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Biomedical subjects

M Cox

Publications and source records attributed to M Cox.

At least 199 records · Page 11Linked to original sources

Some factors affecting accuracy of Canadian Home Fitness Test scores.

Factors affecting the accuracy of Canadian Home Fitness Test scores have been evaluated in male and female office workers. At a first attempt, the typical subject underestimates his 10 sec post-exercise pulse count by 1 beat, with a superimposed probable error of 2 beats. However, the modest experience of pulse counting gained in an employee fitness programme corrects the systematic error, while the probable random error is reduced to approximately 8 beats/min. Taking account also of variations in the fficiency of stepping, the probable error of an Astrand prediction of V O2(max) is approximately 10.3%. Comparison with directly measured values in a subsample of 22 men shows an actual random discrepancy of 9.5%, plus a systematic error of approximately 19% due to an increase of heart rate with anticipation of the maximum test. The Jetté prediction formula has a random discrepancy of approximately 8%, plus a systematic error of approximately 10.6%. Assuming the latter can be corrected by evaluation of a larger population, the fitness scores should give most people an indication of both their initial fitness and responses to a training regimen.

Adult↗

Superiority of demeclocycline over lithium in the treatment of chronic syndrome of inappropriate secretion of antidiuretic hormone.

We evaluated demeclocycline and lithium therapy in 10 patients with the syndrome of inappropriate secretion of antidiuretic hormone. Despite severe water restriction, all patients had hyponatremia (mean +/- S.E.M. serum sodium of 122 +/- 1.1 meq per liter) and elevated urine osmolality (744 +/- 59 mOsm per kilogram) before treatment. Demeclocycline (600 to 1200 mg daily) restored serum sodium concentration to 139 +/- 1.1 meq per liter within five to 14 days, permitting unrestricted water intake in all patients. In three patients given lithium carbonate (900 mg daily) the serum sodium concentration, urine osmolality and urine volume were unchanged; since two patients had adverse central-nervous-system symptoms during lithium therapy, further study of this agent was abandoned. A patient with an unusual 22-year history of the syndrome was unresponsive to lithium, whereas long-term treatment with demeclocyline was markedly effective. Demeclocycline is superior to lithium in the treatment of the syndrome and may obviate the need for severe water restriction.

Adult↗

Tetracycline-induced inhibition of Na+ transport in the toad urinary bladder.

The effects of three tetracyclines, demethylchlortetracycline (DMC), minocycline (MNC), and oxytetracycline (OTC), on Na+ transport (measured as short-circuit current) were examined in toad urinary bladders mounted in modified Ussing chambers. During a 1-h incubation period serosal DMC (but not MNC or OTC) inhibited basal Na+ transport, whereas MNC (but not DMC or OTC) inhibited ADH-stimulated Na+ transport. MNC also inhibited cyclic AMP-stimulated Na+ transport. During longer incubation periods all three drugs inhibited basal Na+ transport. The DMC-induced inhibition of basal Na+ transport and the MNC-induced inhibition of ADH-stimulated Na+ transport were paralleled by an inhibition of the active conductance of the bladders. Thus, although all three drugs inhibit basal Na+ transport, only MNC inhibits ADH-stimulated Na+ transport. This effect does not correlate with the known effects of the tetracyclines on ADH-stimulated water flow or with drug-protein binding, and may be related to the greater lipid solubility of MNC.

Animals↗

Detection of barbiturates by latex agglutination inhibition.

A latex-agglutination inhibition test was developed and evaluated for the detection of barbiturates, primarily in urine, but it has applicability to serum. The 2-h test was performed with samples free of gross debris in a 37 degree C heat block and the reaction between the barbiturate antibody and the barbiturate-latex, at pH 7.3, was inhibited by urines containing secobarbital, amobarbital, pentobarbital, butabarbital, or phenobarbital. For laboratory standards the test was particularly sensitive to secobarbital (300 microgram/litre) and relatively insensitive to amobarbital (5000 microgram/litre). In clinical specimens some barbiturates were detected at levels as low as 150 microgram/litre. The test was specific, and negative endpoints were frequently noted in as little as 30 min. The effects of variables (antiserum dilution, urine specific gravity, heat block temperature, sample size, and type of barbiturate) on the degree of agglutination were also determined.

Agglutination Tests↗

Insulin-mediated Na+ transport in the toad urinary bladder.

The characteristics of insulin-induced Na+ transport in the toad urinary bladder were determined and compared to those of aldosterone. Bladders were mounted in modified Ussing chambers, and standard short-circuit current techniques were employed to measure transepithelial Na+ transport. Insulin added to the serosal medium is much more effective than insulin added to the mucosal medium. Serosal insulin concentrations from 10(1) to 10(3) muU/ml increase both the initial rate and the final level of Na+ transport achieved, whereas concentrations from 10(3) to 10(5) muU/ml increase only the initial rate of Na+ transport. Insulin-induced Na+ transport probably does not require glucose. Both insulin- and aldosterone-induced Na+ transport are directly proportional to serosal (but not mucosal) K+ concentration over the physiologic range (2.0-7.0 meq/liter). However, cycloheximide abolishes aldosterone- but not insulin-induced Na+ transport. In addition, insulin stimulates Na+ transport after a maximal response to aldosterone, and aldosterone stimulates Na+ transport after a maximal response to insulin. Thus, although they have several similar characteristics, insulin and aldosterone have at least partially independent mechanisms of action on Na+ transport in the toad urinary bladder.

Aldosterone↗

Impaired renal tubular potassium secretion in systemic lupus erythematosus.

Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.

Acetazolamide↗

Acute hyperkalemia induced by hyperglycemia: hormonal mechanisms.

Two insulin-requiring diabetics with isolated hyporeninemic hypoaldosteronism cpontaneously developed hyperkalemia that was aggravated whenever blood glucose concentration rose. Acute glucose infusions raised the serum potassium concentration in these patients with combined insulin and aldosterone deficiency but lowered, or did not change, the serum potassium concentration in normal subjects and in patients with either aldosterone or insulin deficiency alone. The paradoxical hyperkalemic response to glucose in patients with combined hormonal deficiency was blunted by prior administration of desoxycorticosterone acetate and abolished by prior administration of insulin. Our studies emphasize the crucial roles played by insulin and aldosterone in regulating the serum potassium concentration in man, and the need to avoid hyperglycemia in patients with combined insulin and aldosterone deficiency.

Acute Disease↗