INT27803

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Context Info
Confidence 0.38
First Reported 1989
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 16
Total Number 17
Disease Relevance 5.94
Pain Relevance 4.64

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
skin 2
cholinergic neurons 1
forearm 1
neurons 1
serotonergic neurons 1
ACOT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Serotonin 48 100.00 Very High Very High Very High
narcan 2 100.00 Very High Very High Very High
bradykinin 57 99.92 Very High Very High Very High
algil 3 99.86 Very High Very High Very High
5HT 50 99.76 Very High Very High Very High
imagery 12 99.36 Very High Very High Very High
qutenza 4 99.28 Very High Very High Very High
acular 6 98.96 Very High Very High Very High
antagonist 8 98.60 Very High Very High Very High
Morphine 3 98.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nicotine Addiction 106 99.86 Very High Very High Very High
Dilated Cardiomyopathy 40 99.48 Very High Very High Very High
Increased Venous Pressure Under Development 88 99.46 Very High Very High Very High
Sleep Disorders 105 99.34 Very High Very High Very High
Diabetes Mellitus 71 98.68 Very High Very High Very High
Hypersensitivity 150 97.36 Very High Very High Very High
Atherosclerotic Plaque 2 92.80 High High
INFLAMMATION 6 89.80 High High
Stroke 5 86.80 High High
Pruritus 5 84.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In older smokers, both ACh and SNP responses were significantly attenuated in comparison with nonsmokers.
Regulation (responses) of ACh associated with nicotine addiction
1) Confidence 0.38 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2515430 Disease Relevance 0.53 Pain Relevance 0.10
A comparison of dynamic changes in NO in response to ACh between the DCM and the control groups is shown in FigureĀ 5.
Regulation (response) of ACh associated with dilated cardiomyopathy
2) Confidence 0.29 Published 2010 Journal European Heart Journal Section Body Doc Link PMC2995954 Disease Relevance 0.44 Pain Relevance 0
In the present study we have focused on the functional aspects of the human peripheral microcirculation and studied the responses to ACh, SNP, and local heating in the forearm skin.
Regulation (responses) of ACh in skin
3) Confidence 0.28 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2515430 Disease Relevance 0.98 Pain Relevance 0.04
Fifty per cent inhibition of output occurred in the presence of concentrations of greater than or equal to 300 mumol/l (morphine and ethylketocyclazocine) and 338 (317, 353; 95 per cent c.l., n = 6) mumol/l (pethidine). (3) ACh output was inhibited by infusion of 100 mumol/l naloxone or 10 mumol/l naltrexone, but was not affected by lower concentrations of either antagonist. (4) These results suggest that the therapeutic concentrations of morphine and pethidine likely to occur in vivo would not affect placental ACh output into fetal vessels.
Regulation (affected) of ACh in vessels associated with antagonist, narcan, algil and morphine
4) Confidence 0.24 Published 1989 Journal Placenta Section Abstract Doc Link 2674931 Disease Relevance 0 Pain Relevance 1.08
It had little effect on tissue levels of ACh, nitric oxide, and histamine assayed in dermal dialysate collected from malathion-exposed and control-treated skin.
Neg (little) Regulation (effect) of ACh in skin
5) Confidence 0.23 Published 2004 Journal J. Appl. Physiol. Section Abstract Doc Link 15333628 Disease Relevance 0 Pain Relevance 0.05
The effects of the intra-arterial infusions of the endothelium-dependent vasodilators ACh, BK, 5HT and the nitric oxide donor SNP on forearm blood flow are shown in Table 1 and Figure 1.
Regulation (effects) of ACh in forearm associated with 5ht and bradykinin
6) Confidence 0.15 Published 2005 Journal Vascular Health and Risk Management Section Body Doc Link PMC1993953 Disease Relevance 0 Pain Relevance 0.27
The effects of ACh, BK, and 5HT were significantly attenuated by the concomitant infusion of the selective ?
Regulation (effects) of ACh associated with 5ht and bradykinin
7) Confidence 0.15 Published 2005 Journal Vascular Health and Risk Management Section Body Doc Link PMC1993953 Disease Relevance 0.14 Pain Relevance 0.44
The results showed that both Keto and L-NAME each attenuated the vasodilation induced by exogenous ACh (ACh control = 79 +/- 4% maximal CVC, Keto = 55 +/- 7% maximal CVC, L-NAME = 46 +/- 6% maximal CVC; P < 0.05, ACh vs.
Regulation (control) of ACh associated with acular and increased venous pressure under development
8) Confidence 0.14 Published 2005 Journal J. Appl. Physiol. Section Abstract Doc Link 15649880 Disease Relevance 0.33 Pain Relevance 0.53
We made similar observations in the present investigation, as both the Ach and SNP responses were blunted in the presence of NIDDM.
Regulation (responses) of Ach associated with diabetes mellitus
9) Confidence 0.08 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2663449 Disease Relevance 0.59 Pain Relevance 0.09
In mammals, two cholinesterases exist: AChE, which selectively hydrolyzes ACh, and butyrylcholinesterase, which hydrolyzes other choline esters in addition to ACh.
Regulation (hydrolyzes) of ACh
10) Confidence 0.08 Published 2007 Journal Current Genomics Section Body Doc Link PMC2647161 Disease Relevance 0.40 Pain Relevance 0.03
CMi(His+) units were most responsive to histamine and to PGE(2) and less to serotonin, ACh, bradykinin, and capsaicin.
Regulation (responsive) of ACh associated with qutenza, bradykinin and serotonin
11) Confidence 0.07 Published 2003 Journal J. Neurophysiol. Section Abstract Doc Link 12611975 Disease Relevance 0.71 Pain Relevance 1.19
The effects of SD on N1 and P300 could thus be an effect of reduced cortical ACh levels caused by inhibition of the cholinergic neurons by AD.
Regulation (effect) of ACh in cholinergic neurons associated with adenocard and sleep disorders
12) Confidence 0.06 Published 2007 Journal Cell Mol Life Sci Section Body Doc Link PMC2778638 Disease Relevance 0.22 Pain Relevance 0.15
It is plausible that different levels of 5-HT differentially activate SER-4 in different neurons to modulate ACh neurotransmission.
Regulation (modulate) of ACh in neurons
13) Confidence 0.00 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2860991 Disease Relevance 0.12 Pain Relevance 0.06
To understand how serotonergic neurons regulate ACh neurotransmission, we analyzed the role of 5-HT signal from specific neurons.
Regulation (regulate) of ACh in serotonergic neurons
14) Confidence 0.00 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2860991 Disease Relevance 0.22 Pain Relevance 0.07
q, EGL-8 phospholipase C and SLO-1 BK channel signaling to modulate ACh neurotransmission and that either reduced or excessive EAT-6 function may lead to increased ACh neurotransmission.
Regulation (modulate) of ACh
15) Confidence 0.00 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2860991 Disease Relevance 0.38 Pain Relevance 0.24
To identify receptors responsible for modulation of ACh neurotransmission by exogenous 5-HT, we analyzed available deletion mutants of these genes by the aldicarb assay.
Regulation (modulation) of ACh
16) Confidence 0.00 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2860991 Disease Relevance 0.27 Pain Relevance 0.04
Although the mechanism by which Na+,K+-ATPase regulates the abundance of synaptic vesicles is unclear, our genetic analyses shed some light on a possible role of EAT-6 in regulation of ACh neurotransmission.
Spec (possible) Regulation (regulation) of ACh in synaptic vesicles
17) Confidence 0.00 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2860991 Disease Relevance 0.53 Pain Relevance 0.26

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