INT20720

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Context Info
Confidence 0.35
First Reported 1990
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 7
Disease Relevance 2.66
Pain Relevance 2.25

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

cytosol (ACOT1) lipid metabolic process (ACOT1) cytoplasm (ACOT1)
Anatomy Link Frequency
neuronal 2
nerve 2
motor neurons 2
ACOT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Neurotransmitter 15 100.00 Very High Very High Very High
Morphine 1 99.92 Very High Very High Very High
Clonidine 1 98.88 Very High Very High Very High
tetrodotoxin 2 97.60 Very High Very High Very High
Pain 64 96.64 Very High Very High Very High
agonist 28 94.92 High High
Neuronal excitability 1 94.64 High High
central sensitization 1 88.80 High High
Analgesic 19 86.56 High High
conotoxin 3 86.40 High High
Disease Link Frequency Relevance Heat
Paralysis 27 98.04 Very High Very High Very High
Pain 74 96.64 Very High Very High Very High
Hypersensitivity 60 96.44 Very High Very High Very High
Targeted Disruption 30 93.08 High High
Pulmonary Disease 96 91.52 High High
Neurogenic Inflammation 1 85.88 High High
Increased Venous Pressure Under Development 3 84.72 Quite High
Cancer 1 73.52 Quite High
INFLAMMATION 10 73.40 Quite High
Nociception 5 72.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The two inhibitors of ACh release, morphine (0.3 microM) and clonidine (0.4 microM), antagonized EC(50) AFB(1)-induced contractions, and apamin, a drug that increases neuronal excitability, facilitated the EC(50) AFB(1)-induced contractile effect.
Negative_regulation (inhibitors) of Localization (release) of ACh in neuronal associated with neuronal excitability, clonidine and morphine
1) Confidence 0.35 Published 2002 Journal Toxicol In Vitro Section Abstract Doc Link 12206819 Disease Relevance 0 Pain Relevance 0.34
Both NE and ACh release decreased with the age of the patients.
Negative_regulation (decreased) of Localization (release) of ACh
2) Confidence 0.30 Published 1990 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 2156061 Disease Relevance 0.07 Pain Relevance 0.32
Drugs block M2, increasing Ach release, and thus increasing bronchoconstrictor responses.
Negative_regulation (block) of Localization (release) of Ach
3) Confidence 0.13 Published 2009 Journal The Open Respiratory Medicine Journal Section Body Doc Link PMC2684714 Disease Relevance 0.34 Pain Relevance 0.11
Ipratropium bromide and oxitropium bromide are nonselective blockers; consequently, they block M2 receptors, thereby increasing Ach release at nerve endings, which may reduce the degree of blockade or the duration of action [4].
Negative_regulation (block) of Localization (release) of Ach in nerve
4) Confidence 0.12 Published 2009 Journal The Open Respiratory Medicine Journal Section Body Doc Link PMC2684714 Disease Relevance 0.28 Pain Relevance 0.06
The unc-17(e245) mutant significantly reduces ACh release, and therefore is resistant to aldicarb-induced paralysis [25], [26].
Negative_regulation (reduces) of Localization (release) of ACh associated with paralysis
5) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2860991 Disease Relevance 0.71 Pain Relevance 0
These results suggest that 5-HT signaling inhibits ACh release by the motor neurons [17].
Negative_regulation (inhibits) of Localization (release) of ACh in motor neurons
6) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2860991 Disease Relevance 0.30 Pain Relevance 0.11
Therefore, BTX-A blocks the release of more neurotransmitters than ACh, and has been shown to affect neurotransmission in CNS tracts that are involved in pain transmission or modulation [68].
Negative_regulation (blocks) of Localization (release) of ACh associated with pain and neurotransmitter
7) Confidence 0.01 Published 2007 Journal Trials Section Body Doc Link PMC2151066 Disease Relevance 0.95 Pain Relevance 1.30

General Comments

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