ライフサイエンスコーパス: 5-HIAA

1 5-HIAA levels were measured in urine spot sample of ever

2 5-HIAA were significantly higher in septic shock patient

3 formation of 5-hydroxyindole-3-acetic acid (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) from

4 metabolites, 5-hydroxyindole-3-acetic acid (5-HIAA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in is

5 acetic acid and 5-hydroxyindole acetic acid (5-HIAA) in the medial prefrontal cortex (PFC), nucleus a

6 its metabolite 5-hydroxyindole acetic acid (5-HIAA) were decreased at 60 min after IBO administratio

7 y tryptamine, 5-hydroxyindole-3-acetic acid (5-HIAA), tryptophane, and 2-phenethylamine (PEA) in rat

8 abolites such as 5-hydoxyindole acetic acid (5-HIAA), which is present in 200-1000 times the concentr

9 its metabolite 5-hydroxyindole acetic acid (5-HIAA).

10 5-HT metabolite 5-hydroxyindole acetic acid (5-HIAA).

11 ion of 5-HT and 5-hydroxyindole acetic acid (5-HIAA).

12 5-HT metabolite, 5-hydroxyindolacetic acid (5-HIAA) but is more than 100 times lower in concentratio

13 major metabolite 5-hydroxyindolacetic acid (5-HIAA), and (2) the ability of the serotonin releasing

14 inal fluid (CSF), 5-hydroxyindolacetic acid (5-HIAA), are strongly associated with suicidal and viole

15 inal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA) and fenfluramine-induced plasma prolactin levels

16 tonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) as a GPR35 ligand.

17 gression and CSF 5-hydroxyindoleacetic acid (5-HIAA) concentration with that between aggression and t

18 eir behavior and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in CSF had been assessed regularl

19 ic acid (HVA) or 5-hydroxyindoleacetic acid (5-HIAA) concentrations in the cerebrospinal fluid 12 mon

20 ntrations of CSF 5-hydroxyindoleacetic acid (5-HIAA) have been consistently associated with suicidal

21 behavior and CSF 5-hydroxyindoleacetic acid (5-HIAA) in newborns was explored.

22 ted the level of 5-hydroxyindoleacetic acid (5-HIAA) in perforated and nonperforated appendicitis pat

23 5-HT metabolite 5-hydroxyindoleacetic acid (5-HIAA) in several regions including the prefrontal cort

24 d its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the PVN.

25 /mL; P<.01), and 5-hydroxyindoleacetic acid (5-HIAA) levels were significantly higher (mean +/- SD, 1

26 ne the impact of 5-hydroxyindoleacetic acid (5-HIAA) on septic shock as a novel biomarker.

27 5-hydroxyindoleacetic acid (5-HIAA), a biomarker of pharmacodynamic activity, was me

28 level of urinary 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin.

29 mmatory mediator 5-hydroxyindoleacetic acid (5-HIAA), a serotonin metabolite.

30 llic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) and

31 rations of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), and kynurenic acid (KA) were measured by HPLC-m

32 , its metabolite 5-hydroxyindoleacetic acid (5-HIAA), and norepinephrine in the raphe nuclei.

33 llic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and serotonin (5-HT) by high performance liquid

34 -HT) metabolite, 5-hydroxyindoleacetic acid (5-HIAA), at the highest dose.

35 onin catabolite, 5-hydroxyindoleacetic acid (5-HIAA), but not that of the norepinephrine catabolite,

36 erotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), dopamine (DA), norepinephrine (NE), and glutami

37 tonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA), fewer 5-HT(1A) autoreceptors and reduced cortic

38 oncentrations of 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), or 3-methoxy-4-hydroxy

39 mary metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in prefrontal cortex and hippocampus of "K"-tre

40 was assayed for 5-hydroxyindoleacetic acid (5-HIAA), norepinephrine, 3-methoxy-4-hydroxyphenylgycol,

41 its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were determined using HPLC.

42 onin, or urinary 5-hydroxyindoleacetic acid (5-HIAA), while topographic localization is by Octreoscan

43 lite interferant 5-hydroxyindoleacetic acid (5-HIAA).

44 tonin metabolite 5-hydroxyindoleacetic acid (5-HIAA).

45 its metabolite, 5-hydroxyindoleacetic acid (5-HIAA); levels of TPH2; and 5-HT(1A) receptor binding.

46 es of serotonin (5-hydroxyindoleacetic acid [5-HIAA]), dopamine (homovanillic acid [HVA]), and norepi

47 icantly decreased plasma 5-HT (P < 0.05) and 5-HIAA (P < 0.0001) concentrations.

48 ased levels of serotonin (5-HT; p<0.05), and 5-HIAA/5-HT ratios (p<0.05) in the raphe; serotonin leve

49 serotonin transporters in the brainstem and 5-HIAA concentrations in CSF.

