatum by quinolinic acid.
3  destined to die following administration of quinolinic acid.
4 radation toward the production of neurotoxic quinolinic acid.
5  administration of the NMDA receptor agonist quinolinic acid.
6 tivity promotes the production of neurotoxic quinolinic acid.
7 e associated with increased plasma levels of quinolinic acid.
8 n, probably as a consequence of formation of quinolinic acid.
9 way that ultimately degrades kynurenine into quinolinic acid.
10 DO and generates the neuroactive metabolite, quinolinic acid.
11 hanced ability to modify the accumulation of quinolinic acid.
12 eiving striatal injections of the neurotoxin quinolinic acid.
13 associated with CSF KYN, kynurenic acid, and quinolinic acid.
14 tive cells in cultures after incubation with quinolinic acid.
15 ytes, occurred during longer incubation with quinolinic acid.
16 location were measured after the infusion of quinolinic acid (120 nmol) into rat striatum.
17 way (tryptophan, kynurenine, kynurenic acid, quinolinic acid, 3-hydroxykynurenine, and their associat
18 te and dihydroxyacetone phosphate, affording quinolinic acid, a central intermediate in the biosynthe
19 ing inorganic phosphate, 2 mol of water, and quinolinic acid, a central intermediate in the biosynthe
20                                              Quinolinic acid, a macrophage/microglia-derived excitoto
21 r an intrastriatal injection of low doses of quinolinic acid, a N-methyl-D-aspartate receptor agonist
22       This study investigated the sources of quinolinic acid, a neurotoxic tryptophan-kynurenine path
23  brain macrophages and microglia can release quinolinic acid, a neurotoxin and NMDA (N-methyl-D-aspar
24                           Here, we show that quinolinic acid accumulated in human gliomas and was ass
25 ults are consistent with the hypothesis that quinolinic acid accumulation in brain tissue contributes
26  used to examine the mechanisms of increased quinolinic acid accumulations and determine the relation
27                                        Since quinolinic acid acts as a potent excitotoxin, the early
28                                           As quinolinic acid acts as an N-methyl-D-aspartate (NMDA) r
29  AP-1, whose binding peaked about 6 hr after quinolinic acid administration, and E2F-1, which was onl
30  death induced by intrastriatal injection of quinolinic acid, an N-methyl-D-aspartate glutamate recep
31 on resulting from intrastriatal injection of quinolinic acid, an NMDA receptor agonist, and kainic ac
32                                Although both quinolinic acid and 3-nitropropionic acid destroy medium
33 h are activated by the tryptophan metabolite quinolinic acid and blocked by kynurenic acid.
34           Our study results revealed highest quinolinic acid and highest BTP- levels in the subsample
35 d to neurotoxicity through the generation of quinolinic acid and immunosuppression and can alter brai
36 OD-1 activity significantly protects against quinolinic acid and kainic acid neurotoxicity in the mou
37 m is activated, leading to the production of quinolinic acid and kynurenic acid which can modulate N-
38 with neurotoxicity through the generation of quinolinic acid and other toxins.
39 cluding the neurotoxic NMDA receptor agonist quinolinic acid and the neuroprotective NMDA receptor an
40 ) to Cu(I) and Fe(II), respectively, whereas quinolinic acid and the nonphenolic kynurenine catabolit
41 f tryptophan metabolism includes an agonist (quinolinic acid) and an antagonist (kynurenic acid) at t
42 KP metabolites (kynurenine and kynurenic and quinolinic acids), and cytokines (SI markers) were measu
43 ed by increased kynurenine/tryptophan ratio, quinolinic acid, and 3-hydroxykynurenine in both the dis
44 of neurotoxins (tumor necrosis factor-alpha, quinolinic acid, and nitric oxide) in plasma and CSF wer
45                                        Thus, quinolinic acid arising from macrophages and microglia d
46 ) metabolism by exploiting microglia-derived quinolinic acid as an alternative source of replenishing
47 duct profiling and affects the production of quinolinic acid at a junction of the metabolic pathway.
48    Small excitotoxin lesions were made using quinolinic acid at bilateral sites within the dorsolater
49 brains of 2-day-old rats were incubated with quinolinic acid at concentrations known to kill neurons.
50 replication is a significant driver of local quinolinic acid biosynthesis.
