INT69985

From wiki-pain
Revision as of 14:23, 21 September 2012 by Daniel (Talk | contribs)

(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to: navigation, search
Context Info
Confidence 0.50
First Reported 1997
Last Reported 2010
Negated 3
Speculated 4
Reported most in Body
Documents 21
Total Number 24
Disease Relevance 13.26
Pain Relevance 6.31

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 (TNF) extracellular space (TNF) extracellular region (TNF)
plasma membrane (TNF) intracellular (TNF) extracellular matrix organization (TNF)
Anatomy Link Frequency
B-cell 2
TNF (Homo sapiens)
Pain Link Frequency Relevance Heat
Bioavailability 40 99.96 Very High Very High Very High
rheumatoid arthritis 266 99.90 Very High Very High Very High
imagery 14 99.90 Very High Very High Very High
Inflammation 228 99.78 Very High Very High Very High
cytokine 189 99.72 Very High Very High Very High
abatacept 39 98.46 Very High Very High Very High
Hippocampus 7 98.40 Very High Very High Very High
Arthritis 339 95.00 High High
Adalimumab 113 92.48 High High
Etanercept 65 91.72 High High
Disease Link Frequency Relevance Heat
Cancer 62 100.00 Very High Very High Very High
Necrosis 43 100.00 Very High Very High Very High
Fever 6 100.00 Very High Very High Very High
Serositis 5 100.00 Very High Very High Very High
Appetite Loss 3 100.00 Very High Very High Very High
Rheumatoid Arthritis 267 99.90 Very High Very High Very High
INFLAMMATION 220 99.78 Very High Very High Very High
Disease 252 99.60 Very High Very High Very High
Cognitive Disorder 6 99.10 Very High Very High Very High
Alzheimer's Dementia 5 96.20 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A series of VCT were simulated assuming different TNF bioavailability ranges induced by the two different treatments and a natural biological variation of ?
Positive_regulation (simulated) of Negative_regulation (assuming) of TNF associated with bioavailability
1) Confidence 0.50 Published 2007 Journal PLoS Computational Biology Section Body Doc Link PMC2041971 Disease Relevance 0.19 Pain Relevance 0.15
TNF inhibitors do not appear to significantly increase the risk of reactivating chronic viral infections.
Spec (appear) Positive_regulation (increase) of Negative_regulation (inhibitors) of TNF
2) Confidence 0.49 Published 2010 Journal Semin. Arthritis Rheum. Section Body Doc Link 19117595 Disease Relevance 0.13 Pain Relevance 0
It has also been observed that patients with elevated CRP or greater amounts of inflammation on MRI may respond better to TNF inhibitors (Maksymowych et al. 2006; van der Heijde et al. 2006b).
Spec (may) Positive_regulation (respond) of Negative_regulation (inhibitors) of TNF associated with inflammation and imagery
3) Confidence 0.49 Published 2007 Journal Core Evidence Section Body Doc Link PMC3012440 Disease Relevance 0.87 Pain Relevance 0.93
The western blot and immunofluorescence experiments further suggested a possible mechanism for the B8-mediated inhibition of TNF?
Spec (possible) Positive_regulation (mechanism) of Negative_regulation (inhibition) of TNF
4) Confidence 0.49 Published 2008 Journal J Inflamm (Lond) Section Body Doc Link PMC2525633 Disease Relevance 0.05 Pain Relevance 0.18
The treatment was well tolerated and induced rapid control of fever, anorexia and serositis, together with downregulation of interleukin (IL)-6, soluble TNF receptors (sTNFR) and IL-1ra, and the acute-phase proteins C-reactive protein (CRP) and serum amyloid A (SAA).
Positive_regulation (induced) of Negative_regulation (downregulation) of TNF associated with appetite loss, alzheimer's dementia, serositis and fever
5) Confidence 0.49 Published 1997 Journal Br. J. Rheumatol. Section Abstract Doc Link 9189062 Disease Relevance 1.88 Pain Relevance 0.59
as a key mediator of inflammation in RA has led to the development of TNF-?
Positive_regulation (led) of Negative_regulation (development) of TNF associated with inflammation and rheumatoid arthritis
6) Confidence 0.49 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212575 Disease Relevance 2.04 Pain Relevance 0.68
Uncontrolled studies have demonstrated TNF inhibition to be effective for this particular sub-group (Henrickson and Reiff 2004; Tse et al 2005).
Positive_regulation (effective) of Negative_regulation (inhibition) of TNF
7) Confidence 0.45 Published 2008 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721362 Disease Relevance 0.61 Pain Relevance 0.71
While it is expected that individual cells will vary in their level of response, it is unexpected to find a lack of correlation between genes such as TNF and IL1?
