INT15844

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Context Info
Confidence 0.67
First Reported 1984
Last Reported 2009
Negated 1
Speculated 2
Reported most in Abstract
Documents 7
Total Number 11
Disease Relevance 4.20
Pain Relevance 3.47

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 (ENG) cell motility (ENG) cell adhesion (ENG)
nucleolus (ENG) nucleus (ENG) cytoplasm (ENG)
Anatomy Link Frequency
plasma 6
pituitary 6
ARC 2
neutrophils 2
ENG (Homo sapiens)
Pain Link Frequency Relevance Heat
Dopamine 4 100.00 Very High Very High Very High
Central nervous system 3 98.60 Very High Very High Very High
Inflammation 28 98.04 Very High Very High Very High
opioid receptor 27 97.40 Very High Very High Very High
IPN 30 97.08 Very High Very High Very High
addiction 6 96.24 Very High Very High Very High
depression 3 95.20 Very High Very High Very High
local anesthetic 1 92.72 High High
dexamethasone 8 92.16 High High
antinociception 15 91.92 High High
Disease Link Frequency Relevance Heat
Stress 53 99.98 Very High Very High Very High
Aids-related Complex 5 98.94 Very High Very High Very High
INFLAMMATION 28 98.04 Very High Very High Very High
Inflammatory Pain 30 97.08 Very High Very High Very High
Hyperalgesia 75 96.52 Very High Very High Very High
Nociception 24 96.32 Very High Very High Very High
Respiratory Failure 3 95.20 Very High Very High Very High
Apoptosis 5 94.80 High High
Vomiting 3 94.24 High High
Heart Rate Under Development 1 68.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results indicate that: 1. secretion of beta-END-LI varies during different phases of the estrous cycle, 2. acute stress is a potent activator for beta-END-LI secretion, 3. no apparent increase of beta-END-LI in the blood plasma of ewes subjected to prolonged stress concomitant with accumulation of this material in pituitary (Polkowska and Przekop, 1988) supports the idea, that prolonged stress augments the synthesis of beta-END-LI but not its release.
Positive_regulation (activator) of Localization (secretion) of END in plasma associated with stress
1) Confidence 0.67 Published 1990 Journal Exp. Clin. Endocrinol. Section Abstract Doc Link 2245820 Disease Relevance 0.50 Pain Relevance 0.05
These results indicate that: 1. secretion of beta-END-LI varies during different phases of the estrous cycle, 2. acute stress is a potent activator for beta-END-LI secretion, 3. no apparent increase of beta-END-LI in the blood plasma of ewes subjected to prolonged stress concomitant with accumulation of this material in pituitary (Polkowska and Przekop, 1988) supports the idea, that prolonged stress augments the synthesis of beta-END-LI but not its release.
Positive_regulation (augments) of Localization (release) of END in plasma associated with stress
2) Confidence 0.45 Published 1990 Journal Exp. Clin. Endocrinol. Section Abstract Doc Link 2245820 Disease Relevance 0.43 Pain Relevance 0
The present study evaluated the hypothesis that increased plasma levels of epinephrine (EPI) stimulate immunoreactive beta-endorphin (i beta END) secretion in humans experiencing a mild stress.
Positive_regulation (stimulate) of Localization (secretion) of END in plasma associated with stress
3) Confidence 0.38 Published 1989 Journal J. Clin. Endocrinol. Metab. Section Abstract Doc Link 2527244 Disease Relevance 0.24 Pain Relevance 0.09
We found the significant increase in MTT reduction by neutrophils in the presence of M-ENK and beta-END both before and after the culture.
Positive_regulation (increase) of Localization (presence) of beta-END in neutrophils
4) Confidence 0.15 Published 2002 Journal Mediators Inflamm Section Abstract Doc Link PMC1781664 Disease Relevance 0.58 Pain Relevance 0.42
Also, these effects could not be enhanced by increasing END release through stress or by modifying POMC-MIDGE-NLS to code for multiple copies of END (Fig. 5, Fig. 6).
Positive_regulation (increasing) of Localization (release) of END associated with stress
5) Confidence 0.11 Published 2009 Journal Mol Pain Section Body Doc Link PMC2797781 Disease Relevance 0.55 Pain Relevance 0.46
Here, we examined whether swim stress can stimulate the secretion of END, possibly overcoming the variability in its leukocytic content, and increase its anti-hyperalgesic actions.
Positive_regulation (stimulate) of Localization (secretion) of END associated with stress and hyperalgesia
6) Confidence 0.07 Published 2009 Journal Mol Pain Section Body Doc Link PMC2797781 Disease Relevance 0.95 Pain Relevance 0.32
Our major objective was to enhance the production and release of END in inflamed tissue using POMC-MIDGE-NLS to provide continuous relief of inflammatory pain.


Positive_regulation (enhance) of Localization (release) of END associated with ipn
7) Confidence 0.07 Published 2009 Journal Mol Pain Section Body Doc Link PMC2797781 Disease Relevance 0.70 Pain Relevance 0.97
However, whereas AVP merely synergizes with CRH in the pituitary, it seems to be essential for the release of hypothalamic beta-END by CRH.
Spec (seems) Positive_regulation (essential) of Localization (release) of beta-END in pituitary
8) Confidence 0.06 Published 1991 Journal Neuroendocrinology Section Abstract Doc Link 1766548 Disease Relevance 0 Pain Relevance 0
To further investigate the phenotype of activated neurons in the ARC, the present study examined whether beta-endorphin (beta-END) and/or dopamine (DA) neurons are activated by mating, and if so, whether activation is involved in the mating-induced acute release of PRL and the establishment of the twice-daily surges of PRL.
Spec (whether) Positive_regulation (mating-induced) of Localization (release) of beta-END in ARC associated with dopamine and aids-related complex
9) Confidence 0.00 Published 2000 Journal Neuroendocrinology Section Abstract Doc Link 10940735 Disease Relevance 0.25 Pain Relevance 0.13
These results demonstrate that 1) the responses of beta-END-LI, PRL, and GH are not an artifact of the sampling procedure; 2) PRL release during suckling is independent of beta-END-LI release by the pituitary; and 3) suckling stimulates the release of ACTH, beta-END, and beta-lipotropin from the anterior pituitary.
Positive_regulation (stimulates) of Localization (release) of beta-END in pituitary
10) Confidence 0.00 Published 1984 Journal Endocrinology Section Abstract Doc Link 6323136 Disease Relevance 0 Pain Relevance 0.50
These results demonstrate that 1) the responses of beta-END-LI, PRL, and GH are not an artifact of the sampling procedure; 2) PRL release during suckling is independent of beta-END-LI release by the pituitary; and 3) suckling stimulates the release of ACTH, beta-END, and beta-lipotropin from the anterior pituitary.
Neg (independent) Positive_regulation (independent) of Localization (release) of beta-END in pituitary
11) Confidence 0.00 Published 1984 Journal Endocrinology Section Abstract Doc Link 6323136 Disease Relevance 0 Pain Relevance 0.52

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