INT9347

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Context Info
Confidence 0.81
First Reported 1992
Last Reported 2009
Negated 1
Speculated 2
Reported most in Abstract
Documents 58
Total Number 60
Disease Relevance 26.13
Pain Relevance 31.53

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
spinal cord 4
microglia 4
hypothalamus 4
spleen 3
vagal nerves 2
Il1b (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammation 149 100.00 Very High Very High Very High
cytokine 83 100.00 Very High Very High Very High
noradrenaline 34 100.00 Very High Very High Very High
Thermal hyperalgesia 12 100.00 Very High Very High Very High
Inflammatory mediators 3 100.00 Very High Very High Very High
dexamethasone 5 99.92 Very High Very High Very High
lidocaine 8 99.88 Very High Very High Very High
substance P 31 99.84 Very High Very High Very High
Calcitonin gene-related peptide 1 99.84 Very High Very High Very High
Enkephalin 55 99.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 127 100.00 Very High Very High Very High
Hyperalgesia 41 100.00 Very High Very High Very High
Cancer 15 100.00 Very High Very High Very High
Necrosis 14 100.00 Very High Very High Very High
Colitis 50 99.88 Very High Very High Very High
Inflammatory Bowel Disease 25 99.68 Very High Very High Very High
Intervertebral Disk Displacement 4 99.48 Very High Very High Very High
Myelitis 12 99.28 Very High Very High Very High
Nervous System Injury 9 99.20 Very High Very High Very High
Bone Cancer 5 99.18 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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.
Localization (release) of irIL-1 beta associated with tetrodotoxin, beta blocker, calcium channel, lidocaine and conotoxin
1) Confidence 0.81 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.32
In this study, we have investigated the release of immunoreactive interleukin-1 beta (irIL-1 beta) from the rat hypothalamus in vitro.
Spec (investigated) Localization (release) of irIL-1 beta in hypothalamus
2) Confidence 0.81 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.19
The present evidence suggests that irIL-1 beta released by rat hypothalamic explants following KCl depolarization is neuronal in origin.
Localization (released) of irIL-1 beta in neuronal
3) Confidence 0.81 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.31
Inhibition by interleukin-1 beta of noradrenaline release in rat spleen: involvement of lymphocytes, NO and opioid receptors.
Localization (release) of interleukin-1 beta in spleen associated with narcan, noradrenaline and opioid receptor
4) Confidence 0.80 Published 1995 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Title Doc Link 7630433 Disease Relevance 0 Pain Relevance 0.57
Methionine-enkephalin and leucine-enkephalin increase interleukin-1 beta release in mixed glia cultures.
Localization (release) of interleukin-1 beta associated with narcan and enkephalin
5) Confidence 0.80 Published 2002 Journal Neuropeptides Section Title Doc Link 12507434 Disease Relevance 0.09 Pain Relevance 1.09
Mixed glia cultures deprived of microglia (by shaking and incubating with L-leucine methyl ester) did not release IL-1 beta, which indicates microglia as a source of the changes in IL-1 beta release.
Neg (not) Localization (release) of IL-1 beta in microglia
6) Confidence 0.80 Published 2002 Journal Neuropeptides Section Abstract Doc Link 12507434 Disease Relevance 0.08 Pain Relevance 1.02
The aim of this study was to evaluate the effects of methionine-enkephalin (ME) and leucine-enkephalin (LE) on the baseline and LPS-activated release of IL-1 beta in rat mixed glia cultures.
Localization (release) of IL-1 beta associated with enkephalin
7) Confidence 0.80 Published 2002 Journal Neuropeptides Section Abstract Doc Link 12507434 Disease Relevance 0.09 Pain Relevance 1.07
Corticotropin-releasing hormone (CRH) and interleukin-1 beta (IL-1 beta) can release these opioids.
Localization (release) of IL-1 beta associated with opioid
8) Confidence 0.80 Published 1996 Journal Eur. J. Pharmacol. Section Abstract Doc Link 8891603 Disease Relevance 0.17 Pain Relevance 0.80
Corticotropin-releasing hormone (CRH) and interleukin-1 beta (IL-1 beta) can release these opioids.
