Oxidative titrations of Rhus vernicifera laccase and its specific interaction with hydrogen peroxide.
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Biomedical subjects
Publications and source records attributed to M Goldberg.
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The electron transfer reaction between the "blue" single copper protein azurin (from Pseudomonas aeruginosa) and the hexacyanoiron (II/III) couple has been studied. Equilibrium constants for the reduction of azurin were measured spectrophotometrically in the temperature range 5-33 degrees C (K = 1.1 X 10(-2) at 25 degrees C, deltaH degrees = 10.9 kcal/mol, 0.1 M potassium phosphate, pH 7.0, I = 0.22). The enthalpy change was also determined by microcalorimetry and from the analysis of chemical relaxation amplitudes. Following a temperature-jump perturbation of this equilibrium, only a single relaxation was observed. The reciprocal of the relaxation time increased linearly as oxidized azurin was reacted with increasing amounts of ferrocyanide, yet reached saturation when reduced azurin was titrated with ferricyanide. This behavior as well as the analysis of the relaxation amplitudes led to the following scheme for this system: see article. At 25 degrees C the rate constants for the electron transfer were k+3=6.4s-1 and k-3=45s-1, the association constants K1=54 M-1 and K2-1=610 M-1. The activation and overall thermodynamic parameters as well as the individual thermodynamic values for the different steps were combined to construct a self-consistent energy profile for the reaction.
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Analgesic abuse nephropathy is seldom considered as a cause in patients presenting with chronic renal disease. In a three-year period 450 patients were seen with chronic renal failure. Of these 103 had interstitial renal disease as the cause of their failure. Twenty of these 103 were due to chronic analgesic abuse, which indicates that need for a greater awareness of this problem. The spectrum of clinical and roentgenographic aspects of analgesic abuse nephropathy are discussed. What constitutes analgesic abuse, helpful clinical findings, frequency of other medical illnesses, and the low incidence of documented renal infection prior to onset of renal failure are discussed. Intravenous pyelographic findings related to visualization, renal size, corticomedullary margins and pelvicalyceal changes are also discussed and demonstrated.
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The effects of hyperglycemia and hyperinsulinemia on renal handling of sodium, calcium, and phosphate were studied in dogs employing the recollection micropuncture technique. Subthreshold sustained hyperglycemia resulted in an isonatric inhibition of proximal tubular sodium, fluid, calcium, and phosphate reabsorption by 8-14%. Fractional excretion of sodium and phosphate, however, fell (P is less than 0.01) indicating that the increased delivery of these ions was reabsorbed in portions of the nephron distal to the site of puncture and in addition net sodium and phosphate transport was enhanced resulting in a significant antinatriuresis and antiphosphaturia. The creation of a steady state plateau of hyperinsulinemia while maintaining the blood glucose concentration of euglycemic levels mimicked the effects of hyperglycemia on proximal tubular transport and fractional excretion of sodium and calcium. Tubular fluid to plasma insulin ratio fell, similar to the hyperglycemic studies. These results suggest that the effects of hyperglycemia on renal handling of sodium and calcium may be mediated through changes in plasma insulin concentration. In contrast to hyperglycemia, however, hyperinsulinemia cuased a significant fall in tubular fluid to plasma phosphate ratio with enhanced proximal tubular phosphate reabsorption (P is less than 0.02). This occurred concomitantly with a significant inhibition of proximal tubular sodium transport. These data indicate that insulin has a direct effect on proximal tubular phosphate reabsorption, and this effect of insulin is masked by the presence of increased amounts of unreabsorbed glucose in the tubule that ensues when hyperinsulinemia occurs secondary to hyperglycemia. Fractional excretion of phosphate fell significantly during insulin infusion but unlike the hyperglycemic studies, the fall in phosphate excretion could be entirely accounted for by enhanced proximal reabsorption.
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.
Four patients with chronic illnesses and stable hyponatremia and plasma hypotonicity had normal urinary diluting capacity, with excretion of greater than 80% of a standard water load (20 ml/kg) within 4 hours and maintenance of a urine osmolality less than 100 mosmol/kg, during sustained water diuresis. Administration of a chronic salt load did not correct the hyponatremia. However, it was stabilized after treatment of the underlying medical condition. These subjects may represent a true resetting of the osmostat or a variant of the syndrome of inappropriate antidiuretic hormone secretion.
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The purpose of this paper is to investigate whether an antibody directed against the exocrine secretion, saliva, is able to induce a modification in vivo within the specific cells of the submaxillary glands which synthesize this secretion. The salivary antigens synthesized within the glandular acinar cells are secreted into their respective lumen and are not present in the general circulation or in the intercellular spaces of the gland. When heterologous anti-saliva antibodies are injected into mice, they induce marked lesions within the acinar cells of the submaxillary glands. When different antibodies recognizing different salivary components are injected, they all induce similar modifications; it is not yet possible to distinguish whether different cells are involved in the synthesis of the different salivary components. The lesions described seem specific since other organs studied, such as the pancreas and the stomach, are unaffected. The different possible mechanisms of this cytotoxic effect are discussed.
Rats receiving a carbohydrate rich cariogenic diet (Stephan 580) showed structural modifications of their salivary glands when compared to a control group. These observations suggested that a disturbance of the after birth organogenesis sequences occurred during the experimental period for the submandibular glands. The elaboration of elaboration of secretion granules was strongly decreased in the parotid acinar cells. Such an indirect action of the hyperglucidic diet could contribute to the carious process development by modifying the oral environment.
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Ultra-thin sections of dental tissues, fixed in glutaraldehyde and osmium tetroxide, embedded without previous demineralization in Epon, were contrasted the grids with an alcian blue solution after previous oxidation periodic acid or hydrogen peroxide. Correlations with histochemical results obtained with the optical microscope, other results obtained with ruthenium red and phosphotungstic acid and controls made after enzymatic digestion with chondroitinase AC suggest that this technique is specific for the detection of acid mucopolysaccharides in those calcified tissues studied.
A double-blind crossover study was undertaken to delineate the renal tubular sites of action of bumetanide and to compare its effects upon electrolyte excretion to that of furosemide in six nephrotic patients with various degrees of renal insufficiency. Bumetanide was found to be a potent oral natriuretic agent without producing changes in either GFR or effective renal plasma flow. The natriuresis was associated with inhibition of proximal tubular transport as evidenced by an increased distal delivery (CH2O+CNA+K) and inhibition of sodium transport in the loop of Henle as shown by a fall in CH2O/CH2O+CC1 during sustained water diuresis and an unchanged TCH2O with continued hydropenia. The increases in free-water clearance induced by furosemide and bumetanide were equivalent, but bumetanide produced significantly higher flow rate, greater solute delivery from the proximal tubule, and a greater natriuresis. The data indicate that at the dosages used, bumetanide has a proportionately greater inhibitory effect than furosemide in both the proximal tubule and the ascending limb of the loop of Henle.
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