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)

The effect of 310 courses of corticotropin, methylprednisolone, prednisone, and dexamethasone were studied in 62 patients with generalized myasthenia gravis who were poorly responsive to anticholinesterase medication and most of whom required assisted respiration. Improvement in strength and response to anticholinesterase medication occurred in 91% of the courses, and was moderate or marked in 63%. The incidence, degree, and duration of improvement appeared to be dose related. High doses of dexamethasone (20 mg orally each day for 10 days, repeated if necessary), which had 75% more glucocorticoid effect than any other regimen studied, produced the highest incidence of both improvement (100%) and moderate-to-marked improvement (75%), and the greatest duration of improvement (more than 3 months after 40% of the courses). The duration of improvement following intensive courses of any of the corticosteroids was approximately doubled by the subsequent administration of smaller doses of dexamethasone or prednisone on alternate days. Most patients with severe disease relapsed after 3 to 6 months of corticosteroid treatment, but increase in the dose of corticosteroid, and daily administration, which was more effective than alternate-day administratin, almost always again resulted in improvement. Corticotropin and corticosteroids were equally effective before and after thymectomy. High doses of corticotropin and corticosteroid produced an initial exacerbation of the disease in 80% of the courses, which was moderate or marked in 57%. Reduction in dose reduced the incidence of severe exacerbation, but did not prevent it, and also resulted in slower and less marked improvement. Withholding anticholinesterase medication did not prevent exacerbation or increase improvement, and afforded no advantage, though it was usually helpful to reduce the dose of this medication. Because of the hazard of initial exacerbation and the occurrence of other serious side effects in 15% of the patients. (bleeding ulcer, vertebral compression, aseptic necrosis of the femoral head or tibia, and subcapsular cataracts), it is recommended that corticosteroid treatment be limited to myasthenic patients who are not responding satifactorily to anticholinesterase medication, that smaller doses be employed in patients whose disease is not life threatening, and that higher doses be reserved for patients who are critically ill and are being managed, at least initially, in an intensive care unit.
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PMID:Corticotropin and corticosteroids in generalized myasthenia gravis: comparative studies and role in management. 18 90

At least seven radioactive peptides, which fractionated on Biogel P6, were found in rat neurointermediate lobes after incubation for 6 h with [14C]proline. Only three of these could be tentatively identified; one as alpha-melanocyte-stimulating hormone (alpha-MSH) and two as forms of corticotrophin-like intermediate lobe peptide (CLIP). One other cross-reacted partially with a beta-malanocyte-stimulating hormone (beta-MSH) antiserum, was acidically charged and eluted on Biogel P6 in roughly the same position as ACTH. The other three peptides showed no resemblance to alpha-MSH, CLIP, beta-MSH or ACTH.
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PMID:Incorporation of 14C-labelled amino acids into corticotrophin-like intermediate lobe peptide and alpha-melanocyte-stimulating hormone by the rat pituitary neurointermediate lobe in vitro, and the identification of four new pars intermedia peptides. 18 28

The intravenous injection of L-Dopa (15 mg/kg) to monkeys (Macaca mulatta) failed to alter plasma concentrations of ACTH and of 11-deoxy-cortisol. When cortisol synthesis was blocked with iv metyrapone, potentiation of ACTH secretion by L-Dopa became apparent. Simultaneous injection of L-Dopa and metyrapone resulted in a marked increase in plasma ACTH from 93 +/- 18 pg/ml to 432 +/- 80 pg/ml, whereas plasma 11-deoxycortisol increased from 1.5 +/- 0.2 mug/100 ml to 14.6 +/- 1.0 mug/100 ml 90 min after treatment. Throughout the experiment the rise in ACTH and in 11-deoxycortisol following coadministration of L-Dopa and metyrapone was significantly (P less than 0.01) higher than that produced by metyrapone administration alone. The results suggest that acute administration of L-Dopa in monkeys enhances the response of ACTH to metyrapone. L-Dopa (or one of its metabolites) probably acts upon a noradrenergic or a dopaminergic system located in the hypothalamus to alter the release of hypothalamic corticotropin regulatory factor(s) and thereby enhance the release of ACTH.
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PMID:Potentiation of the ACTH response to metyrapone by L-dopa in the monkey. 18 48

A patient with Cushing's disease due to a chromophobe adenoma was studied for 243 days before pituitary surgery and evidence for periodicity in cortisol steroid production was found with cycles occurring every 85.8 days (peak-to-peak length), associated with laboratory remissions and paradoxical response to dexamethasone. The autonomy of ACTH secretion was suggested by the nonresponsiveness to repeated lysine-vasopressin stimulation tests and lack of increase in urinary 170HCS following metyrapone. A distinct response of the hyperplastic glands (as demonstrated by percutaneous adrenal venography) was obtained on several B1-24 corticotropin stimulation. The patient's hypercortisolism disappeared following removal of the chromophobe adenoma through transphenoidal hypophysectomy.
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PMID:Periodic remission in Cushing's disease with paradoxical dexamethasone response: an expression of periodic hormonogenesis. 18 34

