INT135835

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Context Info
Confidence 0.21
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Abstract
Documents 1
Total Number 2
Disease Relevance 2.44
Pain Relevance 0.41

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

cell death (PLP1) structural molecule activity (PLP1)
PLP1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Central nervous system 2 91.24 High High
Inflammation 2 89.72 High High
Multiple sclerosis 2 89.04 High High
Demyelination 4 75.00 Quite High
anesthesia 2 44.56 Quite Low
Disease Link Frequency Relevance Heat
Multiple Sclerosis 10 99.84 Very High Very High Very High
Central Nervous System Disease 2 91.24 High High
Demyelinating Disease 8 90.80 High High
INFLAMMATION 2 89.72 High High
Disease 4 75.00 Quite High
Injury 4 75.00 Quite High
Alzheimer's Dementia 2 72.96 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To study the immunological mechanisms causing axonal degeneration, we induced experimental autoimmune encephalomyelitis (EAE) in wildtype Lewis rats and Lewis rats with a slowly progressive myelin degeneration due to proteolipid protein (PLP) overexpression.
Positive_regulation (overexpression) of Gene_expression (overexpression) of proteolipid protein associated with multiple sclerosis
1) Confidence 0.21 Published 2006 Journal Acta Neuropathol. Section Abstract Doc Link 16718350 Disease Relevance 1.22 Pain Relevance 0.20
To study the immunological mechanisms causing axonal degeneration, we induced experimental autoimmune encephalomyelitis (EAE) in wildtype Lewis rats and Lewis rats with a slowly progressive myelin degeneration due to proteolipid protein (PLP) overexpression.
Positive_regulation (overexpression) of Gene_expression (overexpression) of PLP associated with multiple sclerosis
2) Confidence 0.21 Published 2006 Journal Acta Neuropathol. Section Abstract Doc Link 16718350 Disease Relevance 1.22 Pain Relevance 0.20

General Comments

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