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Biomedical subjects

M Goldberg

Publications and source records attributed to M Goldberg.

At least 667 records · Page 37Linked to original sources
PubMed1978

Reductant-dependent electron distribution among redox sites of laccase.

Rhus laccase (monophenol monooxygenase, monophenol,dihydroxyphenylalanine:oxygen oxidoreductase, EC 1.14.18.1) an O2/H2O oxidoreductase containing four copper ions bound to three redox sites (type 1, type 2, and type 3 Cu pair), was titrated anaerobically with several reductants having various chemical and thermodynamic properties. The distribution of electron equivalents among the redox sites was found to be reductant dependent. When the data for titration by various reductants of the type 3 site were plotted against those of the type 1 site according to the Nernst formalism, the slope n varied from 2.0 to 1.0. The redox potential of the reductant's first oxidation step is qualitatively correlated with the value of n and is suggested as the factor that modulates the electron distribution. Such a behavior implies a nonequilibrium situation. A very good simulation of the data was provided by an analysis assuming a formally variable cooperativity between the two type 3 copper ions. This apparent variability is suggested to result from a process whereby sufficiently strong reductants induce a transition of the type 3 site from a cooperative two-electron acceptor to a pair of independent one-electron acceptors. This uncoupled state of the type 3 site is considered metastable. Other possible models were also investigated. Summarizing the available data, we conclude that the two-electron accepting behavior of the 330-nm chromophore is the exception rather than the rule.

Anaerobiosis↗
PubMed1978

Mechanism of lithium-induced hypercalciuria in rats.

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.

Animals↗
PubMed1978

Dissociation of tubular sites of action of saline, PTH and DbCAMP on renal phosphate reabsorption.

The effects of saline expansion, parathyroid hormone (PTH) administration and dibutyryl cyclic 3'5'-adenosine monophosphate (DbCAMP) infusion on renal phosphate reabsorption were examined in acutely thyroparathyroidectomized (TPTX), phosphate infused dogs by the recollection micropuncture technique. Saline expansion reduced whole kidney phosphate reabsorption from a mean of 66.1 to 50.4% of filtered load. This response was entirely accounted for by an inhibition of proximal tubular phosphate reabsorption which fell from a mean of 35 to 21% of the filtered phosphate load. Both PTH and DbCAMP produced a fall in whole kidney phosphate reabsorption comparable to saline. However, this effect was the sum of inhibition of both proximal tubular and distal nephron phosphate reabsorption. These studies demonstrate the important role of the distal nephron in modulating urinary phosphate excretion.

Animals↗
PubMed1978

[Glycoproteins and proteoglycans in the predentin and dentin matrix in the rat: an ultrastructural study].

The ultrastructural distribution of the protein-polysaccharides was studied in the predentinal and dentinal matrices of the rat. Used for the indentification of the glycoproteins, the chromic-phosphotungstic acid mixture (Rambourt, 1967) weakly contrasted the predentine, underlined the mineralization front and impregnated the dentinal matrix. Alcian blue (Goldberg et al., 1977) as well as bismuth nitrate (Serafini-Fracassini and Smith, 1966), cationic stains for the proteoglycans, produced a strong contrast in the predentine, whereas in the dentine, which appeared clear, only 100 to 150 A granules associated with the periodic collagen striations were stained. This inverse variation between non collagenous proteoglycans and glycoproteins is discussed in relation to the mineralization process.

Animals↗
PubMed1978

[Concentration and characterization of a liver cell proliferation factor from partially hepatectomized rat livers (author's transl)].

An extract of rat liver, made 12 h after partial hepatectomy, was injected into untreated rats. The synthesis of DNA in the liver cells of the injected animals showed a 3.3 fold increase in comparison with controls. A similar increase was observed in the mitosis index. Injection of liver extracts from normal rats showed no effect when compared with the injection of NaCl. The effect of the active extract was not altered by neuraminidase treatment. Trypsin-chymotrypsin treatment, howerver, removes the activity. The active factor must therefore be either a protein or a protein-like substance. The molecular weight of the factor was shown to be between about 30 000 and 50 000 by molecular filtration. The specific activity after molecular filtration was raised by a factor of 100. The factor is inert with respect to the proliferation of kidney and spleen. It is apparently not species-specific, however, since it also causes increased proliferation of liver cells in normal mice.

Animals↗
PubMed1978

Laryngeal granuloma secondary to gastro--esophageal reflux.

Approximately 60 per cent of patients with gastro-esophageal reflux have symptoms related to aspiration of acid and/or bile into the airway. Though many instances of lower airway involvement have been well documented, no mass lesion secondary to gastro-esophageal reflux involving the larynx has ever been demonstrated clinically. The purpose of this presentation is to define a recurrent granuloma of the posterior two-thirds of the left vocal cord, which appeared the result of gastro-esophageal reflux, including both bile and acid content. The relationship between the laryngeal granuloma and the gastro-esophageal reflux was both clinical and pathological; in particular, the histology of the lesion with its intact mucous membrane appeared virtually identical to that found in active reflux esophagitis.

Gastroesophageal Reflux↗