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Biomedical subjects

L Finberg

Publications and source records attributed to L Finberg.

At least 55 records · Page 3Linked to original sources

Taurine and osmoregulation: taurine is a cerebral osmoprotective molecule in chronic hypernatremic dehydration.

We studied the effect of 8-wk dietary taurine depletion on the vulnerability to hypernatremic dehydration in postweanling kittens. While experimental taurine depletion was not associated with increased susceptibility to acute hypernatremia (1.5 M NaCl/NaHCO3, 35 ml/kg body weight, single injection), there was an increase in mortality (five of seven versus one of seven, p = 0.05) and seizure activity (three of seven versus none of seven, p = 0.08) in taurine-depleted compared to taurine-replete kittens rendered chronically hypernatremic over 96 h. Furthermore, there was a significant decrease in brain cell water (517.4 +/- 21.7 versus 671.6 +/- 32.3 ml/100 g fat-free dry weight, p less than 0.05), derived almost exclusively from the intracellular compartment (352.5 +/- 12.3 versus 483.8 +/- 34.6 ml/100 g fat-free dry weight, p less than 0.05) that correlated with the reduction in the cerebral taurine content in the taurine-depleted versus control kittens during chronic hypernatremic dehydration. These results suggest that taurine is an important cerebral osmoprotective molecule. This aminoacid constitutes nearly 50% of the adaptable intracellular osmolal pool whose concentration varies in the course of osmoregulating in response to perturbations in the extracellular fluid tonicity.

Animals↗

Abnormal antidiuretic hormone secretion in patients with systemic lupus erythematosus.

There have been anecdotal reports describing patients with systemic lupus erythematosus (SLE) and inappropriately elevated secretion of antidiuretic hormone (ADH), but no systematic studies of ADH and its metabolism in SLE have been performed. We measured plasma ADH levels in 36 stable SLE patients with normal renal function and examined the relationship of the circulating ADH concentration to clinical disease activity and effective extracellular fluid volume as reflected by peripheral plasma renin activity (PRA) and plasma aldosterone concentration. The mean ADH level was elevated, 11.4 +/- 1.0 microU/ml (normal 0.4-1.4 microU/ml), while mean PRA and aldosterone were 5.4 +/- 0.6 ng/ml/h and 10.6 +/- 1.6 ng/100 ml, respectively. When patients were divided into two groups according to disease duration, those with SLE for 2 years or more had significantly higher plasma ADH levels (13.9 +/- 1.4 vs. 7.7 +/- 0.9 microU/ml; p less than 0.001 and urinary osmolality (697 +/- 63 vs. 445 +/- 49 mosm/kg; p less than 0.02) compared to those with SLE of less than 2 years duration. No differences in serum Na+, K+, PRA, plasma aldosterone concentration, C3, or 24-hour urinary protein excretion were noted between these two groups. Six patients with SLE for less than 2 years underwent a standard water load (20 ml/kg); in 3/6 there was a paradoxical increase in the plasma ADH concentration. These findings indicate that SLE is associated with elevated plasma ADH levels that increase with prolonged disease duration. This abnormality is unrelated to the usual serologic indices of SLE activity, effective extracellular fluid volume status, or any apparent renal unresponsiveness to ADH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Severely deficient binding of 1,25-dihydroxyvitamin D to its receptors in a patient responsive to high doses of this hormone.

A 1.6-yr-old Hispanic boy with sparse hair, muscle weakness, severe growth retardation, and rickets was found to have hypocalcemia, secondary hyperparathyroidism, and high circulating 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels. One year of treatment with a high dose of 1,25-(OH)2D3 (20 micrograms, orally, daily) resulted in marked subjective and radiological improvement; there was a parallel improvement in serum calcium, phosphorus, PTH, alkaline phosphatase, and osteocalcin concentrations. Soluble extracts from cultured skin fibroblasts did not bind [3H]1,25-(OH)2D3 using standard methods. To evaluate the possibility of receptors with abnormally low affinity, we tested for binding with [3H]1,25-(OH)2D3 concentrations higher than those usually used. In one experiment, there was a suggestion of low affinity binding. Hormone receptors with abnormally low affinity for 1,25-(OH)2D may explain this patients resistance to 1,25-(OH)2D. Therapy to maintain extremely high serum 1,25-(OH)2D3 concentrations markedly improved mineral homoeostasis, but did not affect the hair disorder.

Calcitriol↗