INT142616

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Context Info
Confidence 0.43
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 1.56
Pain Relevance 1.16

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

extracellular space (Igf1) extracellular region (Igf1)
Anatomy Link Frequency
plasma 2
sensory neurons 2
proximal 2
Igf1 (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 6 99.98 Very High Very High Very High
Calcitonin gene-related peptide 11 98.40 Very High Very High Very High
agonist 3 95.56 Very High Very High Very High
Inflammation 6 88.80 High High
ischemia 1 66.64 Quite High
Bioavailability 1 51.92 Quite High
tolerance 17 49.48 Quite Low
long-term potentiation 24 5.00 Very Low Very Low Very Low
GABAergic 16 5.00 Very Low Very Low Very Low
gABA 14 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 6 99.16 Very High Very High Very High
Metabolic Syndrome 11 91.76 High High
INFLAMMATION 6 88.80 High High
Targeted Disruption 12 77.48 Quite High
Disorder Of Lipid Metabolism 15 71.88 Quite High
Non-genital Cutaneous Warts 6 66.88 Quite High
Cv Unclassified Under Development 1 66.64 Quite High
Diabetes Mellitus 19 63.28 Quite High
Insulin Resistance 14 56.36 Quite High
Sprains And Strains 1 49.76 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Stimulation of sensory neurons by capsaicin increases tissue levels of IGF-I, thereby reducing reperfusion-induced apoptosis in mice.
Negative_regulation (reducing) of Positive_regulation (increases) of IGF-I in sensory neurons associated with qutenza and apoptosis
1) Confidence 0.43 Published 2007 Journal Neuropharmacology Section Title Doc Link 17360009 Disease Relevance 0.49 Pain Relevance 0.82
Furthermore, low levels of serum IGF-I were significantly related with the metabolic syndrome according to the World Health Organization.[19] However, our findings are consistent with the animal studies demonstrating low insulin sensitivity in mice with liver specific deletion of the IGF-I gene that is reversed by treatment with recombinant human IGF-I.[34] Raised blood pressure and slightly enhanced plasma insulin concentrations have been reported in mice with a mutant IGF-I allele causing a marked decrease in circulating IGF-I levels.[20]
Negative_regulation (decrease) of Positive_regulation (circulating) of IGF-I in plasma associated with metabolic syndrome
2) Confidence 0.39 Published 2008 Journal International Journal of Diabetes in Developing Countries Section Body Doc Link PMC2772007 Disease Relevance 0.43 Pain Relevance 0.03
We have shown that the IGF-1-mediated increase in VEGF isoforms using the proximal splice site is inhibited by blocking PKC and SRPK1/2, and that this can be overcome by the use of a PKC inhibitor or mimicked by a PKC agonist or overexpression of SRPK1.
Negative_regulation (inhibited) of Positive_regulation (increase) of IGF-1-mediated in proximal associated with agonist
3) Confidence 0.35 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2820781 Disease Relevance 0 Pain Relevance 0.05
Increasing the IGF1/IGFBP5 ratio through exogenous IGF1 prevented the effects of MD, suggesting that reduced IGF1 signalling is a necessary step for eliciting the plastic changes evoked by MD.
Negative_regulation (prevented) of Positive_regulation (Increasing) of IGF1
4) Confidence 0.24 Published 2008 Journal Philosophical Transactions of the Royal Society B: Biological Sciences Section Body Doc Link PMC2674480 Disease Relevance 0.33 Pain Relevance 0.13
Increasing the IGF1/IGFBP5 ratio through exogenous IGF1 prevented the effects of MD, suggesting that reduced IGF1 signalling is a necessary step for eliciting the plastic changes evoked by MD.
Negative_regulation (prevented) of Positive_regulation (Increasing) of IGF1
5) Confidence 0.24 Published 2008 Journal Philosophical Transactions of the Royal Society B: Biological Sciences Section Body Doc Link PMC2674480 Disease Relevance 0.33 Pain Relevance 0.13

General Comments

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