We have studied whether endogenous alpha-MSH has a function in stimulating intra-uterine growth in the rat. The approach used was to determine whether or not this hormone is present during the intra-uterine growth spurt, and if binding of endogenous foetal alpha-MSH by antibodies would inhibit this growth. Antibodies against alpha-MSH or ACTH 1-24, either purified or non-purified, induced immunofluorescence in the intermediate lobe of adult male control rats. Using purified anti-alpha-MSH, fluorescence appeared in the foetal intermediate lobe on day 18 of pregnancy, the day that biologically active MSH was first seen. A negative correlation was observed between the pituitary MSH content and foetal body weight only on day 19 of pregnancy. Injection of purified anti-alpha-MSH induced a drop in foetal body weight, but no effect on placental weight was observed. Purified anti-acth 1-24 had no effect upon body weight but caused an increase in placental weight. These results support our previous findings and indicate that endogenous MSH has a function in the stimulation of foetal growth.
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PMID:Stimulation of intra-uterine growth in rat by alpha-melanocyte-stimulating hormone. 18 10

Isolated adrenocorticotropin deficiencies are rare. Two cases are reported, one, with hypoglycaemia, the other with weakness and hypotension, with a review of the published cases during the past twenty years. The adrenal defect impairs severely the glucocorticoid secretion while aldosteron is normal. Tetracosactid stimulates adrenal secretion. ACTH activity measurable in serum is very low and not affected by metyrapone. Other pituitary secretions are normal. The hypothalamic or pituitary level of the defect will be situated when CRH test available.
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PMID:[Adrenal insufficiencies caused by isolated corticotropic deficiency. 2 cases]. 18 90

A novel approach to affinity columns is described that is based on the high avidity of biotinylated molecules for avidin attached to solid supports. Biocytin amide [Nepsilon-(+)-biotinyllysine amide] was coupled to the COOH-terminal carboxyl group of corticotropin(1-24) [ACTH(1-24)] to form [biocytin25]ACTH(1-25) amide. The ability of this peptide to stimulate steroidogenesis of bovine adrenocortical cells was within experimental error identical to that of ACTH(1-24). The peptide also binds to avidin and avidin-Sepharose, forming stable complexes. Thus, with biotin as the anchor, the adrenocorticotropically active segment of the ACTH molecule was attached to a solid support in a targeted manner. The general applicability of this principle for the attachment of peptides and proteins to solid supports is discussed.
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PMID:An approach to the targeted attachment of peptides and proteins to solid supports. 18 17

The mechanism of the corticotropin (ACTH) action was studied. It was found that daily injections of ACTH-zinc-phosphate (5 un./100 g) to intact albino rats for 14 days result in a disturbance of the hepatocytes ultrastructure. When the hormone was injected in combination with sodium ribonucleate (5 mg/100 g), the deviations were less pronounced, injections of the hormones to adrenalectomized rats did not change the ultrastructure of hepatocytes.
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PMID:[Ultrastructural changes in the livers of rats following multiple injections of corticotropin and sodium ribonucleinate]. 18 63

Two cases of intrathoracic tumor, different in histology and accompanied by hyperamylasemia, were studied ultrastructurally, histochemically, and biochemically. The ultrastructure of the tumor cell cytoplasm showed many zymogen granules in case 1 and smaller cored granules in addition to zymogen granules in case 2. Both tumors contained not only a large amount of amylase, which was electrophoretically of saliva type with three components, but also significant amounts of immunoreactive ACTH and beta-MSH. Starch film and immunofluorescence showed that the tumor cells stored amylase. It was concluded from these findings that the tumor cells ectopically producing amylase, which showed differentiation toward the cells with zymogen production, could differentiate toward the cells of ACTH-MSH system at the same time.
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PMID:Ultrastructural, histochemical, and biochemical studies of two cases with amylase, ACTH, and beta-MSH producing tumor. 18 72

Plasma 16 beta-hydroxydehydroepiandrosterone (16 beta-OH-DHEA) levels were measured by radioimmunoassay in normal and pathological conditions in man. 16 beta-OH-DHEA levels in normal subjects rose sharply during adolescence and then declined slowly throughout adult life: 192 pg/ml age 7-11, 395 pg/ml age 15-19, 330 pg/ml age 20-39, 261 pg/ml age 40-59, and 124 pg/ml over 60-years-old. No marked difference was seen between male and female subjects. 16 beta OH-DHEA rose significantly (p less than .01) during adrenocorticotropin (ACTH) stimulation, declined (p less than .005) during dexamethasome suppression and during gonadal suppression, rose (p less than .05) during gonadal stimulation and following administration of WIN 24540, an inhibitor of 3 beta-o1-dehydrogenase (p less than .005). 16 beta-OH-DHEA levels in adrenal venous blood were higher than in inferior vena cava blood but the levels in hepatic venous blood were not higher than in arterial blood. These results indicate that 16 beta-OH-DHEA is secreted directly by the adrenal cortex and probably the gonads. 16 beta-OH-DHEA levels were elevated in normal pregnant women, pregnant women with toxemia and in patients with Cushing's disease, ectopic ACTH-producing tumor and congenital adrenal hyperplasia but not in patients with low-renin essential hypertension.
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PMID:Plasma 16 beta-hydroxydehydroepiandrosterone in normal and pathological conditions in man. 18 75


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