INT134197

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Context Info
Confidence 0.44
First Reported 2005
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 11
Total Number 12
Disease Relevance 4.82
Pain Relevance 1.76

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

immune system process (AHR) cell morphogenesis (AHR) DNA binding (AHR)
response to stress (AHR) cytoplasm (AHR) signal transducer activity (AHR)
Anatomy Link Frequency
macrophages 1
eosinophils 1
bile 1
AHR (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 109 99.60 Very High Very High Very High
Bile 2 98.92 Very High Very High Very High
corticosteroid 4 98.50 Very High Very High Very High
Nicotine 192 98.02 Very High Very High Very High
cINOD 4 86.96 High High
B1 receptor 14 72.04 Quite High
antagonist 52 71.60 Quite High
b2 receptor 70 71.16 Quite High
bradykinin 91 68.68 Quite High
cytokine 12 54.32 Quite High
Disease Link Frequency Relevance Heat
Asthma 191 99.74 Very High Very High Very High
Occupational Lung Diseases 46 99.66 Very High Very High Very High
INFLAMMATION 112 99.60 Very High Very High Very High
Mycobacterial Infection 162 84.36 Quite High
Cough 11 80.80 Quite High
Pressure And Volume Under Development 9 80.40 Quite High
Liver Cancer 1 78.48 Quite High
Rhinitis 8 77.08 Quite High
Injury 2 73.52 Quite High
Pulmonary Disease 16 72.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Aryl hydrocarbon receptor-mediated regulation of the human estrogen and bile acid UDP-glucuronosyltransferase 1A3 gene.
Regulation (regulation) of Aryl hydrocarbon receptor in bile associated with bile
1) Confidence 0.44 Published 2008 Journal Arch. Toxicol. Section Title Doc Link 18677463 Disease Relevance 0.09 Pain Relevance 0.18
Since the transcription of CYP1A1 is under the control of the aryl hydrocarbon receptor (AhR), we examined the ability of sulindac to activate the receptor.
Regulation (control) of AhR
2) Confidence 0.22 Published 2006 Journal Carcinogenesis Section Abstract Doc Link 16531450 Disease Relevance 0.13 Pain Relevance 0.16
Thus, the lack of efficacy of anti-IL-5 on AHR via granule protein inhibition was incompletely understood.
Regulation (efficacy) of AHR
3) Confidence 0.16 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2843899 Disease Relevance 0.74 Pain Relevance 0.03
Recently, the role of the eosinophil in asthma has been questioned as anti-IL-5, which effectively depleted eosinophils from the blood and induced sputum in mild atopic subjects with asthma, but had no effect on AHR [7].
Neg (no) Regulation (effect) of AHR in eosinophils associated with asthma
4) Confidence 0.14 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2843899 Disease Relevance 1.03 Pain Relevance 0.07
On the next day, we measured their PC400 to carbachol to determine if the postantigen-induced AHR was affected.
Regulation (affected) of AHR
5) Confidence 0.12 Published 2005 Journal Environ Health Perspect Section Body Doc Link PMC1257560 Disease Relevance 0 Pain Relevance 0
To determine if multiple exposures to PbTx-3 affected antigen-induced responses, we challenged sheep in the morning with 20 breaths of 100 pg/mL PbTx-3 for 3 consecutive days and then on the fourth day challenged the animals with allergen to determine if the antigen-induced EAR, LAR, and AHR were affected.
Regulation (affected) of AHR
6) Confidence 0.12 Published 2005 Journal Environ Health Perspect Section Body Doc Link PMC1257560 Disease Relevance 0 Pain Relevance 0.10
To determine if toxin exposure would enhance the response to allergen and/or affect the postantigen-induced AHR, we exposed three sheep to PbTx-3 (20 breaths of 100 pg/mL) for 3 consecutive days and then, on the day 4, measured the response to allergen challenge.
Regulation (affect) of AHR
7) Confidence 0.12 Published 2005 Journal Environ Health Perspect Section Body Doc Link PMC1257560 Disease Relevance 0 Pain Relevance 0.03
Although inhaled corticosteroids reduce airway inflammation in mild-to-moderate asthmatics,[5758] they are ineffective in normalizing AHR or abolishing airway inflammation in severe asthmatics despite prolonged courses of treatment.[5960]
Regulation (ineffective) of AHR associated with corticosteroid, inflammation and occupational lung diseases
8) Confidence 0.09 Published 2007 Journal Annals of Thoracic Medicine Section Body Doc Link PMC2732069 Disease Relevance 0.93 Pain Relevance 0.27
One of the hypotheses of the present study is that long-term exposure to nicotine can induce activation of airway MAPK-mediated inflammatory signal pathways and subsequently cause AHR via up-regulation of kinin receptors.
Regulation (regulation) of AHR associated with inflammation and nicotine
9) Confidence 0.09 Published 2010 Journal Respir Res Section Body Doc Link PMC2845563 Disease Relevance 0.67 Pain Relevance 0.47
B inflammatory signal pathways in AHR along with an up-regulation of kinin receptors [20,22,23].
Regulation (regulation) of AHR associated with inflammation
10) Confidence 0.09 Published 2010 Journal Respir Res Section Body Doc Link PMC2845563 Disease Relevance 0.62 Pain Relevance 0.45
This suggests that an unaffected AHR/ARNT transcription factor complex that is likely to occur in the IRGM wild-type gene promoter, may decrease innate immune responses mediated by macrophages.
Neg (unaffected) Regulation (unaffected) of AHR in macrophages
11) Confidence 0.06 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2735778 Disease Relevance 0.28 Pain Relevance 0
Inversely, and based on our luciferase reporter gene assays, the loss of the potential PAX5, AHR and ARNT transcription factor binding sites predicted for the IRGM variant ?
Regulation (sites) of AHR
12) Confidence 0.06 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2735778 Disease Relevance 0.32 Pain Relevance 0

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