INT99690

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Context Info
Confidence 0.58
First Reported 2001
Last Reported 2011
Negated 0
Speculated 1
Reported most in Body
Documents 30
Total Number 31
Disease Relevance 14.56
Pain Relevance 4.79

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 (VEGFA) growth (VEGFA) extracellular region (VEGFA)
proteinaceous extracellular matrix (VEGFA) cytoplasm (VEGFA)
Anatomy Link Frequency
PGE2 4
cardiac myocytes 2
gastric juices 2
internal 2
foot 2
VEGFA (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 31 99.98 Very High Very High Very High
Morphine 27 99.84 Very High Very High Very High
Kinase C 8 99.80 Very High Very High Very High
fluoxetine 6 98.60 Very High Very High Very High
Opioid 10 98.56 Very High Very High Very High
Inflammatory mediators 11 98.04 Very High Very High Very High
narcan 3 97.12 Very High Very High Very High
Eae 1 92.64 High High
nud 141 90.24 High High
antidepressant 5 89.44 High High
Disease Link Frequency Relevance Heat
Systemic Lupus Erythematosus 63 99.72 Very High Very High Very High
Pre-eclampsia 118 99.50 Very High Very High Very High
Hypoxia 37 99.50 Very High Very High Very High
Cancer 459 98.66 Very High Very High Very High
Syndrome 18 98.60 Very High Very High Very High
Fibromyalgia 4 98.56 Very High Very High Very High
INFLAMMATION 223 97.84 Very High Very High Very High
Renal Cancer 131 97.84 Very High Very High Very High
Gastritis 87 97.52 Very High Very High Very High
Myeloid Leukemia 27 94.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Phosphatidyl inositol-3 kinase and protein kinase C-mediated activation of the VEGF promoter was also inhibited by morphine.
Negative_regulation (inhibited) of Positive_regulation (activation) of VEGF promoter associated with kinase c and morphine
1) Confidence 0.58 Published 2001 Journal J. Mol. Cell. Cardiol. Section Abstract Doc Link 11735263 Disease Relevance 0.71 Pain Relevance 1.11
Transfection of HUVECs with a human VEGF promoter-luciferase construct showed that hypoxia-induced transcriptional activation of VEGF was markedly inhibited by morphine sulfate (P<0.05).
Negative_regulation (inhibited) of Positive_regulation (activation) of VEGF associated with hypoxia and morphine
2) Confidence 0.43 Published 2001 Journal J. Mol. Cell. Cardiol. Section Abstract Doc Link 11735263 Disease Relevance 0.75 Pain Relevance 1.08
Serum levels of VEGF were determined in 47 SLE patients, including 26 patients with systemic involvement, 21 cases without internal organ manifestations, and in 30 healthy subjects (Fig. 1).
Spec (determined) Negative_regulation (determined) of Positive_regulation (levels) of VEGF in internal associated with systemic lupus erythematosus
3) Confidence 0.43 Published 2007 Journal Arch Immunol Ther Exp (Warsz) Section Body Doc Link PMC2765643 Disease Relevance 0.77 Pain Relevance 0
VEGF was detected in pretreatment serum in 67% of patients tested, increased by day 8 to 52%, and decreased to 93% (67% undetectable) 2 hours after bevacizumab administration.
Negative_regulation (decreased) of Positive_regulation (increased) of VEGF
4) Confidence 0.42 Published 2010 Journal Journal of Oncology Section Body Doc Link PMC2875768 Disease Relevance 0.46 Pain Relevance 0
VEGF was detected in pretreatment serum in 67% of patients tested, increased by day 8 in 52%, and decreased in 93% (67% undetectable) 2 h after bevacizumab.
Negative_regulation (decreased) of Positive_regulation (increased) of VEGF
5) Confidence 0.42 Published 2010 Journal J Angiogenes Res Section Body Doc Link PMC2902424 Disease Relevance 0.65 Pain Relevance 0.03
sVEGFR1-heterodimerization of surface VEGFRs is expected to present an alternative way for sVEGFR1 to modulate VEGF signal transduction even when interstitial free VEGF levels remain high, by effectively reducing the availability of functional endothelial surface VEGFR dimers for VEGF activation, assuming that VEGFR heterodimers with sVEGFR1 cannot signal.
Negative_regulation (reducing) of Positive_regulation (activation) of VEGF
6) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.07 Pain Relevance 0
MNTX inhibited MS, DAMGO and VEGF induced tyrosine phosphorylation (transactivation) of VEGF receptors 1 and 2.
Negative_regulation (inhibited) of Positive_regulation (induced) of VEGF
7) Confidence 0.39 Published 2006 Journal Microvasc. Res. Section Abstract Doc Link 16820176 Disease Relevance 0.06 Pain Relevance 0.68
Interestingly, the patients with PDR/CRVO showed increase of VEGF, but not DME/BRVO which had a significant increase of IL-6, IL-8, and MCP-1 (Figure 1).
Negative_regulation (showed) of Positive_regulation (increase) of VEGF
8) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2780733 Disease Relevance 1.19 Pain Relevance 0.03
We also show that activation of 5-HT1A receptors is sufficient to induce VEGF expression and that a 5-HT1A antagonist blocks both the increase in VEGF and behavioral effects induced by fluoxetine.
Negative_regulation (blocks) of Positive_regulation (increase) of VEGF associated with antagonist and fluoxetine
9) Confidence 0.38 Published 2009 Journal Neuropsychopharmacology Section Abstract Doc Link 19553916 Disease Relevance 0.15 Pain Relevance 0.94
M NS398 demonstrated inhibition of COX-2 expression following VEGF activation (fig 2C).
Negative_regulation (inhibition) of Positive_regulation (activation) of VEGF
10) Confidence 0.36 Published 2008 Journal Gut Section Body Doc Link PMC2582343 Disease Relevance 0 Pain Relevance 0
The selective inhibitor of COX-2, NS398 (1 µM), abolished COX-2 mRNA and protein expression in HIMECs following VEGF activation (not shown).
Negative_regulation (abolished) of Positive_regulation (activation) of VEGF
11) Confidence 0.36 Published 2008 Journal Gut Section Body Doc Link PMC2582343 Disease Relevance 0 Pain Relevance 0
Consistent with the gene expression data, curcumin pretreatment of HIMECs inhibited COX-2 protein expression at 1 µM, with increasing effect at 10 µM curcumin, while 20 µM curcumin completely abolished COX-2 expression following VEGF activation (fig 2B).
Negative_regulation (abolished) of Positive_regulation (activation) of VEGF
12) Confidence 0.31 Published 2008 Journal Gut Section Body Doc Link PMC2582343 Disease Relevance 0 Pain Relevance 0
Drugs may also act indirectly by antibody binding of elevated levels of extracellular angiogenic growth factors eg, bevacizumab (Avastin®, Genentech), acting on overexpressed receptors on tumor cells themselves eg, sunitinib, sorafenib (Nexavar®, Bayer) or by inhibiting related pathways such as mTOR upregulation of VEGF and HIF1?
Negative_regulation (inhibiting) of Positive_regulation (upregulation) of VEGF associated with cancer
13) Confidence 0.27 Published 2008 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2727778 Disease Relevance 0.80 Pain Relevance 0
The synergistic mechanism involves MNTX activation of tyrosine phosphatase activity with consequent inhibition of VEGF-induced Src activation.
Negative_regulation (inhibition) of Positive_regulation (activation) of VEGF-induced
14) Confidence 0.24 Published 2010 Journal J Angiogenes Res Section Body Doc Link PMC2831839 Disease Relevance 0 Pain Relevance 0.08
Thus all media were supplemented with 100ng/ml IGF-I (Peprotech Inc., Rocky Hill, NJ, USA) to ensure activation of the mevalonate pathway and expression of VEGF.
Negative_regulation (ensure) of Positive_regulation (activation) of VEGF
15) Confidence 0.23 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.13 Pain Relevance 0
CONCLUSION

