INT22548

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Context Info
Confidence 0.70
First Reported 1984
Last Reported 2011
Negated 25
Speculated 10
Reported most in Abstract
Documents 483
Total Number 493
Disease Relevance 258.78
Pain Relevance 213.07

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

cytosol (Casp3) peptidase activity (Casp3) mitochondrion (Casp3)
nucleolus (Casp3) nucleus (Casp3) intracellular (Casp3)
Anatomy Link Frequency
neuronal 20
apoptotic cell 17
neurons 17
cleavage 13
NAc 12
Casp3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Morphine 1202 100.00 Very High Very High Very High
Spinal cord 261 100.00 Very High Very High Very High
cocaine 202 100.00 Very High Very High Very High
Abeta 24 100.00 Very High Very High Very High
Glutamate 6368 99.98 Very High Very High Very High
ischemia 851 99.98 Very High Very High Very High
Hippocampus 366 99.98 Very High Very High Very High
withdrawal 222 99.98 Very High Very High Very High
Nicotine 105 99.98 Very High Very High Very High
amygdala 79 99.98 Very High Very High Very High
Disease Link Frequency Relevance Heat
Apoptosis 7205 100.00 Very High Very High Very High
Diabetes Mellitus 1123 100.00 Very High Very High Very High
Cancer 944 100.00 Very High Very High Very High
Necrosis 339 100.00 Very High Very High Very High
Cognitive Disorder 107 100.00 Very High Very High Very High
Anxiety Disorder 94 100.00 Very High Very High Very High
Adhesions 73 100.00 Very High Very High Very High
Sepsis 67 100.00 Very High Very High Very High
Peptic Ulcer 4 100.00 Very High Very High Very High
Hypoxia 801 99.98 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Western blot analysis showed that AA significantly suppressed 150/145 kDa subunits of alpha-fodrin breakdown products (FBDP) in cortex, striatum, thalamus and hippocampus at 24 and 48 h post-HI, and also 120 kDa subunit of FBDP in all examined regions except for thalamus, which indicated that AA injection inhibited both calpain and caspase-3 activation.
Positive_regulation (activation) of caspase-3 in thalamus associated with hippocampus and thalamus
1) Confidence 0.70 Published 2009 Journal Brain Dev. Section Abstract Doc Link 18682317 Disease Relevance 0.58 Pain Relevance 0.36
Apoptosis was further confirmed by increased caspase 3 protein levels and positive terminal deoxyuridine nick end labeling histochemistry.
Positive_regulation (increased) of caspase 3 protein associated with apoptosis
2) Confidence 0.70 Published 2004 Journal Pain Section Abstract Doc Link 15494192 Disease Relevance 2.09 Pain Relevance 1.08
As compared to controls, DMI increased the resistance-to-extinction of CPP, attenuated immobility, and increased wall climbing behavior.
Positive_regulation (increased) of CPP
3) Confidence 0.69 Published 2007 Journal Neurobiol Learn Mem Section Abstract Doc Link 17223365 Disease Relevance 0.38 Pain Relevance 0.35
These results show that a morphine-induced CPP is persistent over time and can be reinstated by morphine after extinction.
Positive_regulation (induced) of CPP associated with morphine
4) Confidence 0.69 Published 2002 Journal Behav. Brain Res. Section Abstract Doc Link 12429400 Disease Relevance 0 Pain Relevance 0.61
Lidocaine reduced cytochrome c release and caspase-3 activation in the penumbra at 4 h and diminished DNA fragmentation in the penumbra at 24 h.
Positive_regulation (activation) of caspase-3 associated with lidocaine
5) Confidence 0.69 Published 2004 Journal Neuroscience Section Abstract Doc Link 15099683 Disease Relevance 0.76 Pain Relevance 1.00
Apoptotic changes were evaluated by immunohistochemistry for cytochrome c release and caspase-3 activation and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) for DNA fragmentation.
Positive_regulation (activation) of caspase-3 associated with apoptosis
6) Confidence 0.69 Published 2004 Journal Neuroscience Section Abstract Doc Link 15099683 Disease Relevance 0.69 Pain Relevance 0.84
Cytochrome c release and caspase-3 activation were detected at 4 and 24 h after ischemia and DNA fragmentation was detected at 24 h.
Positive_regulation (activation) of caspase-3 associated with ischemia
7) Confidence 0.69 Published 2004 Journal Neuroscience Section Abstract Doc Link 15099683 Disease Relevance 0.73 Pain Relevance 0.91
During the retention of morphine-induced CPP, a morphine-dose- and time-dependent elevation of DA and its metabolites was observed in the NAc.
Positive_regulation (induced) of CPP in NAc associated with nucleus accumbens, dopamine and morphine
8) Confidence 0.69 Published 2009 Journal Behav. Brain Res. Section Abstract Doc Link 19539657 Disease Relevance 0 Pain Relevance 1.53
However, in adapted mucosa after aspirin, activated caspase 3 and the number of apoptotic cells had returned to basal levels.
