INT165838

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Context Info
Confidence 0.07
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 1.30
Pain Relevance 0.71

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

protein folding (TBCE) cytoskeleton (TBCE) cytoplasm (TBCE)
Anatomy Link Frequency
endothelial cell 1
TBCE (Homo sapiens)
Pain Link Frequency Relevance Heat
Paracetamol 6 99.52 Very High Very High Very High
Inflammation 11 88.96 High High
spastic colon 2 79.12 Quite High
antagonist 10 52.88 Quite High
cytokine 5 17.28 Low Low
Inflammatory response 5 5.00 Very Low Very Low Very Low
Neurotransmitter 3 5.00 Very Low Very Low Very Low
isoflurane 3 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
vagus nerve 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Nash(non-alcoholic Steatohepatitis) 8 97.48 Very High Very High Very High
Injury 15 94.96 High High
Congenital Anomalies 2 93.88 High High
INFLAMMATION 15 88.96 High High
Fatty Liver 1 81.00 Quite High
Bordatella Infection 3 79.64 Quite High
Functional Bowel Disorder 2 79.12 Quite High
Liver Failure 1 64.20 Quite High
Syndrome 8 49.52 Quite Low
Diabetes Mellitus 15 47.36 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Recently, the involvement of intestinal bacterial flora in the regulation of metabolic homeostasis has been the subject of intense interest.55,56 In particular, studies have revealed that NASH is associated with intestinal bacterial overgrowth and increased intestinal permeability, leading to the endotoxin-dependent activation of KCs.55 This effect was also shown with an HF diet in rats.57 Thus, intestinal effects may add to hepatic effects as causal effectors of HF-linked metabolic abnormalities.
Positive_regulation (activation) of KCs associated with nash(non-alcoholic steatohepatitis) and congenital anomalies
1) Confidence 0.07 Published 2010 Journal Clinics (Sao Paulo) Section Body Doc Link PMC2910863 Disease Relevance 0.54 Pain Relevance 0.15
Conclusion: Collectively, our data indicate that Lac, through activation of KCs, inhibited APAP-induced liver sinusoidal endothelial cell damage and improved hepatic congestion, thereby protecting against AILI.
Positive_regulation (activation) of KCs in endothelial cell associated with paracetamol and injury
2) Confidence 0.04 Published 2010 Journal Hepatology Section Abstract Doc Link 20099297 Disease Relevance 0.51 Pain Relevance 0.49
Either agent by itself induced the phosphorylation of p38 compared to control, however, the combination of NE and LPS showed the strongest activation (over 7-fold induction) of p38 in cultured KCs (Fig. 6B).
Positive_regulation (activation) of KCs
3) Confidence 0.02 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2677660 Disease Relevance 0.25 Pain Relevance 0.07

General Comments

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