INT36173

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Context Info
Confidence 0.43
First Reported 1988
Last Reported 2011
Negated 0
Speculated 0
Reported most in Abstract
Documents 17
Total Number 17
Disease Relevance 7.48
Pain Relevance 8.19

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

Anatomy Link Frequency
PGE1 2
tail 1
NG108-15 1
neurons 1
skeletal muscle 1
Gs (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 55 100.00 Very High Very High Very High
Osteoarthritis 12 100.00 Very High Very High Very High
Paracetamol 10 100.00 Very High Very High Very High
cINOD 8 100.00 Very High Very High Very High
Opioid 21 99.80 Very High Very High Very High
anesthesia 1 99.44 Very High Very High Very High
IPN 9 99.30 Very High Very High Very High
orphanin 4 99.24 Very High Very High Very High
nociceptor 4 98.96 Very High Very High Very High
5HT 2 98.76 Very High Very High Very High
Disease Link Frequency Relevance Heat
Osteoarthritis 10 100.00 Very High Very High Very High
Disease 4 100.00 Very High Very High Very High
Nociception 20 99.82 Very High Very High Very High
Diabetes Mellitus 23 99.62 Very High Very High Very High
Aggression 2 99.36 Very High Very High Very High
Weight Loss 12 99.34 Very High Very High Very High
Hepatotoxicity 2 98.68 Very High Very High Very High
Vibrio Infection 4 98.64 Very High Very High Very High
Ganglion Cysts 35 98.44 Very High Very High Very High
Adverse Drug Reaction 4 97.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The present study confirms that GS is a selective drug for osteoarthritis, as effective on the symptoms of the disease as NSAIDs but significantly better tolerated.
Positive_regulation (tolerated) of GS associated with cinod, disease and osteoarthritis
1) Confidence 0.43 Published 1998 Journal Arzneimittelforschung Section Abstract Doc Link 9638313 Disease Relevance 0.89 Pain Relevance 0.69
The present study confirms that GS is a selective drug for osteoarthritis, as effective on the symptoms of the disease as NSAIDs but significantly better tolerated.
Positive_regulation (effective) of GS associated with cinod, disease and osteoarthritis
2) Confidence 0.43 Published 1998 Journal Arzneimittelforschung Section Abstract Doc Link 9638313 Disease Relevance 0.89 Pain Relevance 0.69
Nocistatin and prepro-nociceptin/orphanin FQ 160-187 cause nociception through activation of Gi/o in capsaicin-sensitive and of Gs in capsaicin-insensitive nociceptors, respectively.
Positive_regulation (activation) of Gs in nociceptors associated with nociception, qutenza, nociceptor and orphanin
3) Confidence 0.25 Published 2003 Journal J. Pharmacol. Exp. Ther. Section Title Doc Link 12665541 Disease Relevance 0.50 Pain Relevance 1.03
As expected, fasted and glucose-induced activation of hepatic GS is also comparable between MCL Cre + and MLC Cre – mice (Figure 3C).
Positive_regulation (activation) of GS
4) Confidence 0.20 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3017066 Disease Relevance 0.18 Pain Relevance 0.09
Deprivation of GS by peridural anesthesia disturbs maternal behaviour in parturient ewes, especially in primiparae.
Positive_regulation (Deprivation) of GS associated with anesthesia
5) Confidence 0.20 Published 1988 Journal Psychoneuroendocrinology Section Abstract Doc Link 3287420 Disease Relevance 0.23 Pain Relevance 0.10
Substitution of the carboxyl-terminal tail of the prostacyclin receptor with the corresponding region of the mDP receptor (IPN-VII/DPC) produced a receptor with increased coupling to both Gs and Gq.
Positive_regulation (increased) of Gs in tail associated with ipn
6) Confidence 0.16 Published 2003 Journal J. Recept. Signal Transduct. Res. Section Abstract Doc Link 12680591 Disease Relevance 0 Pain Relevance 0.57
This property might explain the dose-dependent effects of PGI2 on capsaicin-activated currents: PKC-dependent sensitization of TRPV1 occurs downstream of Gq-coupled IP receptor activation at high concentrations (1000 nM) of PGI2 (1.5 min) while long (6.5 min) treatment with low concentrations (100 nM) of PGI2 causes potentiation of TRPV1 activity through Gs activation.
Positive_regulation (activation) of Gs associated with qutenza
7) Confidence 0.15 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0.07 Pain Relevance 0.38
Adenylyl cyclase supersensitivity in opioid-withdrawn NG108-15 hybrid cells requires Gs but is not mediated by the Gsalpha subunit.