51                                Increased CSF quinolinic acid concentration on admission in children w
52                                          CSF quinolinic acid concentration progressively increased af
53                                              Quinolinic acid concentration was measured by gas chroma
54                                          CSF quinolinic acid concentration was not associated with ag
55                         Although overall CSF quinolinic acid concentration was not associated with sh
56                                Increased CSF quinolinic acid concentrations also correlated with high
57  infant syndrome had increased admission CSF quinolinic acid concentrations compared with children wi
58  of 94 HIV-1-infected patients, elevated CSF quinolinic acid concentrations correlated with worsening
59 d in TBI of all severities and that elevated quinolinic acid concentrations in both the cerebrospinal
60                                    In brain, quinolinic acid concentrations in HIV-infected patients
61        The highest kynurenic, picolinic, and quinolinic acid concentrations were observed in white wi
62                                              Quinolinic acid correlated negatively with composite cog
63 8% p < 0.0001), with a similar age-dependent quinolinic acid elevation (+24% p < 0.001).
64 bsamples with lower or no immune activation (quinolinic acid: F = 21.027, p < 0.001 [ANOVA]; BTP: F =
65 etabolites in both pathways are converted to quinolinic acid for NAD biosynthesis or to acetyl-CoA fo
66 acid phosphoribosyltransferase (QPRT) to use quinolinic acid for NAD(+) synthesis and prevent apoptos
67 -hydroxyanthranilate 3,4-dioxygenase-derived quinolinic acid formed in the final step of the canonica
68                             The synthesis of quinolinic acid from tryptophan is a critical step in th
69 hat significant predictors of BTP levels are quinolinic acid, glomerular filtration rate and age.
70 que with encephalitis showed that almost all quinolinic acid (&gt;98%) was synthesized locally within th
71                   Pathologic accumulation of quinolinic acid has been found in neurodegenerative diso
72  necrosis factor-alpha (TNFalpha), gp120 and quinolinic acid have been implicated as agents for the c
73             Direct measures of the amount of quinolinic acid in brain derived from blood in a macaque
74 in the interferon-gamma-induced synthesis of quinolinic acid in primary cultures of cultured human pe
75 production of neurotoxic kynurenines such as quinolinic acid in TBI of all severities and that elevat
76 ne, kynurenic acid, 3-hydroxy kynurenine and quinolinic acid in the plasma of 19 healthy controls (HC
77  kynurenine pathway, based on high levels of quinolinic acid, in patients with IBD compared with cont
78 vels of tryptophan metabolites-especially of quinolinic acid-indicated a high activity of tryptophan
79 te whether BTP might non-invasively indicate quinolinic acid-induced impaired blood-brain barrier int
80  be a new non-invasive biomarker to indicate quinolinic acid-induced impaired blood-brain barrier int
81                                    Moreover, quinolinic acid-induced internucleosomal DNA fragmentati
82 pared with sham-operated controls, rats with quinolinic acid-induced medial striatal lesions showed a
83 sponses, suppresses ionomycin, glutamate, or quinolinic acid-induced necrotic death of cells includin
84         Excitotoxic cell death stimulated by quinolinic acid injection into the striatum has a long h
85  of kynurenine to the potentially neurotoxic quinolinic acid instead of the neuroprotective kynurenic
86  areas of encephalitis, rather than entry of quinolinic acid into the brain from the meninges or bloo
87 r, monkeys received unilateral injections of quinolinic acid into the previously implanted striatum t
88                                              Quinolinic acid is a common intermediate in the biosynth
89                                              Quinolinic acid is a product of tryptophan degradation a
90 catabolize tryptophan, it is unclear whether quinolinic acid is produced in gliomas and whether it is
91 ncrease in the macrophage-derived neurotoxin quinolinic acid is seen following severe TBI in children
92                              To test whether quinolinic acid is toxic to oligodendrocytes, glial cell
93                        The kynurenic acid-to-quinolinic acid (KA/QA) ratio significantly mediated ass
94                                          The quinolinic acid: kynurenine ratio decreased in aged surg
95                                 In contrast, quinolinic acid lead to a reduction in OCT-1, beginning
96 n of IDO1 pathway metabolites kynurenine and quinolinic acid led to activation of beta-catenin and pr
97                                     Finally, quinolinic acid lesion of striatal projection neurons de
98 ed CPP, rats received bilateral infusions of quinolinic acid (lesion group) or vehicle (sham group) i
99                                              Quinolinic acid lesions decreased the number of NeuN-pos
100    The present study examined the effects of quinolinic acid lesions of the dorsal anterior cingulate
101                                          BLA quinolinic acid lesions significantly disrupted PPI 1 we
102                                          CSF quinolinic acid levels were also elevated in all infecte
103 nificant correlations between elevated serum quinolinic acid levels with those in CSF and brain paren
104                               The neurotoxin quinolinic acid may impair blood-brain barrier integrity
105    These findings raise the possibility that quinolinic acid may play a role in secondary injury afte
106                                              Quinolinic acid might be specifically implicated in the
107 table isotope-labeled precursors tryptophan, quinolinic acid, nicotinic acid, and nicotinamide were a
108 tory behavior were recorded before and after quinolinic acid or radiofrequency (RF) lesions were made
109                                              Quinolinic acid phosphoribosyl transferase (QAPRTase, EC
110                                              Quinolinic acid phosphoribosyltransferase (QAPRTase, EC
111  but not nonneoplastic astrocytes, expressed quinolinic acid phosphoribosyltransferase (QPRT) to use
112                           Because a required quinolinic acid phosphoribosyltransferase (QPRTase) is n
113 , kynurenic acid (Pinteraction = 0.008), and quinolinic acid (Pinteraction = 0.033) with HF and the a
114 tic mechanism in which productive binding of quinolinic acid precedes that of PRPP.
