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Biomedical subjects

E Reiss

Publications and source records attributed to E Reiss.

At least 109 records · Page 6Linked to original sources
PubMed1974

Serological and cellular immune activity of peptidoglucomannan fractions of Candida albicans cell walls.

A two-stage extraction of isolated cell walls of C. albicans resulted in 45% solubilization into antigens of high molecular weight leaving a wall residue which also had antigenic properties. Ice-cold dilute alkali removed 25% of the defatted cell walls. The extract was nondialyzable, had a glucose-to-mannose ratio of 2:3 and an amino acid content of 7.32%, and was designated peptidoglucomannan (PGM). An additional 26% of the walls resistant to stage I were solubilized by sonic treatment yielding a fraction having a glucose-to-mannose ratio of 6:1, termed soluble mannoglucan (sMG). The residue after extraction and sonic treatment contained 10.9% mannose, which was the insoluble mannoglucan. The gel permeation behavior of PGM and sMG on BioGel A5M was similar; each contained two components, one estimated to exceed 5 x 10(6) molecular weight and a second smaller species. The soluble cell wall fractions were active in immunodiffusion and carried antigenic group specificity. Immunoelectrophoresis of PGM, sMG, and mannan revealed some heterogeneity. The insoluble mannoglucan had agglutinating activity. A distinctive immunodiffusion pattern of cell wall antigens was formed with the serum of a leukemic patient with candidiasis. All three cell wall antigens and mannan elicited delayed-type hypersensitivity as measured by skin-test and specific inhibition of macrophage migration. A dose of 25 mug of PGM was sufficient to inhibit 89.9% migration in the peritoneal exudates of guinea pigs immunized with cell walls, and 10 mug of PGM inhibited 91.7% migration in guinea pigs immunized with insoluble mannoglucan.

Amino Acids↗
PubMed1973

Evidence for secondary hyperparathyroidism in idiopathic hypercalciuria.

Circulating levels of immunoreactive parathyroid hormone (PTH) were measured in 40 patients with idiopathic hypercalciuria (IH) before and during reversal of hypercalciuria with thiazide, and in four normal subjects before and during induction of hypercalciuria with furosemide. 26 patients with IH had elevated serum PTH levels. The remaining patients had normal levels. Although the correlation was not complete, high PTH levels were generally found in patients who had more severe average urinary calcium losses. When initially elevated. PTH levels fell to normal or nearly normal values during periods of thiazide administration lasting up to 22 months. When initially normal, PTH levels were not altered by thiazide. Reversal of hyperparathyroidism by thiazide could not be ascribed to the induction of hypercalcemia, since serum calcium concentration failed to rise in a majority of patients. Renal hypercalciuria produced by furosemide administration elevated serum PTH to levels equivalent to those observed in patients with IH. The findings in this study help to distinguish between several current alternative views of IH and its relationship to hyperparathyroidism. Alimentary calcium hyperabsorption cannot be the major cause of IH with high PTH levels, because this mechanism could not elevate PTH. Idiopathic hypercalciuria cannot be a variety of primary hyperparathyroidism, as this disease is usually defined, because PTH levels are not elevated in all patients and, when high, are lowered by reversal of hypercalciuria. Primary renal loss of calcium could explain the variable occurrence of reversible hyperparathyroidism in IH, since renal hypercalciuria from furosemide elevates serum PTH in normal subjects. Consequently, a reasonable working hypothesis is that IH is often due to a primary renal defect of calcium handling that leads, by unknown pathways, to secondary hyperparathyroidism.

Calcium↗
PubMed1973

Activation of renal cortical adenylate cyclase by circulating immunoreactive parathyroid hormone fragments.

Three distinct immunoreactive species of parathyroid hormone (PTH) are present in human serum. One has an estimated mol wt of 9,500 and probably represents glandular hormone, the second 7,000-7,500 mol wt, and the third 4,500-5,000 mol wt. In order to assess the biological activity of these circulating forms of PTH, we determined their ability to activate renal cortical adenylate cyclase. The 9,500 mol wt and 4,500-5,000 mol wt fractions produced four- to sixfold increases in cyclic 3',5'-AMP accumulation above control; the 7,000-7,500 mol wt fraction was inactive. None of the fragments had any effects on phosphodiesterase activity. Antiserum to bovine PTH did not block the activation of adenylate cyclase by either the gragments or bovine PTH. The data suggest that a large proportion of circulating immunoreactive human PTH is biologically active and that the biologically and immunologically active sites of the hormone are distinct.

Adenylyl Cyclases↗
PubMed1972

Circadian rhythm in serum parathyroid hormone concentration in human subjects: correlation with serum calcium, phosphate, albumin, and growth hormone levels.

A circadian variation in serum calcium, albumin and PTH concentration in normal subjects has been demonstrated. The levels of the three blood constituents were remarkably constant during the day, but striking night and early morning changes occurred. Serum calcium levels were highest at 8:00 p.m. and reached a nadir between 2:00 and 4:00 a.m. Serum albumin levels were parallel to those of serum calcium. PTH levels began to rise after 8:00 p.m., reached the highest levels between 2:00 and 4:00 a.m., and fell to baseline values by 8:00 a.m. The nocturnal fall in serum calcium levels appears to be secondary to dilution of serum proteins by increasing blood volume. The nocturnal rise in PTH levels appears to be independent of serum calcium levels within the normal range but it can be abolished by induced hypercalcemia. Serum phosphate levels were lowest between 8:00 a.m. and 10:00 a.m. and highest between 2:00 a.m. and 4:00 a.m. The data presented suggest that circadian changes in serum phosphate levels are not mediated in toto by parathyroid hormone but they are exaggerated when the secretion of this hormone is inhibited. They are independent of growth hormone levels and activity but they are greatly modified during a prolonged fast.

Adult↗
PubMed1971

On the pathogenesis of hyperparathyroidism in chronic experimental renal insufficiency in the dog.

Healthy adult dogs were subjected to stepwise reduction of nephron population so as to create the transition from normal renal function to advanced renal insufficiency. Studies were performed at each level of renal function. Glomerular filtration rate (GFR), renal phosphate clearance, and serum radioimmunoassayable parathyroid hormone (PTH) levels were measured. Two groups of animals were studied. In one, phosphorous intake was maintained at 1200 mg/day. As GFR declined, fractional phosphate excretion rose reciprocally, and PTH levels increased over 20-fold. In the second group, phosphorous intake was maintained at less than 100 mg/day. As GFR fell, fractional phosphate excretion changed little, and no increment in PTH levels occurred. The data suggest that the control system regulating phosphate excretion contributes importantly to the pathogenesis of secondary hyperparathyroidism in advancing renal insufficiency.

Animals↗