INT97903

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Context Info
Confidence 0.17
First Reported 2001
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 16
Total Number 18
Disease Relevance 5.60
Pain Relevance 4.57

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

cytosol (FGFR1) extracellular region (FGFR1) cytoplasmic membrane-bounded vesicle (FGFR1)
plasma membrane (FGFR1) nucleus (FGFR1) cytoplasm (FGFR1)
Anatomy Link Frequency
neuronal 3
neuroblasts 1
middle cerebral artery 1
lymphocyte 1
skeletal muscle 1
FGFR1 (Homo sapiens)
Pain Link Frequency Relevance Heat
metalloproteinase 8 99.96 Very High Very High Very High
Dismenorea 3 99.88 Very High Very High Very High
opioid receptor 3 98.16 Very High Very High Very High
substance P 1 98.16 Very High Very High Very High
antagonist 33 97.52 Very High Very High Very High
narcan 3 97.08 Very High Very High Very High
adenocard 27 95.96 Very High Very High Very High
agonist 97 95.12 Very High Very High Very High
dorsal root ganglion 4 95.08 Very High Very High Very High
Spinal cord 1 94.76 High High
Disease Link Frequency Relevance Heat
Dysmenorrhea 3 99.88 Very High Very High Very High
Necrosis 10 99.60 Very High Very High Very High
Cancer 14 99.42 Very High Very High Very High
Middle Cerebral Artery Infarction 53 99.30 Very High Very High Very High
Injury 7 99.28 Very High Very High Very High
Death 116 98.96 Very High Very High Very High
Adhesions 3 98.96 Very High Very High Very High
Ganglion Cysts 4 95.08 Very High Very High Very High
Stress 14 95.00 High High
Hepatotoxicity 6 94.00 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This study was designed to evaluate if adenomyosis expresses bFGF and FGF-R, and if present, to compare bFGF and FGF-R expression in adenomyosis and autologous endometrium.
Negative_regulation (compare) of FGF-R in endometrium associated with dismenorea
1) Confidence 0.17 Published 2001 Journal Menopause Section Abstract Doc Link 11528364 Disease Relevance 0.46 Pain Relevance 0.27
GAPDH: glyceraldehyde 3-phosphate dehydrogenase; HBMEC: human brain microvascular endothelial cells; HFN: human foetal neurons; INI1: integrase interactor 1; MCAO: middle cerebral artery occlusion; MMP11: matrix metalloproteinase; OGD: oxygen-glucose deprivation; PAK1: p21-activated kinase 1.


