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Context Info
Confidence 0.30
First Reported 1998
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 3.68
Pain Relevance 0.36

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

Anatomy Link Frequency
T cells 2
IFNA1 (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 5 99.70 Very High Very High Very High
opioid receptor 4 99.48 Very High Very High Very High
analgesia 2 64.52 Quite High
Opioid 2 63.72 Quite High
narcan 1 48.36 Quite Low
cytokine 53 44.96 Quite Low
dexamethasone 1 44.68 Quite Low
Inflammation 49 36.96 Quite Low
chemokine 11 10.36 Low Low
rheumatoid arthritis 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Urological Neuroanatomy 5 100.00 Very High Very High Very High
Infection 137 99.24 Very High Very High Very High
Dengue 127 98.80 Very High Very High Very High
Disease 56 94.80 High High
Systemic Lupus Erythematosus 61 94.56 High High
Hepatitis C Virus Infection 37 92.32 High High
Targeted Disruption 3 86.28 High High
Rheumatic Diseases 1 80.96 Quite High
Fever 25 76.92 Quite High
Autoimmune Disease 37 72.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Further detailed whole-cell clamping analyses on neuronal mechanisms in rat brain tissue slices showed that the inhibitory effect of rhIFN-alpha on N-methyl-D-aspartate-induced membrane current responses of MPO neurons was mediated not only by opioid receptors but also by the local production of reactive oxygen intermediates, nitric oxide and prostanoids, possibly due to neuron-glial cell interaction.
Positive_regulation (mediated) of Negative_regulation (effect) of rhIFN-alpha in MPO associated with urological neuroanatomy and opioid receptor
1) Confidence 0.30 Published 1998 Journal Neuroimmunomodulation Section Abstract Doc Link 9730683 Disease Relevance 0.44 Pain Relevance 0.31
induced transcription factor STAT1 and its binding to DNA response elements, thereby increasing the induction of ISGs and enhancing the inhibitory effect of IFN?
Positive_regulation (enhancing) of Negative_regulation (effect) of IFN
2) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2975710 Disease Relevance 0.35 Pain Relevance 0
We detected a large number of IFN response genes induced in both cell line infections and in dengue patients (see Figure 3C).
Positive_regulation (induced) of Negative_regulation (number) of IFN associated with dengue and infection
3) Confidence 0.16 Published 2007 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2100376 Disease Relevance 1.54 Pain Relevance 0
Although the direct TLR antagonists have not been studied in human patients, inhibitors of IFN-?
Neg (not) Positive_regulation (studied) of Negative_regulation (inhibitors) of IFN associated with antagonist
4) Confidence 0.15 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 1.16 Pain Relevance 0.05
expression induced by TCR and CD28 stimulation in human T cells, a moderate and transient reduction of IFN-?
Positive_regulation (stimulation) of Negative_regulation (reduction) of IFN in T cells
5) Confidence 0.05 Published 2006 Journal Arthritis Res Ther Section Body Doc Link PMC1526596 Disease Relevance 0 Pain Relevance 0
Interestingly the two functions of NSs complement each other: first, the specific inhibition of IFN-ß gene transcription is implemented as early as 3–4 h post-infection (p.i.) a time at which IFN-ß would normally be synthesized.
Positive_regulation (implemented) of Negative_regulation (inhibition) of IFN associated with infection
6) Confidence 0.03 Published 2010 Journal Veterinary Research Section Body Doc Link PMC2896810 Disease Relevance 0.19 Pain Relevance 0

General Comments

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