Alendronate, a nitrogen containing bisphosphonate, reduced secreted VEGF at the mRNA, protein, and secretory levels in growth plate chondrocytes indicating that bisphosphonates inhibit cellular turnover at the chondro-osseous junction by reducing VEGF induced vascular invasion.

Negative_regulation (reducing) of Positive_regulation (induced) of VEGF in growth plate
16) Confidence 0.23 Published 2009 Journal The Open Orthopaedics Journal Section Body Doc Link PMC2761671 Disease Relevance 0.16 Pain Relevance 0
These data indicate that bevacizumab causes side effects typical of inhibition of the VEGF pathway in patients with RCC; similar events are observed at a similar incidence in patients treated with TKIs such as sunitinib, which inhibit VEGF receptors as well as other TKIs, although such agents also cause non-VEGF-specific events such as hand-foot syndrome and myelosuppression (Motzer et al 2007).
Negative_regulation (inhibit) of Positive_regulation (cause) of VEGF in foot associated with syndrome and renal cancer
17) Confidence 0.21 Published 2008 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721410 Disease Relevance 0.93 Pain Relevance 0.04
In contrast, inhibition of IKK signaling did not prevent VEGF up-regulation in response to LTA.
Negative_regulation (prevent) of Positive_regulation (up-regulation) of VEGF
18) Confidence 0.15 Published 2009 Journal J. Dent. Res. Section Abstract Doc Link 19767581 Disease Relevance 0.07 Pain Relevance 0.12
SU5416 is a small molecule antiangiogenic agent that inhibits vascular endothelial growth factor (VEGF) stimulation of the KDR tyrosine kinase receptor.
Negative_regulation (inhibits) of Positive_regulation (stimulation) of VEGF
19) Confidence 0.15 Published 2002 Journal Clin. Cancer Res. Section Abstract Doc Link 12231519 Disease Relevance 0.17 Pain Relevance 0
Furthermore, incadronate disodium significantly prevented transcriptional activation of nuclear factor-kappaB and activator protein-1 and the subsequent up-regulation of VEGF mRNA levels in AGE-exposed EC.
Negative_regulation (prevented) of Positive_regulation (regulation) of VEGF mRNA
20) Confidence 0.12 Published 2007 Journal Immun Ageing Section Body Doc Link PMC1845171 Disease Relevance 0.94 Pain Relevance 0.11

General Comments

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