INT67130

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Context Info
Confidence 0.57
First Reported 1996
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 7
Total Number 8
Disease Relevance 1.36
Pain Relevance 6.42

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
microglia 4
glial cell 2
vagal nerves 2
Il1b (Rattus norvegicus)
Pain Link Frequency Relevance Heat
substance P 12 99.84 Very High Very High Very High
narcan 3 99.84 Very High Very High Very High
tetrodotoxin 16 99.72 Very High Very High Very High
antagonist 3 99.62 Very High Very High Very High
Enkephalin 11 99.54 Very High Very High Very High
Dorsal horn 3 99.24 Very High Very High Very High
Calcium channel 1 98.60 Very High Very High Very High
conotoxin 1 97.64 Very High Very High Very High
nMDA receptor antagonist 1 97.54 Very High Very High Very High
ischemia 8 97.16 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pancreatitis 6 97.82 Very High Very High Very High
Cv Unclassified Under Development 8 97.16 Very High Very High Very High
Myelitis 3 95.40 Very High Very High Very High
Nociception 3 93.28 High High
Neurodegenerative Disease 1 91.00 High High
Nervous System Injury 1 89.08 High High
Apoptosis 1 84.40 Quite High
INFLAMMATION 1 83.72 Quite High
Hyperalgesia 1 52.72 Quite High
Pain 2 43.04 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We conclude that: (1) pancreatic ischemic preconditioning reduces the severity of ischemia/reperfusion-induced pancreatitis; (2) this effect seems to be related, at least in part, to the improvement of pancreatic blood flow and the reduction in the release of proinflammatory interleukin-1beta; (3) sensory and vagal nerves are involved in protective effect of ischemic preconditioning against pancreatic damage.
Negative_regulation (reduction) of Localization (release) of interleukin-1beta in vagal nerves associated with ischemia and pancreatitis
1) Confidence 0.57 Published 2003 Journal Eur. J. Pharmacol. Section Abstract Doc Link 12892840 Disease Relevance 0.61 Pain Relevance 0.28
Following application of lipopolysaccharide (LPS) to an ex vivo dorsal horn slice preparation, we observed rapid secretion of IL-1beta which was prevented by inhibition of glial cell metabolism and by inhibitors of either p38 mitogen-activated protein kinase (MAPK) or caspase 1.
Negative_regulation (prevented) of Localization (secretion) of IL-1beta in glial cell associated with dorsal horn
2) Confidence 0.57 Published 2006 Journal J. Neurochem. Section Abstract Doc Link 16942597 Disease Relevance 0.66 Pain Relevance 0.49
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.
Negative_regulation (inhibited) of Localization (release) of irIL-1 beta associated with tetrodotoxin, beta blocker, calcium channel, lidocaine and conotoxin
3) Confidence 0.43 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.33
ME and LE increased LPS-induced IL-1 beta release, which was not blocked by naloxone.
Negative_regulation (blocked) of Localization (release) of IL-1 beta associated with narcan and enkephalin
4) Confidence 0.43 Published 2002 Journal Neuropeptides Section Abstract Doc Link 12507434 Disease Relevance 0.09 Pain Relevance 1.09
The sodium channel inhibitor tetrodotoxin, the NMDA and non-NMDA receptor antagonists d(-)-2-amino-5-phosphonopentanoic acid (AP-5) plus 6-cyano-7-nitroquinoxaline-2,3-dione-disodium (CNQX) almost completely abolished IL-1 beta-evoked [(3)H]purine release.
Negative_regulation (abolished) of Localization (release) of IL-1 beta associated with tetrodotoxin, nmda receptor antagonist and sodium channel
5) Confidence 0.41 Published 2004 Journal J. Neuroimmunol. Section Abstract Doc Link 15145601 Disease Relevance 0 Pain Relevance 0.42
Whereas, IL-1 receptor antagonist and cycloheximide inhibited IL-1beta-evoked secretion of SP-like immunoreactivity (SP-li), actinomycin D decreased it significantly but did not entirely abolish it.
Negative_regulation (inhibited) of Localization (secretion) of IL-1beta-evoked associated with antagonist and substance p
6) Confidence 0.06 Published 2003 Journal Eur. J. Neurosci. Section Abstract Doc Link 14622206 Disease Relevance 0 Pain Relevance 0.47
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.
Negative_regulation (reduced) of Localization (release) of IL-1 beta in microglia associated with tetrodotoxin
7) Confidence 0.05 Published 2009 Journal Glia Section Abstract Doc Link 19115387 Disease Relevance 0 Pain Relevance 1.63
Phenytoin attenuated by approximately 50% the release of IL-1 alpha, IL-1 beta, and TNF-alpha from LPS-stimulated microglia, but had minimal effects on the release of IL-2, IL-4, IL-6, IL-10, MCP-1, and TGF-alpha.
Negative_regulation (attenuated) of Localization (release) of IL-1 beta in microglia
8) Confidence 0.05 Published 2009 Journal Glia Section Abstract Doc Link 19115387 Disease Relevance 0 Pain Relevance 1.71

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