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Biomedical subjects

R Isaac

Publications and source records attributed to R Isaac.

At least 19 recordsLinked to original sources
PubMed1984

Effects of an acute calcium load on plasma ACTH, cortisol, aldosterone and renin activity in man.

Plasma adrenocorticotrophin (ACTH), cortisol and aldosterone increased during and after iv administration of calcium gluconate in 4 normal subjects, one patient with hypoparathyroidism and one patient with hypothyroidism. On the other hand, there was a decrease in plasma renin activity but only in the normal subjects. Plasma ACTH and cortisol responses to calcium were abolished whereas plasma aldosterone response persisted in 2 normal subjects pre-treated with dexamethasone. The results observed after calcium administration were compared to those observed after infusion of the solvent only in 6 normal subjects and 4 thyroidectomized patients who were studied twice at 3 day intervals. Plasma ACTH, cortisol and aldosterone were higher when calcium was administered. Plasma renin activity was not statistically different whether or not calcium had been injected in the subjects studied twice. These results demonstrate a direct effect of calcium on ACTH and aldosterone secretion which is not mediated by calcitonin and parathyroid hormone. The stimulatory effect of calcium on cortisol secretion depends on the increase in plasma ACTH.

Adrenocorticotropic Hormone↗
PubMed1983

Endocrine, histological, and biochemical studies of adrenocorticotropin-producing islet cell carcinoma of the pancreas in childhood with characterization of proopiomelanocortin.

Two 8-yr-old children, a boy and girl, are described with Cushing's syndrome secondary to ectopic ACTH-secreting pancreatic islet cell carcinomas. The girl, seen 28 yr ago, had strong presumptive evidence of ectopic ACTH production and hypercalcemia. The boy, studied recently, had strikingly elevated concentrations of plasma ACTH (1,500 pg/ml) and beta-lipotropin (beta LPH; 2,500 pg/ml) and showed no suppression of urinary 17-hydroxycorticoids or cortisol with low and high dose dexamethasone. He had increased plasma calcitonin (257 pg/ml), glucagon (442 pg/ml), lactate dehydrogenase (497 IU/liter), and alpha-fetoprotein (5,144 pg/ml). He also had hypokalemic alkalosis with elevated plasma deoxycorticosterone (70 ng/ml) and PRA (6.9 ng/ml.h) but normal plasma aldosterone (8.2 ng/dl) and 18-hydroxycorticosterone (7.6 ng/dl). Preoperative localization of the tumor was accomplished by computed tomographic scan of the abdomen with concurrent barium enema. Cell-free translation of the tumor mRNA produced authentic proopiomelanocortin of 35,000 mol wt, indicating that the ACTH and beta LPH were produced by the tumor from a common precursor. After removal of a large amount of metastatic tissue from the boy, clinical progression of the remaining tumor was monitored by measuring plasma ACTH and beta LPH. Episodic secretion of ACTH and beta LPH was demonstrated by taking frequent plasma samples while suppressing pituitary ACTH with oral dexamethasone. Chemotherapy and radiation proved ineffective in controlling the growth of his tumor.

Adenoma, Islet Cell↗
PubMed1980

Effects of calcitonin on basal and thyrotropin-releasing hormone-stimulated prolactin secretion in man.

Plasma PRL fell in nine healthy subjects and four patients with hyperprolactinemia after iv administration of salmon calcitonin (CT). The maximum fall was observed 30--60 min after the infusion. There was no change in the plasma concentrations of the other anterior pituitary hormones tested (GH, FSH, LH, and TSH). In five healthy subjects, TRH was injected 60 min after the CT infusion. This protocol was repeated in the same subjects at 3-day intervals, except CT was not administered. Plasma PRL before TRH injection was clearly lower when CT had been administered. Plasma concentrations of the other anterior pituitary hormones did not change. PRL and TSH responses to TRH were markedly inhibited when CT had been previously infused. These observations are in agreement with preceeding studies showing a similar effect of CT on the plasma concentration of various other polypeptide hormones. This general effect of CT could be attributed to a change in intracellular calcium of the secreting cells.

Adenoma↗
PubMed1978

Effect of parathyroid hormone on plasma prolactin in man.

The iv infusion of parathyroid extract or the synthetic fragments of 1-34 bovine or human parathyroid hormone produced a rapid and marked increase of plasma PRL in normal subjects. The stimulation of the release of endogenous parathyroid hormone by administration of disodium EDTA also resulted in a parallel increase of plasma PRL. Parathyroid hormone did not act via plasma cAMP, as the plasma level reached by this nucleotide was too small to produce PRL release. The ingestion of L-dopa 2 h before parathyroid hormone infusion suppressed the PRL response, suggesting that dopamine and parathyroid hormone interact at a common site. As it has been recently shown that PRL stimulates the renal synthesis of 1,25-dihydroxycholecalciferol, the present data suggest that the effect of parathyroid hormone on this synthesis may be due to the increase in plasma PRL.

