INT129856

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Context Info
Confidence 0.68
First Reported 2005
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 26
Total Number 28
Disease Relevance 16.21
Pain Relevance 4.75

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

signal transduction (TNFRSF11A) cell-cell signaling (TNFRSF11A)
Anatomy Link Frequency
osteoclasts 4
monocytes 4
neutrophils 4
erythrocyte 2
endothelial cells 2
TNFRSF11A (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 106 99.68 Very High Very High Very High
Inflammation 273 99.62 Very High Very High Very High
rheumatoid arthritis 465 99.58 Very High Very High Very High
Arthritis 36 99.00 Very High Very High Very High
aspirin 23 96.44 Very High Very High Very High
Pain 23 94.96 High High
Inflammatory response 7 86.64 High High
Analgesic 1 86.28 High High
Osteoarthritis 80 85.04 High High
Restless leg syndrome 60 84.56 Quite High
Disease Link Frequency Relevance Heat
Edema 2 100.00 Very High Very High Very High
Cancer 137 99.76 Very High Very High Very High
Respiratory Syncytial Virus 232 99.68 Very High Very High Very High
INFLAMMATION 277 99.62 Very High Very High Very High
Rheumatoid Arthritis 465 99.58 Very High Very High Very High
Necrosis 75 99.52 Very High Very High Very High
Arthritis 26 99.00 Very High Very High Very High
Hypercalcemia 57 98.88 Very High Very High Very High
Osteoporosis 105 98.44 Very High Very High Very High
Death 11 97.00 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The presence of a functional RANK protein at the cell surface of neutrophils pretreated by SFs from patients with RA, as demonstrated by RANK-L activation of the NF-?
Positive_regulation (activation) of RANK in neutrophils associated with rheumatoid arthritis
1) Confidence 0.68 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906801 Disease Relevance 0.76 Pain Relevance 0.42
In the in vitro studies, ox-LDL dose-dependently increased the activation of NF-kB in monocytes, but not in lymphocytes derived from healthy volunteers.
Positive_regulation (activation) of NF-kB in monocytes
2) Confidence 0.64 Published 2005 Journal J. Am. Coll. Cardiol. Section Body Doc Link 16139128 Disease Relevance 0.13 Pain Relevance 0
The increase in circulating NF-kB was mainly due to the activation of monocytes.
Positive_regulation (increase) of NF-kB in monocytes
3) Confidence 0.64 Published 2005 Journal J. Am. Coll. Cardiol. Section Body Doc Link 16139128 Disease Relevance 0.15 Pain Relevance 0
The incubation of monocytes with the sera derived from the UA patients induced a significant increase in NF-kB activation compared with the sera derived from the control subjects.
Positive_regulation (activation) of NF-kB in monocytes
4) Confidence 0.64 Published 2005 Journal J. Am. Coll. Cardiol. Section Body Doc Link 16139128 Disease Relevance 0.11 Pain Relevance 0
CONCLUSIONS: The data suggest that the activation of NF-kB in monocytes of UA patients is, at least in part, induced by circulating molecules such as ox-LDL, which has been found to be particularly elevated in UA patients.


Positive_regulation (activation) of NF-kB in monocytes
5) Confidence 0.64 Published 2005 Journal J. Am. Coll. Cardiol. Section Body Doc Link 16139128 Disease Relevance 0.10 Pain Relevance 0
BACKGROUND: Nuclear factor-kB might be involved in atherosclerosis, as is suggested by the presence of activated NF-kB in human atherosclerotic lesions.
Positive_regulation (activated) of NF-kB
6) Confidence 0.64 Published 2005 Journal J. Am. Coll. Cardiol. Section Body Doc Link 16139128 Disease Relevance 0.19 Pain Relevance 0
Such conditions include familial expansile osteolysis, expansile skeletal hyperphosphatasia, and a familial form of early-onset Paget's disease of bone (PDB2), all from constitutive activation of RANK, and juvenile Paget's disease from OPG deficiency.
Positive_regulation (activation) of RANK in juvenile
7) Confidence 0.63 Published 2007 Journal J. Clin. Endocrinol. Metab. Section Body Doc Link 17284635 Disease Relevance 0 Pain Relevance 0
The present data on the increased RANK-L expression by RA neutrophils, together with the presence of neutrophils at the pannus-bone interface [34], suggest that through cell-cell interactions such inflammatory neutrophils could activate RANK-expressing osteoclasts and bone resorption.
Positive_regulation (increased) of RANK in osteoclasts associated with inflammation, rheumatoid arthritis and hypercalcemia
8) Confidence 0.49 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906801 Disease Relevance 0.81 Pain Relevance 0.29
The presence of a functional RANK protein at the cell surface of neutrophils pretreated by SFs from patients with RA, as demonstrated by RANK-L activation of the NF-?
Positive_regulation (presence) of RANK protein in neutrophils associated with rheumatoid arthritis
9) Confidence 0.49 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906801 Disease Relevance 0.71 Pain Relevance 0.40
The present data on the increased RANK-L expression by RA neutrophils, together with the presence of neutrophils at the pannus-bone interface [34], suggest that through cell-cell interactions such inflammatory neutrophils could activate RANK-expressing osteoclasts and bone resorption.
Positive_regulation (activate) of RANK in osteoclasts associated with inflammation, rheumatoid arthritis and hypercalcemia
10) Confidence 0.49 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906801 Disease Relevance 0.79 Pain Relevance 0.28
ODFR, in particular the hydroxyl radical, cause lipid peroxidation, resulting in structural damage and activation of the vascular endothelium, increased vascular permeability and systemic capillary endothelial swelling [2,3,5].
Positive_regulation (increased) of ODFR in vascular endothelium associated with edema
11) Confidence 0.49 Published 2006 Journal Thromb J Section Body Doc Link PMC1540420 Disease Relevance 0.95 Pain Relevance 0.57
B) secondary to the stimulation of RANK by RANK-L is associated with the phosphorylation of the inhibitory I-?
Positive_regulation (stimulation) of RANK
12) Confidence 0.46 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906801 Disease Relevance 0.76 Pain Relevance 0.38
During the immune response, mature dendritic cells express receptor activator of nuclear factor-kappa-B (RANK) and tumor necrosis factor receptor-associated factor 6 (TRAF6) [15,16].
Positive_regulation (activator) of RANK in dendritic cells associated with necrosis and cancer
13) Confidence 0.46 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906801 Disease Relevance 1.25 Pain Relevance 0.28
After 2 days of incubation of healthy blood neutrophils in medium containing 80% SF from patients with RA and 20% CM, membrane RANK-L significantly increased and was detected on 13.4% ± 4.7% of cells (n = 5) (versus 2.5% ± 0.8% neutrophils in CM alone, a percentage similar to that of freshly isolated neutrophils).
Positive_regulation (increased) of RANK in neutrophils associated with rheumatoid arthritis
14) Confidence 0.46 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906801 Disease Relevance 0.76 Pain Relevance 0.42
Differential expression of RANK, RANK-L, and osteoprotegerin by synovial fluid neutrophils from patients with rheumatoid arthritis and by healthy human blood neutrophils