Spec (find) Positive_regulation (find) of Negative_regulation (lack) of TNF
8) Confidence 0.36 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2711328 Disease Relevance 0.06 Pain Relevance 0
Then abatacept and rituximab were recommended for the treatment of the patients who do not respond adequately to TNF inhibitors.
Neg (not) Positive_regulation (respond) of Negative_regulation (inhibitors) of TNF associated with abatacept
9) Confidence 0.35 Published 2009 Journal Clin Calcium Section Abstract Doc Link 19252247 Disease Relevance 0.53 Pain Relevance 0.33
CONCLUSION: Although rituximab does not seem to be effective in patients with AS that does not respond to TNF blockers, it had significant efficacy in TNF blocker-naive patients.
Neg (not) Positive_regulation (respond) of Negative_regulation (blockers) of TNF
10) Confidence 0.33 Published 2010 Journal Arthritis Rheum. Section Body Doc Link 20461780 Disease Relevance 0 Pain Relevance 0
RESULTS: For axial AS, 175 patients received TNF blockers (men 78%, mean disease duration 12.4 +/- 9.1 yrs); 100 patients (of 143 with available data) had an increased CRP (> 10 mg/l).
Positive_regulation (received) of Negative_regulation (blockers) of TNF
11) Confidence 0.33 Published 2007 Journal J. Rheumatol. Section Body Doc Link 17722225 Disease Relevance 0.08 Pain Relevance 0
If this is so, TNF will drive IL-1 production and TNF blockade will be sufficient to control this TNF–IL-1 pathway (Fig. 1).
Positive_regulation (sufficient) of Negative_regulation (blockade) of TNF
12) Confidence 0.31 Published 2001 Journal Arthritis Res Section Body Doc Link PMC128880 Disease Relevance 0.44 Pain Relevance 0.26
Do we need new treatment that goes beyond tumor necrosis factor blockers for rheumatoid arthritis?
Positive_regulation (goes) of Negative_regulation (blockers) of tumor necrosis factor associated with necrosis, cancer and rheumatoid arthritis
13) Confidence 0.31 Published 2005 Journal Ann. N. Y. Acad. Sci. Section Title Doc Link 16127017 Disease Relevance 1.31 Pain Relevance 0.48
The vaccine-specific response in these patients was similar to that in patients never exposed to TNF inhibitors, suggesting that distant exposure to TNF inhibitors was unlikely to contribute to the observed B-cell dysfunctions.
Positive_regulation (exposure) of Negative_regulation (inhibitors) of TNF in B-cell
14) Confidence 0.28 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2911904 Disease Relevance 0.16 Pain Relevance 0.04
downregulatory effect observed in genetically high IL-10 producing patients might be explained by the regulatory feedback mechanism that controls the production of both cytokines, which would lead to a decrease in the TNF?
Positive_regulation (lead) of Negative_regulation (decrease) of TNF associated with cytokine
15) Confidence 0.25 Published 2006 Journal Arthritis Res Ther Section Body Doc Link PMC1526590 Disease Relevance 0.40 Pain Relevance 0.15
Interestingly, P2Y2 stimulation mediated greater inhibition of TNF?
Positive_regulation (mediated) of Negative_regulation (inhibition) of TNF
16) Confidence 0.19 Published 2010 Journal Cellular Signalling Section Body Doc Link PMC2806525 Disease Relevance 0 Pain Relevance 0.11
To our surprise we found that PAR2 activation was able to strongly mediate an inhibition of TNF?
Positive_regulation (mediate) of Negative_regulation (inhibition) of TNF
17) Confidence 0.19 Published 2010 Journal Cellular Signalling Section Body Doc Link PMC2806525 Disease Relevance 0.23 Pain Relevance 0.38
The potential for GPCRs to mediate the inhibition of TNF?
Positive_regulation (mediate) of Negative_regulation (inhibition) of TNF
18) Confidence 0.19 Published 2010 Journal Cellular Signalling Section Body Doc Link PMC2806525 Disease Relevance 0.32 Pain Relevance 0.07
However, although these agents may be effective in a number of patients who fail to respond to TNF blockade, they only rarely induce remission and overall 50% response rates do not exceed those with the TNF inhibitors.
Neg (fail) Positive_regulation (respond) of Negative_regulation (blockade) of TNF
19) Confidence 0.17 Published 2006 Journal Arthritis Res. Ther. Section Abstract Doc Link 16899109 Disease Relevance 0.33 Pain Relevance 0.22
In a recent study, Yun and colleagues showed that EGCG treatment resulted in dose-dependent inhibition of TNF?
Positive_regulation (resulted) of Negative_regulation (inhibition) of TNF
20) Confidence 0.15 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2888220 Disease Relevance 0.89 Pain Relevance 0.34

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox