INT151122

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Context Info
Confidence 0.35
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 8
Disease Relevance 3.58
Pain Relevance 0.92

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
lung 2
microglia 2
hepatocytes 1
Litaf (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammatory mediators 28 99.40 Very High Very High Very High
cytokine 33 97.68 Very High Very High Very High
Inflammation 67 96.72 Very High Very High Very High
metalloproteinase 97 89.12 High High
Neurotransmitter 4 84.56 Quite High
Catecholamine 4 82.48 Quite High
Inflammatory stimuli 3 77.36 Quite High
ischemia 26 76.60 Quite High
Central nervous system 12 76.24 Quite High
Inflammatory response 5 73.44 Quite High
Disease Link Frequency Relevance Heat
Adult Respiratory Distress Syndrome 51 99.96 Very High Very High Very High
Lung Injury 39 99.96 Very High Very High Very High
INFLAMMATION 96 99.40 Very High Very High Very High
Cancer 12 98.96 Very High Very High Very High
Necrosis 12 98.68 Very High Very High Very High
Pneumonia 9 96.72 Very High Very High Very High
Pulmonary Disease 6 90.52 High High
Death 9 85.52 High High
Nonarteritic Anterior Ischaemic Optic Neuropathy 12 82.92 Quite High
Body Weight 15 82.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
rAION induces an early increase in estrogen expressed transcript-1 (EET-1), but EET-1 expression is not affected by systemic estrogen pretreatment.
Positive_regulation (increase) of EET-1
1) Confidence 0.35 Published 2007 Journal Molecular Vision Section Abstract Doc Link PMC2185481 Disease Relevance 0.79 Pain Relevance 0.11
We show here that NE dose-dependently enhanced LPS-induced COX-2 protein levels in primary rat microglia (Fig. 1A).
Positive_regulation (induced) of LPS-induced in microglia
2) Confidence 0.07 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819253 Disease Relevance 0 Pain Relevance 0
Moreover, addition of PD98059, a MAPK kinase inhibitor, significantly suppressed the LPS-induced NF-kappaB nuclear translocation and GM-CSF production, suggesting that the PPF-attenuated GM-CSF production in hepatocytes may be attributed to its suppressive effect on MAPK/ERK signaling pathway.
Positive_regulation (induced) of LPS-induced in hepatocytes
3) Confidence 0.06 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 18387647 Disease Relevance 0.27 Pain Relevance 0.12
An immunosuppressive role has been suggested for NE in vitro since it attenuates LPS-induced microglial production of tumour necrosis factor (TNF)?
Positive_regulation (induced) of LPS-induced associated with necrosis and cancer
4) Confidence 0.06 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819253 Disease Relevance 0.62 Pain Relevance 0.24
Resveratrol effects on mPGES-1 expression seem to be independent on its ability to reduce COX activity/PGE2 formation since other COX inhibitors were unable to modify LPS-induced mPGES-1 upregulation in microglial cells despite their potent inhibitory effects on PGE2 production (Figs. 6 and 7).
Positive_regulation (upregulation) of LPS-induced in microglial cells
5) Confidence 0.06 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2100038 Disease Relevance 0 Pain Relevance 0
However, the functions of c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) in LPS-induced lung injury remain unclear.
Positive_regulation (functions) of LPS-induced in lung associated with lung injury
6) Confidence 0.03 Published 2004 Journal Respir Res Section Body Doc Link PMC538282 Disease Relevance 1.30 Pain Relevance 0.36
In addition, these MAP kinase inhibitors substantially reduced LPS-induced production of inflammatory mediators, such as CINC, MMP-9, and nitric oxide.
Positive_regulation (induced) of LPS-induced associated with inflammatory mediators
7) Confidence 0.02 Published 2004 Journal Respir Res Section Abstract Doc Link PMC538282 Disease Relevance 0.40 Pain Relevance 0.05
In the present study, we determined: (1) the in vivo relation between activation of JNK or ERK and LPS-induced acute lung injury; (2) the inhibition of JNK or ERK resulted in reductions of LPS-induced increases in lung injury parameters, such as total protein content and LDH activity in BAL fluid, neutrophil influx into the lungs, and proinflammatory gene products, such as CINC, MMP-9 and NO; and (3) the activation of JNK is involved in the LPS signaling pathway leading to NF-?
Positive_regulation (activation) of LPS-induced in lung associated with lung injury, metalloproteinase and adult respiratory distress syndrome
8) Confidence 0.01 Published 2004 Journal Respir Res Section Body Doc Link PMC538282 Disease Relevance 0.20 Pain Relevance 0.04

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