Functional links between bone remodeling and the immune system in chronic inflammatory arthritis are mediated, in part, by the ligand of receptor activator of nuclear factor-kappa-B (RANK-L).

Positive_regulation (activator) of RANK in neutrophils associated with inflammation, rheumatoid arthritis and arthritis
15) Confidence 0.46 Published 2007 Journal Arthritis Res Ther Section Title Doc Link PMC1906801 Disease Relevance 0.99 Pain Relevance 0.41
This article reviewed the factors implicated, such as receptor activator of nuclear factor-kappaB (RANK), receptor activator of nuclear factor-kappaB ligand (RANKL), osteoprotegerin (OPG), macrophage inflammatory protein-1alpha (MIP-1alpha), SDF-1 and Wnt pathway.
Positive_regulation (activator) of RANK in macrophage associated with inflammation
16) Confidence 0.45 Published 2007 Journal Zhongguo Shi Yan Xue Ye Xue Za Zhi Section Abstract Doc Link 18088497 Disease Relevance 0.73 Pain Relevance 0.14
CONTEXT: A middle-aged woman with recent-onset painful swollen fingers and widespread periostitis, elevated serum alkaline phosphatase (ALP) activity and erythrocyte sedimentation rate, and accelerated skeletal turnover was found not to have mutations in the gene sequences for exon 1 of receptor activator of nuclear factor-kappaB (RANK), osteoprotegerin (OPG), or sequestosome-1.
Positive_regulation (activator) of nuclear factor-kappaB in erythrocyte associated with pain and periostitis
17) Confidence 0.43 Published 2007 Journal J. Clin. Endocrinol. Metab. Section Abstract Doc Link 17284635 Disease Relevance 0.25 Pain Relevance 0.09
CONTEXT: A middle-aged woman with recent-onset painful swollen fingers and widespread periostitis, elevated serum alkaline phosphatase (ALP) activity and erythrocyte sedimentation rate, and accelerated skeletal turnover was found not to have mutations in the gene sequences for exon 1 of receptor activator of nuclear factor-kappaB (RANK), osteoprotegerin (OPG), or sequestosome-1.
Positive_regulation (activator) of RANK in erythrocyte associated with pain and periostitis
18) Confidence 0.43 Published 2007 Journal J. Clin. Endocrinol. Metab. Section Abstract Doc Link 17284635 Disease Relevance 0.25 Pain Relevance 0.09
The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1.
Positive_regulation (activation) of NF-kB in endothelial cells associated with aspirin
19) Confidence 0.35 Published 2006 Journal Vascul. Pharmacol. Section Abstract Doc Link 16600694 Disease Relevance 0.33 Pain Relevance 0.29
Together, the findings indicate that in endothelial cells aspirin and PPAR-alpha activators reduce the high glucose-increased expression of MCP-1 by a mechanism that includes the inhibition of reactive oxygen species, and decrease of AP-1 and NF-kB activation.
Positive_regulation (activation) of NF-kB in endothelial cells associated with aspirin
20) Confidence 0.35 Published 2006 Journal Vascul. Pharmacol. Section Abstract Doc Link 16600694 Disease Relevance 0 Pain Relevance 0.16

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