115 ed by microglial cells, as expression of the quinolinic acid-producing enzyme 3-hydroxyanthranilate o
116 anthranilate-3,4-dioxygenase responsible for quinolinic acid production was studied by performing tim
117                           Moreover, rates of quinolinic acid production were reported to be 2.2 micro
118 ical attention or age-related differences in quinolinic acid production.
119  forms nicotinate mononucleotide (NAMN) from quinolinic acid (QA) and 5-phosphoribosyl 1-pyrophosphat
120 tide, carbon dioxide, and pyrophosphate from quinolinic acid (QA) and 5-phosphoribosyl 1-pyrophosphat
121                    Kynurenic acid (KynA) and quinolinic acid (QA) are neuroactive kynurenine pathway
122 o, rats were given the NMDA receptor agonist quinolinic acid (QA) by intrastriatal infusion, and the
123 sic striatal neurons by a local injection of quinolinic acid (QA) dramatically enhances the magnitude
124 tum with either 6-hydroxydopamine (6OHDA) or quinolinic acid (QA) exaggerated their dystonic attacks.
125 th some animals also receiving intrastriatal quinolinic acid (QA) injections to ablate medium spiny n
126                                              Quinolinic acid (QA) is a common intermediate in the bio
127                                              Quinolinic acid (QA) is a metabolite of tryptophan degra
128 cal lesions, by using either the excitotoxin quinolinic acid (QA) or the complex II mitochondria inhi
129 mon architecture for both nicotinic acid and quinolinic acid (QA) phosphoribosyltransferases (PRTase)
130 ng copper deprivation, exhibits increases in quinolinic acid (QA) production and NAD(+) levels.
131 genes of the kynurenine pathway required for quinolinic acid (QA) production from tryptophan are pres
132 eptor agonist N-methyl-D-aspartate (NMDA) or quinolinic acid (QA) were studied.
133 selective detection of endogenous neurotoxin quinolinic acid (QA) whose elevated level in serum is ma
134 nd neurotoxic (3-hydroxykynurenine (3HK) and quinolinic acid (QA)) kynurenine pathway metabolites wer
135                                    Levels of quinolinic acid (QA), a potent NMDA agonist, are elevate
136             Three metabolites were measured: quinolinic acid (QA), an excitotoxin; kynurenic acid (KA
137 her KTR was associated with a 0.46 SD higher quinolinic acid (QA), and 0.31 SD higher 3-hydroxykynure
138 inic acid (NAc) and its metabolic precursor, quinolinic acid (QA), are produced in yields as high as
139   The enzyme NadA catalyzes the synthesis of quinolinic acid (QA), the precursor of the universal nic
140 ydrating enzyme involved in the synthesis of quinolinic acid (QA), the universal precursor of the ess
141 s, kynurenine (KYN), kynurenic acid (KA) and quinolinic acid (QA), were examined in terms of their ef
142 n stem cell transplants into the striatum of quinolinic acid (QA)-lesioned rats.
143 enase (IDO), KYN, kynurenic acid (KynA), and quinolinic acid (QA)-were assessed at baseline (pre-infu
144  days later by an intrastriatal injection of quinolinic acid (QA).
145 astriatal administration of the NMDA agonist quinolinic acid (QA).
146 drial complex II activity or the excitotoxin quinolinic acid (QA).
147 e metabolites were measured: the excitotoxin quinolinic acid (QA); the protective receptor antagonist
148 eived unilateral injection (1 microliter) of quinolinic acid (QA, 40 micrograms in 0.1 M phosphate bu
149 events triggered by intrastriatally injected quinolinic acid (QA, 60 nmol) and kainic acid (KA, 2.5 n
150  5-phosphoribosyl 1-pyrophosphate (PRPP) and quinolinic acid (QA, pyridine 2,3-dicarboxylic acid).