Localization (release) of interleukin-1 beta associated with opioid
9) Confidence 0.80 Published 1996 Journal Eur. J. Pharmacol. Section Abstract Doc Link 8891603 Disease Relevance 0.17 Pain Relevance 0.81
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.
Localization (release) of IL-1beta in muscle associated with hyperalgesia and inflammation
10) Confidence 0.78 Published 2007 Journal J Pain Section Abstract Doc Link 16949880 Disease Relevance 1.24 Pain Relevance 1.08
Extensive microglial cell activation in the dorsal horn, as determined by immunoreactivity for phosphorylated p38 MAPK, was found to correlate with the occurrence of IL-1beta secretion.
Localization (secretion) of IL-1beta in dorsal horn associated with dorsal horn
11) Confidence 0.78 Published 2006 Journal J. Neurochem. Section Abstract Doc Link 16942597 Disease Relevance 0.60 Pain Relevance 0.68
Following nerve injury, spinal cord glia become activated and secrete a number of inflammatory cytokines, including interleukin-1 (IL-1), which exists as two genetically distinct proteins, IL-1alpha and IL-1beta.
Localization (secrete) of IL-1beta in spinal cord associated with nervous system injury, inflammation, cytokine and spinal cord
12) Confidence 0.78 Published 2009 Journal Exp. Neurol. Section Abstract Doc Link 19341730 Disease Relevance 0.59 Pain Relevance 0.92
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.
Localization (released) of IL-1beta in spinal cord associated with nociception, inflammation, spinal cord and cytokine
13) Confidence 0.78 Published 2006 Journal J. Neurochem. Section Abstract Doc Link 16942597 Disease Relevance 0.66 Pain Relevance 0.62
Further, bone cancer activates spinal glial cells, which may release IL-1beta and other cytokines and contribute to hyperalgesia.
Localization (release) of IL-1beta in spinal associated with hyperalgesia, bone cancer and cytokine
14) Confidence 0.78 Published 2005 Journal Pain Section Abstract Doc Link 16154703 Disease Relevance 1.23 Pain Relevance 1.00
Proinflammatory cytokines, such as interleukin-1beta and tumour necrosis factor-alpha, are released by activated glial cells in the spinal cord and play a major role in pain facilitation.
Localization (released) of interleukin-1beta in spinal cord associated with pain, necrosis, cancer, spinal cord and cytokine
15) Confidence 0.78 Published 2005 Journal Eur. J. Neurosci. Section Abstract Doc Link 16262636 Disease Relevance 0.70 Pain Relevance 0.65
In this study we analyzed the role of substance P (SP) from afferent nerves in ileum contractibility and in the release of inflammatory mediators (neurotensin, Il-1beta, and TNF-alpha) in ileal mucosa and muscularis layers after a 10-Gy gamma-irradiation of the abdomen.
Localization (release) of Il-1beta in nerves associated with inflammatory mediators and substance p
16) Confidence 0.78 Published 2003 Journal Dig. Dis. Sci. Section Abstract Doc Link 12741457 Disease Relevance 0.17 Pain Relevance 0.53
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.
Localization (secretion) of IL-1beta in glial cell associated with dorsal horn
17) Confidence 0.78 Published 2006 Journal J. Neurochem. Section Abstract Doc Link 16942597 Disease Relevance 0.66 Pain Relevance 0.48
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.
Localization (release) of interleukin-1beta in vagal nerves associated with ischemia and pancreatitis
18) Confidence 0.78 Published 2003 Journal Eur. J. Pharmacol. Section Abstract Doc Link 12892840 Disease Relevance 0.61 Pain Relevance 0.28
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.
Localization (release) of irIL-1 beta associated with tetrodotoxin, beta blocker, calcium channel, lidocaine and conotoxin
19) Confidence 0.75 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.30
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.
Localization (release) of irIL-1 beta associated with tetrodotoxin, beta blocker, calcium channel, lidocaine and conotoxin
20) Confidence 0.75 Published 1996 Journal Neurosci. Lett. Section Abstract Doc Link 8971800 Disease Relevance 0 Pain Relevance 0.31

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