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)

A study was made of the effects of exogenous adrenocorticotropin (ACTH) on the levels of blood components in 109 dairy replacement calves and the statistical correlations between these effects and the growth rates of the calves from birth to six months. Blood samples were taken from a jugular vein before ACTH was injected and then at two, four, six and eight hours afterwards, and analysed for plasma cortisol concentration, total white cell counts, packed cell volume, haemoglobin, plasma glucose, sodium, potassium, magnesium and inorganic phosphorus, erythrocyte sodium, potassium and magnesium, serum ionised calcium and total protein and total plasma calcium concentration. The injection of 1.1 +/- 0.02 iu/kg of ACTH intramuscularly resulted in a peak plasma cortisol concentration after two hours which had not returned to normal after eight hours. It also resulted in leucocytosis, lymphopenia, neutrophilia, eosinopenia and hypophosphataemia; the mean changes were repeatable (P < 0.05) in 49 of the calves tested two months later. The weight gains to six months of age could be predicted from the degree of the changes in several blood constituents. Significant partial regression coefficients were found for the change in glucose concentration (0 to four hours), absolute neutrophil count (0 to two hours), absolute lymphocyte count (0 to four hours) and loge absolute eosinophil count (0 to two hours). The multiple regression sum of squares was highly significant (P < 0.0001), and the multiple coefficient of determination was 0.305. It was concluded that the changes in these blood components after an injection of ACTH might be used to predict the weight gains of dairy replacement calves.
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PMID:Responses of calves to injections of ACTH and their relationship with growth rate. 852 81

Cortisone acetate, hydrocortisone, and hydrocortisone acetate depress the resistance of mice to pneumococcal and influenza viral infections, although hydrocortisone acetate is somewhat less effective than the free alcohol, when given subcutaneously. Pituitary adrenocorticotropin, even in highly purified form and in oil and beeswax, does not significantly alter the resistance of mice to these experimental infections, even when given in doses which may cause profound eosinopenia, lymphopenia, and weight loss, and which are at the limit of tolerance of the animals. Corticosterone depresses resistance to pneumococcal infections significantly, but fails to alter resistance to influenza viral infections. The findings suggest that murine adrenals may produce one of the known adrenal steroids such as corticosterone along with another steroid, or may produce a steroid other than cortisone, hydrocortisone, or corticosterone. When resistance is decreased by adrenal steroids, survival time is invariably shortened, and the effect of the steroid hormones is frequently demonstrable within the 1st day after infection with pneumococci, making it unlikely that the depression of resistance that is seen is primarily due to depression of antibody formation. A single dose of 5 mg. of cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward. Growth hormone (somatotropic hormone) in highly purified form, and in the doses used, did not overcome the weight loss induced by cortisone, but the animals treated with growth hormone and cortisone regained their lost weight more rapidly than those receiving cortisone alone. Growth hormone alone caused a slight increase in the rate of gain in weight over controls. Growth hormone alone did not increase resistance to infection, and did not increase the survival time, in mice infected with either pneumococci or influenza virus. Growth hormone in various dosages failed to overcome the effect of cortisone in depressing resistance to these infections. Cortisone, hydrocortisone, corticosterone, and corticotropin did not alter significantly the titers of influenza virus attained in the murine lungs during the first 2 days after infection, but cortisone and hydrocortisone markedly delayed the rate at which virus titers declined during the subsequent 6 days. Corticosterone and corticotropin delayed the rate at which the titers declined but slightly, and growth hormone had no apparent effect, as compared with controls. Growth hormone did not overcome the effect of cortisone and hydrocortisone on viral titers. No detectable antibody was found as late as 6 days after infection, in controls or in hormone-treated animals.
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PMID:The effect of adrenal steroids, corticotropin, and growth hormone on resistance to experimental infections. 1311 66

Purified alpha-corticotropin has been reported to exercise the following biological effects: (a) stimulation of the adrenal glands in normal and hypophysectomized rats, (b) production of blood eosinopenia in hypophysectomized rats, (c) maintenance of muscle glycogen in hypophysectomized rats, (d) inhibition of growth-promoting activity of somatotropin, (e) stimulation of melanocytes in the skin of frogs, (f) mobilization of fat into the liver of fasted mice, (g) stimulation of the accessory sex glands of castrated-hypophysectomized male rats, (h) induction of deciduoma formation in hypophysectomized-oophorectomized rats, and (i) elevation of the total red cell volume in hypophysectomized rats. alpha-Corticotropin has also been shown for the first time to act in synergism with lactogenic hormone as an essential galactopoietic hormone. The ability of alpha-corticotropin to elicit biological responses in the absence of the adrenal cortex is discussed.
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PMID:Corticotropins (ACTH). X. Biological investigations on alpha-corticotropin. 1341 72

The treatment with adrenocorticotropic hormone of guinea pigs sensitized with heat-killed tubercle bacilli caused suppression of their skin reactivity to tuberculin. Similar animals treated with saline did not show this change. Normal guinea pigs treated with adrenocorticotropic hormone showed suppression of inflammation, but not necrosis, produced by intracutaneous oil of turpentine. There was slight, but probably not significant, diminution of inflammation during saline administration. Tuberculin complement-fixing antibody titers were not altered by either adrenocorticotropic hormone or saline administration. Adrenocorticotropic hormone produced marked eosinopenia and lymphopenia in guinea pigs.
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PMID:The effect of adrenocorticotropic hormone on inflammation due to tuberculin hypersensitivity and turpentine and on circulating antibody levels. 1488 23