Positive_regulation (requires) of Gs in NG108-15 associated with narcan and opioid
8) Confidence 0.12 Published 1998 Journal J. Pharmacol. Exp. Ther. Section Title Doc Link 9694942 Disease Relevance 0.48 Pain Relevance 0.79
It will be interesting to compare Gs-mediated signaling from the RASSLs based on the 5HT-4 receptor and the MC4R for receptor-specific differences in Gs protein activation in the same cell types in vivo.
Positive_regulation (activation) of Gs associated with 5ht
9) Confidence 0.09 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1930153 Disease Relevance 0 Pain Relevance 0.13
These studies suggest that the excitatory opioid supersensitivity of GM1-treated DRG neurons is due primarily to increased efficacy of excitatory opioid-receptor activation of Gs.
Positive_regulation (activation) of Gs in neurons associated with ganglion cysts and opioid
10) Confidence 0.05 Published 1998 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 9668346 Disease Relevance 0.68 Pain Relevance 1.02
Evaluation of the functional interaction between PGE1 receptors and Gs by means of receptor-stimulated, cholera toxin-catalyzed ADP-ribosylation of Gs alpha revealed a significant increase in the ability of PGE1 receptors to activate Gs alpha (3.3-fold increase in EC50; p < 0.05) in cells chronically exposed to morphine.
Positive_regulation (increase) of Gs in PGE1 associated with vibrio infection and morphine
11) Confidence 0.05 Published 1995 Journal J. Neurochem. Section Abstract Doc Link 7760024 Disease Relevance 0.46 Pain Relevance 0.79
Evaluation of the functional interaction between PGE1 receptors and Gs by means of receptor-stimulated, cholera toxin-catalyzed ADP-ribosylation of Gs alpha revealed a significant increase in the ability of PGE1 receptors to activate Gs alpha (3.3-fold increase in EC50; p < 0.05) in cells chronically exposed to morphine.
Positive_regulation (Evaluation) of Gs in PGE1 associated with vibrio infection and morphine
12) Confidence 0.05 Published 1995 Journal J. Neurochem. Section Abstract Doc Link 7760024 Disease Relevance 0.49 Pain Relevance 0.73
Total skeletal muscle glycogen synthase (GS) activity increased by 31% in the F group (P < .01) and by 17% in the P group (nonsignificant) after 6 months of treatment, but was still less than the activity in normal-weight controls (aged 28.0 +/- 6.3 years; body mass index, 23.5 +/- 2.2).
Positive_regulation (increased) of GS in skeletal muscle associated with obesity
13) Confidence 0.05 Published 1995 Journal Metab. Clin. Exp. Section Abstract Doc Link 8786726 Disease Relevance 1.22 Pain Relevance 0.20
We found that this configuration increases the potential field focality (see GS plots and maps in Figure 8), and that the stimulation focality improved as the surface conductance gGS of the ground surface increased, the best focality being obtained in the limit case of an infinitely conductive ground/electrolyte interface (modeled with a homogeneous Dirichlet condition).
Positive_regulation (conductance) of gGS
14) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2652101 Disease Relevance 0 Pain Relevance 0
After adjustment for fasting glucose, insulin, weight loss, and diabetic state, a positive effect of F remained on the total GS activity, which accounted for 27% of the variation (P < .05).
Positive_regulation (effect) of GS associated with weight loss and diabetes mellitus
15) Confidence 0.03 Published 1995 Journal Metab. Clin. Exp. Section Abstract Doc Link 8786726 Disease Relevance 1.14 Pain Relevance 0.10
CONCLUSION: The difference in opiate-induced functional adaptive alteration of Gs is at least one biochemical mechanism of developing opiate tolerance and dependence.


Positive_regulation (opiate-induced) of Gs
16) Confidence 0.03 Published 1999 Journal Zhongguo Yao Li Xue Bao Section Body Doc Link 10678140 Disease Relevance 0 Pain Relevance 0
These results indicate that: BT is a potent inducer of P450s and phase II metabolizing enzymes; and the increase of AA-GS conjugate and aggravation of AA hepatotoxicity by BT may be related to induction of P450s.
Positive_regulation (increase) of AA-GS associated with paracetamol and hepatotoxicity
17) Confidence 0.01 Published 2000 Journal J Appl Toxicol Section Abstract Doc Link 11180262 Disease Relevance 0.24 Pain Relevance 0.89

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