INT15990

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Context Info
Confidence 0.31
First Reported 1989
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 8.53
Pain Relevance 1.37

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

mitochondrion (Gfm1) intracellular (Gfm1) translation (Gfm1)
GTPase activity (Gfm1)
Anatomy Link Frequency
frontal cortex 1
hippocampus 1
respiratory 1
Gfm1 (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 10 99.06 Very High Very High Very High
Hippocampus 8 96.80 Very High Very High Very High
ischemia 11 94.60 High High
tolerance 1 94.12 High High
Substantia nigra 17 92.36 High High
Inflammation 75 84.24 Quite High
Inflammatory response 26 79.52 Quite High
alcohol 37 60.16 Quite High
midbrain 26 55.04 Quite High
Glutamate 19 34.48 Quite Low
Disease Link Frequency Relevance Heat
Parkinson's Disease 114 100.00 Very High Very High Very High
Neurodegenerative Disease 34 99.92 Very High Very High Very High
Death 131 99.90 Very High Very High Very High
Stress 49 98.96 Very High Very High Very High
Sprains And Strains 148 98.76 Very High Very High Very High
Hypoxia 49 98.68 Very High Very High Very High
Apoptosis 136 98.44 Very High Very High Very High
Aging 93 98.32 Very High Very High Very High
Syndrome 17 97.92 Very High Very High Very High
Urological Neuroanatomy 24 96.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition, pretreatment with buthionine sulfoximine increased the amount of 3'-hydroxyacetanilide bound to mitochondrial proteins.
mitochondrial Binding (bound) of
1) Confidence 0.31 Published 1991 Journal Chem. Res. Toxicol. Section Abstract Doc Link 1782350 Disease Relevance 0.32 Pain Relevance 0.16
However, subcellular fractionation techniques revealed that the acetaminophen treatment produced greater levels of covalent binding to mitochondrial proteins than 3'-hydroxyacetanilide.
mitochondrial Binding (binding) of associated with paracetamol
2) Confidence 0.22 Published 1989 Journal J. Biol. Chem. Section Abstract Doc Link 2524496 Disease Relevance 0.17 Pain Relevance 0.59
The fact that the ADH transgene augmented the ethanol-induced cytosolic accumulation of pro-caspase-9 and cytochrome C further substantiated the critical role of acetaldehyde in ethanol-induced mitochondrial damage, which is consistent with the ADH-accentuated mitochondrial O2•?
mitochondrial Binding (damage) of
3) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2807457 Disease Relevance 1.23 Pain Relevance 0.06
To evaluate mitochondrial integrity and function, mitochondrial O2•?
mitochondrial Binding (integrity) of
4) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2807457 Disease Relevance 0.06 Pain Relevance 0.06
Interestingly, the interaction of the signalling molecule NO with the mitochondrial respiratory chain has been implicated as an important physiological indicator for how cells respond to hypoxic stress [19,40].
mitochondrial Neg (NO) Binding (interaction) of in respiratory associated with stress and hypoxia
5) Confidence 0.01 Published 2008 Journal Biochemical Journal Section Body Doc Link PMC2637578 Disease Relevance 0.93 Pain Relevance 0.09
Parkin has also been recognized as a mitochondrial protection factor.
mitochondrial Binding (recognized) of
6) Confidence 0.01 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.57 Pain Relevance 0.03
Mitochondrial dysfunction has been recognized as a more marked phenomenon, in terms of complex I syndrome, in brain areas as hippocampus and frontal cortex in rats, human cortex in Parkinson's disease and dementia with Lewy bodies, and substantia nigra in Parkinson disease.
Mitochondrial Binding (recognized) of in frontal cortex associated with parkinson's disease, dementia, syndrome, substantia nigra, urological neuroanatomy, hippocampus and disease
7) Confidence 0.00 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2947925 Disease Relevance 1.31 Pain Relevance 0.09
However, induction of cell death via mitochondrial association was specific only to the PB1-F2 protein of the laboratory strain of PR8 in these studies and is not a general property of all PB1-F2 proteins.
mitochondrial Binding (association) of associated with sprains and strains and death
8) Confidence 0.00 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2908617 Disease Relevance 1.31 Pain Relevance 0.11
We show here that the ability to cause cell death through PB1-F2 mediated mitochondrial interactions is specific to the laboratory strain A/Puerto Rico/8/34 (H1N1; PR8) among the viruses studied, arguing this function is not a likely contributor to pathogenicity in humans with most epidemiologically relevant strains.
mitochondrial Binding (interactions) of associated with sprains and strains and death
9) Confidence 0.00 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2908617 Disease Relevance 1.33 Pain Relevance 0.08
Mitochondrial dysfunction has been recognized as a more marked phenomenon, in terms of complex I syndrome, in brain areas as hippocampus and frontal cortex in rats, human cortex in Parkinson's disease and dementia with Lewy bodies, and substantia nigra in Parkinson disease.
Mitochondrial Binding (recognized) of in hippocampus associated with parkinson's disease, dementia, syndrome, substantia nigra, urological neuroanatomy, hippocampus and disease
10) Confidence 0.00 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2947925 Disease Relevance 1.31 Pain Relevance 0.09

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