INT22402
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
BACKGROUND: The source and regulatory mechanisms that elevate beta-endorphin (beta-EP) approximately twofold higher than circulating plasma levels in the colostrum of lactating mothers are still unknown, and no studies have examined beta-EP availability previously during maturation phases of human milk. | |||||||||||||||
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In prepubertal obese children, the increased plasma beta EP and beta LPH levels with the maintenance of their circadian rhythm and responsivity to hypoglycemia suggest overactivity of anterior pituitary secretion. | |||||||||||||||
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CONCLUSIONS: It is hypothesized that elevated beta-EP concentrations in colostrum and transitional milk of mothers who were vaginally delivered of infants may contribute to postnatal fetal adaptation, to overcoming birth stress of natural labor and delivery, and at the same time to the postnatal development of several related biologic functions of breast-fed infants.
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In normal prepubertal subjects, the circadian rhythms of beta EP and beta LPH secretion and release induced by hypoglycemia suggest the presence of a well developed neuroendocrine control of proopiomelanocortin-related peptide secretion. | |||||||||||||||
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In obese adolescents, in spite of the normal rhythm of beta LPH and cortisol, beta EP levels did not change throughout the day, thus suggesting beta EP secretion from nonpituitary sources in these subjects. | |||||||||||||||
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The evidence for an analgesic effect arising from increased peripheral concentrations of beta-endorphin (beta-EP) in various animal species is controversial, and has not been fully evaluated in the sheep. | |||||||||||||||
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To stimulate beta-EP release, ovine corticotropin-releasing factor (oCRF) and arginine vasopressin (AVP) were injected intravenously (iv) into a group of 12 out of 24 sheep, 15 min prior to minor surgery on all sheep. | |||||||||||||||
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The iv route of administration induced a prompt (mean peak values after 150 min) dose-dependent increase in beta-EP and beta-LPH levels. | |||||||||||||||
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This behavior appeared to be unaffected by a pre-operative increase in peripheral plasma beta-EP, and may indicate that this increase in beta-EP was not sufficiently analgesic to block the cognitive response to the operation, or long-lasting enough to prevent the perception of post-operative soreness. | |||||||||||||||
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In the obese patients, CSF SRIH and beta-EP levels were significantly reduced and increased, respectively, compared with controls (20.6 +/- 2.62, mean +/- s.e.m., vs 34.5 +/- 2.14 pg/ml, P < 0.05, for SRIH and 111.2 +/- 5.00 vs 80.4 +/- 5.32 pg/ml, P < 0.001, for beta-EP). | |||||||||||||||
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Although a potential role of EP(4) receptor in pain has been suggested, a limited number of selective ligands have made it difficult to explore the physiological functions of EP(4) or its potential as a new analgesic target. | |||||||||||||||
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No presence of beta-LPH, beta-EP and ACTH was confirmed, while gamma-EP, alpha-MSH and des-alpha-MSH were detected for the first time in follicular fluid. | |||||||||||||||
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Fluoxetine (15 and 30 mg orally) a blocker of SE reuptake, induced a significant dose-related rise in plasma beta-EP and beta-LPH levels in a group of seven normal men (P less than 0.01) (mean peak values after 150 min). | |||||||||||||||
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Total serum CK levels were found to be significantly higher in the EP group as compared to the controls (p < 0.001), suggesting that this test might be used as a indicator for EP.27 | |||||||||||||||
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ROC curves demonstrated significant discriminatory capability of increased CK for EP diagnosis, suggesting that CK concentrations could be used to predict EP.42 | |||||||||||||||
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Serum values of VEGF were significantly increased in EP, and a combination of three independent markers using the formula VEGF/(PAPP-A × Progesterone) was found to be superior to single marker measurements for discrimination between normal intrauterine pregnancy and EP (sensitivity of 97.7% and specificity of 92.4%).13
CREATINE KINASE (CK) | |||||||||||||||
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In the controls, clonidine induced release of beta-LPH and beta-EP after 30 min (from 8.9 +/- 1.0 to 19.1 +/- 4.6 fmol/ml, P less than 0.01 and from 8.1 +/- 0.6 to 17.9 +/- 4.6, P less than 0.01) and of ACTH after 60 min (from 12.1 +/- 1.8 to 18.1 +/- 1.8, P less than 0.05) while in addicts beta-EP but not beta-LPH showed a significant increase (from 8.5 +/- 0.7 to 19.8 +/- 4.2, P less than 0.05), 90 min after the injection. | |||||||||||||||
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The naturally occurring peptide human beta-endorphin-(1-27) (h beta-EP-(1-27) has been shown to antagonize beta-endorphin (h beta-EP)-induced analgesia. | |||||||||||||||
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Beta-EP had increased by the 5th day (group A: 4.74 +/- 0.42 to 6.91 +/- 0.65 pmol/l, p less than 0.01; group B: 3.60 +/- 0.48 to 5.14 +/- 0.22 pmol/l, p less than 0.05, and remained at 5.05 +/- 0.65 pmol/l on the 10th day (group B: 0.05 less than p less than 0.1) during fasting. | |||||||||||||||
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PGE2 signals via a transmembrane G-protein coupled receptor (EP), of which four types have been identified (EP1-4) [13,15]. | |||||||||||||||
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General Comments
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