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  • INFECTED LIVER CYST IN A PATIENT WITH POLYCYSTIC KIDNEY-DISEASE WESTERN JOURNAL OF MEDICINE Gesundheit, N., Kent, D. L., Fawcett, H. D., EFFRON, M. K., MAFFLY, R. H. 1982; 136 (3): 246-249

    View details for Web of Science ID A1982NG84700018

    View details for PubMedID 7046254

  • RUNNING OUT OF WATER EMERGENCY MEDICINE MAFFLY, R. H. 1979; 11 (6): 56-?
  • EVIDENCE FOR INVOLVEMENT OF MICROTUBULES IN ACTION OF VASOPRESSIN IN TOAD URINARY-BLADDER .1. FUNCTIONAL STUDIES ON EFFECTS OF ANTI-MITOTIC AGENTS ON RESPONSE TO VASOPRESSIN JOURNAL OF MEMBRANE BIOLOGY Taylor, A., Mamelak, M., GOLBETZ, H., MAFFLY, R. 1978; 40 (3): 213-235

    Abstract

    The antimitotic agents colchicine, podophyllotoxin, and vinblastine inhibit the action of vasopressin and cyclic AMP on osmotic water movement in the toad urinary bladder. The alkaloids have no effect on either basal or vasopressin-stimulated sodium transport or urea flux across the tissue. Inhibition of vasopressin-induced water movement is half-maximal at the following alkaloid concentrations: colchicine, 1.8 X 10(-6) M; podophyllotoxin, 5 X 10(-7)M; and vinblastine, 1 X 10(-7)M. The characteristics of the specificity, time-dependence and temperature-dependence of the inhibitory effect of colchicine are similar to the characteristics of the interaction of this drug with tubulin in vitro, and they differ from those of its effect on nucleoside transport. Inhibition of the vasopressin response by colchicine, podophyllotoxin, and vinblastine is not readily reversed. The findings support the view that the inhibition of vasopressin-induced water movement by the antimitotic agents is due to the interaction of these agents with tubulin and consequent interference with microtubule integrity and function. Taken together with the results of biochemical and morphological studies, the findings provide evidence that cytoplasmic microtubules play a critical role in the action of vasopressin on transcellular water movement in the toad bladder.

    View details for Web of Science ID A1978FA08300002

    View details for PubMedID 207871

  • EVIDENCE FOR INVOLVEMENT OF MICROTUBULES IN ACTION OF VASOPRESSIN IN TOAD URINARY-BLADDER .3. MORPHOLOGICAL-STUDIES ON CONTENT AND DISTRIBUTION OF MICROTUBULES IN BLADDER EPITHELIAL-CELLS JOURNAL OF MEMBRANE BIOLOGY Reaven, E., MAFFLY, R., Taylor, A. 1978; 40 (3): 251-267

    View details for Web of Science ID A1978FA08300004

    View details for PubMedID 207872

  • INTERRELATIONSHIPS OF SODIUM-TRANSPORT AND CARBON-DIOXIDE PRODUCTION BY TOAD BLADDER - RESPONSE TO CHANGES IN MUCOSAL SODIUM CONCENTRATION, TO VASOPRESSIN AND TO AVAILABILITY OF METABOLIC SUBSTRATE JOURNAL OF MEMBRANE BIOLOGY Coplon, N. S., Steele, R. E., MAFFLY, R. H. 1977; 34 (2-3): 289-312

    Abstract

    Active sodium transport and CO2 production were measured simultaneously in toad bladders mounted in membrane chambers. The rate of sodium transport was varied by changing the concentration of sodium in the mucosal bath (substitution with choline), by adding vasopressin, by adding metabolic substrates and by adding malonate, and the ratio of the change of sodium transport and CO2 production was determined Mean values for deltaNa/deltaCO2 (equiv/mole) were: Na in equilibrium choline 18.3 +/- 1.1; vasopressin 15.5 +/- 2.8; and pyruvate (corrected for the increment in "nontransport" CO2) 15.4 +/- 3.5. Based on previously determined values for the respiratory quotient (R.Q.), calculated mean values for deltaNa/deltaO2 ranged between 15.5 and 18.5 equiv/mole. It appears that basal metabolism does not contribute to metabolism supporting sodium transport when the rate of sodium transport is varied. "Transport" metabolism appears much more responsive to changes in the availability of endogenous and exogenous substrates than does "nontransport" metabolism. We conclude that "transport" and "nontransport" metabolism are functionally separated in the toad bladder.