151 me animals received unilateral injections of quinolinic acid (QA; 225 nmol) into the ipsilateral stri
152 thletes had significantly elevated levels of quinolinic acid (QUIN) and significantly lower ratios of
153                                   The use of quinolinic acid (Quin) as an Fe(II) ligand was proposed
154 increase the release of the NMDA excitotoxin quinolinic acid (QUIN) from mononuclear cells.
155  kynurenine, 3-hydroxykynurenine (3-HK), and quinolinic acid (QUIN) in rat brain.
156                                              Quinolinic acid (QUIN) is a product of tryptophan metabo
157  (4-Cl-3-HAA), a suppressor of NMDAR agonist quinolinic acid (QUIN), is a promising potential antidep
158 ctive metabolites in this pathway, including quinolinic acid (QUIN), is upregulated in the placenta d
159 d chronic intrastriatal dialytic exposure to quinolinic acid (QUIN), malonate, or a combination of QU
160            Rat striata were exposed to 15 mM quinolinic acid (QUIN), or QUIN plus the nitric oxide sy
161 ted by the neurotoxin and related metabolite quinolinic acid (QUIN), the mitochondrial toxin 3-nitrop
162 ctive metabolites, including the neurotoxin, quinolinic acid (QUIN), the neuroprotective agent, picol
163 bolites, including kynurenic acid (KYNA) and quinolinic acid (QUIN).
164 tion of the neurotoxic tryptophan metabolite quinolinic acid (QUIN).
165 ween neurotoxic [3-hydroxykynurenine (3-HK); quinolinic acid (QUIN)] and neuroprotective [kynurenic a
166         We have previously reported elevated quinolinic acid (QuinA), a neurotoxic kynurenine pathway
167 n kynurenine pathway (KP) metabolites (e.g., Quinolinic acid; QuinA).
168 evels of picolinic acid (PIC), the kynurenic/quinolinic acid ratio (KYNA/QUIN), and PIC/QUIN were low
169 SZ; kynurenic acid and the kynurenic acid to quinolinic acid ratio are decreased in mood disorders (i
170 renic acid concentrations and kynurenic acid/quinolinic acid ratio than low-risk adolescents.
171 al loss caused by intrastriatal injection of quinolinic acid resulted in a comparable increase.
172 nurenine (SMD = -0.60) and kynurenic acid to quinolinic acid (SMD = -0.37) ratios, than healthy contr
173 (ACMS), can nonenzymatically cyclize to form quinolinic acid, the precursor for de novo biosynthesis
174 (ACMS), can nonenzymatically cyclize to form quinolinic acid, the precursor for de novo biosynthesis
175 sed fmo-2 requires the tryptophan metabolite quinolinic acid to change behavior.
176 mage in the mouse brain by (i) administering quinolinic acid to conditional mutant animals lacking CB
177                                 We have used quinolinic acid to create unilateral excitotoxic lesions
178 mulations and determine the relationships of quinolinic acid to encephalitits and systemic responses.
179 DS produce elevated levels of kynurenine and quinolinic acid, two tryptophan catabolites with potent
180                                              Quinolinic acid was associated with AF (OR: 1.15; 95% CI
181                                 Furthermore, quinolinic acid was elevated in neonatally infected rat
182                                              Quinolinic acid was produced by microglial cells, as exp
183 d identified the phagosome as the site where quinolinic acid was stored and metabolized for de novo n
184 als, the levels of the downstream metabolite quinolinic acid were also greatly decreased in liver and
185 these specimens, whereas chitotriosidase and quinolinic acid were elevated in 2 patients.
186 enine, xanthurenic acid, picolinic acid, and quinolinic acid were identified in the hemolymph of LS b
187 ycle intermediates, aromatic amino acids and quinolinic acid were present in significantly higher con
188 bolites kynurenine, 3-hydroxykynurenine, and quinolinic acid were unchanged in the brain and liver of
189 icity of these associations, blood levels of quinolinic acid were unrelated to striatal and limbic vo
190 , anthranilic acid [AA], picolinic acid, and quinolinic acid) were assessed by ultra-high-performance
191 -kynurenine pathway metabolites (kynurenine, quinolinic acid) were measured.
192  oxide (NO) synthesis, and lowered levels of quinolinic acid which is derived from the immunosuppress
193 3-HK, 3-hydroxyanthranilic acid (3-HAA), and quinolinic acid, which are considered neurotoxic owing t
194                                              Quinolinic acid, which is produced by macrophages and mi
195 enase in accelerating the local formation of quinolinic acid within the brain tissue, particularly in

 
Page Top