INT116527

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Context Info
Confidence 0.70
First Reported 2004
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 29
Total Number 30
Disease Relevance 25.79
Pain Relevance 4.87

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

small molecule metabolic process (HMOX1) endoplasmic reticulum (HMOX1) enzyme binding (HMOX1)
transmembrane transport (HMOX1) signal transducer activity (HMOX1) cytosol (HMOX1)
Anatomy Link Frequency
monocytes 10
macrophages 2
plasma 2
endothelial cells 2
ARPE-19 2
HMOX1 (Homo sapiens)
Pain Link Frequency Relevance Heat
rheumatoid arthritis 148 99.60 Very High Very High Very High
Inflammatory response 126 99.20 Very High Very High Very High
Abeta 10 98.62 Very High Very High Very High
Inflammation 493 97.44 Very High Very High Very High
cva 15 92.52 High High
Infliximab 26 91.68 High High
Pain 12 90.56 High High
cytokine 51 88.20 High High
cINOD 30 81.28 Quite High
antagonist 11 78.80 Quite High
Disease Link Frequency Relevance Heat
Rheumatoid Arthritis 148 99.60 Very High Very High Very High
Shock 61 99.60 Very High Very High Very High
Atherosclerosis 23 99.60 Very High Very High Very High
Necrosis 34 99.50 Very High Very High Very High
Toxicity 7 99.48 Very High Very High Very High
Disease 1205 99.40 Very High Very High Very High
Cancer 73 99.32 Very High Very High Very High
INFLAMMATION 618 99.20 Very High Very High Very High
Rheumatic Diseases 52 99.00 Very High Very High Very High
Lung Cancer 12 99.00 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Exposure to either PPI resulted in a strong induction of HO-1 expression on mRNA and protein level, and led to an increased activity of this enzyme.
Positive_regulation (induction) of Gene_expression (expression) of HO-1
1) Confidence 0.70 Published 2006 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 16712795 Disease Relevance 0.18 Pain Relevance 0.06
In human umbilical vein and aortic endothelial cells, 24-48 h treatment with celecoxib induced HO-1 mRNA and protein expression and increased HO-1 enzyme activity.
Positive_regulation (induced) of Gene_expression (expression) of HO-1 in endothelial cells
2) Confidence 0.69 Published 2010 Journal Free Radic. Biol. Med. Section Abstract Doc Link 20083195 Disease Relevance 0.41 Pain Relevance 0.35
Overexpression of HO-1 in arterial walls reduces lesion formation as well as intimal hyperplasia subsequent to vascular injury, supporting its vasoprotective function [17-19].
Positive_regulation (Overexpression) of Gene_expression (Overexpression) of HO-1 associated with vasculitis and hyperplasia
3) Confidence 0.69 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2841098 Disease Relevance 1.64 Pain Relevance 0.18
Vascular proliferation was inhibited by transferring HO-1 gene[18].
Positive_regulation (transferring) of Gene_expression (transferring) of HO-1 gene
4) Confidence 0.69 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2841098 Disease Relevance 1.03 Pain Relevance 0.03
Increased HO-1 and ferritin expression as well as endothelial protection occurred at micromolar concentrations of PETriN which are well within the range of plasma or tissue levels that can be expected during oral therapy.
Positive_regulation (Increased) of Gene_expression (expression) of HO-1 in plasma
5) Confidence 0.61 Published 2004 Journal Herz Section Abstract Doc Link 14968347 Disease Relevance 0.31 Pain Relevance 0.03
Evidence suggests that increased expression of HO-1 can benefit the host in a variety of pathologic conditions, including inflammatory changes, whereas a deficiency in HO-1 expression is associated with vigorous inflammation, as demonstrated by studies of HO-1 knockout mice and observed in a patient with HO-1 deficiency [22,23].
Positive_regulation (increased) of Gene_expression (expression) of HO-1 associated with targeted disruption and inflammation
6) Confidence 0.54 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.98 Pain Relevance 0.18
GLNVA also suppressed accumulation of iROS and up-regulated heme oxygenase-1 expression. 6-OHDA-induced overexpression of nNOS, iNOS, COX-2, and gp91(phox) was also reduced by GLNVA.
Positive_regulation (up-regulated) of Gene_expression (expression) of heme oxygenase-1
7) Confidence 0.49 Published 2007 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 17855475 Disease Relevance 0.65 Pain Relevance 0.16
Supplementation of culture medium with iloprost or prostaglandin E(2) failed to reverse celecoxib-mediated HO-1 induction, indicating a cyclooxygenase-independent mechanism.
Positive_regulation (mediated) of Gene_expression (induction) of HO-1
8) Confidence 0.44 Published 2010 Journal Free Radic. Biol. Med. Section Abstract Doc Link 20083195 Disease Relevance 0.38 Pain Relevance 0.36
