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Biomedical subjects

S Levine

Publications and source records attributed to S Levine.

At least 595 records · Page 33Linked to original sources
PubMed1973

Effect of phloretin on water and solute movement in the toad bladder.

It is generally believed that urea crosses the cell membrane through aqueous channels, and that its movement across the membrane is accelerated in the direction of net water flow (solvent drag effect). The present report presents evidence for a vasopressin-sensitive pathway for the movement of urea, other amides, and certain non-amides, which is independent of water flow. Phloretin, when present at 10(-4) M concentration in the medium bathing the luminal surface of the toad bladder, strongly inhibits the movement of urea, acetamide, and propionamide across the toad bladder, both in the absence and presence of vasopressin. The vasopressin-stimulated movement of formaldehyde and thiourea is also reduced. Osmotic water flow, on the other hand, is not affected; nor is the movement of ethanol and ethylene glycol, or the net transport of sodium. On the basis of these studies we would conclude that the movement of many, if not all, solutes across the cell membrane is independent of water flow, and that a vasopressin-sensitive carrier may be involved in the transport of certain solutes across the cell membrane.

Acetamides↗
PubMed1973

A saturable, vasopressin-sensitive carrier for urea and acetamide in the toad bladder epithelial cell.

The permeability of the toad bladder to a series of isotopically labeled nonelectrolytes was determined in the presence of 150 mM unlabeled acetamide. Under these conditions, overall bladder function was unimpaired, as shown by a normal response to vasopressin of short-circuit current and permeability coefficient of [(3)H]water,[(14)C]ethanol, and [(14)C]propionamide. The permeability of the bladder to isotopic acetamide and urea, however, was significantly depressed by unlabeled acetamide, in both the absence and presence of vasopressin. These experiments indicate a competition between unlabeled and isotopic species for binding sites, and show the existence of a saturable, vasopressin-sensitive carrier for urea and acetamide in the epithelial cell membrane.

Acetamides↗
PubMed1973

Hyperacute allergic encephalomyelitis. A localized form produced by passive transfer and pertussis vaccine.

A hyperacute form of experimental allergic encephalomyelitis (EAE) has been produced previously by administering pertussis vaccine to rats actively immunized with neural antigen or given passive transfer of lymphoid cells from donors with EAE. Now, a localized form of hyperacute EAE has been produced within 1 day of passive transfer. The speed with which pertussis acts tends to exclude antibody production as the mechanism for conversion of EAE to the hyperacute form. With this rapid system, it has been found that pertussis, or its histamine-sensitizing factor, inhibited the host mononuclear cell component of the pervascular lesions. When the immune injury was sufficiently severe (high doses of donor EAE cells), the decrease in the number of mononuclear cells was accompanied by an increase in the amount of fibrin and the number of neutrophils in the lesions. This inverse relationship may be explained by the loss of the protective effect of mononuclear cells on vessels, a concept for which there is increasing evidence.

Acute Disease↗