INT6128

Context Info Confidence 0.70 First Reported 1980 Last Reported 2010 Negated 6 Speculated 16 Reported most in Abstract Documents 256 Total Number 272 Disease Relevance 68.77 Pain Relevance 121.64

small molecule metabolic process (POMC) cell-cell signaling (POMC) cytoplasm (POMC) extracellular space (POMC) generation of precursor metabolites and energy (POMC) signal transduction (POMC)

Anatomy Link Frequency pituitary 61 plasma 26 corticotroph 17 blood 14 nucleus 10 POMC (Homo sapiens)

Pain Link Frequency Relevance Heat Enkephalin 370 100.00 Opioid 323 100.00 narcan 298 100.00 cytokine 239 100.00 Morphine 176 100.00 analgesia 152 100.00 Dopamine 149 100.00 Serotonin 108 100.00 opiate 86 100.00 fluoxetine 82 100.00

Disease Link Frequency Relevance Heat Stress 684 100.00 Cancer 383 100.00 Hypoglycemia 44 100.00 Necrosis 33 100.00 Hypothermia 3 100.00 Nociception 71 99.98 Disease 407 99.96 Thrombosis 1 99.88 Pain 269 99.84 Fibromyalgia 118 99.60

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Electrical stimulation-induced release of beta-endorphin from genetically modified neuro-2a cells.

Positive_regulation (induced) of Localization (release) of beta-endorphin

1) Confidence 0.70 Published 2008 Journal Cell Transplant Section Title Doc Link 18714673 Disease Relevance 0 Pain Relevance 0.14

Using electrical field stimulation we were able to identify a stimulation pattern that significantly increased the release of beta-endorphin-immunoreactive material, although to a limited extent.

Positive_regulation (increased) of Localization (release) of beta-endorphin

2) Confidence 0.70 Published 2008 Journal Cell Transplant Section Abstract Doc Link 18714673 Disease Relevance 0 Pain Relevance 0.16

In this article we address the question of whether the release of beta-endorphin, an opioid with a potent analgesic effect, could be induced by electrically stimulating stably transfected Neuro-2a cells.

Positive_regulation (induced) of Localization (release) of beta-endorphin in Neuro-2a associated with analgesic and opioid

3) Confidence 0.70 Published 2008 Journal Cell Transplant Section Abstract Doc Link 18714673 Disease Relevance 0 Pain Relevance 0.20

Physical exercise stimulates marked concomitant release of beta-endorphin and adrenocorticotropic hormone (ACTH) in peripheral blood in man.

Positive_regulation (stimulates) of Localization (release) of adrenocorticotropic hormone in blood associated with nociceptor

4) Confidence 0.70 Published 1980 Journal Experientia Section Title Doc Link 6254800 Disease Relevance 0.09 Pain Relevance 0.10

Six normal men were treated with oral metyrapone to stimulate the secretion of ACTH, beta-lipotropin, and beta-endorphin.

Positive_regulation (stimulate) of Localization (secretion) of ACTH

5) Confidence 0.70 Published 1985 Journal J. Clin. Endocrinol. Metab. Section Abstract Doc Link 2997256 Disease Relevance 0 Pain Relevance 0.16

The effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects.

Positive_regulation (induced) of Localization (secretion) of ACTH associated with dexamethasone and analgesia

6) Confidence 0.70 Published 1990 Journal Brain Res. Section Abstract Doc Link 2168784 Disease Relevance 0.24 Pain Relevance 0.59

Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release.

Positive_regulation (induced) of Localization (release) of ACTH associated with pain threshold and dexamethasone

7) Confidence 0.70 Published 1990 Journal Brain Res. Section Abstract Doc Link 2168784 Disease Relevance 0.27 Pain Relevance 0.65

Suppression of electroacupuncture(EA)-induced beta-endorphin and ACTH release by hydrocortisone in man.

Positive_regulation (induced) of Localization (release) of beta-endorphin associated with anesthesia and electroacupuncture

8) Confidence 0.70 Published 1983 Journal Acta Endocrinol. Section Title Doc Link 6310920 Disease Relevance 0 Pain Relevance 0.47

BACKGROUND: In the pituitary of lower species, pro-opiomelanocortin is expressed in corticotroph cells of the anterior and in melanotroph cells of the neurointermediate lobe; enzymatic processing in the corticotrophs results in the release of adrenocorticotropic hormone, beta-lipotropin, or beta-endorphin.

