INT94863

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Context Info
Confidence 0.65
First Reported 2001
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 27
Total Number 27
Disease Relevance 10.21
Pain Relevance 4.35

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

signal transduction (Litaf) extracellular region (Litaf) Golgi apparatus (Litaf)
signal transducer activity (Litaf)
Anatomy Link Frequency
microglia 8
retina 2
macrophage 1
hepatocytes 1
alveolar macrophages 1
Litaf (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammation 192 100.00 Very High Very High Very High
cytokine 74 100.00 Very High Very High Very High
Inflammatory mediators 52 99.84 Very High Very High Very High
COX-2 inhibitor 16 99.52 Very High Very High Very High
cINOD 6 99.38 Very High Very High Very High
cerebral cortex 1 97.36 Very High Very High Very High
Central nervous system 36 97.24 Very High Very High Very High
Neurotransmitter 13 95.44 Very High Very High Very High
Locus ceruleus 25 93.16 High High
anesthesia 14 93.08 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 257 100.00 Very High Very High Very High
Cancer 147 100.00 Very High Very High Very High
Necrosis 31 100.00 Very High Very High Very High
Death 33 99.76 Very High Very High Very High
Stroke 73 97.56 Very High Very High Very High
Adult Respiratory Distress Syndrome 68 95.96 Very High Very High Very High
Disease 124 94.88 High High
Neurodegenerative Disease 23 93.64 High High
Schizophrenia 220 89.20 High High
Retina Disease 6 87.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The synthesis pathways for HETEs and EETs are complex exhibiting multiple routes leading to the same compound.
Gene_expression (synthesis) of EET
1) Confidence 0.65 Published 2010 Journal Cancer Metastasis Rev Section Body Doc Link PMC2962793 Disease Relevance 0 Pain Relevance 0.03
However, estrogen receptors and EET-1 are both expressed at significant levels in male retinas [29].
Gene_expression (expressed) of EET-1 in retinas
2) Confidence 0.59 Published 2007 Journal Molecular Vision Section Body Doc Link PMC2185481 Disease Relevance 0.85 Pain Relevance 0.34
However, we also determined that retinal EET-1 expression is not estrogen responsive (data not shown), suggesting that in the CNS and retina, estrogen does not modulate the inflammatory roles of EET-1 following infarct.
Gene_expression (expression) of EET-1 in retina associated with inflammation and central nervous system
3) Confidence 0.59 Published 2007 Journal Molecular Vision Section Body Doc Link PMC2185481 Disease Relevance 1.03 Pain Relevance 0.34
rAION induces an early increase in estrogen expressed transcript-1 (EET-1), but EET-1 expression is not affected by systemic estrogen pretreatment.
Gene_expression (expression) of EET-1
4) Confidence 0.40 Published 2007 Journal Molecular Vision Section Abstract Doc Link PMC2185481 Disease Relevance 0.78 Pain Relevance 0.10
A similar lack of inhibition of LPS-induced cytokine expression by another COX-2 inhibitor, NS-398, was observed in vitro.
Gene_expression (expression) of LPS-induced associated with cox-2 inhibitor and cytokine
5) Confidence 0.15 Published 2009 Journal Int. J. Androl. Section Abstract Doc Link 18522674 Disease Relevance 0.60 Pain Relevance 0.30
However, celecoxib had no effect on COX-2 protein levels or LPS-induced expression of the inflammatory mediators interleukin-1beta, tumour necrosis factor-alpha or inducible nitric-oxide synthase.
Gene_expression (expression) of LPS-induced associated with necrosis, inflammatory mediators and cancer
6) Confidence 0.15 Published 2009 Journal Int. J. Androl. Section Abstract Doc Link 18522674 Disease Relevance 0.60 Pain Relevance 0.28
The results of semi-quantitative RT-PCR demonstrated that PPF pretreatment significantly suppressed the LPS-induced toll-like receptor (TLR)-4, CD14, tumor necrosis factor (TNF)-alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF) gene expression.
Gene_expression (expression) of LPS-induced in macrophage associated with necrosis and cancer
7) Confidence 0.12 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 18387647 Disease Relevance 0.38 Pain Relevance 0.20
In short, LC is a NSAID with inhibitory action on the expression of LPS-induced NOS, effect that was not seen with INDO in our experimental conditions.
Gene_expression (expression) of LPS-induced associated with cinod
8) Confidence 0.12 Published 2001 Journal Nitric Oxide Section Abstract Doc Link 11292364 Disease Relevance 0.05 Pain Relevance 0.15
On the other hand, exogenous PGE2 protects neurons from LPS-induced cell death by reduction of NO and reactive oxygen species [53].
Gene_expression (protects) of LPS-induced in neurons associated with death
9) Confidence 0.09 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819253 Disease Relevance 0.67 Pain Relevance 0.25
Propofol pretreatment attenuates LPS-induced granulocyte-macrophage colony-stimulating factor production in cultured hepatocytes by suppressing MAPK/ERK activity and NF-kappaB translocation.
Gene_expression (production) of LPS-induced in hepatocytes associated with cytokine
10) Confidence 0.08 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Title Doc Link 18387647 Disease Relevance 0.28 Pain Relevance 0.31
Pretreatment with 100 microM PPF for 24 h prior to LPS stimulation was performed to investigate the modulatory effect on LPS-induced inflammatory gene production.
Gene_expression (production) of LPS-induced associated with inflammation
11) Confidence 0.08 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 18387647 Disease Relevance 0.36 Pain Relevance 0.22
An immunosuppressive role has been suggested for NE in vitro since it attenuates LPS-induced microglial production of tumour necrosis factor (TNF)?
Gene_expression (production) of LPS-induced associated with necrosis and cancer
12) Confidence 0.08 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819253 Disease Relevance 0.62 Pain Relevance 0.24
NE enhances LPS-induced production of COX-2 mRNA and protein in primary rat microglial cells
Gene_expression (production) of LPS-induced in microglial cells
13) Confidence 0.08 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819253 Disease Relevance 0 Pain Relevance 0
Norepinephrine enhances the LPS-induced expression of COX-2 and secretion of PGE2 in primary rat microglia

