INT71442

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Context Info
Confidence 0.58
First Reported 1997
Last Reported 2002
Negated 0
Speculated 1
Reported most in Abstract
Documents 9
Total Number 13
Disease Relevance 6.53
Pain Relevance 2.78

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

mitochondrion (Pars2) ligase activity (Pars2) cytoplasm (Pars2)
Anatomy Link Frequency
diaphragm 1
neurons 1
neutrophil 1
Pars2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
anesthesia 12 99.92 Very High Very High Very High
Glutamate 3 98.72 Very High Very High Very High
Inflammation 8 98.60 Very High Very High Very High
ischemia 24 98.40 Very High Very High Very High
Inflammatory response 4 97.84 Very High Very High Very High
Eae 8 95.16 Very High Very High Very High
Neuropathic pain 7 93.76 High High
Sciatic nerve 2 93.64 High High
Dorsal horn neuron 3 85.44 High High
Spinal cord 4 84.64 Quite High
Disease Link Frequency Relevance Heat
Reperfusion Injury 16 99.80 Very High Very High Very High
Renal Disease 4 99.12 Very High Very High Very High
Brain Injury 4 99.12 Very High Very High Very High
INFLAMMATION 12 98.60 Very High Very High Very High
Cv Unclassified Under Development 20 98.40 Very High Very High Very High
Pressure And Volume Under Development 4 98.32 Very High Very High Very High
Drug Induced Neurotoxicity 7 98.08 Very High Very High Very High
Shock 4 97.96 Very High Very High Very High
Stress 4 97.44 Very High Very High Very High
Sepsis 8 97.28 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Therefore, we propose that PARS activation contributes to renal reperfusion injury and that PARS inhibitors may be beneficial in renal disorders associated with oxidative stress-mediated injury.
Negative_regulation (inhibitors) of PARS associated with stress, reperfusion injury, injury and renal disease
1) Confidence 0.58 Published 2000 Journal FASEB J. Section Abstract Doc Link 10744621 Disease Relevance 0.66 Pain Relevance 0.07
Inhibition of PARS activity, demonstrated by a reduction in poly(ADP-ribose) polymer formation, also reduces neutrophil recruitment and levels of nitrotyrosine, an indicator of peroxynitrite generation.
Negative_regulation (Inhibition) of PARS in neutrophil
2) Confidence 0.58 Published 2000 Journal J. Neurochem. Section Abstract Doc Link 10820212 Disease Relevance 0.55 Pain Relevance 0.30
Taken together, our results demonstrate that PARS inhibition reduces ischemic damage and local inflammation associated with reperfusion and may be of interest for the treatment of neonatal stroke.
Negative_regulation (inhibition) of PARS associated with inflammation and stroke
3) Confidence 0.51 Published 2000 Journal J. Neurochem. Section Abstract Doc Link 10820212 Disease Relevance 0.70 Pain Relevance 0.29
In our experimental study, the effects of poly(ADP-ribose) synthetase (PARS) inhibition on the diaphragmatic Ca(2+)-ATPase, malondialdehyde (MDA), and 3-nitrotyrosine (3-NT) levels and additionally histopathology of the diaphragm in lipopolysaccharide (LPS)-induced endotoxemia are investigated.Thirty-two male Wistar rats, weighing between 180-200 g were randomly divided into four groups.
Negative_regulation (inhibition) of PARS in diaphragm associated with endotoxemia
4) Confidence 0.49 Published 2002 Journal Pharmacol. Res. Section Abstract Doc Link 12208123 Disease Relevance 0.18 Pain Relevance 0
In the present study, we examined whether the inhibition of the nitric oxide (NO)-activated poly(ADP-ribose) synthetase (PARS), a nuclear enzyme critical to glutamate-induced neurotoxicity, would both reduce the incidence of dark neurons and attenuate behavioral manifestations of neuropathic pain in CCI rats.
Spec (whether) Negative_regulation (inhibition) of PARS in neurons associated with glutamate, drug induced neurotoxicity, eae and neuropathic pain
5) Confidence 0.44 Published 1997 Journal Pain Section Abstract Doc Link 9313276 Disease Relevance 0.89 Pain Relevance 0.96
Both renal damage and PARS activation were attenuated by administration of PARS inhibitors during reperfusion.
Negative_regulation (inhibitors) of PARS
6) Confidence 0.43 Published 2000 Journal FASEB J. Section Abstract Doc Link 10744621 Disease Relevance 0.33 Pain Relevance 0.10
The aim of this study was to investigate whether PARS inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo.
Negative_regulation (inhibitors) of PARS associated with reperfusion injury and ischemia
7) Confidence 0.43 Published 2000 Journal FASEB J. Section Abstract Doc Link 10744621 Disease Relevance 0.71 Pain Relevance 0.17
The PARS inhibitors also significantly increased GFR and reduced FE(Na), suggesting the recovery of both glomerular and tubular function, respectively, with a more pronounced recovery of tubular function.
Negative_regulation (inhibitors) of PARS
8) Confidence 0.43 Published 2000 Journal FASEB J. Section Abstract Doc Link 10744621 Disease Relevance 0.58 Pain Relevance 0.15
We examined the effect of inhibiting PARS on the (a) degree of cerebral injury, (b) process of inflammatory responses, and (c) functional outcomes in a neonatal rat model of focal ischemia.
Negative_regulation (inhibiting) of PARS associated with inflammatory response, ischemia and brain injury
9) Confidence 0.43 Published 2000 Journal J. Neurochem. Section Abstract Doc Link 10820212 Disease Relevance 0.63 Pain Relevance 0.25
We demonstrate that administration of 3-aminobenzamide, a PARS inhibitor, leads to a significant reduction of infarct volume: 63 +/- 2 (untreated) versus 28 +/- 4 mm(3) (treated).
Negative_regulation (inhibitor) of PARS
10) Confidence 0.43 Published 2000 Journal J. Neurochem. Section Abstract Doc Link 10820212 Disease Relevance 0.61 Pain Relevance 0.29
The first group (control; n=8) received saline solution and the second (LPS group; n=8) 10 mgkg(-1) LPS i.p. 3-Aminobenzamide (3-AB) as a PARS inhibitor; was given to the third group (C+3-AB, n=8) 20 min before administration of saline solution while the fourth group (LPS+3-AB, n=8) received 3-AB 20 min before LPS injection.
Negative_regulation (inhibitor) of PARS
11) Confidence 0.36 Published 2002 Journal Pharmacol. Res. Section Abstract Doc Link 12208123 Disease Relevance 0.16 Pain Relevance 0.08
PARS inhibitors should further be investigated as a new thearapetic alternative in sepsis treatment.
Negative_regulation (inhibitors) of PARS associated with sepsis
12) Confidence 0.31 Published 2002 Journal Pharmacol. Res. Section Abstract Doc Link 12208123 Disease Relevance 0.28 Pain Relevance 0.07
PARS inhibition with 3-AB prevented not only lipid peroxidation but also the decrease of Ca(2+)-ATPase activity in endotoxemia.
Negative_regulation (inhibition) of PARS associated with endotoxemia
13) Confidence 0.31 Published 2002 Journal Pharmacol. Res. Section Abstract Doc Link 12208123 Disease Relevance 0.25 Pain Relevance 0.08

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