Adult↗
PubMed1977

The effect of povidone iodine on plaque and salivary bacteria. A double-blind crossover trial.

A double blind crossover trial was carried out to assess the effect of povidone iodine on plaque accumulation in vivo and to measure the total salivary aerobes and anaerobes throughout the study. When compared to the placebo preparation, povidone iodine was without effect on plaque accumulation in all the subjects and there was a progressive increase in plaque throughout the 10-day periods. A 30 to 40 % overall reduction in aerobes and anaerobes occurred with the active preparation which was significant. There appears to be no indication for the use of povidone iodine as an adjunct to oral hygiene or in the treatment of chronic gingivitis.

Bacteria↗
PubMed1976

Cyclic peroxides and the thiobarbituric assay.

Several monocyclic peroxide compounds and two acyclic hydroperoxides have been tested for activity in the thiobarbituric acid test. All cyclic peroxides tested which have beta dioxygen functionality on non-tertiary carbons gave positive thiobarbituric acid tests at 532 nm. (epsilon = 10(3) --10(4)) Two acyclic unsaturated hydroperoxides which were derived from gamma-linolenic acid also gave positive thiobarbituric acid tests. In addition to the 532-nm-absorbing species, all peroxidic compounds tested showed a transient absorption at 450 nm during the thiobarbituric acid test. The species responsible for this 450 nm absorption appears to be an intermediate in a series reaction sequence. This intermediate is converted, in time, to the 532-nm-absorbing species. Thiobarbituric acid assay of the crude autoxidation product mixture of gamma-linolenic acid also shows this transient 450-nm-absorbing species. Added ferric ion enhances the 532 nm abosrbance of the thiobarbituric acid assay of cyclic peroxides.

Methods↗
PubMed1976

Effect of salmon calcitonin on renal excretion of adenosine 3', 5' monophosphate in man.

Intravenous infusion of salmon calcitonin in six healthy subjects produced an increase in the plasma levels and urinary excretion of cyclic AMP. Cyclic AMP clearance diminished but remained higher than inulin clearance. Salmon calcitonin was also infused in six hypertensive patients with normal glomerular filtration rate. Arterial and renal venous plasma concentration of cyclic AMP were clearly raised. The difference between both these concentrations was not significant in the control periods but became marked during the treatment and post treatment periods demonstrating a net extraction of cyclic AMP from plasma by the kidneys. Renal extraction of cyclic AMP was lower than its urinary excretion in the control periods whereas it was clearly higher after salmon calcitonin was given. This shows that salmon calcitonin stimulates the production of cyclic AMP in extra-renal tissues and that the excess of cyclic AMP formed is catabolized by the kidneys.

Adult↗
PubMed1976

[Renal production and excretion of AMPc after intravenous infusion of salmon calcitonin in man].

Intravenous infusion of salmon calcitonin in man produced an increase in the plasma levels and urinary excretion of cyclic AMP. This study demonstrates a net extraction of cyclic AMP from plasma by the kidneys but salmon calcitonin does not act only on the kidney and stimulates the production of cyclic AMP in extra renal tissues. The excess of cyclic AMP formed is catabolized by the kidneys.

Adult↗
PubMed1975

Increased plasma calcitonin in early acute renal failure.

1. High plasma immunoreactive calcitonin concentrations were observed in ten of eleven patients with acute renal failure, particularly in the oliguric phase. 2. Immunoreactive calcitonin decreased progressively with time, independently of recovery of renal function. 3. Radioimmunoassay curves obtained with serial dilutions of plasma from these patients were parallel to or superimposed upon those obtained with calcitonin standards.

Acute Kidney Injury↗
PubMed1975

Influence of calcium infusion on calcitonin and parathyroid hormone concentrations in normal and hemodialyzed subjects.

Plasma calcitonin and parathyroid hormone concentrations were compared before and after calcium infusion in both hemodialyzed patients and control subjects. Levels of both hormones were significantly higher in patients with chronic renal failure. In the uremic group, calcium infusion inhibited parathyroid hormone secretion but did not affect calcitonin. In the control group, calcium infusion stimulated calcitonin secretion but had no effect on parathyroid hormone.

Adult↗
PubMed1973

Defining death.

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Death↗