Positive_regulation (activated) of caspase 3 in apoptotic cells associated with aspirin and apoptosis
9) Confidence 0.68 Published 2000 Journal Am. J. Physiol. Gastrointest. Liver Physiol. Section Abstract Doc Link 10859212 Disease Relevance 0.75 Pain Relevance 0.33
Secondly, there is a path where receptors form groups in a death-receptor path, forming death-inducing signaling complex and finally activating the Casp8 and Casp3 (caspase-3) genes [23].
Positive_regulation (activating) of caspase-3 associated with death
10) Confidence 0.67 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2872860 Disease Relevance 1.11 Pain Relevance 0.08
These findings suggest that morphine exposure during the first embryonic days may enhance the susceptibility of neuroblasts to apoptosis by upregulating the ratio of Bax to Bcl-2 protein expression and increasing downstream caspase-3 activity.
Positive_regulation (increasing) of caspase-3 in neuroblasts associated with apoptosis and morphine
11) Confidence 0.67 Published 2010 Journal J. Mol. Neurosci. Section Abstract Doc Link 19936637 Disease Relevance 0.10 Pain Relevance 0.64
Our experimental evidence suggests that APAP-induced nephro-toxicity is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome C release.
Positive_regulation (activation) of caspase-3 associated with toxicity and paracetamol
12) Confidence 0.67 Published 2010 Journal Toxicology Section Abstract Doc Link 19922764 Disease Relevance 0.62 Pain Relevance 0.62
In parallel, superoxide and hydrogen peroxide levels in mitochondria were decreased, cytochrome c release into the cytosol was reduced at 1 h after reperfusion, and activation of caspase-3 and -9 was subsequently attenuated.
Positive_regulation (activation) of caspase-3
13) Confidence 0.67 Published 2009 Journal J. Neurotrauma Section Abstract Doc Link 19196076 Disease Relevance 0.91 Pain Relevance 0.74
These results showed an increased ratio of Bax/Bcl-2 and activated caspase-3 in hippocampus and dorsal lumbar spinal cord of animals treated with pain and IMO stress; these effects were reduced in ADX animals.
Positive_regulation (increased) of caspase-3 in spinal cord associated with stress, pain, hippocampus and spinal cord
14) Confidence 0.67 Published 2008 Journal Neuroscience Section Abstract Doc Link 18822355 Disease Relevance 1.76 Pain Relevance 1.06
High glucose also causes a 2 fold increase in Bax expression, which induced cytochrome C release which in turn stimulates apoptosis activating factor, caspase 9 and caspase 3 [41].
Positive_regulation (activating) of caspase 3 associated with apoptosis
15) Confidence 0.67 Published 2008 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC2570581 Disease Relevance 1.20 Pain Relevance 0.03
Brain histopathology showed myelin disintegration and caspase-3 activation in glial cells, whereas, grey matter changes were sparse.
Positive_regulation (activation) of caspase-3 in glial cells
16) Confidence 0.67 Published 2007 Journal Neurotoxicology Section Abstract Doc Link 16930716 Disease Relevance 0.69 Pain Relevance 0.08
In a model of peripheral neuropathy, obtained by the loose ligation of the rat sciatic nerve (CCI), we describe a nerve apoptotic state that encompasses the release of cytochrome C in the cytosol, the activation of caspase 3, and the fragmentation of the genome.
Positive_regulation (activation) of caspase 3 in CCI associated with sciatic nerve, peripheral neuropathy and apoptosis
17) Confidence 0.66 Published 2007 Journal Eur. J. Neurosci. Section Abstract Doc Link 17714181 Disease Relevance 1.48 Pain Relevance 0.55
Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury.
Positive_regulation (Activation) of CPP32-like in neuronal associated with anesthesia, neurodegenerative disease and brain injury
18) Confidence 0.66 Published 1997 Journal J. Neurosci. Section Title Doc Link 9295387 Disease Relevance 0.74 Pain Relevance 0.24
Caspase-3 mRNA levels, estimated by semiquantitative RT-PCR, were elevated fivefold in ipsilateral cortex and twofold in hippocampus by 24 hr after TBI.
Positive_regulation (elevated) of Caspase-3 mRNA in hippocampus associated with hippocampus and brain injury
19) Confidence 0.66 Published 1997 Journal J. Neurosci. Section Abstract Doc Link 9295387 Disease Relevance 0.84 Pain Relevance 0.29
Reducing Na(+) entry with the VSSC blocker, tetrodotoxin (TTX), attenuated apoptotic neuronal death via a reduction in caspase-3 activation.
Positive_regulation (activation) of caspase-3 in neuronal associated with tetrodotoxin, apoptosis and death
20) Confidence 0.66 Published 2004 Journal Neuroscience Section Abstract Doc Link 15145071 Disease Relevance 1.73 Pain Relevance 0.38

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