INT145537

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Context Info
Confidence 0.18
First Reported 2003
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 3
Total Number 4
Disease Relevance 4.86
Pain Relevance 0.59

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 (PECAM1) extracellular space (PECAM1) cell adhesion (PECAM1)
plasma membrane (PECAM1)
Anatomy Link Frequency
vasculature 4
neuronal 2
leukocytes 2
PECAM1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 100 99.08 Very High Very High Very High
Multiple sclerosis 82 86.36 High High
Potency 2 79.12 Quite High
Opioid 1 50.60 Quite High
chemokine 37 5.00 Very Low Very Low Very Low
5HT 23 5.00 Very Low Very Low Very Low
Nicotine 20 5.00 Very Low Very Low Very Low
metalloproteinase 17 5.00 Very Low Very Low Very Low
cytokine 11 5.00 Very Low Very Low Very Low
Inflammatory response 10 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Nicotine Addiction 369 100.00 Very High Very High Very High
Adhesions 193 100.00 Very High Very High Very High
INFLAMMATION 114 99.08 Very High Very High Very High
Chronic Obstructive Pulmonary Disease 44 97.66 Very High Very High Very High
Emphysema 2 89.76 High High
Multiple Sclerosis 93 86.36 High High
Disease 80 79.52 Quite High
Periodontal Disease 22 78.12 Quite High
Thrombocytopenia 5 73.60 Quite High
Increased Venous Pressure Under Development 34 70.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As much of the pulmonary tissue destruction in COPD is thought to be due to the recruitment and activation of inflammatory cells, several researchers have examined the influence of smoking on adhesion molecule expression and release by the endothelial cells comprising the pulmonary vasculature, and recruited alveolar inflammatory cells.
Regulation (influence) of Localization (release) of adhesion molecule in vasculature associated with nicotine addiction, inflammation, chronic obstructive pulmonary disease and adhesions
1) Confidence 0.18 Published 2003 Journal Tob Induc Dis Section Body Doc Link PMC2669563 Disease Relevance 2.01 Pain Relevance 0.17
As much of the pulmonary tissue destruction in COPD is thought to be due to the recruitment and activation of inflammatory cells, several researchers have examined the influence of smoking on adhesion molecule expression and release by the endothelial cells comprising the pulmonary vasculature, and recruited alveolar inflammatory cells.
Spec (examined) Regulation (influence) of Localization (release) of adhesion molecule in vasculature associated with nicotine addiction, inflammation, chronic obstructive pulmonary disease and adhesions
2) Confidence 0.18 Published 2003 Journal Tob Induc Dis Section Body Doc Link PMC2671531 Disease Relevance 2.01 Pain Relevance 0.17
Our findings, together with evidence reviewed in prior sections, suggest a broader hypothesis, namely, that platelet interaction with leukocytes at the endothelium of the BBB is responsible for the release of PECAM-1 to the circulation, and associated infiltration of leukocytes.
Regulation (responsible) of Localization (release) of PECAM-1 in leukocytes
3) Confidence 0.16 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2829540 Disease Relevance 0.61 Pain Relevance 0.21
These results indicate that OBCAM is a synaptic cell adhesion molecule concerning synaptogenesis and its surface localization is dynamically regulated in response to neuronal activity.
Regulation (regulated) of Localization (localization) of adhesion molecule in neuronal associated with adhesions
4) Confidence 0.00 Published 2007 Journal Brain Res. Section Abstract Doc Link 17658490 Disease Relevance 0.23 Pain Relevance 0.05

General Comments

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