INT158837

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Context Info
Confidence 0.37
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 6
Disease Relevance 4.69
Pain Relevance 0.44

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

mitochondrion (POLG) cell death (POLG) aging (POLG)
DNA binding (POLG) nucleotidyltransferase activity (POLG) DNA metabolic process (POLG)
POLG (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 2 99.68 Very High Very High Very High
imagery 14 95.92 Very High Very High Very High
peripheral neuropathy 3 95.60 Very High Very High Very High
Migraine 2 71.52 Quite High
headache 7 70.40 Quite High
Neuropathic pain 3 46.32 Quite Low
cerebral cortex 1 25.00 Low Low
Thalamus 1 25.00 Low Low
depression 6 5.00 Very Low Very Low Very Low
Osteoarthritis 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Myalgia 2 99.68 Very High Very High Very High
Disease 17 99.28 Very High Very High Very High
Muscle Weakness 2 99.04 Very High Very High Very High
Fatigue 2 98.36 Very High Very High Very High
Premature Ovarian Failure 2 98.00 Very High Very High Very High
Dementia 36 97.44 Very High Very High Very High
Encephalopathy 3 97.12 Very High Very High Very High
Deafness 3 96.92 Very High Very High Very High
Diabetes Mellitus 18 96.52 Very High Very High Very High
Mitochondrial Disorders 15 96.52 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We suggest that POLG1 p.R722H mutation causes a late-onset neurological phenotype as a homozygous state, whereas the onset of the disease can be earlier in patients with compound heterozygosity for POLG1 p.R722H and other pathogenic POLG1 mutations.
POLG1 Binding (heterozygosity) of associated with disease
1) Confidence 0.37 Published 2010 Journal BMC Neurol Section Body Doc Link PMC2873323 Disease Relevance 0.37 Pain Relevance 0
We suggest that POLG1 p.R722H mutation causes a late-onset neurological phenotype as a homozygous state, whereas the onset of the disease can be earlier in patients with compound heterozygosity for POLG1 p.R722H and other pathogenic POLG1 mutations.
POLG1 Binding (heterozygosity) of associated with disease
2) Confidence 0.37 Published 2010 Journal BMC Neurol Section Body Doc Link PMC2873323 Disease Relevance 0.37 Pain Relevance 0
Our patient A1 manifested with all these typical features associated with POLG1 mutations.
POLG1 Binding (associated) of
3) Confidence 0.37 Published 2010 Journal BMC Neurol Section Body Doc Link PMC2873323 Disease Relevance 1.53 Pain Relevance 0.05
Polg-1 deficiency causes severe mtDNA depletion, but not a developmental arrest
Polg-1 Binding (deficiency) of
4) Confidence 0.36 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.28 Pain Relevance 0.09
POLG is today recognized as a major human disease gene, possibly accounting for up to 25% of all patients with mitochondrial diseases (3,4).
POLG Binding (recognized) of associated with mitochondrial disorders and disease
5) Confidence 0.30 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 1.23 Pain Relevance 0.10
The latter clinical phenotypes resemble those associated with recessive POLG1 mutations.
POLG1 Binding (associated) of
6) Confidence 0.17 Published 2009 Journal Brain Section Abstract Doc Link 19304794 Disease Relevance 0.91 Pain Relevance 0.20

General Comments

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