INT48954

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Context Info
Confidence 0.53
First Reported 1994
Last Reported 2009
Negated 1
Speculated 0
Reported most in Abstract
Documents 13
Total Number 13
Disease Relevance 8.16
Pain Relevance 6.44

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
endothelial cell 4
muscle 2
spinal cord 2
microglia 2
nerve 2
Il1b (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cytokine 26 100.00 Very High Very High Very High
Inflammation 20 100.00 Very High Very High Very High
noradrenaline 10 100.00 Very High Very High Very High
Hyperalgesia 10 100.00 Very High Very High Very High
lidocaine 2 99.88 Very High Very High Very High
Enkephalin 11 99.70 Very High Very High Very High
tetrodotoxin 10 99.60 Very High Very High Very High
narcan 3 98.92 Very High Very High Very High
antagonist 2 98.72 Very High Very High Very High
Calcium channel 2 98.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 15 100.00 Very High Very High Very High
Hyperalgesia 11 100.00 Very High Very High Very High
Colitis 20 99.88 Very High Very High Very High
Diabetes Mellitus 26 99.36 Very High Very High Very High
Nociception 5 98.52 Very High Very High Very High
Myelitis 3 97.40 Very High Very High Very High
Adhesions 2 96.36 Very High Very High Very High
Inflammatory Bowel Disease 10 95.92 Very High Very High Very High
Myalgia 2 94.24 High High
Shock 4 93.60 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our results demonstrate under conditions in vivo that active colitis is associated with enhanced interleukin-1 beta release into the colonic lumen whereas such release does not occur in remission, supporting the concept that ulcerative colitis flare-ups involve increased interleukin-1 beta production.
Positive_regulation (enhanced) of Localization (release) of interleukin-1 beta in lumen associated with colitis and inflammatory bowel disease
1) Confidence 0.53 Published 1995 Journal Clin. Sci. Section Abstract Doc Link 8549067 Disease Relevance 0.92 Pain Relevance 0
It was found that (1) tissue explants release sizable amounts of irIL-1 beta (ranging from 0.43 to 0.52 pg/mg of wet tissue) in 20 min incubations; (2) basal release in significantly increased by depolarization induced with 56 mM KCl; (3) K(+)-induced irIL-1 beta release is inhibited by the specific blocker of N-type calcium channels, omega-conotoxin, and by verapamil, but not by nifedipine; (4) K(+)-induced release is also inhibited by the Na+ channel blockers tetrodotoxin and lidocaine; (5) irIL-1 beta release is significantly increased by noradrenalin; such increase is antagonized by verapamil and the beta-blocker propranolol, but not by the alpha-blocker phentolamine.
Positive_regulation (-induced) of Localization (release) of irIL-1 beta associated with tetrodotoxin, beta blocker, calcium channel, lidocaine and conotoxin
2) Confidence 0.50 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.32
In the present experiments, we found that: (1) selective inhibition of glia metabolism with intrathecal (i.t.) administration of fluorocitrate (1 nmol) results in a marked, but reversible, attenuation of the persistent thermal and mechanical hyperalgesia produced by intraplantar zymosan (5 mg); (2) selective inhibition of the inducible form of nitric oxide synthase (iNOS) with i.t. aminoguanidine (1 pmol-1 nmol) resulted in a dose-dependent inhibition of the persistent thermal, but not mechanical hyperalgesia produced by intraplantar zymosan (5 mg); (3) i.t. coadministration of interleukin 1 beta (IL1 beta; 10 ng) and interferon gamma (IFN; 1000 U) resulted in expression of the message for iNOS 8 hr after administration assessed using reverse-transcription polymerase chain reaction (RT-PCR) and Southern blot analysis; and (4) i.t. administration of lipopolysaccharide (LPS; 150 micrograms) produced a time-dependent thermal hyperalgesia compared with saline treated-rats (15 microliters).
Positive_regulation (resulted) of Localization (coadministration) of interleukin 1 beta associated with hyperalgesia, thermal hyperalgesia and intrathecal
3) Confidence 0.49 Published 1994 Journal Neuropharmacology Section Abstract Doc Link 7532831 Disease Relevance 0.72 Pain Relevance 0.65
The release of IL-1beta and IL-6, known to mediate hyperalgesia elsewhere, is delayed in muscle inflammation compared with cutaneous inflammation, whereas TNF-alpha is not elevated during muscle inflammation.