Background

Gene_expression (expression) of LPS-induced in microglia
14) Confidence 0.08 Published 2010 Journal J Neuroinflammation Section Title Doc Link PMC2819253 Disease Relevance 0.15 Pain Relevance 0.32
Our study shows that NE increases LPS-induced COX-2 expression and PGE2 secretion by primary rat neonatal microglia in vitro.
Gene_expression (expression) of LPS-induced in microglia
15) Confidence 0.08 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819253 Disease Relevance 0.68 Pain Relevance 0.46
The ability of resveratrol to reduce PGE2 production comes from the modulation of multiple events in the COX/PGE2 pathway: 1) resveratrol is a potent inactivator of the peroxidase reaction of COX-1 [43], and thus is considered a relatively selective inhibitor of this isozyme; 2) resveratrol significantly diminished LPS-induced expression of mPGES-1 (Figs. 3 and 4), the most important terminal synthase responsible for PGE2 synthesis in activated microglia [42]; and 3) production of 8-iso-PGF2?
Gene_expression (expression) of LPS-induced in microglia
16) Confidence 0.06 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2100038 Disease Relevance 0.38 Pain Relevance 0.09
This suggests that LPS-induced microglial expression of mPGES-1 proceeds through molecular mechanisms which are different from the ones involved in COX-2 induction, providing for the first time evidence that the expression of mPGES-1 and COX-2 are not always coupled as suggested by other authors [75,76].
Gene_expression (expression) of LPS-induced
17) Confidence 0.06 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2100038 Disease Relevance 0 Pain Relevance 0
Since previous studies have shown the ability of antioxidants to modify gene expression of pro-inflammatory mediators in activated microglia [31,45], we studied the effects of Trolox C on LPS-induced COX-2 and mPGES-1 expression.
Gene_expression (expression) of LPS-induced in microglia associated with inflammatory mediators
18) Confidence 0.06 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2100038 Disease Relevance 0.10 Pain Relevance 0.05
It is important to emphasize that resveratrol did not modified basal COX-1 or LPS-induced COX-2 expression in microglia.
Gene_expression (expression) of LPS-induced in microglia
19) Confidence 0.06 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2100038 Disease Relevance 0 Pain Relevance 0
Results from control experiments using other highly selective COX-1 inhibitors (SC-560 and VAS), in addition to resveratrol, indicate that COX-1 isoform is not only important in LPS-induced PGE2 synthesis, but it is also a key source of free radicals in microglia.
Gene_expression (synthesis) of LPS-induced in microglia
20) Confidence 0.06 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2100038 Disease Relevance 0.21 Pain Relevance 0.03

General Comments

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