50 on and decreased mucosal SERT expression and 5-HIAA.

51 Hyperthermia-enhanced 5-HT and 5-HIAA depletion resulting from D-Fen exposure was depen

52 ough hyperthermic rats have greater 5-HT and 5-HIAA depletions than the hypothermic rats.

53 ficantly and substantially depleted 5-HT and 5-HIAA in all brain regions examined.

54 ficantly and substantially depleted 5-HT and 5-HIAA in all brain regions examined.

55 T treatment significantly decreased 5-HT and 5-HIAA in certain brain areas, but to a much lesser exte

56 sue levels of dopamine, DOPAC, HVA, 5-HT and 5-HIAA in multiple brain regions.

57 EN-treated rats showed decreases in 5-HT and 5-HIAA in the hippocampus, frontal cortex, somatosensory

58 dicted 5-HIAA levels in the NA, and 5-HT and 5-HIAA levels in the raphe.

59 re positively associated with raphe 5-HT and 5-HIAA levels, and negatively associated with 5-HT level

60 aled significant elevations in NE, 5-HT, and 5-HIAA as compared with the control group injected with

61 so increased tissue levels of DOPAC, HVA and 5-HIAA by 169, 221 and 134% of basal levels in nucleus a

62 he adult, basal levels of DA, DOPAC, HVA and 5-HIAA in n. accumbens did not differ across prenatal tr

63 379268, mPFC tissue levels of DOPAC, HVA and 5-HIAA were increased in a dose-dependent manner.

64 terized by increases in DOPAC, HVA, MHPG and 5-HIAA coupled with decreases in DA, NE and 5-HT.

65 d induced increase in DOPAC/DA, MHPG/NE, and 5-HIAA/5-HT ratio.

66 Important sources of serotonin and 5-HIAA are platelets and mast cells.

67 -1-induced increases of MHPG, tryptophan and 5-HIAA in hypothalamus and brain stem were not significa

68 The authors assayed 5-HIAA in "leftover" CSF from 193 neurologically normal

69 ignificantly lower levels of median baseline 5-HIAA (98.8 vs. 256 mg/24 h), posttreatment 5-HIAA (50.

70 The association between 5-HIAA levels and severity indices was analyzed.

71 ce of excessive 5-HT degradation assessed by 5-HIAA levels, 5-HIAA:5-HT ratio, or both.

72 ring their effects on mitochondria-catalyzed 5-HIAA or DOPAC formation and hamster ethanol intake rev

73 mol/ml; HVA 318.0 pmol/ml) than in controls (5-HIAA 298.0 pmol/ml; HVA 552.0 pmol/ml).

74 CSF 5-HIAA concentrations, however, did not correlate with s

75 CSF 5-HIAA was assayed in a subgroup of subjects.

76 d the association between aggression and CSF 5-HIAA concentrations in a group of 64 patients who had

77 the correlation between cholesterol and CSF 5-HIAA concentrations was not significant.

78 d with both plasma total cholesterol and CSF 5-HIAA concentrations.

79 associations with suicidal behavior and CSF 5-HIAA were found.

80 None of the subjects from the highest CSF 5-HIAA concentration quartile were dead or missing.

81 Changes in CSF 5-HIAA significantly correlated with increases in "activ

82 affects brain neurochemistry, increasing CSF 5-HIAA and decreasing MHPG.

83 Thus, we show that not only low CSF 5-HIAA and a blunted fenfluramine-induced prolactin resp

84 These data seemingly confirm that low CSF 5-HIAA and fenfluramine-induced plasma prolactin reflect

85 died, with 46% of the subjects with low CSF 5-HIAA concentrations dead or presumed dead.

86 ls with greater beta-CIT binding and low CSF 5-HIAA concentrations displayed greater aggressiveness a

87 These findings suggest that low CSF 5-HIAA concentrations quantified early in life is a powe

88 n, and highly rejected infants had lower CSF 5-HIAA and HVA than low-rejection infants.

89 aggressive group had significantly lower CSF 5-HIAA concentrations than the nonaggressive group.

90 captured more than once possessed lower CSF 5-HIAA concentrations, were rated as more aggressive, an

91 e abusive mothers in adulthood had lower CSF 5-HIAA than the abused females who did not.

92 ramine may be more sensitive than lumbar CSF 5-HIAA concentration in detecting a relationship between

93 isorders were compared with their lumbar CSF 5-HIAA concentrations and with their prolactin responses

94 nfluramine challenge but not with lumbar CSF 5-HIAA concentrations in these subjects.

