INT203372

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Context Info
Confidence 0.40
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 9.24
Pain Relevance 1.11

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

extracellular region (Igfals) cell adhesion (Igfals) nucleus (Igfals)
Anatomy Link Frequency
glial cell 1
lateral 1
neurons 1
spinal cord 1
LMNs 1
Igfals (Mus musculus)
Pain Link Frequency Relevance Heat
Spinal cord 115 99.78 Very High Very High Very High
Inflammation 134 87.48 High High
Central nervous system 52 86.28 High High
cytokine 38 86.28 High High
antagonist 16 69.36 Quite High
Inflammatory response 58 65.52 Quite High
chemokine 10 65.52 Quite High
Inflammatory mediators 18 60.56 Quite High
imagery 1 55.68 Quite High
positron emission tomography 4 55.36 Quite High
Disease Link Frequency Relevance Heat
Motor Neuron Diseases 813 100.00 Very High Very High Very High
Dementia 7 100.00 Very High Very High Very High
Frontotemporal Lobar Degeneration 5 100.00 Very High Very High Very High
Death 119 98.40 Very High Very High Very High
Disease 356 97.76 Very High Very High Very High
Stroke 8 96.84 Very High Very High Very High
Lifespan 14 90.24 High High
Congenital Anomalies 19 90.00 High High
Targeted Disruption 69 88.80 High High
Apoptosis 62 88.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
VEGF polymorphisms have been associated with an increased risk for ALS in some, but not all populations.23 Therefore VEGF deficiency may play a role in the pathogenesis of ALS.
Positive_regulation (increased) of ALS associated with motor neuron diseases
1) Confidence 0.40 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785861 Disease Relevance 0.88 Pain Relevance 0.08
It is possible that glial cell activation in ALS could lead to vessel leakage.
Positive_regulation (activation) of ALS in glial cell associated with motor neuron diseases
2) Confidence 0.31 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2075163 Disease Relevance 0.77 Pain Relevance 0.29
in ALS is supported by the use of thalidomide and lenalidomide to successfully inhibt TNF-?
Positive_regulation (supported) of ALS associated with motor neuron diseases
3) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2827549 Disease Relevance 1.09 Pain Relevance 0.15
Recently, TDP-43 has been found to be the main protein that accumulates in frontotemporal lobar degeneration with ubiquitin positive inclusions (FTLD-U) and in amyotrophic lateral sclerosis (ALS) [29].
Positive_regulation (accumulates) of ALS in lateral associated with dementia, frontotemporal lobar degeneration and motor neuron diseases
4) Confidence 0.15 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC2989316 Disease Relevance 1.03 Pain Relevance 0
Nevertheless, several studies have suggested that SOD1 mutations in neurons alone are insufficient to cause ALS and that dysfunction in support glia may contribute to disease development and progression [129-132].
Positive_regulation (cause) of ALS in neurons associated with disease and motor neuron diseases
5) Confidence 0.07 Published 2009 Journal Mol Neurodegener Section Body Doc Link PMC2784760 Disease Relevance 1.03 Pain Relevance 0.18
However, despite a raised incidence of mutations in NF genes in ALS subjects, a comprehensive study has excluded mutations in NF genes as a primary cause for ALS [56].
Positive_regulation (cause) of ALS associated with motor neuron diseases
6) Confidence 0.04 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 1.21 Pain Relevance 0
Possibly owing to earlier clinical manifestations of defects in LMNs and their easier accessibility to experimenters, however, most investigations of ALS, including previous genomics studies [2-4], focus on the spinal cord and LMNs, leaving ALS-related responses and defects of cellular maintenance in the motor cortex under-investigated.
Positive_regulation (leaving) of ALS-related in LMNs associated with motor neuron diseases and spinal cord
7) Confidence 0.04 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 0.79 Pain Relevance 0.11
The comprehensive analysis described here provides a full molecular portrait of the changes occurring in the motor cortex of SALS patients and provides new leads for the development of effective ALS therapies.
Positive_regulation (effective) of ALS in cortex associated with motor neuron diseases
8) Confidence 0.04 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 1.10 Pain Relevance 0.18
FALS – familial ALS
Positive_regulation (familial) of ALS associated with motor neuron diseases
9) Confidence 0.04 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 0.55 Pain Relevance 0
Possibly owing to earlier clinical manifestations of defects in LMNs and their easier accessibility to experimenters, however, most investigations of ALS, including previous genomics studies [2-4], focus on the spinal cord and LMNs, leaving ALS-related responses and defects of cellular maintenance in the motor cortex under-investigated.
Positive_regulation (leaving) of ALS-related in spinal cord associated with motor neuron diseases and spinal cord
10) Confidence 0.01 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 0.79 Pain Relevance 0.11

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