INT48081

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Context Info
Confidence 0.80
First Reported 1995
Last Reported 2010
Negated 0
Speculated 2
Reported most in Abstract
Documents 46
Total Number 48
Disease Relevance 21.59
Pain Relevance 22.40

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

extracellular space (Il1b) aging (Il1b) extracellular region (Il1b)
Anatomy Link Frequency
brain 6
macrophages 3
peritoneal macrophages 3
THP-1 2
neutrophils 2
Il1b (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 256 100.00 Very High Very High Very High
cytokine 119 100.00 Very High Very High Very High
Spinal cord 61 100.00 Very High Very High Very High
chemokine 58 100.00 Very High Very High Very High
Enkephalin 49 99.92 Very High Very High Very High
agonist 28 99.84 Very High Very High Very High
narcan 34 99.34 Very High Very High Very High
antagonist 40 99.00 Very High Very High Very High
orphanin 24 98.56 Very High Very High Very High
Analgesic 19 98.26 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 243 100.00 Very High Very High Very High
Endometriosis 90 100.00 Very High Very High Very High
Cancer 30 100.00 Very High Very High Very High
Necrosis 28 100.00 Very High Very High Very High
Apoptosis 42 99.88 Very High Very High Very High
Injury 30 99.36 Very High Very High Very High
Bone Cancer 2 99.36 Very High Very High Very High
Burns 24 99.28 Very High Very High Very High
Infection 70 98.60 Very High Very High Very High
Crystal Associated Disease 8 98.44 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Modulatory effects of [Met5]-enkephalin on interleukin-1 beta secretion from microglia in mixed brain cell cultures.
Localization (secretion) of interleukin-1 beta in brain associated with narcan and enkephalin
1) Confidence 0.80 Published 1995 Journal J. Neuroimmunol. Section Title Doc Link 7499497 Disease Relevance 0 Pain Relevance 0.85
In the present study, functional interactions between [Met5]-enkephalin (ME), naloxone and lipopolysaccharide (LPS) on interleukin-1 beta (IL-1 beta) immunostaining and secretion have been assessed in mixed brain cell cultures from embryonic day 17 mice.
Localization (secretion) of IL-1 beta in brain associated with narcan and enkephalin
2) Confidence 0.80 Published 1995 Journal J. Neuroimmunol. Section Abstract Doc Link 7499497 Disease Relevance 0 Pain Relevance 0.60
Despite increasing IL-1 beta release into the media, ME (10(-8) M) did not induce morphological changes in microglia.
Localization (release) of IL-1 beta in microglia associated with enkephalin
3) Confidence 0.80 Published 1995 Journal J. Neuroimmunol. Section Abstract Doc Link 7499497 Disease Relevance 0 Pain Relevance 0.82
The enhanced release of IL-1 beta caused by ME or LPS was partially blocked by naloxone.
Localization (release) of IL-1 beta associated with narcan and enkephalin
4) Confidence 0.80 Published 1995 Journal J. Neuroimmunol. Section Abstract Doc Link 7499497 Disease Relevance 0 Pain Relevance 0.82
Adding ME alone or together with LPS to the culture increased the release of IL-1 beta after 48 h in a concentration-dependent fashion.
Localization (release) of IL-1 beta associated with enkephalin
5) Confidence 0.80 Published 1995 Journal J. Neuroimmunol. Section Abstract Doc Link 7499497 Disease Relevance 0 Pain Relevance 0.71
In the present study, functional interactions between [Met5]-enkephalin (ME), naloxone and lipopolysaccharide (LPS) on interleukin-1 beta (IL-1 beta) immunostaining and secretion have been assessed in mixed brain cell cultures from embryonic day 17 mice.
Localization (secretion) of interleukin-1 beta in brain associated with narcan and enkephalin
6) Confidence 0.80 Published 1995 Journal J. Neuroimmunol. Section Abstract Doc Link 7499497 Disease Relevance 0 Pain Relevance 0.60
IL-4, -10, or -13 significantly inhibited the release of both tumor necrosis factor (TNF)-alpha (60, 53, and 100%, respectively) and IL-1beta (80, 100, and 100%, respectively) by mice peritoneal macrophages obtained after local (i.p.) injection of zymosan.
Localization (release) of IL-1beta in peritoneal macrophages associated with necrosis and cancer
7) Confidence 0.78 Published 2003 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 12490580 Disease Relevance 0.37 Pain Relevance 0.80
This analgesic effect could be related to a peripheral mechanism, probably via the inhibition of the release of the pro-inflammatory cytokines TNF-alpha and IL-1beta by resident peritoneal macrophages.
Localization (release) of IL-1beta in peritoneal macrophages associated with inflammation, analgesic and cytokine
8) Confidence 0.78 Published 2003 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 12490580 Disease Relevance 0.38 Pain Relevance 0.76
When cultured and stimulated by tumor necrosis factor alpha, these peritoneal macrophages also secreted less RANTES and less IL-1beta protein.