Our recent study [26] showed that tumor necrosis factor (TNF) suppresses HO-1 expression in human monocytes, leading to augmentation of inflammatory responses, and that clinical efficacy of anti-TNF therapy is associated with restoration of HO-1 expression in circulating monocytes from patients with RA [26].
Positive_regulation (restoration) of Gene_expression (expression) of HO-1 in monocytes associated with necrosis, inflammatory response, cancer and rheumatoid arthritis
9) Confidence 0.39 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.67 Pain Relevance 0.47
Inverse correlation between HO-1 and TLR4 mRNA in PBMCs from BD patients
Positive_regulation (between) of Gene_expression (mRNA) of HO-1 associated with disease
10) Confidence 0.39 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.65 Pain Relevance 0.04
Over-expression of HO-1 protein was confirmed by immunoblotting analysis 24 hours after transfection with pHO-1 (human HO-1 expression vector) into monocytes.
Positive_regulation (Over) of Gene_expression (expression) of HO-1 protein in monocytes
11) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.32 Pain Relevance 0.04
No effect of forced HO-1 expression on TLR2 and TLR4 mRNA in human PBMCs
Positive_regulation (forced) of Gene_expression (expression) of HO-1
12) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.16 Pain Relevance 0.05
Our recent study [26] showed that tumor necrosis factor (TNF) suppresses HO-1 expression in human monocytes, leading to augmentation of inflammatory responses, and that clinical efficacy of anti-TNF therapy is associated with restoration of HO-1 expression in circulating monocytes from patients with RA [26].
Positive_regulation (leading) of Gene_expression (expression) of HO-1 in monocytes associated with necrosis, inflammatory response, cancer and rheumatoid arthritis
13) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.81 Pain Relevance 0.51
Over-expression of HO-1 protein was confirmed by immunoblotting analysis 24 hours after transfection with pHO-1 (human HO-1 expression vector) into monocytes.
Positive_regulation (expression) of Gene_expression (expression) of HO-1 protein in monocytes
14) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.32 Pain Relevance 0.04
Abundant expression of HO-1 was identified in synovial tissues of patients with RA, in the absence of elevated serum HO-1 levels [24,25].
Positive_regulation (elevated) of Gene_expression (levels) of HO-1 associated with rheumatoid arthritis
15) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.66 Pain Relevance 0.45
In our previous study [26] we showed that TNF suppresses HO-1 expression levels in human peripheral monocytes, thereby accelerating inflammatory responses; this suggests that excessive TNF levels contribute to defective HO-1 expression.
Positive_regulation (contribute) of Gene_expression (expression) of HO-1 in monocytes associated with inflammatory response
16) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 1.09 Pain Relevance 0.12
Our previous studies [24,25] have demonstrated elevated serum HO-1 levels in patients with adult onset Still's disease and hemophagocytic syndrome, and aberrant expression of HO-1 in synoviocytes from patients with RA.
Positive_regulation (elevated) of Gene_expression (levels) of HO-1 associated with hemophagocytic lymphohistiocytosis, rheumatoid arthritis and disease
17) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.90 Pain Relevance 0.17
Taken together, our findings suggest that highly expressed TLR4 might contribute to reduced HO-1 expression, leading to an activation of the innate immune system in BD, although other factors including TNF may be involved in the defective HO-1.
Spec (might) Positive_regulation (contribute) of Gene_expression (expression) of HO-1 in immune system associated with disease
18) Confidence 0.36 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.92 Pain Relevance 0.10
The magnitude of LPS-induced HO-1 suppression (calculated as the gap in HO-1 mRNA between PBMCs subjected to 6 hours of LPS treatment and untreated PBMCs [?
Positive_regulation (calculated) of Gene_expression (suppression) of HO-1
19) Confidence 0.34 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.52 Pain Relevance 0.03
The magnitude of LPS-induced HO-1 suppression (calculated as the gap in HO-1 mRNA between PBMCs subjected to 6 hours of LPS treatment and untreated PBMCs [?
Positive_regulation (induced) of Gene_expression (suppression) of HO-1
20) Confidence 0.34 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2374472 Disease Relevance 0.52 Pain Relevance 0.03

General Comments

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