Negative_regulation (deprivation) of OGD in middle cerebral artery associated with middle cerebral artery infarction and metalloproteinase
2) Confidence 0.09 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC2194693 Disease Relevance 0.20 Pain Relevance 0.05
In vitro oxygen-glucose deprivation (OGD)
Negative_regulation (deprivation) of OGD
3) Confidence 0.08 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC2194693 Disease Relevance 0.40 Pain Relevance 0
Immunosuppression of bFGF in newborn animals greatly reduced their number, suggesting that the factor was required in vivo. bFGF was present in the DRG and spinal cord, as well as in skeletal muscle, the peripheral projection site of P-neurons, as revealed by tracer DiIC(18)3.
Negative_regulation (Immunosuppression) of bFGF in skeletal muscle associated with dorsal root ganglion and spinal cord
4) Confidence 0.06 Published 2001 Journal J. Neurosci. Section Abstract Doc Link 11698599 Disease Relevance 0.30 Pain Relevance 0.69
Shortly after OGD (6–24 hours), there is a reduction in the proliferative and migratory activity of precursors, whereas later (2 to 5 days after the insult), these cells start to proliferate and migrate into the damaged cortex.
Negative_regulation (reduction) of OGD in cortex
5) Confidence 0.06 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2669296 Disease Relevance 0.11 Pain Relevance 0.03
We have studied the proliferative and migratory behavior of neuroblasts activated by oxygen/glucose deprivation (OGD) in an organotypic model which includes the neurogenic SVZ and the cortex.
Negative_regulation (deprivation) of OGD in neuroblasts
6) Confidence 0.06 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2669296 Disease Relevance 0.34 Pain Relevance 0.03
However, SAM is a weak inhibitor of CYP2E1.
Negative_regulation (inhibitor) of SAM
7) Confidence 0.03 Published 2005 Journal Biochem. Pharmacol. Section Abstract Doc Link 15763544 Disease Relevance 0.08 Pain Relevance 0.11
Since the K(i) for SAM inhibition of CYP2E1 activity is relatively high, inhibition of CYP2E1 activity is not likely to play a major role in the ability of SAM to protect against the hepatotoxicity produced by toxins requiring metabolic activation by CYP2E1 such as acetaminophen, ethanol, carbon tetrachloride, thioacetamide and carcinogens.
Negative_regulation (inhibition) of SAM associated with paracetamol and hepatotoxicity
8) Confidence 0.03 Published 2005 Journal Biochem. Pharmacol. Section Abstract Doc Link 15763544 Disease Relevance 0.09 Pain Relevance 0.13
In microsomes engineered to express individual human P450s, SAM produced a type II binding spectrum with CYP2E1-, but not with CYP3A4-expressing microsomes, and SAM was a weaker inhibitor against the metabolism of a specific CYP3A4 substrate than a specific CYP2E1 substrate.
Negative_regulation (inhibitor) of SAM
9) Confidence 0.03 Published 2005 Journal Biochem. Pharmacol. Section Abstract Doc Link 15763544 Disease Relevance 0.05 Pain Relevance 0.13
SAM was a non-competitive inhibitor of CYP2E1 catalytic activity and its inhibitory actions could not be mimicked by methionine, SAH or MTA.
Negative_regulation (inhibitor) of SAM associated with adenocard
10) Confidence 0.02 Published 2005 Journal Biochem. Pharmacol. Section Abstract Doc Link 15763544 Disease Relevance 0 Pain Relevance 0.16
-AR activation may include several mechanisms of excitatory inhibition during OGD.
Negative_regulation (inhibition) of OGD
11) Confidence 0.02 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3017519 Disease Relevance 0.74 Pain Relevance 0.55
We have shown that exposure to lipopolysaccharide (LPS) immediately prior to oxygen-glucose deprivation (OGD) heavily aggravated cell death in the neuronal subregions, CA1, CA3 and the dentate gyrus (DG) [17].
Negative_regulation (oxygen-glucose deprivation) of OGD in neuronal associated with death
12) Confidence 0.02 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3017519 Disease Relevance 1.05 Pain Relevance 0.64
g/mL; Sigma-Aldrich) for 24 h followed by oxygen-glucose deprivation (OGD) and thereafter transfer to fresh medium for 48 h; Oxygen-glucose deprivation (OGD) = preincubation without LPS for 24 h, followed by OGD and thereafter transfer to fresh medium for 48 h.
Negative_regulation (oxygen-glucose deprivation) of OGD
13) Confidence 0.02 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3017519 Disease Relevance 0.15 Pain Relevance 0.26
We found that OGD-induced damage in neuronal cell survival rate and LDH leakage could be improved by MP pretreatment (3 microM) within 20 min of OGD, which was abolished by concomitant incubation with non-selective opioid receptor antagonist naloxone (Nal, 50 microM).
Negative_regulation (abolished) of OGD in neuronal associated with antagonist, narcan and opioid receptor
14) Confidence 0.02 Published 2008 Journal Neurosci. Lett. Section Abstract Doc Link 18706478 Disease Relevance 0.09 Pain Relevance 0.46
These results demonstrated that MP can reduce OGD-induced neuronal injuries, and the down-regulation of cPKCgamma membrane translocation might be involved in the neuroprotection.
Negative_regulation (reduce) of OGD in neuronal associated with injury
15) Confidence 0.02 Published 2008 Journal Neurosci. Lett. Section Abstract Doc Link 18706478 Disease Relevance 0.15 Pain Relevance 0.24
To further elucidate the role of cPKCgamma in MP-induced neuroprotection, we found that cPKCgamma membrane translocation inhibitor, Go6983 (6 nM) did not affect MP-induced neuroprotection while Go6983 alone exhibited a significant inhibition on OGD-induced increment in LDH leakage and decrease in cell survival rate.
Negative_regulation (inhibition) of OGD
16) Confidence 0.02 Published 2008 Journal Neurosci. Lett. Section Abstract Doc Link 18706478 Disease Relevance 0.07 Pain Relevance 0.29
Current data suggest that the action of thalidomide is related to several different mechanisms, including suppression of tumor necrosis factor, effects on basic fibroblast growth factor, vascular endothelial growth factor, interleukins and interferons, downregulation of selected cell surface adhesion molecules, and changes in the lymphocyte subsets.
Negative_regulation (downregulation) of basic fibroblast growth factor in lymphocyte associated with necrosis, cancer and adhesions
17) Confidence 0.02 Published 2004 Journal Eur. J. Haematol. Section Abstract Doc Link 14962263 Disease Relevance 1.13 Pain Relevance 0.08
Therefore oxidative stress
               was found in combination with S-adenosylmethionine (SAM) depletion, as SAM is the
               methyl donor for nicotinamide N-methylation and most other important methylation
                   reactions.7,61,63–66 Accordingly, reduced SAM levels were found in
               chronic neurodegeneration.67–70
               LD/DDI further lowered SAM concentrations,71 as O-methylation of LD by COMT elevates homocysteine.58,64,72 Consequently, one may suggest combining central COMT inhibition with
               central blocking of monoaminooxidase-B. 
Negative_regulation (reduced) of SAM associated with stress and catechol-o-methyltransferase
18) Confidence 0.01 Published 2009 Journal Patient Prefer Adherence Section Body Doc Link PMC2778405 Disease Relevance 0.18 Pain Relevance 0.44

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