Neg (not) Positive_regulation (elevated) of Localization (release) of IL-1beta in muscle associated with hyperalgesia and inflammation
4) Confidence 0.49 Published 2007 Journal J Pain Section Abstract Doc Link 16949880 Disease Relevance 1.30 Pain Relevance 1.15
It was found that (1) tissue explants release sizable amounts of irIL-1 beta (ranging from 0.43 to 0.52 pg/mg of wet tissue) in 20 min incubations; (2) basal release in significantly increased by depolarization induced with 56 mM KCl; (3) K(+)-induced irIL-1 beta release is inhibited by the specific blocker of N-type calcium channels, omega-conotoxin, and by verapamil, but not by nifedipine; (4) K(+)-induced release is also inhibited by the Na+ channel blockers tetrodotoxin and lidocaine; (5) irIL-1 beta release is significantly increased by noradrenalin; such increase is antagonized by verapamil and the beta-blocker propranolol, but not by the alpha-blocker phentolamine.
Positive_regulation (increased) of Localization (release) of irIL-1 beta associated with tetrodotoxin, beta blocker, calcium channel, lidocaine and conotoxin
5) Confidence 0.47 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.35
ME and LE increased LPS-induced IL-1 beta release, which was not blocked by naloxone.
Positive_regulation (induced) of Localization (release) of IL-1 beta associated with narcan and enkephalin
6) Confidence 0.46 Published 2002 Journal Neuropeptides Section Abstract Doc Link 12507434 Disease Relevance 0.09 Pain Relevance 1.08
These data suggest a critical role for the cytokine IL-1beta and caspase 1 rapidly released by activated microglia in enhancing nociceptive transmission in spinal cord inflammation.
Positive_regulation (role) of Localization (released) of IL-1beta in spinal cord associated with nociception, inflammation, spinal cord and cytokine
7) Confidence 0.45 Published 2006 Journal J. Neurochem. Section Abstract Doc Link 16942597 Disease Relevance 0.67 Pain Relevance 0.65
RESULTS: IL-6 and IL-1beta secretion from the nerve was significantly elevated on the 3rd day post-operation (DPO).
Positive_regulation (elevated) of Localization (secretion) of IL-1beta in nerve
8) Confidence 0.45 Published 2009 Journal Brain Behav. Immun. Section Body Doc Link 19486649 Disease Relevance 0.13 Pain Relevance 0
An interleukin-1 beta-induced noradrenaline release in the spleen is mediated by brain corticotropin-releasing factor: an in vivo microdialysis study in conscious rats.
Positive_regulation (mediated) of in brain Localization (release) of interleukin-1 beta in spleen associated with noradrenaline
9) Confidence 0.45 Published 1994 Journal Brain Behav. Immun. Section Title Doc Link 8003768 Disease Relevance 0 Pain Relevance 0.40
In active colitis, the release of interleukin-1 beta was detected in 17 out of 19 patients (median 500 pg/min, interquartiles 270-1582 pg/min, P < 0.01 compared with control subjects and patients with inactive colitis).
Positive_regulation (detected) of Localization (release) of interleukin-1 beta associated with colitis
10) Confidence 0.39 Published 1995 Journal Clin. Sci. Section Abstract Doc Link 8549067 Disease Relevance 1.22 Pain Relevance 0.07
The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70).
Positive_regulation (increase) of Localization (release) of IL-1 beta in endothelial cell associated with diabetes mellitus, shock and adhesions
11) Confidence 0.34 Published 2003 Journal Eur. J. Pharmacol. Section Abstract Doc Link 14642793 Disease Relevance 1.56 Pain Relevance 0.08
The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70).
Positive_regulation (increase) of Localization (release) of interleukin-1 beta in endothelial cell associated with diabetes mellitus, shock and adhesions
12) Confidence 0.34 Published 2003 Journal Eur. J. Pharmacol. Section Abstract Doc Link 14642793 Disease Relevance 1.55 Pain Relevance 0.08
TTX (0.3 microM) reduced, but to a smaller extent, the release of IL-1 alpha, IL-1 beta, and TNF-alpha from activated microglia.
Positive_regulation (activated) of Localization (release) of IL-1 beta in microglia associated with tetrodotoxin
13) Confidence 0.06 Published 2009 Journal Glia Section Abstract Doc Link 19115387 Disease Relevance 0 Pain Relevance 1.62

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