INT20892

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Context Info
Confidence 0.48
First Reported 1985
Last Reported 2007
Negated 0
Speculated 0
Reported most in Abstract
Documents 21
Total Number 22
Disease Relevance 2.54
Pain Relevance 15.82

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
neutrophils 5
IGKV1D-39 (Homo sapiens)
Pain Link Frequency Relevance Heat
Enkephalin 148 99.92 Very High Very High Very High
Opioid 15 99.84 Very High Very High Very High
narcan 32 99.78 Very High Very High Very High
agonist 18 99.76 Very High Very High Very High
Morphine 6 99.66 Very High Very High Very High
Potency 6 99.42 Very High Very High Very High
opiate 9 99.30 Very High Very High Very High
antagonist 8 99.28 Very High Very High Very High
opioid receptor 15 93.40 High High
Inflammation 29 84.92 Quite High
Disease Link Frequency Relevance Heat
Sepsis 3 99.06 Very High Very High Very High
Disease 10 99.04 Very High Very High Very High
Sleep Disorders 98 98.98 Very High Very High Very High
Adult Respiratory Distress Syndrome 12 98.28 Very High Very High Very High
INFLAMMATION 35 84.92 Quite High
Vomiting 4 29.60 Quite Low
Adhesions 41 5.00 Very Low Very Low Very Low
Anxiety Disorder 4 5.00 Very Low Very Low Very Low
Pressure And Volume Under Development 3 5.00 Very Low Very Low Very Low
Necrosis 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Another opiate antagonist, nalorphine, as well as the opiate agonist, morphine, also inhibited O2- release in the same concentration range.
Localization (release) of O2 associated with antagonist, agonist, opiate and morphine
1) Confidence 0.48 Published 1985 Journal Life Sci. Section Abstract Doc Link 2995744 Disease Relevance 0.08 Pain Relevance 0.92
Neutrophils were pre-incubated with the range of concentrations of (-) naloxone that is administered in models of experimental sepsis (10(-6) - 10(-4.5) M). (-) Naloxone inhibited O2- release in a dose dependent manner. 02- produced by a cell-free xanthine-xanthine oxidase system was not inhibited by (-) naloxone, indicating that (-) naloxone was not scavanging O2-.
Localization (release) of O2 in Neutrophils associated with narcan and sepsis
2) Confidence 0.42 Published 1985 Journal Life Sci. Section Abstract Doc Link 2995744 Disease Relevance 0.10 Pain Relevance 0.76
Using the superoxide dismutase inhibitable reduction of cytochrome c assay, we studied, the effect of (-) naloxone on N-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulated superoxide (O2-) release from human neutrophils.
Localization (release) of O2 in neutrophils associated with narcan
3) Confidence 0.42 Published 1985 Journal Life Sci. Section Abstract Doc Link 2995744 Disease Relevance 0.09 Pain Relevance 0.55
Leu-enkephalin induced baseline reactivity was dependent upon progressive increase in the magnitude of change on O2- release (i.e., the higher the baseline the higher the magnitude of change in O2- generation).
Localization (release) of O2 associated with enkephalin
4) Confidence 0.35 Published 1990 Journal Brain Behav. Immun. Section Abstract Doc Link 2159354 Disease Relevance 0 Pain Relevance 0.91
The present work describes the ability of Met- and Leu-enkephalin to modulate the superoxide anion (O2-) release from unstimulated human polymorphonuclear cells (PMN) and from PMN stimulated with phorbol myristate acetate (PMA).
Localization (release) of O2 associated with enkephalin
5) Confidence 0.35 Published 1990 Journal Brain Behav. Immun. Section Abstract Doc Link 2159354 Disease Relevance 0 Pain Relevance 0.37
Both opioid peptides stimulated O2- release by PMN from donors with low baseline reactivity in a concentration-dependent manner.
Localization (release) of O2 associated with opioid
6) Confidence 0.35 Published 1990 Journal Brain Behav. Immun. Section Abstract Doc Link 2159354 Disease Relevance 0 Pain Relevance 0.55
PMNs collected from donors with medium baseline reactivity incubated with Leu-enkephalin regardless of concentration released less O2- than control, nontreated PMNs.
Localization (released) of O2 associated with enkephalin
7) Confidence 0.35 Published 1990 Journal Brain Behav. Immun. Section Abstract Doc Link 2159354 Disease Relevance 0 Pain Relevance 0.77
