INT29845

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Context Info
Confidence 0.62
First Reported 1988
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 11
Total Number 12
Disease Relevance 3.69
Pain Relevance 6.63

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

mitochondrion (Sds) lyase activity (Sds) cellular amino acid metabolic process (Sds)
cytoplasm (Sds)
Anatomy Link Frequency
plasma 4
neuronal 1
liver 1
neurons 1
spinal cord 1
Sds (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 10 100.00 Very High Very High Very High
Paracetamol 62 99.82 Very High Very High Very High
Glutamate 3 99.76 Very High Very High Very High
primary afferent fibers 2 99.58 Very High Very High Very High
Spinal cord 50 99.04 Very High Very High Very High
alcohol 10 99.00 Very High Very High Very High
Adelta 2 98.96 Very High Very High Very High
c fibre 4 98.36 Very High Very High Very High
nMDA receptor antagonist 2 97.96 Very High Very High Very High
Neuronal excitability 2 96.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hepatotoxicity 13 99.66 Very High Very High Very High
Necrosis 8 99.32 Very High Very High Very High
Spasticity 2 97.72 Very High Very High Very High
Depression 8 94.52 High High
Nephrotoxicity 6 94.24 High High
Toxicity 15 93.68 High High
Injury 4 93.64 High High
Nociception 10 64.04 Quite High
Pain 6 43.96 Quite Low
Disseminated Intravascular Coagulation 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
APAP treatment resulted in elevation of SDH activity and BUN to 2,490 U/ml and 47 mg/dl, respectively.
Positive_regulation (elevation) of SDH associated with paracetamol
1) Confidence 0.62 Published 2000 Journal Toxicol Pathol Section Abstract Doc Link 11026606 Disease Relevance 0.47 Pain Relevance 1.12
Either simultaneous or 2 h delayed treatment with 5beta-S significantly decreased the APAP-induced SDH increase while only the simultaneous pretreatment prevented the BUN elevation. 5beta-S alone did not increase liver glutathione content.
Positive_regulation (increase) of SDH in liver associated with paracetamol
2) Confidence 0.50 Published 2004 Journal Toxicology Section Abstract Doc Link 15363587 Disease Relevance 0.24 Pain Relevance 1.00
CFB pretreatment also diminished elevation in plasma SDH activity produced by CHCl3 in CD-1 mice, while BUN was significantly elevated in both groups, indicating that CFB did not protect against CHCl3-induced nephrotoxicity.
Positive_regulation (elevation) of SDH in plasma associated with nephrotoxicity
3) Confidence 0.46 Published 1998 Journal Toxicology Section Abstract Doc Link 9699788 Disease Relevance 0.38 Pain Relevance 0.20
Challenge with BrB significantly elevated plasma SDH activity in C57Bl6J mice.
Positive_regulation (elevated) of SDH in plasma
4) Confidence 0.43 Published 1998 Journal Toxicology Section Abstract Doc Link 9699788 Disease Relevance 0.39 Pain Relevance 0.16
As in the present study, a greater proportion of SDH neurons received GABAAR- versus GlyR-mediated inhibition.
Positive_regulation (proportion) of SDH in neurons
5) Confidence 0.36 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0.10 Pain Relevance 0.16
This analysis showed that GABAARs underlying the mIPSCs had an identical unitary conductance in the SDH and DDH (22.7 ± 1.7 vs. 22.4 ± 2.0 pS, n = 8 and n = 11, respectively).
Positive_regulation (conductance) of SDH
6) Confidence 0.32 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0 Pain Relevance 0.10
In mice subjected to glutathione depletion by pretreatment with phorone (diisopropylidene acetone, 200 mg/kg i.p. in 10 ml/kg olive oil) paracetamol (acetaminophen, 300 mg/kg p.o. in 10 ml/kg tylose 2 h later) led to a marked hepatotoxicity as evidenced by increased plasma activities of the liver-specific enzymes sorbitol dehydrogenase (SDH) and glutamate-pyruvate-transaminase (GPT) 3 and 24 h after treatment.
Positive_regulation (increased) of SDH in plasma associated with glutamate, paracetamol and hepatotoxicity
7) Confidence 0.26 Published 1988 Journal J Appl Toxicol Section Abstract Doc Link 2846674 Disease Relevance 0.35 Pain Relevance 0.38
YGW also decreased the elevated activities of ALT and SDH and reduced the necrosis induced by AA and CCl4.
Positive_regulation (elevated) of SDH associated with necrosis and paracetamol
8) Confidence 0.24 Published 2000 Journal Am. J. Chin. Med. Section Abstract Doc Link 10999434 Disease Relevance 0.27 Pain Relevance 0.67
YGW dramatically abolished the elevated activities of alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) and reduced the necrosis induced by AlOH.
Positive_regulation (elevated) of SDH associated with necrosis and alcohol
9) Confidence 0.24 Published 2000 Journal Am. J. Chin. Med. Section Abstract Doc Link 10999434 Disease Relevance 0.26 Pain Relevance 0.68
At 24 h after APAP, hepatotoxicity was evident in control mice by elevated plasma sorbitol dehydrogenase activity (SDH) and histologic evidence of hepatic degeneration and necrosis.
Positive_regulation (elevated) of SDH in plasma associated with necrosis, paracetamol and hepatotoxicity
10) Confidence 0.24 Published 1999 Journal J. Toxicol. Environ. Health Part A Section Abstract Doc Link 10522648 Disease Relevance 0.52 Pain Relevance 0.72
In the absence of GluR2, high-frequency stimulation (HFS) of small-diameter primary afferent fibers induced LTP that is enhanced and non-saturating in the SDH at both primary afferent Adelta- and/or C-fibers monosynaptic and polysynaptic pathways, whereas neuronal excitability and paired-pulse depression were normal.
Positive_regulation (enhanced) of SDH in neuronal associated with c fibre, depression, neuronal excitability, adelta, primary afferent fibers and long-term potentiation
11) Confidence 0.21 Published 2008 Journal Pain Section Abstract Doc Link 17826911 Disease Relevance 0.39 Pain Relevance 0.75
The LTP could be induced in the presence of the NMDA receptor antagonist d-AP5, and L-type Ca(2+) channel blockers, suggesting that Ca(2+)-permeable-AMPARs are sufficient to induce LTP in the SDH neurons of adult mouse spinal cord.
Positive_regulation (induce) of SDH in spinal cord associated with nmda receptor antagonist, long-term potentiation and spinal cord
12) Confidence 0.21 Published 2008 Journal Pain Section Abstract Doc Link 17826911 Disease Relevance 0.32 Pain Relevance 0.69

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