INT21846

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Context Info
Confidence 0.78
First Reported 1985
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 27
Total Number 29
Disease Relevance 5.14
Pain Relevance 9.22

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytoskeleton (Spna1) molecular_function (Spna1) cytoplasm (Spna1)
Anatomy Link Frequency
hypothalamus 3
neuronal 3
neurons 3
brain 2
T cells 2
Spna1 (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 35 100.00 Very High Very High Very High
Glutamate 4 100.00 Very High Very High Very High
gABA 39 99.98 Very High Very High Very High
opiate 4 99.88 Very High Very High Very High
Morphine 31 99.82 Very High Very High Very High
Spinal cord 17 99.76 Very High Very High Very High
opioid receptor 1 99.54 Very High Very High Very High
Antinociceptive 3 99.46 Very High Very High Very High
Opioid 12 98.62 Very High Very High Very High
tetrodotoxin 13 98.22 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 4 99.44 Very High Very High Very High
Cancer 404 98.88 Very High Very High Very High
Disease 110 98.48 Very High Very High Very High
Increased Venous Pressure Under Development 9 98.08 Very High Very High Very High
Influenza Virus Infection 246 96.80 Very High Very High Very High
Sprains And Strains 85 96.08 Very High Very High Very High
Death 19 95.88 Very High Very High Very High
Pox Virus Infection 46 94.24 High High
Immunization 104 90.12 High High
Amyloid Plaque 2 86.72 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Insulin release from the SPH-IPNs exhibited sensitivity towards pH and ionic strength.
Localization (release) of SPH
1) Confidence 0.78 Published 2008 Journal Int J Pharm Section Abstract Doc Link 17976932 Disease Relevance 0 Pain Relevance 0.07
The possibility that the release of HA from the mouse hypothalamus is regulated by glucose concentration and that activation of neuronal Na+ channels is involved in the enhancement of the HA release by low glucose concentrations warrants further attention.
Localization (release) of HA in neuronal
2) Confidence 0.71 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0.09
The rate of the HA release was dependent on the absolute concentration of glucose and not on an abrupt change in the concentration.
Localization (release) of HA
3) Confidence 0.71 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0.07
When slices of the hypothalamus were incubated in high K+ medium, a temperature- and Ca2+-dependent HA release was observed.
Localization (release) of HA in hypothalamus
4) Confidence 0.71 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0.09
The possibility that the release of HA from the mouse hypothalamus is regulated by glucose concentration and that activation of neuronal Na+ channels is involved in the enhancement of the HA release by low glucose concentrations warrants further attention.
Localization (release) of HA in neuronal
5) Confidence 0.70 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0.09
At low concentrations of glucose, the K+ (20 mM)-induced HA release from the hypothalamic slices was also enhanced.
Localization (release) of HA
6) Confidence 0.70 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0.10
The effect of glucose concentration on the in vitro release of histamine (HA) was examined, using two different preparations of the mouse hypothalamus.
Localization (release) of HA in hypothalamus
7) Confidence 0.62 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0
Tetrodotoxin (10 microM) inhibited the enhancing effect of a low glucose concentration (2 mM) on the HA release by 60%, in both preparations of the hypothalamus.
Localization (release) of HA in hypothalamus associated with tetrodotoxin
8) Confidence 0.62 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0.10
The HA and tele-methylhistamine released from whole blocks of the hypothalamus into the medium linearly increased during 2-h incubation in normal Krebs-Ringer bicarbonate solution in the absence of external depolarizing stimuli.
Localization (released) of HA in external
9) Confidence 0.62 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0
The release of HA from this preparation depended on the temperature and Ca2+ in the medium and was progressively increased with decrease in the glucose concentration from 11.5 to 1 mM.
Localization (release) of HA
10) Confidence 0.62 Published 1986 Journal J. Neurochem. Section Abstract Doc Link 2430060 Disease Relevance 0 Pain Relevance 0.06
These results suggest that the acute morphine treatment increases the turnover of neuronal HA via opioid receptors, and this opiate also releases HA from a slowly turning over pool(s).
Localization (releases) of HA in neuronal associated with opiate, opioid receptor and morphine
11) Confidence 0.54 Published 1985 Journal J. Neurochem. Section Abstract Doc Link 4031857 Disease Relevance 0 Pain Relevance 0.81
HA is also known as an NMDA (N-methyl-D-glutamate) receptor agonist [2] and is released under mental stress from astrocytes by the activation of ?
Localization (released) of HA in astrocytes associated with stress, glutamate and agonist
12) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808336 Disease Relevance 1.12 Pain Relevance 0.10
The enhancement of HA release induced by DAGO (10(-6) M) was blocked completely by naloxone (10(-6) M) but not by tetrodotoxin (10(-6) M).
Localization (release) of HA associated with tetrodotoxin and narcan
13) Confidence 0.29 Published 1988 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2855235 Disease Relevance 0 Pain Relevance 0.80
DAGO (10(-7) and 10(-6) M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release.
Localization (release) of HA
14) Confidence 0.29 Published 1988 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2855235 Disease Relevance 0 Pain Relevance 0.80
DAGO (10(-7) and 10(-6) M) significantly increased the K+ (30 mM)-evoked HA release from mouse cerebral cortical slices without influencing on the spontaneous HA release.
Localization (release) of HA
15) Confidence 0.29 Published 1988 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2855235 Disease Relevance 0 Pain Relevance 0.80
These results suggest that opioids with mu agonist activity increase brain HA turnover by facilitating HA release from nerve endings.
Localization (release) of HA in nerve associated with agonist and opioid
16) Confidence 0.26 Published 1988 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2855235 Disease Relevance 0 Pain Relevance 0.68
These results suggest that in DBA mice, antinociceptive doses of morphine inhibit HA release in brain, and promote the release of HA from spinal cord.
Localization (release) of HA in brain associated with antinociceptive, spinal cord and morphine
17) Confidence 0.24 Published 1990 Journal Brain Res. Section Abstract Doc Link 2207651 Disease Relevance 0.14 Pain Relevance 1.32
These results suggest that in DBA mice, antinociceptive doses of morphine inhibit HA release in brain, and promote the release of HA from spinal cord.
Localization (release) of HA in brain associated with antinociceptive, spinal cord and morphine
18) Confidence 0.24 Published 1990 Journal Brain Res. Section Abstract Doc Link 2207651 Disease Relevance 0.14 Pain Relevance 1.32
The effects of morphine on the levels of histamine (HA), its metabolite tele-methylhistamine (t-MH) and on t-MH synthesis rates (thought to be indicative of neuronal HA release) were investigated in brain regions and spinal cords of DBA/2J (DBA) and C57/BL6 (C57) mice, two strains known to differ in their sensitivity to morphine.
Localization (release) of HA in spinal cords associated with sprains and strains and morphine
19) Confidence 0.24 Published 1990 Journal Brain Res. Section Abstract Doc Link 2207651 Disease Relevance 0.18 Pain Relevance 0.67
secreting splenocytes specific to the HA peptide pool were observed in the immunized animals as compared to control mice.
Localization (secreting) of HA peptide
20) Confidence 0.23 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2646145 Disease Relevance 0.22 Pain Relevance 0.07

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