In cells stimulated with PMA, Met-enkephalin caused additional O2- release, while Leu-enkephalin was ineffective in triggering already stimulated cells.
Localization (release) of O2 associated with enkephalin
8) Confidence 0.35 Published 1990 Journal Brain Behav. Immun. Section Abstract Doc Link 2159354 Disease Relevance 0 Pain Relevance 0.91
Opioid antagonist naloxone (10(-5) M) abrogated the effect of MENK on O2- release.
Localization (release) of O2 associated with antagonist, narcan, enkephalin and opioid
9) Confidence 0.34 Published 1995 Journal Neuropeptides Section Abstract Doc Link 8837964 Disease Relevance 0 Pain Relevance 1.26
DADLE (delta receptor agonist) increased O2- release in 10(-11) M concentration, while DAGO (mu receptor agonist) had no effect in any concentration examined.
Localization (release) of O2 associated with agonist
10) Confidence 0.29 Published 1995 Journal Neuropeptides Section Abstract Doc Link 8837964 Disease Relevance 0 Pain Relevance 1.24
Aminopeptidase inhibition by bestatin did not influence O2- release from MENK treated PMNs.
Localization (release) of O2 associated with enkephalin
11) Confidence 0.29 Published 1995 Journal Neuropeptides Section Abstract Doc Link 8837964 Disease Relevance 0 Pain Relevance 1.20
In lower MENK concentrations, where MENK alone had no effect on O2- release, inhibition of enkephalinase by thiorphan significantly increased O2- production, while in higher concentrations, where MENK alone was effective, inhibition of enkephalinase had no effect.
Localization (release) of O2 associated with enkephalin
12) Confidence 0.29 Published 1995 Journal Neuropeptides Section Abstract Doc Link 8837964 Disease Relevance 0 Pain Relevance 1.10
While MENK predominantly stimulated, TGG suppressed O2- release.
Localization (release) of O2 associated with enkephalin
13) Confidence 0.29 Published 1995 Journal Neuropeptides Section Abstract Doc Link 8837964 Disease Relevance 0 Pain Relevance 1.27
Using human neutrophils as a source of O-2, and an assay for O-2 based upon the reduction of cytochrome C, we found that prostaglandin D2 (PGD2), leucine enkephalin (LE), and methionine enkephalin (ME) inhibited O-2 release.
Localization (release) of O-2 in neutrophils associated with enkephalin
14) Confidence 0.18 Published 1986 Journal J. Surg. Res. Section Abstract Doc Link 3023754 Disease Relevance 0.27 Pain Relevance 0.68
Another peptide, thyrotropin releasing hormone (TRH), had no effect on O-2 release.
Localization (release) of O-2
15) Confidence 0.18 Published 1986 Journal J. Surg. Res. Section Abstract Doc Link 3023754 Disease Relevance 0.23 Pain Relevance 0.67
The Escherichia coli product, N-formyl methionyl leucyl phenylalanine (FMLP), was employed to stimulate O-2 release.
Localization (release) of O-2
16) Confidence 0.18 Published 1986 Journal J. Surg. Res. Section Abstract Doc Link 3023754 Disease Relevance 0.25 Pain Relevance 0.68
The effect of enkephalins and prostaglandins on O-2 release by neutrophils.
Localization (release) of O-2 in neutrophils associated with enkephalin
17) Confidence 0.15 Published 1986 Journal J. Surg. Res. Section Title Doc Link 3023754 Disease Relevance 0.28 Pain Relevance 0.72
There was no correlation between the potency of the inhibitory effect on O-2 release and the effect of these agents on the binding of [3H] FMLP to human neutrophils.
Localization (release) of O-2 in neutrophils associated with potency
18) Confidence 0.15 Published 1986 Journal J. Surg. Res. Section Abstract Doc Link 3023754 Disease Relevance 0.22 Pain Relevance 0.65
Control of the release of O-2 may prove beneficial.
Localization (release) of O-2
19) Confidence 0.13 Published 1986 Journal J. Surg. Res. Section Abstract Doc Link 3023754 Disease Relevance 0.30 Pain Relevance 0.57
Before N2O/O2 sedation, patientsÂ’ RSS were determined as 1 but after the administration of N2O/O2, at the T1-6 time points patientsÂ’ RSS were 2 and OAA/S scores of patientsÂ’ were 4 or 5.
Localization (administration) of N2O associated with sleep disorders
20) Confidence 0.13 Published 2007 Journal European journal of dentistry Section Body Doc Link PMC2609910 Disease Relevance 0.32 Pain Relevance 0

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