Localization (secreted) of IL-1beta in peritoneal macrophages associated with necrosis and cancer
9) Confidence 0.78 Published 2003 Journal Gynecol. Obstet. Invest. Section Abstract Doc Link 12624547 Disease Relevance 1.05 Pain Relevance 0.35
Systemic treatment of mice with a panel of melanocortin peptides inhibited IL-1 beta release and PMN accumulation elicited by urate crystals in the murine peritoneal cavity.
Localization (release) of IL-1 beta in peritoneal cavity
10) Confidence 0.78 Published 2003 Journal J. Immunol. Section Abstract Doc Link 12626592 Disease Relevance 0.29 Pain Relevance 0.48
In vitro M phi activation, determined as release of the CXC chemokine KC and IL-1 beta, was inhibited by the more selective MC3-R agonist gamma(2)-melanocyte stimulating hormone but not by the selective MC1-R agonist MS05.
Spec (determined) Localization (release) of IL-1 beta in melanocyte associated with chemokine and agonist
11) Confidence 0.78 Published 2003 Journal J. Immunol. Section Abstract Doc Link 12626592 Disease Relevance 0.30 Pain Relevance 0.50
In conclusion, some hyperalgesic symptoms observed in this model of bone cancer are mediated by the peripheral release of IL-1beta and may be inhibited by antagonists of type I IL-1 receptors with a similar or greater potency than symptoms produced by inflammation.
Localization (release) of IL-1beta associated with hyperalgesia, inflammation, antagonist, bone cancer and potency
12) Confidence 0.78 Published 2007 Journal Life Sci. Section Abstract Doc Link 17692876 Disease Relevance 1.52 Pain Relevance 1.18
Activation of P2X7 receptors leads to rapid changes in intracellular calcium concentrations, release of the pro-inflammatory cytokine IL-1beta, and following prolonged agonist exposure, the formation of cytolytic pores in plasma membranes.
Localization (release) of IL-1beta in plasma associated with inflammation, agonist and cytokine
13) Confidence 0.78 Published 2009 Journal Neuropharmacology Section Abstract Doc Link 18602931 Disease Relevance 0.35 Pain Relevance 0.45
The Dyn response is mediated by release of IL1beta in the spinal cord to activate an ascending pathway to the brain and in turn releases IL1beta in the brain which activates a descending pathway to the spinal cord.
Localization (release) of IL1beta in brain associated with spinal cord
14) Confidence 0.78 Published 2002 Journal Life Sci. Section Abstract Doc Link 11860156 Disease Relevance 0 Pain Relevance 0.54
Activation of P2X(7) receptors leads to rapid changes in intracellular calcium concentrations, release of the proinflammatory cytokine interleukin-1beta (IL-1beta), and following prolonged agonist exposure, cytolytic plasma membrane pore formation.
Localization (release) of IL-1beta in pore associated with agonist and cytokine
15) Confidence 0.78 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16982702 Disease Relevance 0.43 Pain Relevance 0.44
However, IL-1beta release was significantly increased in CAP/DNFB mice over O/DNFB by 18-fold and by over 30-fold compare to O/O controls.
Localization (release) of IL-1beta
16) Confidence 0.78 Published 1998 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 9878594 Disease Relevance 0.27 Pain Relevance 0.25
Burn trauma promoted cardiac myocyte secretion of tumor necrosis factor (TNFalpha) (175+/-6 pg/mL) compared to that measured in shams (72+/-9 pg/mL, P < 0.05); burn trauma also increased cardiac myocyte secretion of interleukin 1beta (IL-1beta) (sham: 2+/-0.5; burn: 22+/-1 pg/mL, P < 0.05) and IL-6 (sham: 70+/-6; burn: 148+/-16 pg/mL, P < 0.05).
Localization (secretion) of IL-1beta in cardiac myocyte associated with necrosis, cancer, burns and injury
17) Confidence 0.78 Published 2001 Journal Shock Section Abstract Doc Link 11508864 Disease Relevance 2.13 Pain Relevance 0.06
Fittingly, Dyn was not antianalgesic in C3H/HeJ mice, which are genetically deficient in release of IL1beta.
Localization (release) of IL1beta
18) Confidence 0.78 Published 2001 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 11602679 Disease Relevance 0 Pain Relevance 0.74
A-804598 also potently blocked agonist stimulated release of IL-1beta and Yo-Pro uptake from differentiated THP-1 cells that natively express human P2X7 receptors.
Localization (release) of IL-1beta in THP-1 associated with agonist
19) Confidence 0.78 Published 2009 Journal Neuropharmacology Section Abstract Doc Link 18602931 Disease Relevance 0.34 Pain Relevance 0.50
A-740003 potently blocked agonist-evoked IL-1beta release (IC(50) = 156 nM) and pore formation (IC(50) = 92 nM) in differentiated human THP-1 cells.
Localization (release) of IL-1beta in THP-1 associated with agonist
20) Confidence 0.78 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16982702 Disease Relevance 0.74 Pain Relevance 1.00

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