INT10201

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Context Info
Confidence 0.50
First Reported 1991
Last Reported 2008
Negated 1
Speculated 0
Reported most in Abstract
Documents 8
Total Number 8
Disease Relevance 0.97
Pain Relevance 2.21

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 (Agt) aging (Agt) extracellular region (Agt)
extracellular matrix organization (Agt)
Anatomy Link Frequency
Brain 2
nucleus 2
head 2
Agt (Rattus norvegicus)
Pain Link Frequency Relevance Heat
analgesia 5 100.00 Very High Very High Very High
antagonist 53 98.36 Very High Very High Very High
anesthesia 2 98.00 Very High Very High Very High
noradrenaline 4 88.56 High High
agonist 34 88.52 High High
Clonidine 6 82.64 Quite High
Neurotransmitter 9 81.40 Quite High
Intracerebroventricular 2 70.88 Quite High
tail-flick 1 66.84 Quite High
tetrodotoxin 1 65.20 Quite High
Disease Link Frequency Relevance Heat
Stress 58 100.00 Very High Very High Very High
Ureteral Obstruction 3 96.92 Very High Very High Very High
Pressure Volume 2 Under Development 2 55.60 Quite High
INFLAMMATION 28 5.00 Very Low Very Low Very Low
Cancer 22 5.00 Very Low Very Low Very Low
Targeted Disruption 22 5.00 Very Low Very Low Very Low
Pituitary Cancer 11 5.00 Very Low Very Low Very Low
Starvation 10 5.00 Very Low Very Low Very Low
Rheumatoid Arthritis 8 5.00 Very Low Very Low Very Low
Natriuresis 7 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Brain renin angiotensin system (RAS) in stress-induced analgesia and impaired retention.
Positive_regulation (stress-induced) of Localization (retention) of angiotensin system in Brain associated with stress and analgesia
1) Confidence 0.50 Published 1999 Journal Peptides Section Title Doc Link 10447091 Disease Relevance 0.65 Pain Relevance 0.48
Levels of angiotensin release increased from 13.85 +/- 1.53 pg/mg protein to 172.64 +/- 17.49 pg/mg protein with increasing concentrations of K+.
Positive_regulation (increased) of Localization (release) of angiotensin
2) Confidence 0.46 Published 1992 Journal Brain Res. Bull. Section Abstract Doc Link 1617438 Disease Relevance 0 Pain Relevance 0.13
In situ hybridization and Western blot analysis demonstrated angiotensinogen mRNA and angiotensin converting enzyme (ACE) protein localized to PTs and upregulated in obstructed kidneys, respectively, confirming an increased expression of renal RAS in vivo.
Positive_regulation (demonstrated) of Localization (localized) of angiotensinogen mRNA
3) Confidence 0.45 Published 2000 Journal Am. J. Physiol. Renal Physiol. Section Abstract Doc Link 10807582 Disease Relevance 0.27 Pain Relevance 0.10
Involvement of adrenergic and angiotensinergic receptors in the paraventricular nucleus in the angiotensin II-induced vasopressin release.
Positive_regulation (induced) of Localization (release) of angiotensin II in nucleus
4) Confidence 0.43 Published 1992 Journal J. Pharmacol. Exp. Ther. Section Title Doc Link 1469631 Disease Relevance 0 Pain Relevance 0.41
The data indicate that head-up tilt increases AVP secretion in anesthetized rats, that the response is mediated by the vagus and particularly by the arterial baroreceptors, and that circulating angiotensin II contributes to the response.
Positive_regulation (increases) of Localization (secretion) of angiotensin II in head
5) Confidence 0.38 Published 1991 Journal Neuroendocrinology Section Abstract Doc Link 1922676 Disease Relevance 0.06 Pain Relevance 0.05
ANG II-induced AVP release.
Positive_regulation (induced) of Localization (release) of ANG
6) Confidence 0.37 Published 1992 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 1469631 Disease Relevance 0 Pain Relevance 0.50
ANG II-induced AVP release.
Positive_regulation (induced) of Localization (release) of ANG
7) Confidence 0.37 Published 1992 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 1469631 Disease Relevance 0 Pain Relevance 0.46
In reaggregate cell cultures kept in serum-free medium, we found that physiological doses of GnRH stimulate PRL release and, at these doses, neither an angiotensin-converting enzyme inhibitor, nor angiotensin receptor-1 antagonists were capable of inhibiting the GnRH-stimulated PRL release (222).
Neg (neither) Positive_regulation (stimulate) of Localization (release) of angiotensin associated with antagonist
8) Confidence 0.13 Published 2008 Journal Journal of Neuroendocrinology Section Body Doc Link PMC2229370 Disease Relevance 0 Pain Relevance 0.09

General Comments

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