INT70087

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Context Info
Confidence 0.50
First Reported 1997
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 7
Disease Relevance 2.62
Pain Relevance 0.21

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

protein modification process (TGM1) transferase activity, transferring acyl groups (TGM1)
Anatomy Link Frequency
epithelium 1
TGM1 (Homo sapiens)
Pain Link Frequency Relevance Heat
monoamine 1 100.00 Very High Very High Very High
cINOD 1 100.00 Very High Very High Very High
Pain 12 58.80 Quite High
cytokine 6 5.00 Very Low Very Low Very Low
Inflammation 6 5.00 Very Low Very Low Very Low
Inflammatory response 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 13 100.00 Very High Very High Very High
Acquired Immune Deficiency Syndrome Or Hiv Infection 306 99.76 Very High Very High Very High
Toxicity 156 99.52 Very High Very High Very High
Disease 4 93.80 High High
Alzheimer's Dementia 2 81.00 Quite High
Sexually Transmitted Diseases 18 80.96 Quite High
Syndrome 6 79.56 Quite High
Immunodeficiency 6 79.20 Quite High
Sperm Disorder 6 73.12 Quite High
Pain 6 58.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This report evaluated the potential of a total of ten different pharmacological agents to inhibit TGase-induced cross-linking of A beta, including known TGase inhibitors (dansylcadaverine, spermine), non-steroidal anti-inflammatory drugs (indomethacin, meclofenamic acid, diflunisal, salicylic acid), monoamine oxidase inhibitors (tranylcypromine, phenelzine), an acetylcholinesterase inhibitor (tacrine), and an iron chelating agent (deferoxamine).
Negative_regulation (inhibitors) of TGase associated with inflammation, cinod and monoamine
1) Confidence 0.50 Published 1997 Journal Life Sci. Section Abstract Doc Link 9194688 Disease Relevance 0.58 Pain Relevance 0.15
The reduction in the inhibitory activity of LiJ in the presence of SP is mostly linked to its buffering capacity, suggesting that the main antiviral activity of LiJ is mediated by low pH.
Negative_regulation (reduction) of LiJ
2) Confidence 0.23 Published 2008 Journal Retrovirology Section Body Doc Link PMC2259360 Disease Relevance 0.54 Pain Relevance 0.06
Whilst there were no obvious signs of toxicity following a 5 or 30 minute treatment period with up to 50% LiJ, a significant reduction in viability was observed following 60 minutes, with 50% LiJ causing a 75% reduction in viability.
Negative_regulation (reduction) of LiJ associated with toxicity
3) Confidence 0.20 Published 2008 Journal Retrovirology Section Body Doc Link PMC2259360 Disease Relevance 0.38 Pain Relevance 0
To assess the epithelium viability following topical application of LiJ, reconstructed cervicovaginal epithelium cultures were exposed to a topical application of LiJ (100 ?
Negative_regulation (application) of LiJ in epithelium
4) Confidence 0.20 Published 2008 Journal Retrovirology Section Body Doc Link PMC2259360 Disease Relevance 0.16 Pain Relevance 0
LiJ was then carefully removed by washing (2 × 200 ?
Negative_regulation (removed) of LiJ
5) Confidence 0.20 Published 2008 Journal Retrovirology Section Body Doc Link PMC2259360 Disease Relevance 0.15 Pain Relevance 0
ARB prepared the LiJ and SP, tested their pH and physical properties, and ran neutralization assays.
Negative_regulation (prepared) of LiJ
6) Confidence 0.20 Published 2008 Journal Retrovirology Section Body Doc Link PMC2259360 Disease Relevance 0.47 Pain Relevance 0
Furthermore, a 2 hour exposure to 25% LiJ resulted in 65% reduction in viability and 50% LiJ caused 90% toxicity.
Negative_regulation (reduction) of LiJ associated with toxicity
7) Confidence 0.20 Published 2008 Journal Retrovirology Section Body Doc Link PMC2259360 Disease Relevance 0.34 Pain Relevance 0

General Comments

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