95 Post-mortem CSF 5-HIAA, MHPG and HVA were measured by high-performance l

96 Concentrations of CSF 5-HIAA (P = 0.01) and HVA (P < 0.001) were lower in the

97 covered BN women had increased levels of CSF 5-HIAA compared with control women (117 +/- 33 vs 73 +/-

98 ounters came from the lowest quartile of CSF 5-HIAA concentrations and had been rated as more aggress

99 ects came from the 2 lowest quartiles of CSF 5-HIAA concentrations.

100 uicidal behavior, a low concentration of CSF 5-HIAA is related to aggressive behavior but does not sh

101 violence by decreasing concentrations of CSF 5-HIAA via changes in membrane biophysical properties, h

102 The CSF 5-HIAA concentrations were predictive of which subjects

103 ons had a weak positive correlation with CSF 5-HIAA (r = 0.18, P < 0.01).

104 Cholesterol correlated weakly with CSF 5-HIAA concentrations only in late-onset alcoholics afte

105 AAS significantly decreased 5-HIAA levels in the hypothalamus and increased 5-HT lev

106 hrine (Epi) or monoamine catabolites (DOPAC, 5-HIAA) at any ammonia concentrations tested.

107 e diminution of the voltammetric signals for 5-HIAA as well as other common anionic species.

108 Extracellular hippocampal 5-HIAA also decreased during continuous paroxetine and i

109 he frontal cortex, striatum and hippocampus, 5-HIAA ranged from 0 to 93%, 15 to 72% and 0 to 83% of c

110 Mucosal 5-HT, 5-HIAA, and KA concentrations remained unaltered by ATD.

111 ponents of the 5-HT signalling system (5-HT, 5-HIAA, SERT) and TNF-alpha expression were examined in

112 F monoamine concentrations and ratios of HVA/5-HIAA and HVA/MHPG did not significantly change with 6

113 droxyindole acetic acid:5-hydroxytryptamine (5-HIAA:5-HT) ratio.

114 These findings identify 5-HIAA as a GPR35 ligand and neutrophil chemoattractant

115 significantly greater decreases (26-50%) in 5-HIAA in the frontal cortex, hippocampus and somatosens

116 however, there was no significant change in 5-HIAA concentrations (median difference 0, IQR 0-5; p=0

117 Changes in 5-HIAA levels caused by anabolic androgenic steroids are

118 Despite major declines in 5-HIAA levels during therapy in most patients, CVHD did

119 0-fold) in PEA brain level and a decrease in 5-HIAA by more than 90% were observed after administrati

120 nversion to 5-HIAA, or genetic deficiency in 5-HIAA production by platelets and mast cells resulted i

121 Mice deficient in 5-HIAA show a loss of GPR35-mediated neutrophil recruitm

122 Differences in 5-HIAA were maintained after controlling for breed and a

123 0 flow injection experiments or after 2 h in 5-HIAA for PEI-CNT electrodes.

124 25 percent (odds ratio for each increase in 5-HIAA of 25 mg per 24 hours, 1.08 [95 percent confidenc

125 orrelated with a dose-dependent reduction in 5-HIAA, a marker for TPH inhibition, from baseline until

126 mpus of "K"-treated mice showed reduction in 5-HIAA, indicative of either serotonin uptake transporte

127 multiple times or after bathing the slice in 5-HIAA.

128 t and mast cell-derived mediators, including 5-HIAA, cooperate to promote neutrophil recruitment.

129 erotonin uptake and metabolism may influence 5-HIAA-GPR35 function, and we speculate about broader in

130 suppress hamster ethanol intake also inhibit 5-HIAA and DOPAC formation.

131 at concentrations that significantly inhibit 5-HIAA formation, have little or no effect on mitochondr

132 5-HT degradation assessed by 5-HIAA levels, 5-HIAA:5-HT ratio, or both.

133 DOPAC and HVA, and the major 5-HT metabolite 5-HIAA, in rat medial prefrontal cortex (mPFC).

134 of 5-HT (2.12+/-0.30 ng) and its metabolite 5-HIAA (4.24+/-0.11 ng) in maximally stimulated cultures

135 tissue levels of 5-HT and/or its metabolite 5-HIAA tended to decrease during continuous paroxetine,

136 he concentration of the serotonin metabolite 5-HIAA in the caudomedial mesopallium of the auditory fo

137 ntified: serotonin and serotonin metabolite, 5-HIAA, concentrations in body fluids; serotonin 5-HT(1A

138 studies examining the serotonin metabolite, 5-HIAA, showed no association with depression.

139 s, DOPAC, HVA, and the serotonin metabolite, 5-HIAA, were markedly lower in pups.

140 ions of serotonin (5-HT) and the metabolite, 5-HIAA, in the hypothalamus.

141 predictive value, and diagnostic accuracy of 5-HIAA were investigated.