    View details for Web of Science ID A1977DL97600009

    View details for PubMedID 407360

  • HOW TO AVOID COMPLICATIONS OF POTENT DIURETICS JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION MAFFLY, R. H. 1976; 235 (23): 2526-2528
  • URINARY CONCENTRATING MECHANISM NEW ENGLAND JOURNAL OF MEDICINE Jamison, R. L., MAFFLY, R. H. 1976; 295 (19): 1059-1067

    View details for Web of Science ID A1976CJ12300008

    View details for PubMedID 972660

  • EVIDENCE FOR INVOLVEMENT OF MICROTUBULES IN ACTION OF VASOPRESSIN ANNALS OF THE NEW YORK ACADEMY OF SCIENCES Taylor, A., MAFFLY, R., Wilson, L., Reaven, E. 1975; 253 (JUN30): 723-737

    View details for Web of Science ID A1975AH94100055

    View details for PubMedID 1096729

  • EFFECTS OF PROPIONATE AND OTHER SHORT-CHAIN FATTY-ACIDS ON SODIUM-TRANSPORT BY TOAD BLADDER BIOCHIMICA ET BIOPHYSICA ACTA Hess, J. J., Taylor, A., MAFFLY, R. H. 1975; 394 (3): 416-437

    Abstract

    1. Propionate and other unbranched short-chain fatty acids, butyrate, pentanoate, hexanoate and octanoate were found to both stimulate and inhibit active sodium transport by the toad bladder, as measured by the short-circuit current (s.c.c.). 2. Stimulation alone followed addition of low concentrations of fatty acids (0.1-1.0 mM) to either the serosal or mucosal bathing medium; stimulation was also seen after an initial period of inhibition in response to higher concentrations (approx. 5 mM) of some compounds. 3. Inhibition alone followed addition of high concentrations (5-20 mM) of these compounds. The duration and magnitude of the inhibition varied with increasing concentration and chain length of the fatty acid, and was greater following mucosal addition than serosal addition. 4. The inhibitory effect of mucosal propionate increased with decreasing pH of the mucosal bathing medium. 5. Inhibition by the fatty acids was completely reversed upon removing the compound from the bathing medium, and stimulation characteristically followed. 6. In studies designed to evaluate the role of metabolism of the fatty acids in their mucosal inhibitory effects it was found that 14-c-labelled propionate, when added to the mucosal surface of the bladder, was converted to 14-CO2, and mucosal succinate and alpha-oxoglutaric acid at 20 mM inhibited the s.c.c. slightly. However, malonate did not interfere with inhibition by mucosal propionate and two non-metabolizable acids, dimethylpropionate and benzoate, induced inhibition (and no stimulation) of the s.c.c. 7. In the presence of an inhibitory concentration of fatty acid, the ability of the bladder to respond to added pyruvate was reduced in proportion to the reduction in the level of the s.c.c., whereas the natriferic response to vasopressin was largely intact. 8. We conclude that stimulation of sodium transport by propionate and other short-chain fatty acids is due to metabolism of the compounds and provision of energy to the sodium transport mechanism. The basis of the inhibition appears complex. It may in part depend on metabolism of the fatty acids and/or uncoupling of oxidative phosphorylation, with resultant reduction in net ATP production for the sodium transport mechanism. However, the inhibition may also be caused in part by a direct effect on the mucosal entry of sodium into the transporting epithelial cells.

    View details for Web of Science ID A1975AH77400008

    View details for PubMedID 236789

  • EFFECTS OF TRICARBOXYLIC-ACID CYCLE INTERMEDIATES ON SODIUM-TRANSPORT BY TOAD BLADDER JOURNAL OF MEMBRANE BIOLOGY Taylor, A., Hess, J. J., MAFFLY, R. H. 1974; 15 (4): 319-329

    View details for Web of Science ID A1974S693800001

    View details for PubMedID 4209850

  • VASOPRESSIN - POSSIBLE ROLE OF MICROTUBULES AND MICROFILAMENTS IN ITS ACTION SCIENCE Taylor, A., Mamelak, M., Reaven, E., MAFFLY, R. 1973; 181 (4097): 347-350

    Abstract

    Colchicine, vinblastine, podophyllotoxin, and cytochalasin B inhibit the action of vasopressin and cyclic adenosine monophosphate on osmotic water movement across the toad bladder. The findings suggest that microtubules, and possibly microfilaments, play a role in the action of vasopressin, perhaps through involvement in the mechanism of release of secretory material from the bladder epithelial cells.

    View details for Web of Science ID A1973Q162800019

    View details for PubMedID 4352609

  • EFFECTS OF PROPIONATE ON SODIUM-TRANSPORT BY TOAD BLADDER - EVIDENCE FOR A METABOLIC MODE OF ACTION BIOCHIMICA ET BIOPHYSICA ACTA Taylor, A., Hess, J. J., MAFFLY, R. H. 1973; 298 (2): 376-392

    View details for Web of Science ID A1973P191000022

    View details for PubMedID 4198138

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