ライフサイエンスコーパス: 5-HIAA

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

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

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

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

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

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

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

8 5-HT metabolite 5-hydroxyindole acetic acid (5-HIAA).

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

10 5-HT metabolite, 5-hydroxyindolacetic acid (5-HIAA) but is more than 100 times lower in concentratio

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

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

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

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

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

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

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

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

19 5-HT metabolite 5-hydroxyindoleacetic acid (5-HIAA) in several regions including the prefrontal cort

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

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

22 5-hydroxyindoleacetic acid (5-HIAA), a biomarker of pharmacodynamic activity, was me

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 379268, mPFC tissue levels of DOPAC, HVA and 5-HIAA were increased in a dose-dependent manner.

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

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

58 -1-induced increases of MHPG, tryptophan and 5-HIAA in hypothalamus and brain stem were not significa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 0-fold) in PEA brain level and a decrease in 5-HIAA by more than 90% were observed after administrati

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

109 0 flow injection experiments or after 2 h in 5-HIAA for PEI-CNT electrodes.

110 25 percent (odds ratio for each increase in 5-HIAA of 25 mg per 24 hours, 1.08 [95 percent confidenc

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

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

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

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

115 5-HT degradation assessed by 5-HIAA levels, 5-HIAA:5-HT ratio, or both.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 5-HIAA (98.8 vs. 256 mg/24 h), posttreatment 5-HIAA (50.3 vs. 324 mg/24 h) and posttreatment 5-HIAA t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 302.0 pmol/ml) compared to dogs that warned (5-HIAA 244.0 pmol/ml; HVA 400.0 pmol/ml).

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