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Biomedical subjects

D Fraser

Publications and source records attributed to D Fraser.

At least 217 records · Page 12Linked to original sources
PubMed1974

Interaction of mycoplasma with viruses. I. Primary adsorption of virus is ionic in mechanism.

We have studied the adsorption of the Gourlay Acholeplasma virus MVL-1 to the host cell Acholeplasma laidlawii JA-1. Successful adsorption depends primarily on some unknown action of the serum factor in the medium, but evaluation of various physical parameters indicates clearly that given this factor the kinetics is pseudo first order (K = 3 x 10(-9) cm(3)/min) and the mechanism ionic. Chiefly important are the ionic strength of the cation and pH (optimal Na(+) = 0.08 M, pH = 6). The system seems indifferent to whether the cation is Na, K, NH(4), Ca, or Mg. There is little effect of temperature over the range 0 to 42 C. The diffusion constant of the virus, calculated from its geometry or its maximum adsorption rate, is consistent with its reported size and shape.

Adsorption↗
PubMed1973

Surface structure of intact cells and spheroplasts of pseudomonas aeruginosa.

This report describes the ultrastructural features of Pseudomonas aeruginosa after freeze-etching of intact cells and enzymatically prepared spheroplasts. Freeze-etching of intact cells revealed two convex layers of the cell wall and particles within the hydrophobic interior of the cell membrane. Areas of the membrane free of particles were sometimes elevated in the form of rather large dome-shaped structures. Spheroplasts were formed from intact cells by the addition of trypsin to a reaction mixture of lysozyme and ethylenediaminetetraacetic acid. Spheroplasts contained the outer lipoid layer of the cell wall. It was possible to observe this cell wall layer in freeze-etch preparations of spheroplasts. The spheroplast membrane like that of intact cells was cleaved along a central plane to expose particles and particle-free areas.

Cell Membrane↗
PubMed1973

Pathogenesis of hypocalcemia in primary hypomagnesemia: normal end-organ responsiveness to parathyroid hormone, impaired parathyroid gland function.

Hypocalcemia is a frequent feature of hypomagnesemia in man and several other species. To elucidate the cause of this hypocalcemia, we have studied a child with primary hypomagnesemia and secondary hypocalcemia during magnesium supplementation when he was normomagnesemic and normocalcemic and after magnesium restriction for 16 days when he quickly became hypomagnesemic (0.5 meq/liter) and hypocalcemic (3.4 meq/liter) and had positive Chvostek's and Trousseau's signs. Whether in the normomagnesemic or hypomagnesemic state, intravenous bovine parathyroid extract (PTE) 8 U. S. P. U/kg promptly caused transient increases in the urinary phosphate excretion, renal phosphate clearance and cyclic AMP excretion. The magnitudes of these responses were similar in the two states, and similar to those observed in a hypoparathyroid patient. When the patient was hypomagnesemic and hypocalcemic, intramuscular PTE, 8 U/kg at 8-h intervals for four doses promptly caused hypercalcemia. The findings indicate that the end-organs were responsive to parathyroid hormone. The concentrations of serum parathyroid hormone (PTH) were normal in the normomagnesemic state ranging from 0.15 ng/ml to 0.40 ng/ml. Serum PTH did not increase in the hypomagnesemic state in spite of hypocalcemia. Indeed, PTH became unmeasurable in four consecutive samples at the end of the period of magnesium restriction. The concentrations of serum calcitonin remained unmeasurable (< 0.10 ng/ml) throughout the study, implying that excess calcitonin was not the cause of hypocalcemia in magnesium depletion. The findings in this study support our thesis that magnesium depletion causes impaired synthesis or secretion of parathyroid hormone. This impairment would account for the hypocalcemia observed in the hypomagnesemic state.

Calcitonin↗
PubMed1971

Photodynamic action of proflavine on coliphage T3. I. Kinetics of inactivation.

The photodynamic inactivation of coliphage T3 was studied over a wide range of concentrations of the dye proflavine. With 2 x 10(7) phage/ml, two modes of inactivation were observed. Between 0.25 and 12 to 13 mug/ml, inactivation was biphasic. There was an initial first-order inactivation (Rx1) which became temporally associated with an apparently multiorder process (Rx2) at higher light doses. Dye concentrations above 12 to 13 mug/ml showed only two-target inactivation curves (Rx3), except at high dye concentrations where processes kinetically identical to Rx1 and Rx2 reappeared. Rx2 showed a normal rectangular hyperbolic saturation curve but Rx1 and Rx3 appeared to saturate prematurely. The saturation behavior of Rx1 and Rx2 was independent of phage concentration, but Rx3 was lost at phage titers above 2 x 10(7)/ml. No dark inactivation was seen with Rx1 and Rx2 subsequent to a period of illumination. With Rx3, an exponential dark inactivation was seen for at least 1 hr after a period of illumination. The dye-phage system equilibrated immediately, at any temperature, at proflavine concentrations where Rx1 and Rx2 occurred. With Rx3, prolonged equilibration times were necessary. Moreover, there was a temperature effect. The rate of inactivation at equilibrium was temperature-dependent, whereas the initial rate at which equilibrium was approached was essentially temperature-independent.

Acridines↗
PubMed1971

Photodynamic action of proflavine on coliphage T3. II. Protection by L-cysteine.

Three kinetically different reactions (Rx1, Rx2, and Rx3) have been distinguished in the photoinactivation of phage T3 in the presence of the dye proflavine. The response of these reactions to the presence of the radical trap l-cysteine has been examined. At dye concentrations equal to or less than 2.2 mug/ml, Rx1 was composed of at least two parallel first-order reactions, one cysteine-insensitive (Rx1A) and one cysteine-inhibited (Rx1B). Rx2 was completely cysteine-insensitive (Rx2A). The cysteine sensitivity of these reactions changed abruptly at dye concentrations above 2.2 mug/ml. Rx1A and Rx1B now operated in tandem, rather than simultaneously, with Rx1B being confined to the first 1 min at most. Rx2, on the other hand, was completely cysteine-inhibited (Rx2B). Rx3 was inhibited roughly 75 to 80% by saturating concentrations of cysteine regardless of the time of addition of cysteine. The dark inactivation associated with Rx3 was inhibited roughly 85% whether the radical trap was added during the light or dark regimes. Changes of initial phage titer did not alter the cysteine sensitivity of a reaction.

Acridines↗