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Biomedical subjects

H Osborne

Publications and source records attributed to H Osborne.

23 records · Page 2Linked to original sources
PubMed1980

Functional aspects of endorphins.

Radioimmunoassay of methionine-enkephalin, leucine-enkephalin and beta-endorphin were used in order to study the distribution and release of endorphins. The distribution pattern of enkephalin immunoreactivity in brain, including human brain, is quite different from that of beta-endorphin immunoreactivity. Separation of beta-endorphin and beta-lipotropin by column chromatography revealed that the contribution of beta-lipotropin to beta-endorphin immunoreactivity in brain is very small. In the anterior lobe of the pituitary both beta-endorphin and beta-lipotropin were found, whereas in the intermediate/posterior lobe almost all immunoreactivity was due to beta-endorphin; considerable amounts of enkephalin were also detected. Raising the concentration of potassium ions stimulated the release of met- and leu-enkephalin from striatal slices and the release of beta-endorphin immunoreactive material(s) from hypothalamic slices; both phenomena were dependent upon the presence of calcium ions. Studies of the release of beta-endorphin from isolated rat pituitaries revealed characteristic differences between the anterior and intermediate/posterior lobes; e.g., lysine vasopressin and extracts from the median eminence were highly effective in releasing beta-endorphin from the anterior lobe without affecting the release from the intermediate/posterior lobe; on the other hand, dopamine inhibited beta-endorphin release from the intermediate/posterior lobe without affecting release from the anterior lobe. Increased beta-endorphin levels were found after various stress conditions in rat plasma, as well as after treatment with metyrapone and vasopressin. In normal human plasma significant amounts of beta-endorphin were detected; increased levels were found in Addison's, Nelson's and Cushing's disease. Chronic opiate treatment of rats for 10 days did not affect brain levels of enkephalin or the beta-endorphin content of the hypothalamus, pituitary and plasma. Precipitated withdrawal decreased beta-endorphin in the anterior lobe and hypothalamus and increased beta-endorphin levels in the plasma. Long-term morphine treatment (30 days) decreased enkephalin and beta-endorphin content in some brain areas and in the intermediate/posterior pituitary lobe but not in the anterior lobe.

Animals↗
PubMed1979

Release of beta-endorphin from rat hypothalamus in vitro.

The rate of release of beta-endorphin-like immunoreactivity (beta-EI) from rat hypothalamic slices was increased 3- to 4-fold over the spontaneous release during exposure to a depolarizing concentration of potassium ions. This augmented outflow was abolished in the absence of calcium. The amount of beta-EI released from slices exposed to a second pulse of potassium was reduced by approximately 50% compared to that in the first. 70% of the potassium-induced released immunoreactive material migrated on a calibrated Sephadex G-50 column like synthetic human beta-endorphin. These findings are discussed in terms of a neuronal release of beta-endorphin and may be taken as supportive evidence for a neurotransmitter and/or neurohormonal role of beta-endorphin in the hypothalamus.

Animals↗
PubMed1978

Potassium-induced release of enkephalins from rat striatal slices.

The rate of release of enkephalin from rat striatal slices increased 7--10 fold in response to depolarization by 50 mM potassium ions in vitro. The potassium-evoked release of enkephalins was abolished in a calcium deficient medium. Uptake studies indicated that the potassium-stimulated efflux was not due to the inhibition of an active uptake mechanism for these peptides. These findings provide support for the view that enkephalins may function as neurotransmitters in brain.

Animals↗
PubMedDate not supplied

A novel treatment for chronic pancreatitis.

BACKGROUND: Hereditary pancreatitis is an important cause of chronic pancreatitis, which may result in endocrine and exocrine failure. This may necessitate simultaneous pancreas and kidney transplant (SPK). Bladder drainage of the exocrine secretions may cause problems. AIM: To report one such case and its surgical correction. METHODS: A 20-year-old male with insulin-dependent diabetes mellitus secondary to idiopathic chronic pancreatitis had a SPK with bladder drainage. Urological and metabolic complications secondary to the drainage of pancreatic secretions, rich in proteolytic enzymes required convertion from bladder to enteric drainage. RESULTS: He was able to discontinue his pancreatic enzyme supplements, ceased to have steatorrhoea and gained weight. He was referred to the European Registry of Hereditary Pancreatitis and Familial Pancreatic Cancer (EUROPAC), hereditary pancreatitis was confirmed by genetic analysis. CONCLUSION: Enteric-drained pancreas transplantation is a successful treatment for exocrine as well as endocrine pancreatic failure and should be considered as a treatment option in patients with chronic pancreatitis.

Adult↗