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Biomedical subjects

M A Wallace

Publications and source records attributed to M A Wallace.

49 records · Page 3Linked to original sources
PubMed1983

Regulation of Ca2+-Mg2+-ATPase activity in hepatocyte plasma membranes by vasopressin and phenylephrine.

A high affinity Ca2+-stimulated, Mg2+-dependent ATPase (Ca2+-Mg2+-ATPase) was identified in microsomes and plasma membrane vesicles isolated from rat hepatocytes. The distribution of this enzyme was similar to that of the plasma membrane marker enzymes alkaline phosphodiesterase and 5'-nucleotidase. The Ca2+-Mg2+-ATPase had an apparent half-saturation constant of approximately 75 nM for Ca2+. After incubation of rat hepatocytes with 25 nM vasopressin for 3 min, the activity of Ca2+-Mg2+-ATPase was decreased 15-30%. The effect of vasopressin on the activity of this enzyme was near maximal after incubating hepatocytes with vasopressin for only 15 sec. The concentration of vasopressin needed for half-maximal inhibition of this enzyme in hepatocytes was approximately 6 nM. Treatment of the hepatocytes with 10 microM phenylephrine caused about a 10% decrease in ATPase activity while 10 nM glucagon or 200 microU/ml insulin did not affect the enzyme. These findings suggest that inhibition of the Ca2+-Mg2+-ATPase activity may be part of the mechanism by which vasopressin and alpha-adrenergic agonists elevate cytosolic Ca2+ in hepatocytes.

Animals↗
PubMed1983

The clinical specialist as manager: myth versus realities.

This article advocates combining administrative power and professional power in middle management roles. The usual difficulties of the clinical specialist role with staff and the administrative hierarchy are contrasted with examples of the specialist as head nurse or clinical supervisor. The authors recommend blending clinical specialist-nursing manager roles as a strategy during budgetary cuts to retain clinical expertise in the institutional setting.

Nurse Clinicians↗
PubMed1982

Alpha-adrenergic stimulation of phosphatidylinositol synthesis in human platelets as an alpha-2 effect secondary to platelet aggregation.

Epinephrine and adenosine diphosphate (ADP) stimulated 3H-glycerol uptake into phosphatidylinositol of human platelets. Yohimbine, an alpha-2 adrenoceptor antagonist, markedly reduced epinephrine-stimulated 3H-glycerol uptake into phosphatidylinositol; while prazosin, an alpha-1 antagonist, was without effect. Likewise, yohimbine, but not prazosin, blocked epinephrine-induced platelet aggregation. Furthermore, clonidine, a specific agonist for alpha-2 adrenoceptors, stimulated incorporation of 3H-glycerol into phosphatidylinositol and promoted platelet aggregation in the presence of low concentrations of ADP. These studies indicate that the effects of epinephrine on platelet aggregation and phosphatidylinositol synthesis are mediated through alpha-2 adrenoceptors. Further, since the stimulation of phosphatidylinositol synthesis seen with epinephrine was also observed with ADP, this suggests that the increased 3H-glycerol labeling is an indirect result of platelet aggregation.

Adrenergic alpha-Agonists↗
PubMed1982

Direct stimulation of phosphatidylinositol degradation by addition of vasopressin to purified rat liver plasma membranes.

Rat liver plasma membranes were incubated in Ca2+-free buffer plus 0.5 mM ethyleneglycol-bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) containing 0.5 mg/ml deoxycholate or 50 mU/ml vasopressin or both compounds. The membrane phospholipids were extracted, separated by two-dimensional chromatography and quantitated by phosphorus analysis. Vasopressin significantly enhanced degradation of phosphatidylinositol in the presence of deoxycholate (21% with deoxycholate alone versus 32% in the presence of vasopressin plus deoxycholate). However, no significant effects of deoxycholate or vasopressin were seen on the degradation of phosphatidylcholine, phosphatidylethanolamine or phosphatidylserine. These results indicate that specific degradation of phosphatidylinositol can be seen after direct addition of vasopressin to a plasma membrane preparation.

Animals↗
PubMed1979

Genetic exchanges in the macrocysts of Dictyostelium discoideum.

Crosses were made between strains of Dictyostelium discoideum involving two drug resistance markers and the mating-type locus. Over 6000 progeny from 263 individual germinated macrocysts from four single-factor crosses, five two-factor crosses and one three-factor cross were characterized. In most cases the progeny from a single macrocyst were of one genotype, although in the population of macrocysts from any two-factor cross all possible parental and recombinant genotypes were recovered. There was no evidence of linkage between any of the markers examined. No selection against progeny carrying the methanol or the cycloheximide resistance markers was found in two-factor crosses, but selection against progeny carrying both resistance markers was found in the three-factor cross. Germination of macrocysts in all crosses was poor, only once exceeding 2.5% of the total macrocyst population. A variety of crosses and back-crosses with different parental strains indicated that germination might be influenced by both extrinsic (environmental) and multiple genetic factors. About 10% of the macrocysts yielded progeny spores that were ambivalent in their mating reactions. After extensive recloning these populations could be resolved to the normal matA (formerly A1) and mata (formerly A2) mating-types and might therefore have represented aneuploids. The results obtained with D. discoideum macrocysts differ from those obtained with other cellular slime moulds--Dictyostelium mucoroides, Dictyostelium giganteum and Polysphondylium pallidum--and are reminiscent of the results reported for germinated zygospores of Phycomyces blakesleeanus.

Crosses, Genetic↗