Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Baseline concentrations of beta-endorphin (beta-EP) and monoamine metabolites (MHPG: 3-methoxy-4-hydroxy-phenylglycol, HVA: homovanillic acid, 5-HIAA: 5-hydroxyindoleacetic acid) in lumbar CSF (LCSF) and ventricular CSF (VCSF) were measured in 18 patients with intractable pain; 10 with deafferented pain and 8 with peripheral pain. Control values were obtained from 37 individuals of various ages. Changes in the concentrations of these substances were determined before and after giving stimulations (2-5 V, 0.2-0.5 msec, 40-50 Hz, 20-sec duration) to 6 patients through electrodes implanted in deep brain structures (DBS; posterior limb of the internal capsule in 5 patients and rostral mesencephalic lemniscus medialis in one patient), and to 2 other patients through electrodes implanted in the spinal dorsal column (DCS). The control value of beta-EP in LCSF was 57.6 +/- 24.7 pg/ml, which was not significantly different from that of VCSF. Great variation in the individual control LCSF beta-EP concentrations was found, but it was not related to differences in age. The mean baseline LCSF beta-EP concentration was significantly higher (p less than 0.05) than the control in the patients with deaffernted pain before stimulation. One of the monoamine-metabolites, MHPG, showed higher level in the patients with peripheral pain (p less than 0.01). The LCSF beta-EP concentration was not affected by deep brain stimulation, but was increased by dorsal column stimulation. In one patient with excellent pain relief by stimulation of the posterior limb of the internal capsule, the LCSF HVA and 5-HIAA concentrations were conspicuously increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[beta-Endorphin and monoamine metabolite concentrations in patients with intractable pain--changes before and after deep brain or spinal dorsal column stimulation]. 241 30

We have developed a redox system for brain-enhanced delivery of dexamethasone based on an interconvertible dihydropyridine in equilibrium pyridinium salt carrier. Dexamethasone, when combined with the lipoidal carrier, readily crosses the blood-brain barrier. The carrier, when oxidized, reduces its rate of exit from the brain. The aim of the study was to evaluate the capacity of a dexamethasone-chemical delivery system (DX-CDS) and dexamethasone (DEX) to suppress stress-induced elevations of plasma adrenocorticotropic hormone (ACTH) and corticosterone (CORT). Adult male Sprague-Dawley (CD) rats were administered either DX-CDS (10 mg/kg), an equimolar dose of DEX or the drug vehicle (2-hydroxypropyl-beta-cyclodextrin) by a single tail vein injection. Rats then received either no stress or a restraint stress for a 5- or 15-min duration on days 1, 3, 5 or 7 after drug administration and trunk blood was rapidly collected. To assess peripheral effects of DX-CDS and DEX, 1 ml of blood was removed via orbital puncture and evaluated for total and differential leukocyte counts in a separate group of animals. Both DX-CDS and DEX were effective on day 1 in suppressing, by greater than 95%, ACTH secretion induced by a 5-min stress. However, DX-CDS was effective through day 5 (44% suppression) while DEX was not effective after 24 h. When 15 min of stress was applied, DX-CDS effected a significant ACTH suppression through 7 days while DEX was effective for only 3 days. DX-CDS was effective through day 7 (55%) in suppressing CORT after a 15-min stress while DEX was effective for 3 days only.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for prolonged suppression of stress-induced release of adrenocorticotropic hormone and corticosterone with a brain-enhanced dexamethasone-redox delivery system. 254 77