142 To place the functions of 5-HIAA in context, we summarize the actions of serotonin

143 pression of ethanol intake and inhibition of 5-HIAA (or DOPAC) formation by six structural analogues

144 In contrast, the brain level of 5-HIAA reduced by approximately 53%, but the PEA level w

145 Lower levels of 5-HIAA (P = 0.02) and HVA (P = 0.04) were found in the s

146 Significant increases in levels of 5-HIAA and/or the 5-HIAA/5-HT ratio were found in all ar

147 f conspecific male song had higher levels of 5-HIAA in the caudomedial nidopallium of the auditory fo

148 renatal treatments; however, basal levels of 5-HIAA in this region were significantly elevated in pre

149 relief was associated with reduced levels of 5-HIAA in urine samples.

150 Levels of 5-HIAA were significantly lower in the infants with fami

151 out liver metastases, had elevated levels of 5-HIAA without any evidence of carcinoid syndrome.

152 th carcinoid syndrome had elevated levels of 5-HIAA, but the absolute levels did not correlate with t

153 thout significant effect on tissue levels of 5-HIAA.

154 gic activation, as indicated by the ratio of 5-HIAA to 5-HT.

155 e correlation-the stronger the inhibition on 5-HIAA or DOPAC formation, the greater the ethanol intak

156 did not alter basal levels of brain 5-HT or 5-HIAA in any brain region examined.

157 DOPAC levels but did not alter HVA, 5-HT, or 5-HIAA.

158 less, these patients had higher urinary peak 5-HIAA levels (median, 265 mg per 24 hours [interquartil

159 Plasma 5-HIAA levels and disease severity indices were obtained

160 IAA (50.3 vs. 324 mg/24 h) and posttreatment 5-HIAA time integral (37.3 vs. 192 g/24 h* days) in grou

161 5-HIAA (98.8 vs. 256 mg/24 h), posttreatment 5-HIAA (50.3 vs. 324 mg/24 h) and posttreatment 5-HIAA t

162 However, only posttreatment 5-HIAA levels independently predicted the development or

163 nical markers showed that only posttreatment 5-HIAA levels independently predicted the development or

164 left- and right-hemisphere lesions predicted 5-HIAA levels in the NA, and 5-HT and 5-HIAA levels in t

165 a role for platelet- and mast cell-produced 5-HIAA in cell recruitment to the sites of inflammation

166 Serotonin turnover (ratio 5-HIAA/5-HT) was reduced in exposed females and males af

167 A, HVA/DA) and the serotonin turnover ratio (5-HIAA/5-HT) were significantly elevated in the ventral

168 hile PAR increased NE in the PFC and reduced 5-HIAA in all three structures.

169 so increases intracellular 5-HTP and reduces 5-HIAA.

170 ales had significantly greater telencephalic 5-HIAA, and serotonergic activation, as indicated by the

171 bolism by regulating AMX-2 function and that 5-HIAA may function in the SER-1 signaling pathway.

172 The results indicated that 5-HIAA and PEA were susceptible and effective biomarkers

173 Additional studies reveal that 5-HIAA functions to inhibit egg laying in a manner depen

174 The 5-HIAA concentrations had a wider range than the 5-HT co

175 The difference in the 5-HIAA concentration between the acute appendicitis grou

176 There were also significant increases in the 5-HIAA/5-HT and DOPAC/DA ratios, often used as measures

177 To impede access of the 5-HIAA to the electrode surface, a thin layer of Nafion,

178 ant increases in levels of 5-HIAA and/or the 5-HIAA/5-HT ratio were found in all areas examined inclu

179 This study shows that the 5-HIAA concentration in patients with perforated appendi

180 Thus, the 5-HIAA-GPR35 axis is an eosinophil chemoattractant recep

181 of PEA escalated to about 6-fold, while the 5-HIAA level remained unchanged following a dose of the

182 ogical inhibition of serotonin conversion to 5-HIAA, or genetic deficiency in 5-HIAA production by pl

183 scuss distinct response profiles of GPR35 to 5-HIAA compared to other ligands.

184 n analysis showed that a higher peak urinary 5-HIAA level and previous chemotherapy were predictors o

185 phy, correlating these features with urinary 5-HIAA levels and clinical data collected during therapy

186 ower in the aggressive group (median values: 5-HIAA 202.0 pmol/ml; HVA 318.0 pmol/ml) than in control

187 Mast cells also attract GPR35(+) cells via 5-HIAA.

188 302.0 pmol/ml) compared to dogs that warned (5-HIAA 244.0 pmol/ml; HVA 400.0 pmol/ml).

189 gs with a history of biting without warning (5-HIAA 196.0 pmol/ml; HVA 302.0 pmol/ml) compared to dog