Positive_regulation (results) of in pituitary Localization (release) of adrenocorticotropic hormone in corticotroph

9) Confidence 0.70 Published 2006 Journal Clin J Pain Section Abstract Doc Link 16428944 Disease Relevance 0.07 Pain Relevance 0.15

Therefore, any contribution of the endorphin system to the production of general anesthesia does not appear to require the release of beta-endorphin.

Spec (appear) Positive_regulation (require) of Localization (release) of beta-endorphin associated with anesthesia

10) Confidence 0.70 Published 1984 Journal Anesthesiology Section Abstract Doc Link 6318607 Disease Relevance 0.07 Pain Relevance 0.62

Two different signalling pathways for the induction of immunoreactive beta-endorphin secretion by human peripheral blood mononuclear cells.

Positive_regulation (induction) of Localization (secretion) of beta-endorphin in mononuclear cells

11) Confidence 0.70 Published 1991 Journal Endocrinology Section Title Doc Link 1824933 Disease Relevance 0 Pain Relevance 0.14

Naloxone-induced ACTH release in man is inhibited by clonidine.

Positive_regulation (induced) of Localization (release) of ACTH associated with narcan and clonidine

12) Confidence 0.70 Published 1990 Journal Clin. Exp. Pharmacol. Physiol. Section Title Doc Link 2160341 Disease Relevance 0 Pain Relevance 0.76

This suggests that naloxone causes ACTH release through these same central noradrenergic pathways.

Positive_regulation (causes) of Localization (release) of ACTH associated with narcan

13) Confidence 0.70 Published 1990 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 2160341 Disease Relevance 0 Pain Relevance 0.64

We used the alpha 2-adrenergic agonist, clonidine, as a central nervous system inhibitor of ACTH release to see if it would alter naloxone-induced ACTH secretion in normal human volunteers. 2.

Positive_regulation (induced) of Localization (secretion) of ACTH in central nervous system associated with narcan, agonist, central nervous system and clonidine

14) Confidence 0.70 Published 1990 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 2160341 Disease Relevance 0 Pain Relevance 0.63

We conclude that clonidine, by blocking central noradrenergic pathways, which stimulate corticotropin-releasing hormone secretion, inhibits naloxone-induced ACTH secretion.

Positive_regulation (induced) of Localization (secretion) of ACTH associated with narcan and clonidine

15) Confidence 0.70 Published 1990 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 2160341 Disease Relevance 0 Pain Relevance 0.65

In dispersed monolayer culture, CRF failed to elicit ACTH release from the tumor cells, but dexamethasone caused a paradoxical increase in ACTH secretion in vitro.

Positive_regulation (increase) of Localization (secretion) of ACTH associated with cancer and dexamethasone

16) Confidence 0.70 Published 1988 Journal Horm. Metab. Res. Section Abstract Doc Link 2456259 Disease Relevance 0.72 Pain Relevance 0.17

Inhibition of serotonin-induced ACTH release in man by clonidine.

Positive_regulation (induced) of Localization (release) of ACTH associated with serotonin and clonidine

17) Confidence 0.70 Published 1988 Journal Clin. Exp. Pharmacol. Physiol. Section Title Doc Link 2856056 Disease Relevance 0.15 Pain Relevance 1.03

Fenfluramine, a serotonin releasing agent and uptake inhibitor, causes ACTH release in normal man. 2.

Positive_regulation (causes) of Localization (release) of ACTH associated with serotonin

18) Confidence 0.70 Published 1988 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 2856056 Disease Relevance 0.17 Pain Relevance 0.84

Central serotonergic pathways are hypothesized to be involved in the stimulation of hypothalamic adrenocorticotropic hormone (ACTH) secretagogue release by both circadian- and stress-induced mechanisms.

Positive_regulation (stimulation) of Localization (release) of ACTH associated with stress

19) Confidence 0.70 Published 1997 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 9171947 Disease Relevance 0.10 Pain Relevance 0.62

Fluoxetine produced a small but non-significant increase in Nal-stimulated ACTH and cortisol release in both morning and afternoon studies.

Positive_regulation (increase) of Localization (release) of ACTH associated with narcan and fluoxetine

20) Confidence 0.70 Published 1997 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 9171947 Disease Relevance 0.06 Pain Relevance 1.13

General Comments

This test has worked.